|||||||||||||||||Exon|||||||Intron||Custom| ID|Nickname|Name(*)|Designation|Mode of inheritance(*)|Gene name(*)|Gene symbol(*)|Protein expression of altered gene|Gene synonyms|MGI Gene accession ID|Allele Name|Allele symbol|MGI Allele accession ID|Chromosome(*)|Ensemble Gene ID|Transcript ID|Transcript name|bp coding sequence position|bp cdna sequence position|bp change|Exon ID|Exon number|Amino acid position|Amino acid change|Genomic position|Intron number|Mutation type(*)|Strand type|Coding Sequence|Novelty|Transgene name|Transgene promoter|Transgene expression level|Congenic Gene name|Congenic Gene symbol|Congenic Protein expression of altered gene|Congenic Gene synonyms|Congenic MGI Gene accession ID|Congenic Allele Name|Congenic Allele symbol|Congenic MGI Allele accession ID|Congenic Gene Chromosome|Homozygous phenotype(*)|Heterozygous phenotype(*)|Current genetic background(*)|Female homozygous viable(*)|Female homozygous fertile(*)|Female heterozygotes/hemizygotes fertile|Male homozygous viable(*)|Male homozygous fertile(*)|Male heterozygotes/hemizygotes fertile|Evidence of compromised male fertility|Breeding performance|# generations backcrossed to background strain|# sib-mated generations|Mating scheme|Requires homozygous matings|Date created (dd/mm/yyyy)|Stock stored as|Frozen sperm straw count|Frozen embryo count|Does it Model a Human Condition?|Description of a Human Condition|Keywords|Is the strain available in any form to other researchers?| 1776.0|Bim / IL7r Knockout|C57BL/6-Bcl2l11 IL7r/Wehi||Recessive|BCL2-like 11 (apoptosis facilitator)|Bcl2l11|Reduced|1500006F24Rik, Bim, Bod|MGI:1197519|BCL2-like 11 (apoptosis facilitator); targeted mutation 1.1, Andreas Strasser|Bcl2l11|MGI:2156498|2||||||||||||||||No|||||||||||||Bim/IL-7Ralpha double deficient mice have significantly increased thymocyte numbers, restored near normal numbers of mature T cells in the blood and spleen, and enhanced cytotoxic T cell responses to virus infection in IL-7Ralpha-/- mice compared to IL7R KO alone. These results indicate that Bim cooperates with other proapoptotic proteins in the death of IL-7-deprived T cell progenitors in vivo, but is the major inducer of this pathway to apoptosis in mature T cells.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|03-Aug-2007||0.0|0.0|Unknown||interleukin, T cell, BH3 only, receptor, Lymphoid|Yes| 1776.0|Bim / IL7r Knockout|C57BL/6-Bcl2l11 IL7r/Wehi||Recessive|interleukin 7 receptor|Il7r|Nil|CD127, IL-7 receptor alpha chain, IL-7Ralpha|MGI:96562|interleukin 7 receptor; targeted mutation 1, Immunex|Il7r|MGI:1857198|Unknown||||||||||||||||No|||||||||||||Bim/IL-7Ralpha double deficient mice have significantly increased thymocyte numbers, restored near normal numbers of mature T cells in the blood and spleen, and enhanced cytotoxic T cell responses to virus infection in IL-7Ralpha-/- mice compared to IL7R KO alone. These results indicate that Bim cooperates with other proapoptotic proteins in the death of IL-7-deprived T cell progenitors in vivo, but is the major inducer of this pathway to apoptosis in mature T cells.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|03-Aug-2007||||Unknown||interleukin, T cell, BH3 only, receptor, Lymphoid|Yes| 4451.0||129/SvEv.OLA x C57BL/6||Dominant||||||||||||||||||||||||||||||||||||||||129/Sv x 129/OLA x C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|20-Feb-2009|Cryopreserved sperm|100.0|0.0|Unknown|||Yes| 4958.0|EGFP|C57BL/6-Gt(ROSA)26Sor Alpl|MGI:2177588|4|||||||||||||||||gene trap ROSA 26, Philippe Soriano; targeted mutation 1, Martyn Goulding|||||||||||||Expression of GFP in all cells.|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|18-Dec-2009||0.0|0.0|Unknown||GFP, B cell|Yes| 705.0||NOD.B6-Tg(ML5sHEL)5Ccg/Dvs||Recessive|||Unknown||||||Unknown||||||||||||||||No|transgene insertion 5, Christopher C Goodnow|mouse metallothionein I|High||||||||||Mice homozygous for the TgN(ML5sHEL)5Ccg transgene express a soluble form of hen egg lysozyme.||NOD/lt|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|02-May-2007||0.0|0.0|Unknown||hen egg lysozyme (HEL), autoimmunity, B cell|Yes| 5277.0|MIP-GFP|NOD.Cg-Tg(Ins1-EGFP)1Hara||Dominant||||||||||||||||||||||||||transgene insertion 1, Manami Hara|mouse insulin 1 gene|High|||||||||||The MIP-GFP mice develop normally and are indistinguishable from control animals with respect to glucose tolerance and pancreatic insulin content. Histological studies showed that the MIP-GFP mice had normal islet architecture with coexpression of insulin and GFP in the beta-cells of all islets. Observed GFP expression in islets from embryonic day E13.5 through adulthood.|NOD/Lt|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|28-Oct-2010||0.0|0.0|Unknown||islet, beta cell, insulin, GFP|Possibly| 846.0|Traf2 KO|C57BL/6-Traf2||Recessive|Tnf receptor-associated factor 2|Traf2|Nil||MGI:101835|targeted mutation 1.1, Robert Brink|Traf2|MGI:3511496|2||||||||||||||||No|||||||||||||Embryonic lethal||C57BL/6|No|No|Yes|No|No|Yes|No|Unknown||||No|23-May-2007||0.0|0.0|Unknown||TNF, receptor, B cell, embryonic lethal|Yes| 1553.0||BALB/c-IL9 Tg(iFABPp-IL9)/AnuApb||Recessive|interleukin 9|Il9|Nil|Il-9, P40|MGI:96563|interleukin 9; targeted mutation 1, Andrew NJ McKenzie|Il9|MGI:2656470|13||||||||||||||||Yes|Interleukin 9|rat intestinal fatty acid binding protein (nucleotides -1178 - +28) - iFABP , i-FABP linked to nucleotides 3–2,150 of the human growth hormone (hGH) gene (except for its 5' regulatory sequences). |High||||||||||Restricted expression of IL9 transgene to intestine - duodenum and proximal jejunum.||BALB/c|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|06-Jul-2007|Cryopreserved sperm|90.0|0.0|Unknown||T cell, inflamation, interleukin, anaphylaxis, mast cell, allergy|Yes| 10315.0|Rpl41 (7) 445bpΔ|C57BL/6NCrl-Rpl41/AnuApb||Semi-dominant|ribosomal protein L41|Rpl41|||MGI:1915195||||10|||||||||||||||||||||||||||||Unknown|Unknown|C57Bl/6N|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Good||||No|07-Mar-2023|Cryopreserved sperm|76.0|0.0|Unknown|||Possibly| 6779.0|SIGMA-J20|B6.Cg-Tg(PDGFB-APPSwInd)20Lms/JAusb||Dominant||||||||||||||||||||||||||transgene insertion 20, Lennart Mucke |human platelet derived growth factor, B polypeptide (PDGFB) promoter|highest level of expression occurring in the neocortex and hippocampus||||||||||Unknown|At five to seven months of age diffuse amyloid beta peptides deposition in the dendate gyrus and neocortex forms|C57BL6|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown|12||hemizygous males are bred to wildtype siblings or to C57BL/6J inbred females. Pups born of carrier females have shown an increased mortality rate in our colonies.|No|12-Jan-2012||0.0|0.0|Unknown||amyloid protein , neocortex, hippocampus, seizures, Alzheimer's|Yes| 6808.0|Dudley|SJL/Mrit-Gck/MritApb||Dominant|Glucokinase|Gck|Unknown|Gk, hexokinase 4, HK4, MODY2|MGI:1270854|Glucokinase;MRI32562|Gck||11|||||||||||||||||||||||||||||Growth retardationDramatic hyperglycemia|HyperglycemiaHyperinsulinemiaGlucose intolerant|SJL|Yes|No|Yes|Yes|No|Yes|No|Good||||No|01-Feb-2012|Cryopreserved sperm|60.0|0.0|Yes|Maturity onset diabetes of the young 2|Diabetes, Glucokinase, ENU|Yes| 7634.0||SJL/ASAM||Dominant|unknown|unknown|Reduced||||||Unknown|||||||||||||||||||||||||||||Unknown|The mice displays a slight growth retardation phenotype.|SJL/J|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Good||||No|07-Apr-2014|Cryopreserved sperm|80.0|0.0|Unknown|||Yes| 3536.0||B6.SJL-Tg(Nes-cre)1Kln||Dominant|||Unknown||||||Unknown||||||||||||||||No|transgene insertion 1, Rudiger Klein |rat nestin (Nes)|||||||||||Normal.|||Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|29-Jul-2008||0.0|0.0|Unknown||Cre recombinase, Nestin|Yes| 6655.0|HICAM|B6.129S4-Icam1/J/Ausb||Recessive|intercellular adhesion molecule 1 |Icam1|Nil|CD54, Icam-1, Ly-47, MALA-2, MGC:6195|MGI:96392|intercellular adhesion molecule 1; targeted mutation 1, Jose Carlos Gutierrez Ramos|Icam1|MGI:1857292|9|||||||||||||||||||||||||||||Abnormal cardiac muscle contractility:*Lipopolysaccharide (LPS) treatment does not result in a decrease in left ventricular contractility as is seen in wild-type, indicating a lack of LPS-induced myocardial dysfunction.||BALB/c|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|02-Dec-2011||0.0|0.0|Unknown||Intercellular adhesion molecule 1 (ICAM-1), lymphocyte function associated 1 (LFA-1), Mac-1|Yes| 5939.0|Nf1bCond/NestinCre/Rosa26||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5938.0|Nf1BCond/NesCreERT2||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 3924.0|CC|BALB/c-Tg(Col1a2-cre/ESR1)7Cpd/AnuApb||Dominant||||||||||||||||||||||||||transgene insertion 7, Christopher P Denton|Col1a2 enhancer|fibroblast-specific expression, restricted to collagen||||||||||Normal|Normal|BALB/c|Yes|Yes|Yes|Yes|Yes|Yes|No|Excellent|5||Backcross to balb/c|No|14-Oct-2008|Cryopreserved sperm|87.0|0.0|No||epidermis, inducible, fribroblast, collagen|Yes| 4774.0|5AT129|ENU5AT:129||Recessive||||||||||||||||||||||||||transgene insertion 3, Christopher C Goodnow|Rat insulin promoter|||||||||||Heightened susceptibility to autoimmune diabetes on the transgenically sensitized TCR x insHEL background (see figure). Phenotype Screen: Urine glucose|Normal|C57BL/6 x B10BR x CBA|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|06-Sep-2009|Cryopreserved sperm|60.0|0.0|Yes|Type I Diabetes|ENU, JDRF, T cell, autoimmunity|Possibly| 4774.0|5AT129|ENU5AT:129||Recessive||||||||||||||||||||||||||transgene insertion 1, Mark M Davis||||||||||||Heightened susceptibility to autoimmune diabetes on the transgenically sensitized TCR x insHEL background (see figure). Phenotype Screen: Urine glucose|Normal|C57BL/6 x B10BR x CBA|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|06-Sep-2009|Cryopreserved sperm|||Yes|Type I Diabetes|ENU, JDRF, T cell, autoimmunity|Possibly| 10320.0||C57Bl/6-TFF3(CreGFP)GRP78/Apb||Semi-dominant|trefoil factor 3, intestinal|Tff3|||MGI:104638||||17|ENSMUSG00000024029 ||||||||||||||||||||||||||||Normal|Normal|C57Bl/6J|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|29-Mar-2023|Cryopreserved sperm|54.0|0.0|Unknown|||Possibly| 10320.0||C57Bl/6-TFF3(CreGFP)GRP78/Apb||Semi-dominant|heat shock protein 5|Hspa5|| Grp78, Hsce70, mBiP, |MGI:95835||||2|ENSMUSG00000026864 ||||||||||||||||||||||||||||Normal|Normal|C57Bl/6J|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|29-Mar-2023|Cryopreserved sperm|||Unknown|||Possibly| 10319.0||C57BL/6J-Gt(Rosa26)Sor(LPfCSPrev-mCherry)Anu/N||Semi-dominant|Rosa26|||||PfCSP|||Unknown|||||||||||||||||||||||||||||N/A mice maintained as Hets|Expression of membrane P. falciparum circumsporzoite protein|C57Bl/6J|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|25-Mar-2023||0.0|0.0|Unknown|||Possibly| 6826.0|APP KO|B6.129-App/Apb||Recessive|amyloid beta (A4) precursor protein|App|Nil|Abeta, Adap, appican, betaAPP, Cvap, E030013M08Rik, protease nexin II|MGI:88059|amyloid beta (A4) precursor protein; targeted mutation 1, David R Borchelt|App|MGI:2136847|16|||||||||||||||||||||||||||||Abnormal active avoidance behavior: age-related impairment in conditioned avoidance tests, seen at 10 months of age, but not at 4 months of age.Abnormal spatial learning: impairment in watermaze test of spatial learning, both at 4 and 10 months of age.Decreased grip strength: significantly reduced grip strength.Abnormal locomotor activation: decreased locomotor activityHypoactivity.Gliosis: reactive gliosis was observed throughout the cortical layers of the neocortex and extensive astrogliosis was seen in the CA1 region of the hippocampus, however did not observe neuronal cell damage.Astrocytosis: reactive astrocytosis in many brain areas, but predominantly in the cortex and hippocampus at 14 weeks of age.Abnormal neuron morphology: the branching of dendrites of both cortical and hippocampal neurons was much less extensive, however did not show any loss of cells in the cortex or the hippocampus.Abnormal long term potentiation: impairment of ability of high frequency stimuli to induce LTP which correlated with extent of gliosis in stratum radiatum.Decreased body weight: body weight was 15-20% less at all ages compared with that of controls.||C57BL/6|Yes|Unknown|Yes|Yes|Unknown|Yes|No|Unknown||||No|27-Feb-2012|Cryopreserved sperm|50.0|0.0|Yes|Alzheimer's disease (AD)|amyloid, tau, locomotion, neuron|Yes| 4579.0||SJL.129S7-Ifngr1/AnuApb||Recessive|interferon gamma receptor 1|Ifngr1|Unknown|CD119, Ifgr, IFN-gamma R, IFN-gammaR, Ifngr, Nktar|MGI:107655|targeted mutation 1, Michel Aguet|Ifngr1|MGI:1857286|10||||||||||||||||Yes|||||||||||||Abnormal immune system||SJL/J|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|10|||No|08-Mar-2009|Cryopreserved sperm|60.0|0.0|Unknown||cytokine, interleukin, infection, immunoglobulin, macrophage|Yes| 5279.0|MacBlue|NOD.B6-Tg(Csf1r-Gal4VP16/UAS-ECFP)||Dominant||||||||||||||||||||||||||Gal4VP16 transcriptional activator , enhanced cyan fluorescent protein (ECFP)|Csf1r and Gal4|||||||||||Expression of ECFP in macrophages.ECFP expression in transgenic embryos was first detectable at 8 dpc in the blood islands of the proximal yolk sac.ECFP<+> macrophages were concentrated in areas of increased apoptotic cell death, such as necrotic zones of the developing limb, consistent with their proposed scavenger function.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|28-Oct-2010||0.0|0.0|Unknown||Gal4, Csf1r, macrophage, phagocyte, mononuclear phagocyte system (MPS), enhanced cyan fluorescent protein (ECFP)|Possibly| 7635.0||SJL/ASAM||Dominant|unknown|unknown|Reduced||||||Unknown|||||||||||||||||||||||||||||Unknown|The mice displays a slight growth retardation phenotype.|SJL/J|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Good||||No|07-Apr-2014|Cryopreserved sperm|55.0|0.0|Unknown|||Yes| 4779.0|wildtype control|129/Sv-Ifngr(WT)||Recessive|||Unknown||||||Unknown||||||||||||||||Yes|||||||||||||Control strain for conducting experiments with 129/Sv-Ifngr1 strain||129|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|06-Sep-2009|Cryopreserved sperm|100.0|0.0|No||infection, interleukin, splenocyte|Yes| 777.0|ID3∆ ID1∆|B6.129-Idd3<-> Idd1<->||Dominant|insulin dependent diabetes susceptibility 3|Idd3|Unknown|Idd-3|MGI:96405||||3||||||||||||||||Yes|||||||||||||||129 x C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|18-May-2007||0.0|0.0|Unknown||insulin, diabetes, autoimmunity|Yes| 777.0|ID3∆ ID1∆|B6.129-Idd3<-> Idd1<->||Dominant|insulin dependent diabetes susceptibility 1|Idd1|Unknown|Idd-1|MGI:96400||||17|||||||||||||||||||||||||||||||129 x C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|18-May-2007||||Unknown||insulin, diabetes, autoimmunity|Yes| 5187.0||ENU18WT:020b||Recessive|Unknown||Unknown||||||Unknown|||||||||||||||||||||||||||||Unknown||C57BL/6JAnu|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|02-Aug-2010|Cryopreserved sperm|40.0|0.0|Unknown||ENU, Wellcome Trust|Possibly| 5188.0||ENU18WT:035b||Recessive|Unknown||Unknown||||||Unknown|||||||||||||||||||||||||||||Unknown||C57BL/6JAnu|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|02-Aug-2010|Cryopreserved sperm|20.0|0.0|Unknown||ENU, Wellcome Trust|Possibly| 4919.0|CD9 -/-|FVB/N.B6(129)-CD9/AusbApb||Recessive|CD9 antigen|Cd9|Nil|Tspan29|MGI:88348|targeted mutation 1, Claude Boucheix|Cd9|MGI:2180795|6|||||||||||||||||||||||||||||Reduced female fertility: 40 - 50% of females fail to produce litters.Decreased litter size.Impaired fertilization: impaired sperm - egg fusion.||FVB/N|Yes|Yes|Yes|Yes|Yes|Yes|No|Poor|10|||No|20-Oct-2009|Cryopreserved sperm|135.0|0.0|Unknown||fertility, tetraspan, CD151|Yes| 780.0|Munc18c KO|C57BL/6-Stxbp3a||Recessive|syntaxin binding protein 3A|Stxbp3a|Nil|MGC:86097, Munc-18c, Stxbp3, Sxtbp3|MGI:107362|targeted mutation 1, Yoshikazu Tamori|Stxbp3a|MGI:3528591|3||||||||||||||||No|||||||||||||Homozygous null mice display embryonic or perinatal lethality with reduced embryonic growth and malformation of the intermediate zone of the cerebral cortex.Decreased embryo size: at E13.5, homozygous mice are 17% shorter.Decreased birth body size: at birth pups are 30% shorterAbnormal cerebral cortex morphology:* contained poorly formed neural fibers and greater number of cellular components in the intermediate zone of the cerebral cortex.||C57BL/6|No|No|Yes|No|No|Yes|Yes|Poor||||No|19-May-2007||0.0|0.0|Unknown||embryonic lethal, size, growth, neuronal|Yes| 4994.0|4AT6|ENU4AT:006||Recessive|||||||||Unknown|||||||||||||||||transgene insertion 3, Christopher C Goodnow|Rat insulin promoter|||||||||||Heightened susceptibility to autoimmune diabetes on the transgenically sensitized TCR x insHEL background.Phenotype Screen: Urine glucose|Normal|C57BL/6 x B10BR x CBA|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|28-Jan-2010|Cryopreserved sperm|75.0|0.0|Yes|Type I Diabetes|ENU, JDRF, T cell, autoimmunity|No| 4994.0|4AT6|ENU4AT:006||Recessive||||||||||||||||||||||||||transgene insertion 1, Mark M Davis||||||||||||Heightened susceptibility to autoimmune diabetes on the transgenically sensitized TCR x insHEL background.Phenotype Screen: Urine glucose|Normal|C57BL/6 x B10BR x CBA|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|28-Jan-2010|Cryopreserved sperm|||Yes|Type I Diabetes|ENU, JDRF, T cell, autoimmunity|No| 7340.0|MommeD42|FVB/NJ-Brd1 Tg(Hba1-Gfp)1Ew/QimrApb||Dominant|bromodomain containing 1|Brd1|Unknown||MGI:1924161|bromodomain containing 1; modifiers of murine metastable epiallele D42|Brd1|MGI:5515395|15|ENSMUSG00000022387|ENSMUST00000109381|Brd1-001|||T to A||||Unknown to Unknown||||||Yes|transgene insertion 1, Emma Whitelaw|human alpha-globin promoter and enhancer region|||||||||||Homozygous lethality (~10.5 dpc)|Percentage of cells expressing the GFP transgene is decreased (enhancer of variegation).|FVB/NJ|No|No|Yes|No|No|Yes|No|Good||||No|27-May-2013|Cryopreserved sperm|50.0|0.0|Unknown||epigenetics, modifier, ENU|Yes| 2467.0||B6.CBA-Tg(hGMCSF-KBM)457/AnuApb||Dominant|||||||||Unknown||||||||||||||||No|human GMCSF (GM-CSF)|human GM-CSF promoter and enhancer (10.5kb)|||||||||||Express human GM-CSF. hGM-CSF detected in serum by ELISA. Murine GM-CSF used as internal control.|||Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|16-Jan-2008|Cryopreserved sperm|40.0|0.0|No||T cell, lymphocyte, transcription, chromatin remodelling, NF-kappaB|Yes| 6564.0|iNOSΔ|B6.129P2-Nos2/JAusb||Recessive|nitric oxide synthase 2, inducible|Nos2|Nil|iNOS, Nos-2, NOS-II, Nos2a|MGI:97361|nitric oxide synthase 2, inducible; targeted mutation 1, Victor E Laubach|Nos2|MGI:1857228|11|||||||||||||||||||||||||||||Abnormal surfactant physiology:*Following infection with mycoplasma, the numbers of large surfactant aggregates is decreased and higher protein to lipid ratios are present in the bronchoalveolare lavage fluid compared to similarly infected wild-type mice.*Following infection with mycoplasma, the minimal surface area on the pulsating bubble is increased and the levels of surfactant protein are decreased compared to similarly infected wild-type mice.Abnormal circadian rhythm:*Mice display a more pronounced diurnal variation of sleep-wake activity.Abnormal sleep pattern:*Mice spend more time in REM sleep during the light phase as a result of an increased number of REM episodes and shortened duration of the inter REM intervals.*Mice display a more pronounced diurnal variation of sleep-wake activity.*Mice spend less time in non-REM sleep during the dark phase.*During the light phase mice spend the same amount of time in non-REM sleep but have a higher number of non-REM episodes of shorter average duration.Abnormal brain wave pattern:*During non-REM sleep the absolute value of slow wave activity is increased.Abnormal inflammatory response:*Unlike in wild-type mice, LPS injection fails to reduce nighttime body temperature relative to saline injected controls. Decreased inflammatory response: *Fever in response to LPS injection is partially reduced compared to wild-type controls. *The fever response to LPS is initiated but not sustained. *However, fever in response to turpentine injection is not different from controls.||unknown|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|13-Sep-2011|Embryo|0.0|0.0|Unknown||iNOS, Inflammatory disorders|Yes| 7644.0||B6/Mrit-135904|B6/Mrit-135904|Dominant|unknown||Unknown||||||Unknown|||||||||||||||||||||||||||||Unknown|Heterozygous mice display a transient growth decrease|C57BL/6|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Good||||No|07-Apr-2014|Cryopreserved sperm|33.0|0.0|Unknown||growth , ENU|Yes| 7643.0||SJL/ASAM||Dominant|unknown|unknown|Reduced||||||Unknown|||||||||||||||||||||||||||||Unknown|The mice displays a slight growth retardation phenotype for a week.|SJL/J|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Good||||No|07-Apr-2014||0.0|0.0|Unknown|||Yes| 709.0|NR4ML5|NOD.NOR-(D4Mit31-D4Mit310) Tg(ML5sHEL)5Ccg||Recessive|insulin dependent diabetes susceptibility 9|Idd9|Nil|Idd-9|MGI:96411|NOR/LtJ|Idd9|MGI:3582457|4||||||||||||||||No|transgene insertion 5, Christopher C Goodnow|mouse metallothionein I|High||||||||||||NOD|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|03-May-2007||0.0|0.0|Unknown||Autoimmunity, B cell, immunoglobulin, hen egg lysozyme (HEL), MHC|Yes| 711.0|NIHL|NOD-Tg(ILK3mHEL)3Ccg||Recessive||||||||||||||||||||||||||transgene insertion 3, Christopher C Goodnow|Rat insulin promoter|||||||||||Pancreatic islet cells express membrane bound hen egg lysozyme.||NOD|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|03-May-2007||0.0|0.0|Unknown||hen egg lysozyme (HEL), tolerance, B cell, autoimmunity|Yes| 850.0|Traf3 floxed|C57BL/6-Traf3||Dominant|Tnf receptor-associated factor 3|Traf3|Normal|CAP-1, CD40bp, CRAF1, LAP1|MGI:108041|targeted mutation 1, Robert Brink|Traf3|MGI:3777324|12||||||||||||||||Yes|||||||||||||Normal||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|23-May-2007||0.0|0.0|Unknown||TNF, receptor, lymphocyte, runting, hypoglycaemia|Yes| 5110.0|KRN 007 Balb/b F2|KRN:007 BALB/b F2||Recessive|Unknown|Unknown|||||||Unknown||||||||||||||||Unknown|transgene insertion KRN, Diane Mathis|Natural TCR alpha and -beta promoter/enhancer elements.|||||||||||Maybe resistant to arthritis induced through serum transfer|Partially resistant to arthritis induced through serum transfer|BALB/b|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Good||||No|07-May-2010|Cryopreserved sperm|29.0|0.0|Yes|Rhematoid arthritis|autoimmune disease, arthritis, ENU|No| 5200.0|ZIKO ; Zfp397 KO LacZ|STOCK Zfp397/Apb||Recessive|zinc finger protein 397|Zfp397|Nil||MGI:1916506|zinc finger protein 397; gene trap W131C06, German Gene Trap Consortium|Zfp397|MGI:4123642|18||||||||||||||||No|||||||||||||Normal|Normal|mixed|Yes|Yes|Yes|Yes|Yes|Yes|No|Excellent||||No|05-Aug-2010|Cryopreserved sperm|50.0|0.0|No||centromere, kinetochore, zinc finger, SCAN domain|No| 10324.0|Lcp1 I232F - founder 3|C57BL/6NCrl-Lcp1Anu/Apb||Recessive|lymphocyte cytosolic protein 1|Lcp1|||MGI:104808||||14|||||||||||||||||||||||||||||||C57Bl/6N|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|14-Apr-2023|Cryopreserved sperm|11.0|0.0|Unknown|||Possibly| 1760.0|Bcl-2-Bcl-w - double knockout|C57BL/6-Bcl2 Bcl2l2/Wehi||Recessive|B-cell leukemia/lymphoma 2|Bcl2|Nil|Bcl-2|MGI:88138|targeted mutation 1, Dennis Y Loh|Bcl2|MGI:2156165|1||||||||||||||||Yes|||||||||||||||C57BL/6|No|No|Yes|No|No|Yes|No|Unknown||||No|02-Aug-2007||0.0|0.0|Unknown||Pro-survival, Mitochondria, BH3|Yes| 1760.0|Bcl-2-Bcl-w - double knockout|C57BL/6-Bcl2 Bcl2l2/Wehi||Recessive|Bcl2-like 2|Bcl2l2|Nil|Bcl-w, bclw, Gtrgal2, Gtrosa41|MGI:108052|targeted mutation 1, Suzanne Cory|Bcl2l2|MGI:2158430|14|||||||||||||||||||||||||||||||C57BL/6|No|No|Yes|No|No|Yes|No|Unknown||||No|02-Aug-2007||||Unknown||Pro-survival, Mitochondria, BH3|Yes| 7595.0||SJL/ASAM||Dominant|unknown|unknown|Reduced||||||Unknown|||||||||||||||||||||||||||||Unknown|The mice displays a growth retardation phenotype without other gross abrnomalities. The mice are viable and fertile.|SJL/J|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Good|8|||No|18-Feb-2014|Cryopreserved sperm|50.0|0.0|Unknown||growth retardation, ENU|Yes| 1855.0||AID-cre-IRES-hCD2t||Recessive||||||||||||||||||||||||||Cre recombinase|IRES - hCD2 ?||||||||||||||Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|10-Aug-2007||0.0|0.0|No|||Yes| 5281.0|NODGrzA/8.3|NOD.B6-Gzma Tg(TcraTcrbNy8.3)1Pesa||Recessive|granzyme A |Gzma|Nil|BLT esterase, Ctla-3, Ctla3, H factor, Hanukah factor, Hf, SE1, serine esterase 1, TSP-1, TSP1|MGI:109266|granzyme A; targeted mutation 1, Markus M Simon|Gzma|MGI:2449926|13||||||||||||||||No|transgene insertion 1, Pere Santamaria|TCR alpha and beta enhancers|||||||||||Mice may develop diabetes faster than wildtype.||NOD/Lt|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|28-Oct-2010||0.0|0.0|Yes|insulin-dependent diabetes mellitus (IDDM)|apoptosis, pancreas, islet, T cell|Possibly| 5282.0|NODGrzB/8.3|NOD.B6-Gzmb Tg(TcraTcrbNy8.3)1Pesa||Recessive|granzyme B |Gzmb|Nil|CCP-1/C11, CCP1, Ctla-1, Ctla1, GZB|MGI:109267|granzyme B; targeted mutation 1, Timothy J Ley|Gzmb|MGI:1857156|14||||||||||||||||No|transgene insertion 1, Pere Santamaria|TCR alpha and beta enhancers|||||||||||Mice may develop diabetes faster than wildtype.||NOD/Lt|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|28-Oct-2010||0.0|0.0|Yes|insulin-dependent diabetes mellitus (IDDM)|apoptosis, pancreas, islet, T cell|Possibly| 7476.0|Rhea|FVB/N-MommeD34 Tg(Hba1-Gfp)1Ew||Semi-dominant|rearranged L-myc fusion sequence|Rlf|Reduced||MGI:1924705|rearranged L-myc fusion sequence; modifier of murine metastable epialleles, D34|Rlf|MGI:5515367|4||||||||||Unknown to Unknown||||||Yes|transgene insertion 1, Emma Whitelaw|human alpha-globin promoter and enhancer region|||||||||||Mutant mice show a reduction in survival past weaning. Survivors at weaning are smaller than controls.Postnatal lethality: * few animals survive to weaning * normal litter size at birthDecreased body size: at weaning||FVB/NJ|No|No|Yes|No|No|Yes|No|Good|||MommeD34<+/->;Tg(Hba1-Gfp)3Ew x Tg(Hba1-Gfp)3Ew|No|13-Nov-2013|Cryopreserved sperm|30.0|0.0|Unknown||epigenetics, suppressor of variegation, ENU|Yes| 4860.0||C57BL/6-Tg(H2-K-huCD55,huCD59)/Apb||Dominant||||||||||||||||||||||||||human CD55/CD59 dual construct|H2-K|ubiquitous||||||||||Expression of membrane bound human CD55 and CD59 in all tissues on all cells.|Expression of membrane bound human CD55 and CD59 in all tissues on all cells.|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|24-Sep-2009|Cryopreserved sperm|92.0|0.0|Unknown||complement, skeletal, muscle, ischemia, reperfusion|Yes| 6268.0|del511|C57BL/6-Fasl||Recessive|Fas ligand (TNF superfamily, member 6)|Fasl|Nil|APT1LG1, CD178, CD95L, Fas-L, Tnfsf6|MGI:99255|Fas ligand (TNF superfamily, member 6); targeted mutation 1.1, Andreas Strasser|Fasl|MGI:4366050|1|||||||||||||||||||||||||||||Premature death:*Compared with wild-type mice and Fasl homozygotes.Immune system phenotype:*Mice mount a normal immune response to influenza. Enlarged spleen Increased circulating tumor necrosis factor level: *At 12 to 20 weeks. Enlarged lymph nodes Increased immunoglobulin level Increased IgA level Increased IgE level Increased IgG level Increased IgG1 level Increased IgG2a level Increased IgG2b level Increased IgM level Defective cytotoxic T cell cytolysis: *T cells are less efficient than wild-type cells at killing CH1 cells. Increased susceptibility to systemic lupus erythematosus: *62% of terminally ill mice exhibit systemic lupus erythematosus-like (SLE) autoimmune disease with cellular crescents, protein casts, and compliment in renal glomeruli unlike wild-type mice. *Mice develop more severe SLE-like disease than Fasl homozygotes. *By 57 weeks, 50% of mice develop fatal SLE-like autoimmune kidney disease compared with 15% of Fasl homozygotes. Increased anti-nuclear antigen antibody level: *Higher than in wild-type mice and Fasl homozygotes. Increased anti-double stranded DNA antibody level: *Higher than in wild-type mice and Faslgld homozygotes. Glomerulonephritis: *Mice develop SLE-like glomerulonephritis unlike wild-type mice and more frequently than Fasl homozygotes. Dermatitis: *30% of mice develop severe dermatitis with lesions on the ears and necks unlike wild-type mice.Increased histiocytic sarcoma incidence:*By 78 weeks, 27% of mice develop hepatic tumors with characteristics of histiocytic sarcoma with deposits in the spleen and lungs.Increased liver tumor incidence:*By 78 weeks, 27% of mice develop hepatic tumors with characteristics of histiocytic sarcoma with deposits in the spleen and lungs.||C57BL/6|Yes|Unknown|Yes|Yes|Unknown|Yes|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown||FasL, TNF cytokine family|Yes| 7255.0|MLC:1IGF-1B_2B (Class 1Eb) ; SP1-IGF-1Eb|B6.FVB-Tg(Myl1-SP1/IGF1Ea)1Nros/MarpApb|FVB-Tg(Myl1-SP1/IGF1Ea)1Nros|Semi-dominant||||||||||||||||||||||||||mouse insulin-like growth factor-1|myosin light chain|skeletal muscle||||||||||Unknown|Normal|C57BL/6|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Good||||No|15-Jan-2013|Cryopreserved sperm|50.0|0.0|Unknown|||Possibly| 6661.0|McBride|C;B6-Myd88/ANU/Ausb||Recessive|myeloid differentiation primary response gene 88 |Myd88|Nil||MGI:108005|myeloid differentiation primary response gene 88; targeted mutation 1, Shizuo Akira |Myd88|MGI:2385681|9|||||||||||||||||||||||||||||Decreased B cell proliferation:*Splenocytes showed a defect in proliferation in response to the TLR4 ligand lipopolysaccharide (LPS), bacterial lipopeptide (BLP) that signals through the TLR1-TLR2 heterodimer, the TLR9 ligand unmethylated CpG DNA (CpG) and to the TLR7 ligand resiquimod (R-848).Abnormal dendritic cell physiology:*Dendritic cells produced barely detectable amounts of cytokines in response to LPS or CpG.*Dendritic cells mature only in response to LPS but not CpG.Abnormal macrophage physiology:*Activation of NF-kappaB, JNK, p38 and ERK in bone marrow derived macrophages was delayed in response to LPS and absent in response to BLP and CpG.Abnormal NK cell physiology:*NK and NK-T cell activation is significantly lower compared to C57BL/6 wild-type controls during mouse cytomegalovirus infection.Abnormal T cell physiology:*Thymocytes failed to proliferate in response to IL-1. Abnormal NK T cell physiology: *NK and NK-T cell activation is significantly lower compared to C57BL/6 wild-type controls during mouse cytomegalovirus infection.Abnormal cytokine secretion:*Type 1 IFN, IFNgamma and IL-12 p40 levels are decreased compared to C57BL/6 wild-type controls following sublethal viral infection.*IFNalpha was not secreted after infection with vesicular stomatitis virus (a ssRNA virus).Increased susceptibility to viral infection:*Viral loads and mortality are significantly higher after mouse cytomegalovirus infection compared to C57BL/6 wild-type controls.Decreased B cell proliferation:*Splenocytes showed a defect in proliferation in response to the TLR4 ligand lipopolysaccharide (LPS), bacterial lipopeptide (BLP) that signals through the TLR1-TLR2 heterodimer, the TLR9 ligand unmethylated CpG DNA (CpG) and to the TLR7 ligand resiquimod (R-848).||BALB/c|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|02-Dec-2011||0.0|0.0|Unknown||Myd88, IL-1, IL-18|Yes| 5945.0|NfixCond/NestinCre||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 4924.0|IL21 KO|NOD.B6-IL21||Recessive|interleukin 21|Il21|Nil||MGI:1890474|targeted mutation 1, Lexicon Genetics|Il21|MGI:3528994|3||||||||||||||||No|||||||||||||Decreased germinal center B cell number:* the percentage of GC B cells that make up the total B cell population in the spleen of immunized mice is reduced by two-thirdsAbnormal CD4-positive T cell morphology:* the percentage of follicular T helper cells (defined as CXCR5+ICOS+CD4+ T cells) is reduced by a third.Abnormal spleen germinal center morphology:* the number of actively proliferating T cells found within GC is reduced 3- to 4- fold.* the percentage of follicular T helper cells (defined as CXCR5+ICOS+CD4+ T cells) is reduced by a third.Decreased spleen germinal center number:* there is a paucity of GC in the spleen of mice after immunization with sheep red blood cells (SRBC).Decreased CD4-positive T cell number:* Il-17+ CD4+ cells are absent from lamina propria and spleen in mutants.Abnormal T cell differentiation:* when naive TH cells are subjected to TH17 differentiation, a deficit in generation of Il-17-producing cells is observed with an increased number of Foxp3+ cells compared to wild-type.* one week after immunization with MOG peptide in CFA, restimulation of spleen cells with TPA or MOG peptide results in production of almost no Il-17 producing cells, showing impaired TH17 differentiation.Abnormal gamma-delta T cell morphology:*lamina propria and splenic TCRgd+ T cells show <10-fold decrease in Il-17-expressing cells compared to wild-type cells.Abnormal interleukin level:* CNS-infiltrating and splenic CD4+ T cells produce interferon gamma, in contrast to CD4+ T cells from controls which produce predominantly Il-17.||C57BL/6 x NOD|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|29-Oct-2009||0.0|0.0|Unknown||interleukin, Immunoglobulin, B cell, T cell, CD4, germinal centre, IL17|Yes| 10326.0|Tex9 flox/flox|C57BL/6J-Tex9<(em1)MGMP>/Apb||Dominant|testis expressed gene 9|Tex9||tsec-1|MGI:1201610||Tex9 flox||9|||||||||||||||||||||||||||||Normal|Normal|C57Bl/6J|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|19-Apr-2023|Cryopreserved sperm|50.0|0.0|Unknown|||No| 68.0||Socks||Recessive|||Unknown||||||4||||||||||||||||Yes|||||||||||||Dilute coat, white belly spot and "socks", small eyes. Unique phenotype for chromosome location, 34 potential genes in this region.|||Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|06-Feb-2006|Cryopreserved sperm|30.0|0.0|Unknown||melanocyte, migration, coat, ENU|Yes| 644.0|ATM-pKZ1|C57BL/6-Tg(pKZ1) Atm||Recessive|ataxia telangiectasia mutated homolog (human)|Atm|Unknown|C030026E19Rik|MGI:107202|ataxia telangiectasia mutated homolog (human); targeted mutation 1, Philip Leder|Atm|MGI:1926875|9||||||||||||||||Yes|β-galactosidase gene (lacZ) E. coli|chicken β-actin||||||||||||Irradiated Atm heterozygous knock-out mice did demonstrate fewer inversions after exposure to 15 mGy X-radiation than the Atm normal pKZ1 mice.|C57BL/6|Yes|No|Yes|Yes|No|Yes|No|Unknown||||No|25-Apr-2007||0.0|0.0|No||ATM, pKZ1, inversion, radiation, recombination|No| 6900.0|TGFbeta2|STOCK Tgfb2/MarpApb||Recessive|transforming growth factor, beta 2|Tgfb2|Nil|Tgfb-2, Tgf-beta2|MGI:98726|transforming growth factor, beta 2; targeted mutation 1, Thomas Doetschman|Tgfb2|MGI:1888389|1||||||||||||||||||||||||||||||TGFb2-null mice exhibit perinatal mortality and a wide range of developmental defects for a single gene disruption. These include cardiac, lung, craniofacial, limb, spinal column, eye, inner ear and urogenital defects (Sanford et al., 1997.Development 124, 2659-2670).TGFb2 heterozygotes exhibit a 30% increase in nephron number (Sims-Lucas et al., Pediatr Res. 2008 Jun;63(6):607-12). |Black Swiss/129/Ola mixed |No|Unknown|Yes|No|Unknown|Yes|No|Good|||Heterozygotes are crossed to Wildtypes|No|24-May-2012|Cryopreserved sperm|50.0|0.0|Yes|Peters Anomaly|signal transduction, kidney, heart|Yes| 4999.0|ENU9CAT:G1|ENU9CAT::HelxTCR:CBAxB6||Recessive|||||||||Unknown|||||||||||||||||||||||||||||No phenotype.Breeding from this G1 male lead to the 9CAT:051 pedigree.||C57BL/6|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|01-Feb-2010|Cryopreserved sperm|10.0|0.0|Unknown||Sperm, infertility|Yes| 3535.0||C57BL/6J-K/JWehi||Recessive|histocompatibility-2, MHC|H2|Nil|H-2, MHC-II|MGI:95894||||17||||||||||||||||Yes|||||||||||||These mice lack one MHC class I molecule, H-2K. Since they still load and express H2D, these mice are able to mount normal CD8 T cell responses to most pathogenes. They do not show an immuno-compromised phenotype. ||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|29-Jul-2008||0.0|0.0|Unknown||MHC, T cell, cytotoxic, presentation, vaccine|Yes| 6663.0|MORTLOCK|BALB/c.B6-Il13/ANU/Ausb||Recessive|interleukin 13 |Il13|Nil|Il-13 |MGI:96541 |interleukin 13; targeted mutation 2, Andrew NJ McKenzie |Il13|MGI:1931804|11|||||||||||||||||||||||||||||||BALB/c|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|02-Dec-2011||0.0|0.0|Unknown||Th2, IL-13|Yes| 6685.0|Young|B6.BALB/c-Il5/Ausb||Recessive|interleukin 5 |Il5|Nil|Il-5 |MGI:96557|interleukin 5; targeted mutation 1, Manfred A Kopf|Il5|MGI:1861948|11|||||||||||||||||||||||||||||Enlarged placenta:*Knockout females have a significant increase in placenta size in matings with CBA males and the fetal:placental ratio is reduced.Prolonged estrous cycle:*Duration of oestrus in knockouts is moderately extended (5.6 days versus 5 days in controls).Abnormal mating receptivity:*Background Sensitivity: duration of mating interval to achieve mating with syngeneic (B6) versus allogeneic (CBA or BALB/c) males is increased.*After correction for male background, knockout females have significantly lower mating intervals than control females.Increased body weight:*Background Sensitivity: allogeneic matings produce larger pups than syngeneic pups; in CBA F1 pups, at weaning, female and male weights are increased 9.5 and 10%, while in C57BL/6 F1 pups, female and male weights at 6 weeks are increased by 7.9 and 12.2%.*Il5 deficient pups have an increased weight gain trajectory compared to wild-type.*Knockout pups are significantly larger than wild-type pups from birth to adulthood.||BALB/c|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|02-Dec-2011||0.0|0.0|Unknown||IL5, ES cells, Eosinophilia|Yes| 4843.0||ENU6AT:008||Recessive|Unknown||Unknown||||||Unknown|||||||||||||||||||||||||||||Mothers fail to lactate.Pups can be maintained by adding lactating foster mother.|Normal|C57BL/6 x CBA|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|24-Sep-2009|Cryopreserved sperm|20.0|0.0|Unknown||lactation, milk, ENU|Yes| 7048.0|FST KO|STOCK Fst/MarpApb||Recessive|follistatin|Fst|Nil||MGI:95586|follistatin; targeted mutation 1, Martin M Matzuk|Fst|MGI:1857467|13|||||||||||||||||||||||||||||Lifespan and health is affected. FS knock-out mice are liveborn, but die within 6 hours of birth due to respiratory failure because of lung and chest muscle defects. These pups display growth retardation, defects of the hard palate and 13th rib, as well as whisker and tooth abnormalities and shiny taut skin.|Normal|C57BL/6 x 129 x FVB|No|No|Yes|No|No|Yes|No|Good|||Het x Het|No|13-Aug-2012|Cryopreserved sperm|50.0|0.0|No||activin, heparan sulphate proteoglycans, skeletal, muscle, teeth|Possibly| 1936.0||BALB/c-Tg(iFABPp-IL13)/AnuApb||Semi-dominant||||||||||||||||||||||||||interleukin 13|rat intestinal fatty acid binding protein (nucleotides -1178 - +28) - iFABP , i-FABP|High||||||||||Restricted expression of IL13 transgene to intestine - duodenum and proximal jejunum.||Balb/c ?|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|29-Aug-2007|Cryopreserved sperm|150.0|0.0|Unknown||T cell, infection, intestine, interleukin, allergy, gastrointestinal disease, hyperresponsiveness|Yes| 6664.0|JOHNSON|BALB/c.B6-Tlr2/ANU/Ausb||Recessive|toll-like receptor 2|Tlr2|Nil|Ly105|MGI:1346060|toll-like receptor 2; targeted mutation 1, Shizuo Akira|Tlr2|MGI:2178675|3|||||||||||||||||||||||||||||||BALB/c|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|02-Dec-2011||0.0|0.0|Unknown||TLR2, TLR4, Lipopolysaccharide (LPS), Gram-negative bacterial, Gram-positive bacterial|Yes| 4847.0||ENU6CAT:050||Recessive|Unknown||Unknown||||||Unknown|||||||||||||||||||||||||||||Mothers fail to lactate.Pups can be maintained by adding lactating foster mother.|Normal|C57BL/6 x CBA|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|24-Sep-2009|Cryopreserved sperm|30.0|0.0|Unknown||lactation, milk, ENU|Yes| 10328.0||C57BL/6NCrlAnu-Dnajb11Anu/Apb||Recessive|Dnajb11||||||||Unknown|||||||||||||||||||||||||||||Unknown|Unknown|C57Bl/6N|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|02-May-2023|Cryopreserved sperm|55.0|0.0|Unknown|||Yes| 7648.0||B6/Mrit-fech|B6/Mrit-fech|Dominant|Unknown||Unknown||||||Unknown|||||||||||||||||||||||||||||Unknown|Heterozygous mice display a transient growth decrease|C57BL/6|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Good||||No|07-Apr-2014|Cryopreserved sperm|47.0|0.0|Unknown||ENU|No| 5582.0|129SvJ/Emx1||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 190.0||S100 beta-dsRed||Dominant|||Unknown||||||Unknown||||||||||||||||Yes|dsRed|human S100 β gene|||||||||||Cells expressing beta S100 express dsRed||Quackenbush|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|17-Apr-2006||0.0|0.0|Unknown||dsRed, S100|Yes| 7886.0|Osx-Cre R26eYFP Recql4fl/fl|C57BL/6-Recql4 Gt(ROSA)26Sor/Apb Tg(Sp7-tTA,tetO-EGFP/cre)1Amc ||Dominant|RecQ protein-like 4|Recql4|Nil|Recql4fl/fl|MGI:1931028|Recql4 fl/fl|Recql4||15|||||||||||||||||transgene insertion 1, Andrew P McMahon|Osterix (Sp7)|||||||||||Reduced bone mass, shortened bone length|Normal, fertile and viable (floxed line with eYFP reporter of cre activity)|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|generated on pure C57Bl/6 so not backcrossed. Only maintained on C57||Osx-Cre+ve R26eYFP Recql4fl/+ male crossed to Osx-Cre-ve R26eYFPki/ki Recql4fl/fl or fl/+ female|No|30-Apr-2015|Cryopreserved sperm|50.0|0.0|Yes|Rothmund-Thomson Syndrome|Recql4, R26eYFP, Rothmund-Thomson Syndrome|Yes| 7886.0|Osx-Cre R26eYFP Recql4fl/fl|C57BL/6-Recql4 Gt(ROSA)26Sor/Apb Tg(Sp7-tTA,tetO-EGFP/cre)1Amc ||Dominant|gene trap ROSA 26, Philippe Soriano|Gt(ROSA)26Sor||beta geo, Gtrgeo26, Gtrosa26, R26, ROSA26|MGI:104735|gene trap ROSA 26, Philippe Soriano; targeted mutation 1, Frank Costantini|Gt(ROSA)26Sor|MGI:2449038|6|||||||||||||||||||||||||||||Reduced bone mass, shortened bone length|Normal, fertile and viable (floxed line with eYFP reporter of cre activity)|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|generated on pure C57Bl/6 so not backcrossed. Only maintained on C57||Osx-Cre+ve R26eYFP Recql4fl/+ male crossed to Osx-Cre-ve R26eYFPki/ki Recql4fl/fl or fl/+ female|No|30-Apr-2015|Cryopreserved sperm|||Yes|Rothmund-Thomson Syndrome|Recql4, R26eYFP, Rothmund-Thomson Syndrome|Yes| 5162.0|KRN 156|KRN:156||Recessive|Unknown|Unknown|||||||Unknown|||||||||||||||||transgene insertion KRN, Diane Mathis|Natural TCR alpha and -beta promoter/enhancer elements.|||||||||||No arthritis, no GPI autoantibodies in KRN/H2g7 model.||C57BL/6J x BALB/b|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Good||||No|28-Jun-2010|Cryopreserved sperm|18.0|0.0|Unknown||autoimmunity, arthritis, KRN, ENU|Possibly| 4738.0||B6;Cg-H2 Cbl Tg(ILK3mHEL)3Ccg Tg(TcrHEL3A9)1Mmd/AnuApb|B6;Cg-H2 Cbl Tg(ILK3mHEL)3Ccg Tg(TcrHEL3A9)1Mmd|Recessive|Casitas B-lineage lymphoma|Cbl|Unknown|c-Cbl, cbl, Cbl-2|MGI:88279|targeted mutation 1, David D L Bowtell|Cbl|MGI:2180578|9||||||||||||||||Yes|transgene insertion 3, Christopher C Goodnow|For Tg(ILK3mHEL)3Ccg: Rat insulin promoter|||||||||||Defect in T cell function||B10.BR-H2 x C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||5|hom x hom|No|20-Apr-2009|Cryopreserved sperm|105.0|0.0|Unknown||T cell, T cell receptor (TCR), signal transduction|Yes| 4738.0||B6;Cg-H2 Cbl Tg(ILK3mHEL)3Ccg Tg(TcrHEL3A9)1Mmd/AnuApb|B6;Cg-H2 Cbl Tg(ILK3mHEL)3Ccg Tg(TcrHEL3A9)1Mmd|Recessive||||||||||||||||||||||||||transgene insertion 1, Mark M Davis ||||||||||||Defect in T cell function||B10.BR-H2 x C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||5|hom x hom|No|20-Apr-2009|Cryopreserved sperm|||Unknown||T cell, T cell receptor (TCR), signal transduction|Yes| 5195.0||ENU18WT:017b||Recessive|Unknown||Unknown||||||Unknown|||||||||||||||||||||||||||||Unknown||C57BL/6JAnu|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|04-Aug-2010|Cryopreserved sperm|37.0|0.0|Unknown||ENU, Wellcome Trust|Yes| 7376.0|ENU26:032:Birc6|C57BL/6NCrlAnu-Birc6/AnuApb|C57BL/6NCrlAnu-Birc6/AnuApb|Recessive|baculoviral IAP repeat-containing 6|Birc6|Unknown|A430032G04Rik, A430040A19Rik, apollon, Bruce, D630005A10Rik|MGI:1276108|baculoviral IAP repeat-containing 6; mutation 1, The Australian National University|Birc6|MGI:5563506|17|ENSMUSG00000024073|ENSMUST00000024879|Birc6-201|14218|14475|C to T|ENSMUSE00001248145|71|4740|Glutamine to STOP|||||AAGCAACGGTTAAATGGGCTATGCTAGAACAAATCAGAAATCCTTCACCGTGCTTTAAAGA||||||||||||||Probably embryonic lethal|Unknown|C57BL/6NCrlAnu|No|No|Yes|No|No|Yes|No|Good||3|HET x HET|No|17-Jul-2013|Cryopreserved sperm|36.0|0.0|Unknown||embryo, lethal, ENU|Yes| 1987.0|Nkx2-3 KO|B6.129-Nkx2-3||Recessive|NK2 transcription factor related, locus 3 (Drosophila)|Nkx2-3|Unknown|Nkx-2.3, Nkx2.3, tinman|MGI:97348|targeted mutation 1, Richard P Harvey|Nkx2-3|MGI:2448069|19||||||||||||||||No|||||||||||||Homozygotes exhibit postnatal lethality due to acute intestinal malabsorption. Survivors recover well but exhibit splenic and Peyer's patch hypoplasia, intestinal villus malformation, gut truncation and distension, abnormal molar and sublingual gland development, and deranged lymphocyte homing. 30% of homozygotes die within the first 2 weeks due to acute intestinal malabsorptionsurviving homozygotes recover rapidly, are fertile, and appear generally healthy as adults.||129 x C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|05-Sep-2007||0.0|0.0|Unknown||postnatal lethality, intestinal malabsorption, hyoplasia, transcription factor, B cell|Yes| 5193.0||ENU18WT:025b||Recessive|Unknown||Unknown||||||Unknown|||||||||||||||||||||||||||||Unknown||C57BL/6JAnu|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|04-Aug-2010|Cryopreserved sperm|30.0|0.0|Unknown||ENU, Wellcome Trust|Yes| 5194.0||ENU18WT:036a||Recessive|Unknown||Unknown||||||Unknown|||||||||||||||||||||||||||||Unknown||C57BL/6JAnu|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|04-Aug-2010|Cryopreserved sperm|38.0|0.0|Unknown||ENU, Wellcome Trust|Yes| 7649.0||B6/Mrit-pf|B6/Mrit-pf|Dominant|Unknown||Unknown||||||Unknown|||||||||||||||||||||||||||||Unknown|Heterozygous mice display a transient growth decrease|C57BL/6|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Good||||No|07-Apr-2014|Cryopreserved sperm|50.0|0.0|Unknown||ENU|No| 7036.0|zeta-BALB/c 390 ; 14-3-3 zeta deficient (Line 390)|C.129-Ywhaz/Apb||Recessive|tyrosine 3-monooxygenase/tryptophan 5-monooxygenase activation protein, zeta polypeptide|Ywhaz|Nil|1110013I11Rik, 14-3-3 zeta|MGI:109484|tyrosine 3-monooxygenase/tryptophan 5-monooxygenase activation protein, zeta polypeptide; gene trap OST405390, Lexicon Genetics|Ywhaz||15|||||||||||||||||||||||||||||Infertile, reduced survival of KO pups at 21 days|None|BALB/c|Yes|No|Yes|Yes|No|Yes|Yes|Good|10||het x het|No|06-Aug-2012|Cryopreserved sperm|50.0|0.0|Unknown||14-3-3, signal transduction|Possibly| 7779.0|SGTA KO|B6(Cg)-Sgta<(tm1.1Drmcr)><(OzCre-Gt(ROSA)26Sor)>/J|DRMCR|Semi-dominant|Small Glutamine-Rich Tetratricopeptide Repeat (TPR)-Containing, Alpha|SGTA|Nil|alphaSGT, SGT, Vpu-Binding Protein|MGI:1098703 ||||10|MGI:5788685||B6(Cg)-Sgtatm1.1Drmcr/J||||||||||||||||||||||||||Homozygous SGTA knockout mice weigh less than their wildtype littermates. They appear to give birth to fewer young. |Normal/unknown.|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|Yes|Poor||||No|06-Nov-2014|Cryopreserved sperm|67.0|0.0|No||SGTA, small glutamine-rich tetratricopeptide repeat (TPR)-containing, alpha, AR, Androgen receptor|Possibly| 7080.0|Momme D40|FVB/NJ-Uhrf1 Tg(Hba1-Gfp)1Ew/QimrApb||Semi-dominant|ubiquitin-like, containing PHD and RING finger domains, 1|Uhrf1|Unknown|ICBP90, Np95|MGI:1338889|ubiquitin-like, containing PHD and RING finger domains, 1; modifier of murine metastable epialleles, D40|Uhrf1|MGI:5515394|17||||||||||Unknown to Unknown|||||||transgene insertion 1, Emma Whitelaw|human alpha-globin promoter and enhancer region|11 copies||||||||||Lethalhomozygous die E10.5|Normal|FVB/NJ|No|No|Yes|No|No|Yes|No|Good|||MommeD40<+/->;Tg(Hba1-Gfp)1Ew x Tg(Hba1-Gfp)1Ew|No|13-Sep-2012|Cryopreserved sperm|29.0|0.0|Unknown||ENU, variegation, modifier|Possibly| 6665.0|Big Blue|C57BL/6-Tg(TacLIZa)A1Jsh/Ausb||Dominant||||||||||||||||||||||||||transgene insertion A1, Jay M Short||30 copies of the transgene||||||||||||C57BL/6|Yes|Unknown|Yes|Yes|Unknown|Yes|No|Unknown||||No|02-Dec-2011||0.0|0.0|Unknown||lacI, Spontaneous mutation spectrum|Yes| 697.0|TAG (C3SV40T)|FVB/N-Tg(C3-1-TAg)cJeg||Dominant||||||||||||||||||||||||||transgene insertion C, Jeffrey E Green|rat prostatic binding protein C3 promoter (Pbpc3)||||||||||||Mammary gland hyperplasia: at 2 months of age, female mice exhibit atypical ductal hyperplasias unlike in wild-type mice,hyperplastic cells exhibit increased rates of apoptosis compared to cells in wild-type mice.Abnormal prostate physiology:prostate cells exhibit increased proliferation and apoptosis rates compared to in wild-type mice according to their degree of prostate intraepithelial neoplasia.Increased tumor incidence:some mice exhibit mixed tumors of the sweat glands and occasional nasal proliferative or neoplastic lesions develop from the nasal turbinate epithelium unlike in wild-type mice.Adenocarcinoma:at 7 months, 10% to 20% male mice develop adenocarcinomas of the urethral and bulbourethral glands unlike in wild-type miceMammary adenocarcinoma:by 6 months of age female mice develop multiple mammary ductular adenocarcinomas unlike in wild-type mice.at 6 months, 10% of female mice exhibit lung metastasis.adenocarcinoma cells exhibit increased rates of apoptosis compared to cells in wild-type mice.Prostate adenocarcinoma:at 7 months of age, 19% of mice exhibit carcinomas in the ventral lobe and 3% in the dorsolateral lobe unlike in wild-type mice.after 8 months, 40% of mice exhibit carcinomas in the ventral lobe and 13% in the dorsolateral lobe unlike in wild-type mice.the number of apoptotic cells in the prostate is greater than in wild-type mice.at 7 months in the ventral prostate and 11 months in the dorsolateral prostate.however, no metastasis is observed.Prostate intraepithelial neoplasia:at 5 to 6 months, mice develop low to high grade prostate intraepithelial neoplasia (PIN) unlike wild-type mice.low-grade PIN is observed in 83% and 100% of the ventral prostate at 2 to 3 months and 4 to 12 months, respectively, unlike wild-type mice.at 5 months, ventral and dorsolateral lobes exhibit high grade PIN unlike in wild-type mice.high-grade PIN is observed on 88% and 100% of mice at 5 to 8 months and more than 8 months, respectively, unlike in wild-type mice.numbers of PIN lesions increase with age in the ventral and dorsolateral lobes unlike wild-type mice.the number of apoptotic cells in the prostate is greater than in wild-type miceat 2 to 3 months, low-grade prostate intraepithelial neoplasia (PIN) is observed in the ventral and dorsolateral prostates unlike in wild-type mice.at 5 months, high-grade PIN is observed in both lobes unlike in wild-type mice.PIN lesions increase with age.|FVB/N|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|01-May-2007||0.0|0.0|Unknown||Mammary gland, Prostate, tumourigenesis, SV40, hormone, hyperplasia, adenocarcinoma|Yes| 5196.0||ENU18WT:022a||Recessive|Unknown||Unknown||||||Unknown|||||||||||||||||||||||||||||Unknown||C57BL/6JAnu|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|04-Aug-2010|Cryopreserved sperm|49.0|0.0|Unknown||ENU, Wellcome Trust|Yes| 5284.0|B6.CD39.Tg.1079-4.A2AR.KO|C57BL/6-Adora2a Tg(H2-K-Entpd1)||Recessive|adenosine A2a receptor|Adora2a|Nil|A2a, Rs, A2AAR, A2aR, AA2AR|MGI:99402|adenosine A2a receptor; targeted mutation 1, Jiang-Fan Chen|Adora2a|MGI:2155985|10||||||||||||||||No|human CD39|H2-K|||||||||||Unknown||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|28-Oct-2010||0.0|0.0|Yes||ischemia, renal ischemia-reperfusion, purinergic signal, adenosine, T cells, transplantation, kidney|Possibly| 1513.0|eNOSTg|B6.Cg-Tg(Edn1-NOS3)22Yky/Apb|B6.Cg-Tg(Edn1-NOS3)22Yky/Apb|Dominant||||||||||||||||||||||||||transgene insertion 22, Mitsuhiro Yokoyama|mouse Edn1|Active in vascular wall||||||||||Hypotension. Elevated cGMP, plasma nitrate and nitrite levels.||C57BL/6JAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|7|||No|04-Jul-2007|Cryopreserved sperm|90.0|0.0|Unknown||eNOS, connexin, renal arterioles, hypotension|Yes| 3444.0|TCR transgenic - CL4|BALB/c-Tg(TcraCl4,TcrbCl4)1Shrm/Wehi||Dominant||||||||||||||||||||||||||transgene insertion 1, Linda Sherman|Tcra-V promoter, the immunoglobulin heavy-chain enhancer E(H)|||||||||||TCR transgenics are immunocompromised by having a mono-specific T cell receptor however, in a clean envirnoment, mice show no difference in phenoptype from wild-type B6 mice. CL4 - Transgenic mice are viable, fertile, normal in size, normoglycemic and do not display any gross physic or behavioral abnormalities.The TCR expressed from this transgene is specific for influenza virus A/PR/8 hemagglutinin (HA) in the context of the MHC class I molecule H2-Kd. Both thymic and periperal T-cell populations are skewed toward CD8+ cells. The majority of thymocytes and virtually all CD8+ T cells in lymph nodes express the transgenic TCR beta chain. About 40% of peripheral blood CD8+ T cells react with the HA peptide presented by H2-Kd. ||BALB/c|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|17-Jul-2008||0.0|0.0|Unknown||T cell, influenza, autoimmunity, tolerance|Yes| 5285.0|B6.CD39.Tg.1079-4.CD73.KO|C57BL/6-Nt5e Tg(H2-K-Entpd1)||Recessive|5' nucleotidase, ecto|Nt5e|Nil|CD73, ecto-5'-nucleotidase, Nt5|MGI:99782|5' nucleotidase, ecto; targeted mutation 1, Linda F Thompson|Nt5e|MGI:3522017|9||||||||||||||||No|human CD39|H2-K|||||||||||Unknown||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|28-Oct-2010||0.0|0.0|Yes||ischemia, renal ischemia-reperfusion, purinergic signal, adenosine, T cells, transplantation, kidney|Possibly| 3471.0|C3G genetrap|129-Rapgef1/Wehi||Recessive|Rap guanine nucleotide exchange factor (GEF) 1|Rapgef1|Nil|4932418O06Rik, C3G, Grf2|MGI:104580|Rap guanine nucleotide exchange factor (GEF) 1; gene trap 5, Peter Gruss |Rapgef1|MGI:2445403|2||||||||||||||||Yes|||||||||||||Mice homozygous for a gene trap allele exhibit embryonic lethality, altered neuroepithelium morphology, embryonic and extra-embryonic vascular defects, and reduced cell migration and adhesion.|Normal|129/SvPas|No|No|Yes|No|No|Yes|No|Unknown||||No|22-Jul-2008||0.0|0.0|Unknown||cerebral cortex, nucleotide exchange factor, embryonic lethal, Akt/PKB, Ras signalling|Yes| 7087.0|Bim Des RAG|B10.BR.(Cg)-H2 Bcl2l11/Wehi Rag1 Tg(TcraKB5.C20,TcrbKB5.C20)10395Arnd/Apb||Recessive|BCL2-like 11 (apoptosis facilitator)|Bcl2l11|Nil|1500006F24Rik, Bim, Bod|MGI:1197519|BCL2-like 11 (apoptosis facilitator); targeted mutation 1.1, Andreas Strasser|Bcl2l11|MGI:2156498|2||||||||||||||||Yes|transgene insertion 10395, Bernd Arnold||||||||||||Similar phenotype as in C57BL/6 mice (Increased numbers of lymphoid and myeloid cells.)Bim-/- females are bad mothers and should not be used for breeding unless necessary. Bim -/-: blood - increased lymphocytes (B + T cells), granulocytes & monocytes. - decreased platelets - Increased serum Ig. Des-TCR onto Bim-deficient background can be generated but problems to generate RAG-/- mice. This strain is thus HETEROZYGOUS for RAG deficiency|Unknown|B10.BR|Yes|Yes|Yes|Yes|Yes|Yes|No|Poor|10|||Yes|20-Sep-2012|Cryopreserved sperm|50.0|0.0|No||T cell, RAG, Lymphoid, CD8, TCR|Yes| 7087.0|Bim Des RAG|B10.BR.(Cg)-H2 Bcl2l11/Wehi Rag1 Tg(TcraKB5.C20,TcrbKB5.C20)10395Arnd/Apb||Recessive|recombination activating gene 1|Rag1|Normal|Rag-1|MGI:97848||||2|||||||||||||||||||||||||||||Similar phenotype as in C57BL/6 mice (Increased numbers of lymphoid and myeloid cells.)Bim-/- females are bad mothers and should not be used for breeding unless necessary. Bim -/-: blood - increased lymphocytes (B + T cells), granulocytes & monocytes. - decreased platelets - Increased serum Ig. Des-TCR onto Bim-deficient background can be generated but problems to generate RAG-/- mice. This strain is thus HETEROZYGOUS for RAG deficiency|Unknown|B10.BR|Yes|Yes|Yes|Yes|Yes|Yes|No|Poor|10|||Yes|20-Sep-2012|Cryopreserved sperm|||No||T cell, RAG, Lymphoid, CD8, TCR|Yes| 6279.0|FOX03|B6.129-Foxo3||Recessive|forkhead box O3|Foxo3|Nil|1110048B16Rik, 2010203A17Rik, Fkhr2, FKHRL1, Foxo3a|MGI:1890081|forkhead box O3; targeted mutation 1, Noboru Motoyama|Foxo3|MGI:3719789|10|||||||||||||||||||||||||||||Increased sensitivity to xenobiotic induced morbidity/mortality:*All mice die by 4 weeks after injection with the cell cycle specific myelotoxic drug 5-FU in contrast over 60% of wild-type controls survived.Hematopoietic system phenotype:*Unlike red blood cells, the numbers of white blood cells and platelets and the morphology or myeloid and lymphoid cells are similar to controls.*Proliferation and differentiation of hematopoietic progenitors in the bone marrow are similar to controls. Decreased erythrocyte cell number Increased mean corpuscular hemoglobin Increased mean corpuscular volume Reticulocytosis Abnormal hematopoietic stem cell morphology: *Colony formation in long term culture experiments is severely impaired reflecting a defect in hematopoietic stem cell function. *Competitive repopulation assays suggest a defect in hematopoietic stem cell self renewal. *The proportion of cells in G0 is reduced suggesting a defect in quiescence maintenance. *Reactive oxygen species are elevated. *Colony formation in short term cultures is reduced for cells from aged mice but not for cells from young mice. Decreased hematopoietic stem cell number: *In some aged mice but not in young mice.Female infertility||C57BL/6 X 129/sv|Yes|No|Yes|Yes|Unknown|Yes|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown||IL-15, NK cell, Apoptosis|Yes| 5434.0|Meio1|Meio1||Recessive|unknown|unknown|Unknown||||||Unknown|||||||||||||||||||||||||||||Male infertility due to meiotic arrest in male germ cells.|normal|mixed background (C57BL/6J and CBA)|Yes|Yes|Yes|Yes|No|Yes|Yes|Good||||No|15-Feb-2011|Cryopreserved sperm|250.0|0.0|Unknown||infertility, meiosis, sperm|No| 4936.0|Cathepsin-S Knockout|C6;SJL-Ctss/Wehi||Recessive|cathepsin S|Ctss|Nil|Cat S|MGI:107341|cathepsin S; targeted mutation 1, Harold A Chapman|Ctss|MGI:2182133|3||||||||||||||||Yes|||||||||||||Defective CD4 T cell response and humoral responses, but no overt immunodeficiency. Homozygous null mice are resistant to the development of experimental autoimmune myasthenia gravis and showed reduced T and B cell responses to acetylcholine receptor.||C57BL/6 x SJL|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|24-Nov-2009||0.0|0.0|Unknown||T cell, MHC class II, cysteine proteinase, Humoral resposne, arthritis, germinal centre|Yes| 7093.0|F/F x Tlr2; gp130Y757F x Tlr2|STOCK Il6st Tlr2/MarpApb||Dominant|interleukin 6 signal transducer|Il6st|Unknown|CD130, D13Ertd699e, gp130|MGI:96560|interleukin 6 signal transducer; targeted mutation 1, Matthias Ernst|Il6st|MGI:2388478|13||||||||||||||||Yes|||||||||||||Mice develop gastric and inflammation and tumours, as well as splenomegaly and lymphadenopathy.|If the mice are heterozygous for the gp130 knock-in mutation (F+) then the mice appear normal. |C57BL/6 x 129Sv x BALB/c|Yes|No|Yes|Yes|Yes|Yes|No|Good|10||heterozogous x homozygous|No|26-Sep-2012|Cryopreserved sperm|30.0|0.0|Yes|Gastric cancer|gastric, cancer, gp130, tlr|No| 7093.0|F/F x Tlr2; gp130Y757F x Tlr2|STOCK Il6st Tlr2/MarpApb||Dominant|toll-like receptor 2|Tlr2|Nil|Ly105|MGI:1346060|toll-like receptor 2; targeted mutation 1, Shizuo Akira|Tlr2|MGI:2178675|3||||||||||||||||No|||||||||||||Mice develop gastric and inflammation and tumours, as well as splenomegaly and lymphadenopathy.|If the mice are heterozygous for the gp130 knock-in mutation (F+) then the mice appear normal. |C57BL/6 x 129Sv x BALB/c|Yes|No|Yes|Yes|Yes|Yes|No|Good|10||heterozogous x homozygous|No|26-Sep-2012|Cryopreserved sperm|||Yes|Gastric cancer|gastric, cancer, gp130, tlr|No| 349.0|PKZ1|C57BL/6-pKZ1||Dominant||||||||||||||||||||||||||β-galactosidase gene, E. coli (reverse orientation) flanked by the mouse Vκ21C and Jκ5 immunoglobulin recombination signal sequences|chicken β-actin promoter complex|||||||||||Normal.When an inversion event occurs, facilitated by the mouse recombination signal sequences, the lacZ gene is brought into correct juxtaposition with respect to the promoter complex and expression of the E. coli β-galactosidase message can occur (Fig 1). The E. coli β-galactosidase protein can then be detected in tissues in the animals by staining with the chromogenic substrate X-gal. Cells that undergo inversion events exhibit blue staining. The number of inversion events is determined by the ratio of the number of blue staining cells to the total number of cells counted. Inversion events have been detected in a wide range of pKZ1 tissues, with most studies to date concentrating on spleen tissue.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|||pKZ1 mice x C57BL/6|No|29-Sep-2006||0.0|0.0|Unknown||pKZ1, somatic intrachromosomal recombination, SICR, radiation, inversion|Yes| 7099.0|Fst-oEX|B6;D2-Tg(KRT14-Fst)/MarpApb||Dominant||||||||||||||||||||||||||transgene insertion 1, |human keratin-14 (K14)|||||||||||unknown|only one copy required to demonstrate phenotype.Mice demonstrate larger ears, longer tails, reduced body weight, mild dermal and epidermal atrophy and delayed wound healing|B6D2F2|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Good|||Het mouse x wt mouse|No|01-Oct-2012|Cryopreserved sperm|50.0|0.0|Unknown||activin, epidermis, follistatin|Possibly| 3940.0|C3H.DUB/3|C3Arc.MOLD-Oas1b/Arc|C3Arc.MOLD-Oas1bArc|Dominant|2'-5' oligoadenylate synthetase 1B|Oas1b|Normal|Flavivirus resistance, Flv, L1, Mmu-L1, Oias-2, Oias2, Wnv|MGI:97430|minor flavivirus resistance|Oas1b|MGI:1857802|5||||||||||||||||No|||||||||||||Minor resistance to Flavivirus infection.Flv Phenotype – Resistance to infections by Flaviviruses.Tlr4 Phenotype – Toll 4 receptor is responsive to LPS injection.|Flv Phenotype – dominant phenotype, heterozygotes are resistant to infection.Tlr4 phenotype is dominant and heterozygous mice show responsiveness to LPS.|C3H/HeJARC|Yes|Yes|Yes|Yes|Yes|Yes|No|Poor|10||brother x sister|No|17-Oct-2008||0.0|0.0|Unknown||Flavivirus resistance, Lipopolysaccharide (LPS), Toll like receptor|Yes| 6349.0|NPYcre|B6.Cg-Npy/Ausb||Recessive|neuropeptide Y |Npy|Nil|0710005A05Rik |MGI:97374|neuropeptide Y; targeted mutation 1, Tim Karl |Npy|MGI:3811718|6|||||||||||||||||||||||||||||Increased anxiety-related response:*Increased levels of anxiety-related behaviors are detected across different test paradigms with males having more pronounced behaviors.*Males have about a two-thirds reduction and females have a third to a half reduction in time spent in the center of an open field.*Male mice but not female mice show a reduced amount of time in the open arm of an elevated maze test.*Mutant males spend less time in the aversive illuminated compartment of a light-dark test with the ratio of distance traveled in lit areas (to total distance traveled) being half that of sex-matched controls.Decreased exploration in new environment:*vertical activities in a new environment are reduced by two-thirds.*Similar results are obtained in an elevated maze test.Decreased vertical activity:*Vertical activities of mutant mice are reduced by two-third in open field testsHypoactivity:*Mice of both sexes have reduced motor activity in an open field tests(371.1 movements vs. 585.5 movements for males).*Both mutant and wild-type female mice have higher locomotion than male mice of the same genotype (479.8 movements vs. 630.7 movements for wild-type females).*Similar results occur in light-dark field tests.*Mutant mice also have longer resting duration time in an open field test (393.3 seconds vs. 347.2 s in wild-type females).*Male mice have increased resting times compared to female mice (462.7s vs. 381.6s).*Similar resting results occur in light-dark field tests.Increased defecation:*Female mice have increased rates of defecation in elevated maze tests (2.8 vs. 0.1 in controls)||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown||neuropeptide Y, sexually dimorphic impact, anxiety-related disorders|Yes| 3597.0||C57BL/6-Cd36||Recessive|CD36 antigen|Cd36|Nil|FAT, fatty acid translocase, Scarb3|MGI:107899|targeted mutation 1, Maria Febbraio|Cd36|MGI:1931790|5||||||||||||||||Yes|||||||||||||Homozgyous mutant mice exhibit an immunodeficiency phenotype, are susceptible to S. aureus infection and develop ocular pterygium. Mice homozygous for disruptions in this gene display abnormal lipid homeostasis which affects energy utilization in the heart. CD36 null mice have elevated fasting levels and cholesterol, triacylglycerol & non-esterfied free fatty acids and lower fasting serum glucose levels.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|06-Aug-2008||0.0|0.0|Unknown||cholesterol, fatty acid , lipoprotein, glucose, presentation, T cell, Cd8|Yes| 6353.0|IL27ra|B6.Cg-IL27ra/Ausb||Recessive|interleukin 27 receptor, alpha|Il27ra |Nil|IL-27R, Tccr, WSX-1 |MGI:1355318 |interleukin 27 receptor, alpha; targeted mutation 1, Frederic J de Sauvage|Il27ra|MGI:3525439|8|||||||||||||||||||||||||||||Increased lymphocyte cell number:*Increased lymphocyte accumulation within the lung granulomata during M. tuberculosis infection compared to wild-type.Abnormal T-helper 1 physiology:*amount of interferon-gamma production was decreased per lung-derived CD4 T cell and per antigen-specific CD4 T cell, but not in spleen-derived CD4 T cell, after M. tuberculosis infection.Decreased susceptibility to bacterial infection:*Improved control of Mycobacterium tuberculosis growth and improved reduction of bacterial burden in the lungs, spleen, and draining lymph node.Increased lymphocyte cell number:*Increased lymphocyte accumulation within the lung granulomata during M. tuberculosis infection compared to wild-type||C57BL/6|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown||The interleukin-27, T-cell cytokine receptor, Immunopathology|Yes| 7104.0|MT-1/II KO|B6.129-Mt1 Mt2/SaApb||Recessive|metallothionein 1|Mt1|Nil|Mt-1, MT-I|MGI:97171|metallothionein 1; targeted mutation 1, Anna E Michalska|Mt1|MGI:2668454|8|||||||||||||||||||||||||||||Increased circulating alanine transaminase level: in acetaminophen-treated miceAbnormal ion homeostasis: * increased cadmium sensitivity * take up a hunched back posture, ruffed coat and display general lethargyAbnormal lipid homeostasis: acetaminophen-induced lipid peroxidation is increased compared to in similarly treated wild-type mice.Increased sensitivity to xenobiotic induced morbidity/mortality: mice are more sensitive to acetaminophen-induced lethality compared with similarly treated wild-type mice.Increased physiological sensitivity to xenobiotic: * mice exhibit increased susceptibility to acetaminophen-induced hepatotoxicity, alanine aminotransferase, hepatic necrosis, lipid peroxidation, and lethality compared with similarly treated wild-type mice * acetaminophen-induced injuries are not ameliorated by pretreatment with zinc unlike in similarly treated wild-type mice * hepatocytes are more sensitive to acetaminophen and NAPQI-induced oxidative stress compared with similarly treated wild-type cells * however, acetaminophen metabolism is normalIncreased incidence of chemically-induced tumors: increased sensitivity to DMBA/TPA treatment; 100% of treated mice have tumors by 19 weeks, and only 10% of wild-type mice have tumors at 20 weeks, and the average tumor size of treated mice is 2X larger.Abnormal hepatocyte morphology: hepatocytes are more sensitive to acetaminophen and NAPQI-induced oxidative stress indicated by lactate dehydrogenase leakage compared with similarly treated wild-type cells.Hepatic necrosis: in acetaminophen-treated micetumorigenesis.Increased tumor incidence: 90% of mice with tumors by 13 weeks (earliest tumors by 9 weeks).Increased incidence of chemically-induced tumors: increased sensitivity to DMBA/TPA treatment; 100% of treated mice have tumors by 19 weeks, and only 10% of wild-type mice have tumors at 20 weeks, and the average tumor size of treated mice is 2X larger.|Normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|10|||No|09-Oct-2012|Cryopreserved sperm|10.0|0.0|Unknown||Zinc, cadmium, diet|Yes| 7104.0|MT-1/II KO|B6.129-Mt1 Mt2/SaApb||Recessive|metallothionein 2|Mt2|Nil|Mt-2, MT-II|MGI:97172|metallothionein 2; targeted mutation 1, Anna E Michalska|Mt2|MGI:2668455|8|||||||||||||||||||||||||||||Increased circulating alanine transaminase level: in acetaminophen-treated miceAbnormal ion homeostasis: * increased cadmium sensitivity * take up a hunched back posture, ruffed coat and display general lethargyAbnormal lipid homeostasis: acetaminophen-induced lipid peroxidation is increased compared to in similarly treated wild-type mice.Increased sensitivity to xenobiotic induced morbidity/mortality: mice are more sensitive to acetaminophen-induced lethality compared with similarly treated wild-type mice.Increased physiological sensitivity to xenobiotic: * mice exhibit increased susceptibility to acetaminophen-induced hepatotoxicity, alanine aminotransferase, hepatic necrosis, lipid peroxidation, and lethality compared with similarly treated wild-type mice * acetaminophen-induced injuries are not ameliorated by pretreatment with zinc unlike in similarly treated wild-type mice * hepatocytes are more sensitive to acetaminophen and NAPQI-induced oxidative stress compared with similarly treated wild-type cells * however, acetaminophen metabolism is normalIncreased incidence of chemically-induced tumors: increased sensitivity to DMBA/TPA treatment; 100% of treated mice have tumors by 19 weeks, and only 10% of wild-type mice have tumors at 20 weeks, and the average tumor size of treated mice is 2X larger.Abnormal hepatocyte morphology: hepatocytes are more sensitive to acetaminophen and NAPQI-induced oxidative stress indicated by lactate dehydrogenase leakage compared with similarly treated wild-type cells.Hepatic necrosis: in acetaminophen-treated micetumorigenesis.Increased tumor incidence: 90% of mice with tumors by 13 weeks (earliest tumors by 9 weeks).Increased incidence of chemically-induced tumors: increased sensitivity to DMBA/TPA treatment; 100% of treated mice have tumors by 19 weeks, and only 10% of wild-type mice have tumors at 20 weeks, and the average tumor size of treated mice is 2X larger.|Normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|10|||No|09-Oct-2012|Cryopreserved sperm|||Unknown||Zinc, cadmium, diet|Yes| 7663.0||ENU17China14 ||Recessive|Unknown|Unknown|||||||Unknown|||||||||||||||||||||||||||||Reduced numbers of marginal zone B cells|Normal|C57BL/6NCrlAnu|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|11-Apr-2014|Cryopreserved sperm|21.0|0.0|Unknown||ENU, B cell, lymphocyte|No| 3487.0||C57BL/6-IL1rap||Recessive|interleukin 1 receptor accessory protein|Il1rap|Unknown|6430709H04Rik, IL-1R AcP, IL-1RAcP|MGI:104975|interleukin 1 receptor accessory protein; targeted mutation 1, Mark A Labow |Il1raptm1Roml|http://www.informatics.jax.org/javawi2/servlet/WIFetch?page=alleleDetail&key=3262|16||||||||||||||||Yes|||||||||||||Normal.Decreased IL-6 secretion in response to IL-1 injections||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|23-Jul-2008||0.0|0.0|Unknown||interleukin, signal transduction, receptor, NF-kappaB|Yes| 5432.0|11B6115b|ENU11B6:115b||Recessive|Unknown|Unknown|||||||Unknown|||||||||||||||||||||||||||||Increased susceptibility to TB||C57BL/6J x C57BL/10|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||6|Sib x sib|No|14-Feb-2011|Cryopreserved sperm|30.0|0.0|Unknown||Infection|Possibly| 713.0|NID5ML5|NOD-Idd5 Tg(ML5sHEL)5Ccg||Dominant|insulin dependent diabetes susceptibility 5|Idd5|Unknown|Idd-5|MGI:96407|C57BL/10|Idd5|MGI:2389023|1||||||||||||||||Yes|transgene insertion 5, Christopher C Goodnow||High||||||||||||NOD|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|03-May-2007||0.0|0.0|Unknown||hen egg lysozyme (HEL), auotimmunity, B cell, immunoglobulin, diabetes|Yes| 7085.0|floxed CYP27B1 |B6.129-Cyp27b1/Apb||Dominant|cytochrome P450, family 27, subfamily b, polypeptide 1|Cyp27b1|Normal|1alpha(OH)ase, 25-hydroxyvitamin D3 1alpha-hydroxylase, 25(OH)D 1alpha-hydroxylase, Cp2b, Cyp1, Cyp27b, Cyp40, P450c1, P450VD1alpha, Pddr, Vdd1, Vddr, VddrI|MGI:1098274|cytochrome P450, family 27, subfamily b, polypeptide 1; targeted mutation 1.1, Rene St-Arnaud|Cyp27b1|MGI:2656261|10|||||||||||||||||||||||||||||Normal|Normal|C57BL6/J|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|>4|||No|18-Sep-2012|Cryopreserved sperm|50.0|0.0|Yes|pseudovitamin D-deficiency rickets|Vitamin D3, rickets, cytochrome P450|Yes| 1740.0|Aire knockout 384|C57BL/6-Aire/Wehi||Recessive|autoimmune regulator (autoimmune polyendocrinopathy candidiasis ectodermal dystrophy)|Aire|Unknown||MGI:1338803||||10||||||||||||||||No|||||||||||||Some disturbance of the medullary epithelial compartment, but at the phenotypic level their T cell compartment appeared relatively normal in the thymus and periphery. An increase in the number of activated T cells was evident, and autoantibodies against several organs were detected. At the histological level, lymphocytic infiltration of several organs indicated the development of autoimmunity, although symptoms were mild.Male infertility.They are immuno-compromised. They suffer mild auto-immune disease and the immune response to some infectious agents is impaired. The -/- C57BL/6 LINE of aireKO mice suffers very mild autoimmune symtoms, particularly in the eye and possibly in the epididymis. Other strains may have more severe autoimmune symptoms. Fertility of homozygous males is variable. |Hetrozygotes are apparently unaffected. |C57BL/6|Yes|Yes|Yes|Yes|No|Yes|No|Unknown||||No|01-Aug-2007||0.0|0.0|Yes|APECED (autoimmune polyendocrinopathy-candidiasis-ectodermal dystrophy)|Antigens, Autoimmunity, TRA, tolerance, T cell|Yes| 5287.0|B6.CD73KO/B6.A2ARKO|C57BL/6-Nt5e Adora2a||Recessive|5' nucleotidase, ecto|Nt5e|Nil|CD73, ecto-5'-nucleotidase, Nt5|MGI:99782|5' nucleotidase, ecto; targeted mutation 1, Linda F Thompson|Nt5e|MGI:3522017|9||||||||||||||||No|||||||||||||Unknown||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|28-Oct-2010||0.0|0.0|Yes||ischemia, renal, purinergic, hypoxia, Ectonucleotidase, transplantation|Possibly| 5287.0|B6.CD73KO/B6.A2ARKO|C57BL/6-Nt5e Adora2a||Recessive|adenosine A2a receptor|Adora2a|Nil|A2a, Rs, A2AAR, A2aR, AA2AR|MGI:99402|adenosine A2a receptor; targeted mutation 1, Jiang-Fan Chen|Adora2a|MGI:2155985|10||||||||||||||||No|||||||||||||Unknown||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|28-Oct-2010||||Yes||ischemia, renal, purinergic, hypoxia, Ectonucleotidase, transplantation|Possibly| 5290.0|CBA/B6/129sv-TgN(HUEPCR)-PAR1 KO|CBA;B6;129-F2r Tg(H2-K-EPCR)||Recessive|coagulation factor II (thrombin) receptor|F2r|Nil|Cf2r, Par1, thrombin receptor, ThrR|MGI:101802|coagulation factor II (thrombin) receptor; targeted mutation 1, Andrew J Connolly|F2r|MGI:1857306|13||||||||||||||||No|human protein C receptor, endothelial|H2-K|Strong, endothelial cells and neutrophils||||||||||Unknown||C57BL/6 x CBA|Yes|Unknown|Yes|Yes|Unknown|Yes|No|Unknown||||No|28-Oct-2010||0.0|0.0|Unknown||thrombin, receptor, transplantation, inflammation|Possibly| 3561.0||C57BL/6-Mnt||Recessive|max binding protein|Mnt|Normal|Rox|MGI:109150||||11||||||||||||||||No|LoxP, Hygro||||||||||||Normal.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|01-Aug-2008||0.0|0.0|Unknown||Max, tumour suppressor, cell cycle, proliferation, transcription repressor|Yes| 5291.0|B6.EPCR/TBM.Tg.|CBA;B6-Tg(H2-K-TBM) Tg(H2-K-EPCR)||Recessive||||||||||||||||||||||||||Thrombomodulin|H2-K|Strong, endothelial cells and neutrophils||||||||||Unknown||CBA x C57BL/6|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|28-Oct-2010||0.0|0.0|Unknown||transplantation, thrombin, inflammation, receptor|Possibly| 5291.0|B6.EPCR/TBM.Tg.|CBA;B6-Tg(H2-K-TBM) Tg(H2-K-EPCR)||Recessive||||||||||||||||||||||||||human protein C receptor, endothelial|H2-K|Strong, endothelial cells and neutrophils||||||||||Unknown||CBA x C57BL/6|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|28-Oct-2010||||Unknown||transplantation, thrombin, inflammation, receptor|Possibly| 6203.0|IFNg|B6.129S7-Ifng/J||Recessive|interferon gamma|Ifng |Nil|Ifg, IFN-gamma|MGI:107656|interferon gamma; targeted mutation 1, Timothy Stewart |Ifng|MGI:1857184|10|||||||||||||||||||||||||||||Increased sensitivity to xenobiotic induced morbidity/mortality:*Increase in mortality following a single dose of N-methyl-N-nitrosourea (MNU) compared to similarly treated wild-type controls.Increased susceptibility to bacterial infection induced morbidity/mortality:*Die by 6 - 10 weeks after infection with the avirulent BCG strain of Mycobacterium bovis.Increased susceptibility to parasitic infection induced morbidity/mortality:*Most mice die by 9 days after infection with 1x10<6> Cryptosporidium parvum oocysts.Immune system phenotype:*Do not exhibit defects on either IgE isotype switch or IgE production. Stomach inflammation: *5 weeks after Helicobacter pylori infection, mice have a significantly decreased gastritis inflammation score compared to infected wild-type mice. Increased leukocyte cell number: *Following infection with BCG. Increased NK T cell number: *Unlike in wild-type mice, treatment with LPS and DGalN fails to decrease NK T cell numbers. Increased granulocyte number: *In the blood, bone marrow and spleen following infection with BCG. Increased monocyte cell number: *Following infection with BCG. Abnormal spleen morphology Abnormal spleen red pulp morphology: *Following infection with BCG, the normal follicular structure of the red and white pulp is lost and the red pulp is replaced with extramedullary hematopoietic tissue. Enlarged spleen: *Develop splenomegaly after infection with BCG. Abnormal spleen white pulp morphology: *Following infection with BCG, the normal follicular structure of the red and white pulp is lost and the lymphocytic populations of the white pulp are replaced with sheets of leukocytes. Pale spleen: *Spleens become paler as BCG infection proceeds. Abnormal circulating cytokine level: *Increase in circulating levels of CSF3 after infection with BCG especially in moribund mice. Increased circulating interleukin-6 level: *Following infection with BCG. Enlarged mesenteric lymph nodes: *In C. parvum infected mice. Abnormal dendritic cell physiology: *Increase in IL12 and decrease in IL10 secretion following LPS stimulation. Abnormal Langerhans cell physiology: *Enhancement in hapten induced Langerhan cell migration to the draining lymph nodes. Abnormal dendritic cell antigen presentation: *Dendritic cells show a greater ability to stimulate T cell proliferation in vitro. Abnormal dendritic cell chemotaxis: *Enhancement in the ability of dendritic cells to transmigrate across a membrane in response to RANTES in vitro. *Enhancement in LPS induced dendritic cell migration to the spleen. Abnormal macrophage recruitment: *5 days after muscle injury fewer macrophages are present at the injury site compared to similarly treated wild-type mice. Abnormal type IV hypersensitivity reaction: *In OVA fed mice only a modest decrease in the delayed type hypersensitivity response to injected OVA is seen in contrast this reaction is strongly decreased in similarly treated wild-type controls. Increased susceptibility to type IV hypersensitivity reaction: *Display a more severe delayed type hypersensitivity reaction in response to sheep IgG. Abnormal humoral immune response: *The magnitude of the OVA specific antibody response to subcutaneous OVA challenge is reduced. *However, following oral OVA exposure OVA antibody levels in response to subcutaneous OVA challenge are essentially unchanged unlike in wild-type controls where oral exposure reduces antibody levels. Abnormal immunoglobulin level: *IgG responses are restricted to IgG1 and IgG2b. Abnormal cytokine secretion: Decreased interferon-gamma secretion: *Splenocytes fail to produce IFN-gamma in response to H. pylori antigen stimulation. Decreased interleukin-10 secretion: *Splenocytes from Helicobacter pylori infected mice produce 4-fold less IL-10 when cultured in the presence of H. pylori antigen. *By bone marrow dendritic cells following LPS stimulation. Increased interleukin-12 secretion: *By bone marrow dendritic cells following LPS stimulation. Increased interleukin-4 secretion: *Splenocytes from Helicobacter pylori infected mice produce significantly more IL-4 than splenocytes from wild-type controls when cultured in the presence of H. pylori antigen. Abnormal immune tolerance: *Oral exposure to antigen (OVA) fails to reduce the responsiveness of mice to subsequent subcutaneous exposure to the same antigen. Glomerulonephritis: *Increased susceptibility to induced accelerated antiglomerular basement membrane nephritis as determined by increased albuminuria and more severe pathological changes. Increased susceptibility to bacterial infection: *Following infection with BCG mice display an increased bacterial load throughout the infect in contrast to wild-type mice where bacterial numbers peak at 17 days post infection and decline thereafter. *Following infection with BCG mice develop numerous granulomatous lesions in the liver and necrosis of both the liver and spleen. Increased susceptibility to parasitic infection: *Background Sensitivity: mice on a C57BL/6 background lose weight and develop soft gelatinous stools over the course of a C. parvum infection while mice on a BALB/c background do not. *Background Sensitivity: in C. parvum infected mice on a C57BL/6 background, but not on a BALB/c background, the gastrointestinal tract is heavily colonized with parasites, the small intestines are distended and filled with gelatinous fluid, mesenteric lymph nodes are enlarged and in about 50% of mice gallbladders are enlarged. Decreased length of allograft survival: *Decrease in survival times of heart transplants from CBA mice after a 30 day course of anti-CD4 and anti-CD8 mAb. *Only 10% of heart grafts survive more than 100 days compared to 36% of grafts in wild-type mice.Increased fear-related response:*Background Sensitivity: increase in the number of defecations following a sound stimulus suggesting an enhancement of fear related responses in mice on a C57BL/6 background but not in mice on a BALB/c background.*Prolonged freeze time and longer time to return to normal open field activity patterns following a startle stimulus relative to wild-type controls.*Make fewer entries and spend less time in the open arms of an elevated maze relative to wild-type controls.Abnormal response to new environment:*Background Sensitivity: increase in the number of defecations in a novel environment compared to wild-type controls in mice on a C57BL/6 background but not in mice on a BALB/c background.*The number of rearings is decreased in a novel environment.*Initial locomotor activity is decreased; however, overall distance traveled is not different from controls.Decreased vertical activity:*In a novel environment.Abnormal redox activity:*Unlike in wild-type mice, treatment with LPS and DGalN or TNF-alpha and interferon-gamma fails to increase the production of reactive oxygen species in hepatocytes.Abnormal urine homeostasis:*1 day after induction of accelerated antiglomerular basement membrane nephritis no increase in total urinary nitrate or nitrate levels is detected unlike in similarly treated wild-type controls. Albuminuria: *Increase in albuminuria on days 2, 3,and 4 following induction of accelerated antiglomerular basement membrane nephritis.Abnormal nitric oxide homeostasis:*Unlike in wild-type mice, treatment with LPS and DGalN fails to increase nitric oxide levels.Abnormal response to injury:*Decrease in the number and area of regenerating muscle fibers 5 and 10 days after muscle injury.*Fibrotic lesions are sometimes seen after injury.*5 days after muscle injury fewer macrophages are present at the injury site compared to similarly treated wild-type mice. Decreased susceptibility to injury: *Following a 48 h exposure to hyperoxia (98-99% oxygen) neutrophil migration into the lung air space and the increase in pulmonary alveolar permeability are decreased indicating a decrease susceptibility to the early phase of hyperoxia induced lung injury. *However, after 84 h of exposure to hyperoxia these measures are not different from similarly exposed to wild-type controls.Skeletal muscle fibrosis:*Fibrotic lesions are sometimes seen after injury.Abnormal muscle regeneration:*Decrease in the number and area of regenerating fibers 5 and 10 days after injury.*Fibrotic lesions are sometimes seen after injury.*However, prior to injury no difference in muscle fiber morphology are detected.Stomach inflammation:*5 weeks after Helicobacter pylori infection, mice have a significantly decreased gastritis inflammation score compared to infected wild-type mice.Extramedullary hematopoiesis:*Following infection with BCG.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown||IFN-gamma, Murine immune system|Yes| 1779.0|NOD.B6 Idd11A|B6.NOD-Idd11/Wehi||Recessive|||Unknown|||insulin dependent diabetes susceptibility 11; NOD/ShiLt|Idd11NOD/ShiLt>|MGI:3036810|4||||||||||||||||Yes|||||||||||||Non obese diabetic (NOD) mice exhibit a susceptibility to Spontaneous development of type 1 diabetes. It is best to best to begin monitoring development of glycosuria at weekly intervals starting at 10 wks of age.||NOD|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|03-Aug-2007||0.0|0.0|Unknown||Diabetes, congenic, insulin, non obese|Yes| 6766.0|Ert2/Stat3flox/gp130F |STOCK Stat3 Tg(Gpa33-cre/ERT2)/LudApb||Recessive|signal transducer and activator of transcription 3|Stat3|Normal|1110034C02Rik, Aprf|MGI:103038|signal transducer and activator of transcription 3; targeted mutation 2, Shizuo Akira|Stat3|MGI:1926816|11|||||||||||||||||cre recombinase|glycoprotein A33 (transmembrane)|||||||||||Gastric polyps, maybe developing later and fewer than gp130 ff mice, and maybe additional phenotypes in other tissues.|Unknwon|Mixed|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|16-Dec-2011|Cryopreserved sperm|50.0|0.0|Unknown||signal transduction, polyposis|Yes| 6352.0|Y1fCOL3.6?|B6.Cg-Npy1r Tg(Col1a1-cre)2Bek/Ausb||Dominant|neuropeptide Y receptor Y1|Npy1r|Normal|Npyr, Y1-R|MGI:104963|neuropeptide Y receptor Y1; targeted mutation 1, William P Gray|Npy1r|MGI:3053795|8|||||||||||||||||transgene insertion 2, Barbara E Kream|rat Col1a1 promoter|||||||||||Increased diameter of femur:*With an increase in total tissue area, marrow area, periosteal perimeter and endosteal perimeter.Increased bone mineral content:*Whole body and lumbar vertebraeIncreased bone mineral densityIncreased bone trabecula numberIncreased trabecular bone thicknessAbnormal bone ossification:*Bone formation rate in cancellous and cortical bone is increased compared to in wild-type mice.Abnormal osteoblast physiology:*Mice exhibit increased osteoblast activity compared to in wild-type mice.Increased bone strengthIncreased diameter of femur:*With an increase in total tissue area, marrow area, periosteal perimeter and endosteal perimeter.||Mixed - mice|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Yes| 1814.0|SOCS2 / Ghrhr|Un-Socs2 Ghrhr/Wehi||Recessive|suppressor of cytokine signaling 2|Socs2|Nil|CIS2, Cish2, cytokine-inducible SH2 protein 2, D130043N08Rik, JAB, SOCS-2, SSI-2, STAT-induced STAT inhibitor 2|MGI:1201787|targeted mutation 1, Walter and Eliza Hall Institute of Medical Research|Socs2|MGI:1934557|10||||||||||||||||Yes|||||||||||||The Ghrhr mutation deletes the SOCS2 -/- phenotype.|||Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|06-Aug-2007||0.0|0.0|Unknown||Growth hormone, signal transduction, dwarf, phosphorylation|Yes| 1814.0|SOCS2 / Ghrhr|Un-Socs2 Ghrhr/Wehi||Recessive|growth hormone releasing hormone receptor|Ghrhr|Nil|Ghrfr|MGI:95710|little|Ghrhr|MGI:1856425|6|||||||||||||||||||||||||||||The Ghrhr mutation deletes the SOCS2 -/- phenotype.|||Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|06-Aug-2007||||Unknown||Growth hormone, signal transduction, dwarf, phosphorylation|Yes| 115.0|Ben|C57BL/6JSfdAnu-Tg(IghelMG6)6Ccg/AnuApb|C57BL/6JSfdAnu-Tg(IghelMG6)6Ccg/AnuApb|Dominant||||||||||||||||||||||||||transgene insertion 6, Christopher C Goodnow||High||||||||||B cells express immunoglobulin specific for Hen Egg Lysozyme.||C57BL/6JAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||16||No|06-Feb-2006|Cryopreserved sperm|17.0|0.0|No||Hen Egg Lysozyme, HEL, autoimmunity, tolerance, IgM, IgG, B cell|Yes| 783.0|DYN KO|B6.129-Pdyn(tm1(cre)Czer||Recessive|prodynorphin|Pdyn|Nil|Dyn|MGI:97535|targeted mutation 1, Christoph Schwarzer|Pdyn|MGI:3715202|2||||||||||||||||No|||||||||||||Dyn-/- mice were no different from wild types with regards to body weight and basaland fasting-induced food intake, but fecal output was increased – suggestingdecreased nutrient absorption – and they had significantly less white fat andlost more weight during a 24-hour fast. The neuroendocrine and thermalresponses to fasting were at least as pronounced in Dyn-/- as in wild types, andthere was no stimulatory effect of dynorphin knockout on 24-hour energyexpenditure (kcal heat produced) or physical activity. However, Dyn-/- miceshowed increased circulating concentrations of 3,4-dihydroxyphenlacetic acidand 3,4-dihydroxyphenylglycol, suggesting increased activity of sympatheticnervous system. The respiratory exchange ratio of male but not female Dyn-/-mice was reduced, demonstrating increased fat oxidation. Interestingly,expression of the orexigenic acting neuropeptide Y in the hypothalamic arcuatenucleus was reduced in Dyn-/- mice. However, fasting-induced increases in preprodynorphinexpression in the arcuate nucleus, the paraventricular nucleusand the ventromedial hypothalamus but not the lateral hypothalamus wereabolished by deletion of Y1 but not Y2 receptors. Ablation ofdynorphins results in increases in fatty acid oxidation in male mice, reductionsin adiposity and increased weight loss during fasting||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|8|||No|19-May-2007||0.0|0.0|Unknown||neuropeptide, body weight, adipose, fatty acid, bone density, glucose|Yes| 784.0|NPY KO|B6.129-Npy|MGI:3811718|6||||||||||||||||No|||||||||||||A significant reduction of food intake after 24 or 48 h fasting.High fat diet did not appear to influence bodyweight or food intake in the NPY knockout young adult NPY knockout mice is the increase (≈30%) in mild seizures when exposed to an unfamiliar environmentsignificant increase in an anxiogenic-like phenotype of these mice NPY−/− mice exhibit significant higher ethanol consumption and lower sensitivity to ethanol compared to control mice with NPY-overexpressing mice showing opposite effects The lack of NPY in NPY−/− mice causes an exaggerated autotomy, a self-mutilation behavior possibly related to pain sensation, in agreement with the analgesic effects of NPY.Increased anxiety-related response:* increased levels of anxiety-related behaviors are detected across different test paradigms with males having more pronounced behaviors.* males have about a two-thirds reduction and females have a third to a half reduction in time spent in the center of an open field.* male mice but not female mice show a reduced amount of time in the open arm of an elevated maze test.* mutant males spend less time in the aversive illuminated compartment of a light-dark test with the ratio of distance traveled in lit areas (to total distance traveled) being half that of sex-matched controls.Decreased exploration in new environment:* vertical activities in a new environment are reduced by two-thirds.* similar results are obtained in an elevated maze test.Decreased vertical activity:* vertical activities of mutant mice are reduced by two-third in open field tests.Hypoactivity:* mice of both sexes have reduced motor activity in an open field tests(371.1 movements vs. 585.5 movements for males)* both mutant and wild-type female mice have higher locomotion than male mice of the same genotype (479.8 movements vs. 630.7 movements for wild-type females)* similar results occur in light-dark field testsmutant mice also have longer resting duration time in an open field test (393.3 seconds vs. 347.2 s in wild-type females)* male mice have increased resting times compared to female mice (462.7s vs. 381.6s).* similar resting results occur in light-dark field testsIncreased defecation:* female mice have increased rates of defecation in elevated maze tests (2.8 vs. 0.1 in controls).||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|19-May-2007||0.0|0.0|Unknown||neuropeptide, receptor, obesity, neuronal|Yes| 785.0|PYY KO|B6.129-Pyy||Recessive|peptide YY|Pyy|Nil||MGI:99924|targeted mutation 1, H Herzog|Pyy|MGI:3664105|11||||||||||||||||No|Cre recombinase||||||||||||Abnormal body weight:* male mutants do not show significant changes is body weight on a high-fat diet from 4 weeks of age compared to wild type mice.Increased body weight:* on a normal chow diet, female mutants from 4 to 28 weeks of age have significantly increased body weights compared to wild type (area under curve (AUC): wild type, 505g/24 weeks vs Pyy-null, 554g/24 weeks).* females show a marked increase in body weight between 15 and 28 weeks (AUC: mutants 344 g/15-28 weeks; wild type 307.6 g/ 15-28 weeks).Increased susceptibility to age related obesity:* female mutants, not males, develop late-onset obesityIncreased lean body mass:* both 14-week-old male and female mice show a significant increase in whole body lean mass.Increased circulating insulin level:* male and female chow-fed animals show higher serum insulin levels than controls during glucose tolerance test period.* fasting and glucose-induced serum insulin levels are elevated significantly above those observed in wild type mice fed a high fat diet (mutant >200 pmol/l/min vs wild type ~150 pmol/l/min).Increased circulating insulin-like growth factor I level:* male mutants have significantly higher serum levels of IGF-1 when fed a normal chow dietIncreased circulating testosterone level:* in regular chow-fed male mutants, serum testosterone levels are elevated to a statistically significant degree.Impaired glucose tolerance:on a high-fat diet, male mutants are less glucose-tolerant than wild type but difference disappears when data are normalized for bodyweight.Increased white adipose tissue amount:weight of all white fat adipose tissue deposits in females are increased at 28 weeks of age, consistent with increase in body fat.Decreased adipose tissue amount:* females show a decrease in whole body fat mass at 14 weeksIncreased adipose tissue amount:* chow-fed females show a significant 50% increase in fat mass at 28 weeks of age.Abnormal gonadal fat pad:* males fed on a high-fat diet from 4 weeks of age show significant increases in weight of gonadal white fat depositsAbnormal hypothalamus physiology:* 14-week old female mutants show a 51% increase in Pomc expression vs controls in the arcuate nucleus consistent with reduced food intake, while males show a 21% decrease in Npy expression and a 25% increase in Pomc, associated with increased lean mass and serum hormone levels; Ghrh is increased 32% in the ventromedial hypothalamic nucleus of mutants.Behavior/neurological phenotype:* mutants show no alterations in motor activity over a 14 day observation period||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|19-May-2007||0.0|0.0|Unknown||body weight, neuropeptide, adipose, insulin|Yes| 788.0|Y2f|B6.129-Npy2r||Recessive|neuropeptide Y receptor Y2|Npy2r|Normal|NPY-Y2 receptor|MGI:108418|targeted mutation 1, Herbert Herzog|Npy2r|MGI:2447395|3||||||||||||||||No|||||||||||||Normal||129/Sv x C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|19-May-2007||0.0|0.0|Unknown||neuropeptide, obesity, adipose, receptor|Yes| 1638.0|Chloe|C57BL/6-Acan||Recessive|aggrecan|Acan|Normal|Agc1, Cspg1|MGI:99602|aggrecan; targeted mutation 1, Amanda J Fosang|Acan|MGI:3577026|7||||||||||||||||Yes|||||||||||||Mutants develop normally with no skeletal abnormalities but do not accumulate aggregan in cartilage even though Agc1 is not cleaved by matrix metalloproteases||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|17-Jul-2007||0.0|0.0|Unknown||Cartilage, Skeletal, metalloproteinase (MMP), collagen, cleavage|Yes| 7529.0|Sost|C57BL/NTac-Sost|MGI:3797839|11|||||||||||||||||||||||||||||Skeleton phenotype: • mice exhibit normal osteoclast activity.Increased compact bone area.Abnormal osteoblast morphology:• 3-fold increase in bone formation at the distal femur.• increased bone formation at the endocortical surface of the femur midshaft.Abnormal trabecular bone morphology:• lower trabecular separation, increased osteoblast surface and reduced structure model index at 6 months.Increased trabecular bone volume:• at 6 monthsIncreased bone trabecula number:• at 6 monthsIncreased trabecular bone connectivity density:• at 6 monthsIncreased bone mass:• 3-foldAbnormal bone ossification:• 2-fold increase in bone formation at the distal femur.Abnormal bone mineralization:• increased mineral apposition rateAbnormal compact bone morphology:• tibial cortical bone area, bone thickness, and polar moment of inertia are increased compared to in wild-type mice.Increased bone mass:• in the tibiaAbnormal osteoblast physiology:• osteocyte apoptosis is reduced compared to in wild-type mice||C57BL/6|Yes|Unknown|Yes|Yes|Unknown|Unknown|No|Unknown||||No|04-Dec-2013||0.0|0.0|Unknown||sclerosis, mineralization, osteoclast|Yes| 3586.0|C57BL/6.NOD/Lt-KRN|B6.NOD-Tg(TcraR28,TcrbR28)KRNDim||Dominant||||||||||||||||||||||||||transgene insertion KRN, Diane Mathis|natural TCR alpha and -beta promoter/enhancer elements.|||||||||||A single founder (KRN) in which TCRalpha and Tcrbeta transgenes were cointegrated was identified. These constructs together express a T cell receptor that recognizes the 41-61 peptide of bovine pancreas ribonuclease (RNase) in the context of Ak. These mice develop spontaneous rheumatoid arthritis (RA) joint disease highly reminiscent of man. The trigger for the murine disorder is chance recognition of a NOD-derived major histocompatibility complex (MHC) class II molecule by the transgenic TCR.||C57BL/6 x NOD/Lt|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|05-Aug-2008||0.0|0.0|Yes||Rheumatoid arthritis, autoimmunity, TCR, T cell, CD4, B cell|Yes| 792.0|NPY KO x PYY KO|B6.129-Npy Pyy||Semi-dominant|neuropeptide Y|Npy|Nil||MGI:97374|targeted mutation 1, Tim Karl|Npy|MGI:3811718|6||||||||||||||||Yes|||||||||||||Locomotor and exploratory behaviour was decreased in male and female PYY+NPY-/- mice during the photo- and scotophase.Significant decreases in water and food intake were seen in male and female PYY+NPY-/- mice during the photophase.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|19-May-2007||0.0|0.0|Unknown||neuropeptide, receptor, obesity, insulin, circadian, locomotion|Yes| 792.0|NPY KO x PYY KO|B6.129-Npy Pyy||Semi-dominant|peptide YY|Pyy|Nil||MGI:99924|targeted mutation 1, H Herzog|Pyy|MGI:3664105|Unknown|||||||||||||||||||||||||||||Locomotor and exploratory behaviour was decreased in male and female PYY+NPY-/- mice during the photo- and scotophase.Significant decreases in water and food intake were seen in male and female PYY+NPY-/- mice during the photophase.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|19-May-2007||||Unknown||neuropeptide, receptor, obesity, insulin, circadian, locomotion|Yes| 6678.0|ELTON|B6.129S5-Tpsb2/Ausb||Recessive|tryptase beta 2|Tpsb2|Nil|Mcp-6, Mcp6, Mcpt6, MMCP-6 |MGI:96942|tryptase beta 2; targeted mutation 1, Roberto Adachi|Tpsb2|MGI:3722523|17|||||||||||||||||||||||||||||Increased susceptibility to bacterial infection:*A substantially reduced ability to combat K. pneumoniae infections of their peritoneal cavities.*Produced normal-sized litters, showed no obvious developmental abnormality, and had a normal lifespan when maintained in a pathogen-free animal facility.*The peritoneal mast cells showed no substantial alteration in their size or shape or in the numbers, size and density of their secretory granules.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|02-Dec-2011||0.0|0.0|Unknown||mMCP-6, Tryptase|Yes| 808.0|Y2 KO x NPY KO|B6.129-Npy Npy2r||Recessive|neuropeptide Y receptor Y2|Npy2r|Nil|NPY-Y2 receptor|MGI:108418|targeted mutation 1.1, Herbert Herzog|Npy2r|MGI:2447398|3||||||||||||||||Yes|||||||||||||||129/Sv x C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|21-May-2007||0.0|0.0|Unknown||Neuropeptide, obesity, adipose, neuronal|Yes| 808.0|Y2 KO x NPY KO|B6.129-Npy Npy2r||Recessive|neuropeptide Y|Npy|Nil||MGI:97374|targeted mutation 1, Tim Karl|Npy|MGI:3811718|6|||||||||||||||||||||||||||||||129/Sv x C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|21-May-2007||||Unknown||Neuropeptide, obesity, adipose, neuronal|Yes| 811.0|Y1Y5f|B6.129-Npy1r Npy5r||Recessive|neuropeptide Y receptor Y1|Npy1r|Normal|Npyr, Y1-R|MGI:104963|targeted mutation 1, William P Gray|Npy1r|MGI:3053795|8||||||||||||||||Yes|||||||||||||Normal||C57BL/6 x 129|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|21-May-2007||0.0|0.0|Unknown||Neuropeptide, adipose, body weight, insulin, obesity|Yes| 811.0|Y1Y5f|B6.129-Npy1r Npy5r||Recessive|neuropeptide Y receptor Y5|Npy5r|Unknown|Y5R|MGI:108082||||8|||||||||||||||||||||||||||||Normal||C57BL/6 x 129|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|21-May-2007||||Unknown||Neuropeptide, adipose, body weight, insulin, obesity|Yes| 5632.0|B612954 PKd||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6346.0|Vavbcl69|C57BL/6-Tg(Vav-BCL2)1Jad||Semi-dominant||||||||||||||||||||||||||transgene insertion 1, Jerry M Adams|mouse Vav promoter|Overexpression||||||||||Abnormal lymphocyte cell number:*The ratio of CD4 cells per B cell is 25% to 50% lower than in wild-type mice. Increased B cell number: *5-fold higher in the spleen at 18 weeks. Increased T cell number: *Mice exhibit higher splenic T cell numbers than in wild-type and Tg(BCL2)22Wehi or Tg(BCL2)36Wehi mice. Increased CD4-positive T cell number: *The increase in CD4+ T cells is greater than the increase in CD8+ T cells. Increased CD8-positive T cell number: *The increase in CD4+ T cells is greater than the increase in CD8+ T cells.Abnormal class switch recombination:*The total number of B cells that undergo class switching is 50-fold higher than in wild-type mice.Abnormal somatic hypermutation frequency:*22 of 23 clones isolated from class-switching cells harbor on average about 6 somatic mutations compared to in wild-type cells where no mutations are found.Enlarged spleenAbnormal spleen germinal center morphology:*Mice exhibit a larger pool of cycling B cells with a germinal center phenotype than in wild-type mice.*At 18 weeks, mice exhibit an increased in germinal center size and number compared to in wild-type mice.*However, expansion of germinal centers is dependent on CD4 T cell help. Increased spleen germinal center number: *At 18 weeks. Increased spleen germinal center size: *At 18 weeks.Enlarged lymph nodesGlomerulonephritis:*At 40 weeks, 15% to 25% of mice develop autoimmune glomerulonephritis.Increased tumor incidence:*12% of mice develop plasma cell tumors. Increased lymphoma incidence: *Less than 10% of mice develop lymphoblastic lymphomas. B cell derived lymphoma: *Less than 10% of mice develop large cell B lymphomas. Follicular lymphoma: *At 18 months, 37% to 50% of mice develop monoclonal follicular lymphoma. Increased histiocytic sarcoma incidence: *In less than 10% of mice. Thymic lymphoma: *In less than 10% of mice.Abnormal renal glomerular capsule:*Bowman epithelium proliferates to form crescents in the most advanced cases.Abnormal renal glomerulus morphology:*Mice develop hypercellular glomeruli that contain amorphous, eosinophilic deposits.*Most capillaries are no longer patent.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown||Bcl-2, Hematopoietic system|Yes| 7046.0|FST Flox|B6.129-Fst/MarpApb||Dominant|follistatin|Fst|||MGI:95586|follistatin; targeted mutation 2, Martin M Matzuk|Fst|MGI:3040645|13|||||||||||||||||||||||||||||Normal|Normal|C57BL/6J x 129S7|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|13-Aug-2012|Cryopreserved sperm|70.0|0.0|No||activin, ovary, granulosa|Possibly| 3425.0|Crlf1 KO|B6.129-Crlf1/Wehi||Recessive|cytokine receptor-like factor 1|Crlf1|Nil|CLF-1, CRLM3, cytokine receptor like molecule 3, NR6.1|MGI:1340030|targeted mutation 1, Warren S Alexander|Crlf1|MGI:2387956|8||||||||||||||||Yes|||||||||||||Mice homozygous for a targeted mutation fail to suckle effectively and do not survive beyond 24 hrs after birth. Newborns exhibit reduced numbers of hematopoietic progenitor cells as well as a significant reduction in the number of motoneurons in the lumbar spinal cord and facial nucleus.Neonatal lethality: at birth, homozygotes are present at the expected Mendelian frequency; however, no homozygotes survive beyond 24 hrs after birth.Absent gastric milk in neonates: newborn homozygotes contain no milk in their stomachs.Abnormal suckling behavior: newborn homozygotes open and close their mouths but fail to suckle effectively, despite the absence of gross or histologic abnormalities in brain (i.e. cortex and hippocampus), olfactory bulb, as well as facial or mouth tissues.Decreased motor neuron number:* newborn homozygotes display a significantly reduced number of motoneurons in the lumbar spinal cord, with no apparent change in the brachial or thoracic cord.* newborn homozygotes also exhibit a significant decrease in the number of motoneurons in the facial but not hypoglossal nucleus; sensory neurons of the dorsal root ganglia remain unaffected.Impaired hematopoiesis:* newborn homozygotes display reduced numbers of hemopoietic progenitor cells in the bone marrow and spleen* no differences in the numbers and lineage commitment of progenitor cells are observed in neonatal liver.||129/Sv x C57BL/6|Yes|No|Yes|Yes|No|Yes|No|Poor||||No|15-Jul-2008||0.0|0.0|Unknown||cytokine signalling, haemopoietic progenitor, soluble receptor, suckling|Yes| 5614.0|B16A (Nod Cg Tg)||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 7259.0|HSA-Cre-ER T2|B6.129S2-Tg(ACTA1-cre/ERT2)97.16Mtz/NrosMarpApb|B6.129S2-Tg(ACTA1-cre/ERT2)97.16Mtz/Nros|Semi-dominant||||||||||||||||||||||||||transgene insertion 97.16, Daniel Metzger|human skeletal alpha-actin (ACTA1)|||||||||||Unknown|Normal|C57BL/6|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Good||||No|15-Jan-2013|Cryopreserved sperm|50.0|0.0|Unknown||Cre recombinase, tamoxifen, skeletal muscle|Possibly| 5289.0|B6.TBM.Tg.1142-7.PAR1.KO|C57BL/6-F2r Tg(H2-K-TBM)||Recessive|coagulation factor II (thrombin) receptor|F2r|Nil|Cf2r, Par1, thrombin receptor, ThrR|MGI:101802|coagulation factor II (thrombin) receptor; targeted mutation 1, Andrew J Connolly|F2r|MGI:1857306|13||||||||||||||||No|human thrombomodulin|H2-K|vascular endothelium and neutrophils||||||||||Unknown||C57BL/6|Yes|Unknown|Yes|Yes|Unknown|Yes|No|Unknown||||No|28-Oct-2010||0.0|0.0|Unknown||thrombin, anticoagulant, acute vascular rejection (AVR), collagen, pulmonary thromboembolism, transplantation|Possibly| 3562.0||C57BL/6-Mnt||Recessive|max binding protein|Mnt|Nil|Rox|MGI:109150||||11||||||||||||||||No|||||||||||||Postnatal lethality * homozygotes die within a few days of birthtumorigenesisAltered tumor susceptibility* MEFs infected with c-Myc and H-Ras viruses develop higher numbers of transformed foci* transformed cells capable of anchorage independent growthCellularAbnormal cell physiology * at early passages show improved growth rates and higher cell densities* enter more quickly into S phase* higher apoptosis levels in culture 24 hours after serum withdrawl* faster development of immortalized cell linesGrowth/SizeDecreased embryo size * apparent by E13.5||C57BL/6|No|No|Yes|No|No|Yes|No|Unknown||||No|01-Aug-2008||0.0|0.0|Unknown||Max, tumour suppressor, cell cycle, proliferation, transcription repressor|Yes| 4935.0|Cathepsin-S Knockout|C3H-Ctss/Wehi||Recessive|cathepsin S|Ctss|Nil|Cat S|MGI:107341|cathepsin S; targeted mutation 1, Harold A Chapman|Ctss|MGI:2182133|3||||||||||||||||Yes|||||||||||||Defective CD4 T cell response and humoral responses, but no overt immunodeficiency. Homozygous null mice are resistant to the development of experimental autoimmune myasthenia gravis and showed reduced T and B cell responses to acetylcholine receptor.||C3H|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|24-Nov-2009||0.0|0.0|Unknown||T cell, MHC class II, cysteine proteinase, Humoral resposne, arthritis, germinal centre|Yes| 7432.0|Y20A|B6.129-Atp4b Tg(Atp4b*Y20A)/Ird/Apb||Dominant|ATPase, H+/K+ exchanging, beta polypeptide|Atp4b|Nil|H+,K+-ATPase, H+/K+-ATPase beta, H,K-ATPase-Beta|MGI:88114|ATPase, H+/K+ exchanging, beta polypeptide; targeted mutation 1, Ian R van Driel|Atp4b|MGI:2158258|8|||||||||||||||||Mutated form of H+/K+ ATPase β subunit|CMV|moderate to high||||||||||Gastric Parietal cells of these mice lacked a tubulovesicular compartment, and the H/K ATPase was resident exclusively on the apical plasma membrane. Despite the inability of the H/K ATPase to be endocytosed, the gastric acid secretory response to histamine or an antagonist was very similar to that of wild-type mice,|normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|>10|||No|10-Sep-2013|Cryopreserved sperm|50.0|0.0|Unknown||gastric acid, gastric proton pump, stomach, endocytosis|Possibly| 36.0|Dopey ; ENU3strain:031|B6;NOD-Ddr2/AnuApb|B6;NOD-Ddr2/AnuApb|Recessive|discoidin domain receptor family, member 2|Ddr2||Ntrkr3|MGI:1345277|mutation 1, The Australian National University|Ddr2|MGI:5008734|1|ENSMUSG00000026674|ENSMUST00000170800|Ddr2-202||||||||171932145|6|||TCTCTTCTCTCCTCTTCCCATGGCCTGAGCAGCATGACTGAAGGGCTAGGCCAGTTGACT|Yes|||||||||||||Dwarf, short face||C57BL/6JSfdAnu x NOD/Lt.Cg-H2|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||8||No|06-Feb-2006|Cryopreserved sperm|47.0|0.0|Unknown||Dawrf, ENU, craniofacial|Yes| 1947.0|C57BL/6-TLR-4 ; Teague|B6;129P2-Tlr4/AnuApb|B6;129P2-Tlr4|Recessive|toll-like receptor 4|Tlr4|Nil|lipopolysaccharide response, Lps, Rasl2-8|MGI:96824|toll-like receptor 4; targeted mutation 1, Shizuo Akira|Tlr4|MGI:1860885|4||||||||||||||||Yes|||||||||||||Homozygotes for spontaneous or targeted mutations are hyporesponsive to bacterial lipopolysaccharide and more susceptible to infection by gram negative bacteria.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|01-Sep-2007|Cryopreserved sperm|140.0|0.0|Unknown||infection, T cell, inflammation, eosinophil, hyperresponsiveness|Yes| 5586.0|3G||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 4704.0|NODβ2M-/- β2Mb homozygous 8.3TCRαβ|NOD.B6-B2m Tg(B2mb)1Rms Tg(TcraTcrbNY8.3)1Pesa/MarpApb||Recessive|beta-2 microglobulin|B2m|Unknown|beta 2 microglobulin, beta2-m, Ly-m11|MGI:88127|targeted mutation 1, Rudolf Jaenisch|B2m|MGI:1927183|2||||||||||||||||Yes|transgene insertion 1, Robyn M Slattery||||||||||||||NOD|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|07-Apr-2009|Cryopreserved sperm|50.0|0.0|Unknown||Autoimmunity, insulin, MHC II, beta cell|Yes| 4704.0|NODβ2M-/- β2Mb homozygous 8.3TCRαβ|NOD.B6-B2m Tg(B2mb)1Rms Tg(TcraTcrbNY8.3)1Pesa/MarpApb||Recessive||||||||||||||||||||||||||transgene insertion 1, Pere Santamaria||||||||||||||NOD|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|07-Apr-2009|Cryopreserved sperm|||Unknown||Autoimmunity, insulin, MHC II, beta cell|Yes| 1761.0|Caspase-9 knockout|C57BL/6-Casp/Wehi||Recessive|caspase 9|Casp9|Nil|Caspase-9, ICE-LAP6, Mch6|MGI:1277950|targeted mutation 1, Richard A Flavell|Casp9|MGI:2158755|4||||||||||||||||No|||||||||||||Perinatal lethality: normal mendelian ratio at E16.5 but fewer than 3% of the pups born are homozygotes.Abnormal neural tube closure: failure of neural tube closure in hindbrain region apparent by E10.5 and persists.Abnormal brain morphology.Abnormal brain development: enlargement of the proliferative zone in the forebrain and midbrain with resultant protrusion of brain mass.Abnormal embryonic neuroepithelial layer differentiation:* lacking pyknotic clusters* lamina terminalis of the forebrain is thicker with increased number and density of cells.Abnormal forebrain development.Abnormal telencephalon development: E16.5 expanded midbrain displaces telencephalic vesicles.Exencephaly: by E16.5 prominent exencephaly of the entire cranial tissues with enlarged and irregularly shaped protruding brain masses.Abnormal brain ventricle morphology: stenosis of the cerebral ventricles, lateral and third ventricles obstructed by E13.5.Abnormal lateral ventricle morphology.Abnormal third ventricle morphology.Abnormal telencephalon morphology: heterotopias and discontinuities of the proliferative ventricular zone lead to invagination and complete interruption of the telencephalic wall.Abnormal cerebral cortex morphology.Abnormal midbrain morphology.Decreased neuron apoptosis:* E13 olfactory epithelium has lower levels of olfactory receptor neuron apoptosis than normal.* absence of activated caspase 3 in the developing brain as assessed by immunohistochemistry with antibody CM1.* nearly 10 fold reduction in TUNEL-positive cells in E12.5 neuroepithelium.* fewer TUNEL-positive cells in the E16.5 spinal cord and E12.5 dorsal root ganglia although there is no change in TUNEL staining in E12.5 liver.Normal apoptosis in interdigital webbing retraction.Abnormal thymocyte apoptosis: thymocytes are delayed in apoptotic response to anti-CD3 + andi-CD28, etoposide, gamma irradiation, and dexamethasone, but have normal apoptotic response to Fas stimulation.||C57BL/6|No|No|Yes|No|No|Yes|No|Unknown|10|||No|02-Aug-2007||0.0|0.0|Unknown||Bcl-2, mitochondria, apoptosome, caspase, Apaf-1, caspase-2|Yes| 841.0|OT2; OTII|C57BL/6-Tg(TcraTcrb)425Cbn||Dominant||||||||||||||||||||||||||transgene insertion 425, Frank Carbone||||||||||||Homozygous mice are viable and fertile. In these mice there is a four-fold increase in the CD4 to CD8 peripheral T-cell ratio, and lymph node T-cells demonstrate a dose-dependent proliferative response to the specific ovalbumin ligand.T cells express T cell receptor specific for chicken ovalalbumin residues 323 - 339 in the context of H2-Ab1 (I-A)Transgenic mice express the mouse alpha-chain and beta-chain T-cell receptor that pairs with the CD4 coreceptor and is specific for chicken ovalbumin 323-339 in the context of I-A b. Homozygous transgenic mice are viable and fertile. In these mice there is a four-fold increase in the CD4 to CD8 peripheral T-cell ratio, and lymph node T-cells demonstrate a dose-dependent proliferative response to the specific ovalbumin ligand.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|23-May-2007||0.0|0.0|Unknown||receptor (TCR), CD4, ovalbumin, thymic selection|Yes| 7047.0|βA Flox|B6.129S7-Inhba/MarpApb||Dominant|inhibin beta-A|Inhba||activin|MGI:96570|inhibin beta-A; targeted mutation 3, Martin M Matzuk|Inhba|MGI:3758877|13|||||||||||||||||||||||||||||Normal|Normal|C57BL/6 x 129S7|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|13-Aug-2012|Cryopreserved sperm|50.0|0.0|No||activin, ovary|Possibly| 4602.0||MRL/MpJ-Fas/MarpApb||Recessive|Fas (TNF receptor superfamily member 6)|Fas|Unknown|APO-1, CD95, TNFR6, Tnfrsf6|MGI:95484|lymphoproliferation|Fas|MGI:1856334|19||||||||||||||||Yes|||||||||||||Premature death, decreased B cell number, decreased CD4 and CD8 -positive T cell number, decreased activated T cell number, increased double-negative T cell number, enlarged spleen and lymph nodes, abnormal leukocyte rolling - increased adhesion, development of anti-nuclear antibodies, glomerulonephritis. ||MRL/MpJ|Yes|No|Yes|Yes|No|Yes|No|Unknown||||No|13-Mar-2009|Cryopreserved sperm|115.0|0.0|Unknown||autoimmunity, T cell, B cell, leukocyte adhesion, glomerulonephritis|Yes| 7260.0|MLC-IGF/F08 (MLC=mIGF-1-8) |B6(Cg)-Tg(Myl1-Igf1)1Nros/MarpApb|B6(Cg)-Tg(Myl1-Igf1)1Nros|Semi-dominant||||||||||||||||||||||||||transgene insertion 1, Naida Rosenthal|myosin light chain|||||||||||Unknown|Normal|C57BL/6|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Good||||No|15-Jan-2013|Cryopreserved sperm|50.0|0.0|Unknown||Igf1, muscle|Possibly| 1738.0|VavP-BCL2-45|C57BL/6-Tg(Vav-BCL2)45Jad/Wehi||Dominant|||||||||Unknown||||||||||||||||No|transgene insertion 45, Jerry M Adams|mouse Vav promoter|High, haemopoietic cells|||||||||||Abnormal lymphocyte cell number:* the ratio of CD4 cells per B cell is 25% to 50% lower than in wild-type mice.Increased B cell number: 5-fold higher in the spleen at 18 weeksIncreased T cell number:* mice exhibit higher splenic T cell numbers than in wild-type and Tg(BCL2)22Wehi or Tg(BCL2)36Wehi mice.Increased CD4-positive T cell number:* the increase in CD4+ T cells is greater than the increase in CD8+ T cells.Increased CD8-positive T cell number:* the increase in CD4+ T cells is greater than the increase in CD8+ T cells.Abnormal class switch recombination:* the total number of B cells that undergo class switching is 50-fold higher than in wild-type mice.Abnormal somatic hypermutation frequency:* 22 of 23 clones isolated from class-switching cells harbor on average about 6 somatic mutations compared to in wild-type cells where no mutations are found.Enlarged spleen:Abnormal spleen germinal center morphology:* mice exhibit a larger pool of cycling B cells with a germinal center phenotype than in wild-type mice.* at 18 weeks, mice exhibit an increased in germinal center size and number compared to in wild-type mice.* however, expansion of germinal centers is dependent on CD4 T cell help.Increased spleen germinal center number: at 18 weeks.Increased spleen germinal center size: at 18 weeks.Enlarged lymph nodes.Glomerulonephritis:* at 40 weeks, 15% to 25% of mice develop autoimmune glomerulonephritis.Increased tumor incidence:* 12% of mice develop plasma cell tumorsLymphoma: less than 10% of mice develop lymphoblastic lymphomas.B cell derived lymphoma:* less than 10% of mice develop large cell B lymphomasFollicular lymphoma:* at 18 months, 37% to 50% of mice develop monoclonal follicular lymphoma.Thymic lymphoma: in less than 10% of miceHistiocytic sarcoma: in less than 10% of mice.|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|01-Aug-2007||0.0|0.0|Unknown||B cell, Bcl-2, Vav, progenitor, lymphoma, germinal centre|Yes| 847.0|Traf2 floxed|C57BL/6-Traf2||Dominant|Tnf receptor-associated factor 2|Traf2|Normal||MGI:101835|targeted mutation 1, Robert Brink|Traf2|MGI:3511494|2||||||||||||||||Yes|||||||||||||Normal||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|23-May-2007||0.0|0.0|Unknown||B cell, TNF, receptor, lymph node|Yes| 7280.0|B6 gamma -/-|C57Bl/6-Fcer1g/J|HOGA|Semi-dominant|FceR gamma chain|FceRIg|Nil||MGI:95496|Fc receptor, IgE, high affinity I, gamma polypeptide; targeted mutation 1, Jeffrey V Ravetch|Fcer1g|MGI:2162818|1||||||||||Unknown to Unknown|||||||||||||||||||normal|normal|C57BL/6J|Yes|Yes|Yes|Yes|Yes|Yes|Yes|Good|12|||Yes|15-Feb-2013|Cryopreserved sperm|50.0|0.0|Yes|immune complex disease and allergy|Fc receptor, antibody, immune complex, inflammation, arthritis, thrombocytopenia, osteopetrosis, allergy|Possibly| 75.0|Theodor|ENU4AT:011||Recessive|Unknown||||||||Unknown||||||||||||||||Yes|||||||||||||Low IgG2a response to B. pertussis|||Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|18-Aug-2004|Cryopreserved sperm|30.0|0.0|Unknown||ENU, Wellcome Trust, memory, immunization, T cell, B cell|Yes| 4601.0||NOD.B6-Socs3/WehiApb||Dominant|suppressor of cytokine signaling 3|Socs3|Normal|CIS3, Cish3, cytokine-inducible SH2 protein 3, E2a-Pbx1 target gene in fibroblasts 10, EF-10, SOCS-3, SSI-3, STAT-induced STAT inhibitor 3|MGI:1201791|targeted mutation 2, Warren S Alexander|Socs3|MGI:2663917|11||||||||||||||||Yes|||||||||||||Normal. When crossed with Cre expressing strain allows deletion of Socs3 in tissue specific manner.||NOD|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|7||Socs3 x NOD|No|13-Mar-2009|Cryopreserved sperm|130.0|0.0|Unknown||cytokine signalling, G-CSF, STAT3, neutrophil|Yes| 843.0|SW{HEL}-H|C57BL/6-Igh||Dominant||||||||||||||||||||||||||immunoglobulin heavy chain complex; targeted mutation 1, Robert Brink||||||||||||B cells express immunoglobulin Heavy chain that recognises hen egg lysozyme.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|23-May-2007||0.0|0.0|Unknown||Immunoglobulin, Hen egg lysozyme (HEL), self-tolerance, autoimmunity, B cell|Yes| 4598.0||B6.129-Apc Myb||Semi-dominant|adenomatosis polyposis coli|Apc|Nil|Min|MGI:88039|multiple intestinal neoplasia|Apc|MGI:1856318|18||||||||||||||||Yes|||||||||||||For Myb Homozygous null fetuses are severely anemic due to defects in fetal hepatic hematopoiesis. Embryonic lethal at E15.5For Apc Homozygotes are embryonic lethal.|For Apc heterozygous mutants develop intestinal polyps and colorectal cancer, associated with anemia from intestinal bleeding.For Myb are viable and fecund|C57BL/6 x 129|No|No|Yes|No|No|Yes|No|Unknown|||Apc Myb x Apc Myb|No|13-Mar-2009||0.0|0.0|Unknown||colon, transcription factor, epithelium, intestinal polyps|Yes| 4598.0||B6.129-Apc Myb||Semi-dominant|myeloblastosis oncogene|Myb|Unknown|c-myb|MGI:97249|targeted mutation 1, S Steven Potter|Myb|MGI:2662859|10|||||||||||||||||||||||||||||For Myb Homozygous null fetuses are severely anemic due to defects in fetal hepatic hematopoiesis. Embryonic lethal at E15.5For Apc Homozygotes are embryonic lethal.|For Apc heterozygous mutants develop intestinal polyps and colorectal cancer, associated with anemia from intestinal bleeding.For Myb are viable and fecund|C57BL/6 x 129|No|No|Yes|No|No|Yes|No|Unknown|||Apc Myb x Apc Myb|No|13-Mar-2009||||Unknown||colon, transcription factor, epithelium, intestinal polyps|Yes| 6426.0|Blys2tg|B6.Cg-Tg(Tnfsf13b)1Fma/Ausb||Dominant||||||||||||||||||||||||||transgene insertion 1, Fabienne Mackay|human liver-specific alpha-1-antitrypsin promoter|||||||||||Increased B cell number:*Splenic B cell numbers are about twice that of controls. Increased transitional stage B cell number: *Numbers of T1 B cells in the spleen are increased almost 3-fold while T2 numbers are almost about doubled. Increased marginal zone B cell number: *The number of splenic marginal zone B cells is increased by about 3-fold.Abnormal B cell activation:*B cells have a vigorous response to T cell independent antigens producing much higher levels of IgG1, IgG2a, IgG2b, IgG3, and IgA class immunoglobulins than controls.Abnormal spleen marginal zone morphology:*The size of the marginal zone is increasedAbnormal marginal zone B cell physiology:*Marginal zone B cells (MZB) mediate autoimmune disease in these transgenic mice as demonstrated by auto-antibody production when MZB are transferred into transgenic mice on a B-cell deficient background.*MZB from transgenic mice have higher integrin adhesion activity.Increased anti-double stranded DNA antibody level:*Anti-dsDNA antibodies of the IgM class, IgA class, and all IgG subclasses are found in circulation.*Titers of these auto-antibodies increase with.*Splenectomy at three weeks of age significantly reduces IgG auto-antibodies and partially reduces auto-antibodies in the other subclasses.Glomerulonephritis:*Kidneys of 10-month old mice have necrotic lesions.*Immunohistology of kidneys with severe lesions reveal numerous glomerular deposits of IgG.Proteinuria:*All 8-month old mice have proteinuria in their urine with most having 100-300 mg/dl.|||Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown||BAFF, Autoimmune disorders|Yes| 848.0|Traf3 KO|C57BL/6-Traf3||Recessive|Tnf receptor-associated factor 3|Traf3|Unknown|CAP-1, CD40bp, CRAF1, LAP1|MGI:108041|targeted mutation 1.1, Robert Brink|Traf3|MGI:3777325|12||||||||||||||||Yes|||||||||||||Not analysed||C57BL/6|Yes|Unknown|Yes|Yes|Unknown|Yes|No|Unknown||||No|23-May-2007||0.0|0.0|Unknown||TNF, receptor, lymphocyte, hypoglycaemia|Yes| 6876.0|BRINP3 Targeted|C57BL/6-Fam5c/Marp||Recessive|family with sequence similarity 5, member C|Fam5c||DBC3, B830045N13Rik|MGI:2443035||||1|||||||||||||||||||||||||||||Normal|Normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|23-Apr-2012|Cryopreserved sperm|50.0|0.0|Unknown|||Possibly| 1712.0|Rag2 gammaC|C57BL/6-IL2rg Rag2||Recessive|interleukin 2 receptor, gamma chain|Il2rg|Nil|[g]c, CD132, common cytokine receptor gamma chain, common gamma chain, gamma C receptor, gamma(c), gc|MGI:96551|interleukin 2 receptor, gamma chain; targeted mutation 1, University of Cologne|Il2rg|MGI:1861947|X||||||||||||||||Yes|||||||||||||Severely immunocompromised throughout life.The common gamma (gc) KO mouse lacks functional receptors for many cytokines including IL-2, IL-4, IL-7, IL-9, and IL-15. As a consequence lymphocyte development is greatly compromised. The mouse lacks Natural Killer (NK) cells and produces only a small number of T and B cells. To eliminate the residual T and B cells this mouse was crossed to the recombinase activating gene 2 (Rag-2) deficient mouse. The double knock-out should now lack T cells, B cells, and NK cells. A preliminary analysis of this strain showed no detectable NK1.1+ cells, B220+ B cells or Thy1+ T cells in the spleen. A small number of the 1-3 million cells obtained were CD45 low and probably are cells in the macrophage/monocyte lineage. Functional tests, performed by Drs. Elias Hadaad and Pierre Henkart of NIH, for NK killing activity in the spleen, with or without poly I:C stimulation, were negative.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|26-Jul-2007||0.0|0.0|Unknown||T cell, B cell, immunodeficient, transplantation|Yes| 1712.0|Rag2 gammaC|C57BL/6-IL2rg Rag2||Recessive|recombination activating gene 2|Rag2|Unknown|Rag-2|MGI:97849|recombination activating gene 2; targeted mutation 1, Frederick W Alt|Rag2|MGI:1858556|2|||||||||||||||||||||||||||||Severely immunocompromised throughout life.The common gamma (gc) KO mouse lacks functional receptors for many cytokines including IL-2, IL-4, IL-7, IL-9, and IL-15. As a consequence lymphocyte development is greatly compromised. The mouse lacks Natural Killer (NK) cells and produces only a small number of T and B cells. To eliminate the residual T and B cells this mouse was crossed to the recombinase activating gene 2 (Rag-2) deficient mouse. The double knock-out should now lack T cells, B cells, and NK cells. A preliminary analysis of this strain showed no detectable NK1.1+ cells, B220+ B cells or Thy1+ T cells in the spleen. A small number of the 1-3 million cells obtained were CD45 low and probably are cells in the macrophage/monocyte lineage. Functional tests, performed by Drs. Elias Hadaad and Pierre Henkart of NIH, for NK killing activity in the spleen, with or without poly I:C stimulation, were negative.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|26-Jul-2007||||Unknown||T cell, B cell, immunodeficient, transplantation|Yes| 647.0|AMY|Un-Tg(APPswe,PSEN1dE9)85Dbo||Dominant||||||||||||||||||||||||||transgene insertion 85, David R Borchelt|mouse prion promoter||||||||||||Amyloidosis.Amyloid beta deposits.||Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|25-Apr-2007||0.0|0.0|Yes|Alzheimer disease|alzheimer's disease, amyloid beta protein, plaque|No| 186.0|P2-IRES-tauLacZ|B6.129-Olfr17||Dominant|olfactory receptor 17|Olfr17|Unknown|GA_x6K02T2PBJ9-9470146-9471093, MOR263-5, P2|MGI:109148|targeted mutation 1, Peter Mombaerts|Olfr17|MGI:2179510|7||||||||||||||||No|||||||||||||P2 odorant receptor neurons express LacZ||C57BL/6 x 129|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|17-Apr-2006||0.0|0.0|Unknown||odorant receptor, LacZ, olfactory|Yes| 187.0||VR1-IRES-tau:GFP||Dominant||||||||||||||||||||||||||||||||||||||A subpopulation of vomeronasal neruons innervating the rostral accessory olfactory bulb express GFP||C57BL/6 x 129|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|17-Apr-2006||0.0|0.0|Unknown||GFP, olfactory, neuron|Yes| 185.0||OMP-tau:GFP||Recessive|olfactory marker protein|Omp|Nil||MGI:97436|targeted mutation 3, Peter Mombaerts|Omp|MGI:3692201|7||||||||||||||||Yes|||||||||||||All primary olfactory neurons express GFP||129/Sv x C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|17-Apr-2006||0.0|0.0|Unknown||GFP, olfactory neurons|Yes| 1787.0|Bax / Bak knockout|129-Bak1 Bax/Wehi||Recessive|BCL2-antagonist/killer 1|Bak1|Nil|Bak, N-Bak|MGI:1097161|targeted mutation 1, Craig B Thompson|Bak1|MGI:2159364|17||||||||||||||||Yes|||||||||||||Mice lacking bax display limited phenotypic abnormalities. Bak(-/-) mice were found to be developmentally normal and reproductively fit and failed to develop any age-related disorders. However, when Bak-deficient mice were mated to Bax-deficient mice to create mice lacking both genes, the majority of bax(-/-) bak(-/-) animals died perinatally with fewer than 10% surviving into adulthood. bax(-/-)bak(-/-) mice displayed multiple developmental defects, including persistence of interdigital webs, an imperforate vaginal canal, and accumulation of excess cells within both the central nervous and hematopoietic systems. Thus, Bax and Bak have overlapping roles in the regulation of apoptosis during mammalian development and tissue homeostasis. Those that survive are runted and grey.||129/Sv|No|No|Yes|No|No|Yes|No|Unknown||||No|03-Aug-2007||0.0|0.0|Unknown||Bcl2, interdigital web, hyperplasia|Yes| 1787.0|Bax / Bak knockout|129-Bak1 Bax/Wehi||Recessive|Bcl2-associated X protein|Bax|Unknown||MGI:99702|targeted mutation 1, Stanley J Korsmeyer|Bax|MGI:1857429|7|||||||||||||||||||||||||||||Mice lacking bax display limited phenotypic abnormalities. Bak(-/-) mice were found to be developmentally normal and reproductively fit and failed to develop any age-related disorders. However, when Bak-deficient mice were mated to Bax-deficient mice to create mice lacking both genes, the majority of bax(-/-) bak(-/-) animals died perinatally with fewer than 10% surviving into adulthood. bax(-/-)bak(-/-) mice displayed multiple developmental defects, including persistence of interdigital webs, an imperforate vaginal canal, and accumulation of excess cells within both the central nervous and hematopoietic systems. Thus, Bax and Bak have overlapping roles in the regulation of apoptosis during mammalian development and tissue homeostasis. Those that survive are runted and grey.||129/Sv|No|No|Yes|No|No|Yes|No|Unknown||||No|03-Aug-2007||||Unknown||Bcl2, interdigital web, hyperplasia|Yes| 645.0||IL-12 KO||Dominant|not sure if alpha or beta||Unknown||||||1||||||||||||||||Yes||||||||||||||||No|No|No|Yes|No|Yes|No|Unknown||||No|25-Apr-2007||0.0|0.0|Unknown|||Yes| 7345.0|PTEN lox P locus/MMTV CRE|B6.129P2-Pten Tg(MMTV-Cre)4Mam/Apb||Dominant|phosphatase and tensin homolog|Pten|||MGI:109583|phosphatase and tensin homolog; targeted mutation 2, Tak W Mak|Pten|MGI:2182005|19|||||||||||||||||transgene insertion 4, Lothar Hennighausen|mouse mammary tumor virus (MMTV) long terminal repeat|||||||||||Neoplastic proliferation of prostate and skin tissues|Susceptible to tumour development|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|28-May-2013|Cryopreserved sperm|45.0|0.0|Unknown||Cre recombinase, pten, prostate, hyperplasia|Yes| 7666.0|Depdc5-w|B6;C-Depdc5/AnuApb|B6.Cg;C-Depdc5/AnuApb|Recessive|DEP domain containing 5|Depdc5|Unknown||MGI:2141101|DEP domain containing 5; mutation 1, Walter and Eliza Hall Institute|Depdc5|MGI:5648439|5|ENSMUSG00000021431|ENSMUST00000091641|Snrnp48-201|794|828|A to G|ENSMUSE00000117800|7|265|Aspartic acid to Glycine|||||CTGGCAGGAAGAGCAGGGGAGAGCAGGAGACGCTGCTGAGAAGAATGAAGAAAGGCGGTCA||||||||||||||Unknown|Unknown|C57BL/6NCrlAnu|Yes|Unknown|Yes|Yes|Unknown|Yes|No|Good||G3|Het x Het|No|28-Apr-2014|Cryopreserved sperm|72.0|0.0|Unknown||ENU|Possibly| 175.0|OVE550|FVB/N-Tg(Cryaa-Tgfbr2*)550/Apb||Dominant||||||||||||||||||||||||||truncated TGFβ receptor II, kinase deficient|αA-crystallin, Cryaa|||||||||||Nuclear cataract, characterised by rapid apoptosis and death of terminally differentiating lens fibres cells at E18.||FVB/N|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|17-Apr-2006|Cryopreserved sperm|50.0|0.0|Unknown||cataract, lens fibres, eye|Yes| 7084.0|MommeD33|FVB/NJ-MommeD33 Tg(Hba1-Gfp)1Ew||Semi-dominant|suppressor of variegation 3-9 1|Su-var39h|Unknown||MGI:1099440|suppressor of variegation 3-9 1; modifier of murine metastable epialleles, D33|Suv39h1|MGI:5515387|X||||||||||Unknown to Unknown|||||||transgene insertion 1, Emma Whitelaw|human alpha-globin promoter and enhancer region|||||||||||homo viable|Normal|FVB/NJ|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|||MommeD33<+/->;Tg(Hba1-Gfp)1Ew x Tg(Hba1-Gfp)1Ew|No|14-Sep-2012|Cryopreserved sperm|30.0|0.0|Unknown||ENU, epigenetics, modifier|Possibly| 5214.0|mIMPα4FL (low level expression)|C57BL/6-Tg(EGFP-Kpna4 full length)low||Dominant|karyopherin (importin) alpha 4|Kpna4|Unknown|IPOA3|MGI:1100848||||Unknown||||||||||||||||Yes|EGFP fused to full length Kpna4|Protamine 1|low level expression||||||||||Fertility maybe reduced||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|30-Aug-2010|Cryopreserved sperm|40.0|0.0|Unknown||importin, testis, nuclear transport, fertility, protamine 1|No| 4099.0||KRN:187||Recessive|||||||||Unknown||||||||||||||||Yes|transgene insertion KRN, Diane Mathis|Natural TCR alpha and -beta promoter/enhancer elements.|||||||||||Hypo response post arthritogenic serum transfer||C57BL/6 x NODk x C57BL/10 x Balb/b|Yes|Yes|Yes|Yes|Yes|Yes|No|Poor||1||No|04-Dec-2008|Cryopreserved sperm|75.0|0.0|Yes||Autoimmunity, Arthritis, KRN, ENU, Serum transfer|No| 1812.0|C57BL/6. Socs2 KO|C57BL/6-Socs2/Wehi||Recessive|suppressor of cytokine signaling 2|Socs2|Nil|CIS2, Cish2, cytokine-inducible SH2 protein 2, D130043N08Rik, JAB, SOCS-2, SSI-2, STAT-induced STAT inhibitor 2|MGI:1201787|targeted mutation 1, Walter and Eliza Hall Institute of Medical Research|Socs2|MGI:1934557|10||||||||||||||||Yes|||||||||||||SOCS-2(-/-) mice grew significantly larger than their wild-type littermates. Increased body weight became evident after weaning and was associated with significantly increased long bone lengths and the proportionate enlargement of most organs. Characteristics of deregulated growth hormone and insulin-like growth factor-I (IGF-I) signalling, including decreased production of major urinary protein, increased local IGF-I production, and collagen accumulation in the dermis, were observed in SOCS-2-deficient mice, indicating that SOCS-2 may have an essential negative regulatory role in the growth hormone/IGF-I pathway. ||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|06-Aug-2007||0.0|0.0|Unknown||Growth, weight, growth hormone, STAT, JAK, gigantism|Yes| 5552.0|Dravid|C57BL/6-Prf1 Tg(TcraTcrb)1100Mjb/AnuApb||Recessive|perforin 1 (pore forming protein)|Prf1|Nil|perforin, Pfp, Prf-1|MGI:97551|targeted mutation 1, Sandoz Pharmaceutical|Prf1|MGI:1857235|10|||||||||||||||||transgene insertion 1100, Michael J Bevan||High - 49 Copies||||||||||Unknown||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|10-Aug-2011|Cryopreserved sperm|45.0|0.0|Unknown||T cell receptor, CD8, ovalbumin, Natural Killer cell|No| 7344.0|PBCre|B6;DBA2-Tg(Pbsn-cre)4Prb/Apb||Dominant||||||||||||||||||||||||||transgene insertion 4, Pradip Roy-Burman|rat Pbsn|||||||||||| Cre recombinase is expressed postnatally in prostatic epithelium with the highest level of expression in the lateral lobe of the prostate gland. A very low level of transgene expression was detected in the seminal vesicles, testes, and ovaries.|(C57BL/6 x DBA/2)F1|No|Yes|Unknown|No|Yes|Unknown|No|Unknown||||No|28-May-2013|Cryopreserved sperm|54.0|0.0|Unknown||Cre recombinase, prostate, epithelium|Possibly| 706.0||NOD.Cg-Igh-6 Tg(IghelMD4)4Ccg/Dvs||Recessive|immunoglobulin heavy chain 6 (heavy chain of IgM)|Igh-6|Nil|BCR, Ig mu, Igh-M, Igh6, IgM, muH, muMT|MGI:96448|targeted mutation 1, University of Cologne|Igh-6|MGI:1857187|12||||||||||||||||Yes|||||||||||||Do not express endogenous IgM, viable, fertile, normal in size, and do not display any gross physical or behavioral abnormalities.All B lymphocytes in NOD.Igh-6 deficient transgenic mice express Ig molecules specific for HEL.||NOD|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|02-May-2007||0.0|0.0|Unknown||autoimmunity, B cell, immunoglobulin, Hen egg lysozyme|Yes| 6775.0|DBC3 Flpe ; BRINP3 Flpe|C57BL/6-Brinp3/Marp||Recessive|family with sequence similarity 5, member C|Fam5c|Normal|DBC3, Fam5c, Brinp3|MGI:2443035|bone morphogenetic protein/retinoic acid inducible neural specific 3; targeted mutation 1.1, Phillip I Bird|Brinp3|MGI:5604621|1|||||||||||||||||||||||||||||Normal|Normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Excellent||||No|11-Jan-2012|Cryopreserved sperm|50.0|0.0|Unknown|||Possibly| 4079.0||ENU6PH:058||Recessive|||||||||Unknown||||||||||||||||Yes|||||||||||||Hypo IgE response following allergic challenge.||C57BL/6 x C57BL/10|Yes|Yes|Yes|Yes|Yes|Yes|No|Poor||6||No|04-Dec-2008|Cryopreserved sperm|15.0|0.0|Unknown||allergic challenge, ENU, Immunoglobulin, IgE|No| 1785.0|Cathepsin D knockout|Un-Ctsd||Recessive|cathepsin D|Ctsd|Nil|CatD, CD|MGI:88562|targeted mutation 1, Cristoph Peters|Ctsd|MGI:2182078|7||||||||||||||||Yes|||||||||||||Mice homozygous for a null mutation die in a state of anorexia at ~P26, displaying severe atrophy of the intestinal mucosa, and massive destruction of the thymus and spleen with loss of T and B cells; near the terminal stage, affected mice have seizures, display retinal atrophy, and become blind.|||Yes|No|Yes|Yes|No|Yes|No|Unknown||||No|03-Aug-2007||0.0|0.0|Unknown||atrophy, intestinal mucosa, thymus, seizures, retinal, T cell, B cell|Yes| 1816.0|Oct2 deltaC|B6.129-Pou2f2/Wehi||Recessive|POU domain, class 2, transcription factor 2|Pou2f2|Normal|Oct-2, Oct2a, Oct2b, Otf-2, Otf2|MGI:101897|POU domain, class 2, transcription factor 2; targeted mutation 1, Lynn M Corcoran|Pou2f2|MGI:3037094|7||||||||||||||||No|||||||||||||Neonatal lethality: homozygous mice die shortly after birth.Decreased B cell number: in adult Rag-1 deficient mice in which the immune system has been reconstituted with fetal liver stem cells from mutants the proportion of B cells is significantly reduced.Decreased B-1 B cell number: these mice also lack peritoneal B-1 cells.Arrested B cell differentiation: in adult Rag-1 deficient mice in which the immune system has been reconstituted with fetal liver stem cells from mutants peripheral B cells appear mature but behave as immature B cells in response to B cell receptor signaling.Decreased immunoglobulin level: in adult Rag-1 deficient mice in which the immune system has been reconstituted with fetal liver stem cells from mutants an 8 - 10 fold reduction in immunoglobulin concentrations is seen.||C57BL/6|No|No|Yes|No|No|Yes|No|Unknown||||No|06-Aug-2007||0.0|0.0|Unknown||POU domain, B cell, Lymphocyte, C terminal domain, DNA binding|Yes| 5593.0|A2Kb ||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5594.0|Actm0va (actin0va)||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 703.0|NR4MD4|NOD.NOR-(D4Mit31-D4Mit310) Tg(IghelMD4)4Ccg||Dominant|insulin dependent diabetes susceptibility 9|Idd9|Unknown|Idd-9|MGI:96411|NOR/LtJ|Idd9|MGI:3582457|4||||||||||||||||Yes|transgene insertion 4, Christopher C Goodnow||High||||||||||||NOD|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|02-May-2007||0.0|0.0|Unknown||Immunoglobulin, diabetes, autoimmunity, hen egg lysozyme (HEL)|Yes| 1730.0|B6 Bclw -/- 228|B6.129-Bcl2l2/Wehi||Recessive|Bcl2-like 2|Bcl2l2|Nil|Bcl-w, bclw, Gtrgal2, Gtrosa41|MGI:108052|targeted mutation 1, Suzanne Cory|Bcl2l2|MGI:2158430|14||||||||||||||||Yes|||||||||||||Most tissues exhibited typical histology, and hematopoiesis was unaffected, presumably due to redundant function with other pro-survival family members. Although female reproductive function was normal, the males were infertile. The testes developed normally, and the initial, prepubertal wave of spermatogenesis was largely unaffected. The seminiferous tubules of adult males, however, were disorganized, contained numerous apoptotic cells, and produced no mature sperm. Both Sertoli cells and germ cells of all types were reduced in number, the most mature germ cells being the most severely depleted.|||Yes|Yes|Yes|Yes|No|Yes|Yes|Unknown||||No|01-Aug-2007||0.0|0.0|Unknown||spermatogenesis, seminiferous tubules, Sertoli cells, Germ cells, pro-survival|Yes| 774.0|NIDM5MD4ML5|NOD-Idd5 Tg(IghelMD4)4Ccg Tg(ML5sHEL)5Ccg||Dominant|insulin dependent diabetes susceptibility 5|Idd5|Nil|Idd-5|MGI:2389023|C57BL/10|Idd5|MGI:2389023|1||||||||||||||||Yes|transgene insertion 4, Christopher C Goodnow||High|||||||||||||Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|18-May-2007||0.0|0.0|Unknown||Autoimmunity, B cell, Hen Egg Lysozyme (HEL), immunoglobulin|Yes| 774.0|NIDM5MD4ML5|NOD-Idd5 Tg(IghelMD4)4Ccg Tg(ML5sHEL)5Ccg||Dominant||||||||||||||||||||||||||transgene insertion 5, Christopher C Goodnow|mouse metallothionein I||||||||||||||Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|18-May-2007||||Unknown||Autoimmunity, B cell, Hen Egg Lysozyme (HEL), immunoglobulin|Yes| 7609.0|Pax7|B6.D2-Tg(Pax7-EGFP)#Tajb/Ausb||Dominant||||||||||||||||||||||||||transgene insertion, Shahragim Tajbakhsh|Pax7|muscle||||||||||Expression of nGFP in muscle satellite cells.|Expression of nGFP in muscle satellite cells.|C57BL/6|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|28-Feb-2014||0.0|0.0|Unknown||muscle|Yes| 1824.0||B6.129-H2-Ab1||Recessive|histocompatibility 2, class II antigen A, beta 1|H2-Ab1|Nil|A beta, Abeta, H-2Ab, H2-Ab, I-Ab, I-Abeta, Ia-2, Ia2, IAb, Rmcs1|MGI:103070|targeted mutation 1, Michael J Grusby|H2-Ab1|MGI:2158420|17||||||||||||||||Yes|||||||||||||Homozygotes for targeted null mutations exhibit depletion of mature CD4+ T cells, deficiency in cell-mediated immune responses, and increased susceptibility to viral infections.Decreased CD4-positive T cell number.Increased CD8-positive T cell number.Abnormal level of surface class II molecules: MHC II complex is not expressed on the surface of cells.Decreased IgG1 level.Decreased IgM level.Abnormal response to transplant:* skin grafts from OVA expressing transgenic mice ( Tg(CAG-OVA)916Jen) are indistinguishable from wild-type donor skin grafts for the first 40 days.* rejection starts occurring after 40 days with 25% of the transgenic grafts being completely lost after 115 days.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|||The colony is maintained by brother x sister mating of homozygotes.|No|06-Aug-2007||0.0|0.0|Unknown||Transplantation, T cell, CD8, immunoglobulin, CD4|Yes| 781.0|VAMP2 KO|C57BL/6-Vamp2<->||Recessive|vesicle-associated membrane protein 2|Vamp2|Nil|Syb-2, Syb2, synaptobrevin II|MGI:1313277||||11||||||||||||||||Yes|||||||||||||Homozygous null mutants show 10X reduction in synaptic vesicle fusion and hypertonic sucrose-induced fusion and >100X reduction in fusion triggered by fast Ca2+. Newborn pups are rounded in appearance, with humped shoulders, and die immediately.||C57BL/6|No|No|Yes|No|No|Yes|No|Poor||||No|19-May-2007||0.0|0.0|Unknown||neuron, synaptic vesicle, embryonic lethal|Yes| 776.0||B6.Cg-Tg(Fabp4-cre)1Rev/J||Dominant||||||||||||||||||||||||||transgene insertion 1, Ronald M Evans|fatty acid binding protein 4, adipocyte, mouse (Fabp4)|||||||||||Transgene expressed in brown and white adipose tissue.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|18-May-2007||0.0|0.0|Unknown||Hepatocyte, liver, cre, adipose tissue|Yes| 5247.0|ENU11B6 45a|ENU11B6:045a||Recessive|Unknown|Unknown|||||||Unknown|||||||||||||||||||||||||||||Increased susceptibility to infection with TB||C57BL/6JAnu|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Good|0|5|Sib x sib|No|19-Oct-2010|Cryopreserved sperm|20.0|0.0|Unknown||infection model, ENU, tuberculosis|No| 8574.0|MMTV-Neu/FVB/N|FVB-Tg(MMTVneu)/WehiVccc||Dominant||||||||||||||||||||||||||transgene insertion 202, William Muller|MMTV (mouse mammary tumor virus)|||||||||||These mice develop tumours at approximately 6 - 8 months. Mammary adenocarcinoma.Metastatic potential.||FVB/N|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|27-Sep-2018||0.0|87.0|Yes||Her2, breast cancer, signal transduction, c-erbB2, tyrosine kinase, adenocarcinoma|Yes| 4932.0|Aire knockout 384|BALB/c-Aire/Wehi||Recessive|autoimmune regulator (autoimmune polyendocrinopathy candidiasis ectodermal dystrophy)|Aire|Unknown||MGI:1338803||||10||||||||||||||||No|||||||||||||Some disturbance of the medullary epithelial compartment, but at the phenotypic level their T cell compartment appeared relatively normal in the thymus and periphery. An increase in the number of activated T cells was evident, and autoantibodies against several organs were detected. At the histological level, lymphocytic infiltration of several organs indicated the development of autoimmunity, although symptoms were mild.Male infertility.||BALB/c|Yes|Yes|Yes|Yes|No|Yes|No|Unknown||||No|19-Nov-2009||0.0|0.0|Yes|APECED (autoimmune polyendocrinopathy-candidiasis-ectodermal dystrophy)|Antigens, Autoimmunity, TRA, tolerance, T cell|Yes| 786.0|PY1 KO|B6.129-Npy1r||Recessive|neuropeptide Y receptor Y1|Npy1r|Nil|Npyr, Y1-R|MGI:104963|targeted mutation 1.1, William P Gray|Npy1r|MGI:3053796|8||||||||||||||||Yes|||||||||||||Homozygotes for targeted null mutations exhibit moderate obesity, mild hyperinsulinemia, reduced activity and energy expenditure, lowered fast-induced refeeding, hyperalgesia, increased neuropathic pain, and resistance to barbiturates.Increased litter size:* average litter size is 7.64 +/- 0.51 compared to 4.86 +/- 0.32 in wild-type mice.Decreased B cell number: all B cell subsets reducedDecreased transitional stage B cell number: type 1 and type 2 cells both reduced.Decreased mature B cell number.Abnormal T cell number.Decreased CD8-positive T cell number: slightly reduced in the spleen.Increased single-positive T cell number:Increased CD4-positive T cell number: significantly increased in the lymph nodes.Increased CD8-positive T cell number: significantly increased in the lymph nodes.Abnormal immune system organ morphology.Abnormal spleen morphology.Decreased marginal zone B cell number.Abnormal splenic cell ratio: reduced B cell numbers among splenocytes.Small spleen.Abnormal lymph node cell ratio: reduced numbers of B cells.Abnormal immune system physiology.Abnormal immune cell physiology.Abnormal T cell activation: hyper responsive to activation.Abnormal antigen presenting cell physiology: antigen presentation defective as tested by mixed lymphocyte response tests.Abnormal immunoglobulin level.Decreased IgG2a level: both baseline levels and levels in response to antigen are reduced.Increased immunoglobulin level: in response to antigenIncreased IgA level.Increased IgG2b level.Increased IgM level.Abnormal macrophage physiology: levels of Il12 released are reduced.* levels of TNF released are reduced.Abnormal T-helper 1 physiology: impaired* protected against Th1 cell mediated inflammatory conditions such as those resulting from sodium dextran sulfate treatmentAbnormal inflammatory response.Decreased circulating interleukin-12 level: decreased levels released by macrophage.Decreased circulating tumor necrosis factor level: decreased levels released by macrophage.Decreased interferon-gamma secretion: reduced productionDecreased susceptibility to type IV hypersensitivity reaction:* swelling reduced to 55% that of controls* reduced proliferation of lymph node cells* reduced production of IFN-gammaIncreased aggression towards mice:* territorial aggression but not spontaneous aggression is increased in homozygous mutants* injection of an Htr1a agonist reduces aggressive behavior in a dose-dependent mannerHyperactivity: homozygous males display increased movement in an open field test.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|19-May-2007||0.0|0.0|Unknown||neuropeptide, body weight, adipose, insulin, obesity, T cell|Yes| 787.0|Y2 KO|B6.129-Npy2r||Recessive|neuropeptide Y receptor Y2|Npy2r|Nil||MGI:108418|targeted mutation 1.1, Herbert Herzog|Npy2r|MGI:2447398|3||||||||||||||||No|||||||||||||Homozygotes for targeted null mutations exhibit reduced food intake, body weight, and adiposity, elevated plasma pancreatic polypeptide levels, increased cancellous bone volume, and heightened sensitivity to pentobarbital-induced sedation.||C57BL/6 x 129|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|19-May-2007||0.0|0.0|Unknown||neuropeptide, obesity, adipose|Yes| 4811.0|ENU8BAT:070:Banjora|C57BL6-Tg<(ILK3mHEL)3Ccg><(TcrHEL3A9)1Mmd>/AnuApb||Recessive|||||||||Unknown|||||||||||||||||transgene insertion 3, Christopher C Goodnow|Rat insulin promoter|Expression of the inserted sequence specifically to pancreatic islet beta cells||||||||||Mice carrying the ins-HEL gene have a subclinical predisposition to diabetes due to islet cell failure. Mice carrying the insHEL and TCR transgenes have asubclinical predisposition to autoimmune destruction of the beta cell. Screening mice by urine glucose test. High glucose levels indicate diabetes and thus autoimmunity. "Early onset diabetes" definition changed during screen from approx 80 days to 40 days.||C57BL/6 x CBA x C57BL/10BR|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|||Breed diabetic Double transgenic with a non transgenic sib for next generation|No|24-Sep-2009|Cryopreserved sperm|45.0|0.0|Yes|Type I Diabetes|ENU, Singapore, autoimmunity, T cell, B cell, glucose|Possibly| 4811.0|ENU8BAT:070:Banjora|C57BL6-Tg<(ILK3mHEL)3Ccg><(TcrHEL3A9)1Mmd>/AnuApb||Recessive||||||||||||||||||||||||||transgene insertion 1, Mark M Davis||||||||||||Mice carrying the ins-HEL gene have a subclinical predisposition to diabetes due to islet cell failure. Mice carrying the insHEL and TCR transgenes have asubclinical predisposition to autoimmune destruction of the beta cell. Screening mice by urine glucose test. High glucose levels indicate diabetes and thus autoimmunity. "Early onset diabetes" definition changed during screen from approx 80 days to 40 days.||C57BL/6 x CBA x C57BL/10BR|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|||Breed diabetic Double transgenic with a non transgenic sib for next generation|No|24-Sep-2009|Cryopreserved sperm|||Yes|Type I Diabetes|ENU, Singapore, autoimmunity, T cell, B cell, glucose|Possibly| 4086.0||ENU8PH:025 , Cletus||Recessive|||||||||Unknown||||||||||||||||Yes|||||||||||||Alopecia (Hair loss).||C57BL/6 x C57BL/10 x Balb/b|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||3||No|04-Dec-2008|Cryopreserved sperm|60.0|0.0|Unknown||Alopecia, Hair loss, follicle, ENU|No| 3416.0|RIP-OVA|C57BL/6-Tg(Ins2-OVA)59Wehi/Wehi||Dominant|||Unknown||||||Unknown||||||||||||||||No|transgene insertion 59, Walter and Eliza Hall Institute of Medical ResearchTg(Ins2-OVA)59Wehi|rat insulin 2|High - 49 Copies||||||||||Mice bearing this transgene express a secreted form of ovalbumin from the full-length chicken ovalbumin cDNA under control of the rat insulin 2 promoter||C57BL/6-H2-K|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|14-Jul-2008||0.0|0.0|Unknown||ovalbumin, T cell, CD8, autoimmunity, cytotoxic|Yes| 3426.0|anti-Hy transgenic strain|C57BL/6-Tg(TcraH-Y,TcrbH-Y)71Vbo||Dominant||||||||||||||||||||||||||transgene insertion 71, Harald von Boehmer||||||||||||Cells expressing the H-Y antigen were frequent in female but not male transgenic offspring, despite the fact that peripheral T cells in animals of both sexes expressed both transgenes, T cells in male (but not female) mice had an abnormal CD4/CD8 phenotpye: over 90% of T cells in male transgenic mice were CD4-8- or expressed only low levels of CD8 molecules and the numbers of CD4+8- T cells were very small. This was due to deletion of autospecific thymocytes expressing high levels of CD8 molecules predominantly CD4+8+.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|15-Jul-2008||0.0|0.0|Unknown||T cell, autoimmunity, selection, thymus, CD4 , CD8|Yes| 790.0|Y4f|B6.129-Ppyr1||Recessive|pancreatic polypeptide receptor 1|Ppyr1|Normal|Npy4r, NYYR-D, Y4|MGI:105374|targeted mutation 1, Herbert Herzog|Ppyr<1tm1Hhz>|MGI:2183928|14||||||||||||||||Yes|||||||||||||Normal||129/Sv x C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|19-May-2007||0.0|0.0|Unknown||neuropeptide, obesity, mammary, receptor|Yes| 791.0|Y1f|B6.129-Npy1r||Dominant|neuropeptide Y receptor Y1|Npy1r|Normal|Npyr, Y1-R|MGI:104963|targeted mutation 1, William P Gray|Npy1r|MGI:3053795|8||||||||||||||||Yes|||||||||||||Normal||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|19-May-2007||0.0|0.0|Unknown||neuropeptide, receptor, obesity, hippocampal, neuroproliferative|Yes| 807.0|NPY KO x DYN KO|B6.129-Npy Pdyn||Recessive|neuropeptide Y|Npy|Nil||MGI:97374|targeted mutation 1, Tim Karl|Npy|MGI:3811718|6||||||||||||||||Yes|Cre recombinase||||||||||||Unknown||C57BL/6 x 129|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|21-May-2007||0.0|0.0|Unknown||neuropeptide, receptor, obesity, neuronal|Yes| 807.0|NPY KO x DYN KO|B6.129-Npy Pdyn||Recessive|prodynorphin|Pdyn|Nil|Dyn|MGI:97535|targeted mutation 1, Christoph Schwarzer|Pdyn|MGI:3715202|2|||||||||||||||||||||||||||||Unknown||C57BL/6 x 129|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|21-May-2007||||Unknown||neuropeptide, receptor, obesity, neuronal|Yes| 7121.0|Id3Fva∆|FVB/N(Cg)-Id3/AusbApb||Recessive|inhibitor of DNA binding 3|Id3|Nil|bHLHb25, HLH462, Idb3|MGI:96398|inhibitor of DNA binding 3; targeted mutation 1, Cornelis Murre|Id3|MGI:3046425|4|||||||||||||||||||||||||||||Id3 nulls do not breed.Although ID3 deficiency (Id3(-/-) mice) had no noticeable impact on epididymal histology, the targeted mutation adversely affected sperm motility parameters. Moreover, principal component analysis of microarray data indicated that the gene expression signatures for tissues obtained from Id3(-/-) mice and their genotypic controls were distinct from each other in each epididymal region. The predominant effect of the Id3 null mutation was in the cauda region where the expression of many transcription factors, including Hoxb8 and Bclaf1, was markedly affected.Abnormal T cell differentiation: * the total number of thymocytes is unchanged however the percent and total number of CD4 single positive cells is significantly decreased and the percent and total number of CD8 single positive cells is slightly decreased * after 5 generations of backcrossing onto a C57BL/6J background slightly increased compared to wild-typeAbnormal double-positive T cell morphology: a small but consistent increase in CD5 expression is seen compared to wild-type littermates|None|FVB/N|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|6||Heterozygous pairs|No|31-Oct-2012|Cryopreserved sperm|50.0|0.0|Unknown||transcription factor, DNA binding, helix-loop-helix|Yes| 3467.0|Asb1 KO|C57BL/6-Asb1/Wehi||Recessive|ankyrin repeat and SOCS box-containing 1|Asb1|Nil|1700029O08Rik, 1700054C17Rik, mKIAA1146|MGI:1929735|targeted mutation 1, Walter and Eliza Hall Institute of Medical Research|Asb1|MGI:2178847|1||||||||||||||||Yes|||||||||||||Homozygous mutation of this gene results in spleen hypocellularity, decreased spermatogenesis, and thickening of the epithelial layer of the skin in male animals.Abnormal testis morphology:* in 31% of homozygous mutant testes, clusters of tubules completely lack developing spermatocytes.* however, this abnormal testicular morphology has no impact on male fertility.Abnormal spermatogenesis: mutant testes frequently show less complete filling of the seminiferous tubules, suggesting reduced spermatogenesis.Hematopoietic system phenotype:* homozygotes show normal hemopoiesis, both at steady state and in response to several forms of hematopoietic stress* also, mutants exhibit no abnormalities of mature blood cells or their progenitors.Small spleen: homozygotes show normal splenic architecture but a mild reduction in spleen size.Spleen hypoplasia: reduced spleen size reflects a slightly reduced cellularity without loss of any specific cell subset.Thickened epidermis:*56% of male homozygotes display thickening of the epithelial layer of skin, either in discrete patches or in a generalized distribution; only 14% of control C57BL/6 male mice exhibit epithelial thickening.* epithelial thickening is associated with squamous differentiation and some keratin formation; however, mutants show no consistent infiltration of cells in the underlying dermis.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|22-Jul-2008||0.0|0.0|Unknown||signal transduction, SOCS, spermatogenesis, ankyrin repeat|Yes| 8573.0|UBC-Cre/ERT2 Tg x FVB/N ; iCre|FVB/N.Cg-Tg(UBC-cre/ERT2)1Ejb/VcccApb||Dominant||||||||||||||||||||||||||transgene insertion 1, Eric J Brown|human ubiquitin C (UBC) promoter||||||||||||Mice display tamoxifen-inducible Cre activity in all tissue types. |FVB/N|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|27-Sep-2018||0.0|30.0|Unknown||Cre recombinase, inducible, tamoxifen|Yes| 1750.0|Lck-Cre|B6.129-Tg(Lck-cre)157Jxm/WehiAnuApb||Dominant||||||||||||||||||||||||||targeted mutation I57, Jamey Marth; transgene insertion I57, Jamey Marth|mouse proximal Lck promoter|active in thymocytes and splenocytes||||||||||Normal||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||10|sib x sib|No|02-Aug-2007|Cryopreserved sperm|82.0|0.0|Unknown||Cre recombinase, loxP, T cell, lymphocyte, expression|Yes| 812.0|Y1Y5 KO|B6.129-Npy1r Npy5r||Recessive|neuropeptide Y receptor Y1|Npy1r|Unknown||MGI:104963||||8||||||||||||||||Yes|||||||||||||Unknown||C57BL/6 x 129|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|21-May-2007||0.0|0.0|Unknown||Neuropeptide, adipose, body weight, insulin, obesity|Yes| 812.0|Y1Y5 KO|B6.129-Npy1r Npy5r||Recessive|neuropeptide Y receptor Y5|Npy5r|Unknown|Y5R|MGI:108082||||8|||||||||||||||||||||||||||||Unknown||C57BL/6 x 129|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|21-May-2007||||Unknown||Neuropeptide, adipose, body weight, insulin, obesity|Yes| 813.0|Y1Y2Y4 KO|B6.129-Npy1r Npy2r Ppyr1||Recessive|neuropeptide Y receptor Y1|Npy1r|Nil|Npyr, Y1-R|MGI:104963|targeted mutation 1.1, William P Gray|Npy1r|MGI:3053796|8||||||||||||||||Yes|||||||||||||Unknown||C57BL/6 x 129|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|21-May-2007||0.0|0.0|Unknown||neuropeptide, obesity, adipose, neuronal, mammary|Yes| 813.0|Y1Y2Y4 KO|B6.129-Npy1r Npy2r Ppyr1||Recessive|neuropeptide Y receptor Y2|Npy2r|Unknown|NPY-Y2 receptor|MGI:108418|targeted mutation 1.1, Herbert Herzog|Npy2r|MGI:2447398|3|||||||||||||||||||||||||||||Unknown||C57BL/6 x 129|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|21-May-2007||||Unknown||neuropeptide, obesity, adipose, neuronal, mammary|Yes| 813.0|Y1Y2Y4 KO|B6.129-Npy1r Npy2r Ppyr1||Recessive|pancreatic polypeptide receptor 1|Ppyr1|Nil|Npy4r, NYYR-D, Y4|MGI:105374|targeted mutation 1.1, Herbert Herzog|Ppyr1|MGI:2183929|14|||||||||||||||||||||||||||||Unknown||C57BL/6 x 129|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|21-May-2007||||Unknown||neuropeptide, obesity, adipose, neuronal, mammary|Yes| 1751.0|SOCS|B6.129-Socs1/Wehi||Recessive|suppressor of cytokine signaling 1|Socs1|Normal|Cish1, Cish7, JAB, JAK-binding protein, JAK2-binding protein, SOCS-1, SSI-1, STAT-induced STAT inhibitor 1|MGI:1354910|suppressor of cytokine signaling 1; targeted mutation 3, Walter and Eliza Hall Institute of Medical Research|Socs1|MGI:2656917|16||||||||||||||||No|||||||||||||Normal||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|02-Aug-2007||0.0|0.0|Unknown||inflammatory disease, T cell, cytokine, signal transduction, phosphorylation|Yes| 5199.0|tghFS288(mFS WT)|129/C57BL6/FVB/N-Tg(hFST<288>)/Marp||Dominant||||||||||||||||||||||||||Human follistatin-288 splice variant|endogenous human promoter|unknown||||||||||Unknown|Hemizygous: normal Note: An abnormal phenotype is not observed until these mice are bred onto a mouse follistatin knockout background|129 x C57BL/6J|Yes|Yes|Yes|Yes|Yes|Yes|No|Excellent||||No|04-Aug-2010|Cryopreserved sperm|50.0|0.0|No||FST315, FST288, angiogenesis, ovary|Possibly| 1777.0|B6.Bim Knockout clone 339 del|C57BL/6-Bcl2l11/Wehi||Recessive|BCL2-like 11 (apoptosis facilitator)|Bcl2l11|Reduced|1500006F24Rik, Bim, Bod|MGI:1197519|BCL2-like 11 (apoptosis facilitator); targeted mutation 1.1, Andreas Strasser|Bcl2l11|MGI:2156498|2||||||||||||||||No|||||||||||||Increased numbers of lymphoid and myeloid cells. Spleen and lymph modes are 2-3-fold bigger than in wt. Sternum is sticking out. Bim-/- females are bad mothers and should not be used for breeding unless necessary.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|03-Aug-2007||0.0|0.0|Unknown||Lymphoid, Myeloid, Sternum, T cell, B cell|Yes| 7206.0|classII-mOVA|C57BL/6-Tg(H2-Ab1-TFRC/OVA)3Cbn/Apb|C57BL/6-Tg(H2-Ab1-TFRC/OVA)3Cbn|Dominant||||||||||||||||||||||||||ovalbumin residues 139-385 fused to transferrin receptor membrane domain|MHC class II|moderate||||||||||NormalClass II mOVA mice express a membrane-bound form of ovalbumin (transferrin receptor membrane domain and OVA residues 139-385) under the control of the MHC class II promoter. OVA expression is directed to the membranes of cells that express MHC class II, such as B cells, macrophages and dendritic cells.|Normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|09-Nov-2012|Cryopreserved sperm|45.0|0.0|No||MHC, ovalbumin, B cell|Yes| 3477.0|CBA.Rip-H2-Kb (lineage 50-1)|CBA-Tg(Ins2-H2-K)/Wehi||Dominant||||||||||||||||||||||||||H-2Kb heavy chain|rat insulin 2|In beta cells||||||||||Spontaneous, non-immune diabetes by 4-6 weeks of age. Diabetes is generally more severe in males (mean=23.0, sd=4.0 mmol/l at 6 weeks) compared to females (mean=16.8, sd=2.2 at 6weeks). Also appears to be more severe in homozygous compared to heterozygous mice although no formal analysis of the latter has been performed. Diabetes is stable and sufficiently mild that most heterozygous mice can be maintained to 40 weeks of age without parenteral insulin.|Diabetes is stable and sufficiently mild that most heterozygous mice can be maintained to 40 weeks of age without parenteral insulin.|CBA|Yes|No|Yes|Yes|No|Yes|No|Unknown|||Maintained as heterozygous line (CBA +/+ female x 50-1/CBA T/+ male)|No|22-Jul-2008||0.0|0.0|Unknown||autoimmunity, islet cells, transplantation, insulin|Yes| 2744.0|SXR|B6.CBA-Tg(Sox3)1Pqt/Apb||Dominant||||||||||||||||||||||||||transgene insertion 1, Paul Q Thomas|Sox3 promoter|2 copies; High with aberrant expression in gonads and CNS||||||||||Transgenic line only maintained as hemizygous. |High Sox3 expression with aberrant expression in gonads and CNS. Heterozygous females will develop phenotypically as males in approximately 80% of cases. These animals also have occasional dwarfism as well as a tendency to develop hydrocephalus due to CNS abnormalities. Sex-reversed XX tg/+ males are sterile|CBA x C57BL/6|No|No|Yes|No|No|Yes|No|Good|||Tg/+ Male mated to a wildtype female|No|10-Feb-2008|Cryopreserved sperm|120.0|0.0|Yes||Sex reversal, gonads, Sox3, Sry, Brain development|Yes| 3553.0||C57BL/6.129-Mpl||Recessive|myeloproliferative leukemia virus oncogene|Mpl|Nil|c-mpl, c-mpl-I, c-mpl-II, CD110, thrombopoietin receptor, TPO-R|MGI:97076|targeted mutation 1, Warren S Alexander|Mpl|MGI:2660811|4||||||||||||||||No|||||||||||||Mice homozygous for targeted mutations at this locus are unable to produce normal amounts of megakaryocytes and platelets. Decreased hematopoietic stem cell number - in clonal culture of bone marrow, total progenotor cell number was 38%- 44% of wildtype. Neutrophil-CFC, neutrophil-macrophage-CFC and pure erythroid-CFC were present at approximately 50% of normal levels. Abnormal megakaryocyte progenitor cell morphology -mice are deficient in megakaryocyte progenitor cellsDecreased platelet cell number - mice had only 6% the number platelets detected in controlsAbsent megakaryocytes - mutant mice displayed a loss of megakaryocytes in the spleen and bone marrow||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|31-Jul-2008||0.0|0.0|Unknown||megakaryocyte, platelet, thrombocytopenia, Thrombopoetin (TPO) receptor|Yes| 6743.0|KIf3LoxP|Klf3-LoxP conditional/Ausb||Recessive||Klf3|||||||Unknown|||||||||||||||||||||||||||||None||BL6/129SV/J|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|02-Dec-2011||0.0|0.0|Unknown|||Possibly| 7513.0|Epo-R-Cre R26eYFP Recql4fl/fl|STOCK Epor Recql4 Gt(ROSA)26Sor/StVApb|STOCK Epor Recql4 Gt(ROSA)26Sor/StVApb|Dominant|erythropoietin receptor|Epor|Normal||MGI:95408|erythropoietin receptor; targeted mutation 1, Ursula Klingmuller|Eportm1(EGFP/cre)Uk|MGI:3052727|9|||||||||||||||||||||||||||||Epo-R-Cre ki/+ R26eYFPki/ki Recql4fl/fl - no apparent phenotype|Epo-R-Cre ki/+ R26eYFPki/ki Recql4fl/+ - no apparent phenotype|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|generated on a C57bl6 background||Epo-R-Creki/+ male with Cre negative female; homozygous R26eYFP; Recql4fl/+ both|No|26-Nov-2013|Cryopreserved sperm|50.0|0.0|Yes|Rothmund-Thomson syndrome|Epo-R-Cre, R26eYFP, Recql4|Possibly| 7513.0|Epo-R-Cre R26eYFP Recql4fl/fl|STOCK Epor Recql4 Gt(ROSA)26Sor/StVApb|STOCK Epor Recql4 Gt(ROSA)26Sor/StVApb|Dominant|gene trap ROSA 26, Philippe Soriano|Gt(ROSA)26Sor|Unknown|beta geo, Gtrgeo26, Gtrosa26, R26, ROSA26 |MGI:104735|gene trap ROSA 26, Philippe Soriano; targeted mutation 1, Frank Costantini|Gt(ROSA)26Sortm1(EYFP)Cos|MGI:2449038|6|||||||||||||||||||||||||||||Epo-R-Cre ki/+ R26eYFPki/ki Recql4fl/fl - no apparent phenotype|Epo-R-Cre ki/+ R26eYFPki/ki Recql4fl/+ - no apparent phenotype|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|generated on a C57bl6 background||Epo-R-Creki/+ male with Cre negative female; homozygous R26eYFP; Recql4fl/+ both|No|26-Nov-2013|Cryopreserved sperm|||Yes|Rothmund-Thomson syndrome|Epo-R-Cre, R26eYFP, Recql4|Possibly| 7513.0|Epo-R-Cre R26eYFP Recql4fl/fl|STOCK Epor Recql4 Gt(ROSA)26Sor/StVApb|STOCK Epor Recql4 Gt(ROSA)26Sor/StVApb|Dominant|RecQ protein-like 4|Recql4|Normal||MGI:1931028 |RecQ protein-like 4; targeted mutation 1.1, TaconicArtemis|Recql4|MGI:5645319|15|||||||||||||||||||||||||||||Epo-R-Cre ki/+ R26eYFPki/ki Recql4fl/fl - no apparent phenotype|Epo-R-Cre ki/+ R26eYFPki/ki Recql4fl/+ - no apparent phenotype|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|generated on a C57bl6 background||Epo-R-Creki/+ male with Cre negative female; homozygous R26eYFP; Recql4fl/+ both|No|26-Nov-2013|Cryopreserved sperm|||Yes|Rothmund-Thomson syndrome|Epo-R-Cre, R26eYFP, Recql4|Possibly| 4110.0||KRN:153||Recessive|||||||||Unknown||||||||||||||||Yes|transgene insertion KRN, Diane Mathis|natural TCR alpha and -beta promoter/enhancer elements.|||||||||||No arthritis in KRN/H2g7 model||C57BL/6 x NODk x C57BL/10 x Balb/b|Yes|Yes|Yes|Yes|Yes|Yes|No|Poor||||No|05-Dec-2008|Cryopreserved sperm|30.0|0.0|Yes||Autoimmunity, Arthritis, KRN, ENU|No| 3595.0||C57BL/6.129-Rag1 Ly5.1||Recessive|recombination activating gene 1|Rag1|Nil|Rag-1|MGI:97848|targeted mutation 1, Peter Mombaerts|Rag1|MGI:1857241|2||||||||||||||||No|||||||||||||Homozygotes for targeted null mutations exhibit arrested development of T and B cell maturation at the CD4-8- thymocyte or B220+/CD43+pro-B cell stage due to inability to undergo V(D)J recombination. Mice homozygous for the Rag1tm1Mom mutation produce no mature T cells or B cells. Their phenotype can be described as a "non-leaky" severe combined immune deficiency (Prkdcscid/Prkdcscid) (Prkdcscid mice produce some B cells and IgM). They have no CD3+ or T cell receptor (TCR) alpha-beta positive cells. The thymus of the mutant mice contains 15 to 130 times fewer cells than heterozygous or wildtype siblings. The thymocytes are CD8-CD4- and most are IL2 receptor positive. Neither the spleen nor bone marrow contain any IgM or IgD staining cells, indicating an absence of mature B cells. These and other data suggest that B cell and T cell development has been arrested at an early stage. Macroscopically, the mutants are indistinguishable from heterozygotes or normal wildtype siblings. ||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|06-Aug-2008||0.0|0.0|Unknown||Lymphocytes, T cell, Cd4, B cell|Yes| 7230.0|KRasG12D|B6.129-Kras/JMarpApb||Dominant|v-Ki-ras2 Kirsten rat sarcoma viral oncogene homolog|Kras|Normal|Ki-ras, K-ras, Kras2, Kras-2|MGI:96680|v-Ki-ras2 Kirsten rat sarcoma viral oncogene homolog; targeted mutation 4, Tyler Jacks|Kras|MGI:2429948|6|||||||||||||||||||||||||||||Normal until mice crossed with Cre expressing strain.Expression of adenovirus controlled Cre recombinase results in lung tun our development.Treatment with adenoviral Cre injection results in ovarian endometriosis like lesions.Abnormal peritoneum morphology: * 47% of mutants develop peritoneal endometriosis following ovarian intrabursal injection of an adenovirus expressing Cre * however, mice injected with adenovirus expressing Cre directly into the peritoneum do not develop peritoneal endometriosis.||C57BL/6|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|22-Nov-2012|Cryopreserved sperm|50.0|0.0|Unknown||lung, ovary, adenocarcinoma, Cre|Yes| 7358.0|ENU25 26 TNPO3|C57BL/6NCrlAnu-Tnpo3/AnuApb|C57BL/6NCrlAnu-Tnpo3/AnuApb|Recessive|transportin 3|TNPO3|Unknown|5730544L10Rik, C430013M08Rik, D6Ertd313e |MGI:1196412|transport in 3; mutation 1, The Australian National University|Tnpo3|MGI:5563403|6|ENSMUSG00000012535|ENSMUST00000012679|Tnpo3-001|1508|1910|A to T|ENSMUSE00001238723|12|503|Leucine to STOP|||||CCGGAATCCCCAGTTCCTGGACCCTGTATTGGGCTATTTGATGAAAGGCCTGTGTGAAAAG||||||||||||||Homozygous mutation appears lethal|Heterozygous mice appear healthy and normal|C57BL/6NCrlAnu|No|No|Yes|No|No|Yes|No|Good||Generation 4|HET x HET|No|20-Jun-2013|Cryopreserved sperm|36.0|0.0|Unknown||lethal, embryo, ENU|Possibly| 3522.0|NOD.B6-Idd14|NOD.B6-Idd14||Recessive|||Unknown|||insulin dependent diabetes susceptibility 14|Idd14|MGI:99416|13||||||||||||||||Yes|||||||||||||Non obese diabetic (NOD) mice exhibit a susceptibility to Spontaneous development of type 1 diabetes.||NOD|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|28-Jul-2008||0.0|0.0|Unknown||T cell, diabetic, autoimmunity|Yes| 1755.0|Bmf Del/376|C57BL/6-Bmf/Wehi||Recessive|Bcl2 modifying factor|Bmf|Nil||MGI:2176433|BCL2 modifying factor; targeted mutation 1.1, Andreas Villunger|Bmf|MGI:3778610|2||||||||||||||||Yes|||||||||||||Abnormal spleen morphology.Enlarged spleen: significantly enlarged at 12 months.Spleen hyperplasia: increased by more than 50%.Abnormal immune system cell morphology.Abnormal B cell morphology: increased immature B cell number.Increased pre-B cell number: significantly elevated numbers in bone marrow while pro-B cell numbers are normal.Increased transitional stage B cell number:* both T1 and T2 transitional B cells are elevated* increased T1 transitional B cells in inguinal lymph nodesIncreased mature B cell number: * mature B cell numbers are elevated.* increased numbers in inguinal lymph nodes* increased numbers in peripheral bloodIncreased follicular B cell number: elevated while marginal B cell numbers are normal.Decreased B cell apoptosis: highly resistant to apoptosis caused by dexamethasone.Increased immunoglobulin level: total serum levels elevated at 8-10 weeks but not at 1 year of age.Decreased T cell apoptosis:* double positive T cells with increased resistance to the apoptotic effects of dexamethasone* thymocytes and double positive T cells resistant to the apoptotic effects of suberoylanilide hydroxamic acidTumorigenesis: no B cell neoplasia through 18 months of ageThymic lymphoma: increased susceptibility to gamma irradiation induced thymic lymphomas made up of double positive or CD8 single positive cells.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|02-Aug-2007||0.0|0.0|Unknown||Bcl-2, BH3 only, B cell, cell death, stress|Yes| 1361.0|IL21 KO|B6.129-IL21||Recessive|interleukin 21|Il21|Nil||MGI:1890474|targeted mutation 1, Lexicon Genetics|Il21|MGI:3528994|3||||||||||||||||No|||||||||||||Decreased germinal center B cell number:* the percentage of GC B cells that make up the total B cell population in the spleen of immunized mice is reduced by two-thirdsAbnormal CD4-positive T cell morphology:* the percentage of follicular T helper cells (defined as CXCR5+ICOS+CD4+ T cells) is reduced by a third.Abnormal spleen germinal center morphology:* the number of actively proliferating T cells found within GC is reduced 3- to 4- fold.* the percentage of follicular T helper cells (defined as CXCR5+ICOS+CD4+ T cells) is reduced by a third.Decreased spleen germinal center number:* there is a paucity of GC in the spleen of mice after immunization with sheep red blood cells (SRBC).Decreased CD4-positive T cell number:* Il-17+ CD4+ cells are absent from lamina propria and spleen in mutants.Abnormal T cell differentiation:* when naive TH cells are subjected to TH17 differentiation, a deficit in generation of Il-17-producing cells is observed with an increased number of Foxp3+ cells compared to wild-type.* one week after immunization with MOG peptide in CFA, restimulation of spleen cells with TPA or MOG peptide results in production of almost no Il-17 producing cells, showing impaired TH17 differentiation.Abnormal gamma-delta T cell morphology:*lamina propria and splenic TCRgd+ T cells show <10-fold decrease in Il-17-expressing cells compared to wild-type cells.Abnormal interleukin level:* CNS-infiltrating and splenic CD4+ T cells produce interferon gamma, in contrast to CD4+ T cells from controls which produce predominantly Il-17.||129/SvEvBrd x C57BL6/J|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|22-Jun-2007||0.0|0.0|Unknown||interleukin, Immunoglobulin, B cell, T cell, CD4, germinal centre, IL17|Yes| 4997.0|ENU6AT:HELxTCR:line057:CBA:F2 ; Diablo|C57BL/6J: B10.BR/SgSnJ-Tg(ILK3mHEL)<3Ccg>Tg(TcrHEL3A9)<1Mmd>||Recessive|||||||||Unknown|||||||||||||||||transgene insertion 3, Christopher C Goodnow|Rat insulin promoter|||||||||||Heightened susceptibility to autoimmune diabetes on the transgenically sensitized TCR x insHEL background.Phenotype Screen: Urine glucose|Normal|C57BL/6 x B10BR x CBA|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|28-Jan-2010|Cryopreserved sperm|75.0|0.0|Yes|Type I Diabetes|ENU, JDRF, T cell, autoimmunity|Possibly| 4997.0|ENU6AT:HELxTCR:line057:CBA:F2 ; Diablo|C57BL/6J: B10.BR/SgSnJ-Tg(ILK3mHEL)<3Ccg>Tg(TcrHEL3A9)<1Mmd>||Recessive||||||||||||||||||||||||||transgene insertion 1, Mark M Davis||||||||||||Heightened susceptibility to autoimmune diabetes on the transgenically sensitized TCR x insHEL background.Phenotype Screen: Urine glucose|Normal|C57BL/6 x B10BR x CBA|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|28-Jan-2010|Cryopreserved sperm|||Yes|Type I Diabetes|ENU, JDRF, T cell, autoimmunity|Possibly| 4516.0||ENU8C:011||Recessive|||||||||Unknown||||||||||||||||Yes|||||||||||||Subclinical autoimmune susceptibility. Antinuclear autoantibodies: homogeneous nuclear.|||Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|26-Feb-2009|Cryopreserved sperm|60.0|0.0|Unknown||autoimmunity, Antinuclear antibodies (ANA), ENU, Wellcome Trust|Yes| 7244.0|CMV-cre|C57BL/6-Tg(CMV-cre)1Cgn/WehiArcApb||Dominant||||||||||||||||||||||||||transgene insertion 1, University of Cologne|human cytomegalovirus (CMV) promoter||||||||||||Cre recombinase under the control of a human cytomegalovirus (CMV) promoter, active in most cells and tissues.|C57BL/6|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|11-Dec-2012|Embryo|0.0|0.0|Unknown||CMV, Cre recombinase, ubiquitous, deleter|Yes| 5297.0|CD39 KO|C57BL/6-Entpd1||Recessive|ectonucleoside triphosphate diphosphohydrolase 1|Entpd1|Nil|Cd39, ectoapyrase, NTPDase-1|MGI:102805|ectonucleoside triphosphate diphosphohydrolase 1; targeted mutation 1, Robert D Rosenberg|Entpd1|MGI:2182811|19||||||||||||||||No|||||||||||||Cardiac fibrosis.Abnormal blood flow velocity: terminal erythrocyte velocity is increased (17.1+/-5.2 compared to 3.3+/-3.3 mm per second in wild-type mice).Abnormal vascular endothelial cell physiology: ATPase and ADPase activities are substantially decreased compared to in wild-type mice.Decreased platelet cell number: platelet count is 20% lower than in wild-type mice (538+/-78x103 per mm3 compared to 740+/-81x103 per mm3 in wild-type mice).Decreased platelet aggregation: * in vitro, platelets fail to aggregate in response to ADP, collagen or low doses of thrombin. * however, treatment with a soluble potato ATPase restores aggregation response.Increased bleeding time: * bleed time is increased to greater than 20 minutes in 4 mice and greater than 7 minutes in 7 mice compared to 1.0+/-0.2 minutes in heterozygous mice. * treatment with ferric chloride revealed a delay in platelet plug formation with no thrombi formation after 20 minutes compared to 100% in wild-type mice.Abnormal neutrophil physiology: * polymorphonuclear (PMN) cells fail to convert etheno-AP into etheno-AMP as do wild-type PMNs. * following activation, the supernatant surrounding PMNs accumulate 1.6+/-0.09-fold more ATP than from wild-type PMNs. * unactivated PMN supernatant accumulates more ATP than wild-type.Fibrosis: mice exhibit increased fibrin deposits in the lungs, heart and spleen and in some mice the liver, kidney and brainPulmonary fibrosis: fibrin deposits are present in the lungs and worsen after thrombogenic challenge.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|05-Nov-2010|Cryopreserved sperm|50.0|0.0|Unknown||vascular adenosine triphosphate diphosphohydrolase, platelet, coagulation|Possibly| 5367.0|NODTNFR1|NOD.Cg-Tnfrs1a||Recessive|tumor necrosis factor receptor superfamily, member 1a|Tnfrsf1a|Unknown|CD120a, p55, p55-R, TNF receptor alpha chain, TNF-alpha-R1, TNF-alphaR1, TNF-R-I, TNF-R1, TNF-R55, TNFalpha-R1, TNFAR, Tnfr-2, Tnfr1, TNFR60, TNFRI, TNFRp55|MGI:1314884|tumor necrosis factor receptor superfamily, member 1a; targeted mutation 1, Horst Bluethmann|Tnfrsf1a|MGI:1861040|6||||||||||||||||No|||||||||||||Absent follicular dendritic cells: organized follicular dendritic cell networks are absent.Abnormal Peyer's patch morphology: the typical subepithelial dome areas fail to form.Abnormal Peyer's patch follicle morphology: B cells are present but no organized follicles are seen and organized follicular dendritic cell networks are absent.Decreased Peyer's patch number: * average of 2 - 4 per mouse compared to 6 - 8 in wild-type mice * however, T cell populations in the thymus and T and B cell populations in the spleen and lymph nodes are normal.Abnormal lymph node B cell domain: B cell follicles and follicular dendritic cell network formation are impaired in mesenteric and peripheral lymph nodes; however B cells are present and B and T cell areas are segregated.Abnormal immune system physiology.Increased susceptibility to type I hypersensitivity reaction: significant reduction in bronchoalveolar lavage leukocytosis in an ovalbumin-induced allergic asthma model.Decreased interleukin-6 secretion: LPS-induced IL-6 secretion is reduced about 3-fold compared to wild-type mice; however TNF secretion is similar to wild-type.Increased susceptibility to bacterial infection: * infection with as few as 250 colony forming units of Listeria monocytogenes results in 100% mortality by 6 days after infection, all wild-type mice survive this treatment. * D-galactosamine sensitized homozygotes can survive 100-fold higher concentrations of LPS than wild-type; however without D-galactosamine sensitization both types of mice show similar sensitivity to LPS-induced mortality. * however, homozygotes are able to control infections of lymphocytic choriomeningitis virus.Increased susceptibility to parasitic infection: * T. gondii-exposed mice exhibit increased bacterial load compared with similarly treated wild-type mice * however, recruitment and intracerebral cell movement is normal in T. gondii-exposed mice.||NOD|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|21-Dec-2010||0.0|0.0|Unknown||TNF, infection, LPS|Yes| 7246.0|MLC-hAP|C57BL/6-Tg(Myl1-AP)1Nros/MarpApb||Semi-dominant||||||||||||||||||||||||||human alkaline phosphatase|myosin light chain (MLC)|||||||||||Unknown|Normal.Expression of human alkaline phosphatase in skeletal muscle.|C57BL/6|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Good||||No|12-Dec-2012|Cryopreserved sperm|70.0|0.0|Unknown|||Possibly| 1640.0|Bailey|C57BL/6-Col2a1||Recessive|procollagen, type II, alpha 1|Col2a1|Normal|Col2a, Col2a-1, Del1|MGI:88452||||15||||||||||||||||Yes|||||||||||||Mice have shortened and deformed limbs.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|17-Jul-2007||0.0|0.0|Unknown||Collagen, cartilage, limb, Skeletal|Yes| 5947.0|NfixKO||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 4478.0||129-Nos2/AnuApb||Recessive|nitric oxide synthase 2, inducible|Nos2|Unknown|iNOS, Nos-2, NOS-II, Nos2a|MGI:97361|nitric oxide synthase 2, inducible; targeted mutation 1, John S Mudgett|Nos2|MGI:2158791|11||||||||||||||||No|||||||||||||||129|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|10|||No|22-Feb-2009|Cryopreserved sperm|120.0|0.0|Unknown||infection, macrophage, interferon|Yes| 7254.0|FTL-BALB/C|BALB/c-Tg(fos-tau/LacZ)/Apb||Dominant||||||||||||||||||||||||||FOS-TAU-LACZ|C-FOS|Distribution and expression similar to engogenous c-fos||||||||||Normal|Normal|BALB/c|Yes|Yes|Unknown|Yes|Yes|Unknown|No|Excellent|>30||FTL+ FEMALE X FTL+ MALE|No|09-Jan-2013|Cryopreserved sperm|40.0|0.0|No||c-fos, functionally activated neurons, BALB/c, marker mice, neuronal activation, LacZ, beta-galactosidase|Yes| 5298.0|CD39.Tg|C57BL/6-Tg(H2-K-ENTPD1)||Dominant||||||||||||||||||||||||||human ectonucleoside triphosphate diphosphohydrolase-1|H2-K||||||||||||Human CD39 (hCD39) is widely expressed in transgenic mice.hCD39 prolongs bleeding times and protects against induced thrombosis.AMP and adenosine levels are increased in hCD39 transgenic mice.hCD39 protects transgenic mouse cardiac grafts from Ab-mediated rejection.|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|05-Nov-2010|Cryopreserved sperm|50.0|0.0|Unknown||transplantation, ischemia-reperfusion injury (IRI), thrombosis, AMP and adenosine, rejection|Possibly| 350.0|p75|129-Ngfr||Recessive|nerve growth factor receptor (TNFR superfamily, member 16)|Ngfr|Unknown|LNGFR, p75, p75 neurotrophin receptor, p75NGFR, p75NTR, Tnfrsf16|MGI:97323|targeted mutation 1, Rudolf Jaenisch|Ngfr|MGI:1857226|11||||||||||||||||No|||||||||||||Viable and fertile.Homozygotes for targeted mutations exhibit increased perinatal lethality, skin abnormalities, growth retardation, reduced sensory nerve innervation, elevated pain threshold, ataxia, reduced sciatic nerve diameter, and blood vessel abnormalities.Decreased sensory innervation by calcitonin gene-related peptide- and substance P-immunoreactive fibers.The defective innervation was correlated with loss of heat sensitivity and associated with the development of ulcers in the distal extremities. Complicated by secondary bacterial infection, the ulcers progressed to toenail and hair loss. ||129|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|29-Sep-2006||0.0|0.0|Unknown||sensory, nerve, receptor, dorsal root ganglia|Yes| 1706.0|Gin|C57BL/6-Tg(Col2a1-cre)1Asz||Dominant||||||||||||||||||||||||||transgene insertion 1, Attila Aszodi|Cartilage specific Col2a1 gene promoter|||||||||||Normal.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|25-Jul-2007||0.0|0.0|Unknown||collagen, cartilage|Yes| 5615.0|B2ca||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5616.0|B2M||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 2745.0|NSXR|B6.CBA-Tg(Sox3-EGFP)NrPqt/Apb||Dominant||||||||||||||||||||||||||transgene insertion Nr, Paul Q Thomas|Sox3 promoter|High level of expression at restricted regions in CNS||||||||||N/A as transgenic line is maintained at hemizygous state state|High level of expression at restricted regions in CNS. Hydrocephalus with at least 10% penetrance.|CBA x C57BL/6|No|No|Yes|No|No|Yes|No|Poor|||Tg/+ male to wt female|No|10-Feb-2008|Cryopreserved sperm|130.0|0.0|Unknown||Sry, Sox3, CNS development, Brain development|Yes| 6334.0|STAT6/Blimp424|C57BL/6-Prdm1 Stat6||Semi-dominant|PR domain containing 1, with ZNF domain |Prdm1 |Normal|Blimp-1, Blimp1, PRDI-BF1|MGI:99655|PR domain containing 1, with ZNF domain; targeted mutation 1, Stephen L Nutt |Prdm1|MGI:3510704|10|||||||||||||||||||||||||||||||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown||Blimp-1, Antibody-secreting cells (ASCs), STAT6, IL-4|Yes| 6334.0|STAT6/Blimp424|C57BL/6-Prdm1 Stat6||Semi-dominant|signal transducer and activator of transcription 6|Stat6|Nil||MGI:103034 |signal transducer and activator of transcription 6; targeted mutation 1, Shizuo Akira|Stat6|MGI:2386746|10|||||||||||||||||||||||||||||||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|13-Sep-2011||||Unknown||Blimp-1, Antibody-secreting cells (ASCs), STAT6, IL-4|Yes| 3558.0||C57BL/6-Tg(TcraHsv2.3,TcrbHsv2.3)L118-1Cbn Ptprc/Wehi||Recessive||||||||||||||||||||||||||transgene insertion L118-1, Francis R Carbone |a 2 kb fragment of the H-2Kb and a 700 bp fragment including the Igh enhancer.|||||||||||TCR transgenics are immunocompromised by having a mono-specific T cell receptor however, in a clean envirnoment, mice show no difference in phenoptype from wild-type B6 mice.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|01-Aug-2008||0.0|0.0|Unknown||T cell, CD4 , CD8, T cell receptor (TCR), herpes Simplex Virus (HSV), selection, thymus|Yes| 5299.0|B6.TBM.Tg|C57BL/6-Tg(H2-K-THBD)||Dominant||||||||||||||||||||||||||human thrombomodulin|H2-K|Strong on peripheral blood lymphocytes|||||||||||hTBM transgenic mice were indistinguishable from WT littermates in appearance, size, level of activity and fertility.Transgenically expressed hTBM protects against pulmonary arterial thromboembolism.Transgenically expressed hTBM protects against venous thrombosis.Transgenically expressed hTBM reduces the inflammatory infiltrate after IVC ligation.Transgenically expressed hTBM reduces HMGB1 levels.Transgenically expressed hTBM prolongs cardiac graft survival and reduces infiltrating T cells.|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|05-Nov-2010|Cryopreserved sperm|50.0|0.0|Unknown||coagulation, rejection, thrombosis, xenotransplantation, T cell|Possibly| 3582.0||Rb(12.T17<16>65Dn)2Cje||Dominant|||Increased|Ts(Rb(12.17<16>))2Cje||Robertsonian translocation, Chr 12 and T1716Dn, Charles J Epstein 2|Rb(12.T17<16>65Dn)2Cje|MGI:3531161|Unknown||||||||||||||||Yes|||||||||||||This strain has three copies of most of the genes on mouse Chromosome16 that are homologues of human Chromosome 21 genes. Transmission of the chromosome 16 segmental trisomy through the female germline is significantly improved over Ts65Dn (43% versus 24%). Dendritic spines on granule cells in the fascia dentata are enlarged in size and decreased in density (Villar AJ, et al. 2005). Unlike Ts65Dn, males are fertile. Mice are 20% smaller in size than controls. This strain serves a model for Down syndrome.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|04-Aug-2008||0.0|0.0|Yes||Trisomy, Down Syndrome, Chromosome 21|Yes| 8575.0|LGN-VenusC|B6.Cg-Gpsm2/FumaVcccApb||Dominant|G-protein signalling modulator 2 (AGS3-like, C. elegans)|Gpsm2||6230410J09Rik, LGN, Pins|MGI:1923373|G-protein signalling modulator 2 (AGS3-like, C. elegans); targeted mutation 1.1, Fumio Matsuzaki|Gpsm2|MGI:3850859|3|||||||||||||||||||||||||||||Normal||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|27-Sep-2018||0.0|40.0|Unknown||Neuroepithelial progenitors, spindle orientation|Yes| 6738.0|Klf3-8-bY-FV|FVBn-tm.Klf8GT. tg(bYAC)/Ausb||Recessive||Klf3,Klf8,bYAC||||||||||||||||||||||||||||||||||||Embryonic lethalDouble homozygous is 100% embryonic lethal. Klf3KO homozygote is 50% embryonic lethal. KlfKO/Klf8 het is 90% embryonic lethal. Klf8KO has no obvious pheontype. bYAC expresses human globin genes- no affect on mouse.||FVBn|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|02-Dec-2011||0.0|0.0|Unknown|||Possibly| 7362.0|Grhl3 flox|B6.129S1-Grhl3/MarpApb||Recessive|grainyhead-like 3 (Drosophila)|Grhl3|Normal||MGI:2655333|grainyhead-like 3 (Drosophila); targeted mutation 3.1, Stephen M Jane|Grhl3|MGI:5306651|4|||||||||||||||||||||||||||||Normal|Normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Excellent|||fl/fl x fl/fl|No|26-Jun-2013|Cryopreserved sperm|37.0|0.0|Unknown||squamous cell carcinoma (SCC), signalling, transcription factor|Possibly| 7136.0|LRRK1|C57BL/6N-Lrrk1/JAusb|C57BL/6N-Lrrk1/JAusb|Recessive||LRRK1|||MGI:4940302|||||||||||||||||||||||||||||||||||C57BL/6N|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|02-Nov-2012||0.0|0.0|Unknown|||Possibly| 7082.0|Momme D31|FVB/NJ-Trim28 Tg(Hba1-Gfp)1Ew/QimrApb||Semi-dominant|tripartite motif-containing 28 |Trim28|Unknown|KAP-1, KRIP-1, Tif1b|MGI:109274|tripartite motif-containing 28; modifier of murine metastable epialleles, D31|Trim28|MGI:5515385|7||||||||||Unknown to Unknown|||||||transgene insertion 1, Emma Whitelaw|human alpha-globin promoter and enhancer region|11 copies||||||||||Death at E6-E8|Normal|FVB/NJ|No|No|Yes|No|No|Yes|No|Good|||MommeD31<+/->;Tg(Hba1-Gfp)1Ew x Tg(Hba1-Gfp)1Ew|No|13-Sep-2012|Cryopreserved sperm|40.0|0.0|Unknown||ENU, epigenetics, modifier|Possibly| 3538.0||C57BL/6-Prdm1 / Pou2af1||Recessive|PR domain containing 1, with ZNF domain|Prdm1|Unknown|Blimp1, PRDI-BF1|MGI:99655|targeted mutation 1, Stephen L Nutt|Prdm1|MGI:3510704|10||||||||||||||||Yes|Green Fluorescent Protein (GFP)||||||||||||Blimp T/T mice die late in gestation, regardless of OBF-1 genotype ||C57BL/6|No|No|Yes|No|No|Yes|No|Unknown||||No|29-Jul-2008||0.0|0.0|Unknown||B cell, antibody, antibody secreting cells, embryonic lethal, differentiation|Yes| 3538.0||C57BL/6-Prdm1 / Pou2af1||Recessive|POU domain, class 2, associating factor 1|Pou2af1|Unknown|Bob-1, BOB.1, Bob1, OBF-1, OBF.1, OCA-B, OCAB|MGI:105086|targeted mutation 1, Patrick Matthias|Pou2af1|MGI:2388055|9|||||||||||||||||||||||||||||Blimp T/T mice die late in gestation, regardless of OBF-1 genotype ||C57BL/6|No|No|Yes|No|No|Yes|No|Unknown||||No|29-Jul-2008||||Unknown||B cell, antibody, antibody secreting cells, embryonic lethal, differentiation|Yes| 7257.0|MLC:2IGF-1B_3D (Class 2Eb) ; SP2-IGF-1Eb|B6.FVB-Tg(Myl1-SP2/IGF1Eb)1Nros/MarpApb|B6.FVB-Tg(Myl1-SP2/IGF1Eb)1Nros|Semi-dominant||||||||||||||||||||||||||mouse insulin-like growth factor-1|myosin light chain|skeletal muscle||||||||||Unknown|Normal|C57BL/6|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Good||||No|15-Jan-2013|Cryopreserved sperm|50.0|0.0|Unknown||E-peptide, extracellular matrix|Possibly| 7258.0|MLC-Cre|B6.FVB-Tg(Myl1-cre)13Nros/MarpApb|B6.FVB-Tg(Myl1-cre)13Nros|Semi-dominant||||||||||||||||||||||||||Tg(Myl1-cre)13Nros|myosin light chain (MLC)|||||||||||Unknown|Normal.Expression of cre recombinase in skeletal muscle.|C57BL/6|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Good||||No|15-Jan-2013|Cryopreserved sperm|54.0|0.0|Unknown||Cre recombinase, muscle|Possibly| 7310.0|K5rTA-Rae1-32|C57BL/6-Tg(K5-rTA)04Cbn Tg(TetO-RaeT1e)32Cbn/Apb||Dominant||||||||||||||||||||||||||tetracycline-regulated transcriptional transactivator|bovine keratin-5|||||||||||In these mice following oral doxycyline treatment, rTA expresssion induced in the skin activates the TetO promoter driving RaeT1e expression in the skin.Following doxycycline treatment, RaeT1e expression is weak in these mice.|As for homozygous mice.|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||4|Tg Tg x Tg Tg|No|09-Apr-2013|Cryopreserved sperm|45.0|0.0|Yes||etinoic acid early transcript 1E, doxycyline inducible|Yes| 7310.0|K5rTA-Rae1-32|C57BL/6-Tg(K5-rTA)04Cbn Tg(TetO-RaeT1e)32Cbn/Apb||Dominant||||||||||||||||||||||||||retinoic acid early transcript 1E|CMV minimal promoter and 7 TetO sequences|||||||||||In these mice following oral doxycyline treatment, rTA expresssion induced in the skin activates the TetO promoter driving RaeT1e expression in the skin.Following doxycycline treatment, RaeT1e expression is weak in these mice.|As for homozygous mice.|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||4|Tg Tg x Tg Tg|No|09-Apr-2013|Cryopreserved sperm|||Yes||etinoic acid early transcript 1E, doxycyline inducible|Yes| 3589.0|Balb/c-Blimp KO|BALB/c-Prdm1/Wehi||Recessive|PR domain containing 1, with ZNF domain|Prdm1|Unknown|Blimp1, PRDI-BF1|MGI:99655|targeted mutation 1, Stephen L Nutt|Prdm1|MGI:3510704|10||||||||||||||||Yes|Green Fluorescent Protein (GFP)||||||||||||Prenatal lethality - homozygotes die late in gestation.||BALB/c|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|05-Aug-2008||0.0|0.0|Unknown||B cell, Lymphocyte, transcription factor, expression, maturation|Yes| 5008.0|Hbdd5.1|C57BL/6-Ptprc Hbb||Dominant|||||||||||||||||||||||||||||protein tyrosine phosphatase, receptor type, C|Ptprc||B220, CD45, Ly-5, Lyt-4, T200|MGI:97810|protein tyrosine phosphatase, receptor type, C; a variant|Ptprc|MGI:4819849|1|C57BL/6 mice express the a allele of Ptprc and the d allele of hemoglobin beta chain. Both alleles are homozygous.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|22-Feb-2010|Cryopreserved sperm|100.0|0.0|Unknown||erythroid, haemoglobin|Possibly| 5008.0|Hbdd5.1|C57BL/6-Ptprc Hbb||Dominant|||||||||||||||||||||||||||||hemoglobin beta chain complex|Hbb|||MGI:96020|hemoglobin beta chain complex; d|Hbb|MGI:1858119|7|C57BL/6 mice express the a allele of Ptprc and the d allele of hemoglobin beta chain. Both alleles are homozygous.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|22-Feb-2010|Cryopreserved sperm|||Unknown||erythroid, haemoglobin|Possibly| 7363.0|RhoGEF19 flox|B6.129S1-Arhgef19/Marp||Recessive|Rho guanine nucleotide exchange factor (GEF) 19|Arhgef19|Normal|6430573B13Rik, WGEF|MGI:1925912|Rho guanine nucleotide exchange factor (GEF) 19, targeted mutation 1 Stephen Jane|Arhgef19||4|||||||||||||||||||||||||||||Normal|Normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Excellent|||fl/fl x fl/fl|No|27-Jun-2013|Cryopreserved sperm|47.0|0.0|Unknown||Rho, signal transduction|Possibly| 3625.0||C57BL/6.129S4-Cxcl10||Recessive|chemokine (C-X-C motif) ligand 10|Cxcl10|Nil|C7, CRG-2, gIP-10, Ifi10, INP10, IP-10, IP10, mob-1, Scyb10|MGI:1352450|targeted mutation 1, Andrew D Luster|Cxcl10|MGI:2180678|5||||||||||||||||Yes|||||||||||||Abnormal cytokine secretion * only CCL2 levels are elevated in corneas relative to wild-type or Cxcl9-null mice after HSV-1 infectionIncreased susceptibility to experimental autoimmune encephalomyelitis * higher incidence and greater severity of experimental autoimmune encephalomyelitisCNS inflammation * experimental autoimmune encephalomyelitis involves meningeal and brain parenchyma after 15 days* monocytes lymphocytes and some granulocytes are involved* increased levels of IFN-gamma, Il-2 and TGF-Beta1 in lymph nodesIncreased susceptibility to viral infection * 7 days after infection (day 7 pi) with herpes simplex virus type I (HSV-1), homozygotes have significantly higher HSV-1 titers in the cornea * virus shedding in the tear film is elevated at day 7 pi but not at early points relative to Cxcl9 homozygotes or wild-type controls* mice usually succumb to infection between days 7 and 9 pi||C57BL/6 x 129|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|12-Aug-2008||0.0|0.0|Unknown||T cell, Asthma, inflammation, autoimmunity, chemokine|Yes| 1743.0|Bcl-x KO|C57BL/6-Bcl2l1/Wehi||Recessive|Bcl2-like 1|Bcl2l1|Nil|Bcl(X)L, bcl-x, Bcl-XL, Bcl-Xs, BclX|MGI:88139|BCL2-like 1; targeted mutation 1, Dennis Y Loh|Bcl2l1|MGI:2158303|2||||||||||||||||No|||||||||||||Homozygous null mutants die at embryonic day 13 with extensive apoptotic cell death, hypomorphic mutants have severe reproductive defects due to abnormal germ cell development. Mice lacking the gamma isoform show immune defects.|Decreased platelet cell number:* platelet counts are significantly lower than controls (860x10<3>/microliter vs 1100x10<3>/microliter).Abnormal platelet physiology:* platelet half-life is significantly reduced compared to controls (57 hours to 30 hours).|C57BL/6|No|No|Yes|No|No|Yes|No|Unknown||||No|01-Aug-2007||0.0|0.0|Unknown||embryonic lethal, Bcl-2, cell death, neuron, lymphocyte|Yes| 1783.0|Cathepsin B knockout|B6.129-Ctsb/Wehi||Recessive|cathepsin B|Ctsb|Nil||MGI:88561|targeted mutation 1, Jan Deussing|Ctsb|MGI:2182129|14||||||||||||||||Yes|||||||||||||Homozygotes for targeted null mutations are born normal without gross abnormalities. Homozygous mutant has resistance to induced pancreatitis. ||129 x C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|03-Aug-2007||0.0|0.0|Unknown||T cell, cytotoxic, protease, perforin, CD8|Yes| 1762.0|E mu-myc|C57BL/6-Tg(IghMyc)22Bri/Wehi||Dominant||||||||||||||||||||||||||transgene insertion 22, Ralph L Brinster|Igh (E mu) enhancer and Myc promoter||||||||||||Mice invariably develop lymphomas, 90% succumbing in the first 5 mo of life. to almost invariably develop lymphomas, 90% succumbing in the first 5 mo of life. The tumors typically presented as rapidly progressive lymphadenopathy with thymic involvement and were highly malignant by transplantation assay. Morphologically, they were lymphoblastic lymphomas, usually accompanied by lymphoid leukemia and granulocytosis, and were distinct from the tumors that arose much later in 37% of nontransgenic mice of the same (C57BL/6 x SJL)F2 genetic background.Premature death: mice die at 6 to 15 weeks of age with 94% of mice dying by 4 months of age.Increased tumor incidence: mice occasionally develop thyoma without involvement of peripheral lymphoid organsLeukemia: mice develop multicentric lymphosarcoma associated with leukemia.Lymphoma:* 13 of 15 mice develop lymphomas* mice develop multicentric lymphosarcoma associated with leukemia.B cell derived lymphoma: lymphomas develop from single B-lymphoid clones at different stages of differentiation.Sarcoma: mice develop multicentric lymphosarcoma associated with leukemia.Abnormal lymphopoiesis: mice exhibit an increased in the number of lymphoblasts in lymph tissues and the blood compared to wild-type mice.Enlarged spleen: two-fold.Enlarged thymus.Enlarged lymph nodes.|C57BL/6 x SJL|Yes|No|Yes|Yes|No|Yes|No|Unknown||||No|02-Aug-2007||0.0|0.0|Unknown||B cell, lymphoma, c-myc, B cell|Yes| 1757.0|Bmf Deleted Line 372|C57BL/6-Bmf/Wehi||Recessive|Bcl2 modifying factor|Bmf|Normal||MGI:2176433|BCL2 modifying factor; targeted mutation 1, Andreas Villunger|Bmf|MGI:3778609|2||||||||||||||||Yes|||||||||||||Normal||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|02-Aug-2007||0.0|0.0|Unknown||Bcl-2, BH3 only, B cell, cell death, stress|Yes| 6210.0|KO50/266|B6.129S2-Bcl2l11 Trp53||Recessive|transformation related protein 53|Trp53|Nil|p44, p53|MGI:98834|transformation related protein 53; targeted mutation 1, Tyler Jacks|Trp53|MGI:1857263|11|||||||||||||||||||||||||||||||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown||p53, bcl-2|Yes| 6210.0|KO50/266|B6.129S2-Bcl2l11 Trp53||Recessive|BCL2-like 11 (apoptosis facilitator)|Bcl2l11|Nil|1500006F24Rik, Bim, Bod |MGI:1197519|BCL2-like 11 (apoptosis facilitator); targeted mutation 1, Andreas Strasser|Bcl2l11|MGI:2156494|2|||||||||||||||||||||||||||||||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|13-Sep-2011||||Unknown||p53, bcl-2|Yes| 3548.0||C57BL/6-Tg(Cd11c-mOVA) Cst3||Recessive|cystatin C|Cst3|Nil|CysC, cystatin C|MGI:102519|cystatin C; targeted mutation 1, S Karlsson|Cst3|MGI:2182140|2||||||||||||||||Yes|membrane bound ovalbumin (chicken) mOVA|CD11c (mouse)|||||||||||Normal. Transgenic mice express membrane bound ovalbumin under the control of the CD11c promoter.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|30-Jul-2008||0.0|0.0|Unknown||Dendritic cell, presentation, T cell, CD8, cysteine protease|Yes| 7761.0|Nsun2-GGTC|B6.129-Nsun2/Ausb||Recessive|NOL1/NOP2/Sun domain family member 2|Nsun2|Nil|Misu|MGI:107252|NOL1/NOP2/Sun domain family member 2; gene trap D014D11, German Gene Trap Consortium|Nsun2|MGI:3873208|13|||||||||||||||||||||||||||||Alopecia:• cyclic alopecia develops at around 10 months• normal pelage develops after birthAbnormal hair cycle:• a reduced number of hair follicle bulge stem cells are found in S- or G2/M-phase at the initiation of anagen (day 21 of age)• progression of hair follicle cells through the cell cycle is slower• a 2 fold increase in bulge stem cells is found during telogenAbnormal hair cycle anagen phase:• delayed entry of hair follicles into first and second synchronized hair cycleDecreased body size:• appreciably smaller than controlsMale infertility:• males are sterile||C57BL/6|Yes|Yes|Yes|Yes|No|Yes|No|Unknown||||No|09-Oct-2014||0.0|0.0|Unknown||testis, hair, RNA methyltransferase|Yes| 5102.0|129.Cat-L|129-Ctsl/Wehi||Recessive|cathepsin L|Ctsl|Nil|1190035F06Rik, Cat L, major excreted protein, MEP|MGI:88564|||MGI:2136432|13||||||||||||||||Yes|||||||||||||Homozygotes for mutant alleles may exhibit partial or complete hair-loss, skin defects, impaired T cell maturation, dilated cardiomyopathy, and high postnatal mortality. Mutant males for some alleles show both normal and atrophic seminiferous tubules and reduced sperm production.||129|Yes|No|Yes|Yes|No|Yes|Yes|Unknown||||No|29-Apr-2010||0.0|0.0|Unknown||Coat, T cell, seminiferous tubules, Hair loss, alopecia, skin, dermis|Yes| 1770.0|C3H.Cat-L|C3H-Ctsl/Wehi||Recessive|cathepsin L|Ctsl|Nil|1190035F06Rik, Cat L, major excreted protein, MEP|MGI:88564|cathepsin L; targeted mutation 1, Christoph Peters|Ctsl|MGI:2136432|13||||||||||||||||Yes|||||||||||||Homozygotes for mutant alleles may exhibit partial or complete hair-loss, skin defects, impaired T cell maturation, dilated cardiomyopathy, and high postnatal mortality. Mutant males for some alleles show both normal and atrophic seminiferous tubules and reduced sperm production.||C3H|Yes|No|Yes|Yes|No|Yes|Yes|Unknown||||No|03-Aug-2007||0.0|0.0|Unknown||Coat, T cell, seminiferous tubules, Hair loss, alopecia, skin, dermis|Yes| 5173.0|Cx40.350 ; Tie2Cx40.350|B6;CBA-Tg(Tie2-Gja5)/ABS||Dominant|gap junction protein, alpha 5|Gja5|Increased|connexin 40, Cx40, Gja-5|MGI:95716||||Unknown|||||||||||||||||overexpression of Cx40|Tie2 endothelial specific|||||||||||Unknown|unknown|N3 B6|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Good|3|||No|06-Jul-2010|Cryopreserved sperm|45.0|0.0|Yes|hypertension|connexins, hypertension, gap junctions|Possibly| 6535.0|IR1?|B6.129S2-Ifnar1/ScrAusb||Recessive|interferon (alpha and beta) receptor 1 |Ifnar1|Nil|Ifar, IFN-alpha/betaR, Ifrc|MGI:107658|interferon (alpha and beta) receptor 1; targeted mutation 1, Michel Aguet|Ifnar1|MGI:1930950|16|||||||||||||||||||||||||||||Abnormal osteoclast morphology:*Osteoclastogenesis is enhanced.Impaired NK cell cytolysis:*Natural killer cells from polyI:C-treated mice do not display cytotoxicity towards B16 melanoma cells.Decreased interferon-alpha secretion:*Following infection with Leishmania.Decreased interferon-beta secretion:*Following infection with Leishmania.Abnormal response to infection:*Murine cytomegalovirus replication in macrophages is increased greater than 10,000-fold compared to that in wild-type macrophages.Increased tumor growth/size:*In mice treated with polyI:C the reduction in tumor growth of injected B16 melanoma cells is less than in polyI:C treated control mice.Decreased bone mineral density||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown||IFN|Yes| 5152.0||ENU7B6:039 (ANA)||Recessive|Unknown||||||||Unknown|||||||||||||||||||||||||||||Screened phenotype = positive for anti-nuclear antibodies||C57BL/6JStdAnu X CBA/CaJ|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|2|1||No|11-Jun-2010|Cryopreserved sperm|40.0|0.0|Unknown||Antinuclear antibodies, autoimmune disease, ENU, Wellcome Trust, NIH|Yes| 4957.0|BALB/c-Homo Rosa EGFP|BALB/c-Gt(ROSA)26Sor Alpl|MGI:2177588|4|||||||||||||||||gene trap ROSA 26, Philippe Soriano; targeted mutation 1, Martyn Goulding|||||||||||||Expression of GFP in all cells.|BALB/c|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|18-Dec-2009||0.0|0.0|Unknown||GFP, B cell|Yes| 1771.0|Cathepsin-S/Cathepsin-L Knockout|Un-Ctsl Ctss/Wehi||Dominant|cathepsin L|Ctsl|Nil|1190035F06Rik, Cat L, major excreted protein, MEP|MGI:88564|cathepsin L; targeted mutation 1, Christoph Peters|Ctsl|MGI:2136432|3||||||||||||||||No|||||||||||||Deficient CD4 T cell generation (but not "visibly" immunocompromised). Periodic partial hair loss. |||No|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|03-Aug-2007||0.0|0.0|Unknown||T cell, CD4, Lymphocyte|Yes| 1771.0|Cathepsin-S/Cathepsin-L Knockout|Un-Ctsl Ctss/Wehi||Dominant|cathepsin S|Ctss|Nil|Cat S|MGI:107341|cathepsin S; targeted mutation 1, Harold A Chapman|Ctss|MGI:2182133|3||||||||||||||||No|||||||||||||Deficient CD4 T cell generation (but not "visibly" immunocompromised). Periodic partial hair loss. |||No|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|03-Aug-2007||||Unknown||T cell, CD4, Lymphocyte|Yes| 6225.0|Ly5.1/gBT-1/Rel|B6.129-Ptprc Rel Tg(TcraHsv2.3,TcrbHsv2.3)L118-1Cbn||Semi-dominant|protein tyrosine phosphatase, receptor type, C|Ptprc|Normal|B220, CD45, Ly-5, Lyt-4, T200 |MGI:97810|protein tyrosine phosphatase, receptor type, C; a variant|Ptprc|MGI:4819849|1|||||||||||||||||transgene insertion L118-1, Francis R Carbone||||||||||||||C57BL/6 then Ly5.1|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown||Ly-5, c-rel proto-oncogene, NF-kappaB, herpes simplex virus type 1 (HSV-1), gBT-I|Yes| 6225.0|Ly5.1/gBT-1/Rel|B6.129-Ptprc Rel Tg(TcraHsv2.3,TcrbHsv2.3)L118-1Cbn||Semi-dominant|reticuloendotheliosis oncogene|Rel|Normal|c-Rel|MGI:97897|reticuloendotheliosis oncogene; targeted mutation 1, Rodrigo Bravo |Rel|MGI:3639342|11|||||||||||||||||||||||||||||||C57BL/6 then Ly5.1|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|13-Sep-2011||||Unknown||Ly-5, c-rel proto-oncogene, NF-kappaB, herpes simplex virus type 1 (HSV-1), gBT-I|Yes| 1782.0|Cathepsin-S Knockout|B6;129-Ctss/Wehi||Recessive|cathepsin S|Ctss|Nil|Cat S|MGI:107341|cathepsin S; targeted mutation 1, Harold A Chapman|Ctss|MGI:2182133|3||||||||||||||||Yes|||||||||||||Defective CD4 T cell response and humoral responses, but no overt immunodeficiency. Homozygous null mice are resistant to the development of experimental autoimmune myasthenia gravis and showed reduced T and B cell responses to acetylcholine receptor.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|03-Aug-2007||0.0|0.0|Unknown||T cell, MHC class II, cysteine proteinase, Humoral resposne, arthritis, germinal centre|Yes| 1809.0||Cathepsin H knockout||Recessive|cathepsin H|Ctsh|Unknown|Cat H|MGI:107285||||1||||||||||||||||Yes|||||||||||||Normal|||Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|06-Aug-2007||0.0|0.0|Unknown||Protease|Yes| 1810.0|Cathepsin W knockout|Un-Ctsw||Recessive|cathepsin W|Ctsw|Nil|lymphopain|MGI:1338045|cathepsin W; targeted mutation 1, Christine T N Pham|Ctsw|MGI:3046638|19||||||||||||||||Yes|||||||||||||Normal|||Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|06-Aug-2007||0.0|0.0|Unknown||T cell, CD8, cysteine protease, Cytotoxic|Yes| 6916.0|FVBNJ-Momme D23|FVB/NJ-Smchd1 Tg(HBA1-Gfp)3Ew/Apb||Semi-dominant|SMC hinge domain containing 1|Smchd1||4931400A14Rik, mKIAA0650, MommeD1|MGI:1921605|SMC hinge domain containing 1; modifiers of murine metastable epiallele D1|Smchd1|MGI:5515369|17||||||||||Unknown to Unknown|||||||transgene insertion 3, Emma Whitelaw|Human α-Globin (-570 to +37) (4.1kb of enhancer)|36 copies||||||||||Lethal|Normal|FVB/NJ|No|No|Yes|No|No|Yes|No|Good||||No|25-Jun-2012|Cryopreserved sperm|40.0|0.0|Unknown||ENU, DNA methylation, epigenetic|Possibly| 205.0|Nkx2-5 KO|C57BL/6-Nkx2-5/Apb||Dominant|NK2 transcription factor related, locus 5 (Drosophila)|Nkx2-5|Nil|Csx, Nkx-2.5, Nkx2.5, tinman|MGI:97350|targeted mutation 4, Richard P Harvey|Nkx2-5|MGI:3655239|17||||||||||||||||Yes|||||||||||||Arrested cardiac development, death E9.5-10|atrial septal abormalities, AV conduction defect|C57BL/6|No|No|Yes|No|No|Yes|No|Unknown||||No|20-Apr-2006|Cryopreserved sperm|40.0|0.0|Unknown||heart, cardiac, embryonic lethal, homeobox, septal, valvular|Yes| 1818.0|Ts1Cje|B6.Cg-Ts(16C-tel)1Cje||Dominant|||Unknown|||trisomy, Chr 12 translocation to Chr 16, Charles J Epstein|Ts(1216)1Cje|MGI:3623022|12||||||||||||||||Yes|||||||||||||Down Syndrome. Behavioral and learning difficulties.|||Yes|Yes|Yes|Yes|Yes|Yes|Yes|Unknown||||No|06-Aug-2007||0.0|0.0|Unknown||Down Syndrome, Behaviour, Learning, Hippocampus, Trisomy|Yes| 6227.0|B6PLT16|C57BL/6-Bcl2l1||Semi-dominant|BCL2-like 1|Bcl2l1|Reduced|Bcl(X)L, bcl-x, Bcl-XL, Bcl-Xs, BclX|MGI:88139|BCL2-like 1; platelet 16|Bcl2l1|MGI:3847886|2|||||||||||||||||||||||||||||Partial prenatal lethality:*Very few fetuses survive until birth.|Decreased platelet cell number:*Platelet counts are significantly lower than controls (596x10<3>/microliter vs 1100x10<3>/microliter).Increased megakaryocyte cell number:*Megakaryocyte numbers are marginally elevated compared to controls.Abnormal platelet physiology:*Platelet half-life is significantly reduced compared to controls (57 hours to 30 hours).|C57BL/6|No|No|Yes|No|No|Yes|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown||Platelet, Bcl-x|Yes| 1817.0|Rac2 knockout|C57BL/6-Rac2/Wehi||Recessive|RAS-related C3 botulinum substrate 2|Rac2|Nil||MGI:97846|targeted mutation 1, Mary C Dinauer and David A Williams|Rac2|MGI:1857701|15||||||||||||||||Yes|||||||||||||Homozygotes for a targeted null mutation exhibit peripheral blood lymphocytosis, reductions in peritoneal B-1a lymphocytes, marginal zone lymphocytes, and IgM-secreting plasma cells, decreased levels of serum IgM and IgA, and abnormal T cell migration.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|9|||No|06-Aug-2007||0.0|0.0|Unknown||B cell, lymphocyte, immunoglobulin, lymphocytosis, GTPase|Yes| 1833.0|Blimp1 / Rag 2 knockout|C57BL/6-Prdm1 Rag2/Wehi||Recessive|PR domain containing 1, with ZNF domain|Prdm1|Unknown|Blimp1, PRDI-BF1|MGI:99655|targeted mutation 1, Stephen L Nutt|Prdm1|MGI:3510704|10||||||||||||||||Yes|Green Fluorescent Protein (GFP)||||||||||||Blimp-1 homozygotes die late gestation.Rag 2 homzygotes are immunocompromised ||C57BL/6|No|No|Yes|No|No|Yes|No|Unknown||||No|08-Aug-2007||0.0|0.0|Unknown||B cell, T cell, transcription, differentiation|Yes| 1833.0|Blimp1 / Rag 2 knockout|C57BL/6-Prdm1 Rag2/Wehi||Recessive|recombination activating gene 2|Rag2|Unknown|Rag-2|MGI:97849|recombination activating gene 2; targeted mutation 1, Frederick W Alt|Rag2|MGI:1858556|2|||||||||||||||||||||||||||||Blimp-1 homozygotes die late gestation.Rag 2 homzygotes are immunocompromised ||C57BL/6|No|No|Yes|No|No|Yes|No|Unknown||||No|08-Aug-2007||||Unknown||B cell, T cell, transcription, differentiation|Yes| 7762.0|Nsun2-EuComm|C57BL/6N-Nsun2/Ausb||Recessive|NOL1/NOP2/Sun domain family member 2|Nsun2|Nil|Misu|MGI:107252|NOL1/NOP2/Sun domain family member 2; targeted mutation 1a, Wellcome Trust Sanger Institute|Nsun2|MGI:4432654|13|||||||||||||||||||||||||||||Decreased body size:• appreciably smaller than controlsMale infertilitybehavior/neurologicaldecreased grip strength ( J:175295 ) WTSI (J:175295)hyperactivity ( J:175295 ) WTSI (J:175295)craniofacialabnormal cranium morphology ( J:175295 )WTSI (J:175295)abnormal tooth morphology ( J:175295 )WTSI (J:175295)abnormal snout morphology ( J:175295 ) WTSI (J:175295)short snout ( J:175295 ) WTSI (J:175295)upturned snout ( J:175295 ) WTSI (J:175295)growth/sizedecreased percent body fat ( J:175295 ) WTSI (J:175295)decreased total body fat amount ( J:175295 )WTSI (J:175295)abnormal tooth morphology ( J:175295 )WTSI (J:175295)abnormal snout morphology ( J:175295 ) WTSI (J:175295)short snout ( J:175295 ) WTSI (J:175295)upturned snout ( J:175295 ) WTSI (J:175295)decreased lean body mass ( J:175295 )WTSI (J:175295)decreased body weight ( J:165965 , J:175295 )WTSI (J:175295) EuPh (J:165965)decreased body length ( J:175295 )WTSI (J:175295)hematopoietic systemincreased erythrocyte cell number ( J:175295 )WTSI (J:175295)decreased mean corpuscular hemoglobin ( J:175295 )WTSI (J:175295)decreased mean corpuscular volume ( J:175295 )WTSI (J:175295)homeostasis/metabolismdecreased circulating glucose level ( J:175295 )WTSI (J:175295)decreased circulating cholesterol level ( J:175295 ) WTSI (J:175295)decreased circulating HDL cholesterol level ( J:175295 ) WTSI (J:175295)decreased circulating LDL cholesterol level ( J:175295 ) WTSI (J:175295)decreased circulating free fatty acid level ( J:175295 ) WTSI (J:175295)decreased circulating glycerol level ( J:175295 ) WTSI (J:175295)decreased circulating amylase level ( J:175295 ) WTSI (J:175295)decreased energy expenditure ( J:175295 ) WTSI (J:175295)increased energy expenditure ( J:175295 ) WTSI (J:175295)increased carbon dioxide production ( J:175295 ) WTSI (J:175295)increased oxygen consumption ( J:175295 ) WTSI (J:175295)improved glucose tolerance ( J:175295 ) WTSI (J:175295)integumentabnormal hair cycle anagen phase ( J:175295 ) WTSI (J:175295)limbs/digits/tailabnormal humerus morphology ( J:175295 )WTSI (J:175295)abnormal deltoid tuberosity morphology ( J:175295 )WTSI (J:175295)skeletonabnormal cranium morphology ( J:175295 )WTSI (J:175295)abnormal humerus morphology ( J:175295 )WTSI (J:175295)abnormal deltoid tuberosity morphology ( J:175295 )WTSI (J:175295)abnormal spine curvature ( J:175295 )WTSI (J:175295)kyphosis ( J:175295 )WTSI (J:175295)lordosis ( J:175295 ) WTSI (J:175295)decreased bone mineral content ( J:175295 )WTSI (J:175295)decreased bone mineral density ( J:175295 )WTSI (J:175295)abnormal joint morphology ( J:175295 )WTSI (J:175295)vision/eyeabnormal cornea morphology ( J:175295 )WTSI (J:175295)abnormal lens morphology ( J:175295 )WTSI (J:175295)cataracts ( J:175295 )WTSI (J:175295)||C57BL/6|Yes|Yes|Yes|Yes|No|Yes|No|Unknown||||No|09-Oct-2014||0.0|0.0|Unknown||testis, hair, RNA methyltransferase|Yes| 1853.0|PGK-Cre|Un-Tg(Pgk1-cre)1Lni||Dominant||||||||||||||||||||||||||transgene insertion 1, Peter Lonai|Phosphoglycerate kinase|dominant maternal control||||||||||Normal|||Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|10-Aug-2007||0.0|0.0|Unknown||Maternally expressed, oogenesis, Cre recombinase|Yes| 7289.0|TCRF5|B6(Cg)-Tg(Cd2-TcraF5,CD2-TcrbF5)1Kio/AnuApb|B6(Cg)-Tg(Cd2-TcraF5,CD2-TcrbF5)1KioAnu|Dominant||||||||||||||||||||||||||transgene insertion 1, Dimitris Kioussis|CD2 minigene|||||||||||This clone is CD8+ and recognises amino acids 366-374 of the nucleoprotein (NP 366-374) of influenza virus (A/NT/60/68), in the context of Class I MHC Db (Townsend et al., 1986). The usage of V beta 11 makes this TcR reactive to Class II IE molecules and an endogenous ligand recently identified as a product of the endogenous mammary tumour viruses (Mtv) 8, 9, and 11 (Dyson et al., 1991). The development of F5 transgenic T cells and their function in mice of the appropriate MHC (C57BL/10 H-2b, IE-) or in mice expressing Class II MHC IE (e.g., CBA/Ca H-2k and BALB/c H-2d) and the endogenous Mtv ligands. Positive selection of CD8+ T cells expressing the V beta 11 is seen in C57BL/10 transgenic mice (H-2b). Peripheral T cells from these mice are capable of killing target cells in an antigen-dependent manner after a period of in vitro culture with IL-2. In the presence of Class II MHC IE molecules and the endogenous Mtv ligand, most of the single-positive cells carrying the transgenic T-cell receptor are absent in the thymus. Unexpectedly, CD8+ peripheral T-cells in these (H-2k or H-2d) F5 mice are predominantly V beta 11 positive and also have the capacity to kill targets in an antigen-dependent manner. This is true even following backcrossing of the F5 TcR transgene to H-2d scid/scid mice, in which functional rearrangement of endogenous TcR alpha- and beta-chain genes is impaired.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|18-Mar-2013|Cryopreserved sperm|27.0|0.0|No||T cell receptor, T cell, influenza, cytotoxic, CD8|Yes| 4724.0|Gpx1 -/-|B6.129-Gpx1/MarpApb||Recessive|glutathione peroxidase 1|Gpx1|Unknown|cellular GPx, CGPx, Gpx, GPx-1, GSHPx-1|MGI:104887|targeted mutation 1, Ismail Kola|Gpx1|MGI:2388705|9||||||||||||||||Yes|||||||||||||Homozygotes for targeted null mutations show increased sensitivity to the oxidative stress agents paraquat and hydrogen peroxide and to ischemia/reperfusion and cold-induced brain injury. Mutants also show paradoxical bradykinin-induced vasoconstriction.||C57BL/6 x 129|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|09-Apr-2009|Cryopreserved sperm|100.0|0.0|Unknown||oxidative stress, hydrogen peroxide (H2O2), neurodegeneration, NF-kappaB|Yes| 1846.0||Un-Tg(ACTB-ECFP)1Nagy/Wehi||Dominant||||||||||||||||||||||||||transgene insertion CK6, Andras Nagy|chicken beta actin promoter coupled with the cytomegalovirus (CMV) immediate early enhancer|||||||||||Hemizygous transgenic mice are viable, fertile, normal in size, and do not display any gross physical or behavioral abnormalities. All tissues from these animals display fluorescence in all cell types under appropriate lighting conditions, except in erythrocytes and adipocytes where fluorescence is negligible or absent.|||Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|10-Aug-2007||0.0|0.0|Unknown||Fluorescent marker, GFP, CFP|Yes| 1852.0||Jaw1 knockout||Recessive|lymphoid-restricted membrane protein|Lrmp|Unknown|D6Int3, D6Int4, D6Int5, D6Int7, D6Int8, Jaw1|MGI:108424||||6||||||||||||||||Yes|||||||||||||Males are sterile. Females are normal.||C57BL/6|Yes|Yes|Yes|Yes|No|Yes|Yes|Unknown||||No|10-Aug-2007||0.0|0.0|Unknown||T cell, B cell, Lymphocyte, diabetes|Yes| 1854.0||5'endothelial Cre ER-T||Dominant||||||||||||||||||||||||||Cre recombinase|||||||||||||||Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|10-Aug-2007||0.0|0.0|Unknown|||Yes| 308.0|Inbred Athymic Nude|BALB/c-Foxn1/Arc||Recessive|forkhead box N1|Foxn1|Unknown|D11Bhm185e, Hfh11, whn|MGI:102949|nude|Foxn1|MGI:1856108|11||||||||||||||||Yes|||||||||||||Postnatal lethality:some mice die within 1 week of birth55% mortality within 2 weeksPremature death:100% mortality by 25 weeksDecreased body size and weight.Postnatal growth retardation.Abnormal T cell differentiation.Athymia.Abnormal cell-mediated immunity.Abnormal liver morphology:liver lobes were atrophied and covered with red scarsvariable degrees of severity, typically increasing with age at time of death.Small ovaryCoiled sperm flagellum: many sperm had coiled tailsAbnormal estrous cycle: many females exhibited continuous dioestrus and metaoestrus phasesFemale infertility: severely reduced fertilityReduced male fertility.Asthenozoospermia.Nude: sparse hair growth around 5 weeks of agein some mice, cephalo-caudal migration of an irregular band of short sparse hairThin skin:reduction in skin thickness at 3 weeks of age, corresponding to the catagen stage of normal skinAbsent vibrissae: absent at birthShort and wavy vibrissae: older mice show repeated growth and loss of short and wavy vibrissae.|Have hair. Enlarged thymus|BALB/c|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|03-May-2006||0.0|0.0|Unknown||hair loss, alopecia, thymus, T cell, hair keratinization|Yes| 4735.0|Analiese|ENU5WT:035||Recessive|||Unknown|||Analiese|||Unknown||||||||||||||||Yes|||||||||||||Screened phenotype = positive for anti-nuclear antibodies||C57BL/6 x C57BL/10.Br|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||9||No|19-Apr-2009|Cryopreserved sperm|40.0|0.0|Unknown||autoimmunity, ENU, Wellcome Trust|Yes| 7305.0|RIP-mOVA|C57BL/6-Tg(Ins2-TFRC/OVA)Wehi/WehiApb||Dominant||||||||||||||||||||||||||transgene insertion, Walter and Eliza Hall Institute of Medical Research|rat insulin 2|||||||||||Normal. Mice express OVA in the pancreas beta cells and kidney proximal tubular cells. There is low level expression in the testes. No thymic expression detected but when crossed to OT-I TCR Tg mice, the OT-I T cells were deleted indicating low levels of OVA expression in the thymus.|Normal|C57BL/6|No|Unknown|Yes|No|Unknown|Yes|No|Good||>30|Tg x C57BL/6|No|05-Apr-2013|Cryopreserved sperm|50.0|0.0|No||pancreas, autoimmunity, ovalbumin|Yes| 4543.0||C57BL/6-Eed||Recessive|embryonic ectoderm development|Eed|Nil|l(7)5Rn, l7Rn5|MGI:95286|lethal, Chr 7, Rinchik 5, 3354SB|Eed|MGI:1856856|7||||||||||||||||Yes|||||||||||||Lethal shortly after implanatation, extra-embryonic tissue defects||C57BL/6|No|No|Yes|No|No|Yes|No|Good|2||Het x WT|No|01-Mar-2009||0.0|0.0|No||polycomb group proteins, polycomb repressive complex 2, histone, methylation|Yes| 6645.0|NOD.BID|NOD.B6-Bid/WehiStvApb||Dominant|BH3 interacting domain death agonist|Bid|Nil|2700049M22Rik|MGI:108093|BH3 interacting domain death agonist; targeted mutation 1.1, Andreas Strasser|Bid|MGI:4440571|6|||||||||||||||||||||||||||||Homozygous null mutants survive with little or no liver damage after injection with antibody against Fas, whereas wild-type mice normally die from hepatocellular apoptosis and hemorragic necrosisHomozygous null mice develop spontaneous type 1 diabetes at the same incidence as wild-type NOD mice.|Normal|NOD/Lt|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|10|10|Sister x Brother (hom x hom)|Yes|14-Nov-2011|Cryopreserved sperm|50.0|0.0|No||type 1 diabetes, beta cell apoptosis, NOD mouse, BH3-interacting , domain death agonist|Possibly| 7341.0|MommeD43|FVB/NJ-Setdb1 Tg(Hba1-Gfp)1Ew/QimrApb||Dominant|SET domain, bifurcated 1|Setdb1|Unknown|ESET, KMT1E, mKIAA0067|MGI:1934229|SET domain, bifurcated 1; modifiers of murine metastable epiallele D43|Setdb1||3|ENSMUSG00000015697|ENSMUST00000015841|Setdb1-005|||||||||||||Yes|transgene insertion 1, Emma Whitelaw|human alpha-globin promoter and enhancer region|||||||||||Normal|Percentage of cells expressing the GFP transgene is decreased (enhancer of variegation).|FVB/NJ|Yes|Unknown|Yes|Yes|Unknown|Yes|No|Good||||No|27-May-2013|Cryopreserved sperm|45.0|0.0|Unknown||epigenetics, modifier, ENU|Yes| 1731.0|Eµ-BCL2-36|B6.Cg-Tg(Bcl2)36Wehi/Wehi||Dominant||||||||||||||||||||||||||transgene insertion 36, Walter and Eliza Hall Institute of Medical Research|Emu immunoglobulin heavy chain enhancer and SV40 promoter.||||||||||||Increased B cell number: mutants show an excess of B lymphocytesIncreased T cell number: mutants have an excess of T lymphocytes.Abnormal B cell physiology: * transgenic spleen B cells show prolonged in vitro survival in culture compared to wild-type splenocytes.Increased immunoglobulin level:* mice display increased serum immunoglobulin concentrationsAbnormal T cell physiology:* transgenic T cells show prolonged in vitro survival in culture compared to wild-type T lymphocytes.Increased susceptibility to autoimmune disorder:* some transgenic mice develop a systemic autoimmune-like disease.T cell derived lymphoma:* a few mice develop fatal clonal T cell tumors.|C57BL/6|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|01-Aug-2007||0.0|0.0|Unknown||autoimmune disease, lymphoma, plasmacytoma, B cell, T cell|Yes| 4702.0|NOD.MRL(C3)-Fas/LtJ|NOD.Cg-Fas/Apb||Recessive|Fas (TNF receptor superfamily member 6)|Fas|Unknown|APO-1, CD95, TNFR6, Tnfrsf6|MGI:95484|lymphoproliferation|Fas|MGI:1856334|19||||||||||||||||Yes|||||||||||||Mutations in this locus affect immune function and homozygotes show varying severity of lymphadenopathy, splenomegaly, lymphocytic infiltrations, elevated immunoglobulin levels, autoantibodies, impaired clonal deletion of T cells, and lupus-like disease.||NOD/LtJ|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|07-Apr-2009|Cryopreserved sperm|95.0|0.0|No||Autoimmunity, systemic lupus erythromatosis (SLE)|Yes| 291.0||CBA/CaH-Tg(Il5)1Glx||Dominant||||||||||||||||||||||||||Interleukin 5, IL5|locus control region (LCR) from the gene encoding the T-cell surface antigen CD2||||||||||| The IL-5 mice are macroscopically normal apart from an enlarged spleen which contains numerous eosinophiles at various stages of differentiation. Homozygous mice have higher numbers of eosinophils than heterozygotes but are difficult to breed.|Heterozygous mice have about 8 copies of the IL-5 gene and show a life long blood and tissue eosinophilia.|CBA/CaH|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|03-May-2006||0.0|0.0|Unknown||eosinophil, immune surveillance, infection, tumour, il-5|Yes| 6230.0|Bak/Bmf/472 |B6.129-Bak1 Bcl2l11 Bmf||Recessive|BCL2-antagonist/killer 1|Bak1|Nil|Bak, N-Bak|MGI:1097161|BCL2-antagonist/killer 1; targeted mutation 1, Craig B Thompson|Bak1|MGI:2159364|17|||||||||||||||||||||||||||||||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown||bak, Bim, Bcl2-modifying factor (Bmf)|Yes| 6230.0|Bak/Bmf/472 |B6.129-Bak1 Bcl2l11 Bmf||Recessive|BCL2-like 11 (apoptosis facilitator)|Bcl2l11|Nil|1500006F24Rik, Bim, Bod|MGI:1197519|BCL2-like 11 (apoptosis facilitator); targeted mutation 1, Andreas Strasser|Bcl2l11|MGI:2156494|2|||||||||||||||||||||||||||||||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|13-Sep-2011||||Unknown||bak, Bim, Bcl2-modifying factor (Bmf)|Yes| 6230.0|Bak/Bmf/472 |B6.129-Bak1 Bcl2l11 Bmf||Recessive|BCL2 modifying factor|Bmf|Nil||MGI:2176433|BCL2 modifying factor; targeted mutation 1, Roger J Davis|Bmf|MGI:4421178|2|||||||||||||||||||||||||||||||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|13-Sep-2011||||Unknown||bak, Bim, Bcl2-modifying factor (Bmf)|Yes| 4517.0|anda|ENU8C:014||Recessive|||||||||Unknown||||||||||||||||Yes|||||||||||||Subclinical autoimmune susceptibility. Antinuclear autoantibodies: homogeneous nuclear.|||Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|26-Feb-2009|Cryopreserved sperm|50.0|0.0|Unknown||autoimmunity, Antinuclear antibodies (ANA), ENU, Wellcome Trust|Yes| 5154.0|RRFUR|BALB/c-FLii Gt(ROSA)26Sor/AnuApb||Recessive|flightless I homolog (Drosophila)|Flii|Nil|Fliih|MGI:1342286|flightless I homolog (Drosophila); targeted mutation 1, Hugh D Campbell|Flii|MGI:2179825|11|||||||||||||||||gene trap ROSA 26, Philippe Soriano; targeted mutation 1.1, Hugh D Campbell|SV40|Human FLII is not expressed until genetic exposure to Cre recombinase||||||||||Normal. Rescue of embryonic lethal phenotype of Flii strain.|Normal|BALB/c|Yes|Yes|Yes|Yes|Yes|Yes|No|Excellent|4||Hom x Hom|No|15-Jun-2010|Cryopreserved sperm|39.0|0.0|Unknown||ROSA, gelsolin, wound|Yes| 5215.0|mIMPα4FL (very low level expression)|C57BL/6-Tg(EGFP-Kpna4 full length)verylow||Dominant|karyopherin (importin) alpha 4|Kpna4|Unknown|IPOA3|MGI:1100848||||Unknown||||||||||||||||Yes|EGFP fused to full length Kpna4|Protamine 1|very low level expression||||||||||Fertility maybe reduced||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|30-Aug-2010|Cryopreserved sperm|20.0|0.0|Unknown||importin, testis, nuclear transport, fertility, protamine 1|No| 4116.0|Crimpy|ENU12WT:012a||Semi-dominant|||||||||Unknown||||||||||||||||Yes|||||||||||||First coat appears as wavy or crimped. Affected mice shed coat at 3-5 weeks. New coat growth is short, dense and dull. |||Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|05-Dec-2008|Cryopreserved sperm|30.0|0.0|Unknown||Coat, Fur, Wavy, Crimped, ENU|Yes| 5603.0|Ancient 2||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5605.0|Ancient Group 1||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5305.0|Galectin-3 KO|129/Sv;B6;SJL-Lgals3||Recessive|lectin, galactose binding, soluble 3|Lgals3|Nil|gal3, galectin-3, L-34, Mac-2|MGI:96778|lectin, galactose binding, soluble 3; targeted mutation 1, Francoise Poirier|Lgals3|MGI:2183057|14||||||||||||||||No|||||||||||||Normal||129/Sv x C57BL/6 x SJL|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|05-Nov-2010||0.0|0.0|Unknown||implantation|Possibly| 1759.0|Bcl-2 KO|C57BL/6-Bcl2/Wehi||Recessive|B-cell leukemia/lymphoma 2|Bcl2|Nil|Bcl-2|MGI:88138|targeted mutation 1, Dennis Y Loh|Bcl2|MGI:2156165|1||||||||||||||||No|||||||||||||Homozygotes are runted because they develop polycystic kidney disease. They normally die within 6 weeks from birth. They are also profoundly lymphopenic and they turn grey at the second hair follicle cycle because of the death of melanocyte precursors. These defects are corrected by the concomitant loss of Bim.Postnatal lethality: about 50% die between 1 and 6 weeks after birth.Abnormal coat color: hair color turns gray postnatally between 4 and 5 weeks, however skin is normal.Decreased body size.Decreased body weight: body weight is 30-90% of controls.Small ears.Decreased lymphocyte cell number: number of lymphocytes in the peripheral blood, bone marrow, thymus, spleen, and lymph nodes decreases with age, while the number of segmented neutrophils and other hematopoietic lineages is normal.Decreased pre-B cell number: more than 80% reduction of B220+ surface immunoglobulin-negative pre-B cells in the bone marrow.Decreased mature B cell number: more than 80% reduction of B220+/surface immunoglobulin-positive mature B cells in the bone marrow.Decreased CD8-positive T cell number: accelerated decrease over time in the percentage of CD4-CD8+ cells in the periphery.Decreased thymocyte number.Abnormal T cell differentiation.Abnormal kidney morphology: kidneys have a nonsmooth surface, are pale, and exhibit interstitial hyperproliferation.Abnormal kidney cortex: disarray of the cortex structureDecreased renal glomerulus number.Abnormal kidney medulla morphology: disarray of the medulla structure.Small kidney.Dilated renal tubules: dilated renal tubules with hypertrophic epithelium.Polycystic kidney: kidneys exhibit a polycystic appearancerespiratory system.Abnormal nose morphology: rounder nose.||C57BL/6|Yes|No|Yes|Yes|No|Yes|No|Unknown||||No|02-Aug-2007||0.0|0.0|Unknown||T cell, Lymphocyte, Coat, polycystic kidney|Yes| 1811.0|K5-mOVA|Un-Tg(K5-mOVA)||Dominant||||||||||||||||||||||||||membrane bound chicken ovalbumin|Keratin 5|||||||||||Normal. Mice express membrane bound ovalbumin in keratinocytes.|||Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|06-Aug-2007||0.0|0.0|Unknown||Ovalbumin, T cell, keratinocyte, epidermis, graft rejection|Yes| 4600.0|Epo-R-Cre pRbfl/fl|B6.129-Epor Rb1/Apb||Dominant|retinoblastoma 1|Rb1|Unknown|pRb, Rb, Rb-1|MGI:97874|targeted mutation 3, Tyler Jacks|Rb1|MGI:2450162|14||||||||||||||||Yes|||||||||||||Compound mutant: Mild anaemia. Single Epo-R-Cre – lethal as homozygous, heterozygous maintained only. Single pRbfl/fl – no phenotype until Cre exposed||C57BL/6 x 129|Yes|Yes|Yes|Yes|Yes|Yes|No|Excellent|5||Epor -ve Rb1 female x Epor +ve Rb1 het male|No|13-Mar-2009|Cryopreserved sperm|39.0|0.0|Unknown||anaemia, MDS, mitochondria, erythroid differentiation|Yes| 4600.0|Epo-R-Cre pRbfl/fl|B6.129-Epor Rb1/Apb||Dominant|erythropoietin receptor|Epor|Unknown||MGI:95408|erythropoietin receptor; targeted mutation 1, Ursula Klingmuller|Epor|MGI:3052727|9|||||||||||||||||||||||||||||Compound mutant: Mild anaemia. Single Epo-R-Cre – lethal as homozygous, heterozygous maintained only. Single pRbfl/fl – no phenotype until Cre exposed||C57BL/6 x 129|Yes|Yes|Yes|Yes|Yes|Yes|No|Excellent|5||Epor -ve Rb1 female x Epor +ve Rb1 het male|No|13-Mar-2009|Cryopreserved sperm|||Unknown||anaemia, MDS, mitochondria, erythroid differentiation|Yes| 7343.0|MommeD45|FVB/NJ-Klf1 Tg(Hba1-Gfp)1Ew/QimrApb||Dominant|Kruppel-like factor 1 (erythroid)|Klf1|Normal|Eklf, Nan|MGI:1342771|Kruppel-like factor 1 (erythroid); modifiers of murine metastable epiallele D45|Klf1|MGI:5752592|8|ENSMUSG00000054191|ENSMUST00000067060|Klf1-201|||A to G||||Unknown to Unknown||||||Yes|transgene insertion 1, Emma Whitelaw|human alpha-globin promoter and enhancer region|||||||||||GFP transgene expression levels are increased (suppressor of variegation) in MommeD45.|GFP transgene expression levels are increased (suppressor of variegation) in MommeD45.|FVB/NJ|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|27-May-2013|Cryopreserved sperm|45.0|0.0|Unknown||epigenetics, modifier, ENU|Yes| 5084.0|Cas-L KO|C57BL/6-Nedd9/AnuApb||Recessive|neural precursor cell expressed, developmentally down-regulated gene 9|Nedd9|Nil|Cas-L, CasL, E230025G09Rik, HEF1|MGI:97302|neural precursor cell expressed, developmentally down-regulated gene 9; targeted mutation 1, Mineo Kurokawa|Nedd9|MGI:3700233|13||||||||||||||||No|||||||||||||Abnormal B cell number.Increased follicular B cell number: follicular zone B cells (FOB, B-2 cells) are concomitantly increased.Decreased lymphocyte cell number: there are reduced lymphocyte numbers in peripheral lymphoid organs in mutants.Decreased marginal zone B cell number: marginal zone B cell numbers are reduced in mutants, as shown by reduced CD1d cell numbers or IgMIgD cell numbers.Spleen hypoplasia: splenocyte number is ~50% of wild-type; both B and T cell numbers are reduced, with B cells more affected.Lymph node hypoplasia: total number of lymphocytes and numbers of T and B cells is significantly reduced compared to wild-type.Abnormal follicular B cell physiology: follicular zone B cells show aberrant migration and adhesion in response to chemotactic stimuli, compared to wild-type cells.Abnormal leukocyte migration: mutant splenocytes injected into wild-type hosts show abnormal homing with numbers of homing mutant cells found in spleen and lymph nodes decreased compared to wild-type cells.Abnormal T cell physiology: splenic T cells show attenuated responses to chemotactic (CXCL12 and CCL21) stimuli.|Normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|09-Apr-2010|Cryopreserved sperm|50.0|0.0|Unknown||Lymphocyte, migration, integrin, marginal zone (MZB), adhesion|Yes| 5627.0|B6.129-Tg(APPSw)40Btla/J ||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 3414.0|RIP-mOVA|C57BL/6-Tg(Ins2-TFRC/OVA)296Wehi/wehi||Dominant||||||||||||||||||||||||||transgene insertion 296, Walter and Eliza Hall Institute of Medical Research|rat insulin 2|Limited to pancreas||||||||||Express membrane bound ovalbumin in pancreas.||C57BL/6-H2-K|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|14-Jul-2008||0.0|0.0|Unknown||ovalbumin, T cell, membrane bound, pancreas|Yes| 5533.0|B6NT|C57BL/6-Tg(Nup98-Top1)/MarpApb||Dominant||||||||||||||||||||||||||Nup98-top1 fusion|Topoisomerase I|||||||||||Normal.Normal blood counts at 6mo, no anemia, lymphopenia or thrombocytopenia in mice aged to 600 days|Normal|C57BL/6J|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|||sibling matings; transgenic male with wildtype female|No|07-Jul-2011|Cryopreserved sperm|60.0|0.0|No||Nup98, AML, nucleoprotein, leukaemogenic|Possibly| 5611.0|AtF3ko||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5612.0|B Arrestin KO||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 1980.0|Smad1f x Myl2VCre|129;Swiss-Smad Myl2||Recessive|MAD homolog 1 (Drosophila)|Smad1|Nil|Madh1, Madr1, Smad 1|MGI:109452|MAD homolog 1 (Drosophila); targeted mutation 2, Elizabeth J Robertson|Smad1|MGI:2155484|8||||||||||||||||Yes|||||||||||||Deletion of Smad1 and Myl2 in myosin light polypeptide 2, regulatory, cardia c, slow expressing cells.|||No|No|Yes|No|No|Yes|No|Unknown||||No|04-Sep-2007||0.0|0.0|Unknown||myosin, cardiomyopathy, mesoderm, chamber, Cre recombinase|Yes| 1980.0|Smad1f x Myl2VCre|129;Swiss-Smad Myl2||Recessive|myosin, light polypeptide 2, regulatory, cardiac, slow|Myl2|Unknown|MLC-2, MLC-2v, Mlc2v, Mylpc|MGI:97272|myosin, light polypeptide 2, regulatory, cardiac, slow; targeted mutation 1, Kenneth R Chien|Myl2|MGI:2385922|5|||||||||||||||||||||||||||||Deletion of Smad1 and Myl2 in myosin light polypeptide 2, regulatory, cardia c, slow expressing cells.|||No|No|Yes|No|No|Yes|No|Unknown||||No|04-Sep-2007||||Unknown||myosin, cardiomyopathy, mesoderm, chamber, Cre recombinase|Yes| 1976.0||C57BL/6J-TgN(A<2>KHLA)6HsdArc||Recessive||||||||||||||||||||||||||Human HLA A<2> specific for H-2K?||||||||||||||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|Yes|Unknown||||No|04-Sep-2007||0.0|0.0|Unknown||T cell, lymphocyte, alloreactive, MHC|Yes| 4797.0|PLJ|PLJ||Dominant||||||||||||||||||||||||||||||||||||||Normal||PLJ|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|06-Sep-2009|Cryopreserved sperm|110.0|0.0|Unknown||PLJ|Yes| 4926.0||B6;129-Gfpt2/Apb||Recessive|glutamine fructose-6-phosphate transaminase 2|Gfpt2|Unknown|GFAT2|MGI:1338883|glutamine fructose-6-phosphate transaminase 2; gene trap 352F9, Centre for Modeling Human Disease|Gfpt2|MGI:4965721|11||||||||||||||||No|||||||||||||Normal|Normal|C57BL/6 x 129|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|11-Nov-2009|Cryopreserved sperm|90.0|0.0|Unknown||glucosamine, hexosamine|Yes| 4986.0|K14-Frem1|C57BL/6-Tg(KRT14-Frem1)||Dominant||||||||||||||||||||||||||Fras1 related extracellular matrix protein 1|keratin 14 (K14)|||||||||||Unknown||C57BL/6|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|27-Jan-2010|Cryopreserved sperm|63.0|0.0|Unknown|||Yes| 7353.0|Gnat2c.518A>G|BALB/c-Gnat2/MelbApb||Recessive|guanine nucleotide binding protein, alpha transducing 2|Gnat2|Normal|Gnat-2, Gt-2, Tcalpha |MGI:95779|Gnat2c.518A>G|||3|||||||||||||||||||||||||||||This mouse shows no evidence of cone photoreceptor function as measured by the electroretinogram. This lack of function probably results from a misfolding of the Gnat2 protein. There is also retinal remodelling, opsin mislocalisation by 3 months, increasing in severity by 12 months. At 12 months there is evidence of cone photoreceptor cell loss. At these late ages, there is also evidence of rod phototreceptor functional loss. |Unknown|BALB/c|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|approximately 4|unknown||No|17-Jun-2013|Cryopreserved sperm|50.0|0.0|Yes|Achromatopsia, ACHM4|retina, cone photoreptor, achromatopsia, eye, vision|No| 276.0|TgN(IGF-1)|FVB-Tg(Myl1-Igf1)1Nros||Recessive||||||||||||||||||||||||||transgene insertion 1, Naida Rosenthal| regulatory elements from the rat myosin light chain (MLC)-1/3 locus|MSkeletal muscle specific||||||||||||FVB|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|01-May-2006||0.0|0.0|Unknown||insulin like growth factor, IGF 1, IGF-1, muscle|Yes| 1988.0|Nkx2-5Cre x Nodal flox|129-Nkx2-5 Nodal/Apb||Recessive|Nodal|Nodal|Unknown||MGI:97359||||10||||||||||Unknown to Unknown||||||Yes|||||||||||||Deletion of Nodal in Nkx2-5 expressing cells.|||No|No|Yes|No|No|Yes|No|Unknown||||No|05-Sep-2007|Cryopreserved sperm|50.0|0.0|Unknown||heart, ventricle, mesoderm|Yes| 1988.0|Nkx2-5Cre x Nodal flox|129-Nkx2-5 Nodal/Apb||Recessive|NK2 transcription factor related, locus 5 (Drosophila)|Nkx2-5|Unknown|Csx, Csx, Nkx-2.5, Nkx2.5, tinman|MGI:97350|NK2 transcription factor related, locus 5 (Drosophila); targeted mutation 2, Richard P Harvey|Nkx2-5|MGI:2448972|17|||||||||||||||||||||||||||||Deletion of Nodal in Nkx2-5 expressing cells.|||No|No|Yes|No|No|Yes|No|Unknown||||No|05-Sep-2007|Cryopreserved sperm|||Unknown||heart, ventricle, mesoderm|Yes| 1984.0|T-box 2|129-Tbx2||Recessive|T-box 2|Tbx2|Nil||MGI:98494|T-box 2; targeted mutation 1, Virginia Papaioannou|Tbx2|MGI:3505715|11||||||||||||||||Yes|||||||||||||Embryonic lethality during organogenesis: at E12.5 some homozygous embryos are dead.Abnormal atrioventricular canal morphology: at E10.5 the atrioventricular canal fails to constrict in some mutant embryos. embryonic lethality throughout fetal growth and development.|||No|No|Yes|No|No|Yes|No|Unknown||||No|05-Sep-2007||0.0|0.0|Unknown||embryonic lethal, ventricle, aorta, polydactyly, craniofacial, ventricle|Yes| 1989.0|MesP1Cre x PitX2flox|Un.129-Pitx2 Mesp1||Recessive|paired-like homeodomain transcription factor 2|Pitx2|Normal|Brx1, Brx1a, Brx1b, Munc30, Otlx2, Pitx2a, Pitx2b, Pitx2c, Ptx2, Rieg, solurshin|MGI:109340|paired-like homeodomain transcription factor 2; targeted mutation 1, Sally Camper|Pitx2|MGI:1857844|3||||||||||||||||No|||||||||||||Deletion of PitX2 in MesP1 expressing cells|||No|No|Yes|No|No|Yes|No|Unknown||||No|05-Sep-2007||0.0|0.0|No||heart, mesoderm, Cre recombinase|Yes| 1989.0|MesP1Cre x PitX2flox|Un.129-Pitx2 Mesp1||Recessive|mesoderm posterior 1|Mesp1|Normal|bHLHc5|MGI:107785|mesoderm posterior 1; targeted mutation 2, Yumiko Saga|Mesp1|MGI:2176467|7|||||||||||||||||||||||||||||Deletion of PitX2 in MesP1 expressing cells|||No|No|Yes|No|No|Yes|No|Unknown||||No|05-Sep-2007||||No||heart, mesoderm, Cre recombinase|Yes| 1990.0|MesP1Cre x Nodal flox|Un-Nodal Mesp1||Recessive|nodal|Nodal|Nil||MGI:97359||||10||||||||||||||||No|||||||||||||Deletion of Nodal gene in cells expressing MesP1.|||No|No|Yes|No|No|Yes|No|Unknown||||No|05-Sep-2007||0.0|0.0|No||heart, mesoderm, Cre recombinase|Yes| 1990.0|MesP1Cre x Nodal flox|Un-Nodal Mesp1||Recessive|Mesoderm posterior 1|Mesp1|Normal|bHLHc5|MGI:107785|mesoderm posterior 1; targeted mutation 2, Yumiko Saga|Mesp1|MGI:2176467|7|||||||||||||||||||||||||||||Deletion of Nodal gene in cells expressing MesP1.|||No|No|Yes|No|No|Yes|No|Unknown||||No|05-Sep-2007||||No||heart, mesoderm, Cre recombinase|Yes| 4526.0||B6.CBA-Tg(hGMCSF-CK1m)394/AnuApb||Dominant||||||||||||||||||||||||||human GMCSF (GM-CSF)|human GM-CSF promoter and enhancer (10.5kb)|||||||||||Express human GM-CSF. hGM-CSF detected in serum by ELISA. Murine GM-CSF used as internal control.|||Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|27-Feb-2009|Cryopreserved sperm|30.0|0.0|Unknown||T cell, lymphocyte, transcription, chromatin remodelling, NF-kappaB|Yes| 6774.0|DBC2 Flpe ; BRINP2 Flpe|C57BL/6-Brinp2/PibMarpApb||Recessive|bone morphogenic protein/retinoic acid inducible neural-specific 2|Brinp2|Normal|DBC2, Fam5b, 6430517E21Rik, mKIAA1747|MGI:2443333|bone morphogenic protein/retinoic acid inducible neural-specific 2; targeted mutation 1.2, Phillip I Bird|Brinp2|MGI:5604617|1|||||||||||||||||||||||||||||Normal|Normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Excellent||||No|11-Jan-2012|Cryopreserved sperm|50.0|0.0|Unknown|||Yes| 7374.0|CB28-KO|B6.129-Calb1/Apb||Dominant|calbindin 1|Calb1||Brain-2, Calb, Calb-1, calbindin, calbindin-D (28k), CalbindinD28K, CB|MGI:88248|calbindin 1; targeted mutation 1, Max-Planck-Institute for Neurobiology|Calb1|MGI:1857460|4|||||||||||||||||||||||||||||Ataxia• mutants do not display ataxia in standard environments; when challenged (with a runway test or rotarod test) coordination is severely disturbed compared to controls• mice display a shaky tremor which usually worsens during movement; controls do not show any tremors|Ataxia• 2-month old heterozygotes show significant deficits in initial trials in a thin horizontal rod test compared to controls but are significantly better than homozygotes; after first 2 sessions, no significant difference remains between mutant groups|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|11-Jul-2013|Cryopreserved sperm|50.0|0.0|Unknown||ataxia, calcium|Yes| 6612.0|ENU19WT 019:G2|ANU:ENU19WT:019:G2||Semi-dominant|Unknown||||||||Unknown|||||||||||||||||||||||||||||Unknown||C57BL/6JAnu|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|11-Oct-2011|Cryopreserved sperm|10.0|0.0|Unknown||ENU|Yes| 1995.0|TgN(IGF) x Chisel KO|B6.129-Smpx Tg(IGF1)||Recessive|small muscle protein, X-linked|Smpx|Nil|chisel, Csl|MGI:1913356|targeted mutation 1, Richard P Harvey|Smpx|MGI:2387819|X||||||||||||||||Yes|insulin like growth factor 1, IGF 1|||||||||||||||Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|07-Sep-2007||0.0|0.0|Unknown||insulin like growth factor, growth factor, muscle, myosin, mesoderm, heart, muscle|Yes| 1815.0||Interferon consensus binding protein knockout||Semi-dominant|interferon regulatory factor 8|Irf8|Unknown|ICSBP, Icsbp1, IRF-8, Myls|MGI:96395||||8||||||||||||||||Yes|||||||||||||Lack CD8+ dendritic cells33% moribund by 50 weeks. Haematological neoplasis, develop leukaemia with age.Abnormal haemopoiesis. Increased susceptibility to viral infection .|9% moribund by 50 weeks. Haematological neoplasia.|129 x C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|06-Aug-2007||0.0|0.0|Unknown||viral infection, CML, Leukaemia, progenitor cells, immunodeficiency|Yes| 2330.0||C57BL/6-Prf1 Ifng Tg(TcraTcrb)1100Mjb||Recessive|perforin 1|Prf1|Nil|perforin, Pfp, Prf-1|MGI:97551|targeted mutation 1, Sandoz Pharmaceutical|Prf1|MGI:1857235|10||||||||||||||||Yes|transgene insertion 1100, Michael J Bevan||||||||||||||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|04-Dec-2007||0.0|0.0|No||T cell, cytotoxic, ovalabbumin, interferon, CD8|No| 2330.0||C57BL/6-Prf1 Ifng Tg(TcraTcrb)1100Mjb||Recessive|interferon gamma|Ifng|Unknown|Ifg, IFN-gamma|MGI:107656|targeted mutation 1, Timothy Stewart|Ifng|MGI:1857184|10|||||||||||||||||||||||||||||||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|04-Dec-2007||||No||T cell, cytotoxic, ovalabbumin, interferon, CD8|No| 7264.0||Ggn KO (-Neo)||Recessive|gametogenetin|Ggn|Unknown|GGN1, GGN2, GGN3|MGI:2181461||||7||||||||||||||||Yes|||||||||||||Embryonic Lethal|Appear normal, not studied extensively.|C57BL/6J x129Sv|No|No|Yes|No|No|Unknown|No|Unknown||||No|21-Jan-2013|Cryopreserved sperm|50.0|0.0|Unknown||Sperm, testis, embryonic lethal|Possibly| 7247.0|MLC:2IGF-1A_1C (Class 2Ea) ; SP2-IGF-1Ea|STOCK Tg(Myl1-Igf1)1Nros/MarpApb||Semi-dominant||||||||||||||||||||||||||mouse insulin-like growth factor-1|myosin light chain|||||||||||Transgenic IGF-1 propeptides are retained in skeletal muscle.E peptides bind to heparin agarose.IGF-1 E peptide moieties bind to extracellular matrix.|Normal|C57BL/6|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Good||||No|12-Dec-2012|Cryopreserved sperm|60.0|0.0|Unknown||insulin like growth factor, extracellular matrix, serum, circulation|Possibly| 3482.0|C57BL/6.CD45 -/-|C57BL/6-Ptprc/Wehi||Recessive|protein tyrosine phosphatase, receptor type, C|Ptprc|Nil|B220, CD45, Cd45, Ly-5, Lyt-4, T200|MGI:97810|targeted mutation 1, Victor L J Tybulewicz|Ptprc|MGI:3579087|1||||||||||||||||No|||||||||||||Increased NK cell number:* four- and fivefold increase in the percentage of NK1.1+CD49b+TCR-Beta- NK cells in the spleen and liver, respectively, however percentage of NK precursors was normal.* increase in the turnover of NK cells in the spleen but not liver.Abnormal NK cell physiology:* NK cells secrete less cytokines and chemokines when immunoreceptor tyrosine-based activation motif (ITAM)-containing surface receptors are stimulated.* no calcium flux in NK cells after Ly49D stimulationAbnormal chemokine physiology: Ly49D-stimulated NK cells produce 100-1000-fold less MIP-1alpha and MIP-1beta than controls.Abnormal cytokine secretion: Ly49D-stimulated NK cells secrete less IFN-gamma.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|23-Jul-2008||0.0|0.0|Unknown||T cell, CD4 , CD8, selection, splenomegaly, thymus|Yes| 5307.0|17FOX 025 B6.129-Tg(FoxP3-GFP)|ENU17FOX:025 Foxp3||Recessive|forkhead box P3|Foxp3|Normal|JM2, scurfin|MGI:1891436|||MGI:3574964|X||||||||||||||||No|||||||||||||Hyper-IgE phenotypedetected at 10 weeks of age or later.Cells from the Foxp3-gfp background strain that express FoxP3 fluoresce green, predominantly T cells|Normal |129 x C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|||Affected x affected|No|08-Nov-2010|Cryopreserved sperm|20.0|0.0|Unknown||lymphopenia, lymphocytopenia, lymphocyte, T cell, hyper IgE, ENU|Possibly| 5307.0|17FOX 025 B6.129-Tg(FoxP3-GFP)|ENU17FOX:025 Foxp3||Recessive|Unknown|Unknown|||||||Unknown||||||||||||||||Unknown|||||||||||||Hyper-IgE phenotypedetected at 10 weeks of age or later.Cells from the Foxp3-gfp background strain that express FoxP3 fluoresce green, predominantly T cells|Normal |129 x C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|||Affected x affected|No|08-Nov-2010|Cryopreserved sperm|||Unknown||lymphopenia, lymphocytopenia, lymphocyte, T cell, hyper IgE, ENU|Possibly| 5949.0|Nodal ||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 3497.0||BALB/c-H2||Dominant|histocompatibility-2, MHC|H2|Unknown|H-2, MHC-II|MGI:95894|k variant|H2|MGI:3579322|17||||||||||||||||Yes|||||||||||||Balb/c is usually H2. The H2 complex contains 3 major classes of highly polymorphic gene sets: class I (H2-K, H2-D, Q, H2-T18 genes), class II (H2-I genes), and class III (H2-S genes). These genes are involved in many processes, including graft rejection, immune response, antigen presentation and complement component.||BALB/c|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|24-Jul-2008||0.0|0.0|Unknown||haplotype, presentation, antigen presentation, T cell|Yes| 7380.0|Batf3 KO|B6.129-Batf3/MelbAnuApb||Recessive|basic leucine zipper transcription factor, ATF-like 3|Batf3|Nil|9130211I03Rik|MGI:1925491|basic leucine zipper transcription factor, ATF-like 3; targeted mutation 1, Kenneth M Murphy|Batf3|MGI:3817232|Unknown|||||||||||||||||||||||||||||Mice that are homozygous for this allele are viable and fertile. Batf3 is highly expressed in CD11c+ CD8α+ conventional dendritic cells (cDCs), with low to absent expression in other immune cells.The deletion of Batf3 prevents development of splenic CD8α+ cDCs, which are important for cross-presentation during infections. Lymph nodes and thymi of Batf3-/- mice lack CD8α+ DCs, and DCs generated from Batf3-/- bone marrow (BM) and spleens are deficient in Toll-like receptor (TLR) 3-induced interleukin (IL)-12 production. These mice also lack CD103+CD11b- DCs in the lung, intestine, mesenteric lymph nodes (MLNs), dermis, and skin-draining lymph nodes. Exhibiting defects in CD8+T cell response priming, including lack of virus-specific responses, results in the inability to reject highly immunogenic syngeneic tumors.||C57BL/6NCrlAnu|Yes|Yes|Yes|Yes|Yes|Unknown|No|Unknown||||No|19-Jul-2013|Cryopreserved sperm|54.0|0.0|Unknown||CD8, T cell, infection, dendritic cell|Yes| 2399.0||MRL/MpJ||Dominant||||||||||||||||||||||||||||||||||||||The MRL/MpJ mice are large but docile to the point that males rarely fight. Mice submitted to APB for sperm cryopreservation bred as a control for MRL/MpJ-Faslpr, also exhibit autoimmune disorders but symptoms are manifested much later in life compared to those the MRL/MpJ-Fas mice. Starting at about three months of age, levels of circulating immune complexes rise greatly in the MRL-Fas mouse but not in the wildtype control, MRL/MpJ. Also beginning at 3 months Fas mice exhibit very severe proliferative glomerulonephritis, whereas in the MRL/MpJ controls usually only mild glomerular lesions are detected. The MRL/MpJ lymphoproliferation wildtype females die at 73 weeks of age and males at 93 weeks. This compares to a lifespan of 17 weeks in the female and 22 weeks for males in the mouse homozygous for Fas. Mice have increased healing ability.|||Yes|Yes|Yes|Yes|Yes|Yes|No|Good|||Sib x Sib|Yes|20-Dec-2007|Cryopreserved sperm|70.0|0.0|No||Fas, lymphocyte, apoptosis, T cell|Yes| 5107.0|Leaden|C57L/JAnuApb||Dominant||||||||||||||||||||||||||||||||||||||Normal|Normal|C57L/JABS|Yes|Yes|Yes|Yes|Yes|Yes|No|Poor||||No|03-May-2010|Cryopreserved sperm|50.0|0.0|Unknown||C57BL/6|Yes| 5618.0|B6 CX3 CR1 and C57||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5619.0|B6 ngfr P75||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5620.0|B6 ROSA26A-EGFP ||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 3498.0||C57BL/6-Phex/Wehi||X-linked|phosphate regulating gene with homologies to endopeptidases on the X chromosome (hypophosphatemia, vitamin D resistant rickets)|Phex|Unknown|HPDR1|MGI:107489|skeletal abnormality 1|Phex|MGI:2429767|X||||||||||||||||No|||||||||||||Hypophosphatemia, skeletal abnormalities consistent with rickets, including increased width of unmineralized epiphyseal growth plate, reduced bone width in the central metaphysis, and increased trabecular bone volume in the proximal metaphysis. Abnormal angulation of the hips and knees. In all affected mice many bones appeared shorter than in wild-type mice and the vertebrae of affected mice were elliptical. In 30 to 50% of affected hemizygous male mice, heterozygous female mice and homozygous female mice, exostoses on the ribs were also observed. Ten of the 11 bone measurements were significantly shorter in mutant mice and appeared independent of sex. Only the mandible length was not significantly shorter. exostoses in bone from affected animals. Ska1 mice had markedly reduced serum phosphate levels and markedly elevated serum alkaline-phosphatase levels, modest reductions in serum calcium were also observed.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|24-Jul-2008||0.0|0.0|Unknown||endopeptidase, calcium, skeletal, phosphate|Yes| 4960.0|TNAP-Cre|129-Alpl/AnuApb||Recessive|alkaline phosphatase, liver/bone/kidney|Alpl|Nil|Akp-2, Akp2, TNSALP, TNAP|MGI:87983|targeted mutation 1, Andras Nagy|alpl|MGI:2177588|4||||||||||||||||Yes|Cre recombinase||||||||||||Perinatal lethal|Normal|129|No|No|Yes|No|No|Yes|No|Unknown||||No|12-Jan-2010|Cryopreserved sperm|75.0|0.0|Unknown||alkaline phosphatase, primordial germ cell, Cre|Yes| 5309.0|18FOX 010a B6.129-Tg(FoxP3-GFP)|ENU18FOX:010a Foxp3||Recessive|forkhead box P3|Foxp3|Normal|JM2, scurfin|MGI:1891436|||MGI:3574964|X||||||||||||||||No|||||||||||||Reduced lymphocyte population / lymphopenia.Phenotype detected by peripheral blood FACS.Cells from the Foxp3-gfp background strain that express FoxP3 fluoresce green, predominantly T cells|Normal |129 x C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|||Affected x affected|No|08-Nov-2010|Cryopreserved sperm|40.0|0.0|Unknown||lymphopenia, lymphocytopenia, lymphocyte, T cell, hyper IgE, ENU|Possibly| 5309.0|18FOX 010a B6.129-Tg(FoxP3-GFP)|ENU18FOX:010a Foxp3||Recessive|DNA cross-link repair 1C, PSO2 homolog (S. cerevisiae)|Dclre1c||Art, Artemis|MGI:2441769||||2|ENSMUSG00000026648|ENSMUST00000061852|Dclre1c-001|656|743|T to C|ENSMUSE00000319676|8|219|Unknown to Unknown|||||TTATGGCTACGAGTATTTATTCACCAACCTAAGCGAGGAGCTGGGAGTTCAGGTTCATGTG|No|||||||||||||Reduced lymphocyte population / lymphopenia.Phenotype detected by peripheral blood FACS.Cells from the Foxp3-gfp background strain that express FoxP3 fluoresce green, predominantly T cells|Normal |129 x C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|||Affected x affected|No|08-Nov-2010|Cryopreserved sperm|||Unknown||lymphopenia, lymphocytopenia, lymphocyte, T cell, hyper IgE, ENU|Possibly| 3504.0|Trif KO|B6.129-Ticam1/Wehi||Recessive|toll-like receptor adaptor molecule 1 |Ticam1|Unknown|TICAM-1, Trif|MGI:2147032|toll-like receptor adaptor molecule 1; targeted mutation 1, Shizuo Akira |Ticam1|MGI:3029019|17||||||||||||||||Yes|||||||||||||Abnormal interleukin level* severely impaired production of IL12p40 and partiallyDecreased circulating interleukin-6 level * following exposure to acid-induced acute lung injury, LPS, or 1-palmitoyl-2-arachidonoyl-phosphatidylcholineDecreased susceptibility to endotoxin shock * mice were resistant to LPS-induced shockDecreased susceptibility to viral infection * following exposure to inactivated H5N1 virus, acute-lung injury and IL6 production are attenuated compared to in wild-type miceAbnormal interleukin level * severely impaired production of IL12p40 and partiallyDecreased circulating interleukin-6 level * following exposure to acid-induced acute lung injury, LPS, or 1-palmitoyl-2-arachidonoyl-phosphatidylcholineDecreased susceptibility to injury * following exposure to acid-induced acute lung injury, mice exhibit alleviated symptoms compared to wild-type mice with decreased changes in elastance, edema, and serum IL6 levels* following exposure to 1-palmitoyl-2-arachidonoyl-phosphatidylcholine, lung function is improved and IL6 production is decreased compared to in similarly treated wild-type mice||C57BL/6 x 129|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|25-Jul-2008||0.0|0.0|Unknown||Toll-like receptor (TLR), MyD88, signal transduction, T cell, receptor|Yes| 323.0|NOD-Scid|NOD.CB17-Prkdc||Recessive|protein kinase, DNA activated, catalytic polypeptide|Prkdc|Unknown|DNA-PK, DNA-PKcs, DNAPDcs, DNPK1, HYRC1, slip, XRCC7|MGI:104779|severe combined immunodeficiency|Prkdc|MGI:1857113|16||||||||||||||||Yes|||||||||||||Mutations at this locus effect genome stability, radiation sensitivity and DNA repair. Homozygotes have severe combined immunodeficiency.No endogenous T- or B- Lymphocyte function. Most homozygotes have no detectable IgM, IgG1, IgG2a, IgG2b, IgG3, or IgA. Thymus, lymph nodes, and splenic follicles are virtually devoid of lymphocytes (Lymphopenia). They have hypogammaglobulinemia, and a normal hematopoietic microenvironment. Normal antigen-presenting cell, myeloid, and NK cell functions are strain dependent. Scid mice accept allogeneic and xenogeneic grafts making them an ideal model for cell transfer experiments. Develops high incidence of thymoma with age.||NOD|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|05-May-2006||0.0|0.0|Yes||scid, T cell, B cell, lymphocyte, thymoma|Yes| 2449.0||Pardon||Recessive|cadherin 23 (otocadherin)|Cdh23|Unknown|ahl, ahl1, bob, mdfw, nmf112, nmf181, nmf252, USH1D|MGI:1890219||||10||||||||||||||||No|||||||||||||Mutant mice exhibit circling behavior, tilting of the head and are deaf.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|14-Jan-2008||0.0|0.0|Unknown||Deafness, ataxia, circling, ear|Yes| 7050.0||B6.129P2-Lipe/MarpApb||Recessive|lipase, hormone sensitive|Lipe|Unknown|4933403G17Rik, HSL|MGI:96790|lipase, hormone sensitive; targeted mutation 1, Rudolf Zechner|Lipe|MGI:2388334|7|||||||||||||||||||||||||||||Abnormal lipid level: diglycerides accumulate in brown fat, white fat, testes, skeletal muscle, and cardiac muscle.Abnormal fatty acid level: shift from reduced short chain fatty acids to elevated long chain fatty acids is seen in the white fat.Abnormal triglyceride level:in white fat the fraction of triglycerides with shorter chain fatty acids is decreased and the fraction with longer chain fatty acids is increased.Decreased triglyceride level: decreased by about 70% in cardiac muscle compared to controls.Decreased liver triglyceride level:decreased by about 90% compared to controls.Increased triglyceride level: increased by about 30% in brown fat compared to controls.Abnormal metabolism: * decrease in the formation of free fatty acids in white and brown fat, skeletal and cardiac muscle, liver, and brain * reduced capacity for hydrolysis of diglycerides in all tissue examined * reduced capacity for hydrolysis of triglycerides only in white fat and testesAbnormal brown adipose tissue physiology: diglycerides accumulate in brown fatAbnormal white adipose tissue physiology: * diglycerides accumulate in white fat * the fraction of triglycerides with shorter chain fatty acids is decreased and the fraction with longer chain fatty acids is increased||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|20-Aug-2012|Cryopreserved sperm|50.0|0.0|Unknown||liver, fatty acid, triglycerides, adipose|Yes| 2451.0||Tsavo||Recessive|transmembrane channel-like gene family 1|Tmc1|Unknown|Beethoven, Bth|MGI:2151016||||19||||||||||||||||Yes|||||||||||||Mutant mice are characterized by progressive degeneration of the cochlear inner hair cells and concomitant deafness. Different alleles causing progressive deafness or profound congenital deafness||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|14-Jan-2008||0.0|0.0|Unknown||Deafness, ear, hearing, cochlea|Yes| 7395.0|B6-Lym1|B6.BALB/c-Nfkb2/WehiAnuApb||Recessive|nuclear factor of kappa light polypeptide gene enhancer in B-cells 2, p49/p100|Nfkb2|Unknown|NF kappaB2, p52|MGI:1099800|nuclear factor of kappa light polypeptide gene enhancer in B cells 2, p49/p100; Lym1|Nfkb2|MGI:4412046|19|||||||||||||||||||||||||||||Increased circulating lymphocytes.A comprehensive histopathological analysis of these mice, however, revealed an absence of peripheral LN (inguinal, brachial, axillary, cervical) and Peyer’s patches. Mesenteric LN were present, but were reduced in size and cellularity.presence of inflammatory cell infiltrates in the lung and liver.The number of mature recirculating B cells was significantly reduced.Nfkb2 bone marrow was almost completely unresponsive to RANKL with osteoclast formation <0.5% of that seen with wt.Mild osteopetrosis, with significantly increased trabecular bone volume|The ability of Nfkb2 cells to form osteoclasts in response to RANKL stimulation was significantly reduced|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|8|||No|12-Aug-2013|Cryopreserved sperm|4.0|0.0|Unknown||noncanonical, p52, signal transduction, lymph node, osteopetrosis, B cell|Yes| 9430.0||C57Bl/6J -Tg<(Ace2-ACE2)1Pqt>/Apb||Semi-dominant|angiotensin converting enzyme 2|Ace2 |||MGI:1917258|mAce2-hACE2|||X|||||||||||||||||transgene insertion 1, Paul Q Thomas|mAce2|||||||||||Normal|Normal|C57Bl/6J|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|21-Sep-2022|Cryopreserved sperm|50.0|0.0|Unknown|||Yes| 3593.0||C57BL/6.129-Tcra||Recessive|T-cell receptor alpha chain|Tcra|Nil|Tcr alpha, Tcralpha|MGI:98553|targeted mutation 1, Peter Mombaerts|Tcra|MGI:1857255|14||||||||||||||||No|||||||||||||Mice homozygous mice for the Tcra targeted mutation are viable and fertile. They are deficient in the alpha beta T-cell receptor. The thymus is devoid of CD4+CD8- and CD4-CD8+ cells. Normal numbers of CD4+CD8+ cells are retained without the IL2 receptor. There are normal numbers of CD4-CD8- cells. ~1% of the thymocytes express the gamma delta TCR. Mice may develop inflammatory bowel disease beginning at ~4-6 months of age. Increased susceptibility to bacterial infection • greatly increased susceptibility to infection with Mycobacterium paratuberculosis. Older mice may have digestive system problems including ulcers and diarrhea. They will have an impaired immune response but should remain healthy under clean conditions ||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|06-Aug-2008||0.0|0.0|Unknown||T cell, T cell receptor (TCR), inflammatory bowel disease, CD4 , CD8|Yes| 4962.0|Ccr1 +/+|129-Ccr1||Recessive|chemokine (C-C motif) receptor 1|Ccr1|Nil|Cmkbr1, MIP-1 alphaR, Mip-1a-R|MGI:104618||||9||||||||||||||||No|||||||||||||Normal.Control for Ccr1 knockout mouse.||129|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|13-Jan-2010|Cryopreserved sperm|50.0|0.0|Unknown||chemokine, RANTES, neutrophil, inflammation|Yes| 2803.0|C57BL/6.Max 41|C57BL/6-Tg(IghMAX)41Wehi/Wehi ||Dominant||||||||||||||||||||||||||human Max|5' intronic enhancer Eu of the immunoglobulin heavy chain locus|||||||||||Excess granulocytes, B cell deficiency, thymic lymphoma.Maximal severity of phenotype according to age.Approx. 30% thymic lymphomas at 6-12 wks.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|22-Feb-2008||0.0|0.0|Unknown||Lymphocyte, myeloid, granulocyte, B cell, lymphoid, thymoma|Yes| 5441.0|Men1 del/wt (Martin C)|B6.129T2-Men1/Apb|B6.129T2-Men1|Recessive|multiple endocrine neoplasia 1|Men1|Nil|menin|MGI:1316736|multiple endocrine neoplasia 1; targeted mutation 2.1, Graham F Kay|Men1|MGI:3810641|19||||||||||||||||No|||||||||||||Embryonic lethal|Tumours with age predominantly in pancreas, pituitary and parathyroids.|C57BL/6|No|No|Yes|No|No|Yes|No|Good|14|1|heterozygote cross wildtype|No|17-Feb-2011|Cryopreserved sperm|50.0|0.0|Yes|Used to model human MEN1|menin, men1, Multiple Endocrine Neoplasia, Type I; MEN1, transcription factor, pancreas, Jun|Yes| 3626.0||B6.129S4-IL2ra||Recessive|interleukin 2 receptor, alpha chain|Il2ra|Nil|CD25, IL-2R alpha chain, Il2r, Ly-43|MGI:96549|targeted mutation 1, Dennis M Willerford|Il2ra|MGI:1857192|2||||||||||||||||Yes|||||||||||||Homozygotes for a targeted null mutation exhibit massive proliferation of polyclonal T and B cells as adults and develop autoimmune disorders including inflammatory bowel disease and hemolytic anemia with age.||C57BL/6 x 129|Yes|No|Yes|Yes|No|Yes|No|Unknown||||No|12-Aug-2008||0.0|0.0|Unknown||T cell, lymphoid hyperplasia, activation, autoimmunity, enlarged lymph nodes and splenomegaly|Yes| 6913.0|ENU23:G1|ANU:ENU23:G1||Recessive|Unknown||||||||Unknown||||||||||||||||Unknown|||||||||||||Unknown|Unknown|C57BL/6Crl|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||1||No|22-Jun-2012|Cryopreserved sperm|1398.0|0.0|Unknown||ENU, random, mutagenesis, screen|Yes| 6911.0|ENU22:G1|ANU:ENU22:G1||Recessive|Unknown||||||||Unknown||||||||||||||||Unknown|||||||||||||Unknown|Unknown|C57BL/6Crl|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||1||No|22-Jun-2012|Cryopreserved sperm|1096.0|0.0|Unknown||ENU, random, mutagenesis, screen|Yes| 7409.0|Amigo2 KO ; TF3111|B6.129/SvEv-Amigo2/TacAnuApb||Recessive|adhesion molecule with Ig like domain 2|Amigo2|||MGI:2145995||||15|||||||||||||||||||||||||||||Unknown||C57BL/6NCrlAnu|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|22-Aug-2013|Cryopreserved sperm|11.0|0.0|Unknown|||Yes| 7435.0|CSTCR|C.B6-Thy1 Tg(TcraTcrbYA26)1/QimrAnuApb||Dominant|thymus cell antigen 1, theta|Thy1||CD90, T25, theta, Thy-1, Thy1.1, Thy 1.2, Thy-1.2, Thy1.2|MGI:98747|thymus cell antigen 1, theta; a variant|Thy1|MGI:3579311|9|||||||||||||||||tansgene insertion 1, Fidel Zavala||||||||||||The mice express a monoclonal TCR specific for SYVPSAEQI in context of H2Kd – these particular mice are backcrossed to Thy1.1||BALB/c|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|16-Sep-2013|Cryopreserved sperm|50.0|0.0|Unknown||TCR, CD8, Plasmodium yoelii|Yes| 4867.0|TNAP:Cre ; TC|BALB/c-Alpl ||Recessive|alkaline phosphatase, liver/bone/kidney|Alpl|Nil|Akp-2, Akp2, TNSALP, TNAP|MGI:87983|targeted mutation 1, Andras Nagy|Alpl|MGI:2177588|4||||||||||||||||Yes|Cre recombinase|TNAP|||||||||||Embryonic Lethal||BALB/c x C57BL/6|No|No|Yes|No|No|Yes|No|Unknown||||No|25-Sep-2009||0.0|0.0|Unknown||alkaline phosphatase, primordial germ cell|Yes| 3326.0|Chop KO|C57BL/6-Ddit3/Wehi||Recessive|DNA-damage inducible transcript 3|Ddit3|Nil|C/EBP homoologous protein 10, chop, CHOP-10, CHOP10, gadd153|MGI:109247|targeted mutation 1, Masakata Mori|Ddit3|MGI:2179046|10||||||||||||||||Yes|||||||||||||Original mutant on 129/C57BL/6 background had larger brains. Decrease neuronal apoptosis in vivo and in vitro.On C57BL/6 background: kidney epithelium, macrophages and thymocytes are resistant to ER stress induced apoptosis.Males are aggressive.|Normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|5||Het x WT C57BL/6|No|15-Jun-2008||0.0|0.0|Unknown||endoplasmic reticulum stress, Bim, pancreatic, neuron, brain|Yes| 5261.0|Col1-EphB4 Tg|C57BL/6-Tg(Col1a1-EphB4)1Mat||Dominant||||||||||||||||||||||||||Mouse Eph receptor B4|collagen, type I, alpha 1 (Col1a1)|Restricted to osteoblasts||||||||||EphB4 transgenic mice expressed 6.7-fold higher levels of Ephb4 transcripts in calvaria and 4.8-fold higher in the long bones as measured by RT-PCR.EphB4 transgenic mice exhibited increased bone mass by 10 weeks of age.Quantitative bone histomorphometry further showed that bone volume, osteoid thickness, mineralizing surface, and bone formation rate were significantly increased in transgenic mice versus wild-type controls (Figure 7C). Serum levels of osteocalcin, a marker of bone formation, were also slightly elevated in EphB4 transgenic mice.Osteoclast number, osteoclast surface, and eroded surface were significantly reduced in EphB4 transgenic mice compared towild-type controls, indicating that osteoclast function was inhibited in these mice.EphB4 transgenic mice showed a decrease in urinary deoxypyridinoline (DPD) crosslinks, a marker for osteoclastic bone resorption, indicating that osteoclast function was suppressed. Such reduced osteoclastic activity is not due to reduction in RANKL or M-CSF or to an increase in OPG since there was no significant difference in Rankl, Csf1, and Opg mRNA levels in bone or RANKL and OPG levels in serum between wild-type and EphB4 transgenic mice.||C57BL/6|Yes|Unknown|Yes|Yes|Unknown|Yes|No|Unknown||||No|21-Oct-2010||0.0|0.0|Unknown||osteoclast, osetoblast, bone resorbtion, collagen|Possibly| 5288.0|B6.PAR1.KO|C57BL/6-F2r||Recessive|coagulation factor II (thrombin) receptor|F2r|Nil|Cf2r, Par1, thrombin receptor, ThrR|MGI:101802|coagulation factor II (thrombin) receptor; targeted mutation 1, Andrew J Connolly|F2r|MGI:1857306|13||||||||||||||||No|||||||||||||Embryonic lethality during organogenesis: * approximately 50% of homozygotes die between E9.0-10.0. * the remaining 50% survive to adulthood and appear grossly normal. * similar frequencies of embryonic lethality are observed in the C57BL/6J and 129/Sv inbred backgrounds.Abnormal cardiovascular system physiology: * at E8.5, homozygotes have beating hearts and a functional vitelline circulation. * by E9.5, approximately half of the mutant embryos display no heart beat.Abnormal cell physiology: notably, in contrast to platelets, homozygous mutant fibroblasts lack thrombin-induced responses.Decreased embryo size: * at E8.5, homozygotes are morphologically indistinguishable from wild-type embryos. * starting at E9.0, mutant embryos become uniformly smaller than wild-type embryos.Abnormal placenta development: at E9.0 and thereafter, homozygotes display a delay in placental development.Embryonic growth retardation: at E9.0 and thereafter, homozygotes display a global developmental delay.Hematopoietic system phenotype: * surviving homozygotes display normal tail bleeding times and no bleeding diathesis relative to wild-type. * in addition, mutant platelets display strong thrombin-induced responses.||C57BL/6|Yes|Unknown|Yes|Yes|Unknown|Yes|No|Unknown||||No|28-Oct-2010||0.0|0.0|Unknown||thrombin, receptor, G-protein, wound, inflammation|Possibly| 3339.0|cbfa2t3 -/-|C57BL/6-Cbfa2t3/Apb||Recessive|core-binding factor, runt domain, alpha subunit 2, translocated to, 3 (human)|cbfa2t3|Nil|ETO-2, MTGR2|MGI:1338013||||8||||||||||||||||Yes|||||||||||||Normal|Normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|3||Hom x Hom|Yes|20-Jun-2008|Cryopreserved sperm|90.0|0.0|No||leukaemia / leukemia, translocation, breast, transcription|Yes| 7051.0|Aire x Met-Kb|STOCK-Aire Tg(sMt1-H2-K)||Recessive|autoimmune regulator (autoimmune polyendocrinopathy candidiasis ectodermal dystrophy)|Aire|||MGI:1338803||||10|||||||||||||||||mouse H2-K (MHC class I)|Sheep metallothionein promoter|variable and slightly lower than wild type H2-K. Expression can be induced with Zinc||||||||||Normal|Normal|B10.BR|Yes|Yes|Yes|Yes|Yes|Yes|No|Excellent|more than 10|||No|20-Aug-2012||0.0|0.0|No||tolerance, liver, CD8 T cells, MHC class I, autoimmunity|Possibly| 4963.0|Sall-GFP|B6.129-Sall1/Apb||Dominant|sal-like 1 (Drosophila)|Sall1|Normal|Msal-3|MGI:1889585|sal-like 1 (Drosophila); targeted mutation 3, Ryuichi Nishinakamura|Sall1|MGI:3603818|8||||||||||||||||No|||||||||||||Embryonic lethal|Normal.GFP labelled Sall1 structures in embryonic kidney.|C57BL/6|No|No|Yes|No|No|Yes|No|Good||||No|15-Jan-2010|Cryopreserved sperm|72.0|0.0|Unknown||Cap mesenchyme, Nephrogenesis|Yes| 4967.0|B6-HIPCre|B6.NOD-Tg(INS-cre)2Rms/MarpApb||Dominant||||||||||||||||||||||||||transgene insertion 2, Robyn M Slattery|human insulin promoter|beta islet cells||||||||||The human insulin promoter (INS) drives cre expression in beta islet cells. Resistance to development of diabetes and hyperglycemia||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|15-Jan-2010|Cryopreserved sperm|100.0|0.0|Yes||Autoimmunity, insulin, Beta cell|Yes| 6200.0|CD14|B6.129S-CD14/J||Recessive|CD14 antigen|Cd14 |Nil||MGI:88318|CD14 antigen; targeted mutation 1, Mason W Freeman|Cd14|MGI:1934009|18|||||||||||||||||||||||||||||Pulmonary edema:*Less protein leakage into bronchoalveolar lavage fluid after lipopolysaccharide inhalation.Abnormal cytokine level:*Keratinocyte derived cytokine levels in lungs are unaffected by low doses of lipopolysaccharide.*Macrophage inflammatory protein-2 levels in lungs are unaffected by low doses of lipopolysaccharide. Abnormal interleukin level: *Il-6 levels in lungs are unaffected by low doses of lipopolysaccharide. Abnormal tumor necrosis factor level: *TNF alpha levels in lungs are unaffected by low doses of lipopolysaccharide.Increased bone mineral content:*Greater mineral content.Increased bone mineral densityIncreased bone mass:*Increased bone area of the tibia.Decreased susceptibility to bone fracture:*Bones resistant to fracture.Pulmonary edema:*Less protein leakage into bronchoalveolar lavage fluid after lipopolysaccharide inhalation.Decreased total body fat amountIncreased lean body mass||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown||CD14, Inflammatory response, TNF-alpha, IL-6|Yes| 6204.0|IFNg |B6.129S7-Ifng/J |||| ifng ||||||||||||||||||||||||||||||||||||"Mice homozygous for the Ifngtm1Ts targeted mutation are viable and fertile. Homozygotes appear normal in a ""clean"" environment but display reduced macrophage function in response to pathogens. Specifically, macrophages show impaired production of antimicrobial products and reduced expression of MHC II antigens. There is also uncontrollable proliferation of splenocytes from homozygotes in response to mitogens and alloantigens and a reduced resting natural killer cell activity. Increased sensitivity to xenobiotic induced morbidity/mortality Increase in mortality following a single dose of N-methyl-N-nitrosourea (MNU) Increased susceptibility to bacterial infection induced morbidity/mortality Die by 6 - 10 weeks after infection with the avirulent BCG strain of Mycobacterium bovis (MGI Ref ID J:47459) Increased susceptibility to parasitic infection induced morbidity/mortality Most mice die by 9 days after infection with 1x106 Cryptosporidium parvum oocysts (MGI Ref ID J:50832) "||C57BL/6|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6915.0|ENU25:G2|ANU:ENU25:G2||Recessive||||||||||||||||||||||||||||||||||||||Unknown|Unknown|C57BL/6Crl|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown|1|||No|22-Jun-2012|Cryopreserved sperm|1438.0|0.0|Unknown||ENU, mutagenesis, screen, random|Yes| 6914.0|ENU25:G1|ANU:ENU25:G1||Recessive|Unknown||||||||Unknown||||||||||||||||Unknown|||||||||||||Unknown|Unknown|C57BL/6Crl|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||1||No|22-Jun-2012|Cryopreserved sperm|497.0|0.0|Unknown||ENU, random, mutagenesis, screen|Yes| 6912.0|ENU24:G1|ANU:ENU24:G1||Recessive|Unknown||||||||Unknown||||||||||||||||Unknown|||||||||||||Unknown|Unknown|C57BL/6Crl|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||1||No|22-Jun-2012|Cryopreserved sperm|471.0|26.0|Unknown||ENU, random, mutagenesis, screen|Yes| 844.0|SW{HEL}-L ; LC2 Ig|C57BL/6-Tg(IgkHyHEL10)1Rbr||Dominant||||||||||||||||||||||||||transgene insertion 1, Robert Brink||||||||||||B cells express immunoglobulin light chain that recognises hen egg lysozyme.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|23-May-2007||0.0|0.0|Unknown||Immunoglobulin, Hen egg lysozyme (HEL), self-tolerance, autoimmunity, B cell|Yes| 3407.0|MHCII I-A o/o|B6.129-H2-Ab1/Wehi||Recessive|histocompatibility 2, class II antigen A, beta 1|H2-Ab1|Nil|A beta, Abeta, H-2Ab, H2-Ab, I-A, I-Abeta, Ia-2, Ia2, IAb, Rmcs1|MGI:103070|histocompatibility 2, class II antigen A, beta 1; targeted mutation 1, Christophe Benoist and Diane Mathis|H2-Ab1|MGI:1927483|17||||||||||||||||Yes|||||||||||||MHC II-deficient mice do not develop CD4 (helper) T cells. This results in impaired cellular and antibody mediated immune responses. Mice do not appear different to C57BL/6 mice when housed in a clean environment. IA/IA mice seem to breed more robustly when first mated at an older age (12 weeks) rather than the standard 8 weeks (observation G. Davey)||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|13-Jul-2008||0.0|0.0|Unknown||MHC Class II, histocompatability, T cell, CD4|Yes| 5617.0|B57||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 3418.0|Max.OT-1 transgenic|C57BL/6-Tg(TcraTcrb)1100Mjb Tg(IghMAX)Wehi/Wehi||Dominant||||||||||||||||||||||||||transgene insertion 1100, Michael J Bevan||||||||||||TCR transgenics are immunocompromised by having a mono-specific T cell receptor however, in a clean envirnoment, mice show no difference in phenoptype from wild-type B6 mice. Max.OT-I T cells are highly diabetogenic when transferred into RIP-mOVA mice.||C57BL/6 x 129|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|14-Jul-2008||0.0|0.0|Unknown||T cell, receptor (TCR), autoimmunity, lymphocyte|Yes| 3418.0|Max.OT-1 transgenic|C57BL/6-Tg(TcraTcrb)1100Mjb Tg(IghMAX)Wehi/Wehi||Dominant||||||||||||||||||||||||||human Max|5' intronic enhancer Eu of the immunoglobulin heavy chain locus|||||||||||TCR transgenics are immunocompromised by having a mono-specific T cell receptor however, in a clean envirnoment, mice show no difference in phenoptype from wild-type B6 mice. Max.OT-I T cells are highly diabetogenic when transferred into RIP-mOVA mice.||C57BL/6 x 129|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|14-Jul-2008||||Unknown||T cell, receptor (TCR), autoimmunity, lymphocyte|Yes| 6231.0|Bak/vavbcl69|B6.129-Bak1 Tg(Vav-BCL2)1Jad||Semi-dominant|BCL2-antagonist/killer 1|Bak1|Nil|Bak, N-Bak|MGI:1097161|BCL2-antagonist/killer 1; targeted mutation 1, Craig B Thompson|Bak1|MGI:2159364|17|||||||||||||||||transgene insertion 1, Jerry M Adams|mouse Vav promoter|Overexpression||||||||||||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown||bak, Bcl-2, Hematopoiesis|Yes| 5622.0|B6;129P2-OmpMomJ||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6234.0|Bax/Bmf|B6.129-Bax Bmf||Recessive|BCL2 modifying factor|Bmf|Nil||MGI:2176433|BCL2 modifying factor; targeted mutation 1, Roger J Davis|Bmf|MGI:4421178|2|||||||||||||||||||||||||||||Male sterility in -/-. Otherwise, grossly normal. Most -/- mice have grey fur compared to +/- and +/+ which are black. Double -/- males should be infertile.||129/Sv|Yes|Unknown|Yes|Yes|No|Yes|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown||Bax, Bmf|Yes| 6234.0|Bax/Bmf|B6.129-Bax Bmf||Recessive|BCL2-associated X protein|Bax|Nil||MGI:99702|BCL2-associated X protein; targeted mutation 1, Stanley J Korsmeyer|Bax|MGI:1857429|7|||||||||||||||||||||||||||||Male sterility in -/-. Otherwise, grossly normal. Most -/- mice have grey fur compared to +/- and +/+ which are black. Double -/- males should be infertile.||129/Sv|Yes|Unknown|Yes|Yes|No|Yes|No|Unknown||||No|13-Sep-2011||||Unknown||Bax, Bmf|Yes| 6805.0|tenascin C KO|129/Sv-Tnc/MelbApb||Recessive|tenascin C|Tnc|Nil|C130033P17Rik, cytotactin, hexabrachion, Hxb, tenascin-C, TN, TN-C|MGI:101922|tenascin C; targeted mutation 1, Reinhard Fassler|Tnc|MGI:2148541|4|||||||||||||||||||||||||||||No abnormal phenotype.|No abnormal phenotype.|129/Sv|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|31-Jan-2012|Cryopreserved sperm|50.0|0.0|Unknown||matrix, fibronectin, RhoA|Yes| 4799.0|Dimit; ENU13NIH:039ab|C57BL/6JAnu-Ighd/AnuApb|C57BL/6JAnu-Ighd/AnuApb|Recessive|immunoglobulin heavy constant delta|Ighd|Unknown|IgD|MGI:96447|dimit|Ighd|MGI:4819235|12|ENSMUSG00000076616|ENSMUST00000103424|Igh-5-201|241|241|T to A|ENSMUSE00000663372|1|74|Isoleucine to Lysine|||||CAGAACTGAACCTCAACCACACTTGCACCATAAATAAACCCAAAAGGAAAGAAAAACCTTT|Yes|||||||||||||Shifted IgD expression measured by flow cytometry||C57BL/JAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|10-Sep-2009|Cryopreserved sperm|37.0|0.0|Unknown||IgD, immunoglobulin, B cell, ENU, NIH|Yes| 4588.0|Seshat ; ENU11B6:169b|C57BL/6JAnu-Cd4/AnuApb|C57BL/6JAnu-Cd4/AnuApb|Recessive|CD4 antigen|Cd4|Unknown|L3T4, Ly-4|MGI:88335|seshat|Cd4|MGI:4819228|6|ENSMUSG00000023274|ENSMUST00000024044|Cd4-001|374|543|T to C|ENSMUSE00000246632|4|125|Valine to Alanine|||||GAACAGGAAAGAGGAGGTGGAGTTGTGGGTGTTCAAAGTGACCTTCAGTCCGGGTACCAGC|Yes|||||||||||||Reduced T cell numbers in peripheral blood. Reduced CD4 expression.||C57BL/6JAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|11-Mar-2009|Cryopreserved sperm|97.0|0.0|Unknown||T cell, CD4, CD8, ENU, NIH, Wellcome Trust|Yes| 3624.0||B6.CBA-Tg(Pou5f1-EGFP)||Dominant|||||||||Unknown||||||||||||||||Yes|Enhanced green fluorescent protein (GFP)|Pou domain, class 5, transcription factor 1 (Pou5f1)|||||||||||Expression of GFP in primordial germ cells||C57BL/6 x CBA|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|12-Aug-2008||0.0|0.0|Unknown||Pou domain, transcription factor, reporter, GFP|Yes| 6256.0|CBA.nu|CBA-Foxn1/Wehi||Recessive|forkhead box N1|Foxn1|Nil|D11Bhm185e, Hfh11, whn|MGI:102949|forkhead box N1; nude |Foxn1|MGI:1856108|11|||||||||||||||||||||||||||||Partial postnatal lethality:*Some mice die within 1 week of birth*55% mortality within 2 weeksPremature death:*100% mortality by 25 weeksSmall ovaryDecreased body size Decreased body weightPostnatal growth retardationAbnormal liver morphology:*Liver lobes were atrophied and covered with red scars.*Variable degrees of severity, typically increasing with age at time of death.Coiled sperm flagellum:*Many sperm had coiled tails.Abnormal estrous cycle:*Many females exhibited continuous dioestrus and metaoestrus phasesFemale infertility:*Severely reduced fertility.Reduced male fertilityAsthenozoospermiaDecreased leukocyte cell numberAthymiaHairless*Sparse hair growth around 5 weeks of age.*In some mice, cephalo-caudal migration of an irregular band of short sparse hair.Absent vibrissae:*Absent at birth.Short vibrissae:*Older mice show repeated growth and loss of short and wavy vibrissae.Wavy vibrissae:*Older mice show repeated growth and loss of short and wavy vibrissae.Thin skin:*Reduction in skin thickness at 3 weeks of age, corresponding to the catagen stage of normal skin.||CBA|Yes|No|Yes|Yes|No|Yes|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Yes| 5158.0|4AT22 ; ANNA|ENU4AT:022||Recessive|Unknown||||||||Unknown|||||||||||||||||transgene insertion 3, Christopher C Goodnow|Rat insulin promoter|||||||||||Anti-nuclear antibodies, high.Both young and older mice.|Normal|C57BL/6 x B10BR X CBA|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|25-Jun-2010|Cryopreserved sperm|15.0|0.0|Yes|Type I Diabetes|ENU, JDRF, T cell, autoimmunity, antinuclear antibody|No| 5158.0|4AT22 ; ANNA|ENU4AT:022||Recessive||||||||||||||||||||||||||transgene insertion 1, Mark M Davis||||||||||||Anti-nuclear antibodies, high.Both young and older mice.|Normal|C57BL/6 x B10BR X CBA|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|25-Jun-2010|Cryopreserved sperm|||Yes|Type I Diabetes|ENU, JDRF, T cell, autoimmunity, antinuclear antibody|No| 6917.0|FVBNJ-Momme D35|FVB/NJ-Smarca5 Tg(HBA1-Gfp)3Ew/Apb||Semi-dominant|SWI/SNF related, matrix associated, actin dependent regulator of chromatin, subfamily a, member 5|Smarca5|||MGI:1935129|SNF2 related chromatin remodeling ATPase 5; modifier of murine metastable epialleles, D35|Smarca5|MGI:5515388|8||||||||||Unknown to Unknown|||||||transgene insertion 3, Emma Whitelaw|Human alpha-globin promoter (-570 to +37) and 4.1kb of enhancer region|36 copies||||||||||Lethal|Normal|FVB/NJ|No|No|Yes|No|No|Yes|No|Good||||No|25-Jun-2012|Cryopreserved sperm|39.0|0.0|Unknown|||Possibly| 1823.0|MHC II-EGFP|C57BL/6-Tg(MHCII-EGFP)||Dominant||||||||||||||||||||||||||MHC class II tagged with Green fluorescent Protein||||||||||||Normal.MHC II positive cells are fluorescent (EGFP+).Phenotype does not differ from a wildtype of the same genetic background.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|06-Aug-2007||0.0|0.0|Unknown||GFP, MHC class II, H2, histocompatability 2|Yes| 6257.0|CD40K|B6.129P2-Cd40||Recessive|CD40 antigen|Cd40|Nil|Bp50, Cd40, p50, Tnfrsf5|MGI:88336|CD40 antigen; targeted mutation 1, Hitoshi Kikutani|Cd40|MGI:1857457|2|||||||||||||||||||||||||||||Hematopoietic system phenotype*Normal thrombogenesis in ferric-chloride-induced injury of mesenteric arterioles.Abnormal dendritic cell physiology:*Impaired production of IL-12 after Mycobacterium tuberculosis infection and after incubation with Hsp7.*Impaired priming of IFN-gamma producing T cells.Increased susceptibility to bacterial infection:*Increased susceptibility to aerosol Mycobacterium tuberculosis infection.*Increased bacterial loads in lung and spleen.*40% of infected mice moribund 3 - 4 weeks postinfection.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown||CD40, CD23, Immunoglobulin, Germinal center formation|Yes| 6270.0|ERTF5/TOM|ERTF5-rttA3-GFP/Tet-O c-myc|||| ERTF5TA c-myc ||||||||||||||||||||||||||||||||||||Contact Researcher This strain carries the human c-myc gene and the rttA3-IRES-GFP cassette which are controlled by the Tet/O and the ERTF5 promoter respectively. The expression of myc is induced in ERTF5 expressing cells only in the presence of doxycycline. No Special monitoring required (This stain should not have any obvious phenotype without treatment of doxycycline.) DOX - The phenotypes of this strain with treatment of doxycycline remain unknown. But this strain may potentially develop tumors in certain tissues upon treatment with doxycycline. ||FVB|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 4848.0|Lenie|ENU6AT:32||Recessive|||||||||Unknown|||||||||||||||||transgene insertion 3, Christopher C Goodnow|Rat insulin promoter|Expression of the inserted sequence specifically to pancreatic islet beta cells||||||||||Male infertility. Mutant found in HEL:TCR ENU library.HEL:TCR transgenes not required for mutant phenotype||C57BL/6 x CBA x C57BL/10BR|Yes|Yes|Yes|Yes|No|Yes|No|Poor||||No|24-Sep-2009|Cryopreserved sperm|30.0|0.0|Yes|Male Infertility|ENU, fertility, sperm|Yes| 4848.0|Lenie|ENU6AT:32||Recessive||||||||||||||||||||||||||transgene insertion 1, Mark M Davis||||||||||||Male infertility. Mutant found in HEL:TCR ENU library.HEL:TCR transgenes not required for mutant phenotype||C57BL/6 x CBA x C57BL/10BR|Yes|Yes|Yes|Yes|No|Yes|No|Poor||||No|24-Sep-2009|Cryopreserved sperm|||Yes|Male Infertility|ENU, fertility, sperm|Yes| 5621.0|B6 ROSAeGFPxCol1a2 ||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6918.0|FVBNJ-Momme D36|FVB/NJ-Smchd1 Tg(HBA1-Gfp)3Ew/Apb||Semi-dominant|SMC hinge domain containing 1|Smchd1||4931400A14Rik, mKIAA0650, MommeD1|MGI:1921605|SMC hinge domain containing 1; modifiers of murine metastable epiallele D36|Smchd1|MGI:5515389|17||||||||||Unknown to Unknown|||||||transgene insertion 3, Emma Whitelaw|Human alpha-globin promoter (-570 to +37) and 4.1kb of enhancer region|36 copies||||||||||Lethal|Normal|FVB/NJ|No|No|Yes|No|No|Yes|No|Good||||No|25-Jun-2012|Cryopreserved sperm|40.0|0.0|Unknown||ENU, GFP, DNA methylation, epigenetic|Possibly| 7457.0|C2(129)|129X1-Cited2/VccriApb|129X1-Cited2|Recessive|Cbp/p300-interacting transactivator, with Glu/Asp-rich carboxy-terminal domain, 2|Cited2|Nil|ER154-like, Mrg1, Msg2, p35srj|MGI:1306784|targeted mutation 1, Juan Pedro Martinez Barbera|Cited2|MGI:2176158|10||||||||||||||||No|||||||||||||Embryos die during gestation (~E15.5). Heart, left-right axis, neural tube, adrenal gland and placental defects.|None|129X1|No|No|Yes|No|No|Yes|No|Good|10|0|C2B6∆ +/- (heterozygous) mated with 129X1|No|22-Oct-2013|Cryopreserved sperm|50.0|0.0|Yes||Cited2, heart, placenta, left-right axis|Yes| 40.0|Flipper|B6;NODAnu-Chkb/AnuApb|B6;NODAnu-Chkb/AnuApb|Recessive|choline kinase beta|Chkb|Unknown|Chetk, Chkl, CK/EK-beta|MGI:1328313|flipper|Chkb|MGI:3847123|15|ENSMUSG00000022617|ENSMUST00000023289|Chkb-201|1|1|A to T|ENSMUSE00000322690|1|1|Methionine to Leucine|||||ATGGCGGCAGACGGGACAGGGGTAGTCGGAGG|No|||||||||||||Homozygotes develop shortened and lateral rotation (valgus?) of radius and ulna leading to short and splayed forelegs. Female homozygotes can breed. Male homozygotes die suddenly during mating with haemorrhages in seminiferous glands (this is currently being re-investigated). Some homozygotes also develop perineal hernias.Chkb Homozygous null mice display progressive muscular weakness and dystrophy in the hindlimbs but have normal nerve and neuromuscular junction morphology.||C57BL/6 x NOD|Yes|Yes|Yes|Yes|Yes|Yes|Yes|Good||||No|06-Feb-2006|Cryopreserved sperm|70.0|0.0|Unknown||limb, rostocaudal muscular dystrophy, kinase, phosphatidylcholine, ENU|Yes| 5625.0|B6.126Tg(myh6-cre/Ers1)1Jmk/J Cardiac Cre||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 2444.0|Lightning ; ENU8B6:045|C57BL/6-Ptprc/AnuApb|C57BL/6-Ptprc/Apb|Recessive|protein tyrosine phosphatase, receptor type, C|Ptprc|Unknown|B220, CD45, Cd45, Ly-5, Lyt-4, T200|MGI:97810|protein tyrosine phosphatase, receptor type, C; lightening|Ptprc|MGI:4441612|1|ENSMUSG00000026395|ENSMUST00000027645|Ptprc-201|1583|1681|T to C|ENSMUSE00000595907|14|528|Phenylalanine to Serine|||||TACAAAATACAACAAGACAAACTGTCAGTTTTATGTAGATAATCTCTACTATTCAACTGAC|No|||||||||||||Homozygous null mutants have defective T-cell maturation.Decreased CD4-positive T cell number: SP4 thymocytes are reduced compared to in wild-type mice.Abnormal T cell differentiation: * mice exhibit enhanced negative selection compared with wild-type mice. * positive selection of T cell is rescued and single positive thymic subsets compared to in Ptprc homozygotes.Decreased double-positive T cell number.Thymus hypoplasia.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|14-Jan-2008|Cryopreserved sperm|39.0|0.0|Unknown||T cell, Ly5, thymocyte, lymphocyte, B cell, ENU|Yes| 8355.0|Srsf3-UbcCreERT2-RFP|C57BL/6N-Srsf3 Tg(UBC-cre/ERT2)1Ejb Tg(RFP)/Apb||Recessive|serine/arginine-rich splicing factor 3|Srsf3||Sfrs3, X16|MGI:98285|serine/arginine-rich splicing factor 3; targeted mutation 1a, Mouse Biology Program, UCDavis|Srsf3|MGI:4462527|17|||||||||||||||||transgene insertion 1, Eric J Brown|human ubiquitin C |||||||||||Constitutive expression of RFP, tamoxifen inducible Srsf3 knockout, no phenotype until induced.|See above|C57BL/6N|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|27-Nov-2017|Cryopreserved sperm|50.0|0.0|Unknown|||Yes| 8355.0|Srsf3-UbcCreERT2-RFP|C57BL/6N-Srsf3 Tg(UBC-cre/ERT2)1Ejb Tg(RFP)/Apb||Recessive||||||||||||||||||||||||||Red Fluorescence Protein||||||||||||Constitutive expression of RFP, tamoxifen inducible Srsf3 knockout, no phenotype until induced.|See above|C57BL/6N|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|27-Nov-2017|Cryopreserved sperm|||Unknown|||Yes| 3423.0|RIP-EYFPss|C57BL/6-Tg(Ins2-EYFP/OVA{257-264}/gB{498-505})/Wehi||Dominant||||||||||||||||||||||||||yellow fluorescent protein (YFP) linked to two class I epitopes: one from OVA (OVA{257–264}) and one from Herpes simplex virus-1 glycoprotein B (gB{498–505})|Rat insulin 2|||||||||||Transgenic mice expressing a hybrid fusion protein under the control of the rat insulin promoter (RIP). This hybrid protein consists of yellow fluorescent protein (YFP) linked to two class I epitopes: one from OVA (OVA257–264) and one from Herpes simplex virus-1 glycoprotein B (gB498–505). The hybrid protein is referred to as YSS and the transgenic line RIP-YSS. YSS was expressed only in Pancreas.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|15-Jul-2008||0.0|0.0|Unknown||T cell, presentation, clonal deletion, autoimmunity, dendritic cell|Yes| 3447.0|SOCS-1 (SOCS box) KO clone 311 (SOCS-1ΔSB)|C57BL/6-Socs1/Wehi||Recessive|suppressor of cytokine signaling 1|Socs1|Normal|cish1, Cish7, JAB, JAK-binding protein, JAK2-binding protein, SOCS-1, SSI-1, STAT-induced STAT inhibitor 1|MGI:1354910|targeted mutation 2, Walter and Eliza Hall Institute of Medical Research|Socs1|MGI:2177057|16||||||||||||||||Yes|||||||||||||The SOCS box is a C-terminal domain shared with over 30 other proteins that links SOCS proteins to an E3 ubiquitin ligase activity and the proteasome. Mice have an increased responsiveness to IFN- and slowly develop a fatal inflammatory disease.Homozygous  mice (SOCS-1ΔSB) were healthy at birth but died prematurely compared with  or wild-type animals. However,the onset of disease was prolonged compared with SOCS-1-/- mice, and it most closely matched that seen previously for SOCS-1-/-/IFN-γ--/ mice. In fact, the predominant disease states seen in SOCS-1ΔSB mice were remarkably similar in frequency and type to those of moribund SOCS-1-/- IFN-γ-/- mice of the same age. Body weight was reduced and extensive inflammatory lesions were seen in skeletal and heart muscle, as well as in the cornea, sometimes with corneal ulceration. The infiltrating cells were predominantly lymphoid cells and macrophages, but the damage to muscle cells was often more severe than that seen in SOCS-1-/-IFN-γ-/- mice. In addition, lymphoid foci were observed in the salivary glands, lungs, and kidneys of mice, and the ratio of granulocytes to mononuclear (lymphoid and erythroid) cells was elevated in the bone marrow. Like SOCS-1-/- mice,  SOCS-1ΔSB mice showed atrophy and dispersion of pancreatic acinar tissue with lymphoid and macrophage infiltration of both the pancreas and dermis and atrophy or thinning of the thymic cortex. Although liver cells did not show fatty degeneration typical of SOCS-1-/- mice, there were areas where the liver trabeculae were thin and widely separated, suggesting previous damage to hepatocytes. This phenotype suggested that SOCS-1/ΔSB acted as a partial loss of function mutant with significantly reduced capacity to inhibit responses to endogenous IFN-γ.Premature death: mice start dying around weaning age with 80% of mice dead by 80 days of age.Decreased body weight: weights drop as mice develop inflammatory disease.Absent spleen germinal center: 55% of mice have no germinal centers in the spleen.Thymus atrophy: is observed in 95% of mice.Increased inflammatory response: mice die from massive generalized inflammation that affects multiple organs.Myocarditis: 90% of mice have inflammation in heart muscle.Pancreas inflammation: is observed in 55% of mice.Salivary gland inflammation: is observed in 61% of mice.Intestinal inflammation: 15% of mice have GI inflammation.Increased incidence of corneal inflammation: is observed in 53% of mice with 16% of mice having inflammatory ulcers.Glomerulonephritis: is observed in 15% of mice th 5% of mice having polycystic disease and 5% necrosis.Liver inflammation: is observed in 35-40% of mice.Muscle inflammation: 90% of mice have inflammation in skeletal muscle.Skin inflammation: is observed in 50% of mice.||C57BL/6|Yes|No|Yes|Yes|No|Yes|No|Poor||||No|17-Jul-2008||0.0|0.0|Unknown||T cell, signal transduction, inflammation, E3 ubiquitin ligase, box|Yes| 5623.0|B6;129S5-Shc1tm1lex/Mmnc - incomplete ||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 7038.0|zeta-C57BL/6 390|B6;129-Ywhaz/Apb||Recessive|tyrosine 3-monooxygenase/tryptophan 5-monooxygenase activation protein, zeta polypeptide|Ywhaz|Nil|1110013I11Rik, 14-3-3 zeta|MGI:109484|tyrosine 3-monooxygenase/tryptophan 5-monooxygenase activation protein, zeta polypeptide; gene trap OST405390, Lexicon Genetics|Ywhaz||15|||||||||||||||||||||||||||||Infertile, reduced survival of KO pups at 21 days|None|C57BL/6|Yes|No|Yes|Yes|No|Yes|Yes|Poor|N/A||het x het|No|06-Aug-2012|Cryopreserved sperm|80.0|0.0|Unknown||14-3-3, signal transduction|Possibly| 5757.0|Emx2||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 7267.0|Tuara|CBA-Stat1/AnuApb||Recessive|signal transducer and activator of transcription 1|Stat1|Unknown||MGI:103063||||1|||||||||||||||||||||||||||||Unknown||CBA|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|29-Jan-2013|Cryopreserved sperm|50.0|0.0|Unknown|||Possibly| 5544.0|ENU18NIH:064a|C57BL/6JAnu-Dock2/AnuApb|C57BL/6JAnu-Dock2/AnuApb|Recessive|dedicator of cyto-kinesis 2|Dock2 |Unknown|CED-5, Hch, MBC |MGI:2149010|dedicator of cyto-kinesis 2; mutation 2, The Australian National University|Dock2|MGI:5563490|11|ENSMUSG00000020143|ENSMUST00000093193|Dock2-001|4311|4380|T to A|ENSMUSE00000376674|43|1437|Tyrosine to STOP|||||CAGATCATAAACTTTTACAAGTCTAATTATGTGCAAAAGTTCCACTACTCCAGGCCTGTGC||||||||||||||Reduced numbers of mature B cells in peripheral blood; reduced numbers of T cells in peripheral blood with increased expression of CD44 protein on CD4<+> and CD8<+> cells.|Unknown|C57BL6/JAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|27-Jul-2011|Cryopreserved sperm|36.0|0.0|No||cell migration, T cell, B cell, lymphocyte|Possibly| 4706.0|OT1xB6Ly5a|C57BL/6-Ptprc Tg(TcraTcrb)1100Mjb/AnuApb||Recessive|protein tyrosine phosphatase, receptor type, C|Ptprc|Unknown|B220, CD45, Cd45, Ly-5, Lyt-4, T200|MGI:97810|protein tyrosine phosphatase receptor type C; a variant|Ptprc|MGI:4819849|1||||||||||Unknown to Unknown||||||Yes|transgene insertion 1100, Michael J Bevan||||||||||||||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|07-Apr-2009|Cryopreserved sperm|25.0|0.0|Unknown||T cell, receptor, lymphocyte|Yes| 5634.0|Bat Gal||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6919.0|FVBNJ-Momme D17|FVB/NJ-MommeD17 Tg(BA1-Gfp)3Ew/Apb||Semi-dominant|Setdb1|SET domain, bifurcated 1|||MGI:1934229|SET domain, bifurcated 1; modifier of murine metastable epialleles, D17|Setdb1|MGI:5515364|3||||||||||Unknown to Unknown|||||||transgene insertion 3, Emma Whitelaw|Human alpha-globin promoter (-570 to +37) and 4.1kb of enhancer region|36 copies||||||||||Lethal.Transgene expressed in red blood cells. Percentage of cells expressing GFP transgene is increased in Momme D17. |Normal|FVB/NJ|No|No|Yes|No|No|Yes|No|Good||||No|25-Jun-2012|Cryopreserved sperm|19.0|0.0|Unknown||ENU, epigenetic, DNA methylation, GFP|Possibly| 7056.0||B6;SWR-Clcn1||Recessive|chloride channel 1|Clcn1|Unknown|Clc1, Clc-1, nmf310, nmf355, NMF355, SMCC1|MGI:88417|chloride channel 1; myotonia|Clcn1|MGI:1855953|6|||||||||||||||||||||||||||||Altered righting response: mice exhibit an arrested development of righting responseAbnormal voluntary movement: * mice exhibit stiffening of hindlimbs when supine with difficulty righting and stiffening of hindlimbs after rapid movement * abnormal phenotype is visible at 2 weeks of age and is progressive * at 2 weeks of age, mice exhibit stiff extensor postures of the limbs when gently dropped from a height of about 10 cm * when tested after 2 hours at 5 degrees Celsius, extensor posture is elicited more easily and its duration is increased by 50% * unlike in wild-type mice, scratching motion with hindlimb is not rapid * when place in an ice water bath mice exhibit a stiff extensor posture of the hindlimbs that is most prominent in the first minute and gradually subsides.Impaired limb coordination: mice are capable of swimming but alternate movements of the hindlimbs are not well coordinated.Abnormal gait: mice exhibit a slightly stiff gait and walk slower than wild-type mice.Muscle phenotype: mice do not display muscle fiber necrosis, grouped atrophy or inflammatory infiltratesIncreased skeletal muscle mass: by day 70, mice exhibit increased muscle bulk in the neck and shoulder girdle muscles compared to wild-type mice.Abnormal muscle physiology: percussion of muscles occasionally produces a sustained local contraction with sustained posturinghowever, muscle weakness is not observed.Abnormal muscle electrophysiology: * mice exhibit myotonic discharges in limbs, abdominal, tongue, and eye muscles. * unlike in wild-type mice, myotonic discharges are detected from anesthetized mice whose muscles are percussed or stretched * unlike in wild-type mice, myotonic discharges continue for several minutes after amputation.Impaired muscle relaxation: mice exhibit myotoniaAxon degeneration: * by 225 days, mice exhibit degeneration of myelinated axons in the ventrolateral funiculus at all levels of the spinal cord. * however, nerve roots and mixed peripheral nerves are not affectedDecreased body weight: at 30 days mice weigh 10% less than wild-type mice and this difference increases to 40% in adulthood.Reduced fertility: mice are not reliable breeders.Kyphosis: * Background Sensitivity: mice usually develop mild dorsal kyphosis on a mixed background * at day 80, mice exhibit thoracic kyphosis at the T3 to T5 level.||C57BL/6|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|21-Aug-2012||0.0|0.0|Unknown||myotonia, muscle, skeletal|Yes| 3469.0|Cystatin KO|B6.129-Cst3/Wehi||Recessive|cystatin C|Cst3|Unknown|CysC, cystatin C|MGI:102519|targeted mutation 1, S Karlsson|Cst3|MGI:2182140|2||||||||||||||||Yes|||||||||||||Normal||129 x C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|22-Jul-2008||0.0|0.0|Unknown||cysteine protease, metastasis, tumourigenesis|Yes| 5112.0|las vegas ; ENU7B6:142|C57BL/6JSfdAnu-Tnfaip3/AnuApb|C57BL/6JSfdAnu-Tnfaip3/AnuApb|Recessive|tumor necrosis factor, alpha-induced protein 3|Tnfaip3|Unknown|A20, Tnfip3, zinc finger protein A20|MGI:1196377|tumor necrosis factor, alpha-induced protein 3; las vegas|Tnfaip3|MGI:5563400|10|ENSMUSG00000019850|ENSMUST00000105527|Tnfaip3-002|974|1162|T to A|ENSMUSE00000098571|5|325|Isoleucine to Asparagine|||||AGGCTGGGACCACGGCACGACTCACCTGATCAACGCTGCAAAATTGGATGAAGCTAACTTA|Yes|||||||||||||Increased myeloid cells, lower % lymphocytes, increased % ofCD44 expressing activated/memory T cells||C57BL/6JSfdAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|10-May-2010|Cryopreserved sperm|60.0|0.0|Unknown||T cell, TNF, CD8, ENU, NIH|Yes| 6920.0|FVBNJ-Momme D13|FVB/NJ-MommeD13 Tg(HBA1-Gfp)3Ew/Apb||Semi-dominant|SET domain, bifurcated 1|Setdb1|Unknown||MGI:1934229|SET domain, bifurcated 1; modifier of murine metastable epialleles, D13|Setdb1|MGI:5515361|3||||||||||Unknown to Unknown|||||||transgene insertion 3, Emma Whitelaw|Human alpha-globin promoter and enhancer region|36 copies||||||||||Lethal.Transgene expressed in red blood cells. Percentage of cells expressing GFP transgene is increased in Momme D13.|Normal|FVB/NJ|No|No|Yes|No|No|Yes|No|Good||||No|25-Jun-2012|Cryopreserved sperm|19.0|0.0|Unknown||ENU, DNA methylation, epigentic, GFP|Possibly| 5637.0|BDNF||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 3473.0|Socs3 - Socs Box del|C57BL/6-Socs3/Wehi||Recessive|suppressor of cytokine signaling 3|Socs3|Unknown|CIS3, Cish3, cytokine-inducible SH2 protein 3, E2a-Pbx1 target gene in fibroblasts 10, EF-10, SOCS-3, SSI-3, STAT-induced STAT inhibitor 3|MGI:1201791|suppressor of cytokine signaling 3; targeted mutation 1, Lorraine Robb|Socs3|MGI:3835162|11||||||||||||||||Yes|||||||||||||Normal. Treatment of the mice with pharmacologic doses of G-CSF, which mimics emergency granulopoiesis and therapeutic use of G-CSF, revealed that SOCS3(Delta SB/Delta SB) mice were hyperresponsive to G-CSF. Compared with wild-type mice, SOCS3(Delta SB/Delta SB) mice developed a more florid arthritis when tested using an acute disease model. ||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|22-Jul-2008||0.0|0.0|Unknown||G-CSF, STAT, IL-6, signal transduction, G-CSF, arthritis|Yes| 1542.0||C57BL/6-Gzmb Prf1 Tg(TcraTcrb)1100Mjb||Recessive|granzyme B|Gzmb|Unknown|CCP-1/C11, CCP1, Ctla-1, Ctla1|MGI:109267|targeted mutation 1, Timothy J Ley|Gzmb|MGI:1857156|14||||||||||||||||Yes|transgene insertion 1100, Michael J Bevan||||||||||||||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|06-Jul-2007||0.0|0.0|Unknown||T cell receptor, CD8, ovalbumin, Natural Killer cell, cytotoxic|Yes| 1542.0||C57BL/6-Gzmb Prf1 Tg(TcraTcrb)1100Mjb||Recessive|perforin 1 (pore forming protein)|Prf1|Unknown|perforin, Pfp, Prf-1|MGI:97551|targeted mutation 1, Sandoz Pharmaceutical|Prf1|MGI:1857235|Unknown|||||||||||||||||||||||||||||||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|06-Jul-2007||||Unknown||T cell receptor, CD8, ovalbumin, Natural Killer cell, cytotoxic|Yes| 4978.0|ENU11B6:108b|C57BL/6JAnu-Morc3/AnuApb||Recessive|microrchidia 3|Morc3|Unknown||MGI:2136841||||16|ENSMUSG00000039456|ENSMUST00000044068|Morc3-201||||||||93860848|10|||TAAACTTGCCAGTCGAAGACATACAGTAAGTACTGAGCACTGAATTTTGACATACCGTTA|Yes|||||||||||||High expression of Ly6c in peripheral blood.Maturation defect in NK cells.|Normal|C57BL/6JAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|22-Jan-2010|Cryopreserved sperm|40.0|0.0|Unknown||B cell, T cell, immunity, NIH|Yes| 7626.0||C57BL/6NCrlAnu-Zfp831/Apb||Recessive|zinc finger protein 831|Zfp831|Unknown|ENSMUSG00000050600, OTTMUSG00000017459|MGI:3641861|mutation 1, The Australian National University|Zfp831||2|ENSMUSG00000050600|ENSMUST00000059452|Zfp831-001|2752|2752|T to C|ENSMUSE00000357407|1|918|Tyrosine to Histidine|||||CTCGGTCAGGTGGCTTCTTTCCTCCCAAGTACCTCCTCAGGTTACCTCAGGGAGAGAACCC||||||||||||||Unknown||C57BL/6NCrlAnu|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|30-Mar-2014|Cryopreserved sperm|22.0|0.0|Unknown||ENU|Yes| 7045.0|Activin BK transgenic ; Inhba BKBK|B6.129S7-Inhba/MarpApb||Dominant|inhibin beta-A|Inhba||activin|MGI:96570|inhibin beta-A; targeted mutation 2, Martin M Matzuk|Inhba|MGI:2386671|13|||||||||||||||||||||||||||||Mice are viable, but manifest poor overall health at 7 weeks of age|Normal|C57BL/6 x 129S|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|Unknown||Homozygous matings|No|06-Aug-2012|Cryopreserved sperm|40.0|0.0|No||activin, TGF-beta|Possibly| 5558.0|Caspase-1 KO|B6;129S2-Casp1/AnuApb||Recessive|caspase 1|Casp1|Nil|Caspase-1, ICE, Il1bc, interleukin 1 beta-converting enzyme|MGI:96544|caspase 1; targeted mutation 1, Tara Seshadri|Casp1|MGI:1927822|9|||||||||||||||||||||||||||||Cellular phenotype: * macrophages and thymocytes from mutant mice retain their capacity to undergo apoptosis upon ex vivo stimulation by several different signals. * in response to ATP, mutant peritoneal macrophages undergo normal apoptosis relative to wild-type. * in response to dexamethasone, aging or gamma irradiation, thymocytes from young homozygotes undergo normal apoptosis relative to wild-type. * in response to LPS and D-galactosamine, homozygotes undergo normal TNF-induced hepatocyte apoptosis and show normal kinetics of death from hepatic failure relative to wild-type mice.Abnormal apoptosis: * mutant peripheral blood neutrophils display retarded constitutive apoptosis relative to wild-type neutrophils * mutant peripheral blood neutrophils show no LPS-mediated inhibition of apoptosis but remain susceptible to Fas-mediated apoptosis.Abnormal cell migration: in homozygotes lacking bioactive IL-1beta, IL-18 fails to induce the expected migration of epidermal Langerhans cells to draining lymph nodes following skin sensitization; as a result, immunostimulatory dendritic cells fail to accumulate in regional lymph nodes resulting in impaired initiation of cutaneous immune responses.Hematopoietic system phenotype: * homozygotes exhibit normal numbers of leukocytes, erythrocytes, and platelets in peripheral blood * freshly isolated mutant thymuses, spleens and lymph nodes contain a normal % of various T cell subsets and B cells relative to wild-type.Immune system phenotype: * in homozygotes, the % of B lymphocytes and the various T lymphocyte subsets found in mutant thymuses, spleens and lymph nodes appear unaffected relative to wild-type. * the size and lymphocyte counts in these lymphoid organs appear normal; myeolopoiesis remains unaffected.Decreased circulating interleukin-1 alpha level: LPS-treated mice show a 5-fold decrease in IL-1alpha levels in vivo.Decreased circulating interleukin-1 beta level: in vivo, homozygous males injected with a high dose of LPS display undetectable levels of mature IL-1beta in their plasma; females are slightly less affected.Decreased circulating interleukin-6 level: after injection with a high dose of LPS, homozygotes display a moderate reduction in IL-6 levels relative to wild-type mice.Decreased circulating tumor necrosis factor level: after injection with a high dose of LPS, homozygotes display a moderate reduction in TNF levels relative to wild-type mice.Abnormal macrophage physiology: ex vivo, thioglycollate-elicited peritoneal macrophages stimulated with LPS and ATP are defective in IL-1beta processing and release.Abnormal neutrophil physiology: * in addition to delayed apoptosis, mutant neutrophils show absence of LPS-stimulated IL-1beta production relative to wild-type. * in response to LPS-mediated acute lung injury, homozygotes show significantly increased total and percent neutrophil counts at 24 and 48 h; however, these numbers decline to wild-type levels by 72 h suggesting a delay in inflammatory neutrophil apoptosis.Decreased T cell apoptosis: in vitro, thymocytes from young homozygotes are resistant to Fas-induced apoptosis as measured by cell viability.Decreased interleukin-1 alpha secretion: surprisingly, homozygous males are also defective in IL-1alpha production, with macrophages releasing only 20-25% of wild-type IL-1alpha levels after stimulation with LPS and ATP ex vivo.Decreased interleukin-1 beta secretion: * homozygotes are impaired in their capacity to produce mature IL-1beta. * ex vivo, mutant peritoneal macrophages stimulated with LPS and ATP release less that 1% of wild-type IL-1beta levels; however, no decrease in pro-IL-1beta synthesis or release is detected. * in culture, mutant cortical neurons exhibit inhibition of hypoxia-mediated generation of mature IL-1beta.Abnormal inflammatory response: in response to LPS-mediated acute lung injury, homozygotes exhibit a prolonged neutrophilic inflammatory response and evidence of caspase-1-independent IL-1beta production in the lung.Decreased susceptibility to endotoxin shock: * strikingly, homozygotes are significantly resistant to the lethal effects of endotoxic shock after a high dose of LPS. * whereas all LPS-treated wild-type mice die within 30 hours after injection, all homozygotes survive for >45 hours, with only 30% of mutants dying during the next 5 days.Reproductive system phenotype: * homozygotes are fertile and produce a normal litter size relative to wild-type. * in addition, post-lactation involution of mammary glands remains grossly normal in mutant post-partum females.Decreased susceptibility to ischemic brain injury: * following right carotid artery ligation, newborn homozygotes (P9-P10) are resistant to moderate, but not to severe cerebral hypoxic-ischemic insults relative to wild-type mice. * under mild lesioning conditions (right carotid ligation plus 40 min 10% O2), newborn homozygotes show attenuated hypoxia-ischemia induced CCL2 (chemokine (C-C motif) ligand 2; also, MCP-1) expression at 8 h post-hypoxia relative to wild-type; no genotype differences in CCL2 production are observed in animals undergoing longer periods of hypoxia-ischemia (severe insult)>Decreased neuron apoptosis: * cultured cerebrocortical neurons from homozygotes are highly resistant to oxygen/glucose deprivation (OGD)-induced neuronal cell death, showing only 50% of lactate dehydrogenase release relative to wild-type neurons. * also, mutant neurons are highly resistant to Ripk2-mediated cell death; transfecting caspase-1 into mutant neurons restores sensitivity to Ripk2-induced apoptosis. * notably, cultured neurons show inhibition of OGD-mediated processing of various members of the caspase pathway, cleavage of Bid, and hypoxia-associated loss of mitochondrial transmembrane potential; in vivo, these findings are confirmed in a cerebral ischemia model.|Decreased interleukin-1 beta secretion: * heterozygotes are slightly impaired in their capacity to produce mature IL-1beta: ex vivo, heterozygous peritoneal macrophages stimulated with LPS and ATP release 50% of wild-type IL-1beta levels * no decrease in pro-IL-1beta synthesis or release is detected|C57BL/6 x 129S2|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|Unknown|2 since arrival at ANU||No|12-Aug-2011|Cryopreserved sperm|9.0|0.0|Unknown||caspase, ICE, inflammation, IL1, LPS|Possibly| 5559.0|Nos2 KO|B6;129S7-Nos2/AnuApb||Recessive|nitric oxide synthase 2, inducible|Nos2|Nil|iNOS, Nos-2, NOS-II, Nos2a|MGI:97361|nitric oxide synthase 2, inducible; targeted mutation 1, John S Mudgett|Nos2|MGI:2158791|11|||||||||||||||||||||||||||||Abnormal osteoclast morphology.Decreased osteoclast cell number: decreased by 25%Abnormal osteoclast differentiation: in vitro differentiation is markedly attenuated.Abnormal osteoclast physiology: resorption activity is considerably decreased.Increased bone mineral density: bone mineral density of the femur is elevated at both 4 and 9 weeks of age.Increased bone volume: total bone volume is increased.Increased compact bone mass: * increased cortical bone mass * trabecular bone thickness and connectivity unchanged from controls.Abnormal tooth hard tissue morphology: distance between cementoenamel junction and alveolar bone crest is greater than for controls from 6 weeks on (without any bacterial challenge).Abnormal response to infection: * do not respond to oral infection with Porphyromas gingivalis by bone loss * serum levels of specific IgG are comparable to controlsAbnormal involution of the mammary gland: * mammary gland regression after removal of pups is delayed * degree of regression at 72 hours is similar to controls * mammary gland development is normal at 10 days into lactation.Abnormal mammary gland physiology: increase in apoptosis levels of involuting mammary glands is delayed.Abnormal lactation: * elevated milk production * pups nourished by mutant mothers weigh more than pups nourished by control mothers.Increased circulating prolactin level: slightly elevated relative to controls.Abnormal cardiovascular system morphology.Abnormal uterine artery morphology: the large arteries of the uterus during pregnancy have thickened arterial walls and smaller lumina.Atherosclerotic lesions: found in about 35% of homozygotes.Abnormal heart ventricle morphology: total ventricle weights are greater than controls for males only.Abnormal cardiovascular system physiology.Abnormal blood circulation: islet blood flow under basal conditions is increased.Increased systemic arterial blood pressure.Increased mean systemic arterial blood pressure: * relative to controls * streptozotocin induced diabetes for 8 days results in a more modest increase in blood pressure than in similar controls.Increased systemic arterial systolic blood pressure: slightly increased at 3 months of age but not later.Increased infarction size: * area of infarction is greater than for controls in non-diabetic mice after ischemia-reperfusion * reperfusion injury is less in diabetic mice than in diabetic controls.Homeostasis/metabolism phenotype: * normal serum insulin. * obese mice on a high fat diet have normal insulin levels.Abnormal blood homeostasis.Increased circulating creatinine level: slightly elevated levels.Abnormal circulating estradiol level: the cyclic changes in estradiol level are abnormal in homozygous mutant females with the peak in estradiol concentration coming later than in 129/SvEv wild-type females.Increased circulating cholesterol level: levels 1.7 times normal at 9 months of age.Increased circulating triglyceride level: elevated plasma triglycerides.Abnormal circulating serum albumin level: slightly reduced at 3 months and tending to decline with age.Abnormal glucose homeostasis.Abnormal circulating glucose level: resistant to hyperglycemia induced by multiple low doses of streptozotocin.Improved glucose tolerance: * hyperglycemic in the first 30 minutes of a glucose tolerance test. * return to fasting glucose levels by 90 minutes when controls are still hyperglycemic.Increased insulin sensitivity.Abnormal hormone level.Decreased adiponectin level.Abnormal adrenocorticotropin level: plasma ACTH levels increase much more modestly after LPS treatment than for controls.Increased renin activity: plasma renin activity is increased.Decreased cerebral infarction size: * volume of infarction 96 hours after middle cerebral artery occlusion is 28% smaller than controls. * volume of infarction is similar to controls 24 hours after cerebral artery occlusion.Decreased susceptibility to kidney reperfusion injury: * protected from renal ischemia-reperfusion injury as indicated by lower serum creatine levels compared to controls * less tubular necrosis, tubular structure is almost normal * better survival rate at 24 hours after surgeriesAbnormal uterus morphology: the lining of the uterus during pregnancy shows a distinct lack of cellularity in homozygous female mutants compared to wild-type females.Abnormal uterine artery morphology: the large arteries of the uterus during pregnancy have thickened arterial walls and smaller lumina.Prolonged diestrus: diestrus length is increased in homozygous mutant females compared to 129/SvEv wild-type mice without an increase in total oestrus cycle length.Decreased litter size: by mid-gestation homozygous female mutants have significantly fewer viable embryos compared to wild-type females.Nervous system phenotype: chronic nerve constriction does not lead to breakdown of small myelinated fibers.Decreased cerebral infarction size: * volume of infarction 96 hours after middle cerebral artery occlusion is 28% smaller than controls * volume of infarction is similar to controls 24 hours after cerebral artery occlusion.Neuron degeneration: * moderate breakdown of larger caliber myelinated fibers 5 days after chronic nerve constriction at a time when controls have far fewer surviving fibers * fiber numbers are declining at 14 days but at a slower rate than for controls * degenerating myelinated fibers persist longer after nerve crush injuryAbnormal peripheral nervous system regeneration: * no regenerative myelinated sprouts at 21 days when they have begun to appear in controls * regenerating fibers are smaller in caliber after nerve crush injury * similar to controls by 6 weeks after nerve crush injury * nerve fiber regeneration is delayed and new fibers are smaller in diameter after nerve transection.Increased eating behavior: consume 1.6 times as much food as controls on a high fat diet.Abnormal motor capabilities/coordination/movement: motor deficiencies improve between 24 and 96 hours after cerebral artery occlusion unlike controls.Abnormal sensory capabilities/reflexes/nociception.Allodynia: tactile allodynia observed at 3 weeks when neuropathic pain is diminishing in controls.Abnormal response to tactile stimuli: tactile hypersensitivity disappears between 5 and 14 days after the start of chronic nerve constriction while it persists through day 14 in controls.Abnormal thermal nociception: * thermal hypersensitivity disappears between 5 and 14 days after the start of chronic nerve constriction while it persists through day 14 in controls * delayed thermal hypersensitivity observed at 3 weeks when neuropathic pain is diminishing in controls.Pancreas inflammation: * low level of islet inflammation as compared to controls when treated with streptozotocin. * islet size is normal.Increased length of allograft survival: * lower rejection rate of CBA/CaJ cardiac grafts * lower levels of apoptosis by all measures usedDecreased susceptibility to kidney reperfusion injury: * protected from renal ischemia-reperfusion injury as indicated by lower serum creatine levels compared to controls * less tubular necrosis, tubular structure is almost normal * better survival rate at 24 hours after surgeries.Increased body weight:body weight is greater than controls for males only.Increased growth rate: experience greater weight gain on a high fat diet.Abnormal digestion: do not respond to gastric luminal acid with as great an increase in gastric blood flow as do controlsvascular resistance is not diminished.Decreased digestive mucosecretion: * mucus accumulation rate about 25% of controls * firmly adherent layer of mucus is thinner than in controlsLiver fibrosis: * fibrotic changes in the livers of mice on a high fat diet particularly around degenerating hepatocytes and the central vein area * collagen fraction is higher than in controls when on a high fat diet.Allodynia: tactile allodynia observed at 3 weeks when neuropathic pain is diminishing in controls.Abnormal response to tactile stimuli: tactile hypersensitivity disappears between 5 and 14 days after the start of chronic nerve constriction while it persists through day 14 in controls.Abnormal thermal nociception: * thermal hypersensitivity disappears between 5 and 14 days after the start of chronic nerve constriction while it persists through day 14 in controls * delayed thermal hypersensitivity observed at 3 weeks when neuropathic pain is diminishing in controls.||C57BL/6 x 129S7|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|Unknown|2 since arrival at ANU||No|12-Aug-2011|Cryopreserved sperm|40.0|0.0|Unknown||infection, LPS, ischemia|Possibly| 5624.0|B6.126Erbb4Tm2Fej/mmcd FloxedErbB4||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5244.0|ENU18NIH 17a; ENU18NIH:017a|C57BL/6JAnu-Tnfsf13b/AnuApb|C57BL/6JAnu-Tnfsf13b/AnuApb|Recessive|tumor necrosis factor (ligand) superfamily, member 13b|Tnfsf13b|Unknown|BAFF, BLyS, D8Ertd387e, TALL-1, zTNF4|MGI:1344376|tumor necrosis factor (ligand) superfamily, member 13b; mutation 1, Australian National University|Tnfsf13b|MGI:5009047|8|ENSMUSG00000031497|ENSMUST00000033892|Tnfsf13b-201|81|81|T to A|ENSMUSE00000638270|1|27|Tyrosine to STOP|||||GAGAAAGGAGAAGATATGAAAGTGGGATATGATCCCATCACTCCGCAGAAGGAGGAGGGTG|Yes|||||||||||||T1 to T2 block in B cell development in spleen and increased % of immature B cells and decreased % of mature B cells in peripheral blood.||C57BL/6JAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||1|Currently breeding at G4. Affected x affected, affected x unaffected, affected x B6|No|15-Oct-2010|Cryopreserved sperm|45.0|0.0|Unknown||B cell, immunoglobulin, spleen, peripheral, ENU|Possibly| 5109.0|APN36|B6;129-Crisp1/Marp||Recessive|Cysteine-rich secretory protien 1 C|Crisp1||Aeg1, CRISP-1|MGI:102553|cysteine-rich secretory protein 1; gene trap CMHD-GT_255A4-3, Centre for Modeling Human Disease|Crisp1|MGI:3879688|17||||||||||||||||Yes|||||||||||||N/A: Only bred to heterozygosity|Normal|C57BL/6J|No|Unknown|Yes|No|Unknown|Unknown|No|Good||||No|05-May-2010|Cryopreserved sperm|50.0|0.0|Unknown||Genetrap, Sperm, fertilization, ES cell|No| 2362.0||B6.AK-H2/AnuApb|B6.AK-H2/Apb|Dominant|histocompatibility-2, MHC|H2|Unknown|H-2, MHC-II|MGI:95894|histocompatibility-2, MHC; k variant|H2|MGI:3579322|17||||||||||||||||Yes|||||||||||||The k variant has been observed in the following strains: C3H, C3H/HeJ, C3H/An, C3H/Bi, C3H/DiSn, C3H/St, CBA, CBA/CaJ, CBA/N, AKR/J, CE/J, C57BR/cdJ, C58/J, MA/J, RF/J, ST/bJ, MRL/MpJ-Fas/J||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|13-Dec-2007|Cryopreserved sperm|120.0|0.0|No||antigen presentation, T cell, lymphocyte, MHC|Yes| 4849.0|ENU6AT:HELxTCR:line014:Infertility:G4|ENU6AT:14:infertility||Recessive|Unknown||Unknown||||||Unknown|||||||||||||||||||||||||||||Male infertility|Normal|C57BL/6 x CBA|Yes|Yes|Yes|Yes|No|Yes|No|Unknown||||No|24-Sep-2009|Cryopreserved sperm|5.0|0.0|Unknown||ENU, sperm, fertility|Yes| 4975.0|Booreana ; Ped11.28 ; ENU11B6:028|B10;B6-Myb/AnuApb|B10;B6-Myb/AnuApb|Recessive|myeloblastosis oncogene|Myb|Unknown|c-myb|MGI:97249|myeloblastosis oncogene; booreana|Myb|MGI:4867909|10|ENSMUSG00000019982|ENSMUST00000020156|Myb-201|923|1189|A to G|ENSMUSE00000644654|8|308|Glutamic acid to Glycine|||||GGAGTTGCTCCTGATGTCAACAGAGAACGAGCTGAAGGGACAGCAGGCATTACCAACACAG|Yes|||||||||||||E14.5 embryo:15x increase in platelet numbers2x increase in stem cells in foetal liver.Increase in primitive RBCDecrease in definitive RBCIncrease in haemopoietic progenitor cellsPups are born and survive to adulthood. Adults display a 5x increase in platelet numbers|Normal|C57BL/6 x C57BL/10|Yes|Unknown|Yes|Yes|Unknown|Yes|No|Unknown||||No|22-Jan-2010|Cryopreserved sperm|30.0|0.0|Unknown||haemopoiesis, stem cell, platelet, differentiation, transcription factor, proliferation, ENU|Yes| 7268.0||SJL/J-Ank1/MriApb|SJL/J-Ank1|Dominant|ankyrin 1, erythroid|Ank1|Unknown|Ank-1, pale|MGI:88024|ankyrin 1, erythroid; MRI98545|Ank1||8|ENSMUSG00000031543|ENSMUST00000121802|Ank1-004|445|699|T to A|ENSMUSE00000995112|5|149|Tyrosine to Asparagine|||||CCCAGTCTCAGAAAGGCTTTACTCCCCTGTACATGGCTGCTCAGGAGAACCACTTGGAAGT||||||||||||||Pre and Perinatal mortality with Jaundice, enlarge spleen and fragmented red blood cells|Heterozygous mice display a microcytic anaemia with increase osmotic fragility, splenomegaly and survival advantage to Plasmodium chabaudi |SJL/J|No|No|Yes|No|No|Yes|No|Good||||No|05-Feb-2013|Cryopreserved sperm|50.0|0.0|Yes|Hereditary spherocytosis|Hereditary spherocytosis, Malaria resistance, microcytosis, ENU|Yes| 7627.0|ENU28:G3|ANU:ENU28:G3||Recessive|Unknown||||||||Unknown|||||||||||||||||||||||||||||Unknown|Unknown|C57BL/6NCrlAnu|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown|1|||No|31-Mar-2014|Cryopreserved sperm|44.0|0.0|Unknown||ENU, mutagenesis, screen, random|Yes| 3488.0|Il-1R KO|C57BL/6-Il1r1||Recessive|interleukin 1 receptor, type I|Il1r1|Nil|CD121a, IL-1 receptor alpha chain, Il1r-1|MGI:96545||||1||||||||||||||||No|||||||||||||Homozygous null mice are grossly normal but fail to respond to IL-1. Mildly immunocompromised||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|23-Jul-2008||0.0|0.0|Unknown||interleukin, IL-6, signal transduction, receptor, T cell|Yes| 5369.0|NODSocs1/Lck|NOD/Lt-Socs1 Socs1 Tg(Lck-cre)157Jxm||Recessive|suppressor of cytokine signaling 1|socs1|Nil|Cish1, Cish7, JAB, JAK-binding protein, JAK2-binding protein, SOCS-1, SSI-1, STAT-induced STAT inhibitor 1|MGI:1354910|targeted mutation 3, Walter and Eliza Hall Institute of Medical Research||MGI:2656917|16||||||||||||||||Yes|transgene insertion I57, Jamey Marth|lymphocyte protein tyrosine kinase (Lck)|||||||||||Decreased B cell number: large reduction in the percentage of non-T cells, mostly B cells, in the lymph nodes.Abnormal T cell subpopulation ratio: * increase in the ratio of mature CD8 single positive:CD4 single positive thymocytes from 1:4 to 1:1. * increase in the ratio of CD8+:CD4+ T cells in the spleen, however total numbers of T cells are unchanged.Abnormal T cell differentiation: enhanced differentiation of thymocytes toward CD8+ T cells.Abnormal T cell activation: almost all peripheral CD8+ T cells but not CD4+ T cells appear as CD44ho, indicating that they exhibit a memory rather than activated phenotype.Abnormal CD4-positive T cell morphology: mature thymocytes, both CD4 single positive and CD8 single positive, are larger in size.Increased CD4-positive T cell number: increase in CD4+ T cells in the blood.Abnormal CD8-positive T cell morphology: mature thymocytes, both CD4 single positive and CD8 single positive, are larger in size.Increased CD8-positive T cell number: * large increase in the percentage and number of CD8 single positive thymocytes at 6 weeks of age. * increase in CD8+ T cells in the bloodAbnormal thymus medulla morphology: enlarged thymic medulla.Thymus hyperplasia: increase in thymus cellularity predominately due to an increase in CD8+ T cell population.Enlarged lymph nodes.Lymph node hyperplasia: lymph nodes contain 2-fold the number of cells in controls.||NOD/Lt|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|21-Dec-2010||0.0|0.0|Unknown||cytokine signalling, T cell, thymus, hyperplasia|Yes| 5369.0|NODSocs1/Lck|NOD/Lt-Socs1 Socs1 Tg(Lck-cre)157Jxm||Recessive|suppressor of cytokine signaling 1|Socs1|Nil|Cish1, Cish7, JAB, JAK-binding protein, JAK2-binding protein, SOCS-1, SSI-1, STAT-induced STAT inhibitor 1|MGI:1354910|suppressor of cytokine signaling 1; targeted mutation 1, Walter and Eliza Hall Institute of Medical Research|Socs1|MGI:1934607|16||||||||||||||||No|||||||||||||Decreased B cell number: large reduction in the percentage of non-T cells, mostly B cells, in the lymph nodes.Abnormal T cell subpopulation ratio: * increase in the ratio of mature CD8 single positive:CD4 single positive thymocytes from 1:4 to 1:1. * increase in the ratio of CD8+:CD4+ T cells in the spleen, however total numbers of T cells are unchanged.Abnormal T cell differentiation: enhanced differentiation of thymocytes toward CD8+ T cells.Abnormal T cell activation: almost all peripheral CD8+ T cells but not CD4+ T cells appear as CD44ho, indicating that they exhibit a memory rather than activated phenotype.Abnormal CD4-positive T cell morphology: mature thymocytes, both CD4 single positive and CD8 single positive, are larger in size.Increased CD4-positive T cell number: increase in CD4+ T cells in the blood.Abnormal CD8-positive T cell morphology: mature thymocytes, both CD4 single positive and CD8 single positive, are larger in size.Increased CD8-positive T cell number: * large increase in the percentage and number of CD8 single positive thymocytes at 6 weeks of age. * increase in CD8+ T cells in the bloodAbnormal thymus medulla morphology: enlarged thymic medulla.Thymus hyperplasia: increase in thymus cellularity predominately due to an increase in CD8+ T cell population.Enlarged lymph nodes.Lymph node hyperplasia: lymph nodes contain 2-fold the number of cells in controls.||NOD/Lt|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|21-Dec-2010||||Unknown||cytokine signalling, T cell, thymus, hyperplasia|Yes| 4734.0|Cbl-b KO:Hamlet:Charles|B6.129-Cblb Tg(IghelMD4)4Ccg Tg(MLsHEL)Ccg/AnuApb||Semi-dominant|Casitas B-lineage lymphoma b|Cblb|Nil|cbl-b|MGI:2146430|targeted mutation 1, Josef M Penninger|Cblb|MGI:2180570|16||||||||||||||||Yes|transgene insertion 4, Christopher C Goodnow||||||||||||Defect in T cell signalling||C57BL/6 x 129|Yes|Yes|Yes|Yes|Yes|Yes|No|Poor||10||No|19-Apr-2009|Cryopreserved sperm|45.0|0.0|No||T cell, Hen Egg Lysozyme (HEL), signal transduction|Yes| 4734.0|Cbl-b KO:Hamlet:Charles|B6.129-Cblb Tg(IghelMD4)4Ccg Tg(MLsHEL)Ccg/AnuApb||Semi-dominant||||||||||||||||||||||||||immunoglobulin kappa chain complex, immunoglobulin heavy chain complex. (IgM and IgD). Genomic clones of H+L genes with normal control elements. soluble HEL (hen egg lysozyme)|H-2K|||||||||||Defect in T cell signalling||C57BL/6 x 129|Yes|Yes|Yes|Yes|Yes|Yes|No|Poor||10||No|19-Apr-2009|Cryopreserved sperm|||No||T cell, Hen Egg Lysozyme (HEL), signal transduction|Yes| 3594.0||C57BL/6-Tlr4 mutant||Recessive|toll-like receptor 4|Tlr4|Unknown|lipopolysaccharide response, Lps, Rasl2-8|MGI:96824||||4||||||||||||||||No|||||||||||||Homozygotes for spontaneous or targeted mutations are hyporesponsive to bacterial lipopolysaccharide and more susceptible to infection by gram negative bacteria.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|06-Aug-2008||0.0|0.0|Unknown||toll-like receptor (TLR), signal transduction, T cell, lipopolysaccharide (LPS), infection|Yes| 6242.0|Bmf/473|B6.129-Bcl2l11 Bmf||Recessive|BCL2-like 11 (apoptosis facilitator)|Bcl2l11|Normal|1500006F24Rik, Bim, Bod|MGI:1197519|BCL2-like 11 (apoptosis facilitator); targeted mutation 2.1, Philippe Bouillet|Bcl2l11|MGI:4366751|2|||||||||||||||||||||||||||||Unknown|Unknown|C57BL/6|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown||Bim, Noxa, Bmf|Yes| 6242.0|Bmf/473|B6.129-Bcl2l11 Bmf||Recessive|BCL2 modifying factor|Bmf|Nil||MGI:2176433|BCL2 modifying factor; targeted mutation 1, Roger J Davis|Bmf|MGI:4421178|2|||||||||||||||||||||||||||||Unknown|Unknown|C57BL/6|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|13-Sep-2011||||Unknown||Bim, Noxa, Bmf|Yes| 5446.0|ENU12NIH:071b N2|C57BL/6JAnu-Hmbs/AnuApb|C57BL/6JAnu-Hmbs/AnuApb|Dominant|hydroxymethylbilane synthase|Hmbs||PBGD, porphobilinogen deaminase, Ups, Uros1|MGI:96112|hydroxymethylbilane synthase; mutation 1, The Australian National University|Hmbs|MGI:5563463|9|ENSMUSG00000032126|ENSMUST00000077353|Hmbs-201|719|905|A to G|ENSMUSE00000216802|11|240|Aspartic acid to Glycine|||||TATCTTGGACCTAGTGAGTGTGTTGCACGATCCTGAAACTCTGCTTCGCTGCATTGCTGAA|Unknown|||||||||||||Autoflourescence during FACs runs|Autoflourescence during FACs runs|C57BL/6JAnu|Yes|Yes|Yes|Yes|Yes|Yes|Yes|Good|1|5|Affected x B6|No|28-Feb-2011|Cryopreserved sperm|46.0|0.0|Unknown||ENU|Possibly| 6245.0|506|C57BL/6-Bcl2l11||Recessive|BCL2-like 11 (apoptosis facilitator)|Bcl2l11|Normal|1500006F24Rik, Bim, Bod|MGI:1197519|BCL2-like 11 (apoptosis facilitator); targeted mutation 3.1, Philippe Bouillet|Bcl2l11|MGI:4366756|2|||||||||||||||||||||||||||||Increased leukocyte cell number:*Smaller increase in white blood cells numbers (<1.5 fold).Increased spleen weight:*Smaller increase in spleen weight.Immune system phenotype:*Normal in vitro survival assays with several cytotoxic stimuli on sorted thymocyte and B cell populations.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown||Bim, Puma|Yes| 7482.0|Cxcr KO|C57BL/6-Cxcr3/MarpAnuApb||Recessive|chemokine (C-X-C motif) receptor 3|Cxcr3||Cd183, Cmkar3, Cxcr3|MGI:1277207|chemokine (C-X-C motif) receptor 3; targeted mutation 1, Wayne W Hancock|Cxcr3|MGI:2180682|X|||||||||||||||||||||||||||||Females:Decreased susceptibility to viral infection induced morbidity/mortality: • most survive infection with lymphocytic choriomeningitis virus which is cleared in 1 month in survivors, controls do not survive.Impaired macrophage chemotaxis:• 45% decrease of monocyte/macrophage in ischemic calf and thigh muscle.Abnormal cellular extravasation: • reduced numbers of CD8+ cells in the brain 7 days after infection with lymphocytic choriomeningitis.• restricted to meninges and choroids plexus until late in infection unlike controls where white matter of the brain near ventricular surfaces will be penetrated by CD8+ cells.• 38% decrease in numbers of CD3+ T cells in ischemic calf and thigh muscles at 7 days but not at 21 days after ischemia.Abnormal interferon level:• increased levels of IFN-gamma in lung tissue and in bronchoalveolar lavage 1 day after treatment with bleomycin, effect dissipates after 3 days.Lung inflammation: • decreased total lymphocyte counts in bronchoalveolar lavage after bleomycin injury.• reduced numbers of CD8+ T cells after bleomycin injury.• reduced numbers of NK cells at day 7 after bleomycin injury, but also in the lungs of unchallenged mice.Decreased susceptibility to viral infection:• lack symptoms of infection at 7 days after infection with lymphocytic choriomeningitis virus.• less susceptibility to lymphocytic choriomeningitis virus.Increased length of allograft survival:• increased cardiac allograft survival.• grafts with fewer Cd4+ and Cd8+ T cells.Abnormal physiological neovascularization: • ischemic capillary density relative to nonischemic density 1.4 fold lower than in controls.• poor recovery of blood flow after schema.Abnormal interferon level: • increased levels of IFN-gamma in lung tissue and in bronchoalveolar lavage 1 day after treatment with bleomycin, effect dissipates after 3 days.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|14-Nov-2013|Cryopreserved sperm|11.0|0.0|Unknown||allograft, macrophage, chemokine|Yes| 5626.0|B6.129 S2.Oprm1 tm1KGf/J (mu-opoid)||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6621.0|ENU19WT 029a:G2|ANU:ENU19WT:029:a:G2||Semi-dominant|Unknown||||||||Unknown|||||||||||||||||||||||||||||Unknown||C57BL/6|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|14-Oct-2011|Cryopreserved sperm|10.0|0.0|Unknown||ENU, Wellcome Trust|Yes| 7058.0|Crisp1 KO|B6;129-Crisp1/Marp||Recessive|Cysteine-rich secretory protien 1 C|Crisp1||Aeg1, CRISP-1|MGI:102553|cysteine-rich secretory protein 1; gene trap CMHD-GT_255A4-3, Centre for Modeling Human Disease|Crisp1|MGI:3879688|17||||||||||||||||Yes|||||||||||||Unknown|Normal|C57BL/6J|No|Unknown|Yes|No|Unknown|Unknown|No|Good||||No|22-Aug-2012|Cryopreserved sperm|50.0|0.0|Unknown||Genetrap, Sperm, fertilization, ES cell|No| 5641.0|Box 1||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5561.0|WT control|B6;129/Sv||Dominant||||||||||||||||||||||||||||||||||||||WT control for researchers experiments||C57BL/6 x 129/Sv|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|12-Aug-2011||0.0|0.0|Unknown||Wildtype control|Yes| 5370.0|377SCID|NOD/Lt.Cg-Tg(Ins2-Cd80)377-6Wehi Prkdc||Dominant|protein kinase, DNA activated, catalytic polypeptide|Prkdc|Unknown|DNA-PK, DNA-PKcs, DNAPDcs, slip, XRCC7|MGI:104779|protein kinase, DNA activated, catalytic polypeptide; severe combined immunodeficiency|Prkdc|MGI:1857113|16||||||||||||||||Yes|CD80 antigen|rat insulin promoter|islet cells||||||||||Introduction of the CD80 transgene into the nonobese diabetic (NOD) genetic background resulted in early spontaneous autoimmunity, but splenocytes from the diabetic animals could only transfer diabetes to NOD recipients that expressed CD80 on their β cells. Islet destruction required continuousCD80 expression by target β cells.||NOD/Lt|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|21-Dec-2010||0.0|0.0|Unknown||islet, autoimmunity, T cell|Yes| 5371.0|B6IL-1R|B6.Cg-Il1r1/JWehi||Recessive|interleukin 1 receptor, type I|Il1r1|Nil|CD121a, IL-1 receptor alpha chain, IL-iR, Il1r-1|MGI:96545|interleukin 1 receptor, type I; targeted mutation 1, Mark A Labow|Il1r1|MGI:1857441|1||||||||||||||||No||||||||||||||||Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|21-Dec-2010||0.0|0.0|Unknown||interleukin, T cell|Yes| 7066.0|Momme D30|FVB/NJ-MommeD30 Tg(Hba1-Gfp)1Ew||Semi-dominant|widely-interspaced zinc finger motifs|Wiz|||MGI:1332638|widely-interspaced zinc finger motifs; modifier of murine metastable epialleles, D30|Wiz|MGI:5515384|17||||||||||Unknown to Unknown|||||||Green Fluorescent Protein|human alpha-globin promoter and enhancer region|||||||||||Unknown|Unknown|FVB/NJ|No|No|Yes|No|No|Yes|No|Good|||MommeD30<+/->;Tg(Hba1-Gfp)1Ew x Tg(Hba1-Gfp)1Ew|No|24-Aug-2012|Cryopreserved sperm|40.0|0.0|Unknown||ENU, epigenetics, suppressor of variegation|Possibly| 5555.0|IL-1RA KO|B6;129S-Il1rn/Anu||Recessive|interleukin 1 receptor antagonist|Il1rn|Nil|IL-1ra|MGI:96547|interleukin 1 receptor antagonist; targeted mutation 1, David Hirsh|Il1rn|MGI:2157398|2|||||||||||||||||||||||||||||Decreased body weight: lower body weight apparent by 6 weeks of age.Decreased circulating interleukin-1 level: decreased serum levels of IL1 after endotoxin exposure.Increased circulating interleukin-6 level: increased basal serum IL6 levels.Abnormal circulating serum amyloid protein level: increased basal serum amyloid P levels.Increased acute inflammation: increased hepatic acute phase protein response to subcutaneous turpentine administration, increased mortality to turpentine abscess induction: 50% of mice died by day 5.Increased susceptibility to endotoxin shock: more susceptible to lipopolysaccharide (LPS) endotoxin challenge.Decreased susceptibility to bacterial infection: less susceptible to experimental Listeria monocytogenes infection.Reduced fertility: decreased number of offspring.Decreased circulating cholesterol level: 3-fold decrease in non-HDL cholesterol when fed high fat diet containing cholate for 12 weeks.|Increased susceptibility to endotoxin shock: more susceptible to lipopolysaccharide (LPS) endotoxin challenge.Decreased susceptibility to bacterial infection: less susceptible to experimental Listeria monocytogenes infection, heterozygotes display an intermediate phenotype.|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|Unknown|2 since arrival to ANU||No|12-Aug-2011||0.0|0.0|Unknown||interleukin, IL-1, LPS, inflammation, endotoxin, infection, cytokine|Possibly| 6623.0|TG2.129T2|129-Tgm2/Apb||Recessive|transglutaminase 2, C polypeptide|Tgm2|Nil|G[a]h, protein-glutamine gamma-glutamyltransferase, TG C, TG2, tissue transglutaminase, tTG, tTGas|MGI:98731|targeted mutation 1.1, Robert M Graham|Tgm2|MGI:3527996|2||||||||||||||||No|||||||||||||Abnormal cell adhesion: fewer homozygous fibroblasts (20% versus 79% of wild-type) adhered to poly-L-coated or fibronectin coated slidesAbnormal T cell physiology: 24 hours after induction of apoptosis by dexamethasone treatment, homozygotes had smaller thymuses due to decreased viability of thymocytes and increased clearance of dead cells compared to controls, however mutants are viable, normal in size and weight, have normal separation of digits and open eyelids and no difference in thymocyte numbers, indicating that developmental apoptosis was not impaired.||129T2|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|18-Oct-2011|Cryopreserved sperm|50.0|0.0|Unknown||transgluatminase, Gh, G-protein, cross linking, T cell|Yes| 823.0|ACTFLPtg|B6.Cg-Tg(ACTFLPe)9205Dym/JAusb||Dominant||||||||||||||||||||||||||transgene insertion 9205, Susan Dymecki|ACTB, actin, beta, human|The FLPe recombinase variant exhibits enhanced thermostability with recombination activity being 4X and 10X that of wildtype FLP at 37°C and 40°C, respectively||||||||||The FLPe recombinase variant exhibits enhanced thermostability with recombination activity being 4X and 10X that of wildtype FLP at 37°C and 40°C, respectively. |Hemizygous transgenic mice are viable, fertile, normal in size, and do not display any gross physical or behavioral abnormalities.|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|21-May-2007||0.0|0.0|Unknown||recombinase, deleter, Cre, actin|Yes| 119.0|c-cbl KO|B6.129S1-Cbl/WlanAnuApb|B6.129S1-Cbl/WlanAnuApb|Recessive|Casitas B-lineage lymphoma|Cbl|Nil|c-Cbl, cbl, Cbl-2|MGI:88279|targeted mutation 1, David D L Bowtell|Cbl|MGI:2180578|9||||||||||||||||Yes|||||||||||||Homozygotes for targeted null mutations exhibit increased thymic CD3 and CD4 expression and tyrosine-phosphorylation, lymphoid hyperplasia, and altered splenic hemopoiesis. Females show increased ductal density and branching in mammary fat pads.Abnormal spleen red pulp morphology- expandedenlarged spleen. Spleen is enlarged about 1.2- to 2-fold compared to wild type mice due to expansion of the red pulpspleen hyperplasia.Increase in the number of megakaryocytes, megakaryoblasts, and myelocytes but no increase in the number of lymphocytes is seen in the spleen.Abnormal adipocyte morphology- adipocyte volume is reduced by about 64% compared to wild type mice.Decreased adipose tissue amount- despite increased caloric intake, a 40-50% decrease in the size of the adipose tissue depots (including both white and brown fat) is seenthis phenotype is more pronounced in males than in females.Increased lean body mass- balances the decrease in adipose tissue resulting in no significant difference in total body weight.Polyphagia.Hyperactivity- about a 4-fold increase in ambulatory activity is seen, especially during the dark phase.Increased body temperature- rectal temperature is increased by 1 degree C independent of time of day or if the mice are fed or fasted overnight. However, circulating levels of triiodothyronine or thyroxine are similar to wild type in both the fed and fasted states.Decreased circulating leptin level- leptin levels are decreased by 66%; however adiponectin levels are similar to wild type.Abnormal gas homeostasis- increased oxygen consumption:whole body oxygen consumption corrected for the difference in lean mass is increased by 22% compared to wild type mice.Abnormal respiratory quotient- reduced respiratory quotientAbnormal glucose homeostasis- decreased circulating insulin level, after an overnight fast insulin levels are decreased relative to wild type but glucose levels are similar to wild type.Improved glucose tolerance- improved glucose tolerance despite decreased insulin levels throughout the test.Increased insulin sensitivity.Abnormal lipid homeostasis- decreased circulating free fatty acid level.Decreased triglyceride level- triglyceride levels in the liver are decreased but those in the quadriceps muscle are similar to wild type muscleAbnormal muscle physiology- glucose clearance in to glycogen is increased in the soleus and extensor digitorum longus muscles but not in the liver.Abnormal muscle cell glucose uptake- glucose uptake into skeletal muscle is increased about 2-fold; however glucose uptake into white and brown adipose tissue is not different from wild type. Basal and insulin-stimulated glucose uptake are increased in soleus muscle explants by 65% and 30%, respectively; however, glucose uptake is not increased in fat explants basal, but not insulin-stimulated, glucose uptake is increased by 30% in extensor digitorum longus muscle explantscellular.Abnormal mitochondrial morphology- a 2-fold increase in the average size of subsarcolemmal mitochondria is seen; however, no increase in mitochondrial area or cristae density is seen in the subsarcolemmal region.Spleen hyperplasia- increase in the number of megakaryocytes, megakaryoblasts, and myelocytes but no increase in the number of lymphocytes is seen in the spleen.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Poor|11|||No|06-Feb-2006|Cryopreserved sperm|145.0|0.0|No||Cbl, tyrosine kinase, TKB, Zap-70, adipose|Yes| 3530.0||Balb/c-Rag1||Recessive|recombination activating gene 1|Rag1|Unknown|Rag-1|MGI:97848||||1||||||||||||||||Yes|||||||||||||Immuncompromised||Balb/c|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|29-Jul-2008||0.0|0.0|Unknown||T cell, B cell, eosinophil, inflammation, interferon|Yes| 2039.0|STAT1 KO|B6;129-Stat1/Apb|B6;129-Stat1/Apb|Recessive|signal transducer and activator of transcription 1|Stat1|Nil||MGI:103063|targeted mutation 1, Robert D Schreiber|Stat1|MGI:1861949|1||||||||||Unknown to Unknown||||||Yes|||||||||||||Increased sensitivity to microbial pathogens and viruses due to impaired responsiveness to interferons.Increased Bone mass.Increased osteoclast cell number.|No phenotype reported.|C57BL/6 x 129/Sv|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|||homozygous x homozygous|Yes|21-Sep-2007|Cryopreserved sperm|115.0|0.0|No||signal transduction, cytokine, JAK, kinase, phosphorylation|Yes| 1861.0|Sox2-Cre|CD1-Tg(Sox2-cre)1Amc||Recessive||||||||||||||||||||||||||transgene insertion 1, Andrew P McMahon|SRY-box containing gene 2 (Sox2)|||||||||||Cre expression in epiblast.||CD1|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|10-Aug-2007||0.0|0.0|Unknown||epiblast, germline, Cre recombinase, maternal inheritance|Yes| 7062.0|Momme D11|FVB/NJ-MommeD11 Tg(Hba1-Gfp)1Ew||Semi-dominant|Kruppel-like transcription factor 1 (erythroid)|Klf1|Unknown||MGI:1342771|Kruppel-like transcription factor 1 (erythroid); modifier of murine metastable epialleles, D11|Klf1|MGI:5752591|8||||||||||Unknown to Unknown|||||||Green Fluorescent Protein|human alpha-globin promoter and enhancer region|||||||||||Homozygous lethality (~E14.5 dpc)|Unknown|FVB/NJ|No|No|Yes|No|No|Yes|No|Good|||MommeD11<+/->;Tg(Hba1-Gfp)1Ew x Tg(Hba1-Gfp)1Ew|No|24-Aug-2012|Cryopreserved sperm|20.0|0.0|Unknown||ENU, epigenetics, suppressor of variegation|Possibly| 5628.0|B6.129P2-Lgr5||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5948.0|NOD.CD45.2||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 840.0|CD40 KO|B6.129P2-Cd40||Recessive|CD40 antigen|Cd40|Nil|Bp50, Cd40, p50, Tnfrsf5|MGI:88336|targeted mutation 1, Hitoshi Kikutani|Cd40|MGI:1857457|2||||||||||||||||No|||||||||||||Mice homozygous for the targeted mutation are viable and fertile. Homozygous mutant mice exhibit impaired immunoglobulin class switching and germinal center formation.Immune system phenotype: normal numbers and ratios of T and B cells.Decreased neutrophil cell number:* in non-SPF facilities compared to wild-type controlsAbsent spleen germinal center: failed to form.Abnormal humoral immune response.Decreased immunoglobulin level:* reduced production of IgG1, IgG2a, IgG2b, IgG3, IgA, IgE in response to thymus-dependent (TD) antigen, dintrophenol-conjugated ovalbumin.* response to thymus-independent (TI) antigens was in tact.Decreased susceptibility to type II hypersensitivity reaction:*in model of accelerated anti-glomerular basement membrane antibody-mediated glomerulonephritis* deposition of IgG and complement in glomeruli not observed* glomeruli almost normal* fibrin deposition in glomeruli not observed* failure to induce proteinuria||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|||Hom x Hom|No|23-May-2007||0.0|0.0|Unknown||B cell, immunoglobulin, hypersensitivity reaction, germinal center, neutrophil, Ig|Yes| 5161.0|ENU14 NIH 17b|ENU14NIH:017b||Recessive|Unknown|Unknown|Unknown||||||Unknown|||||||||||||||||||||||||||||Shaky gait, and uncoordinated|Normal|C57BL/6JAnu|Yes|Yes|Yes|Yes|Unknown|Yes|Yes|Poor||1||No|28-Jun-2010|Cryopreserved sperm|20.0|0.0|Unknown||Uncoordinated, Shaky, Neurological, gait|Possibly| 7064.0|Momme D21|FVB/NJ-MommeD21 Tg(Hba1-Gfp)1Ew||Semi-dominant|modifier of murine metastable epialleles, D21|MommeD21|||||||16|||||||||||||||||Green Fluorescent Protein|human alpha-globin promoter and enhancer region|||||||||||Unknown|Unknown|FVB/NJ|No|No|Yes|No|No|Yes|No|Good|||MommeD21<+/->;Tg(Hba1-Gfp)1Ew x Tg(Hba1-Gfp)1Ew|No|24-Aug-2012|Cryopreserved sperm|50.0|0.0|Unknown||ENU, epigenetics, suppressor of variegation|Possibly| 5474.0|Rosa 26; MF-05|C57BL/6-Gt(ROSA)26Sor/Apb||Recessive||||||||||||||||||||||||||gene trap ROSA 26, Philippe Soriano; targeted mutation 1, Philippe Soriano||||||||||||Normal|Normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|06-Apr-2011|Cryopreserved sperm|50.0|0.0|Unknown||Cre recombinase, expression, genetrap|Yes| 3405.0|C57BL/6. ACT-mOVA - H2b|C57bL/6-H2-K Tg(CAG-OVA)916Jen/Wehi||Dominant|||Normal|||histocompatibility 2, K region; b haplotype mutation 1|H2-K|MGI:3618114|17||||||||||||||||Yes|transgene insertion 916, Marc K Jenkins|chicken β-actin|||||||||||Ubiquitously express membrane bound chicken ovalbumin under the control of chicken β-actin promoter. Breed less well than hets||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|13-Jul-2008||0.0|0.0|Unknown||ovalbumin, autoimmunity, T cell|Yes| 5630.0|B6.129S6-Erap1tm1Luc/J (ERAP) ||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5629.0|B6.129S2.Oprm1tm1Kff/J ||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 3539.0||C57BL/6-Mixl1-lacZ KO||Recessive|Mix1 homeobox-like 1 (Xenopus laevis)|Mixl1|Normal|Mm1, Mml|MGI:1351322|Mix1 homeobox-like 1 (Xenopus laevis); targeted mutation 1, Lorraine Robb |Mixl1|MGI:2387828|1||||||||||||||||No|||||||||||||Embryonic lethal- embryonic lethality during organogenesis - homozygous embryos are present in normal numbers at E7.5, but are absent after E10.5. Embryos with severely disorganized head folds are only rarely recovered at E9-9.5; such embryos have failed to turn or form a heart tube. At E9.5, axial tissue mass present at E8.5 has grown and developed into huge mass of tail bud-like tissue protruding dorsally from caudal region of embryo, giving impression that axis is bifurcated. Abnormal embryogenesis/ development - at E8.5, embryos adopt a flattened disc morphology instead of a lordotic shape. Abnormal primitive streak morphology - by E7, mutants display a thickened primitive streakan excess of mesoderm-like cells accumulates in anterior streak and in region lateral to streak at E7. Abnormal Henson's node morphology - homozygotes lack a recognizable node at E7Abnormal rostral-caudal axis patterning - at E8.5, AP axis is markedly shortenedAbnormal axial mesoderm. Abnormal embryonic tissue morphology - definitive endoderm is specified, but gut morphogenesis is defective in mutants. Abnormal notochord morphology - notochord is replaced by a thick axial mass of flattened neuroectoderm overlying a condensed core of mesodermal tissues. At E9.5, mutants have a poorly organized structure resembling the notochordal plate and a notochord-like structure that ends caudally either in an ectopic protrusion or in a bulbous mass. Abnormal somite development - from two to five somite pairs form in the paraxial mesoderm flanking a thick axial mass of flattened neuroectoderm overlying a condensed core of mesodermal tissues. Enlarged allantois - compared to wild type, allantois is disproportionately large.Abnormal neural fold formation (J:77443)at E8.5, neural folds are small and disorganized with little head mesenchyme found beneath the head folds. Abnormal neural fold elevation formation - in early-neural plate stage (E7.75), elevation of neural folds is retarded and a shallow anterior intestinal portal developscardiovascular system. Abnormal heart tube morphology - heart tube is absent at E8.25. Abnormal foregut morphology - foregut invagination is rudimentary and no hindgut portal is formed by E8.25.||C57BL/6|No|No|Yes|No|No|Yes|No|Unknown||||No|29-Jul-2008||0.0|0.0|Unknown||embryonic lethality, primitive streak, mesoderm, notochord|Yes| 4996.0|4AT22|ENU4AT:22||Recessive|||||||||Unknown|||||||||||||||||transgene insertion 3, Christopher C Goodnow|Rat insulin promoter|||||||||||Anti-nuclear antibodies, high.Both young and older mice.|Normal|C57BL/6 x B10BR|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|28-Jan-2010|Cryopreserved sperm|40.0|0.0|Yes|Type I Diabetes|ENU, JDRF, T cell, autoimmunity, antinuclear antibody|No| 4996.0|4AT22|ENU4AT:22||Recessive||||||||||||||||||||||||||transgene insertion 1, Mark M Davis||||||||||||Anti-nuclear antibodies, high.Both young and older mice.|Normal|C57BL/6 x B10BR|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|28-Jan-2010|Cryopreserved sperm|||Yes|Type I Diabetes|ENU, JDRF, T cell, autoimmunity, antinuclear antibody|No| 4995.0|4AT36 ; jellybean|ENU4AT:036||Recessive|||||||||Unknown|||||||||||||||||transgene insertion 3, Christopher C Goodnow|Rat insulin promoter|||||||||||Heightened susceptibility to autoimmune diabetes on the transgenically sensitized TCR x insHEL background.Phenotype Screen: Urine glucose|Normal|C57BL/6 x B10BR x CBA|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|28-Jan-2010|Cryopreserved sperm|30.0|0.0|Yes|Type I Diabetes|ENU, JDRF, T cell, autoimmunity|No| 4995.0|4AT36 ; jellybean|ENU4AT:036||Recessive||||||||||||||||||||||||||transgene insertion 1, Mark M Davis||||||||||||Heightened susceptibility to autoimmune diabetes on the transgenically sensitized TCR x insHEL background.Phenotype Screen: Urine glucose|Normal|C57BL/6 x B10BR x CBA|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|28-Jan-2010|Cryopreserved sperm|||Yes|Type I Diabetes|ENU, JDRF, T cell, autoimmunity|No| 4898.0|129/Sv|129/Sv Wildtype||Dominant||||||||||||||||||||||||||||||||||||||Normal.||129/Sv|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|09-Oct-2009|Cryopreserved sperm|60.0|0.0|Unknown||129, control|Yes| 6924.0|ENU20:B6:28:b|ANU:ENU20:028:b||Recessive|Unknown|unknown|||||||Unknown||||||||||||||||||||||||||||||We are currently looking for a prostate phenotype.|C57BL/6NCrlAnu|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|28-Jun-2012|Cryopreserved sperm|10.0|0.0|Unknown||ENU|No| 6626.0|MH2|FVB-Tg(TetO-Myh6*R403Q)1Rmgr||Dominant||||||||||||||||||||||||||transgene insertion 1, Robert Graham|tetO-CMV|||||||||||Normal||FVB/N|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|20-Oct-2011||0.0|0.0|Unknown||myosin, familial hypertrophic cardiomyopathy, heart|Possibly| 5652.0|C57BL/6J hPG||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6615.0|PIPP Floxed|C57BL/6J-Inpp5j/Marp||Dominant|inositol polyphosphate 5-phosphatase J|Inpp5j|Unknown|Pib5pa, Pipp|MGI:2158663||||11||||||||||Unknown to Unknown|||||||||||||||||||Normal|Normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|12-Oct-2011|Cryopreserved sperm|50.0|0.0|Unknown|||Possibly| 6887.0|APN178|C57Bl/6N-Gpx3/MarpApb||Recessive|glutathione peroxidase 3|Gpx3 |Unknown|EGPx, extracellular GPx, GPx, plasma GPx |MGI:105102|glutathione peroxidase 3; targeted mutation 1a, Wellcome Trust Sanger Institute |Gpx3 |MGI:4841147|11|||||||||||||||||||||||||||||Unknown|Normal|C57Bl/6N|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Good||||No|03-May-2012|Cryopreserved sperm|50.0|0.0|Unknown|||Possibly| 7271.0|APN182|C57BL/6N Tnfsf13/Marp||Recessive|tumor necrosis factor (ligand) superfamily, member 13|Tnfsf13 |Unknown|2310026N09Rik, APRIL, TALL2, TRDL1|MGI:1916833|tumor necrosis factor (ligand) superfamily, member 13; targeted mutation 1, Wellcome Trust Sanger Institute/Monash Animal Research Platform|Tnfsf13/Marp |MGI:4419527|11|||||||||||||||||||||||||||||Unknown|Normal|C57Bl/6N|Unknown|Unknown|Unknown|Unknown|Unknown|Yes|No|Good||||No|06-Feb-2013|Cryopreserved sperm|50.0|0.0|Unknown|||Possibly| 5376.0|HinsA Triple 427|C57BL/6-H2 Tg(Cd4-CD4)2362Litt Tg(HLA DR4-DQ8)427 Tg(Ins2-INS1)/Apb||Dominant||||||||||||||||||||||||||||||||||||||||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|22-Dec-2010|Cryopreserved sperm|50.0|0.0|Unknown||MHC, B cell, selection, autoimmunity, celiac disease|Yes| 6627.0|tTA|FVB.Cg-(myh6-tTA)6Smbf||Dominant||||||||||||||||||||||||||transgene insertion 6, Section of Myocardial Biology - Fishman Lab|rat Myh6 and tetracycline transactivator sequence|cardiac tissue||||||||||Normal||FVB/N|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|20-Oct-2011||0.0|0.0|Unknown||tetracycline, myocytes|Yes| 7629.0||B6/Mrit-131297|B6/Mrit-131297|Dominant|unknown||Unknown||||||Unknown|||||||||||||||||||||||||||||Unknown|Heterozygous mice display a growth delay for a week.|C57BL/6|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Good||||No|07-Apr-2014|Cryopreserved sperm|50.0|0.0|Unknown|||Yes| 6925.0|APN151|C57BL/6N-A Ptafr/MarpApb||Recessive|platelet-activating factor receptor|Ptafr|Unknown|PAFR, PAF receptor|MGI:106066|platelet-activating factor receptor; targeted mutation 1a, Wellcome Trust Sanger Institute |Ptafr |MGI:4460278|4|||||||||||||||||||||||||||||Unknown|Normal|C57BL/6N|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|28-Jun-2012|Cryopreserved sperm|50.0|0.0|Unknown||ES cell clone|Possibly| 7299.0|RBC16|C;B6-Cpox/MarpApb||Dominant|coproporphyrinogen oxidase|Cpox|Unknown|Cpo|MGI:104841||||16|||||||||||||||||||||||||||||Embryonic lethal at E10.5|Low mean cell volume and mean cell hemoglobin and anemia|BALB/C|No|No|Yes|No|No|Yes|No|Good|||Heterozygous intercrosses|No|26-Mar-2013|Cryopreserved sperm|59.0|0.0|Unknown||Heme biosynthesis, Iron, Hereditary coproporphyria , Erythropoiesis|Possibly| 3555.0||B6.C-Lmo4/Wehi||Recessive|LIM domain only 4|Lmo4|Normal|A730077C12Rik, Crp3, Etohi4|MGI:109360|LIM domain only 4; targeted mutation 1, Stuart Orkin |Lmo4|MGI:3035911|3||||||||||||||||Yes|||||||||||||Normal||C57BL/6 x BALB/c|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|31-Jul-2008||0.0|0.0|No||flox, neural tube, mammary gland, zinc finger LIM domain, transcription factor|Yes| 6628.0|A1A1tg|FVB-Tg(Myh6-Adra1a)A1A1Rmgr||Dominant||||||||||||||||||||||||||transgene insertion A1A1, Robert M Graham| rat alpha-myosin heavy chain promoter|heart||||||||||Premature death: * 83 of 171 die at a mean age of 155 days with a cumulative mortality of 48.5%. * premature death is sudden with no signs of heart failureCardiac fibrosis: develop progressive cardiac fibrosis with age, beginning at 2 months of age.Increased cardiac muscle contractility: exhibit enhanced contractility as evidenced by a 33% increase in fractional shortening, a 72% decrease in left ventricle (LV) internal dimension at end-systole, an 8% decrease in LV internal dimension at end-diastole, an 80% increase in maximum dP/dt, a 76% increase in dP/dt max/LVPinst, and a 104% increase in dP/dt max:dP/dt min.Increased ventricle muscle contractility: * 1-month old mutants exhibit enhanced left ventricle contractility with no change or a slight decrease in LV relaxation, resulting in a marked increase in the ratio of dP/dt max to dP/dt min. * cardiac contractility declines with age and diastolic function is reduced, although older mutants still show an increase in dP/dt max compared to wild-type.Abnormal cardiac muscle relaxation: time constant of isovolumetric relaxation is prolonged by 40%, indicating impaired relaxation.Decreased left ventricle diastolic pressure: LV end-diastolic pressure is significantly lower.Increased heart rate: * heart rate is 16% higher than in controls, however no alterations in systolic or diastolic aortic pressure is seen. * baseline heart rate is increased by 17-27% at 2 months of age, however this difference is no longer seen in older mutants.Decreased QRS amplitude: death is preceded by a marked and progressive decrease in the QRS amplitude.||FVB/N|Yes|Unknown|Yes|Yes|Unknown|Yes|No|Unknown||||No|20-Oct-2011||0.0|0.0|Unknown||alpha(1A)-adrenergic receptor (alpha(1A)-AR), ventricular fibrosis, hypercontractility|Yes| 6629.0|A1A2tg|FVB-Tg(Myh6-Adra1a)A1A2Rmgr||Dominant||||||||||||||||||||||||||transgene insertion A1A2, Robert M Graham| rat alpha-myosin heavy chain promoter|heart||||||||||Premature death: * 83 of 171 die at a mean age of 155 days with a cumulative mortality of 48.5%. * premature death is sudden with no signs of heart failureCardiac fibrosis: develop progressive cardiac fibrosis with age, beginning at 2 months of age.Increased cardiac muscle contractility: exhibit enhanced contractility as evidenced by a 33% increase in fractional shortening, a 72% decrease in left ventricle (LV) internal dimension at end-systole, an 8% decrease in LV internal dimension at end-diastole, an 80% increase in maximum dP/dt, a 76% increase in dP/dt max/LVPinst, and a 104% increase in dP/dt max:dP/dt min.Increased ventricle muscle contractility: * 1-month old mutants exhibit enhanced left ventricle contractility with no change or a slight decrease in LV relaxation, resulting in a marked increase in the ratio of dP/dt max to dP/dt min. * cardiac contractility declines with age and diastolic function is reduced, although older mutants still show an increase in dP/dt max compared to wild-type.Abnormal cardiac muscle relaxation: time constant of isovolumetric relaxation is prolonged by 40%, indicating impaired relaxation.Decreased left ventricle diastolic pressure: LV end-diastolic pressure is significantly lower.Increased heart rate: * heart rate is 16% higher than in controls, however no alterations in systolic or diastolic aortic pressure is seen. * baseline heart rate is increased by 17-27% at 2 months of age, however this difference is no longer seen in older mutants.Decreased QRS amplitude: death is preceded by a marked and progressive decrease in the QRS amplitude.||FVB/N|Yes|Unknown|Yes|Yes|Unknown|Yes|No|Unknown||||No|20-Oct-2011||0.0|0.0|Unknown||alpha(1A)-adrenergic receptor (alpha(1A)-AR), ventricular fibrosis, hypercontractility|Yes| 7633.0||SJL/ASAM||Dominant|unknown|unknown|Reduced||||||Unknown|||||||||||||||||||||||||||||Unknown|The mice displays a slight growth retardation phenotype.|SJL/J|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Good||||No|07-Apr-2014|Cryopreserved sperm|50.0|0.0|Unknown|||Yes| 6921.0|Recql4 fl/fl|C57BL/6-Recql4/Apb||Dominant|RecQ protein-like 4|Recql4|Nil||MGI:1931028|Recql4 fl/fl|||15|||||||||||||||||||||||||||||homozygous fl/fl mice are normal, viable and fertile||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Excellent|generated on pure C57BL/6 so not backcrossed. Only maintained on C57||fl/+ to fl/+|No|27-Jun-2012|Cryopreserved sperm|97.0|0.0|Yes|Rothmund-Thomson Syndrome||Possibly| 10485.0|Wnt4 Flox|B6;129S-Wnt4/BhrEiJ||Dominant|wingless-type MMTV integration site family, member 4|Wnt4|||MGI:98957|wingless-type MMTV integration site family, member 4; targeted mutation 1.1, Richard R Behringer|Wnt4|MGI:3773442|4|ENSMUSG00000036856||||||||||||||||||||||||||||from Jax: This strain contains loxP sites flanking exon 2 of Wnt4 resulting in a Cre-dependent conditional null allele. Homozygotes are normal. See Jax Strain #007032 for more details.|Normal||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|05-Feb-2025|Cryopreserved sperm|50.0|0.0|Yes|mutations in this gene are associated with Mayer-Rokitansky-Kuster-Hauser syndrome and SERKAL syndrome in humans||No| 336.0|Zfp145|129-Zbtb16||Recessive|zinc finger and BTB domain containing 16|Zbtb16|Nil|Green's luxoid, PLZF, Zfp145|MGI:103222|targeted mutation 1, Pier Paolo Pandolfi|Zbtb16|MGI:2182708|9||||||||||||||||Yes|||||||||||||Homozygous mutants exhibit abnormal anterior-posterior patterning, with skeletal abnormalities of the limb, especially the hindlimb, and homeotic transformations of anterior skeletal elements into posterior structures. Males develop infertility due to loss of germline cells with age.||C57BL/6 x 129|Yes|Yes|Yes|Yes|Yes|Yes|Yes|Unknown||||No|05-May-2006||0.0|0.0|Unknown||anterior-posterior patterning, Hox, skeleton, limb, bud, transcription factor, zinc-finger|Yes| 6250.0|UBC-GFP|C57BL/6-Tg(UBC-GFP)30Scha/J||Dominant||||||||||||||||||||||||||transgene insertion 30, Brian Schaefer|human ubiquitin C promoter|||||||||||||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown||GFP, Human ubiquitin C promoter, CD8|Yes| 5655.0|C5aR KO ||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 7665.0|Gsto KO|B6;129/Sv-Gsto1/TacAnuApb||Recessive|glutathione S-transferase omega 1|Gsto1||GSTX, p28|MGI:1342273||||19|||||||||||||||||||||||||||||Unknown||C57BL/6NTac|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|15-Apr-2014|Cryopreserved sperm|48.0|0.0|Unknown|||Yes| 7522.0|TgC100.WT|B6.DBA-Tg(ACTB-APP)1Colm/ArcApb|B6.DBA-Tg(ACTB-APP)1Colm/Arc|Dominant||||||||||||||||||||||||||transgene insertion 1, Colin L Masters|human beta actin|High||||||||||Abnormal emotion/affect behaviour:• old mice exhibit decreased immobility during a forced swim test compared with wild-type mice.Behavioral despair:• young mice exhibit increased immobility during a forced swim test compared with wild-type mice.Decreased startle reflex:• in young mice but not old miceHyperactivity:• in young, but not old, mice exhibit increased activity in an open field test and entries in a Y-maze compared with wild-type mice• at 9 and 22 months, mice exhibit slight hyperactivity compared with wild-type mice||C57BL/6 x DBA|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||26|sib x sib|No|29-Nov-2013|Embryo|0.0|0.0|Yes|Alzheimer's disease|amyloid beta-protein (A beta), APP, Alzheimer's disease , metal, γ-secretase|Yes| 7630.0||SJL/ASAM||Dominant|unknown|unknown|Reduced||||||Unknown|||||||||||||||||||||||||||||Unknown|The mice displays a slight growth retardation phenotype without other gross abrnomalities. The mice are viable and fertile.|SJL/J|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Good||||No|07-Apr-2014|Cryopreserved sperm|50.0|0.0|Unknown|||Yes| 3485.0||C57BL/6-Cd8a||Recessive|CD8 antigen, alpha chain|Cd8a|Unknown|Ly-2, Ly-35, Ly-B, Lyt-2|MGI:88346|targeted mutation 1, Tak Mak|Cd8a|MGI:1857149|6||||||||||||||||Yes|||||||||||||Animals homozygous for a mutation in this gene lack CD8+CD4- cytotoxic T cells in the thymus and spleen and do not mount a cytotoxic response to alloantigens. CD8-positive T cells are absent resulting in an increased susceptibility to viral infection. There is also demyelination of the nerve cells.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|23-Jul-2008||0.0|0.0|Unknown||T cell, CD8, infection, viral, class I MHC, cytotoxic|Yes| 5122.0|Sox10LacZ|C57BL/6-Sox10||Dominant|SRY-box containing gene 10|Sox10|Nil|Sox21|MGI:98358|SRY-box containing gene 10; targeted mutation 1, Michael Wegner|Sox10|MGI:2151173|15|||||||||||||||||||||||||||||lacZ is expressed by all Sox10-expressing cells|lacZ is expressed by all Sox10-expressing cells|C57BL/6|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|12-May-2010||0.0|0.0|Yes|Waardenburg-Hirschsprung disease|neuron, glial, Schwann, ErbB3, pigmentation, melanocyte|Yes| 10477.0|PGR|C57BL/6-Tg(H2-Kb-Tcra,-Tcrb)P25Ktk/J, C57BL/6-Tg(UBC-GFP)30Scha/J, B6.129S7-Rag1tm1Mom/J||Recessive|TCR alpha and TCR beta chains|||||tcr a and b|tcra and tcrb||Unknown|||||||||||||||||Tg(H2-Kb-Tcra,-Tcrb)P25Ktk|H-2Kb promoter|Tg(H2-Kb-Tcra,-Tcrb)P25Ktk||||||||||In these mice all T cells express the same TCR specific for the P25 mycobacterial epitope and GFP on all cells, Mice also lack B cells |same as homozygous mice except that they have B cells |C57Bl/6J|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|23-Jan-2025|Cryopreserved sperm|40.0|0.0|Unknown|||Possibly| 7631.0||SJL/ASAM||Dominant|unknown|unknown|Reduced||||||Unknown|||||||||||||||||||||||||||||Unknown|The mice displays a slight growth retardation phenotype.|SJL/J|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Good||||No|07-Apr-2014|Cryopreserved sperm|53.0|0.0|Unknown|||Yes| 5657.0|C5L2 x C5aR||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5658.0|C8 (C8 Brca1 Co/Co)||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 2774.0|BALB/c.hK14-FLII 36|BALB/c-Tg(hK14-FLII)36/AnuApb||Dominant|||||||||Unknown||||||||||||||||Yes|Human Flightless|Human Keratin 14|||||||||||Not bred to Homozygous state|Normal|BALB/c|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|5||Het FLII transgenic x WT BALB/c|No|16-Feb-2008|Cryopreserved sperm|150.0|0.0|Unknown||human, skin, enhancer element|Yes| 5120.0|endothelin-3+/-|B6.129-Edn3/J||Recessive|endothelin 3|Edn3|Nil|114-CH19, 114CH19, tmgc48|MGI:95285|endothelin 3; targeted mutation 1, Masashi Yanagisawa|Edn3|MGI:1857160|2||||||||||||||||Yes|||||||||||||Postnatal lethality: mice have a mean life span of 21 days, with a range of 4-65 days.Variable body spotting: * extensive white spotting (70 - 80% of body surface) * white regions showed absence of melanin pigment in coat hair and of melanocytes in the hair bulbs.Abnormal colon morphology: distal portion of colon narrow and spastic; proximal portion of colon distended.Aganglionic megacolon: absence of myenteric ganglion neurons in distal, spastic segment of colon.Absent enteric neurons: absence of myenteric ganglion neurons in distal, spastic segment of colon.||C57BL/6|No|No|Yes|No|No|Yes|No|Unknown|10|||No|12-May-2010||0.0|0.0|Yes|Hirschsprung Disease, Susceptibility to, 1; HSCR1 OMIM ID: 142623|enteric neuron, melanocyte, epidermis, colon, migration, ganglion|Yes| 7527.0|NOD.B6Idd11A|NOD.B6-Idd11/ArcApb||Recessive|||Unknown||||||Unknown||||||||||||||||Yes|||||||||insulin dependent diabetes susceptibility 11; C57BL/6|Idd11||4|||NOD|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|29-Nov-2013|Embryo|0.0|0.0|Unknown||Diabetes, congenic, insulin, non obese|Yes| 1758.0|Apaf-1 knockout|C57BL/6-Apaf1||Recessive|apoptotic peptidase activating factor 1|Apaf1|Nil|6230400I06Rik, Apaf1l|MGI:1306796|apoptotic peptidase activating factor 1; gene trap XIX18, Peter Gruss|Apaf1|MGI:1857868|10||||||||||||||||No|||||||||||||Lethality throughout fetal growth and development: embryonic defects apparent by E12.5, die by E17. Decreased apoptosis:* induction of apoptosis in mutant embryonic fibroblasts is similar to controls, but mutant fibroblasts show reduced cell death after prolonged treatment with apoptotic stimuli (anti-Fas antibody, C6-ceramide, and staurosporin).* tissues that normally exhibit apoptosis in developmental stages instead exhibit hyperplasia and/or overgrowth.Abnormal craniofacial bone morphology.Absent ethmoidal bone.Impaired ossification of basisphenoid bone.Absent neurocranium: absence of skull vault.Absent vomer bone.Cleft palate: late and imperfect palatial fusion occursMidline facial cleft.Nervous system phenotype: at E13-14 and E18, numbers of spinal motoneurons and dorsal root ganglion neurons are not different from wild-type.Abnormal brain morphology: brain hyperplasia presumably due to lack of apoptosis in the mantle layer of the developing diencephalon, midbrain, cerebellum and ventricular layer of the choroid plexus of the fourth ventricle; an excess of differentiating neurons is observed in these locations.Abnormal brain development.Abnormal embryonic neuroepithelial layer differentiation: overgrowth resulting in abnormal folding and generation of a mantle layer.Abnormal cortical marginal zone morphology.Abnormal folding of telencephalic vesicles: may be due to intense overgrowth (hyperplasia) of diencephalon and midbrain.Small telencephalic vesicles: may be due to intense overgrowth (hyperplasia) of diencephalon and midbrain.Exencephaly.Hydroencephaly: results from obliteration of the lumen of the neural tube.Choroid plexus hyperplasia: hyperplasia of the choroid plexus of the fourth ventricle is seen.Hypothalamus hyperplasia: abnormal overgrowth of ventral side of hypothalamus through the base of the skull.Diencephalon hyperplasia.Midbrain hyperplasia.Abnormal neuron morphology: at E14 and E18, motoneurons and DRG neurons exhibit degenerative-like changes not seen in wild-type.Abnormal neuron physiology: at E14, developing neurons undergo atypical programmed cell death (PCD) in contrast to type 1 (apoptotic-like) mechanism exhibited in wild-type neurons; apoptotic-like degeneration markers (such as TUNEL labeling) are not observed in dying mutant neurons.Abnormal lens polarity.Small lens.Persistence of hyaloid capillary system: eye vascular endothelial cells obliterate the optic cup at E14.5.Retina hyperplasia:* by E12.5, the retina is noticeably thicker* by E14.5, the hyperplastic retina fills the optic cup and is folded.Interdigital webbing: interdigital webbing in limb buds with reduced apoptosis.Abnormal craniofacial bone morphology.Absent ethmoidal bone.Impaired ossification of basisphenoid bone.Absent neurocranium: absence of skull vault.Absent vomer bone.Cleft palate: late and imperfect palatial fusion occursAbnormal embryonic neuroepithelial layer differentiation: overgrowth resulting in abnormal folding and generation of a mantle layer.||C57BL/6|No|No|Yes|No|No|Yes|No|Unknown||||No|02-Aug-2007||0.0|0.0|Unknown||Caspase, embryonic lethal, cytochrome c, mitochondria, Bcl-2|Yes| 6651.0|RBC13|C;B6-Hbb-b1/WehiMarpApb||Dominant|Hbb-b1 hemoglobin, beta adult major chain|Hbb-b1|Reduced|beta maj, beta major globin, beta1, beta-s|MGI:96021|hemoglobin, beta adult major chain; red blood cell mutant 13|Hbb-b1|MGI:5460881|7|||||||||||||||||||||||||||||Lethal at E18.5 or just after (not present at birth). Embryos are normal until E16.5 where they manifest progressive pallor and reduced fetal liver cellularity.|Microcytic, hypochromic anemia with severe reticulocytosis. Compensatory erythropoiesis with splenic extramedullary hematopoiesis due to red cell destruction. |C57BL/6 and BALB/c|No|No|Yes|No|No|Yes|No|Excellent|||Heterozygote intercross and background strain wild type to heterozygote|No|28-Nov-2011|Cryopreserved sperm|50.0|0.0|Yes|Beta-thalassemia|Beta-thalassemia, Hbb-b1/beta major globin, ENU-mutagenesis|Possibly| 7669.0|ENU31:G1|ANU:ENU31:G1||Recessive|Unknown||||||||Unknown||||||||||||||||Unknown|||||||||||||Unknown|Unknown|C57BL/6NCrlAnu|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||1||No|02-May-2014|Cryopreserved sperm|3828.0|110.0|Unknown||ENU, random, mutagenesis, screen|Yes| 5661.0|Cardiac Cre ||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 1837.0|B-CK|B6.129-Ckb/Wehi||Recessive|creatine kinase, brain|Ckb|Nil|B-CK, Ck-3|MGI:88407|targeted mutation 1, Be Wieringa|Ckb|MGI:3042843|12||||||||||||||||Yes|||||||||||||Homozygous null mice have abnormal hippocampal morphology with enlarged mossy fiber field size and display resistance to pharmacologically induced seizures, reduced habituation and spatial learning impairments and are slightly smaller than wildtype littermates.|||Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|08-Aug-2007||0.0|0.0|Unknown||energy, ATP, brain, learning, mitochondria|Yes| 1848.0||B6.C3-Tg(APPswe,PSEN1dE9)85Dbo||Dominant||||||||||||||||||||||||||transgene insertion 85, David R Borchelt|Each transgene controlled by mouse prion promoter.||||||||||||Cerebral amyloid angiopathy:* exhibits progressive increase in cerebral amyloid angiopathy as early as 6 months* amyloid deposition is observed in leptomeningeal vasculature.Amyloid beta deposits:* sparse deposits observed at 21 weeks of age, however, numerous deposits are observed at 45 and 60 weeks.* deposits are more extensive in females.* level of brain amyloid beta peptide 42 is predominant over 40; levels increase dramatically after 20 weeks of age.* senile plaques detected by thioflavin S or the anti-amyloid beta antibody, 3D6, as early as 4 months of age.* plaques are restricted to cortex and hippocampus at time points up to 12 months of age.* plaques increase in number and size over time.* exhibits an overall increase in soluble and insoluble amyloid beta peptide 40 and 42 between 4 and 12 months.* insoluble amyloid beta42 is increased 2-fold in cerebrum of sucrose-fed mice as compared to water-fed control.* total amyloid beta levels are increased by 3.6 fold in sucrose fed mice.* amyloid beta deposition is increased by 2.9-fold as determined by immunohistochemical and morphometric analysis in sucrose-fed mice.Increased drinking behavior: mice fed sucrose water exhibited increased water consumption.Abnormal spatial learning* transgenic mice fed sucrose water failed to learn Morris water maze test after 5 days of training.* water-fed transgenic mice retained some learning ability over 5 day test period, but did not perform as well in the water maze test as non-transgenic controls.Increased circulating insulin level: fasting plasma insulin levels are increased 3 fold in mice fed sucrose water as compared to water-fed control.Increased circulating cholesterol level: total cholesterol, but not HDL, levels are increased 30% in mice fed sucrose water as compared to water-fed control.Increased circulating triglyceride level: elevated plasma triglyceride levels observed in females at 15 weeks of age.Impaired glucose tolerance: mice fed sucrose water displayed an impaired glucose tolerance as compared to water-fed controlcardiovascular system.Vasculature congestion.Increased body weight:* mice fed sucrose water consistently gained weight over study time period (2 months- 8 months).* sucrose-fed mice increased body weight by 17% over water-fed controls.|C57BL/6 x C3H|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|10-Aug-2007||0.0|0.0|Yes|Alzheimer's Disease|Alzheimer's Disease, Amyloid, plaques, hippocampus, cortex|Yes| 1849.0||B6.129-Tnfrsf1a/JWehi||Recessive|tumor necrosis factor receptor superfamily, member 1a|Tnfrsf1a|Nil|CD120a, p55, p55-R, TNF receptor alpha chain, TNF-R-I, TNF-R1, TNF-R55, TNFAR, Tnfr-2, Tnfr1, TNFR60, TNFRI, TNFRp55|MGI:1314884|targeted mutation 1, Tak Mak|Tnfrsf1a|MGI:1857261|6||||||||||||||||No|||||||||||||Homozygotes for targeted null mutations exhibit disrupted splenic architecture, increased adult liver weights, reduced IgG immune response, deficits in some host defense and inflammatory responses, LPS resistance, and reduced graft-vs-host disease.||C57BL/6 x 129|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|10-Aug-2007||0.0|0.0|Unknown||T cell, Lymphocyte, infection, signal transduction|Yes| 7632.0||SJL/ASAM||Dominant|unknown|unknown|Reduced||||||Unknown|||||||||||||||||||||||||||||Unknown|The mice displays a slight growth retardation phenotype.|SJL/J|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Good||||No|07-Apr-2014||0.0|0.0|Unknown|||Yes| 5339.0||C57BL/6-Tg(CAG-ATP7A)22Jmer/Apb||Dominant||||||||||||||||||||||||||human ATPase, Cu++ transporting, alpha polypeptide|chicken beta-actin|||||||||||The overall phenotype of transgenic mice was normal, and the transgene was transmissible to progeny, but the transgenic mice showed interesting changes in Cu concentration in various organs that were generally consistent with a role for ATP7A in efflux.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|9|||No|11-Dec-2010|Cryopreserved sperm|40.0|0.0|Unknown||copper, Menkes protein, lactation, mammary gland, transport, cuproenzymes|Yes| 5666.0|Cav-1 WT||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5189.0||ENU18WT:007a||Recessive|Unknown||Unknown||||||Unknown|||||||||||||||||||||||||||||Unknown||C57BL/6JAnu|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|02-Aug-2010|Cryopreserved sperm|20.0|0.0|Unknown||ENU, Wellcome Trust|Possibly| 6630.0|ABKO|B6.129X1-Adra1a||Recessive|Adra1a|adrenergic receptor, alpha 1a|Nil|Adra1c|MGI:104773|adrenergic receptor, alpha 1a; targeted mutation 1, Paul C Simpson|Adra1a|MGI:2387663|14|||||||||||||||||||||||||||||Decreased vasoconstriction: homozygotes are chronically hypotensive due to loss of vasoconstriction and consequent reduction of vasomotor tone.Decreased heart rate variability: by ECG telemetry, conscious homozygotes show a 14% reduction in basal heart rate variability, suggesting increased sympathetic balance.Hypotension: * by tail cuff manometer and arterial catheter, conscious homozygotes are hypotensive at rest, with a ~10-15 mm Hg reduction in blood pressure (8-12% of wild-type mice) * tail cuff pressure is also reduced in a smaller cohort of homozygotes in the C57BL/6 background whereas heart rate is slightly but not significantly higher relative to wild-type mice * no differences in body weight, heart weight, heart histology, blood chemistry, blood cell counts, cardiac output or renal function are observed.|Hypotension: heterozygotes are intermediately hypotensive relative to wild-type and homozygous mutant mice|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|20-Oct-2011||0.0|0.0|Unknown||alpha 1-adrenergic receptors, hypotension, blood pressure|Yes| 5340.0|CTR1 Tg|C57BL/6-Tg(SLC31A1)Jmer||Dominant||||||||||||||||||||||||||human Solute carrier family 31, member 1||||||||||||||C57BL/6|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|11-Dec-2010||0.0|0.0|Unknown||copper, transport|Yes| 7636.0||SJL/ASAM||Dominant|unknown|unknown|Reduced||||||Unknown|||||||||||||||||||||||||||||Unknown|The mice displays a slight growth retardation phenotype.|SJL/J|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Good||||No|07-Apr-2014|Cryopreserved sperm|61.0|0.0|Unknown|||Yes| 7637.0||SJL/ASAM||Dominant|unknown|unknown|Reduced||||||Unknown|||||||||||||||||||||||||||||Unknown|The mice displays a slight growth retardation phenotype.|SJL/J|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Good||||No|07-Apr-2014|Cryopreserved sperm|55.0|0.0|Unknown|||Yes| 7639.0||SJL/ASAM||Dominant|unknown|unknown|Reduced||||||Unknown|||||||||||||||||||||||||||||Unknown|The mice displays a slight growth retardation phenotype for a week.|SJL/J|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Good||||No|07-Apr-2014|Cryopreserved sperm|50.0|0.0|Unknown|||Yes| 7641.0||SJL/ASAM||Dominant|unknown|unknown|Reduced||||||Unknown|||||||||||||||||||||||||||||Unknown|The mice displays a slight growth retardation phenotype for a week.|SJL/J|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Good||||No|07-Apr-2014|Cryopreserved sperm|50.0|0.0|Unknown|||Yes| 1859.0|Eµ-myc/Bad ko|Un-Tg(IghMyc)22Bri Bad/Wehi||Dominant|BCL2-associated agonist of cell death|Bad|Nil|Bbc2|MGI:1096330|BCL2-associated agonist of cell death; targeted mutation 1, Stanley J Korsmeyer|Bad|MGI:2675966|19||||||||||||||||Yes|transgene insertion 22, Ralph L Brinster|Lymphoid-specific immunoglobulin heavy chain enhancer (Eμ)|B cell lineage||||||||||Excess pre-B cells in bone marrow. Animals develop high incidence pre-B and B lymphoma - Adult mortality: 80% More than 90% of Emu-myc mice die between 6 and 18 weeks of age (median 11 weeeks). Enlargement of all lymph nodes, spleen, infiltration of thymus (thymoma), bone marrow, liver, lung, weight loss.|||Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|10-Aug-2007||0.0|0.0|No||B cell, Lymphoma, Bcl2, BH3 only|Yes| 3944.0|Line3|FVB/N-Tg(HBA1-GFP)3EW|FVB/N-Tg(HBA1-GFP)3EW|Dominant||||||||||||||||||||||||||Green Fluorescent Protein|α-Globin (-570 to +37) (4.1kb of enhancer)|||||||||||Fluorescence in erythrocytes can be observed by FACS or fluorescent microscopy. The allele is subject to variegation.|Fluorescence in erythrocytes can be observed by FACS or fluorescent microscopy. The allele is subject to variegation|FVB/NJ|Yes|Yes|Yes|Yes|Yes|Yes|No|Poor|||Hom x Hom|No|17-Oct-2008||0.0|0.0|No||metastable epiallele, transgene silencing, green fluorescent protein|Yes| 7642.0||SJL/ASAM||Dominant|unknown|unknown|Reduced||||||Unknown|||||||||||||||||||||||||||||Unknown|The mice displays a slight growth retardation phenotype for a week.|SJL/J|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Good||||No|07-Apr-2014||0.0|0.0|Unknown|||Yes| 5673.0|CD11c-DTR/GFP x C57 ||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5447.0|Minnie ; ENU12NIH 71b CBA|ENU12NIH:071b CBA||Recessive|Unknown|Unknown|Unknown||||||Unknown|||||||||||||||||||||||||||||Small Mice|Normal|C57BL/6JAnu x CBA/CaJ|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|N/A|2|Sib x sib|No|28-Feb-2011|Cryopreserved sperm|40.0|0.0|Unknown||runted, dwarf, small, ENU|Possibly| 5674.0|CD11cDTR||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 7638.0||SJL/ASAM||Dominant|unknown|unknown|Reduced||||||Unknown|||||||||||||||||||||||||||||Unknown|The mice displays a slight growth retardation phenotype for a week.|SJL/J|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Good||||No|07-Apr-2014|Cryopreserved sperm|20.0|0.0|Unknown|||Yes| 7640.0||SJL/ASAM||Dominant|unknown|unknown|Reduced||||||Unknown|||||||||||||||||||||||||||||Unknown|The mice displays a slight growth retardation phenotype for a week.|SJL/J|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Good||||No|07-Apr-2014|Cryopreserved sperm|22.0|0.0|Unknown|||Yes| 5163.0|FVB x FVB.B6; Dirc-1|FVB/N;B6-Dircq1/ArcApb||Dominant||||||||||||||||||||||||||||||||||||||As per parental strain.Once injected with Alloxan mice are resistant to becoming diabetic (check via urine glucose or blood monitor), these mice do not show nephropathy and retinopathy disease consistent with the human conditions as compared to the B6;FVB/N-Dirc-1 strain. |As per parental strain.|FVB/N|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|10|5|Hom x Hom|No|29-Jun-2010|Embryo|0.0|0.0|Yes|Once injected with Alloxan mice become diabetic (check via urine glucose or blood monitor), these mice show nephropathy and retinopathy disease consistent with the human conditions. |diabetic complications, retinopathy, nephropathy|Yes| 7645.0||B6/Mrit-114906|B6/Mrit-114906|Dominant|unknown||Unknown||||||Unknown|||||||||||||||||||||||||||||Unknown|Heterozygous mice display a transient growth decrease|C57BL/6|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Good||||No|07-Apr-2014||0.0|0.0|Unknown||growth , ENU|Yes| 6631.0|ABKO|B6.129P2-Adra1b||Recessive|adrenergic receptor, alpha 1b|Adra1b|Nil|alpha1B-adrenergic receptor|MGI:104774|adrenergic receptor, alpha 1b; targeted mutation 1, Susanna Cotecchia|Adra1b|MGI:2148638|11|||||||||||||||||||||||||||||Abnormal heart left ventricle morphology: left ventricular volume is higher.Decreased vasoconstriction: exhibit a reduction in mesenteric vascular responses to endogenous norepinephrine compared to wild-type, indicating reduced vasoconstriction in response to norepinephrine.Decreased cardiac muscle contractility: * phenylephrine-induced contractions of aortic rings are decreased by 25%. * baseline myocardial contractility is lower, as reflected by dP/dt. * transient bilateral carotid occlusion results in a minimal increase in myocardial contractility instead of the enhanced contractility seen in wild-type.Decreased heart rate: transient bilateral carotid occlusion results in a decrease in heart rate compared to a slight increase in treated wild-type, however baseline heart rate is normal.Abnormal systemic arterial blood pressure: * mean arterial blood pressure response to phenylephrine is decreased by 45% * mean arterial blood pressure response to norepinephrine is also decreased although to a lesser extent than seen with phenylephrine.Decreased systemic arterial blood pressure: exhibit impaired pressor response to a hypotensive stimulus, with marked attenuation in the change in systolic blood pressure and in the percent change in the end-systolic pressure-volume relationship after transient bilateral carotid occlusion.Decreased systemic arterial systolic blood pressure: baseline systolic blood pressure and Ea are lower.Impaired passive avoidance behaviour: 4-5 month old homozygotes show impaired retention of an inhibitory avoidance task after receiving a stressful electric stimuli.Decreased exploration in new environment: 4-5 month old homozygotes show significantly reduced horizontal exploratory activity and a reduced rearing behavior (vertical activity) in the open field.Abnormal baroreceptor physiology: transient bilateral carotid occlusion to test cardiovascular responses to a hypotensive stimuli produced an attenuated pressor response, indicating an abnormal baroreflex activity.||C57BL/6|Yes|Unknown|Yes|Yes|Unknown|Yes|No|Unknown||||No|20-Oct-2011||0.0|0.0|Unknown||alpha1-adrenergic receptor, adrenergic drugs, blood pressure|Yes| 6927.0|ENU18:::B6:G1|ANU:ENU18:G1||Recessive|Unknown||||||||Unknown||||||||||||||||Unknown|||||||||||||Unknown|Unknown|C57BL/6JAnu|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||1||No|02-Jul-2012|Cryopreserved sperm|3067.0|0.0|Unknown||ENU, random, mutagenesis, screen|Yes| 7373.0|ATARI:kk:Cbl-bKO|C57BL/6JSfdAnu-Aire Cblb H2 Tg(ILK3mHEL)3Ccg Tg(TcrHEL3A9)1Mmd/AnuApb||Recessive|autoimmune regulator (autoimmune polyendocrinopathy candidiasis ectodermal dystrophy) |Aire|Nil||MGI:1338803|autoimmune regulator (autoimmune polyendocrinopathy candidiasis ectodermal dystrophy); targeted mutation 1, Leena Peltonen|Aire|MGI:2182940|10|||||||||||||||||transgene insertion 3, Christopher C Goodnow|Rat insulin promoter|Expression of the inserted sequence specifically to pancreatic islet beta cells||||||||||||C57BL/6JSfdAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|||sib x sib|No|08-Jul-2013|Cryopreserved sperm|20.0|0.0|No||Hen egg Lysozyme, tolerance, immunity, T cell, B cell, selection|Yes| 7373.0|ATARI:kk:Cbl-bKO|C57BL/6JSfdAnu-Aire Cblb H2 Tg(ILK3mHEL)3Ccg Tg(TcrHEL3A9)1Mmd/AnuApb||Recessive|Casitas B-lineage lymphoma b|Cblb||Cbl-b|MGI:2146430|Casitas B-lineage lymphoma b; targeted mutation 1, Josef M Penninger|Cblb|MGI:2180570|16|||||||||||||||||transgene insertion 1, Mark M Davis||||||||||||||C57BL/6JSfdAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|||sib x sib|No|08-Jul-2013|Cryopreserved sperm|||No||Hen egg Lysozyme, tolerance, immunity, T cell, B cell, selection|Yes| 6929.0|ENU20:G1|ANU:ENU20:G1||Recessive|Unknown||||||||Unknown||||||||||||||||Unknown|||||||||||||Unknown|Unknown|C57BL/6NCrlAnu|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||1||No|02-Jul-2012|Cryopreserved sperm|392.0|40.0|Unknown||ENU, random, mutagenesis, screen|Yes| 5164.0|B6 x B6FVB; Dirc-1|B6;FVB/N-Dircq1/ArcApb||Dominant||||||||||||||||||||||||||||||||||diabetes induced renal changes 1|Dircq1||6|As per parental strain.Once injected with Alloxan mice become diabetic (check via urine glucose or blood monitor), these mice show nephropathy and retinopathy disease consistent with the human conditions. Mice are identified by conventional genotyping but on induction of diabetes phenotypes relating to type 1 diabetic complication are observed i.e. Excessive urination, weight loss and proteinuria. |As per parental strain.|C57BL/6J|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|10|5|Hom x Hom|No|29-Jun-2010|Embryo|0.0|0.0|Yes|Once injected with Alloxan mice become diabetic (check via urine glucose or blood monitor), these mice show nephropathy and retinopathy disease consistent with the human conditions. |diabetic complications, retinopathy, nephropathy|Yes| 6928.0|ENU19:G1|ANU:ENU19:G1||Recessive|Unknown||||||||Unknown||||||||||||||||Unknown|||||||||||||Unknown|Unknown|C57BL/6JAnu|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||1||No|02-Jul-2012|Cryopreserved sperm|471.0|0.0|Unknown||ENU, random, mutagenesis, screen|Yes| 5166.0|Idd5|NOD.B6-Idd5/ArcApb||Dominant||||||||||||||||||||||||||||||||||||||As per the parental strain (NOD/Lt).Delayed onset of Type 1 diabetes.||NOD/Lt|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|||Hom x Hom|No|29-Jun-2010|Embryo|0.0|0.0|Yes|All of these 4 strains are derived from the Non Obese Diabetes (NOD) model where we have bred a small section of the protective mouse (C57BL/6) into the Idd locus. This generated 4 congenic mouse strains that have enabled us to evaluate the effectiveness of a protective allele in a known Type 1 Diabetic region in the NOD/Lt mouse.||Yes| 4102.0||KRN:231||Recessive|||||||||Unknown||||||||||||||||Yes|transgene insertion KRN, Diane Mathis|Natural TCR alpha and -beta promoter/enhancer elements.|||||||||||No arthritis in KRN/H2g7 model.||C57BL/6 x NODk x C57BL/10 x Balb/b|Yes|Yes|Yes|Yes|Yes|Yes|No|Poor||4||No|04-Dec-2008|Cryopreserved sperm|100.0|0.0|Yes||Autoimmunity, Arthritis, KRN, ENU|No| 32.0|B-thy|C57BL/6JSfdAnu-Trp53/AnuApb|C57BL/6JSfdAnu-Trp53/AnuApb|Semi-dominant|transformation related protein 53|Trp53|Nil|p53|MGI:98834|bthy|Trp53|MGI:3611889|11|ENSMUSG00000059552|ENSMUST00000108658|Trp53-201|412|540|T to C|ENSMUSE00000111826|5|138|Cysteine to Arginine|||||ATAAGCTATTCTGCCAGCTGGCGAAGACGTGCCCTGTGCAGTTGTGGGTCAGCGCCACACC|No||||||||||||||primitive hematopoietic or T cell leukemia,Sudden death,hemorrhage,Thymic lymphomaFibrosarcomaMultinodal lymphomaOsteosarcomaHaemangiosarcomaBrain tumourTeratocarcinoma|C57BL/6JSfdAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||8||No|06-Feb-2006|Cryopreserved sperm|27.0|0.0|Yes||p53, apoptosis, tumour, cell cycle, ENU|Yes| 141.0|Pebbles ; DD6|C57BL/6JSfdAnu-Tg(IghelD4)Ccg/AnuApb||Dominant||||||||||||||||||||||||||transgene insertion 4, Christopher C Goodnow||low level||||||||||Mice express IgD immunoglobulin reactive to Hen Egg lysozyme||C57BL/6JAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|06-Feb-2006|Cryopreserved sperm|20.0|0.0|No||immunoglobulin, hen egg lysozyme, HEL, IgD|Yes| 7646.0||B6/Mrit-107292|B6/Mrit-107292|Dominant|Unknown||Unknown||||||Unknown|||||||||||||||||||||||||||||Unknown|Heterozygous mice display a transient growth decrease|C57BL/6|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Good||||No|07-Apr-2014||0.0|0.0|Unknown||growth , ENU|Yes| 5452.0|PD|B6;129/Sv-Eif2ak2/MarpApb||Recessive|eukaryotic translation initiation factor 2-alpha kinase 2|Eif2ak2|Nil|dsRNA-activated kinase, eIF-2 alpha, eIF-2 alpha, IFN- type I-induced and dsRNA-activated kinase, IFN-induced and double-stranded RNA-activated kinase, Pkr, Prkr, Tik|MGI:1353449|eukaryotic translation initiation factor 2-alpha kinase 2; targeted mutation 1, Charles Weissmann|Eif2ak2|MGI:2182566|17||||||||||||||||No|||||||||||||Normal|Normal|129/Sv x C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|02-Mar-2011|Cryopreserved sperm|50.0|0.0|No||Protein kinase, innate immunity, double stranded RNA, cell signalling, eif2alpha|Yes| 7647.0||B6/Mrit-amp|B6/Mrit-amp|Dominant|unknown||Unknown||||||Unknown|||||||||||||||||||||||||||||Unknown|Heterozygous mice display a transient growth decrease|C57BL/6|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Good||||No|07-Apr-2014|Cryopreserved sperm|50.0|0.0|Unknown||ENU|Yes| 4111.0||KRN:172||Recessive|||||||||Unknown||||||||||||||||Yes|transgene insertion KRN, Diane Mathis|Natural TCR alpha and -beta promoter/enhancer elements.|||||||||||No arthritis in KRN/H2g7 model||C57BL/6 x NODk x C57BL/10 x Balb/b|Yes|Yes|Yes|Yes|Yes|Yes|No|Poor||||No|05-Dec-2008|Cryopreserved sperm|10.0|0.0|Yes||Autoimmunity, Arthritis, KRN, ENU|No| 6926.0||c-mycδKI||Semi-dominant|BCL2-like 11 (apoptosis facilitator)|Bcl2l11|Unknown|1500006F24Rik, Bim, Bod|MGI:1197519||||2|||||||||||||||||||||||||||||Unknown|Unknown|C57BL/6 x 129/Sv|Yes|Yes|Yes|Yes|Yes|Yes|No|Excellent||||No|29-Jun-2012|Cryopreserved sperm|60.0|0.0|Unknown||Bcl2, BH3 domain|No| 5684.0|Chat tm1(cre/ERT)Nat /J||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5685.0|ChAT-Cre||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 7650.0||B6/Mrit-da|B6/Mrit-da|Dominant|Unknown||Unknown||||||Unknown|||||||||||||||||||||||||||||Unknown|Heterozygous mice display a transient growth decrease|C57BL/6|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Good||||No|07-Apr-2014|Cryopreserved sperm|50.0|0.0|Unknown||ENU|No| 5437.0|Gq KO|B6.129-Gnaq/Apb||Semi-dominant|guanine nucleotide binding protein, alpha q polypeptide|Gnaq|Nil|Dsk1, Dsk10, G alpha q, Galphaq, Gq, GqI|MGI:95776||||19|||||||||||||||||||||||||||||Small agouti mouse, gold stomach, black eyes and extremeties.||C57BL/6|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown|6|||No|16-Feb-2011|Cryopreserved sperm|50.0|0.0|No||Platelet|Yes| 6632.0|Kit1|C57BL/6-Tg(Myh6-kit)1.1||Dominant||||||||||||||||||||||||||myosin heavy chain 6 - c-kit|myosin, heavy polypeptide 6, cardiac muscle, alpha|Heart||||||||||Expression of c-kit in heart tissue||C57BL/6|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|20-Oct-2011||0.0|0.0|Unknown||heart, signal transduction, phosphorylation|Yes| 10327.0|Rosa26-Cas9-KI|B6(C)-Gt(ROSA)26Sorem1.1(CAG-cas9*,-EGFP)Rsky/J||Recessive|gene trap ROSA 26, Philippe Soriano|Gt(ROSA)26Sor|||MGI:104735|gene trap ROSA 26, Philippe Soriano; endonuclease-mediated mutation 1.1, Klaus Rajewsky|Gt(ROSA)26Sor|MGI:5750729|6|ENSMUSG00000086429 ||||||||||||||||Transgene CMV_CRE. Knockin R26LSL_Cas9||||||||||||Normal|Normal|C57Bl/6J|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|27-Apr-2023||0.0|0.0|Unknown|||Possibly| 7579.0|Spi6 KO x OT-I|C57BL/6J-SerpinB9 Tg(TcraTcrb)1100Mjb/MarpApb||Dominant|serine (or cysteine) peptidase inhibitor, clade B, member 9|Serpinb9|Nil|PI-9, Spi6|MGI:106603||||13|||||||||||||||||transgene insertion 1100, Michael J Bevan|MGI:3054907|||||||||||Increased apoptosis:• apoptosis is increased in LCMV- and LM-specific CTLs in mutantsAbnormal CD8-positive, alpha-beta cytotoxic T cell morphology:• upon infection with LCMV Armstrong or a strain of Listeria monocytogenes (LM), numbers of LCMV-specific CTLs are reduced 5-fold and LM-specific CTLs are reduced 9-fold compared to control B6 mice.• frequency of CTLs devoid of Gzmb granules is 3 times greater than in controls; number of Gzmb granules per CTL is 2-fold lower than in controls.Abnormal cytotoxic T cell physiology:• apoptosis is increased in LCMV- and LM-specific CTLs in mutants.Defective cytotoxic T cell cytolysis:• deficit in CTL activity is observed in ex vivo activity assay over course of LCMV infection; on day 10, activity is decrease 6-fold compared to controls.Abnormal enzyme/ coenzyme level:• caspase 3 in cytoplasm is increased.Abnormal enzyme/coenzyme activity:• GranzymeB activity is significantly increased in cytoplasm of mutants compared to controls.|Normal|C57BL/6J|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|||Spi6 KO mice mated with OT-I mice|No|28-Jan-2014|Cryopreserved sperm|50.0|0.0|Unknown||T cell, CD8, dendritic cell, MHC I, cross-priming|Yes| 6633.0|Kit2|C57BL/6-Tg(Myh6-kit)1.2||Dominant||||||||||||||||||||||||||myosin heavy chain 6 - c-kit|myosin, heavy polypeptide 6, cardiac muscle, alpha|Heart||||||||||Expression of c-kit in heart tissue||C57BL/6|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|20-Oct-2011||0.0|0.0|Unknown||heart, signal transduction, phosphorylation|Yes| 4771.0|c-cbl KO|C57BL/6-Cbl ||Recessive|Casitas B-lineage lymphoma|Cbl|Nil|c-Cbl, cbl, Cbl-2|MGI:88279|targeted mutation 1, David D L Bowtell|Cbl|MGI:2180578|9||||||||||||||||Yes|||||||||||||Homozygotes for targeted null mutations exhibit increased thymic CD3 and CD4 expression and tyrosine-phosphorylation, lymphoid hyperplasia, and altered splenic hemopoiesis. Females show increased ductal density and branching in mammary fat pads.Abnormal spleen red pulp morphology- expandedenlarged spleen. Spleen is enlarged about 1.2- to 2-fold compared to wild type mice due to expansion of the red pulpspleen hyperplasia.Increase in the number of megakaryocytes, megakaryoblasts, and myelocytes but no increase in the number of lymphocytes is seen in the spleen.Abnormal adipocyte morphology- adipocyte volume is reduced by about 64% compared to wild type mice.Decreased adipose tissue amount- despite increased caloric intake, a 40-50% decrease in the size of the adipose tissue depots (including both white and brown fat) is seenthis phenotype is more pronounced in males than in females.Increased lean body mass- balances the decrease in adipose tissue resulting in no significant difference in total body weight.Polyphagia.Hyperactivity- about a 4-fold increase in ambulatory activity is seen, especially during the dark phase.Increased body temperature- rectal temperature is increased by 1 degree C independent of time of day or if the mice are fed or fasted overnight. However, circulating levels of triiodothyronine or thyroxine are similar to wild type in both the fed and fasted states.Decreased circulating leptin level- leptin levels are decreased by 66%; however adiponectin levels are similar to wild type.Abnormal gas homeostasis- increased oxygen consumption:whole body oxygen consumption corrected for the difference in lean mass is increased by 22% compared to wild type mice.Abnormal respiratory quotient- reduced respiratory quotientAbnormal glucose homeostasis- decreased circulating insulin level, after an overnight fast insulin levels are decreased relative to wild type but glucose levels are similar to wild type.Improved glucose tolerance- improved glucose tolerance despite decreased insulin levels throughout the test.Increased insulin sensitivity.Abnormal lipid homeostasis- decreased circulating free fatty acid level.Decreased triglyceride level- triglyceride levels in the liver are decreased but those in the quadriceps muscle are similar to wild type muscleAbnormal muscle physiology- glucose clearance in to glycogen is increased in the soleus and extensor digitorum longus muscles but not in the liver.Abnormal muscle cell glucose uptake- glucose uptake into skeletal muscle is increased about 2-fold; however glucose uptake into white and brown adipose tissue is not different from wild type. Basal and insulin-stimulated glucose uptake are increased in soleus muscle explants by 65% and 30%, respectively; however, glucose uptake is not increased in fat explants basal, but not insulin-stimulated, glucose uptake is increased by 30% in extensor digitorum longus muscle explantscellular.Abnormal mitochondrial morphology- a 2-fold increase in the average size of subsarcolemmal mitochondria is seen; however, no increase in mitochondrial area or cristae density is seen in the subsarcolemmal region.Spleen hyperplasia- increase in the number of megakaryocytes, megakaryoblasts, and myelocytes but no increase in the number of lymphocytes is seen in the spleen.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Poor||||No|28-Jul-2009||0.0|0.0|No||Cbl, tyrosine kinase, TKB, Zap-70, adipose|Possibly| 4829.0|6AT:35|ENU6AT:035||Recessive|||||||||Unknown|||||||||||||||||transgene insertion 3, Christopher C Goodnow|Rat insulin promoter|Expression of the inserted sequence specifically to pancreatic islet beta cells||||||||||Mice carrying the ins-HEL gene have a subclinical predisposition to diabetes due to islet cell failure. Mice carrying the insHEL and TCR transgenes have asubclinical predisposition to autoimmune destruction of the beta cell. Screening mice by urine glucose test. High glucose levels indicate diabetes and thus autoimmunity. "Early onset diabetes" definition changed during screen from approx 80 days to 40 days.||C57BL/6 x C57BL/10BR|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|||Breed diabetic Double transgenic with a non transgenic sib for next generation|No|24-Sep-2009|Cryopreserved sperm|60.0|0.0|Yes|Type I Diabetes|ENU, JDRF, autoimmunity, T cell, B cell, glucose|No| 4829.0|6AT:35|ENU6AT:035||Recessive||||||||||||||||||||||||||transgene insertion 1, Mark M Davis||||||||||||Mice carrying the ins-HEL gene have a subclinical predisposition to diabetes due to islet cell failure. Mice carrying the insHEL and TCR transgenes have asubclinical predisposition to autoimmune destruction of the beta cell. Screening mice by urine glucose test. High glucose levels indicate diabetes and thus autoimmunity. "Early onset diabetes" definition changed during screen from approx 80 days to 40 days.||C57BL/6 x C57BL/10BR|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|||Breed diabetic Double transgenic with a non transgenic sib for next generation|No|24-Sep-2009|Cryopreserved sperm|||Yes|Type I Diabetes|ENU, JDRF, autoimmunity, T cell, B cell, glucose|No| 7273.0|ENU20 017b ; ENU20:017b|C57BL/6NCrlAnu-Dock2/AnuApb|C57BL/6NCrlAnu-Dock2/AnuApb|Recessive|dedicator of cyto-kinesis 2|Dock2|Unknown|CED-5, Hch, MBC |MGI:2149010|dedicator of cyto-kinesis 2; mutation 3, The Australian National University|Dock2|MGI:5563488|11|ENSMUSG00000020143|ENSMUST00000093193|Dock2-001|3921|3990|T to A|ENSMUSE00000351317|39|1307|Tyrosine to STOP|||||AGCCTGTGCAAGGAACTGGCGGAACAATATGAGATGGAGATCTTTGACTACGAGCTACTCA||||||||||||||Decreased CD4<+> T cells. Increased CD44 expression in CD4 and CD8 T cells.|Normal|C57BL/6NCrlAnu|Yes|Unknown|Yes|Yes|Unknown|Yes|No|Good|0|G6|Het x Het|No|12-Feb-2013|Cryopreserved sperm|25.0|0.0|Unknown||ENU, T cell|Yes| 2775.0||C57BL/6-Tg(hK14-FLII)36||Dominant|||||||||Unknown||||||||||||||||Yes|Human Flightless|Human Keratin 14|||||||||||Not bred to Homozygous state|Normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|5||Het FLII transgenic x WT C57BL/6|No|16-Feb-2008||0.0|0.0|Unknown||human, skin, enhancer, keratin|Yes| 1360.0||NOD.B6 Idd3r450||Dominant|insulin dependent diabetes susceptibility 3|Idd3|Unknown|Idd-3|MGI:96405||||3||||||||||||||||Yes|||||||||||||Idd3 is a diabetes susceptibility QTL mapping to a 145 kb interval on mouse Chromosome 3 around 19.2 cM. Il2 colocalizes with Idd3 and has been suggested as a candidate gene.||NOD|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|22-Jun-2007||0.0|0.0|Unknown||insulin|Yes| 4782.0|WT control|C57BL/6.Tnf Tnfrsf1a Tnfrsf1b WT control||Recessive|tumor necrosis factor|Tnf|Normal|DIF, TNF alpha, TNF-alpha, Tnfa, TNFalpha, Tnfsf1a, tumor necrosis factor-alpha|MGI:104798|targeted mutation 2, Jonathon D Sedgwick|Tnf|MGI:3578747|17||||||||||||||||Yes|Neomycin resistance gene||||||||||||Normal. Control of APB ID#2395||C57BL/6 x 129|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|06-Sep-2009|Cryopreserved sperm|160.0|0.0|Unknown||lymphocyte, inflammation, lipopolysaccharide, neutrophil, innate immunity|Yes| 4782.0|WT control|C57BL/6.Tnf Tnfrsf1a Tnfrsf1b WT control||Recessive|tumor necrosis factor receptor superfamily, member 1a|Tnfrsf1a|Unknown|memTNF, memTNFdelta|MGI:1314884|targeted mutation 1, Immunex Research and Development Corporation|Tnfrsf1a|MGI:1857468|Unknown|||||||||||||||||||||||||||||Normal. Control of APB ID#2395||C57BL/6 x 129|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|06-Sep-2009|Cryopreserved sperm|||Unknown||lymphocyte, inflammation, lipopolysaccharide, neutrophil, innate immunity|Yes| 4782.0|WT control|C57BL/6.Tnf Tnfrsf1a Tnfrsf1b WT control||Recessive|tumor necrosis factor receptor superfamily, member 1b|Tnfrsf1b|Unknown|CD120a, p55, p55-R, TNF receptor alpha chain, TNF-R-I, TNF-R1, TNF-R55, TNFAR, Tnfr-2, Tnfr1, TNFR60, TNFRI, TNFRp55|MGI:1314883|targeted mutation 1, Immunex Research and Development Corporation|Tnfrsf1b|MGI:1860087|Unknown|||||||||||||||||||||||||||||Normal. Control of APB ID#2395||C57BL/6 x 129|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|06-Sep-2009|Cryopreserved sperm|||Unknown||lymphocyte, inflammation, lipopolysaccharide, neutrophil, innate immunity|Yes| 6634.0|Wv1|C57BL/6-Tg(Myh6-Kit)2.1||Dominant||||||||||||||||||||||||||myosin heavy chain 6 - c-kit|myosin, heavy polypeptide 6, cardiac muscle, alpha|Heart||||||||||Expression of c-kit(W-v> allele in heart tissue||C57BL/6|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|20-Oct-2011||0.0|0.0|Unknown||heart, signal transduction, phosphorylation|Yes| 1550.0||BALB/c-Tg(iFABPp-TGFb1) ||Recessive||||||||||||||||||||||||||transforming growth factor, beta 1|at intestinal fatty acid binding protein (nucleotides -1178 - +28) - iFABP , i-FABP linked to nucleotides 3–2,150 of the human growth hormone (hGH) gene (except for its 5' regulatory sequences).|high||||||||||Restricted expression of TGF beta transgene to intestine - duodenum and proximal jejunum.||BALB/c|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|06-Jul-2007|Cryopreserved sperm|150.0|0.0|Unknown||TGF beta, TGFb, allergy|Yes| 7068.0|Momme D32|FVB/NJ-Dnmt1 Tg(Hba1-Gfp)1Ew/QimrApb||Semi-dominant|DNA methyltransferase (cytosine-5) 1|Dnmt1|Unknown|Cxxc9, Dnmt1o, MommeD2, MTase|MGI:94912|DNA methyltransferase 1; modifier of murine metastable epialleles, D32|Dnmt1|MGI:5515386|9||||||||||Unknown to Unknown|||||||Green Fluorescent Protein|human alpha-globin promoter and enhancer region|||||||||||Unknown|Unknown|FVB/NJ|No|No|Yes|No|No|Yes|No|Good|||MommeD32<+/->;Tg(Hba1-Gfp)1Ew x Tg(Hba1-Gfp)1Ew|No|29-Aug-2012|Cryopreserved sperm|39.0|0.0|Unknown||ENU, epigenetics, suppressor of variegation|Possibly| 4739.0|Wink|C.129-Tg(hGM-CSFRb) Csf2rb Csf2rb2/Apb||Dominant|colony stimulating factor 2 receptor, beta, low-affinity (granulocyte-macrophage)|Csf2rb|Unknown|AIC2B, Bc, beta c, CDw131, common beta chain, Csf2rb1, Il3r, Il3rb1, Il5rb|MGI:1339759|targeted mutation 1, Clare L Scott|Csf2rb|MGI:3653883|15||||||||||||||||Yes|human beta common chain receptor for GM-CSF/IL-3/IL-5|pgk|very low||||||||||Normal|Normal|BALB/c|Yes|Yes|Yes|Yes|Yes|Yes|No|Excellent|10|0|Purchased BALB/c mated with transgenic mouse from colony to maintain colony|No|20-Apr-2009|Cryopreserved sperm|120.0|0.0|Unknown||growth factor, interleukin, signal transduction, receptor|Yes| 4739.0|Wink|C.129-Tg(hGM-CSFRb) Csf2rb Csf2rb2/Apb||Dominant|colony stimulating factor 2 receptor, beta 2, low-affinity (granulocyte-macrophage)|Csf2rb2|Unknown|AIC2A, BetaIl3, Bil3, Il3r, Il3rb2|MGI:1339760|targeted mutation 1, C Glenn Begley|Csf2rb2|MGI:3652583|15|||||||||||||||||||||||||||||Normal|Normal|BALB/c|Yes|Yes|Yes|Yes|Yes|Yes|No|Excellent|10|0|Purchased BALB/c mated with transgenic mouse from colony to maintain colony|No|20-Apr-2009|Cryopreserved sperm|||Unknown||growth factor, interleukin, signal transduction, receptor|Yes| 5687.0|ChAT-EGFP x SOD1G93A||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6932.0|Crim1FLOX|B6.129/Ola-Crim1/Uqbr||Recessive|cysteine rich transmembrane BMP regulator 1 (chordin like)|Crim1|Nil||MGI:1354756|Crim1FLOX|||17|||||||||||||||||||||||||||||Normal|Normal|Predominantly C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Excellent|>6|||No|05-Jul-2012||0.0|0.0|Unknown|||Possibly| 221.0|Chisel KO|C57BL/6-Smpx/Apb||Recessive|small muscle protein, X-linked|Smpx|Unknown|chisel, Csl|MGI:1913356|targeted mutation 1, Richard P Harvey|Smpx|MGI:2387819|X||||||||||||||||Yes|||||||||||||Mice homozygous for a null mutation do not exhibit defects in heart or skeletal muscle morphology or development|No reported phenotype|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|25-Apr-2006|Cryopreserved sperm|45.0|0.0|Unknown||myocyte, insulin, heart|Yes| 1937.0||BALB/c.B6-IL13 Ccl11/AnuApb||Recessive|interleukin 13|Il13|Unknown|Il-13|MGI:96541|targeted mutation 2, Andrew NJ McKenzie|Il13|MGI:1931804|11||||||||||||||||Yes|||||||||||||||BALB/c |Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|29-Aug-2007|Cryopreserved sperm|150.0|0.0|Unknown||Eosinophils, IL4, IL5, T cell, infection, stat6|Yes| 1937.0||BALB/c.B6-IL13 Ccl11/AnuApb||Recessive|small chemokine (C-C motif) ligand 11|Ccl11|Nil|eotaxin, Scya11|MGI:103576|chemokine (C-C motif) ligand 11; targeted mutation 1, Marc E Rothenberg|Ccl11|MGI:2384435|11|||||||||||||||||||||||||||||||BALB/c |Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|29-Aug-2007|Cryopreserved sperm|||Unknown||Eosinophils, IL4, IL5, T cell, infection, stat6|Yes| 5693.0|CMV Cre (CreDel)||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 208.0|Tbx5 KO|Tbx5||Recessive|T-box 5|Tbx5|Unknown||MGI:102541|targeted mutation 1.1, Jonathan G Seidman|Tbx5|MGI:2387851|5||||||||||||||||Yes|||||||||||||Embryonic lethal (do not survive past day E10.5), abnormal cardiac and forelimb development. |Model for Holt Oram Syndrome|C57BL/6|No|No|Yes|No|No|Yes|No|Unknown||||No|24-Apr-2006||0.0|0.0|Yes||Holt Oram Syndrome, forelimb, embryonic lethal, cardiac, heart, transcription factor|Yes| 5136.0|A9|C57BL/6-Tg(TcrbB3)8Cbn/CbnApb||Dominant||||||||||||||||||||||||||transgene insertion TcrbB3, Francis R Carbone|Tcrb|More than 10 copies||||||||||The majority of CD8 T cells express the trangenic Vb5.2 T cell receptor.|As for homozygous.|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|||br|No|26-May-2010|Cryopreserved sperm|50.0|0.0|No||TCR tansgenic, cytotoxic T lymphocytes, T cell repertoire|Yes| 6255.0|B6 Caspase -2/9|B6.129-Casp2 Casp9||Recessive|caspase 2|Casp2|Nil|Caspase-2, Ich-1, Nedd2|MGI:97295|caspase 2; targeted mutation 1, David L Vaux|Casp2|MGI:3609949|6|||||||||||||||||||||||||||||Perinatal Abnormal brain development:*At E14.5 a majority of embryos display brain over-growth similar to that found in Casp9 homozygotes.Abnormal T cell physiology:*Thymocytes grown in wildtype hosts have only 10-20% of the DEVD-ase activity of wildtype or thymocytes deficient for only caspase 2.Hematopoietic system phenotype:*Irradiated wildtype hosts reconstituted with E14.5 Casp2 Casp9 double homozygous fetal liver develop normal thymocyte numbers and sub-populations with no thymocyte upregulation of caspases 1, 3, 6, 7, 8, or 9, normal B cell and T cell apoptosis in response to cytokine withdrawal, and normal T cell sensitivity to dexamethasone.*Dexamethasone induced apoptosis of T cells (grown in wildtype hosts from E14.5 fetal liver) is blocked by caspase inhibitors but not by calpain and cathepsin inhibitors.||C57BL/6|No|No|Yes|No|No|Yes|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown||Caspase 2, Caspase 9|Yes| 6255.0|B6 Caspase -2/9|B6.129-Casp2 Casp9||Recessive|caspase 9|Casp9|Nil|Caspase-9, ICE-LAP6, Mch6|MGI:1277950|caspase 9; targeted mutation 1, Richard A Flavell|Casp9|MGI:2158755|4|||||||||||||||||||||||||||||Perinatal Abnormal brain development:*At E14.5 a majority of embryos display brain over-growth similar to that found in Casp9 homozygotes.Abnormal T cell physiology:*Thymocytes grown in wildtype hosts have only 10-20% of the DEVD-ase activity of wildtype or thymocytes deficient for only caspase 2.Hematopoietic system phenotype:*Irradiated wildtype hosts reconstituted with E14.5 Casp2 Casp9 double homozygous fetal liver develop normal thymocyte numbers and sub-populations with no thymocyte upregulation of caspases 1, 3, 6, 7, 8, or 9, normal B cell and T cell apoptosis in response to cytokine withdrawal, and normal T cell sensitivity to dexamethasone.*Dexamethasone induced apoptosis of T cells (grown in wildtype hosts from E14.5 fetal liver) is blocked by caspase inhibitors but not by calpain and cathepsin inhibitors.||C57BL/6|No|No|Yes|No|No|Yes|No|Unknown||||No|13-Sep-2011||||Unknown||Caspase 2, Caspase 9|Yes| 639.0|Vav-rtTA|B6.129-Tg(Vav-rtTA)/Apb||Dominant||||||||||||||||||||||||||reverse tetracycline transactivator|vav|haemopoietic specific expression||||||||||Normal|Normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Excellent|9|0||No|25-Apr-2007|Cryopreserved sperm|40.0|0.0|No||vav, rtTA, haemopoeisis, tetracycline|Yes| 29.0|Babe|C57BL/6JSfdAnu-Agtpbp1/AnuApb|C57BL/6JSfdAnu-Agtpbp1/AnuApb|Recessive|ATP/GTP binding protein 1|Agtpbp1|Unknown|Nna1|MGI:2159437|ATP/GTP binding protein 1; babe|Agtpbp1|MGI:3847121|13|ENSMUSG00000021557|ENSMUST00000022040|Agtpbp1-201|2413|2543|C to T|ENSMUSE00000118960|19|804|Arginine to STOP|||||ACATTTGTTACTACAAAAATCACTTCTCACGAAGCTCAGTTGCCGCAGGCGGACAGAAGGG|No|||||||||||||Lethal dilute ataxia, weakness of the hindlimbs and mild uncoordination (ataxia) which is usually detectable at weaning.||C57BL/6JSfdAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||8||No|06-Feb-2006|Cryopreserved sperm|37.0|0.0|Unknown||Ataxia, Purkinje cell, degeneration, retinal, ENU|Yes| 133.0|Homer|B10.Cg-H2 Tg(Dct-mHELKK)1Rc Tg(TcrHEL3A9)1Mmd/AnuApb|B10.Cg-H2 Tg(Dct-mHELKK)1Rc Tg(TcrHEL3A9)1Mmd/AnuApb|Dominant||||||||||||||||||||||||||transgene insertion 1, Richard J Cornall|dopachrome tautomerase (Dct) ; Trp2, Tyrp2 |Melanocyte specific|histocompatibility-2, MHC|H2||H-2, MHC-II|MGI:95894|histocompatibility-2, MHC; k2 variant|H2|MGI:4936842|17|Mice develop a spontaneous autoimmune disease with striking similarity to human vitiligo vulgaris and Vogt-Koyanagi-Harada syndrome. ||C57BR|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||5||No|06-Feb-2006|Cryopreserved sperm|60.0|0.0|Yes|human vitiligo vulgaris and Vogt-Koyanagi-Harada syndrome|CD4, T cell, vitiligo, melanocyte, autoimmunity|Yes| 133.0|Homer|B10.Cg-H2 Tg(Dct-mHELKK)1Rc Tg(TcrHEL3A9)1Mmd/AnuApb|B10.Cg-H2 Tg(Dct-mHELKK)1Rc Tg(TcrHEL3A9)1Mmd/AnuApb|Dominant||||||||||||||||||||||||||transgene insertion 1, Mark M Davis||||||||||||Mice develop a spontaneous autoimmune disease with striking similarity to human vitiligo vulgaris and Vogt-Koyanagi-Harada syndrome. ||C57BR|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||5||No|06-Feb-2006|Cryopreserved sperm|||Yes|human vitiligo vulgaris and Vogt-Koyanagi-Harada syndrome|CD4, T cell, vitiligo, melanocyte, autoimmunity|Yes| 1532.0||BALB/c-IL9/AnuApb||Recessive|interleukin 9|Il9|Nil|Il-9, P40|MGI:96563|targeted mutation 1, Andrew NJ McKenzie|IL9|MGI:2656470|13||||||||||||||||Yes|||||||||||||Homozygous null mice are viable and show no overt phenotype, however when challenged, aspects of the inflammatory response are shown to be impaired.||BALB/c|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|10|||No|05-Jul-2007|Cryopreserved sperm|160.0|0.0|Unknown||inflammation, T cell, mast cell, asthma, anaphylaxis|Yes| 5400.0|FVB x FVB.B6 ; Dirc-3|FVB/N;B6-Dircq3/ArcApb||Dominant|||||||||||||||||||||||||||||Unknown|Unknown||||diabetes induced renal changes 3|Dircq3||6|As per parental strain.Once injected with Alloxan mice are resistant to becoming diabetic (check via urine glucose or blood monitor), these mice do not show nephropathy and retinopathy disease consistent with the human conditions as compared to the B6;FVB/N-Dirc-3 strain. |As per parental strain.|FVB/N|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|10|5|Hom x Hom|No|31-Jan-2011|Embryo|0.0|0.0|Yes|Once injected with Alloxan mice become diabetic (check via urine glucose or blood monitor), these mice show nephropathy and retinopathy disease consistent with the human conditions. |diabetic complications, retinopathy, nephropathy|Yes| 6264.0|del 362|C57BL/6-Dnmt3l||Dominant|DNA (cytosine-5-)-methyltransferase 3-like |Dnmt3l|Nil|D6Ertd14e, ecat7|MGI:1859287|DNA (cytosine-5-)-methyltransferase 3-like; targeted mutation 1, Hamish S Scott|Dnmt3l|MGI:3574947|10|||||||||||||||||||||||||||||Abnormal seminiferous epithelium morphology:*The epithelium has a vacuolated appearance.Azoospermia:*Germ cells are lost through apoptosis and sloughing with many tubules containing only Sertoli cells.Arrest of male meiosis:*At P14 in first spermatogenic wave a build up of leptotene and zygotene spermatocytes is seen with no cells progressing beyond stage IV.*At P70 only leptotene spermatocytes and spermatogonia are present.*The pachytene synaptonemal complex is not seen.Small gonad:*Adults display severe hypogonadism.Infertility||C57BL/6|Yes|No|Yes|Yes|No|Yes|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown||Dnmt3L, Spermatogenesis|Yes| 7616.0|EphA2 Knockout , EphA2 Reporter|B6.129-Epha2/QimrApb||Recessive|Eph Receptor A2|EphA2||Eck, Myk2, Sek2, Sek-2|MGI:95278|Eph receptor A2; gene trap CN3, Yoichiro Iwakura|Epha2|MGI:2448472|4|||||||||||||||||||||||||||||Abnormal tail morphology:• abnormal blood vessel formation in the tailsAbnormal caudal vertebrae morphology:• ectopic tail vertebra formationShort tail:• varying degrees of short tails, first seen around E12.5-13.5Kinked tail:• 40% exhibit varying degrees of kinky tails, first seen around E12.5-13.5Abnormal axial mesoderm:• aberrant axial mesoderm formationAbnormal neural tube morphology/development:• the wall of the neural tube in tails is thickened and multi-layeredSplit notochord:• notochord is abnormally bifurcated at the caudal end between E11.5 and E12.5 and the bifurcated notochords are abnormally intertwined• notochordal cells are spread broadly into the tail budAbnormal neural tube morphology/development:• the wall of the neural tube in tails is thickened and multi-layeredAbnormal vascular development:• abnormal blood vessel formation in tails, with the number of blood vessels changed and larger vessel caliberskeletonabnormal caudal vertebrae morphology ( J:69393 )• ectopic tail vertebra formationAbnormal sclerotome morphology• ectopic slerotomes form at the caudal tail where the bifurcated notochords form|Normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Poor|10||Homozygous x Homozygous|No|07-Mar-2014|Cryopreserved sperm|50.0|0.0|Unknown||kink tail, notochord|No| 6933.0|ENU19 WT:001:b:B6:G3|ANU:ENU19WT:001:b:G3||Recessive|Unknown||||||||Unknown||||||||||||||||Unknown|||||||||||||Unknown|Unknown|C57BL/6JAnu|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||1||No|05-Jul-2012|Cryopreserved sperm|58.0|0.0|Unknown||ENU, random, mutagenesis, screen|Yes| 4831.0|6CAT:004|ENU6CAT:004||Recessive|||||||||Unknown|||||||||||||||||transgene insertion 3, Christopher C Goodnow|Rat insulin promoter|Expression of the inserted sequence specifically to pancreatic islet beta cells||||||||||Mice carrying the ins-HEL gene have a subclinical predisposition to diabetes due to islet cell failure. Mice carrying the insHEL and TCR transgenes have asubclinical predisposition to autoimmune destruction of the beta cell. Screening mice by urine glucose test. High glucose levels indicate diabetes and thus autoimmunity. "Early onset diabetes" definition changed during screen from approx 80 days to 40 days.||C57BL/6 x C57BL/10BR x CBA|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|||Breed diabetic Double transgenic with a non transgenic sib for next generation|No|24-Sep-2009|Cryopreserved sperm|75.0|0.0|Yes|Type I Diabetes|ENU, JDRF, autoimmunity, T cell, B cell, glucose|No| 4831.0|6CAT:004|ENU6CAT:004||Recessive||||||||||||||||||||||||||transgene insertion 1, Mark M Davis||||||||||||Mice carrying the ins-HEL gene have a subclinical predisposition to diabetes due to islet cell failure. Mice carrying the insHEL and TCR transgenes have asubclinical predisposition to autoimmune destruction of the beta cell. Screening mice by urine glucose test. High glucose levels indicate diabetes and thus autoimmunity. "Early onset diabetes" definition changed during screen from approx 80 days to 40 days.||C57BL/6 x C57BL/10BR x CBA|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|||Breed diabetic Double transgenic with a non transgenic sib for next generation|No|24-Sep-2009|Cryopreserved sperm|||Yes|Type I Diabetes|ENU, JDRF, autoimmunity, T cell, B cell, glucose|No| 6934.0|ENU19 WT:002:b:B6:G3|ANU:ENU19WT:002:b:G3||Recessive|Unknown||||||||Unknown||||||||||||||||Unknown|||||||||||||Unknown|Unknown|C57BL/6JAnu|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||1||No|05-Jul-2012|Cryopreserved sperm|10.0|0.0|Unknown||ENU, random, mutagenesis, screen|Yes| 6935.0|ENU19 WT:005:b:B6:G3|ANU:ENU19WT:005:b:G3||Recessive|Unknown||||||||Unknown||||||||||||||||Unknown|||||||||||||Unknown|Unknown|C57BL/6JAnu|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||1||No|05-Jul-2012|Cryopreserved sperm|20.0|0.0|Unknown||ENU, random, mutagenesis, screen|Yes| 6937.0|ENU19 WT:008:b:B6:G3|ANU:ENU19WT:008:b:G3||Recessive|Unknown||||||||Unknown||||||||||||||||Unknown|||||||||||||Unknown|Unknown|C57BL/6JAnu|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||1||No|05-Jul-2012|Cryopreserved sperm|40.0|0.0|Unknown||ENU, random, mutagenesis, screen|Yes| 7670.0|ENU31:G2|ANU:ENU31:G2||Recessive|Unknown||||||||Unknown||||||||||||||||Unknown|||||||||||||Unknown|Unknown|C57BL/6NCrlAnu|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||1||No|02-May-2014|Cryopreserved sperm|4383.0|0.0|Unknown||ENU, random, mutagenesis, screen|Yes| 1953.0|PDGFRa floxed|Un-Pdgfra||Recessive|platelet derived growth factor receptor, alpha polypeptide|Pdgfra|Normal|CD140a, Pdgfr-2|MGI:97530|targeted mutation 8, Philippe Soriano|Pdgfra|MGI:2449440|5||||||||||||||||Yes|||||||||||||Normal||129S4|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|03-Sep-2007||0.0|0.0|Unknown||cardiac development, neural crest cells, aortic arch, cranial mesenchyme|Yes| 7628.0|EphA1 Knockout|B6.129-Epha1/QimrApb||Recessive|Eph receptor A1|Epha1||5730453L17Rik, Eph, Esk|MGI:107381|Eph receptor A1; targeted mutation 1, Shannon L Duffy|Epha1|MGI:3822370|6|||||||||||||||||||||||||||||A Homozygous (PLAP/PLAP) mouse will result in the normal phenotype displaying PLAP activity however EphA1 expression will be lost.Endometrium inflammation: • mice exhibit endometrium inflammation secondary to hydrometrocolpos.Vaginal inflammation:• mice exhibit inflammation of the vaginal mucosa secondary to hydrometrocolpos.Dilated uterine horn: • mice exhibit dilated, attenuated uterine horns secondary to hydrometrocolpos.Enlarged uterus:• mice exhibit an enlarged uterus due to an accumulation of clear uterine fluid (hydrometrocolpos).Increased uterus weight.Vagina atresia:• 18% of mice exhibit a failure of vaginal opening.• despite normal estrogen receptor expression, beta-estradiol treatment fails to induce precocious vaginal opening in P12 mice unlike in wild-type mice and vaginal opening can not be induced by likewise treating affected adult mice.Hydrometrocolpos: • mice exhibit inflammation of the vaginal mucosa and endometrium with dilated, attenuated uterine horns secondary to hydrometrocolpos.Female infertility: • female mice affected by hydrometrocolpos are sterile.Kinked tail:• up to 80% of mice exhibit a kinky tail due to incorrectly positioned caudal vertebrae.Distended abdomen: • in some mice due to an enlarged uterusAbnormal response/metabolism to endogenous compounds:• treatment with beta-estradiol fails to induce apoptosis in the lower genital tract and precocious vaginal opening unlike in wild-type mice.Skeleton phenotype: • despite a kinky tail, mice exhibit normal skeletal morphology.|Normal PLAP activity with EphA1 expression.|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|10|||No|04-Apr-2014|Cryopreserved sperm|50.0|0.0|Unknown||receptor tyrosine kinase, epithelium, hydrometrocolpos|No| 5202.0|Tmem26 conditional knockout|C57BL/6-Tmem26/UqbrApb||Recessive|Transmembrane protein 26|Tmem26|Nil||MGI:2143537||||10||||||||||||||||Yes|||||||||||||Normal,ubiquitous deletion of floxed region also produces normal animals.|normal|C57BL/6J|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|2 crosses from founder mouse (derived from a C57 cell line) to C57 mice|approx. 7||No|06-Aug-2010|Cryopreserved sperm|47.0|0.0|Unknown|||Yes| 6936.0|ENU19 WT:007:b:B6:G3|ANU:ENU19WT:007:b:G3||Recessive|Unknown||||||||Unknown||||||||||||||||Unknown|||||||||||||Unknown|Unknown|C57BL/6JAnu|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||1||No|05-Jul-2012|Cryopreserved sperm|50.0|0.0|Unknown||ENU, random, mutagenesis, screen|Yes| 148.0|NODScid|NOD;Cg-H2 Prkdc/AnuApb||Recessive|protein kinase, DNA activated, catalytic polypeptide|Prkdc|Nil|DNA-PK, DNA-PKcs, DNAPDcs, slip, XRCC7|MGI:104779|severe combined immunodeficiency|Prkdc|MGI:1857113|16||||||||||||||||Yes|||||||||||||SCID mutation prevents TCR and BCR rearrangements. This prevents maturation of B and T cells at very early stages of development. These mice, therefore lack, T and B cells in periphery. Please refer to MGI allele page for further information using the link above.||NOD|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||19||No|06-Feb-2006|Cryopreserved sperm|165.0|0.0|Yes||SCID, severe combined immunodeficiency, transplant, T cell, B cell|Yes| 1946.0||BALB/c.B6-Gata1 Il5/AnuApb||Recessive|GATA binding protein 1|Gata1|Unknown|Gata-1, Gf-1|MGI:95661|GATA binding protein 1; targeted mutation 6, Stuart Orkin|Gata1|MGI:3037864|X||||||||||||||||Yes|||||||||||||No eosinophils||BALB/c |Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|01-Sep-2007|Cryopreserved sperm|135.0|0.0|Unknown||infection, eosinophil, nematode|Yes| 1946.0||BALB/c.B6-Gata1 Il5/AnuApb||Recessive|interleukin 5|Il5|Unknown|IL-5|MGI:96557|targeted mutation 1, Manfred A Kopf|Il5|MGI:1861948|11|||||||||||||||||||||||||||||No eosinophils||BALB/c |Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|01-Sep-2007|Cryopreserved sperm|||Unknown||infection, eosinophil, nematode|Yes| 5516.0|Gwendolin|B6.(Cg)-Gstp1/Gstp2||Recessive|glutathione S-transferase, pi 1|Gstp1|Nil|Gst p-1, GstpiB|MGI:95865|targeted mutation 1, C Roland Wolf|Gstp1/Gstp2|MGI:3046099|19||||||||||||||||Yes|||||||||||||Mutant mice with null mutations in both Gstp1 and Gstp2 exhibit an increased susceptibility to DMBA and TPA induced skin papillomas. Male mutant mice exhibit an increased body weight with age. Studying allergic airway disease compared with allergic WT mice, eosinophilia, goblet cell hyperplasia, airway remodeling, lung resistance, and IL-5 were enhanced in allergic Gstp-null mice.||C57BL/6 x 129|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|6|||No|01-Jun-2011||0.0|0.0|Unknown||asthma, eosinophil, signal transduction, IL-5, phosphorylation, papilloma|Yes| 5516.0|Gwendolin|B6.(Cg)-Gstp1/Gstp2||Recessive|glutathione S-transferase, pi 2|Gstp2|Nil|Gst p-2, Gst-3, Gst3, GSTpiA|MGI:95864|glutathione S-transferase, pi 2; targeted mutation 1, C Roland Wolf|Gstp1/Gstp2|MGI:3046101|19|||||||||||||||||||||||||||||Mutant mice with null mutations in both Gstp1 and Gstp2 exhibit an increased susceptibility to DMBA and TPA induced skin papillomas. Male mutant mice exhibit an increased body weight with age. Studying allergic airway disease compared with allergic WT mice, eosinophilia, goblet cell hyperplasia, airway remodeling, lung resistance, and IL-5 were enhanced in allergic Gstp-null mice.||C57BL/6 x 129|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|6|||No|01-Jun-2011||||Unknown||asthma, eosinophil, signal transduction, IL-5, phosphorylation, papilloma|Yes| 2442.0|Koy|C57BL/6JSfdAnu-Coro1a/Apb|C57BL/6JSfdAnu-Coro1a/Apb|Recessive|coronin, actin binding protein 1A|Coro1a|Reduced|Clabp, coronin 1, Lmb3, p57|MGI:1345961|coronin, actin binding protein 1A; koyaanisqatsi|Coro1a|MGI:3818509|7|ENSMUSG00000030707|ENSMUST00000106364|Coro1a-002|76|329|G to A|ENSMUSE00000202191|2|26|Glutamic acid to Lysine|||||GACAGCCAGCCAAGGCTGACCAGTGCTATGAGGATGTGCGCGTCTCACAAACCACTTGGGA|Yes|||||||||||||Mice have few peripheral blood CD4 or CD8 T cells. T cells are also reduced in spleen and LN. There is reduced transwell migration of thymocytes and naive mature T cells to SDF (CXCL12) or to ELC (CCL21). Elevated phalloidin staining (elevated F actin). Decreased CD4-positive T cell number: CD4+ T cell numbers in the periphery are significantly decreased about 5-fold.Decreased CD8-positive T cell number: CD8+ T cell numbers in the periphery are significantly decreased about 5-fold.Decreased thymocyte number: the percentage of mature (CD69loCD62Lhi) single-positive thymocytes is decreased in these mice.Abnormal T cell physiology:* in vitro transwell assays demonstrate migration defects in thymic CD4+ T cells' response to sphingosine 1-phosphate, CCL21, and CXCL12.* similar defects are observed in the migratory response of CD4+CD8+ T cells to CXCL12 and of splenic CD4+ T cells to CCL21.|Slight T cell deficit.|C57BL/6JStdAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||5||No|14-Jan-2008|Cryopreserved sperm|185.0|0.0|Yes|Severe Combined Immunodeficiency|T cell, CD8, SCID, CD4, migration, Severe Combined Immunodeficiency, Autosomal Recessive, T Cell-Negative, B Cell-Positive, Nk Cell-Positive, egress|Yes| 6938.0|ENU19 WT:012:a:B6:G3|ANU:ENU19WT:012:a:G3||Recessive|Unknown||||||||Unknown||||||||||||||||Unknown|||||||||||||Unknown|Unknown|C57BL/6JAnu|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||1||No|05-Jul-2012|Cryopreserved sperm|18.0|0.0|Unknown||ENU, random, mutagenesis, screen|Yes| 6466.0|LSM16Δ|C57BL/6-Edc3Ausb ?||Recessive|enhancer of mRNA decapping 3 homolog (S. cerevisiae)|Edc3|Nil|Lsm16, Yjdc|MGI:2142951|enhancer of mRNA decapping 3 homolog (S. cerevisiae); targeted mutation 1, Velocigene|Edc3|MGI:5292973|9|||||||||||||||||||||||||||||Unknown|Unknown|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Yes| 6940.0|ENU19 WT:014:a:B6:G3|ANU:ENU19WT:014:a:G3||Recessive|Unknown||||||||Unknown||||||||||||||||Unknown|||||||||||||Unknown|Unknown|C57BL/6JAnu|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||1||No|05-Jul-2012|Cryopreserved sperm|40.0|0.0|Unknown||ENU, random, mutagenesis, screen|Yes| 5701.0|Crim1 Flox C57 R26R||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 1977.0|SMAD1Δ|Swiss-Smad||Recessive|MAD homolog 1 (Drosophila)|Smad1|Nil|Madh1, Madr1, Smad 1|MGI:109452|MAD homolog 1 (Drosophila); targeted mutation 1, Elizabeth J Robertson|Smad1|MGI:2155483|8||||||||||||||||No|||||||||||||Embryonic lethality during organogenesis: homozygotes are present at the expected Mendelian ratios at E9.5 but die by E10.5.Abnormal embryogenesis/ development: homozygous mutant embryos are often abnormally positioned within the yolk sac.Incomplete embryo turning: at E9.5-E10.0, a subset of homozygotes exhibit incomplete embryo turning.Abnormal mesoderm development: at E7.0, homozygotes display extensive twisting of the newly formed mesoderm along the proximodistal axis.Decreased embryo size: homozygous mutant embryos are often smaller than wild-type embryos.Abnormal embryonic epiblast morphology: by E7.0, homozygotes display extensive twisting of the epiblast along the proximodistal axis.Disorganized embryonic tissue: homozygotes display severe distortion of the embryonic region.Abnormal extraembryonic tissue morphology.Abnormal allantois morphology:* at E8.0, homozygotes exhibit absence of a recognizable allantoic bud; only a small allantoic rudiment is observed at E8.5.* by E9.5, three allantois phenotypes are observed: a balloon-like structure with peripheral blood-filled vessels; a dense structure filled with compact mesenchyme and small blood-filled sacs; occasionally, an allantoic rudiment that fuses peripherally and non-uniformly with the chorionic surface of the placenta.Abnormal chorion morphology: at E8.5, homozygotes show overproliferation of chorionic tissue, as well as aberrant folding of the chorion within the exocoelomic cavity and defective proximal migration.Abnormal extraembryonic endoderm formation:* at E7.0, homozygotes exhibit a localized outpocketing of the visceral endoderm at the posterior embryonic/extraembryonic junction.* despite ruffling of the visceral endoderm at E8.0-E8.5, the emerging AP axis is symmetrical, headfolds and somites form, gross visceral yolk sac morphology and mesoderm appear normal, and the node is clearly defined.Abnormal placenta morphology: homozygotes fail to establish a functional placental connection.Abnormal chorioallantoic fusion: occasionally, an allantoic rudiment fuses peripherally and non-uniformly with the chorionic surface of the placenta.Abnormal umbilical cord morphology: homozygotes fail to form the umbilical connection to the placenta.Decreased primordial germ cell number:* at E8.5, homozygotes show a significant reduction in the number of primordial germ cells.* 6 of 14 (43%) have no PGCs, 5 of 14 (36%) have fewer than ten and 3 of 14 (21%) have less than 25.Distended pericardium: at E9.5-E10.0, a subset of homozygotes exhibit a distended pericardium.Decreased embryo size: homozygous mutant embryos are often smaller than wild-type embryos.Abnormal ventral body wall: at E9.5-E10.0, a subset of homozygotes exhibit delayed ventral closure.|||No|No|Yes|No|No|Yes|No|Unknown||||No|04-Sep-2007||0.0|0.0|Unknown||placenta, mesoderm, allantois, transforming growth factor beta (TGFbeta), embryonic lethal, epiblast, chorion|Yes| 1978.0|Smad1f|Swiss-Smad1||Dominant|MAD homolog 1 (Drosophila)|Smad1|Normal|Madh1, Madr1, Smad 1|MGI:109452|MAD homolog 1 (Drosophila); targeted mutation 2, Elizabeth J Robertson|Smad1|MGI:2155484|8||||||||||||||||No|||||||||||||Normal||Swiss|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|04-Sep-2007||0.0|0.0|Unknown||placenta, mesoderm, transforming growth factor beta (TGFbeta)|Yes| 6939.0|ENU19 WT:012:b:B6:G3|ANU:ENU19WT:012:b:G3||Recessive|Unknown||||||||Unknown||||||||||||||||Unknown|||||||||||||Unknown|Unknown|C57BL/6JAnu|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||1||No|05-Jul-2012|Cryopreserved sperm|50.0|0.0|Unknown||ENU, random, mutagenesis, screen|Yes| 277.0||FVB-Tg(Myl1-Igf1)1Nros||Recessive||||||||||||||||||||||||||transgene insertion 1, Naida Rosenthal|skeletal muscle-specific regulatory elements from the rat myosin light chain (MLC)-1/3 locus|restricted to skeletal muscle||||||||||Transgenic embryos developed normally, and postnatal increases in muscle mass and strength were not accompanied by the additional pathological changes seen in other Igf-1 transgenic models. Expression of GATA-2, a transcription factor normally undetected in skeletal muscle, marked hypertrophic myocytes that escaped age-related muscle atrophy and retained the proliferative response to muscle injury characteristic of younger animals.||FVB|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|02-May-2006||0.0|0.0|Unknown||insulin like growth factor (IGF-1), membrane bound, signal transduction, growth factor, heart, muscle, hypertrophy|Yes| 6269.0|DO11-10|BALB/c-Tg(DO11.10)10Dlo||Semi-dominant||||||||||||||||||||||||||transgene insertion 10, Dennis Y Loh||||||||||||Decreased CD4-positive T cell number:*CD4+ CD8- TCR thymocytes are reduced in absolute numbers after administration of OVA 323-339 peptide.Decreased double-positive T cell number:*CD4+CD8+TCR cells in thymic cortex are reduced by 55% after administration of OVA 323-339 peptide.Abnormal thymus physiology:*20 hours after administration of OVA323-339 peptide, apoptosis, DNA degradation, chromatin condensation, and cell shrinkage occur in the majority of cortical thymocytes.*Apoptosis occurs throughout the thymus including the subcapsular and deep cortical areas.*3 days after administration of peptide the cortical thymus is acellular; however, normal cellularity exists in the medulla.*Peptide administration does not effect small number of thymocytes that express only the beta chain transgene Vb8.||BALB/c|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown||Antigen-reactive thymocyte, TCR|Yes| 6941.0|ENU19 WT:018:a:B6:G3|ANU:ENU19WT:018:a:G3||Recessive|Unknown||||||||Unknown||||||||||||||||Unknown|||||||||||||Unknown|Unknown|C57BL/6JAnu|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||1||No|05-Jul-2012|Cryopreserved sperm|40.0|0.0|Unknown||ENU, random, mutagenesis, screen|Yes| 6943.0|ENU19 WT:019:a:B6:G3|ANU:ENU19WT:019:a:G3||Recessive|Unknown||||||||Unknown||||||||||||||||Unknown|||||||||||||Unknown|Unknown|C57BL/6JAnu|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||1||No|05-Jul-2012|Cryopreserved sperm|36.0|0.0|Unknown||ENU, random, mutagenesis, screen|Yes| 320.0||B6.129-Rag1/Apb||Recessive|recombination activating gene 1|Rag1|Nil|Rag-1|MGI:97848|targeted mutation 1, Peter Mombaerts|Rag1|MGI:1857241|2||||||||||||||||No|||||||||||||Homozygotes for targeted null mutations exhibit arrested development of T and B cell maturation at the CD4-8- thymocyte or B220+/CD43+pro-B cell stage due to inability to undergo V(D)J recombination.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|04-May-2006|Cryopreserved sperm|250.0|0.0|Unknown||T cell, B cell, eosinophil, inflammation, interferon|Yes| 5409.0|NOD.IL-12KO|NOD/Lt-IL12b/ArcApb||Recessive|interleukin 12b|Il12b|Unknown|IL-12 p40, Il-12b, Il-12p40, IL-23 subunit p40|MGI:96540|interleukin 12b; targeted mutation 1, Jeanne Magram|Il12b|MGI:1857201|11||||||||||||||||Yes|||||||||||||Phenotype on NOD/Lt background is unknown to the APB.However, the phenotype on 129 x C57BL/6 is as follows:Decreased circulating interferon-gamma level:* serum levels of IFNG in LPS-injected mice are only 17 +/- 5% of LPS-induced controls.Abnormal macrophage physiology:* fewer than expected macrophages in the dermis of carcinogen treated skin.Abnormal granulocyte physiology:* fewer than expected granulocytes in the dermis of carcinogen treated skin.Abnormal lymphocyte physiology:* lymph node cells from keyhole limpet hemocyanin (KLH) immunized mice are severely impaired in their ability to produce IFNG when cultured with KLH; however, their production of IL4 is increased.Abnormal NK cell physiology:* mean NK lytic activity is about 66% of controls; however when cultured with IL2 lytic activity is similar to controls.Abnormal CD8-positive T cell physiology:* dramatic increase in the number of cytotoxic CD8+ cells in the dermis and epidermis of carcinogen treated skin.Decreased interleukin-17 secretion:* barely detectable levels of IL17 in the skin after carcinogen treatment unlike wild-type mice which express high levels of IL17.Increased susceptibility to bacterial infection:* vaccination does not produce a protective response to M. tuberculosis.Decreased susceptibility to type IV hypersensitivity reaction:* specific foot pad swelling 48 hours after challenge with methylated bovine serum albumin is inhibited by 47 +/- 3% compared to wild-type mice; however, cytotoxic T lymphocyte responses are similar to wild-type.Decreased incidence of chemically-induced tumors:* resistant to induction of papillomas compared to wild-type mice after treatment with DMBA and TPA in a 2 step skin carcinogenesis protocol.* however, there is an increase in the incidence of tumors following intradermal challenge with PDV squamous carcinoma cells.Abnormal CD4-positive T cell physiology:* 75 days after infection Ifng mRNA expression in CD4+ cells is more than 50-fold lower than in wild-type.* 75 days after infection Il4 mRNA expression in CD4+ cells is 100-fold higher than in wild-type.* draining lymph node cells in L. major infected mice produce significantly more IL4 compared to IFNG in contrast to wild-type mice which express more IFNG than IL4.||NOD/Lt|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|10|||No|03-Feb-2011|Embryo|0.0|0.0|Unknown||delayed type hypersensitivity, T cell, Natural killer cell ; NK cell, interferon, granulocyte, autoimmunity|Yes| 6312.0|B6Noxa/339/Ova|Noxa X BIM 216 /Rip-mOva|||| Noxa Bim RipmOVA ||||||||||||||||||||||||||||||||||||Increased numbers of lymphoid and myeloid cells. Spleen and lymph nodes are 2-3-fold bigger than in wt. Sternum is sticking out. Bim-/- females are bad mothers and should not be used for breeding unless necessary. Bim -/-: blood - increased lymphocytes (B + T cells), granulocytes & monocytes. - decreased platelets - Increased serum Ig. Thymus - fewer pre T cells. Age 1 year - lymphadenopathy - 55% -/-, 35% +/- mice sick with kidney disease or cardiac infarction/vasculitis. Fewer -/- females born. When born, often have poorly formed reproductive organs. -/- have protruding sternum. No phenotype with additional loss of noxa. ||C57BL/6|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 7701.0|B3K506 Tcra/b|C57BL/6-Tg(CD2-Tcra, -Tcrb)506/AnuApb||Recessive||||||||||||||||||||||||||T cell receptor alpha, T cell receptor beta|Human CD2|||||||||||Transgenic mice express the rearranged B3K506 Va4.1 and Vβ8.1 chains using the human CD2 promoter.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|12-Jun-2014|Cryopreserved sperm|11.0|0.0|Unknown||T cell, receptor, MHC|Yes| 7699.0|YAe62 Tcrb|C57BL/6-Tg(CD2-Tcrb)62/AnuApb||Recessive||||||||||||||||||||||||||T cell receptor beta|Human CD2|||||||||||YAe62 β mice are biased toward creating TCRs reactive to IAb-3K and the related ligand IAb-P-1K.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|12-Jun-2014|Cryopreserved sperm|11.0|0.0|Unknown||T cell, receptor, MHC|Yes| 7700.0|B3K506 Tcrb|C57BL/6-Tg(CD2-Tcrb)506/AnuApb||Recessive||||||||||||||||||||||||||T cell receptor beta|Human CD2|||||||||||TCRβ Tg mice express the rearranged B3K506 Vβ8.1 chain using the human CD2 promoter.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|12-Jun-2014|Cryopreserved sperm|12.0|0.0|Unknown||T cell, receptor, MHC|Yes| 6310.0|NOD.scid|NOD.CB17-Prkdc/JWehi||Recessive|protein kinase, DNA activated, catalytic polypeptide|Prkdc|Nil|DNA-PK, DNA-PKcs, DNAPDcs, DOXNPH, dxnph, slip, XRCC7|MGI:104779|protein kinase, DNA activated, catalytic polypeptide; severe combined immunodeficiency|Prkdc|MGI:1857113|16|||||||||||||||||||||||||||||Increased circulating glucose level:*Following treatment with streptozotocin, mice exhibit increased glucose serum levels that can be restored to euglycemic levels by engraftment of human islet cells.*Following intraperitoneal injection of human peripheral blood mononuclear cells, 11 of 12 streptozotocin-treated mice engrafted with human islet cells exhibit increased glucose serum levels although not as high as pre-transplantation.Abnormal response to transplant:*While human islet engrafts in streptozotocin-treated mice appear normal after 4 weeks, subsequent injection of human peripheral blood mononuclear cells results in destructive infiltrate into the human islet graft site, inflammation, loss of engrafted islet beta cells, fibrosis, and necrosis after 3 weeks.*However, this rejection is not due to graft versus host disease.||NOD/LtSz |Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown||SCID|Yes| 6333.0|STAT3/Blimp/Mb-1Cre|C57BL/6-Cd79a Prdm1 Stat3||Semi-dominant|CD79A antigen (immunoglobulin-associated alpha)|Cd79a|Nil|Cd79a, Ig alpha, Ig-alpha, Iga, Igalpha, Ly-54, Ly54, mb-1|MGI:101774|CD79A antigen (immunoglobulin-associated alpha); targeted mutation 1, Michael Reth|Cd79a|MGI:3687451|7|||||||||||||||||||||||||||||||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown||Blimp-1, Antibody-secreting cells (ASCs), STAT3, mb1, B cell|Yes| 6333.0|STAT3/Blimp/Mb-1Cre|C57BL/6-Cd79a Prdm1 Stat3||Semi-dominant|PR domain containing 1, with ZNF domain|Prdm1|Normal|Blimp-1, Blimp1, PRDI-BF1|MGI:99655|PR domain containing 1, with ZNF domain; targeted mutation 1, Stephen L Nutt|Prdm1|MGI:3510704|10|||||||||||||||||||||||||||||||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|13-Sep-2011||||Unknown||Blimp-1, Antibody-secreting cells (ASCs), STAT3, mb1, B cell|Yes| 6333.0|STAT3/Blimp/Mb-1Cre|C57BL/6-Cd79a Prdm1 Stat3||Semi-dominant|signal transducer and activator of transcription 3|Stat3|Nil|1110034C02Rik, Aprf|MGI:103038|signal transducer and activator of transcription 3; targeted mutation 1, Valeria Poli|Stat3|MGI:2384507|11|||||||||||||||||||||||||||||||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|13-Sep-2011||||Unknown||Blimp-1, Antibody-secreting cells (ASCs), STAT3, mb1, B cell|Yes| 4117.0|Patchy|ENU12NIH:037a||Semi-dominant|||||||||Unknown||||||||||||||||Yes|||||||||||||White patch on underbelly. One mouse in G2 seen with white patch as well as curly tail.|White patch on underbelly. One mouse in G2 seen with white patch as well as curly tail.||Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|05-Dec-2008|Cryopreserved sperm|20.0|0.0|Unknown||Coat, White patch, Spot, ENU|Yes| 31.0|Blobby|C57BL/6JSfdAnu-Alms1/AnuApb|C57BL/6JSfdAnu-Alms1/AnuApb|Recessive|Alstrom syndrome 1 homolog (human)|Alms1|Unknown||MGI:1934606|blobby|Alms1|MGI:3611799|6|ENSMUSG00000063810|ENSMUST00000072018|Alms1-001|6392|6507|T to A|ENSMUSE00000552223|10|2130|Leucine to STOP|||||TCTTCTTTCTGAAGGTCAGGATTATGAGTTAGAAGAGGTTCAGCATATACCTCAGTCATAC|No|||||||||||||Late onset obesity (apparent at 3-6 months). Homozygous null mice display obesity starting after puberty, hypogonadism, hyperinsulinemia, male-specific hyperglycemia, retinal dysfunction, and late-onset hearing loss.||C57BL/6JStdAnu|Yes|No|Yes|Yes|No|Yes|Yes|Poor||10||No|06-Feb-2006|Cryopreserved sperm|109.0|0.0|Yes||ENU, spermatogenesis, kidney, hyperinsulinemia|Yes| 2368.0|thiana|ENU5AT:149 ||Recessive|||Unknown|||thiana|||Unknown||||||||||||||||Yes|||||||||||||Defective antibody response to immunization: failure to mount a normal Th1 polarized IgG2c antibody response to heat killed B pertussis bacteria. ||C57BL/6 x C57BL/10BR|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|14-Dec-2007|Cryopreserved sperm|43.0|0.0|Unknown||B cell, Th1, antibody, ENU, Wellcome Trust|Yes| 2371.0||ENU7B6:021||Recessive|||||||||Unknown||||||||||||||||Yes|||||||||||||Defective antibody response to immunization: failure to mount a normal Th1 polarized IgG2c antibody response to heat killed B pertussis bacteria. ||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|14-Dec-2007|Cryopreserved sperm|25.0|0.0|No||B cell, antibody, immunization, ENU, Wellcome Trust|Yes| 2778.0|BALB/c.hK14-FLII 5|BALB/c-Tg(hK14-FLII)5/AnuApb||Dominant|||||||||Unknown||||||||||||||||Yes|Human Flightless|Human Keratin 14|||||||||||Not bred to Homozygous state|Normal|BALB/c|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|5||Het FLII transgenic x WT BALB/c|No|16-Feb-2008|Cryopreserved sperm|130.0|0.0|Unknown||human, keratin, enhancer, skin|Yes| 4747.0|Gelsolin KO ; Gen|STOCK Gsn/AnuApb||Recessive|gelsolin|Gsn|Nil||MGI:95851|targeted mutation 1, David J Kwiatkowski|Gsn|MGI:2179509|2||||||||||||||||Yes|||||||||||||Mice homozygous for disruptions in this gene display abnormalities in the immune system, platelet and platelet function, bone density, nervous and circulatory system. In addition, there are background related effects on viability and mammary gland development. Have defects in cell motility, as might be expected for a protein involved in cytoskeletal actin filament regulation.||Unknown|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|||Hom x Hom|No|27-Apr-2009|Cryopreserved sperm|170.0|0.0|Unknown||actin filament, cytoskeleton, wound healing, cell migration, cell adhesion|Yes| 6336.0|Tbx1 BAC|Tbx1 BAC Transgenic|||| Tbx1 ||||||||||||||||||||||||||||||||||||May die suddenly.||CBA x C57Bl/6|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 2463.0||B6.CBA-Tg(hGMCSF-2CK1)1236/AnuApb||Dominant|||||||||Unknown||||||||||||||||No|human GMCSF (GM-CSF)|human GM-CSF promoter and enhancer (10.5kb)|||||||||||Express human GM-CSF. hGM-CSF detected in serum by ELISA. Murine GM-CSF used as internal control.|||Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|16-Jan-2008|Cryopreserved sperm|20.0|0.0|Unknown||T cell, Lymphocyte, transcription, chromatin remodelling, NF-kappaB|Yes| 6942.0|ENU19 WT:018:b:B6:G3|ANU:ENU19WT:018:b:G3||Recessive|Unknown||||||||Unknown||||||||||||||||Unknown|||||||||||||Unknown|Unknown|C57BL/6JAnu|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||1||No|05-Jul-2012|Cryopreserved sperm|30.0|0.0|Unknown||ENU, random, mutagenesis, screen|Yes| 3323.0|Metallic|ENU10B6:031 ||Recessive||||||||||||||||||||||||||||||||||||||Silver / grey coat. Mice appear otherwise healthy and are able to breed.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||1||No|15-Jun-2008|Cryopreserved sperm|45.0|0.0|Unknown||Coat colour, Fur, ENU, Hair, pigmentation|Yes| 2380.0|Jaffa|ENU8B6:085||Recessive|||||||||Unknown||||||||||||||||Yes|||||||||||||Coat colour defect.Dluted coat colour.Irregular coat pigmentation.Affected mice are born with a brown-coloured coat. Mice appear healthy otherwise. ||C57BL/6 x C57BL/10|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|14-Dec-2007|Cryopreserved sperm|90.0|0.0|Unknown||Coat, melanocyte, hair, ENU, pigmentation|Yes| 2466.0||B6.CBA-Tg(hGMCSF-2KB)63/AnuApb||Dominant||||||||||||||||||||||||||human GMCSF (GM-CSF)|human GM-CSF promoter and enhancer (10.5kb)|||||||||||Express human GM-CSF. hGM-CSF detected in serum by ELISA. Murine GM-CSF used as internal control.|||Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|16-Jan-2008|Cryopreserved sperm|30.0|0.0|No||T cell, lymphocyte, transcription, chromatin remodelling, NF-kappaB|Yes| 2468.0||B6.CBA-Tg(hGMCSF-KBM)498/AnuApb||Dominant||||||||||||||||||||||||||human GMCSF (GM-CSF)|human GM-CSF promoter and enhancer (10.5kb)|||||||||||Express human GM-CSF. hGM-CSF detected in serum by ELISA. Murine GM-CSF used as internal control.|||Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|16-Jan-2008|Cryopreserved sperm|30.0|0.0|No||T cell, lymphocyte, transcription, chromatin remodelling, NF-kappaB|Yes| 6337.0|Tbx5 BAC|Tbx5 BAC Transgenic|||| Tbx5 ||||||||||||||||||||||||||||||||||||Phenotype does not differ from a wildtype of the same genetic background.||CBA x C57Bl/6|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6340.0|VAV-bcl-473|VAV-bcl-473|||| bcl2 Bim ||||||||||||||||||||||||||||||||||||Vavbcl69: Excess B cells throughout life. Develop glomerulonephritis, lymphoma and plasmacytoma Enlarged spleens Lymphadenopathy (more white blood cells), larger (2-3fold) spleen and lymph nodes ||C57BL/6|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6342.0|MYC10/200VT|vav-Myc 10 x vav-Myc/CTTG-PU1.200|||| vav-myc PU1 TTA ||||||||||||||||||||||||||||||||||||Tumour development T/+ mice develop thymoma or sub-cutaneous tumours (hystiocytic sarcoma) with a median onset of 41 weeks. T/T mice develop thymoma with a median onset of 13 weeks.||C57BL/6|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 4531.0|TNAP-Cre|C.B6-Alpl/AnuApb||Recessive|alkaline phosphatase, liver/bone/kidney|Alpl|Nil|Akp-2, Akp2, TNSALP, TNAP|MGI:87983|targeted mutation 1, Andras Nagy|Alpl|MGI:2177588|4||||||||||||||||Yes|Cre recombinase|TNAP|||||||||||Embryonic Lethal||Balb/c x C57BL/6|No|No|Yes|No|No|Yes|No|Unknown|8|||No|27-Feb-2009|Cryopreserved sperm|120.0|0.0|Unknown||alkaline phosphatase, primordial germ cell|Yes| 5174.0|Nehmet ; Maat ; ENU15China:011a|C57BL/6JAnu-Cd4/AnuApb|C57BL/6JAnu-Cd4/AnuApb|Recessive|CD4 antigen|Cd4|Unknown|L3T4, Ly-4|MGI:88335|Maat|Cd4|MGI:4819382|6|ENSMUSG00000023274|ENSMUST00000024044|Cd4-001||||||||124816702|8|||GAGGACTGGGACCCTCACGACTACTCTCCTTGTCCCTGGGCAGCGCCAGGCAGCACGAAT|Yes|||||||||||||Low CD4 expression and CD4<+> T cell numbers.High CD8<+> T cell numbers||C57BL/6JAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|08-Jul-2010|Cryopreserved sperm|57.0|0.0|Unknown||T cell, CD4, CD8, selection, ENU, China|Yes| 6350.0|NPYGFP|B6.FVB-Tg(Npy-hrGFP)1LOWl/JAusb||Dominant||||||||||||||||||||||||||transgene insertion 1, Bradford B Lowell|Npy promoter|||||||||||No abnormal phenotype detected:*Hemizygotes are viable and fertile.*When exposed to UV light, brain tissues show GFP fluorescence in patterns consistent with the endogenous mouse Npy gene.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown||Leptin, GABAergic neurons|Yes| 61.0|PieBaldSeizures|ENU3strain:PieBaldSeizures||Recessive|||Unknown||||||16||||||||||||||||Yes|||||||||||||Mostly white coat with small black flecks and mottles (ie piebald). Eyes are black. Mice also show very subtle shaking/trembling but are otherwise healthy. Defect in melanisation. Seizures were seen in C57BL/6 background.|||Yes|Yes|Yes|Yes|Yes|Yes|No|Good||7||No|06-Feb-2006|Cryopreserved sperm|50.0|0.0|Unknown||melanisation, piebald, ENU|Yes| 5714.0|CYP/FGF9||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6944.0|ENU19 WT:019:b:B6:G3|ANU:ENU19WT:019:b:G3||Recessive|Unknown||||||||Unknown||||||||||||||||Unknown|||||||||||||Unknown|Unknown|C57BL/6JAnu|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||1||No|05-Jul-2012|Cryopreserved sperm|90.0|0.0|Unknown||ENU, random, mutagenesis, screen|Yes| 1362.0|IL21RΔ|C57BL/6.129-IL21r||Recessive|interleukin 21 receptor|Il21r|Nil|IL-21R|MGI:1890475|targeted mutation 1, Warren J Leonard|Il21r|MGI:2446509|7||||||||||||||||No|||||||||||||Although mice deficient in the receptor for IL-21 (IL-21R) have normal lymphoid development, after immunization, these animals have higher production of the immunoglobulin IgE, but lower IgG1, than wild-type animals.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|22-Jun-2007||0.0|0.0|Unknown||lymphocyte, immunization, immunoglobulin, receptor, B cell, ICOS, T cell|Yes| 6388.0|ML5TG|C57BL/6-Tg(ML5sHEL)5Ccg/AnuAusb|C57BL/6-Tg(ML5sHEL)5Ccg/AnuAusb|Dominant||||||||||||||||||||||||||transgene insertion 5, Christopher C Goodnow|mouse metallothionein I promoter|||||||||||Abnormal B cell anergy:*Abnormally low levels of anti-hen egg lysozyme (HEL) antibodies are made in response to immunization with HEL.*50-fold lower levels of anti-HEL antibodies occur in response to immunization with HEL coupled with sheep red blood cells, which is a T cell-independent method of activating B cells.Abnormal circulating protein level:*Hen egg lysozyme (HEL) is found in circulation at a median level of 17.3 ng ml<-1>||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown||Immunological tolerance, IgD|Yes| 6945.0|ENU19 WT:021:b:B6:G3|ANU:ENU19WT:021:b:G3||Recessive|Unknown||||||||Unknown||||||||||||||||Unknown|||||||||||||Unknown|Unknown|C57BL/6JAnu|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||1||No|05-Jul-2012|Cryopreserved sperm|9.0|0.0|Unknown||ENU, random, mutagenesis, screen|Yes| 7671.0|ENU26:008:IL7R:B6:G5|C57BL/6NCrlAnu-Il7r/AnuApb||Recessive|interleukin 7 receptor|Il7r|Unknown|CD127, IL-7Ralpha, IL-7 receptor alpha chain|MGI:96562||||15|ENSMUSG00000003882|ENSMUST00000003981|Il7r-201|166|300|T to G|ENSMUSE00000269798|2|56|Threonine to Proline|||||TGGAAGTGGATGGAAGTCAACATTTATTGACTTGTGCTTTTAATGACTCAGACATCAACAC||||||||||||||Unknown|Unknown|C57BL/6NCrlAnu|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|02-May-2014|Cryopreserved sperm|55.0|0.0|Unknown||ENU, B cell, lymphocyte|Yes| 6186.0|GP139A056|B6;129S1-Mpl/Wehi||Recessive|myeloproliferative leukemia virus oncogene|Mpl|Nil|c-mpl, c-mpl-I, c-mpl-II, CD110, hlb219, thrombopoietin receptor, TPO-R|MGI:97076|myeloproliferative leukemia virus oncogene; targeted mutation 1, Warren S Alexander|Mpl|MGI:2660811|4|||||||||||||||||||||||||||||Thrombocytopenic but healthy. Platelet deficiency and hematopoietic stem cell anomalies. Alexander et al. Deficiencies in progenitor cells of multiple hemopoietic lineages and defective megakaryocytopoiesis in mice lacking the thrombopoietin receptor c-Mpl. ||C57BL/6|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown||thrombopoietin (TPO), platelet, megakaryocytes, thrombocytopenic, progenitor cell |Possibly| 6570.0|R5Δ|R5Δ||Recessive||R5||||||||||||||||||||||||||||||||||||||SVEV|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011|Embryo|0.0|0.0|Unknown|||Possibly| 6283.0|FB/MOF8dec|FVB.C-Myst1||Recessive|MYST histone acetyltransferase 1|Myst1|Nil|2010203C02Rik, 5830450F21Rik, D7Ertd629e, KAT8, MOF|MGI:1915023|MYST histone acetyltransferase 1; targeted mutation 1.1, Anne K Voss |Myst1|MGI:3810976|7|||||||||||||||||||||||||||||Complete embryonic lethality before somite formation:*Although embryos implant they cannot develop beyond the E4.5 blastocyst and die by E5.5.Abnormal trophectoderm morphology:*In culture, trophectoderm cells from E.5 embryos exhibit limited growth and spreading compared to wild-type cells.Inner cell mass apoptosis:*Apoptosis in the remnant inner cell masses is increased compared to in wild-type.Abnormal inner cell mass proliferation:*The inner cell mass fails to proliferate and does not form an inner cell mass outgrowth as do wild-type cells.Abnormal chromosome morphology:*Cells exhibit abnormal chromatin distribution that precedes caspase 3 activation.Increased mitotic index||FVB x BALB/c|No|No|Yes|No|No|Yes|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown||Myst1, Embryonic development|Yes| 4499.0|This and That|ENU4AT:017 ||Semi-dominant|||||||||Unknown||||||||||||||||Yes|||||||||||||Defective antibody response to immunization: failure to mount a normal Th1 polarized IgG2c antibody response to heat killed B pertussis bacteria. ||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|25-Feb-2009|Cryopreserved sperm|44.0|0.0|Unknown||Immunization, B cell, IgG2c, ENU, Wellcome Trust|Yes| 85.0||Trembles||Recessive|||Unknown||||||4||||||||||||||||Yes|||||||||||||Non-progressive mild-moderate ataxia evident at weaning. Some affecteds have shaggy fur. Full histology as been requested by APN. Video available. Phenotype unique to this chromosome location||C57BL/6 x NOD|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|06-Feb-2006|Cryopreserved sperm|110.0|0.0|Unknown||Ataxia, Shaking, ENU, Weakness|Yes| 6875.0|BRINP2 Targetted, DBC2 Targetted|B6.Cg-Brinp2/PibMarpApb||Recessive|bone morphogenic protein/retinoic acid inducible neural-specific 2|Brinp2||6430517E21Rik, Fam5b, mKIAA1747|MGI:2443333|bone morphogenic protein/retinoic acid inducible neural-specific 2; targeted mutation 1, Phillip I Bird|Brinp2|MGI:5604614|1|||||||||||||||||||||||||||||Normal|Normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|23-Apr-2012|Cryopreserved sperm|50.0|0.0|Unknown||Membrane attack complex|Yes| 640.0|Gz alpha knockout|C.B6-Gnaz/AnuApb|C.B6-Gnaz/AnuApb|Dominant|guanine nucleotide binding protein, alpha z subunit|Gnaz|Nil|Gz|MGI:95780|targeted mutation 1, I A Hendry|Gnaz|MGI:3575007|10||||||||||||||||No|||||||||||||Hypertolerant to morphine, show anxiety.In previously unexposed female homozygotes reduced analgesia at low morphine doses is seen, a similar but not significant effect was seen in males.With repeated morphine doses mutants develop tolerance faster than wild type mice.Morphine treated homozygotes are able to tolerate higher morphine doses compared to wild type mice (LD50 of 800 mg/kg compared to 700 mg/kg for wild type)however no significant difference in the serum levels of morphine or its metabolites is seenreproductive systemLitters from homozygous parents on the C57BL/6 background had increased mortality that was not seen in litters from heterozygous or mixed strain parentstouch/vibrissae.|Decreased sensitivity to xenobiotic induced morbidity/mortality: morphine treated homozygotes are able to tolerate higher morphine doses compared to wild-type mice (LD50 of 750 mg/kg compared to 700 mg/kg for wild-type).Abnormal chemically-elicited antinociception: with repeated morphine doses heterozygotes develop tolerance faster than wild-type mice but not as quickly as homozygous mutants.|BALB/c|Yes|Yes|Yes|Yes|Yes|Yes|No|Poor|20|||No|25-Apr-2007|Cryopreserved sperm|60.0|0.0|Unknown||morphine, receptor, G protein, tolerance, feeding behaviour|Yes| 5176.0|APN 33 ; VG10452|C57BL/6N-Smcr7||Recessive|Smith-Magenis syndrome chromosome region, candidate region|Smcr7|||2144199|Smith-Magenis syndrome chromosome region, candidate 7 homolog (human); targeted mutation 1, Velocigene|Smcr7|MGI:3808263|11||||||||||||||||Yes|||||||||||||Unknown|Normal|C57BL/6N|No|Unknown|Unknown|No|Unknown|Unknown|No|Good||||No|14-Jul-2010|Cryopreserved sperm|49.0|0.0|Unknown||ES cell|Yes| 2367.0|Mr Hankey ; ENU8CAT:005|B6;CB-Prkdc/AnuApb|B6;CB-Prkdc/AnuApb|Recessive|protein kinase, DNA activated, catalytic polypeptide|Prkdc|Unknown|DNA-PK, DNA-PKcs, DNAPDcs, slip, XRCC7|MGI:104779|hankey|Prkdc|MGI:4820716|16|ENSMUSG00000022672|ENSMUST00000023352|Prkdc-201|1634|1657|T to A|ENSMUSE00000282431|16|545|Leucine to STOP|||||AGGCTGTGACCAGATGGAGGATTTTATTTTAGGAGATGAAACATTTCTCTTTGTGAACTCC|Yes|||||||||||||Diarrhoea.Lymphopenia||C57BL/6JAnu x CBA/CaJ|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|14-Dec-2007|Cryopreserved sperm|51.0|0.0|Unknown||gut, diarrhoea, intestine, ENU|No| 1490.0|CD40 -/-|B6.129-CD40||Recessive|CD40 antigen|Cd40|Nil|Bp50, Cd40, p50, Tnfrsf5|MGI:88336|CD40 antigen; targeted mutation 1, Hitoshi Kikutani|Cd40|MGI:1857457|2||||||||||||||||Yes|||||||||||||Unknown.Phenotype on B6 background described but not for BALB/c background.||BALB/c|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|03-Jul-2007||0.0|0.0|Unknown||immunoglobulin, T cell, B cell, germinal centre|Yes| 6344.0|Mcl-1(33)/v-abl40|vavMcl-1(33)/B6.E� SV-v-abl 40 COPY|||| Mcl1 E�vabl ||||||||||||||||||||||||||||||||||||vabl40 - Low incidences of plasmacytoma. Look out for dragging hind legs, enlarged spleen, enlarged menteric lymph nodes - tumours. Visually check. 1-2% will die at 20 weeks of age, 19-20% will die at 1 year. Mice die as a result of plasmcytoma. Mice will bear one of the following tumours: lymphoma, splenomegaly, messentary associated, abdominal, caecal, Peyer's Patches. They may also suffer from small bowel obstruction, intestinal haemorrhage, hind leg paralysis, intussusception, Mcl-1 - Transgenics may have late onset haematopoietic tumours. Expect onset of tumours from 2 months of age. Will mainly occur in mesenteric lymph node. Abdomen will look/feel enlarged.||C57BL/6|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6298.0|Mcl-1flox/KO50/lckcre|C57BL/6-Mcl1 Trp53 Tg(Lck-cre)548Jxm||Semi-dominant|myeloid cell leukemia sequence 1|Mcl1|Normal|Mcl-1|MGI:101769|myeloid cell leukemia sequence 1; targeted mutation 3, Stanley J Korsmeyer|Mcl1|MGI:2684151|3|||||||||||||||||transgene insertion 548, Jamey Marth|mouse lck promoter|||||||||||||C57BL/6|Yes|Yes|Yes|Yes|No|Yes|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown||Mcl-1, Apoptosis, p53, GalNAc|Yes| 6298.0|Mcl-1flox/KO50/lckcre|C57BL/6-Mcl1 Trp53 Tg(Lck-cre)548Jxm||Semi-dominant|transformation related protein 53|Trp53|Nil|p44, p53|MGI:98834|transformation related protein 53; targeted mutation 1, Tyler Jacks|Trp53|MGI:1857263|11|||||||||||||||||||||||||||||||C57BL/6|Yes|Yes|Yes|Yes|No|Yes|No|Unknown||||No|13-Sep-2011||||Unknown||Mcl-1, Apoptosis, p53, GalNAc|Yes| 2464.0||B6.CBA-Tg(hGMCSF-2CK1)79/AnuApb||Dominant|||||||||Unknown||||||||||||||||No|human GM-CSF|human GM-CSF promoter and enhancer (10.5kb)|||||||||||Express human GM-CSF. hGM-CSF detected in serum by ELISA. Murine GM-CSF used as internal control.||C57BL/6 x CBA|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|16-Jan-2008|Cryopreserved sperm|40.0|0.0|No||T cell, lymphocyte, transcription, chromatin remodelling, NF-kappaB|Yes| 5017.0||BALB/c-SM22/CNX 40 tg1 (N4)||Dominant||||||||||||||||||||||||||||||||||||||||3|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|22-Feb-2010|Cryopreserved sperm|45.0|0.0|Unknown|||No| 1511.0||C57BL/6-Tcra Tg(TcrLCMV)327Sdz/AnuApb||Recessive|T-cell receptor alpha chain|Tcra|Unknown|Tcr alpha, Tcralpha|MGI:98553|targeted mutation 1, Peter Mombaerts|Tcra|MGI:1857255|14||||||||||||||||Yes|transgene insertion 327, Birgit Ledermann||High||||||||||T cell express T cell receptor specific for LCMV P14 protein.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|04-Jul-2007|Cryopreserved sperm|150.0|0.0|Unknown||T cell, receptor, lymphocytic choriomeningitis virus (LCMV)|Yes| 46.0|Kenobi ; ENU5strain:045; ENU5WT:054 |C57BL/6JSfdAnu-Cd79a/AnuApb|C57BL/6JSfdAnu-Cd79a/AnuApb|Recessive|CD79A antigen (immunoglobulin-associated alpha)|Cd79a|Nil|Cd79a, Ig alpha, Ig-alpha, Iga, Ly54, mb-1|MGI:101774|CD79A antigen (immunoglobulin-associated alpha); mutation 1, The Australian National University|Cd79a|MGI:5006856|7|ENSMUSG00000003379|ENSMUST00000003469|Cd79a-001|186|327|G to A|ENSMUSE00000199568|2|62|Tryptophan to STOP|||||AATGGCAGGAACCCTAATATCACATGGTGGTTCAGCCTTCAGTCTAACATCACATGGCCCC|Yes|||||||||||||Immune deficiency. Hypogammaglobulinemia. Absolutely no B cells or pre-B cells.||C57BL/6 x C57BL/10.Br|Yes|Yes|Yes|Yes|Yes|Yes|Yes|Unknown||||No|28-Apr-2004|Cryopreserved sperm|65.0|0.0|Unknown||B-cell antigen receptor, B cell, hypogammaglobulinemia, ENU, Wellcome Trust|Yes| 5002.0|aFO8 aa262|FVB/N-Tg(Prm1-Pebp1)8Mkob/MarpApb||Dominant||||||||||||||||||||||||||phosphatidylethanolamine binding protein 1|Protamine 1|low level expression||||||||||||FVB/N|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown|0|||No|22-Feb-2010|Cryopreserved sperm|60.0|0.0|Unknown||fertility, sperm|No| 5180.0||ENU15CHINA:075b||Recessive|Unknown|Unknown|Unknown||||||Unknown||||||||||||||||Unknown|||||||||||||CD4:CD8 T cell ratio skew. Decreased CD4 population and increased CD8 population|Normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Poor||||No|19-Jul-2010|Cryopreserved sperm|10.0|0.0|Unknown||CD4 , T cell, CD8, immunology, ENU|Possibly| 4574.0|FATT-129Sv/EvTac|129Sv-Lepr/Apb||Semi-dominant|Leptin Receptor|LepR|Unknown|Leprb, LEPROT, leptin receptor gene-related protein, Modb1, OB-RGRP, obese-like, obl, Obr|MGI:104993|FATT|||4||||||||||||||||No|||||||||||||The homozygote mutant has juvenile obesity, florid diabetes. The adult is hypogonadal and does not breed, and had an increased body length (10-20%).|There is a slight change in adipose tissue distribution and liver weight but no other significant changes.|129Sv/EvTac|Yes|No|Yes|Yes|No|Yes|No|Unknown||||No|08-Mar-2009|Cryopreserved sperm|144.0|0.0|Yes||Obesity, diabetes, leptin, receptor|Yes| 5718.0|Dallaglio KO||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5719.0|Dan Blackmore C57||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 4730.0||NOD.B6.Cg-H2 Tg(TLK2mHEL)2Ccg/AnuApb|NODB6.Cg-H2 Tg(TLK2mHEL)2Ccg/AnuApb|Dominant||||||||||||||||||||||||||transgene insertion 2, Christopher C Goodnow|rat thyroglobulin|expression limited to thyroid||||||||||Express low levels of membrane bound HEL in thyroid. Low serum levels of HEL detected.||NOD.Cg-H2 x C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|8|||No|17-Apr-2009|Cryopreserved sperm|95.0|0.0|Unknown||autoimmunity, B cell, tolerance, Hen egg lysozyme (HEL), T cell|Yes| 6947.0|ENU19 WT:023:a:B6:G3|ANU:ENU19WT:023:a:G3||Recessive|Unknown||||||||Unknown||||||||||||||||Unknown|||||||||||||Unknown|Unknown|C57BL/6JAnu|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||1||No|05-Jul-2012|Cryopreserved sperm|59.0|0.0|Unknown||ENU, random, mutagenesis, screen|Yes| 4434.0||ENU7B6:011||Recessive|||||||||Unknown||||||||||||||||Yes|||||||||||||Subclinical autoimmune susceptibility. Antinuclear autoantibodies: homogeneous nuclear.||C57BL/6 x C57BL/10|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||3||No|17-Feb-2009|Cryopreserved sperm|30.0|0.0|Unknown||autoimmunity, antinuclear antibodies (ANA), ENU, Wellcome Trust|Yes| 4577.0||NOD.129S7-H2 Ifngr1/AnuApb||Recessive|interferon gamma receptor 1|Ifngr1|Nil|CD119, Ifgr, IFN-gamma R, IFN-gammaR, Ifngr, Nktar|MGI:107655|targeted mutation 1, Michel Aguet|Ifngr1|MGI:1857286|10||||||||||||||||Yes||||histocompatibility-2, MHC|H2||H-2, MHC-II|MGI:95894|histocompatibility-2, MHC; k2 variant|H2|MGI:4936842|17|Abnormal immune system||NOD|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|10|||No|08-Mar-2009|Cryopreserved sperm|120.0|0.0|Unknown||cytokine, interleukin, infection, immunoglobulin, macrophage|Yes| 4578.0||PLJ.129S7-Ifngr1/AnuApb||Recessive|interferon gamma receptor 1|Ifngr1|Unknown|CD119, Ifgr, IFN-gamma R, IFN-gammaR, Ifngr, Nktar|MGI:107655|targeted mutation 1, Michel Aguet|Ifngr1|MGI:1857286|10||||||||||||||||Yes|||||||||||||Abnormal immune system||PLJ|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|10|||No|08-Mar-2009|Cryopreserved sperm|60.0|0.0|Unknown||cytokine, interleukin, infection, immunoglobulin, macrophage|Yes| 5010.0|Zedd|FVB/n-Luciferase Tg1 (ASD069)||Dominant||||||||||||||||||||||||||||||||||||||||10|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|22-Feb-2010|Cryopreserved sperm|150.0|0.0|Unknown|||Possibly| 5519.0|17China 43b|C57BL/6JAnu-Ptprc/Apb||Dominant|protein tyrosine phosphatase, receptor type, C|Ptprc |Reduced|B220, CD45, Ly-5, Lyt-4, T200|MGI:97810|mutation 1, The Australian National University|Prtprc||1||||||||||||||||No|||||||||||||Blood lymphopenia|Reduced expression of CD45|C57BL/JAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||3|Sib x sib|No|07-Jun-2011|Cryopreserved sperm|50.0|0.0|Unknown||T cell|Possibly| 5373.0|NOD.SCID/BDC2.5|NOD.Cg-Prkdc Tg(TcraBDC2.5,TcrbBDC2.5)1Doi||Dominant|protein kinase, DNA activated, catalytic polypeptide|Prkdc|Unknown|DNA-PK, DNA-PKcs, DNAPDcs, slip, XRCC7|MGI:104779|protein kinase, DNA activated, catalytic polypeptide; severe combined immunodeficiency|Prkdc|MGI:1857113|16|||||||||||||||||transgene insertion 1, Christophe Benoist|||||||||||||InsulitisIncreased activated T cell number|NOD/Lt|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|21-Dec-2010||0.0|0.0|Unknown||T cell, autoimmunity|Yes| 5251.0|FHWMKA|B6.129-Fxn Tg(FXN)CSars/Apb||Recessive|Frataxin|Fxn||Frda|MGI:1096879|frataxin; targeted mutation 1, Michel Koenig|Fxn|MGI:2177162|19||||||||||||||||No|Human FRATAXIN gene|FXN endogenous promoter|||||||||||Homozygous FXN transgene: Normal.Homozygous Fxn knockout: embryonic lethal, but completely complemented by presence of FXN transgene.|Hemizygous FXN transgene: Normal.Heterozygous Fxn knockout: Normal.|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||16|Hemizygous FXN transgene and Homozygous Fxn knockout X Hemizygous FXN transgene and Homozygous Fxn knockout|Yes|20-Oct-2010|Cryopreserved sperm|45.0|0.0|Yes|Friedreich ataxia|Friedreich ataxia, neurodegenerative disease, iron-sulfur clusters|Yes| 5374.0|Hom.NOD.FADD51|NOD/Lt-Tg(Ins2-dnFADD)51Wehi||Dominant||||||||||||||||||||||||||dominant negative Fas associated death domain protein|rat insulin promoter (Ins2) (RIP)|2 - 3 copies||||||||||Islets developed normally in these animals.β cells from the transgenic mice were resistant to killing via the Fas pathway in vitro.A reduced incidence of diabetes was found in mice with higher levels of dominant-negative FADD expression.||NOD/Lt|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|21-Dec-2010||0.0|0.0|Unknown||Fas, apoptosis, T cell, IL-1R, death receptor|Yes| 4918.0|CD9 -/-|B6.129-CD9/AusbApb||Recessive|CD9 antigen|Cd9|Nil|Tspan29|MGI:88348|targeted mutation 1, Claude Boucheix|Cd9|MGI:2180795|6|||||||||||||||||||||||||||||Reduced female fertility: 40 - 50% of females fail to produce litters.Decreased litter size.Impaired fertilization: impaired sperm - egg fusion.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Poor||||No|20-Oct-2009|Cryopreserved sperm|90.0|0.0|Unknown||fertility, tetraspan, CD151|Yes| 6948.0|ENU19 WT:025:b:B6:G3|ANU:ENU19WT:025:b:G3||Recessive|Unknown||||||||Unknown||||||||||||||||Unknown|||||||||||||Unknown|Unknown|C57BL/6JAnu|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||1||No|05-Jul-2012|Cryopreserved sperm|30.0|0.0|Unknown||ENU, random, mutagenesis, screen|Yes| 4606.0|mIMPα4delta|C57BL/6-Tg(EGFP-Kpna4 dominant negative) ||Dominant|karyopherin (importin) alpha 4|Kpna4|Unknown|IPOA3|MGI:1100848||||3||||||||||Unknown to Unknown||||||Yes|EGFP fused to dominant negative Kpna4|Protamine 1|||||||||||Fertility maybe reduced.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|Yes|Good||||No|13-Mar-2009|Cryopreserved sperm|20.0|0.0|Unknown||importin, testis, nuclear transport, protamine 1, fertility|No| 5020.0|N4.WB6.Hep.516Kl/+|N4.WB6.Hep.516Kl/+||Dominant||||||||||||||||||||||||||||||||||||||||8|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|22-Feb-2010|Cryopreserved sperm|120.0|0.0|Unknown|||No| 3472.0|CD11c-mOVA|C57BL/6-Tg(Itgax-mOVA)||Dominant||||||||||||||||||||||||||membrane bound ovalbumin|CD11c (mouse) (Itgax)|||||||||||Normal. Transgenic mice express membrane bound ovalbumin under the control of the CD11c promoter.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|22-Jul-2008||0.0|0.0|Unknown||Dendritic cell, presentation, T cell, CD8|Yes| 5492.0|Ndfip - 2 (SV129 Background)|Ndfip - 2 (SV129 Background)||Recessive|Unknown|Unknown|||||||Unknown|||||||||||||||||||||||||||||Unknown||129Sv|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|02-May-2011|Cryopreserved sperm|40.0|0.0|Unknown|||Possibly| 6810.0|L12SLR1R|SJL.B6-L12SLR1R/MriApb||Recessive|||||||||||||||||||||||||||||Unknown||||||||9|This allele confers normo-susceptibility to Plasmodium chabaudi compared to wildtype SJL.||SJL|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||Yes|01-Feb-2012|Cryopreserved sperm|70.0|0.0|Unknown||Malaria, Red blood cells, Innate immune response|Yes| 6950.0|ENU19 WT:029:a:B6:G3|ANU:ENU19WT:029:a:G3||Recessive|Unknown||||||||Unknown||||||||||||||||Unknown|||||||||||||Unknown|Unknown|C57BL/6JAnu|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||1||No|05-Jul-2012|Cryopreserved sperm|60.0|0.0|Unknown||ENU, random, mutagenesis, screen|Yes| 4520.0||ENU8C:051||Recessive|||||||||Unknown||||||||||||||||Yes|||||||||||||Subclinical autoimmune susceptibility. Antinuclear autoantibodies: homogeneous nuclear.||C57BL/6 x CBA|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|26-Feb-2009|Cryopreserved sperm|150.0|0.0|Unknown||autoimmunity, Antinuclear antibodies (ANA), ENU, Wellcome Trust|Yes| 2780.0|C57BL/6.Flii 2.1A|B6.C-Flii/3AnuApb|B6.C-Flii/3AnuApb|Recessive|flightless I homolog (Drosophila)|Flii|Nil|Fli1, Fliih|MGI:1342286|targeted mutation 1, Hugh D Campbell|Flii|MGI:2179825|11||||||||||||||||Yes|||||||||||||Embryonic lethal|No obvious altered phenotype|C57BL/6|No|No|Yes|No|No|Yes|No|Good|10|11|Het male x WT female|No|16-Feb-2008|Cryopreserved sperm|105.0|0.0|Unknown||gelsolin, embryonic lethal, wound repair, egg cylinder, gastrulation|Yes| 5177.0|17FOX 014 B6.129-Tg(FoxP3-GFP)|ENU17FOX:014 Foxp3||Recessive|forkhead box P3|Foxp3|Normal|JM2, scurfin|MGI:1891436|||MGI:3574964|X||||||||||||||||No|||||||||||||Reduced B cell population, visualised via flow cytometric analysisCells from the Foxp3-gfp background strain that express FoxP3 fluoresce green, predominantly T cells|Normal |129 x C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|||Affected x affected|No|19-Jul-2010|Cryopreserved sperm|20.0|0.0|Unknown||B cell, immunology, ENU|Possibly| 5177.0|17FOX 014 B6.129-Tg(FoxP3-GFP)|ENU17FOX:014 Foxp3||Recessive|Unknown|Unknown|||||||Unknown||||||||||||||||Unknown|||||||||||||Reduced B cell population, visualised via flow cytometric analysisCells from the Foxp3-gfp background strain that express FoxP3 fluoresce green, predominantly T cells|Normal |129 x C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|||Affected x affected|No|19-Jul-2010|Cryopreserved sperm|||Unknown||B cell, immunology, ENU|Possibly| 5784.0|FGF9||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5788.0|Floxed ErbB4 ||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 4827.0|6AT:022|ENU6AT:022||Recessive|||||||||Unknown|||||||||||||||||transgene insertion 3, Christopher C Goodnow|Rat insulin promoter|Expression of the inserted sequence specifically to pancreatic islet beta cells||||||||||Mice carrying the ins-HEL gene have a subclinical predisposition to diabetes due to islet cell failure. Mice carrying the insHEL and TCR transgenes have asubclinical predisposition to autoimmune destruction of the beta cell. Screening mice by urine glucose test. High glucose levels indicate diabetes and thus autoimmunity. "Early onset diabetes" definition changed during screen from approx 80 days to 40 days.||C57BL/6 x C57BL/10BR|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|||Breed diabetic Double transgenic with a non transgenic sib for next generation|No|24-Sep-2009|Cryopreserved sperm|75.0|0.0|Yes|Type I Diabetes|ENU, JDRF, autoimmunity, T cell, B cell, glucose|No| 4827.0|6AT:022|ENU6AT:022||Recessive||||||||||||||||||||||||||transgene insertion 1, Mark M Davis||||||||||||Mice carrying the ins-HEL gene have a subclinical predisposition to diabetes due to islet cell failure. Mice carrying the insHEL and TCR transgenes have asubclinical predisposition to autoimmune destruction of the beta cell. Screening mice by urine glucose test. High glucose levels indicate diabetes and thus autoimmunity. "Early onset diabetes" definition changed during screen from approx 80 days to 40 days.||C57BL/6 x C57BL/10BR|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|||Breed diabetic Double transgenic with a non transgenic sib for next generation|No|24-Sep-2009|Cryopreserved sperm|||Yes|Type I Diabetes|ENU, JDRF, autoimmunity, T cell, B cell, glucose|No| 5117.0|TH-GFP|C57BL/6-Tg(Th-EGFP)21-31Koba||Dominant||||||||||||||||||||||||||transgene insertion 21-31, Kazuto Kobayashi|rat tyrosine hydroxylase gene|High, 10 copies||||||||||Strong GFP fluorescent signal is detected in typical catecholaminergic cell groups and in most dopaminergic neurons of the transgenic adult ventral midbrain. Embryonic expression begins in the dopaminergic neurons of the developing ventral midbrain around E11-E12, is dramatically reduced later in gestation, and gradually resumes postnatally.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|12-May-2010||0.0|0.0|Unknown||Green fluorescent protein (GFP), expression, neuron, tyrosine hydroxylase|Yes| 4714.0|Rolex/129|129-Hccs/MarpApb||X-linked|holocytochrome c synthetase|Hccs|Unknown||MGI:106911|targeted mutation 1, Timothy C Cox|Hccs|MGI:3826866|X||||||||||||||||Yes|||||||||||||NormalHomozygous female or hemizygous males for a conditional allele activated in the heart exhibit fetal lethality associated with abnormal fetal cardiomyocyte morphology and physiology.||129/Sv|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|08-Apr-2009|Cryopreserved sperm|150.0|0.0|Unknown||cardiac, midgestation, mitochondria|Yes| 4646.0||MRL/MpJ-Icam Fas/JMarpApb||Recessive|intercellular adhesion molecule 1|Icam1|Nil|CD54, Icam-1, Ly-47, MALA-2, MGC:6195|MGI:96392|targeted mutation 1, Baylor College of Medicine|Icam1|MGI:1857183|9||||||||||||||||Yes|||||||||||||MRL/MpJ-Fas(lpr) (Fas(lpr)) mice develop a rapidly fatal form of systemic autoimmune disease characterized by glomerulonephritis and vasculitis similar to severe cases of systemic lupus erythematosus in humans. ICAM-1 deficiency resulted in a striking improvement in the survival of Fas(lpr) mice (median +/- SEM survival of Fas(lpr) = 26 +/- 1.7 vs ICAM-1/Fas(lpr) = 47 +/- 2.4 wk, p < 0.0001) and the increased survival was associated with delayed elevations of blood urea nitrogen levels in the ICAM-1/Fas(lpr) mice. Histologic examination of the ICAM-1/Fas(lpr) mice revealed an overall reduction in glomerular disease and a significant reduction in vasculitis in the kidney, lung, skin, and salivary glands when compared with Fas(lpr).||MRL/MpJ|Yes|No|Yes|Yes|No|Yes|No|Unknown|10|||No|22-Mar-2009|Cryopreserved sperm|105.0|0.0|Unknown||adhesion, systemic lupus erythematosus (SLE), autoimmune, leukocyte, rolling|Yes| 4646.0||MRL/MpJ-Icam Fas/JMarpApb||Recessive|Fas (TNF receptor superfamily member 6)|Fas|Unknown|APO-1, CD95, TNFR6, Tnfrsf6|MGI:95484|lymphoproliferation|Fas|MGI:1856334|Unknown|||||||||||||||||||||||||||||MRL/MpJ-Fas(lpr) (Fas(lpr)) mice develop a rapidly fatal form of systemic autoimmune disease characterized by glomerulonephritis and vasculitis similar to severe cases of systemic lupus erythematosus in humans. ICAM-1 deficiency resulted in a striking improvement in the survival of Fas(lpr) mice (median +/- SEM survival of Fas(lpr) = 26 +/- 1.7 vs ICAM-1/Fas(lpr) = 47 +/- 2.4 wk, p < 0.0001) and the increased survival was associated with delayed elevations of blood urea nitrogen levels in the ICAM-1/Fas(lpr) mice. Histologic examination of the ICAM-1/Fas(lpr) mice revealed an overall reduction in glomerular disease and a significant reduction in vasculitis in the kidney, lung, skin, and salivary glands when compared with Fas(lpr).||MRL/MpJ|Yes|No|Yes|Yes|No|Yes|No|Unknown|10|||No|22-Mar-2009|Cryopreserved sperm|||Unknown||adhesion, systemic lupus erythematosus (SLE), autoimmune, leukocyte, rolling|Yes| 4698.0||NOD.Cg-Tg(H2-Ea-Atp4b)1Wehi/WehiApb||Dominant||||||||||||||||||||||||||ATPase, H+/K+ exchanging, beta polypeptide (Atp4b)|1.8-kb fragment encoding nucleotides -1,903 through -39 of the 5' flanking sequence of the MHC Class II gene, H2-Ea (k allele)|||||||||||||NOD/Lt|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|07-Apr-2009|Cryopreserved sperm|155.0|0.0|Unknown||Tolerance, Autoimmunity, Autoantigen|Yes| 6809.0||SJL/Mrit-MRI47495||Dominant|Unknown|Unknown|||||||Unknown|||||||||||||||||||||||||||||Macrocytic anaemia|Macrocytic anaemia|SJL|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|01-Feb-2012|Cryopreserved sperm|70.0|0.0|Unknown||red blood cells, ENU|Yes| 5118.0|Ednrb-Kik|Un-Tg(Ednrb-Kik)||Dominant||||||||||||||||||||||||||Kikume|Endothelin receptor B|Unknown||||||||||Ednrb-expressing cells in the gut express the photoconvertible protein, Kikume.||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|12-May-2010||0.0|0.0|Unknown||endothelin receptor, kikume, fluorescent, gut|Yes| 7063.0|Momme D25|FVB/NJ-MommeD25 Tg(Hba1-Gfp)1Ew||Semi-dominant|modifier of murine metastable epialleles, D25|MommeD25|Unknown||||||3|||||||||||||||||Green Fluorescent Protein|human alpha-globin promoter and enhancer region|||||||||||Unknown|Unknown|FVB/NJ|No|No|Yes|No|No|Yes|No|Good|||MommeD25<+/->;Tg(Hba1-Gfp)1Ew x Tg(Hba1-Gfp)1Ew|No|24-Aug-2012|Cryopreserved sperm|39.0|0.0|Unknown||ENU, epigenetics, suppressor of variegation|Possibly| 867.0|B6.Fas-/-|B6;129P2-Fas/Apb|B6;129P2-Fas/Apb|Recessive|Fas (TNF receptor superfamily member)|Fas|Nil|APO-1, CD95, TNFR6, Tnfrsf6|MGI:95484|targeted mutation 1, Osaka University Medical School|Fas|MGI:1861923|19||||||||||||||||No|||||||||||||Premature death: 50% dead at about 5 months of ageAbnormal hepatocyte morphology: hepatocyte nuclear areas are variable and larger.Liver hyperplasia: * significantly heavier at 12 weeks of age and becomes 50-60% heavier by 16 weeks of age.* number of hepatocytes per each liver lobe is increasedimmune system.Increased leukocyte cell number: 20x higher than in controls, attributable to increased lymphocyte numbers.Increased lymphocyte cell number:* lymphocytosis; progressively accumulate abnromal T cells Thy1<+> B220<+> CD4<-> CD8<->.Increased B cell number: increase in the number of normal B cells.Abnormal T cell clonal deletion:* peripheral clonal deletion of mature T cells against a bacterial superantigen is impaired.Abnormal lymph organ size.Enlarged spleen: spleen becomes progressively larger.Enlarged lymph nodes: lymph nodes become progressively larger.Lymphoid hyperplasia.Increased IgG level: 10-100x higher serum levels of IgG1, IgG2a, IgG2b, and IgG3 at 16 weeks of age.Increased IgG1 level.Increased IgG2a level.Increased IgG2b level.Increased IgG3 level.Increased autoantibody level:* 50-500x higher levels of dsDNA and ssDNA autoantibodies at 16 weeks of age.Increased anti-double stranded DNA antibody level.Increased anti-single stranded DNA antibody level.Increased susceptibility to parasitic infection:* decreased survival after infection with Trypanosoma cruzi even though were able to clear parasites from blood and affected organs.Hypersensitivity:* occasional infiltration of lymphocytes into tissues such as the lungs and liver.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|25-May-2007|Cryopreserved sperm|139.0|0.0|Yes|Autoimmune Lymphoproliferative Syndrome; ALPS|autoimmunity, hepatocyte, lymphocyte, T cell, B cell|Yes| 4776.0|TOMtg|FVB-Tg(tetO-MYC)1Lach/Apb||Dominant||||||||||||||||||||||||||transgene insertion 1, Lewis A Chodosh|bacterial tetracycline-resistance operon|||||||||||Normal||FVB/N|Yes|Yes|Yes|Yes|Yes|Yes|No|Excellent||||No|06-Sep-2009|Cryopreserved sperm|95.0|0.0|No||Mammary Gland, tetracycline, tumourigenesis, Myc, transcription factor|Yes| 9331.0||B6.Cg-Tg<(Tyr-cre/ERT2)13Bos> Braf Pten DSG2/Apb||Semi-dominant|Braf transforming gene|Braf|||MGI:88190|Braf transforming gene; targeted mutation 1, Martin McMahon|Braf|MGI:3711771|6|||||||||||||||||||||||||||||Mice are viable however 10-20% of mice develop spontaneous melanomas within 4 months with an increased risk as mice age due to leaky Cre recombinase expression and the genetic background which is less than the reported incidence for the BRafCA, PtenloxP, Tyr::CreERT2 parental strain on the JAX website.Mice that are hemizygous for the Tg(Tyr-cre/ERT2)13Bos transgene, homozygous for BRafCA and homozygous for PtenloxP should develop melanoma lesions with tamoxifen application.|Mice are viable however 10-20% of mice develop spontaneous melanomas within 4 months with an increased risk as mice age due to leaky Cre recombinase expression and the genetic background which is less than the reported incidence for the BRafCA, PtenloxP, Tyr::CreERT2 parental strain on the JAX website.Mice that are hemizygous for the Tg(Tyr-cre/ERT2)13Bos transgene, homozygous for BRafCA and homozygous for PtenloxP should develop melanoma lesions with tamoxifen application.|C57Bl/6N|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|31-Jan-2022|Cryopreserved sperm|50.0|0.0|Unknown|||Possibly| 9331.0||B6.Cg-Tg<(Tyr-cre/ERT2)13Bos> Braf Pten DSG2/Apb||Semi-dominant|phosphatase and tensin homolog|Pten||MMAC1, TEP1|MGI:109583|phosphatase and tensin homolog; targeted mutation 1, Hong Wu|Pten|MGI:2156086|19|||||||||||||||||||||||||||||Mice are viable however 10-20% of mice develop spontaneous melanomas within 4 months with an increased risk as mice age due to leaky Cre recombinase expression and the genetic background which is less than the reported incidence for the BRafCA, PtenloxP, Tyr::CreERT2 parental strain on the JAX website.Mice that are hemizygous for the Tg(Tyr-cre/ERT2)13Bos transgene, homozygous for BRafCA and homozygous for PtenloxP should develop melanoma lesions with tamoxifen application.|Mice are viable however 10-20% of mice develop spontaneous melanomas within 4 months with an increased risk as mice age due to leaky Cre recombinase expression and the genetic background which is less than the reported incidence for the BRafCA, PtenloxP, Tyr::CreERT2 parental strain on the JAX website.Mice that are hemizygous for the Tg(Tyr-cre/ERT2)13Bos transgene, homozygous for BRafCA and homozygous for PtenloxP should develop melanoma lesions with tamoxifen application.|C57Bl/6N|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|31-Jan-2022|Cryopreserved sperm|||Unknown|||Possibly| 9331.0||B6.Cg-Tg<(Tyr-cre/ERT2)13Bos> Braf Pten DSG2/Apb||Semi-dominant|desmoglein 2|DSG2|||MGI:1196466||DSG2||18|ENSMUSG00000044393 ||||||||||||||||||||||||||||Mice are viable however 10-20% of mice develop spontaneous melanomas within 4 months with an increased risk as mice age due to leaky Cre recombinase expression and the genetic background which is less than the reported incidence for the BRafCA, PtenloxP, Tyr::CreERT2 parental strain on the JAX website.Mice that are hemizygous for the Tg(Tyr-cre/ERT2)13Bos transgene, homozygous for BRafCA and homozygous for PtenloxP should develop melanoma lesions with tamoxifen application.|Mice are viable however 10-20% of mice develop spontaneous melanomas within 4 months with an increased risk as mice age due to leaky Cre recombinase expression and the genetic background which is less than the reported incidence for the BRafCA, PtenloxP, Tyr::CreERT2 parental strain on the JAX website.Mice that are hemizygous for the Tg(Tyr-cre/ERT2)13Bos transgene, homozygous for BRafCA and homozygous for PtenloxP should develop melanoma lesions with tamoxifen application.|C57Bl/6N|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|31-Jan-2022|Cryopreserved sperm|||Unknown|||Possibly| 5181.0|Mif -/- Fas|MRL/MpJ.Cg-Fas Mif/MarpApb||Recessive|Fas (TNF receptor superfamily member 6)|Fas|Unknown|APO-1, CD95, TNFR6, Tnfrsf6|MGI:95484|lymphoproliferation|Fas|MGI:1856334|19||||||||||||||||Yes|||||||||||||MIF<–/–>MRL/lpr mice had significantly less proteinuria than MIF<+/+>MRL/lpr mice.Ab production in the MRL mice was largely unaffected by MIF deficiency.No difference in the percentage of CD4<+> or CD8<+> T cells, B cells (CD3<->B220<+>), CD3<+>CD4<->CD8<->B220<+> double-negative T cells (DNTCs), or CD11b<+>CD11c<+> dendritic cells between MIF<+/+> and MIF<–/–>MRL mice.MIF<–/–>MRL mice were protected from crescentic glomeruli formation as compared to MRL mice.MIF deficiency reduces renal macrophage recruitment and MCP-1 expression.||MRL/MpJ|Yes|Unknown|Yes|Yes|Unknown|Yes|No|Unknown||||No|19-Jul-2010|Cryopreserved sperm|70.0|0.0|Unknown||autoimmunity, T cell, B cell, leukocyte adhesion, glomerulonephritis, macrophage|Yes| 5181.0|Mif -/- Fas|MRL/MpJ.Cg-Fas Mif/MarpApb||Recessive|macrophage migration inhibitory factor|Mif|Nil|Glif|MGI:96982|macrophage migration inhibitory factor; targeted mutation 1, John R David|Mif|MGI:2176337|10||||||||||||||||No|||||||||||||MIF<–/–>MRL/lpr mice had significantly less proteinuria than MIF<+/+>MRL/lpr mice.Ab production in the MRL mice was largely unaffected by MIF deficiency.No difference in the percentage of CD4<+> or CD8<+> T cells, B cells (CD3<->B220<+>), CD3<+>CD4<->CD8<->B220<+> double-negative T cells (DNTCs), or CD11b<+>CD11c<+> dendritic cells between MIF<+/+> and MIF<–/–>MRL mice.MIF<–/–>MRL mice were protected from crescentic glomeruli formation as compared to MRL mice.MIF deficiency reduces renal macrophage recruitment and MCP-1 expression.||MRL/MpJ|Yes|Unknown|Yes|Yes|Unknown|Yes|No|Unknown||||No|19-Jul-2010|Cryopreserved sperm|||Unknown||autoimmunity, T cell, B cell, leukocyte adhesion, glomerulonephritis, macrophage|Yes| 6949.0|ENU19 WT:026:a:B6:G3|ANU:ENU19WT:026:a:G3||Recessive|Unknown||||||||Unknown||||||||||||||||Unknown|||||||||||||Unknown|Unknown|C57BL/6JAnu|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||1||No|05-Jul-2012|Cryopreserved sperm|20.0|0.0|Unknown||ENU, random, mutagenesis, screen|Yes| 657.0|transgenic line MBP-c-myc |B6.129-Tg(Mbp-MYC*)/Apb||Dominant|||||||||Unknown||||||||||||||||Yes|exons 2 and 3 of the human c-myc gene|1.3Kb of the mouse myelin basic protein (Mbp)|very low||||||||||Mice exhibit a transient shivering phenotype over the period corresponding to the peak of central nervous system myelination (4 to 8 weeks postnatally). Thereafter, shivering decreases abruptly and mice go on to live a normal life-span and breed normally.|As for heterozygous, but more pronounced. Death between 4 and 8 weeks has been observed but is rare. |C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|Yes|Excellent|38||transgenic males mated to normal C57BL/6 females between about 7 to 15 weeks of age|No|26-Apr-2007|Cryopreserved sperm|110.0|0.0|Yes||myelination, congenital hypomyelination, leukodystrophy, oligodendrocyte loss, myelin, CNS, shivering|Yes| 4846.0|Pricilla|ENU6CAT:04||Recessive|Unknown||Unknown||||||Unknown|||||||||||||||||||||||||||||Mothers fail to lactate.Pups can be maintained by adding lactating foster mother.|Normal|C57BL/6 x CBA|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|24-Sep-2009|Cryopreserved sperm|160.0|0.0|Unknown||lactation, milk, ENU|Yes| 5113.0|Joey-SCO|C57BL/6JAnu-Etv5/AnuMarpApb|C57BL/6JAnu-Etv5/AnuMarpApb|Recessive|ets variant gene 5|Etv5|Unknown|ERM|MGI:1096867|ets variant gene 5; sco|Etv5|MGI:5563470|16|ENSMUSG00000013089|ENSMUST00000079601|Etv5-202|1234|1414|A to T|ENSMUSE00000560895|12|412|Lysine to STOP|||||AAGAGGTTGCTCGCCGTTGGGGTATCCAGAAGAATCGGCCAGCCATGAACTATGACAAGCT|No|||||||||||||Sertoli cells only.Male infertility.Progressive loss of germ cells following the first wave of spermatogenesis.Germ cells appeared to be preferentially lost in a basal to apical direction from the seminiferous epithelium as detected in 7 week old testis.Reduced testis size, compared to WT, at 8 weeks of age.Etv5 mRNA levels 95% reduced compared to WT males.Etv5 mRNA is unstable.Reduced expression of Etv5 target genes Cxcr4 and Ccl9.Increased incidence of embryonic and perinatal lethality.Reduced body weight.Renal asymmetry.Polydactyly.||C57BL/6JAnu|Yes|Yes|Yes|Yes|No|Yes|No|Unknown||||No|10-May-2010|Cryopreserved sperm|50.0|0.0|Unknown||infertility, sperm, arrest, ENU, sertoli|Yes| 4712.0|T3RWT|B6.129-Tlr3||Dominant|toll-like receptor 3|Tlr3|Unknown||MGI:2156367||||8||||||||||||||||Yes|||||||||||||Wild-type strain used as control for Tlr3 knockout, APB ID#630||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|08-Apr-2009|Cryopreserved sperm|100.0|0.0|Unknown||Lymphocyte, viral infection, hypersensitivity, T cell, stimulation , proliferation|Yes| 5778.0|FGF8Flox/Rosa26/NesCreERT2||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 4475.0||Brooke||Dominant|||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|22-Feb-2009|Cryopreserved sperm|50.0|0.0|Unknown|||Yes| 4845.0||ENU6AT:53||Recessive|Unknown||Unknown||||||Unknown|||||||||||||||||||||||||||||Mothers fail to lactate.Pups can be maintained by adding lactating foster mother.|Normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|24-Sep-2009|Cryopreserved sperm|40.0|0.0|Unknown||lactation, milk, ENU|Yes| 4721.0|TGM2 floxed|C57BL/6-Tgm2/Apb||Recessive|transglutaminase 2, C polypeptide|Tgm2|Normal|G[a]h, protein-glutamine gamma-glutamyltransferase, TG C, TG2, tissue transglutaminase, tTG, tTGas|MGI:98731|targeted mutation 1, Robert M Graham|Tgm2|MGI:3525256|2||||||||||||||||Yes|||||||||||||Normal - no phenotypic analysis * mice were only used to generate the null allele||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|08-Apr-2009|Cryopreserved sperm|59.0|0.0|Unknown||Transgluatminase, Gh, G-protein, cross-linking|Yes| 5723.0|DCCKanga||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5724.0|Dcckanga/Tomato/Satb2Cre||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5456.0|ENU14Ch 036b; ENU14China:036b|C57BL/6JAnu-Cd22/AnuApb|C57BL/6JAnu-Cd22/AnuApb|Recessive|CD22 antigen|Cd22|Reduced|Lyb-8, Lyb8|MGI:88322|CD22 antigen; mutation 1, Australian National University|Cd22|MGI:5009050|7|ENSMUSG00000030577|ENSMUST00000019248|Cd22-201|1536|2116|T to A|ENSMUSE00000359124|7|511|Cysteine to STOP|||||GTCAGCTGTGCTGCCTGCAACCACAAGTGTTCGTGGGCCCTCCCTGTCATCCTGAATGTCC|Yes|||||||||||||Block in B cell maturation and reduced number of B cells in peripheral blood.||C57BL/6JAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|07-Mar-2011|Cryopreserved sperm|47.0|0.0|Unknown||B cell, lymphocyte, immunoglobulin, ENU|Possibly| 108.0|Alison2 ; AL3|C57BL/6JSfdAnu-Tg(AlsHEL)3Ccg/AnuApb|C57BL/6JSfdAnu-Tg(AlsHEL)3Ccg/AnuApb|Dominant||||||||||||||||||||||||||transgene insertion 3, Christopher C Goodnow|liver specific albumin|high||||||||||High ubiquitous expression of soluble Hen Egg Lysozyme (sHEL). Females express approximately 2-fold more sHEL than males of this strain.||C57BL/6JSfdAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||5|Hom xHom|No|06-Feb-2006|Cryopreserved sperm|125.0|0.0|Yes||Hen Egg Lysozyme (HEL), B cell, T cell, tolerance, autoimmunity|Yes| 4731.0|Rama|C57BL/6-Tg(H2-K-sHELdimer)/Apb||Dominant||||||||||||||||||||||||||soluble Hen Egg Lysozyme dimeric molecule|H-2K|Low||||||||||Low serum expression of dimeric soluble HEL.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|17-Apr-2009||0.0|0.0|Unknown||Hen egg lysozyme (HEL), autoimmunity, T cell, B cell, tolerance|Yes| 4803.0|Mal ; ENU8BAT:012|B6(Cg);CBA-Rabl2a/AnuApb||Recessive|RAB, member of RAS oncogene family-like 2A|Rabl2a|||MGI:1915958|RAB, member of RAS oncogene family-like 2; mot|Rabl2|MGI:5469381|15|ENSMUSG00000022621|ENSMUST00000023294|Rabl2a-201|218|311|A to G|ENSMUSE00000128937|5|73|Aspartic acid to Glycine|||||CACAGTAGACGGCAAGACGATCCTTGTGGACTTCTGGGATACAGCAGGCCAGGAGCGGTTC|Yes|||||||||||||Male InfertilityDecreased testis weightOligozoospermiaShort sperm flagellumAsthenozoospermia:• low total motility and minimal progressive motility• however, ultrastructure is normal||C57BL/6 x CBA x C57BL/10BR|Yes|Yes|Yes|Yes|No|Yes|No|Poor||||No|24-Sep-2009|Cryopreserved sperm|115.0|0.0|Yes|Male Infertility|ENU, fertility, sperm|No| 2767.0|BALB/c.Flii<-/-> FLII ; FICR|BALB/c-Flii Tg(FLII)1Hdc/AnuApb|BALB/c-Flii Tg(FLII)1Hdc|Recessive|flightless I homolog (Drosophila)|Flii|Unknown|Fli1, Fliih|MGI:1342286|targeted mutation 1, Hugh D Campbell|Flii|MGI:2179825|11||||||||||||||||Yes|transgene insertion 1, Hugh D Campbell|human flightless promoter|||||||||||Embryonic lethal phenotype of FLii knockout is rescued by human FLII transgene. Ubiquitous expression of human Flightless gene.||BALB/c|Yes|Yes|Yes|Yes|Yes|Yes|No|Poor|||FLii<-/-> FLII x FLii<-/-> FLII|No|15-Feb-2008|Cryopreserved sperm|120.0|0.0|Unknown||human flightless, wound repair, cellular proliferation, cell migration, gelsolin|Yes| 5725.0|DccKangC57||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 4705.0|NOD-HIPCre|NOD-Tg(INS-cre)2Rms/MarpApb||Dominant||||||||||||||||||||||||||transgene insertion 2, Robyn M Slattery|human insulin promoter|beta islet cells||||||||||The human insulin promoter (INS) drives cre expression in beta islet cells. Resistance to development of diabetes and hyperglycemia||NOD|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|07-Apr-2009|Cryopreserved sperm|135.0|0.0|Yes||Autoimmunity, insulin, Beta cell|Yes| 5184.0|Vincent ; KRN 14 Vincent B6 F2|KRN:014 Vincent B6 F2||Recessive|glutamate receptor, ionotropic, kainate 4|Grik4|Unknown|6330551K01Rik, GluRgamma1, KA-1, KA1 |MGI:95817||||9||||||||||||||||Yes|||||||||||||Unknown||C57BL/6JAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|26-Jul-2010|Cryopreserved sperm|45.0|0.0|Unknown||arthritis, inflammation, ENU|Possibly| 7703.0|ENU29:G3|ANU:ENU29:G3||Recessive|Unknown|Unknown|||||||Unknown|||||||||||||||||||||||||||||Unknown|Unknown|C57BL/6NCrlAnu|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown|1|||No|17-Jun-2014|Cryopreserved sperm|138.0|0.0|Unknown||ENU, mutagenesis, screen, random|Yes| 5631.0|B6.129x1BAX||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 7514.0|QSi5|Quackenbush Swiss i5||Dominant||||||||||||||||||||||||||||||||||||||Outbred strain derived from Quackenbusg Swiss.Highly fecund - average litter size 13.4Large litter size.Shorter period between litters.Septum primum or flap valve length (FVL) - long compared to 129 - 1.13mm v 0.6mmMilk yield 3x greater than CBA.||Quackenbush Swiss|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|28-Nov-2013|Embryo|0.0|0.0|Unknown|||Yes| 109.0|Andrew2 ; ML4|C57BL/6JSfdAnu-Tg(ML4sHEL)4Ccg/AnuApb|C57BL/6JSfdAnu-Tg(ML4sHEL)4Ccg/AnuApb|Dominant||||||||||||||||||||||||||transgene insertion 4, Christopher C Goodnow ; soluble HEL (hen egg lysozyme)|zinc inducible mouse metallothionein I|High||||||||||Mice homozygous for the TgN(ML5sHEL)5Ccg transgene express a soluble form of hen egg lysozyme.||C57BL/6JSfdAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||10|sib x sib|No|06-Feb-2006|Cryopreserved sperm|140.0|0.0|No||hen egg lysozyme (HEL), autoimmunity, B cell, T cell, tolerance|Yes| 4737.0||ENU8C:060||Recessive|||||||||Unknown||||||||||||||||Yes|||||||||||||Screened phenotype = positive for anti-nuclear antibodies||C57BL/6 x CBA|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|1|||No|19-Apr-2009|Cryopreserved sperm|70.0|0.0|Unknown||Autoimmunity, ANA, ENU, Wellcome Trust|Yes| 7515.0|QSi5|Quackenbush Swiss i5||Dominant||||||||||||||||||||||||||||||||||||||Highly fecund - large litter sizeShorter time between littersImproved lactation - compared to CBA. Higher milk yield, more efficient milk production.Septum primum or flap valve length (FVL) longer compared to 129T2 - 1.11 mm v 0.6mm.||Quackenbush Swiss|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|28-Nov-2013|Embryo|0.0|0.0|Unknown|||Yes| 5459.0|ENU16Ch:017a, Lyn|C57BL/6JAnu-Lyn/AnuApb|C57BL/6JAnu-Lyn/AnuApb|Recessive|Yamaguchi sarcoma viral (v-yes-1) oncogene homolog |Lyn|Unknown|Hck-2|MGI:96892|Yamaguchi sarcoma viral (v-yes-1) oncogene homolog; mutation 1, Australian Phenomics Facility|Lyn|MGI:5501039|4|ENSMUSG00000042228|ENSMUST00000041377|Lyn-001|1228|1483|A to G|ENSMUSE00000605548|12|410|Threonine to Alanine|||||GGGAAGGTGCGAAGTTCCCTATCAAGTGGACAGCTCCAGAGGCCATCAACTTCGGCTGCTT|No|||||||||||||Very low B cells numbers but High IgM<+>IgD<-> cells.||C57BL/6JAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|07-Mar-2011|Cryopreserved sperm|45.0|0.0|Unknown||B cell, Lymphocyte, ENU, immunoglobulin, kinase, signal transduction|Possibly| 6356.0|KRAS2f|B6.129-Kras/Ausb||Semi-dominant|v-Ki-ras2 Kirsten rat sarcoma viral oncogene homolog|Kras||K-ras, Ki-ras, Kras-2, Kras2 |MGI:96680 |v-Ki-ras2 Kirsten rat sarcoma viral oncogene homolog; targeted mutation 4, Tyler Jacks|Kras|MGI:2429948|6|||||||||||||||||||||||||||||Increased lung tumor incidence:*Treatment with adenoviral Cre to induce oncogenic Kras expression results in lung tumor development, but causes a lower tumor burden and decreased overall tumor area compared to induced mutants on a Spry2-null background.||B6/129|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown||Lung adenocarcinoma, K-ras G12D, Tumor initiation|Yes| 7704.0|H2A.Lap1:NM1|FVB/NJArc-H2afb2 H2afb3 Gm14920/AnuApb||X-linked|H2A histone family, member B2|H2afb2|Nil|EG624153, H2A.Bbd4, H2afb2-ps|MGI:3644980||||X|||||||||||||||||||||||||||||Normal. Small percentage dies when reaches the age of 7-9 months. Under investigation|Normal. Small percentage dies when reaches the age of 7-9 months. Under investigation|FVB/NJArc|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|3||het to wt; homo to wt; homo to homo|No|18-Jun-2014|Cryopreserved sperm|48.0|0.0|Unknown||H2A.Lap1, histone, NM1|Possibly| 7704.0|H2A.Lap1:NM1|FVB/NJArc-H2afb2 H2afb3 Gm14920/AnuApb||X-linked|H2A histone family, member B3|H2afb3||EG624957, H2A.Bbd3, H2afb3-ps|MGI:3644875||||X|||||||||||||||||||||||||||||Normal. Small percentage dies when reaches the age of 7-9 months. Under investigation|Normal. Small percentage dies when reaches the age of 7-9 months. Under investigation|FVB/NJArc|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|3||het to wt; homo to wt; homo to homo|No|18-Jun-2014|Cryopreserved sperm|||Unknown||H2A.Lap1, histone, NM1|Possibly| 7704.0|H2A.Lap1:NM1|FVB/NJArc-H2afb2 H2afb3 Gm14920/AnuApb||X-linked|predicted pseudogene 14920|Gm14920||ENSMUSG00000067441, H2A.Bbd1|MGI:3642445||||X|||||||||||||||||||||||||||||Normal. Small percentage dies when reaches the age of 7-9 months. Under investigation|Normal. Small percentage dies when reaches the age of 7-9 months. Under investigation|FVB/NJArc|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|3||het to wt; homo to wt; homo to homo|No|18-Jun-2014|Cryopreserved sperm|||Unknown||H2A.Lap1, histone, NM1|Possibly| 5740.0|DTA||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5741.0|E2F7-/- (295/09)||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 7673.0|Solox Low x AR 2-/-|B6;CBA-Ifnar2 Tg(sIfnar2)Pjh/MarpApb||Recessive|interferon (alpha and beta) receptor 2|Ifnar2|Nil|Ifnar-2 |MGI:1098243 |interferon (alpha and beta) receptor 2; targeted mutation 1, Paul J Hertzog|Ifnar2|MGI:2680693|16||||||||||Unknown to Unknown|||||||interferon (alpha and beta) soluble receptor 2 low expression ||Low||||||||||Unknown|Unknown|C57BL/6 (tbc)|Yes|Yes|Yes|Yes|Yes|Yes|No|Poor||||No|07-May-2014|Cryopreserved sperm|50.0|0.0|Unknown||septic shock, proinflammatory cytokines, agonist|No| 3340.0|C57BL/6 Tg(IL5)C2|B6.CBACa-Tg(CD2-Il5)5C2Ldt/Apb [cc]|B6.CBACa-Tg(CD2-Il5)5C2Ldt/Apb [cc]|Dominant||||||||||||||||||||||||||transgene insertion 5C2, Lindsay A Dent|the dominant control region (DCR) of the gene encoding human CD2|High - 49 Copies||||||||||Constitutive expression of the IL5 gene is sufficient to induce lifelong high-level eosinophilia. Northern blot analysis identified 11,5 mRNA in the thymus, Peyer's patches, and subcutaneous (pooled inguinal and axillary) lymph nodes. No IL5 mRNA was detected in liver, heart, brain, or skeletal muscle tissues from transgenics, nor in any tissues from normal littermates. Do not maintain as homozygotes. While this is apparently possible, survival of homozygotes likely to be lower.|C57BL/6 IL-5 Tg2 mice are resistant to methylcholanthrene-induced carcinogenesis - see Simson, L, et al., 2007, Regulation of carcinogenesis by IL-5 and CCL11: a potential role for eosinophils in tumor immune surveillance. J. Immunol., 178:4222-4229.|C57BL/6|No|No|Yes|No|No|Yes|No|Excellent|20||Tg male wild type female|No|20-Jun-2008|Cryopreserved sperm|75.0|0.0|Yes||eosinophil, immune surveillance, esistance to helminthic parasites, asthma, allergy|Yes| 4736.0|Anasette|ENU5AT:140 ||Recessive|||Unknown|||Anasette|||Unknown||||||||||||||||Yes|||||||||||||Screened phenotype = positive for anti-nuclear antibodies||C57BL/6 x C57BL/10.Br|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||10||No|19-Apr-2009|Cryopreserved sperm|120.0|0.0|Unknown||Autoimmunity, ANA, ENU, Wellcome Trust|Yes| 9405.0|Six3Cre|C57Bl/6J-Tg<(Six3-cre)69Frty>/GcoJ |MGI:J:69312|Semi-dominant|sine oculis-related homeobox 3|Six3|||MGI:102764|transgene insertion 69, Yasuhide Furuta|Tg(Six3-cre)69Frty|Tg(Six3-cre)69Frty|Unknown|||||||||||||||||||||||||||||The donating investigator has not attempted to make a homozygous colony|heterozygous mice may be bred together|C57Bl/6J|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Jul-2022||0.0|30.0|Unknown|||Possibly| 18.0|Androida|ENU5:028 ||Recessive|||Unknown|||Androida|||Unknown||||||||||||||||Yes|||||||||||||Screened phenotype = positive for anti-nuclear antibodies||C57BL/6 x C57BL/10.Br|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||10||No|19-Aug-2006|Cryopreserved sperm|40.0|0.0|Unknown||ANA, autoimmunity, ENU, Wellcome Trust|Yes| 2781.0|C57BL/6.Flii 1.4A|B6.C-Flii/2AnuApb|B6.C-Flii/2AnuApb|Recessive|flightless I homolog (Drosophila)|Flii|Nil|Fli1, Fliih|MGI:1342286|targeted mutation 1, Hugh D Campbell|Flii|MGI:2179825|11||||||||||||||||No|||||||||||||Embryonic lethality at implantation: no embryos are recovered after E5.5; embryos develop normally until cellularization, the development arrests before completion of gastrulation blastocysts initiate uterine implantation but embryos fail to develop.embryonic growth arrest: development arrests during gastrulation|Enhanced wound healing: 3 days after a 1 cm full-thickness incision was made in the dorsal skin, surface wound area measurements show smaller, more contracted wounds than in wild-type mice. Length of neoepidermis is significantly greater in mutant animals, and percentage or re-epithelialization of wounds is greater at 5 days after wounding. By day 7, healing is comparable in mutants and wild-type|C57BL/6|No|No|Yes|No|No|Yes|No|Unknown|10|11||No|16-Feb-2008|Cryopreserved sperm|105.0|0.0|No||embryonic lethal, gelsolin, wound, cell migration, gastrulation|Yes| 4468.0|HB9-GFP|129-Tg(Mnx1-GFP)1Slp/AnuApb||Dominant||||||||||||||||||||||||||transgene insertion 1, Samuel L Pfaff|Mnx1|||||||||||Enhanced Green Fluorescent protein highlights motoneurons in the spinal cord.||129|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|||sib x sib|Yes|22-Feb-2009|Cryopreserved sperm|135.0|0.0|Unknown||GFP, neuron, transcription|Yes| 9.0|Anaconda|ENU4:006 ||Recessive|||Unknown|||Anaconda|||Unknown||||||||||||||||Unknown|||||||||||||Screened phenotype = positive for anti-nuclear antibodies||C57BL/6 x C57BL/10.Br|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||10||No|20-Apr-2004|Cryopreserved sperm|50.0|0.0|Unknown||autoimmunity, ENU, Wellcome Trust, ANA|Yes| 16.0|Anaya|ENU5:134 ||Recessive|||Nil|||Anaya|||Unknown||||||||||||||||Yes|||||||||||||Phenotypic screen= positive for anti-nuclear antibodies||C57BL/6 x CBA|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|2|||No|20-Apr-2004|Cryopreserved sperm|30.0|0.0|Yes||ANA, autoimmunity, ENU, Wellcome Trust|Yes| 5458.0|ENU16China:051a ; Berty|C57BL/6JAnu-Prkdc/AnuApb|C57BL/6JAnu-Prkdc/AnuApb|Recessive|protein kinase, DNA activated, catalytic polypeptide |Prkdc|Reduced|DNA-PK, DNA-PKcs, DNAPDcs, DOXNPH, dxnph, slip, XRCC7|MGI:104779|rotein kinase, DNA activated, catalytic polypeptide; berty|Prkdc|MGI:5009121|16|ENSMUSG00000022672|ENSMUST00000023352|Prkdc-201|10326|10349|T to A|ENSMUSE00000129337|73|3442|Tyrosine to STOP|||||CAGAAGACAAGTGCAGAAATGGAAGCATATCCAGCACTTGTGGTGGAAAAAATGCTGAGAG|Yes|||||||||||||No B or T cells.||C57BL/6JAnu|Yes|Unknown|Yes|Yes|Unknown|Yes|Yes|Poor||||No|07-Mar-2011|Cryopreserved sperm|48.0|0.0|Unknown||B cell, T cell, lymphocyte, ENU, severe combined immunodeficiency (SCID)|Possibly| 4732.0||B6;B10Br;129-Cblb Tg(IghelMD4)4Ccg/AnuApb||Recessive|Casitas B-lineage lymphoma b|Cblb|Nil|cbl-b|MGI:2146430|targeted mutation 1, Josef M Penninger|Cblb|MGI:2180570|16||||||||||||||||Yes|transgene insertion 4, Christopher C Goodnow||||||||||||T cell signalling defect||C57BL/6 x C57BL/10.Br x 129|Yes|Yes|Yes|Yes|Yes|Yes|No|Poor|1|2||No|19-Apr-2009|Cryopreserved sperm|90.0|0.0|No||T cell, tyrosine kinase, signal transduction, Hen Egg Lysozyme (HEL)|Yes| 7517.0|HA-TetO|C57BL/6-Tg(tetO-CYP19A1)2/MarpApb||Dominant||||||||||||||||||||||||||Human Aromatase ; human cytochrome P450, family 19, subfamily a, polypeptide 1|TetO|||||||||||Normal; no phenotype|Normal; no phenotype|C57BL/6J|No|Yes|Unknown|No|Yes|Unknown|No|Unknown||||No|29-Nov-2013|Cryopreserved sperm|50.0|0.0|Unknown|||Yes| 5743.0|E2F7/E2F8 floxed -/- (339/09)||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5742.0|E2F7/E2F8 flox-/- x K14Cre.FVB ?????||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5744.0|E2F8 flox-/- x K14Cre.FVB (339/09)||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6315.0|OT-II/Puma/Bim |C57BL/6-Bbc3 Bcl2l11 Tg(TcraTcrb)425Cbn||Semi-dominant|BCL2 binding component 3|Bbc3|Nil|PUMA|MGI:2181667|BCL2 binding component 3; targeted mutation 1, Andreas Strasser|Bbc3|MGI:2681654|7|||||||||||||||||transgene insertion 425, Frank Carbone||||||||||||||C57BL/6|Yes|No|Yes|Yes|Yes|Yes|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown||p53, Puma, Bim, TCR|Yes| 6315.0|OT-II/Puma/Bim |C57BL/6-Bbc3 Bcl2l11 Tg(TcraTcrb)425Cbn||Semi-dominant|BCL2-like 11 (apoptosis facilitator)|Bcl2l11|Nil|1500006F24Rik, Bim, Bod|MGI:1197519 |BCL2-like 11 (apoptosis facilitator); targeted mutation 1, Andreas Strasser|Bcl2l11|MGI:2156494|2|||||||||||||||||||||||||||||||C57BL/6|Yes|No|Yes|Yes|Yes|Yes|No|Unknown||||No|13-Sep-2011||||Unknown||p53, Puma, Bim, TCR|Yes| 6703.0|Gt3|B6.129-Gtf2ird1/Ausb||Recessive|general transcription factor II I repeat domain-containing 1 |Gtf2ird1|Nil|Alb-c-myc line 166.8, Alb/c-myc line 166.8, BEN, binding factor for early enhancer, c-myc line 166.8, Cream1, ESTM9, GTF3, MusTRD1, Tg(Alb1-Myc)166.8Sst, WBSCR11|MGI:1861942|general transcription factor II I repeat domain-containing 1; targeted mutation 1, Edna Hardeman|Gtf2ird1|MGI:4454555|5|||||||||||||||||||||||||||||Impaired coordinationAbnormal nervous system physiology:*Mice exhibit evidence of altered GABAergic neuronal function compared with wild-type mice.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|02-Dec-2011||0.0|0.0|Unknown||Williams-Beuren syndrome (WBS), GTF2IRD1|Yes| 9269.0||C57BL/6J-Sfd/AnuApb ||Semi-dominant|mucin 2|Muc2|||MGI:1339364|mucin 2; winnie|Muc2wnn|MGI:3614806|7|ENSMUSG00000025515 |||||||||Unknown to Unknown|||||||This is a missense mutation type||||||||||||spontaneous watery diarrhoea, and high incidence of rectal bleeding and prolapse, suggestive of ulcerative colitis.|Observable phenotype seems to present as normal, same as wildtype|C57Bl/6J|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|03-Sep-2021|Cryopreserved sperm|30.0|0.0|Unknown|||Possibly| 5222.0|C57.Lyn-/-uMT-/-|B6.129-Lyn Ighm/Apb|B6.129-Lyn Ighm/Apb|Recessive|Yamaguchi sarcoma viral (v-yes-1) oncogene homolog|Lyn|Nil|Hck-2|MGI:96892|Yamaguchi sarcoma viral (v-yes-1) oncogene homolog; targeted mutation 1, Ashley R Dunn|Lyn|MGI:2157129|4||||||||||||||||No|||||||||||||Mice are B cell deficient, and do not develop autoimmune disease characteristics of lyn -/- mice.|Not Studied|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|29-Sep-2010|Cryopreserved sperm|50.0|0.0|No||src kinase family, B cell, lymphocyte, signal transduction|Yes| 5222.0|C57.Lyn-/-uMT-/-|B6.129-Lyn Ighm/Apb|B6.129-Lyn Ighm/Apb|Recessive|immunoglobulin heavy constant mu|Ighm||BCR, Ig mu, Igh-M, Igh6, IgM, muH, muMT|MGI:96448|immunoglobulin heavy chain 6 (heavy chain of IgM); targeted mutation 1, University of Cologne|Ighm|MGI:1857187|12||||||||||||||||No|||||||||||||Mice are B cell deficient, and do not develop autoimmune disease characteristics of lyn -/- mice.|Not Studied|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|29-Sep-2010|Cryopreserved sperm|||No||src kinase family, B cell, lymphocyte, signal transduction|Yes| 2353.0||B6.SJL-PtprcPep3/Boy Tg(TcrLCMV)327Sdz Tcra||Recessive|protein tyrosine phosphatase, receptor type, C|Ptprc|Unknown|B220, CD45, CD45 antigen, Cd45, Ly-5, Lyt-4, T200, lymphocyte antigen 5|MGI:97810||Ptprc||1||||||||||||||||Yes|transgene insertion 327, Birgit Ledermann||High||||||||||||C57BL/6 x SJL/J|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|11-Dec-2007||0.0|0.0|No||T cell, receptor, phosphatase, Ly5, cytomegalovirus|No| 2353.0||B6.SJL-PtprcPep3/Boy Tg(TcrLCMV)327Sdz Tcra||Recessive|peptidase C|Pepc|Unknown|Dip-1, Pep-3, Pep3|MGI:97541||Pepc||1|||||||||||||||||||||||||||||||C57BL/6 x SJL/J|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|11-Dec-2007||||No||T cell, receptor, phosphatase, Ly5, cytomegalovirus|No| 2353.0||B6.SJL-PtprcPep3/Boy Tg(TcrLCMV)327Sdz Tcra||Recessive|T-cell receptor alpha chain|Tcra|Nil|Tcr alpha, Tcralpha|MGI:98553|T-cell receptor alpha chain; targeted mutation 1, Peter Mombaerts|Tcra|MGI:1857255|14|||||||||||||||||||||||||||||||C57BL/6 x SJL/J|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|11-Dec-2007||||No||T cell, receptor, phosphatase, Ly5, cytomegalovirus|No| 258.0||C57BL/6-Dpp4||Recessive|dipeptidylpeptidase 4|Dpp4|Nil|Cd26, Dpp-4, THAM|MGI:94919|targeted mutation 1, Nicolai Wagtmann|Dpp4|MGI:2150161|2||||||||||||||||Yes|||||||||||||Homozygous mutants show hypoglycemia, hyperinsulinemia, and increased plasma glucagon-like peptide 1 in glucose tolerance tests.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|30-Apr-2006||0.0|0.0|Unknown||insulin, glucose, CD26, cytokine, immunoglobulin|Yes| 238.0|MLR39|FVB/N-Tg(Cryaa-cre)39Mlr/Apb||Dominant||||||||||||||||||||||||||transgene insertion 39, Mike Robinson|aA-crystallin with tyrosinase cassette|||||||||||Nil. Mice express Cre in lens fibres with very little ectopic expression elsewhere||FVB/N|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|25-Apr-2006|Cryopreserved sperm|70.0|0.0|Unknown||crystallin, lens, eye, epithelial, Pax6|Yes| 6951.0|ENU19 WT:030:a:B6:G3|ANU:ENU19WT:030:a:G3||Recessive|Unknown||||||||Unknown||||||||||||||||Unknown|||||||||||||Unknown|Unknown|C57BL/6JAnu|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||1||No|05-Jul-2012|Cryopreserved sperm|27.0|0.0|Unknown||ENU, random, mutagenesis, screen|Yes| 7519.0|QSi5 - black|Quackenbush Swiss i5 - black||Dominant||||||||||||||||||||||||||||||||||||||Superior fecundity. Large litter size even after 50 generations.Mean length of the septum primum or flap valve length (FVL) is linger in QSI5 mice compared to 129T2 - 1.13mm compared to 0.60mm - the mean length of the septum primum or flap valve length (FVL) is strongly inversely correlated with patent foramen ovale (PFO) incidence.Increased lactation.More efficient milk production.Increased platelet count: QSi5 was found to have a mean platelet count of 1062 × 109/L (SD = 8.2 × 109/L, n = 16) versus that of 581 × 109/L (SD = 79 × 109/L, n = 23) in CBA mice.||Quackenbush Swiss|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|29-Nov-2013|Embryo|0.0|0.0|Unknown||breeding, fecund, platelet, heart, lactation|Yes| 5748.0|EKLF||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5749.0|EKLF/GKLF||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 4098.0||KRN:156||Recessive|||||||||Unknown||||||||||||||||Yes|transgene insertion KRN, Diane Mathis|Natural TCR alpha and -beta promoter/enhancer elements.|||||||||||No arthritis in KRN/H2g7 model. Candidate gene position likely to be Chr 3 or 12.||C57BL/6 x NODk x C57BL/10 x Balb/b|Yes|Yes|Yes|Yes|Yes|Yes|No|Poor||5||No|04-Dec-2008|Cryopreserved sperm|106.0|0.0|Yes||Autoimmunity, Arthritis, KRN, ENU|No| 4605.0|mIMPα4FL (mid level expression)|C57BL/6-Tg(EGFP-Kpna4 full length)mid||Dominant|karyopherin (importin) alpha 4|Kpna4|Unknown|IPOA3|MGI:1100848||||Unknown||||||||||||||||Yes|EGFP fused to full length Kpna4|Protamine 1|mid level expression||||||||||Fertility maybe reduced||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|13-Mar-2009|Cryopreserved sperm|72.0|0.0|Unknown||importin, testis, nuclear transport, fertility, protamine 1|No| 17.0|Andrea|ENU4strain:AT007||Recessive|Unknown||||||||Unknown||||||||||||||||Yes|||||||||||||Homogeneous anti-nuclear antibodies. |||Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|20-Apr-2004|Cryopreserved sperm|10.0|0.0|Yes||ENU, Wellcome Trust, anti-nuclear anitbodies, autoimmunity, T cell, B cell|Yes| 5347.0|B6.hCD4|C57BL/6-Tg(Cd4-CD4)2362Litt/Apb||Dominant||||||||||||||||||||||||||transgene insertion 2362, Dan R Littman|murine Cd4 and human CD4|equivalent to human CD4+ cells|||||||||||CD4 T cells express both the mouse and human CD4 without any adverse effects on phenotype.|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|24|||No|15-Dec-2010|Cryopreserved sperm|50.0|0.0|Unknown||T cell, lymphocyte|Yes| 4716.0||129-Shh/AnuApb||Recessive|sonic hedgehog|Shh|Unknown|Hhg1, Hx, Hxl3, M100081|MGI:98297|targeted mutation 1, Chin Chiang|Shh|MGI:1857796|5||||||||||||||||Yes|||||||||||||Perinatal Lethality, most die just before birth. abnormal dorsal-ventral axis patterning: indistinct midline at E8.5. Notochord degeneration: rostral-to-caudal loss of notochord tissue. Decreased brain size: abnormal forebrain morphology, ventral forebrain structures are lost. Abnormal diencephalon morphology: most of the diencephalon as an identifiable structure is absent. Abnormal telencephalon morphology: the bilateral lobes of the telencephalon are fused to form a single midline structure. Abnormal long bone morphology: absence or fusion of the paired distal limb bones. Abnormal humerus morphology: have a bony extension of the humerus in the forelimb. Absent fibula:the fibula is absent in the hindlimb. Absent tibia: the tibia is absent in the hindlimb. Abnormal axial skeleton morphology: most sclerotomal derivatives are absent. Abnormal craniofacial bone morphology: craniofacial bones are severely affected and almost entirely absent. Decreased rib number: most of the ribs are absent, with only 5-6 rib cartilages remaining. Absent vertebrae: most sclerotomal derivatives including the entire vertebral column are absent, with only 5-6 rib cartilages remaining. Absent cartilage: cartilage is absent at the elbow joint. Abnormal optic vesicle formation: optic vesicles are fused at the midline at E9.5, the optic stalks are deficient or absent, and there is no invagination to form the double-layered optic cups||129SvEv|No|No|Yes|No|No|Yes|No|Unknown|||Het x 129SvEv|No|08-Apr-2009|Cryopreserved sperm|105.0|0.0|Yes||embryonic lethal, limb, craniofacial, neural tube, notochord|Yes| 4717.0|SmoTgR|C57BL/6-Tg(CMV-RFP/Smo)/MarpApb||Dominant||||||||||||||||||||||||||red fluorescent protein tagged to Smoothened|cytomegalovirus (CMV)|||||||||||Animals express red fluorescent protein, are viable and healthy.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|15|2|Mate positive RFP mice with wild type C57BL/6|No|08-Apr-2009|Cryopreserved sperm|90.0|0.0|Unknown||Smoothen, red fluorescent protein (RFP)|Yes| 4922.0|Kylie|NOD.129/Sv-Tg(Csf2rb) Csf2rb Csf2rb Prkdc/Apb||Dominant|colony stimulating factor 2 receptor, beta 1, low-affinity (granulocyte-macrophage)|Csf2rb1|Nil|AIC2B, Bc, beta c, CDw131, common beta chain, Il3r, Il3rb1, Il5rb|MGI:1339759|targeted mutation 1, C Glenn Begley|Csf2rb|MGI:2181245|15||||||||||||||||Yes|colony stimulating factor 2 receptor, beta 1, low-affinity (granulocyte-macrophage)||High||||||||||None detected|Normal|NOD/SCID|Yes|Yes|Yes|Yes|Yes|Yes|No|Excellent|||Matings of 2 transgenic non-sibling mice|Yes|22-Oct-2009|Cryopreserved sperm|105.0|0.0|No||murine beta chain, GM-CSF, receptor, phosphorylation, signal transduction|Yes| 4922.0|Kylie|NOD.129/Sv-Tg(Csf2rb) Csf2rb Csf2rb Prkdc/Apb||Dominant|colony stimulating factor 2 receptor, beta, low-affinity (granulocyte-macrophage)|Csf2rb|Nil|AIC2B, Bc, beta c, CDw131, common beta chain, Csf2rb1, Il3r, Il3rb1, Il5rb|MGI:1339759|targeted mutation 1, Clare L Scott|Csf2rb|MGI:3653883|15|||||||||||||||||||||||||||||None detected|Normal|NOD/SCID|Yes|Yes|Yes|Yes|Yes|Yes|No|Excellent|||Matings of 2 transgenic non-sibling mice|Yes|22-Oct-2009|Cryopreserved sperm|||No||murine beta chain, GM-CSF, receptor, phosphorylation, signal transduction|Yes| 4922.0|Kylie|NOD.129/Sv-Tg(Csf2rb) Csf2rb Csf2rb Prkdc/Apb||Dominant|protein kinase, DNA activated, catalytic polypeptide|Prkdc||DNA-PK, DNA-PKcs, DNAPDcs, slip, XRCC7|MGI:104779|severe combined immunodeficiency|Prkdc|MGI:1857113|16|||||||||||||||||||||||||||||None detected|Normal|NOD/SCID|Yes|Yes|Yes|Yes|Yes|Yes|No|Excellent|||Matings of 2 transgenic non-sibling mice|Yes|22-Oct-2009|Cryopreserved sperm|||No||murine beta chain, GM-CSF, receptor, phosphorylation, signal transduction|Yes| 5346.0|SS-01 ; Vegfd 2.2.36 (SS-01)|B6;129S1/Sv-Figf/Apb||X-linked|c-fos induced growth factor|Figf|Nil|VEGF-D, Vegfd|MGI:108037|c-fos induced growth factor; targeted mutation 1, Marc G Achen|Figf|MGI:3576785|X|||||||||||||||||||||||||||||No abnormal phenotype detected: homozygous females are morphologically normal, can suckle, and have grossly normal lymphatic system morphology and function.Mice have reduced numbers of lymphatic vessels in lungs.|Normal|129S1/Sv x C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|0|||No|15-Dec-2010|Cryopreserved sperm|100.0|0.0|Unknown||growth factor, Vegf, lymphatics|Yes| 7.0|Alberta|C57BL/6JSfdAnu-Lepr/AnuApb|C57BL/6JSfdAnu-Lepr/AnuApb|Recessive|leptin receptor|LepR|Unknown|LEPROT, leptin receptor gene-related protein, OB-RGRP, obese-like, obl, Obr|MGI:104993|alberta|Lepr|MGI:3847119|4|ENSMUSG00000057722|ENSMUST00000037552|Lepr-001||||||||101768248|10|||ACCAACGTGTGTCCTTCCTGACTCCGTAGGTACGTCAGACTATATTATGTATTTTCCTTA|Yes|||||||||||||Homozygotes develop severe obesity evident by 4-8weeks. 50% develop diabetes by 6 weeks of age.Homozygotes don't breed||C57BL/6JSfdAnu|Yes|No|Yes|Yes|No|Yes|Yes|Good||9||No|06-Feb-2006|Cryopreserved sperm|57.0|0.0|Yes||obesity, leptin, diet, ENU|Yes| 7065.0|Momme D41|FVB/NJ-MommeD41 Tg(Hba1-Gfp)1Ew||Semi-dominant|modifier of murine metastable epialleles, D41|MommeD41|||||||16|||||||||||||||||transgene insertion 1, Emma Whitelaw|human alpha-globin promoter and enhancer region|11 copies||||||||||Unknown|Unknown|FVB/NJ|No|No|Yes|No|No|Yes|No|Good|||MommeD41<+/->;Tg(Hba1-Gfp)1Ew x Tg(Hba1-Gfp)1Ew|No|24-Aug-2012||0.0|0.0|Unknown||ENU, epigenetics, suppressor of variegation|Possibly| 3401.0|IL11R KO|B6.129-Il11ra1/Wehi||Recessive|interleukin 11 receptor, alpha chain 1|Il11ra1|Nil|Il-11ra, Il-11ra-alpha, Il11ra, NR1|MGI:107426|targeted mutation 1, Walter and Eliza Hall Institute of Medical Research|Il11ra1|MGI:2177778|4||||||||||||||||No|||||||||||||Normal haemopoeisis. Female mice with a null mutation of the interleukin-11 receptor alpha chain are infertile because of defective decidualization. A temporal analysis revealed IL-11 expression is maximal in the normal pregnant uterus at the time of decidualization, and in situ hybridization studies showed expression of the IL-11 and the IL-11 receptor alpha chain in the developing decidual cells. In both male and female IL-11Ralpha1-/- mice, trabecular bone volume was significantly higher than that of wildtype controls. This was associated with low bone resorption and low bone formation, and the low osteoclast number generated by IL-11Ralpha1-/- precursors was reproduced in ex vivo cultures, whereas elevated osteoblast generation was not.Embryonic lethality during organogenesis:* intercrosses of heterozygotes produce viable homozygous offspring at the expected Mendelian ratios.* however, embryos developing in homozygous mutant mothers appear necrotic at >7.5 dpc, with rare instances (<1%) of intact embryos detected at 9.5 dpc, and no live embryos found after 10.5 dpc.* notably, 2.5 dpc mutant embryos survive normally when transferred in foster uteri, whereas wild-type embryos fail to do so in uteri of mutant mice.Impaired embryo implantation:* at 4.5-7.5 dpc, homozygotes display a normal number of implantation sites relative to wild-type mice.* however, mutants show reduced capillary permeability and blood flow in the uterine vascular bed at the site of blastocyst apposition.Abnormal placenta development:* in most cases, embryos surviving in 9.5 dpc mutant uteri contain fibrinoid material and inflammatory cells in the space normally occupied by the placenta.* in a few cases, embryos surviving in 9.5 dpc mutant uteri display fetal components of the chorioallantoic placenta; however, the decidua basalis is entirely absent, being replaced by multiple layers of trophoblast giant cells, while the decidua capsularis is present but significantly thinner.Abnormal decidualization:* at 4.5 dpc, uteri of pregnant homozygotes display a reduced secondary decidual response to the implanting blastocystat 5.5-7.5 dpc, mutant deciduae are significantly smaller, displaying hemorrhage in the uterine lumen, disruption of the antimesometrium, and overgrowth of giant trophoblast cells in the mesometrial portion of the deciduum.* notably, pseudopregnant homozygotes show reduced deciduoma formation in response to an artificial (oil) stimulus, albeit with partial preservation of mesometrial decidual tissue.Increased trophoblast giant cell number: pregnant homozygotes exhibit a significantly increased number of secondary trophoblast giant cells in the mutant decidua.|Normal|C57BL/6|Yes|No|Yes|Yes|Yes|Yes|No|Good||||No|13-Jul-2008||0.0|0.0|Unknown||infertility, defective decidualization, decidual cells, trabecular bone, IL6, IL-6, osteoclast|Yes| 3946.0|MommeD5|FVB/NJ-Hdac1/Apb|FVB/NJ-Hdac1/Apb|Semi-dominant|histone deacetylase 1|Hdac1|Unknown|HD1, RPD3|MGI:108086|modifier of murine metastable epialleles, D5|Hdac1||4||||||||||||||||Yes|Green Fluorescent Protein|human alpha-globin promoter and enhancer region|||||||||||Lethality/prenatal-perinatalEmbryonic lethality during organogenesis* homozygotes die at or before E14.5EmbryogenesisEmbryonic growth arrest * around E8-9Embryonic growth retardation * developmentally delayed at E10.5Growth/sizeEmbryonic growth retardation* developmentally delayed at E10.5|Percentage of cells expressing the Line3 GFP transgene is decreased (enhancer of variegation).|FVB/NJ|No|No|Yes|No|No|Yes|No|Poor|||MommeD5<+/->;Tg(α-Globin-GFP)3EWh x Tg(α-Globin-GFP)3EWh|No|17-Oct-2008|Cryopreserved sperm|95.0|0.0|No||epigenetics, histone modification|Yes| 5809.0|GHR 569||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 9334.0||B6.B10-H2 Rag1Tg<(ILK3mHEL)3Ccg>/Apb ||Semi-dominant|recombination activating 1|Rag1 |||MGI:97848|recombination activating 1; targeted mutation 1, Peter Mombaerts|Rag1|MGI:1857241|2|||||||||||||||||transgene insertion 3, Christopher C Goodnow ||||||||||||Rag1 KO mice lack mature T and B cells. Hen egg lysozyme expressed on the pancreatic islet beta cells.|same|B10BR N10|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|10-Feb-2022|Cryopreserved sperm|26.0|0.0|Unknown|||Possibly| 9334.0||B6.B10-H2 Rag1Tg<(ILK3mHEL)3Ccg>/Apb ||Semi-dominant|histocompatibility-2, MHC|H2 |||MGI:95894|histocompatibility-2, MHC; k2 variant|H2k2|MGI:4936842|17|||||||||||||||||||||||||||||Rag1 KO mice lack mature T and B cells. Hen egg lysozyme expressed on the pancreatic islet beta cells.|same|B10BR N10|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|10-Feb-2022|Cryopreserved sperm|||Unknown|||Possibly| 6952.0|ENU19 WT:031:a:B6:G3|ANU:ENU19WT:031:a:G3||Recessive|Unknown||||||||Unknown||||||||||||||||Unknown|||||||||||||Unknown|Unknown|C57BL/6JAnu|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||1||No|05-Jul-2012|Cryopreserved sperm|60.0|0.0|Unknown||ENU, random, mutagenesis, screen|Yes| 6704.0|Gt4|B6.129-Gtf2ird1/Ausb||Recessive|general transcription factor II I repeat domain-containing 1|Gtf2ird1|Nil|Alb-c-myc line 166.8, Alb/c-myc line 166.8, BEN, binding factor for early enhancer, c-myc line 166.8, Cream1, ESTM9, GTF3, MusTRD1, Tg(Alb1-Myc)166.8Sst, WBSCR11|MGI:1861942|general transcription factor II I repeat domain-containing 1; targeted mutation 2, Edna C Hardeman MGI ID: MGI:3698407|Gtf2ird1|MGI:3698407|5|||||||||||||||||||||||||||||Abnormal behavior:*Mice display some behavioral and neurological defects that mimic some aspects of the behavioral deficit of Williams syndrome.Craniofacial phenotype:*Unlike human patients with Williams syndrome, mice do not display craniofacial or dental abnormalities.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|02-Dec-2011||0.0|0.0|Unknown||Williams-Beuren syndrome (WBS), GTF2IRD1|Yes| 6814.0|NOD-SBmut10|NOD/Lt-Tn(sb-pTrans-SA-IRESLacZ-CAG-GFP-SD:Neo)10TCB/Apb||Recessive||||||||||||||||||||||||||TgTn(sb-pTrans-SA-IRESLacZ-CAG-GFP-SD:Neo)2TCB||||||||||||unknown|unknown|NOD/Lt|Unknown|Unknown|Unknown|Unknown|Unknown|Yes|No|Excellent||||No|08-Feb-2012|Cryopreserved sperm|50.0|0.0|Unknown|||No| 3947.0|mommeD6|FVB/NJ-MommeD6/Apb||Semi-dominant|||Unknown|||modifiers of murine metastable epiallele D6|MommeD6|MGI:3586553|14||||||||||||||||Yes|Green fluorescent protein (GFP)|human alpha-globin promoter and enhancer region|||||||||||Homozygous lethality (~9.5 dpc)|GFP transgene (Line3) expression levels are increased.|FVB/NJ|No|No|Yes|No|No|Yes|No|Good|||MommeD6<+/->;Tg(Hba1-Gfp)3Ew x Tg(Hba1-Gfp)3Ew|No|17-Oct-2008|Cryopreserved sperm|75.0|0.0|Unknown||epigenetics, embryonic lethal|Yes| 5348.0|NOD.hCD4|NOD-Tg(Cd4-CD4)2362Litt/Apb||Dominant||||||||||||||||||||||||||transgene insertion 2362, Dan R Littman|murine Cd4 and human CD4|equivalent to human CD4+ cells|||||||||||CD4 T cells express both the mouse and human CD4 without any adverse effects on phenotype.|NOD|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|24|||No|15-Dec-2010|Cryopreserved sperm|50.0|0.0|Unknown||T cell, lymphocyte|Yes| 4131.0|Line3c|C57BL/6-Tg(HBA1-GFP)3Ew/Apb||Dominant|||Unknown||||||Unknown||||||||||||||||No|Green Fluorescent Protein (GFP)|α-Globin (-570 to +37) (4.1kb of enhancer)|||||||||||Fluorescence in erythrocytes can be observed by FACS or fluorescent microscopy. The allele is subject to variegation.|Fluorescence in erythrocytes can be observed by FACS or fluorescent microscopy. The allele is subject to variegation|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Poor|||Hom x Hom|No|07-Dec-2008|Cryopreserved sperm|125.0|0.0|No||Metastable epiallele, Transgene silencing, Green fluorescent protein|Yes| 5021.0|N1.C57BL6/J.Hep.516 KI/KI|C57BL/6J-Hep.516 KI/KI||Dominant||||||||||||||||||||||||||||||||||||||||7|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|22-Feb-2010|Cryopreserved sperm|105.0|0.0|Unknown|||No| 4699.0|NOD.Cg-Tg(RIP-Socs1)24Wehi NODPfp|NOD.Cg-Tg(Ins2-Socs1)24Wehi Prf1/WehiApb||Dominant|perforin 1 (pore forming protein)|Prf1|Nil|perforin, Pfn, Pfp, Prf-1|MGI:97551|perforin 1 (pore forming protein); targeted mutation 1, Sandoz Pharmaceutical|Prf1|MGI:1857235|10||||||||||||||||No|suppressor of cytokine signaling 1 (Socs1)|Rat insulin promoter from RIP7 vector|||||||||||90–95% of Pancreatic β cells did not up-regulate class I MHC in response to 100 U/ml IFN-, whereas all other islets cells were responsive, as measured by flow cytometry. SOCS-1 overexpression in Pancreatic β cells prevents progression to diabetes in CD8+ TCR transgenic NOD8.3 mice||NOD|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|07-Apr-2009|Cryopreserved sperm|150.0|0.0|Yes||Tolerance, Autoimmunity, Autoantigen, insulin|Yes| 6322.0|Puma/Bim/OT-1|C57BL/6-Bbc3 Bcl2l11 Tg(TcraTcrb)1100Mjb||Semi-dominant|BCL2 binding component 3|Bbc3|Nil|PUMA|MGI:2181667|BCL2 binding component 3; targeted mutation 1, Andreas Strasser|Bbc3|MGI:2681654|7|||||||||||||||||transgene insertion 1100, Michael J Bevan|a 2-kb fragment of the H-2Kb promoter|||||||||||||C57BL/6|Yes|No|Yes|Yes|Yes|Yes|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown||p53, Bbc3, Bim, Bcl-2, TCR|Yes| 6322.0|Puma/Bim/OT-1|C57BL/6-Bbc3 Bcl2l11 Tg(TcraTcrb)1100Mjb||Semi-dominant|BCL2-like 11 (apoptosis facilitator)|Bcl2l11|Nil|1500006F24Rik, Bim, Bod|MGI:1197519|BCL2-like 11 (apoptosis facilitator); targeted mutation 1, Andreas Strasser|Bcl2l11|MGI:2156494|2|||||||||||||||||||||||||||||||C57BL/6|Yes|No|Yes|Yes|Yes|Yes|No|Unknown||||No|13-Sep-2011||||Unknown||p53, Bbc3, Bim, Bcl-2, TCR|Yes| 5349.0|B6.IAE|C57BL/6-H2/JApb||Recessive|histocompatibility-2, MHC|H2|Nil|H-2, MHC-II|MGI:95894|histocompatibility-2, MHC; targeted deletion, H2 complex|H2|MGI:2658725|17||||||||||||||||No|||||||||||||Mice feature immune system perturbations including a dearth of CD4(+) lymphocytes in the thymus and spleen.Mice are susceptible to infection.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|36||Het x Het|No|15-Dec-2010|Cryopreserved sperm|50.0|0.0|Unknown||T cell, CD4, histocompatibility, MHC, lymphocyte|Yes| 5350.0|NOD.IAE|NOD-H2/JApb||Recessive|histocompatibility-2, MHC|H2|Nil|H-2, MHC-II|MGI:95894|histocompatibility-2, MHC; targeted deletion, H2 complex|H2|MGI:2658725|17||||||||||||||||No|||||||||||||Mice feature immune system perturbations including a dearth of CD4(+) lymphocytes in the thymus and spleen.Mice are susceptible to infection.||NOD|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|41||Het x Het|No|15-Dec-2010|Cryopreserved sperm|50.0|0.0|Unknown||T cell, CD4, histocompatibility, MHC, lymphocyte|Yes| 6719.0|cre1|B6-Tg(CMV-cre)1Cgn/Ausb||Dominant||||||||||||||||||||||||||transgene insertion 1, University of Cologne|human cytomegalovirus (CMV) promoter|||||||||||||C57BL/6|Yes|Unknown|Yes|Yes|Unknown|Yes|No|Unknown||||No|02-Dec-2011||0.0|0.0|Unknown||Cre, Germ cell|Yes| 5316.0|RKO 44|B6;129S1-Ryk/Apb||Recessive|receptor-like tyrosine kinase|Ryk||ERK-3, Vik|MGI:101766|receptor-like tyrosine kinase; targeted mutation 1, Steven A Stacker|Ryk|MGI:2667542|9|||||||||||||||||||||||||||||Neonatal lethality: most mice died within 1 day of birth, though some survived up to 8 days, and 2 to adulthood.Abnormal gait: mice surviving to adulthood dragged their hindlimbs.Short mandible.Abnormal maxilla morphology: in conjunction with shortened nasal bone, resulting in flattened midface.Abnormal neurocranium morphology: slightly smaller and rounder than that of wild-type or heterozygous mutant mice.Short nasal bone: shortened nasal bone, resulting in flattened midface.Cleft secondary palate: * cleft secondary palate observed in 88% of mice * consequence of abnormally high positioning and enlargement of the tongue.Increased tongue size: enlargement observed around E14, resulting in the disruption of the development of the palatal shelf.Short snout.Microcephaly: exhibited by mice that survived to adulthood.Cachexia.Postnatal growth retardation: growth was severely impaired in mice surviving past the first day of life.Cyanosis: mice were largely unable to suckle, became dehydrated, cyanotic, and exhibited gasping respirations.Short ulna: reduced in length.Abnormal hindlimb morphology: hindlimbs were splayed laterally.Short fibula.Short limbs: 18% to 25% reduction in the length of the long bones.Microphthalmia: bilateral microphthalmia was observed in mice that survived to adulthood.||C57BL/6 X 129S1/Sv|No|No|Yes|No|No|Yes|No|Unknown|0|||No|11-Nov-2010|Cryopreserved sperm|50.0|0.0|Unknown||craniofacial, Eph receptor, TGF, receptor protein tyrosine kinases (RTKs)|Yes| 5029.0|Bertolino|DAS||Recessive||||||||||||||||||||||||||||||||||||||||1|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|22-Feb-2010|Cryopreserved sperm|10.0|0.0|Unknown|||No| 6357.0|NOD/SCIDeGFP|NOD.Cg-Prkdc Tg(ActBeGFP)/Ausb|NOD.Cg-Prkdc Tg(ActBeGFP)/Ausb|Recessive|protein kinase, DNA activated, catalytic polypeptide|Prkdc|Nil|DNA-PK, DNA-PKcs, DNAPDcs, DOXNPH, dxnph, slip, XRCC7|MGI:104779|protein kinase, DNA activated, catalytic polypeptide; severe combined immunodeficiency|Prkdc|MGI:1857113|16|||||||||||||||||transgene insertion 1, Research Institute for Microbial Diseases, Osaka University|chicken beta actin promoter|||||||||||The mayority of eGFP expressing mice develop normally.A proportion(7%) of the e-GFP had small bodies,with a body weight of only 50% of the NOD/SCID mice||NOD SCID|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|13-Sep-2011|Embryo|0.0|0.0|Unknown|||Yes| 3948.0|mommeD10|FVB/NJ-Baz1b/Apb|FVB/NJ-Baz1b|Semi-dominant|bromodomain adjacent to zinc finger domain, 1B|Baz1b|Unknown|Wbscr9, WSTF|MGI:1353499|modifier of murine metastable epialleles, D10|Baz1b|MGI:3821601|5||||||||||||||||Yes|Green Fluorescent Protein (GFP)|human alpha-globin promoter and enhancer region|||||||||||Most homozygotes die perinatally. One-fifth will survive to weaning and are occasionally fertile. Surviving homozygotes are mostly male and are small in size. Homozygotes display craniofacial abnormalities.Decreased body size: at weaning.Decreased fetal size: noticable in utero at E18.5.Short mandible: mandibular hypoplasia, particularly posteriorly.Micrognathia: mandibular hypoplasia.Small parietal bone: shortened 12% relative to controls.Short nasal bone: * shortened 12% relative to controls. * flattened.Abnormal palatine bone morphology: reduced in width.Malocclusion.Short snout: upward curvature of the nasal tip.Broad head: widened bulbous forehead.|Heterozygotes display subtle craniofacial abnormalities. Percentage of cells expressing the GFP transgene (Line3) is decreased (enhancer of variegation).Decreased litter size.Small parietal bone: shortened 12% relative to controls.Short nasal bone: * shortened 12% relative to controls. * flattened.Abnormal palatine bone morphology: reduced in width.|FVB/NJ|No|No|Yes|No|No|Yes|No|Good|||MommeD10<+/->;Tg(Hba1-Gfp)3Ew x Tg(Hba1-Gfp)3Ew|No|17-Oct-2008|Cryopreserved sperm|100.0|0.0|Yes|Williams-Beuren Syndrome; WBS|chromatin, epigenetics, Williams-Beuren Syndrome; WBS|Yes| 5330.0|RKO C57BL/6|C57BL/6-Ryk/Apb||Recessive|receptor-like tyrosine kinase|Ryk|Nil|ERK-3, Vik|MGI:101766|receptor-like tyrosine kinase; targeted mutation 1, Steven A Stacker|Ryk|MGI:2667542|9||||||||||||||||Yes|||||||||||||Homozygotes die on the day of birth. Approx. 90% of E18.5 embryos have heart defects, the probable cause of neonatal death. They also have a cleft palate, craniofacial defects, shortened limbs and body axis, inner ear defects and abnormal corpus callosum (brain).Abnormal gait: mice surviving to adulthood dragged their hindlimbs.Short mandible.Abnormal maxilla morphology: in conjunction with shortened nasal bone, resulting in flattened midface.Abnormal neurocranium morphology: slightly smaller and rounder than that of wild-type or heterozygous mutant mice.Short nasal bone: shortened nasal bone, resulting in flattened midface.Cleft secondary palate: * cleft secondary palate observed in 88% of mice * consequence of abnormally high positioning and enlargement of the tongue.Increased tongue size: enlargement observed around E14, resulting in the disruption of the development of the palatal shelf.Short snout.Microcephaly: exhibited by mice that survived to adulthood.Cachexia.Postnatal growth retardation: growth was severely impaired in mice surviving past the first day of life.Cyanosis: mice were largely unable to suckle, became dehydrated, cyanotic, and exhibited gasping respirations.Short ulna: reduced in length.Abnormal hindlimb morphology: hindlimbs were splayed laterally.Short fibula.Short limbs: 18% to 25% reduction in the length of the long bones.Microphthalmia: bilateral microphthalmia was observed in mice that survived to adulthood.|Apparently normal|C57BL/6|No|No|Yes|No|No|Yes|No|Unknown||||No|19-Nov-2010|Cryopreserved sperm|50.0|0.0|Unknown||craniofacial, Eph receptor, TGF, receptor protein tyrosine kinases (RTKs), Wnt signalling, axon guidance|Yes| 9332.0|TBP-DSG2.tm1e|B6.Cg-Tg<(Tyr-cre/ERT2)13Bos> Braf<(tm1)/Mmcm> Pten<(tm1)/Hwu/BosJ>DSG2<(tm1e)>/CcbApb||Semi-dominant|DSG2, BRAF & PTEN||||||||Unknown|||||||||||||||||||||||||||||Mice are viable however 10-20% of mice develop spontaneous melanomas within 4 months with an increased risk as mice age due to leaky Cre recombinase expression and the genetic background which is less than the reported incidence for the BRafCA, PtenloxP, Tyr::CreERT2 parental strain on the JAX website.Mice that are hemizygous for the Tg(Tyr-cre/ERT2)13Bos transgene, homozygous for BRafCA and homozygous for PtenloxP should develop melanoma lesions with tamoxifen application.|Mice are viable however 10-20% of mice develop spontaneous melanomas within 4 months with an increased risk as mice age due to leaky Cre recombinase expression and the genetic background which is less than the reported incidence for the BRafCA, PtenloxP, Tyr::CreERT2 parental strain on the JAX website.Mice that are hemizygous for the Tg(Tyr-cre/ERT2)13Bos transgene, homozygous for BRafCA and homozygous for PtenloxP should develop melanoma lesions with tamoxifen application.|C57Bl/6N|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|31-Jan-2022||0.0|0.0|Unknown|||Possibly| 7710.0|37L1iKO|B6.Cg-Gpr37L1 Gt(ROSA)26Sor/JVccrApb||Recessive|G protein-coupled receptor 37-like 1|Gpr37l1||CAG-18, D0Kist8|MGI:1928503|G protein-coupled receptor 37-like 1; targeted mutation 1d, Wellcome Trust Sanger Institute|Gpr37L1||1|||||||||||||||||gene trap ROSA 26, Philippe Soriano; targeted mutation 1, Tyler Jacks||||||||||||Unknown|Unknown|C57BL/6J|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|25-Jun-2014||0.0|0.0|Unknown|||Possibly| 7676.0|CD4-cre.Egr2f/f.Egr3-/-|B6.129-Egr2 Egr3 Tg(Cd4-Cre)1Cwi/JhmiAnu||Recessive|early growth response 2|Egr2||Egr-2, Krox20, Krox-20, NGF1-B, Zfp-25|MGI:95296|early growth response 2; targeted mutation 3, Patrick Charnay|Egr2|MGI:2183227|10|||||||||||||||||transgene insertion 1, Christopher B Wilson|CD4|||||||||||Egr2 f/f.Egr3-/-.CD4-cre+ mice develop autoimmune disease at around three months of age or older. Egr2 f/f.CD4-cre+ mice develop milder autoimmune disease and at a slower rate. Egr3-/- exhibit some neurological defects.||C57BL/6|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown|>10|||No|09-May-2014|Cryopreserved sperm|21.0|0.0|Unknown|||Yes| 7676.0|CD4-cre.Egr2f/f.Egr3-/-|B6.129-Egr2 Egr3 Tg(Cd4-Cre)1Cwi/JhmiAnu||Recessive|early growth response 3|Egr3|Nil|Pilot|MGI:1306780|early growth response 3; targeted mutation 1, Jeffrey Milbrandt|Egr3|MGI:2180063|14|||||||||||||||||||||||||||||Egr2 f/f.Egr3-/-.CD4-cre+ mice develop autoimmune disease at around three months of age or older. Egr2 f/f.CD4-cre+ mice develop milder autoimmune disease and at a slower rate. Egr3-/- exhibit some neurological defects.||C57BL/6|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown|>10|||No|09-May-2014|Cryopreserved sperm|||Unknown|||Yes| 6331.0|Sey|C57BL/6-Pax6||Semi-dominant|paired box gene 6|Pax6|Nil|1500038E17Rik, AEY11, Dey, Dickie's small eye, Gsfaey11, Pax-6|MGI:97490|paired box gene 6; small eye|Pax6|MGI:1856155|2|||||||||||||||||||||||||||||Complete neonatal lethality:*Mice die soon after birth because of inability to breathe during suckling.Anophthalmia:*At E15, homozygotes have no visible eyes.Abnormal nasal cavity morphologyShort snout:*Defects in nasal cavity development results in shortened, imperforate snout.|Abnormal optic cup morphology:*At E15, fissure of optic cup is often delayed in closing.*At E15, there is folding at the margin of the optic cup resulting in a keyhole-shaped opening.Microphthalmia:*At E15 heterozygotes have smaller eyes than wild-type.|C57BL/6|No|No|Yes|No|No|Yes|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown||Sey, Aniridia (AN) locus|Yes| 5756.0|Emx1CreERT2||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 7520.0|QSi5 - albino|Quackenbush Swiss i5 - albino||Dominant||||||||||||||||||||||||||||||||||||||Superior fecundity. Large litter size even after 50 generations.Mean length of the septum primum or flap valve length (FVL) is linger in QSI5 mice compared to 129T2 - 1.13mm compared to 0.60mm - the mean length of the septum primum or flap valve length (FVL) is strongly inversely correlated with patent foramen ovale (PFO) incidence.Increased lactation.More efficient milk production.Increased platelet count: QSi5 was found to have a mean platelet count of 1062 × 109/L (SD = 8.2 × 109/L, n = 16) versus that of 581 × 109/L (SD = 79 × 109/L, n = 23) in CBA mice.||Quackenbush Swiss|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|29-Nov-2013|Embryo|0.0|0.0|Unknown||breeding, fecund, platelet, heart, lactation|Yes| 6953.0|ENU19 WT:034:a:B6:G3|ANU:ENU19WT:034:a:G3||Recessive|Unknown||||||||Unknown||||||||||||||||Unknown|||||||||||||Unknown|Unknown|C57BL/6JAnu|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||1||No|05-Jul-2012|Cryopreserved sperm|56.0|0.0|Unknown||ENU, random, mutagenesis, screen|Yes| 9387.0||C57Bl/6J-Prox1/Apb||Dominant|prospero homeobox 1|Prox1|Normal||MGI:97772| -11kb enhancer|||1|||||||||||||||||LacZ|Hsp68|||||||||||Presence of the transgene drives LacZ expression, chiefly in lymphatic vessels and valves.|Presence of the transgene drives LacZ expression, chiefly in lymphatic vessels and valves.|C57Bl/6J|Yes|Yes|Yes|Yes|Yes|Yes|No|Excellent||||No|19-May-2022|Cryopreserved sperm|40.0|0.0|No|||No| 6954.0|ENU19 WT:035:a:B6:G3|ANU:ENU19WT:035:a:G3||Recessive|Unknown||||||||Unknown||||||||||||||||Unknown|||||||||||||Unknown|Unknown|C57BL/6JAnu|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||1||No|05-Jul-2012|Cryopreserved sperm|30.0|0.0|Unknown||ENU, random, mutagenesis, screen|Yes| 10329.0||C57BL/6-Osxp53(fl/fl>pRbR26/Apb||Semi-dominant|Osx-Cre p53fl/fl pRbfl/fl R26-Adar1|||||Osx-Cre p53fl/fl pRbfl/fl R26-Adar1|||Unknown|||||||||||||||||Osx-Cre|Sp7|||||||||||Homozygous viable and fertile; stock maintained as Cre negative line with all other alleles homozygous. When crossed to Osx-Cre will develop osteosarcoma|Heterozygous viable and fertile; stock maintained as Cre negative line with all other alleles homozygous. When crossed to Osx-Cre will develop osteosarcoma|C57Bl/6N|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|09-May-2023|Cryopreserved sperm|40.0|0.0|Unknown|||Possibly| 86.0|T-wimp|C57BL/6JSfdAnu-Lcp2/AnuApb|C57BL/6JSfdAnu-Lcp2/AnuApb|Recessive|lymphocyte cytosolic protein 2|Lcp2|Reduced|SLP-76, SLP76, twm|MGI:1321402|t-wimp|Lcp2|MGI:3614800|11|ENSMUSG00000002699|ENSMUST00000052413|Lcp2-001||||||||33978410|12|||TGCAGCCCTCAGCCCCATTGGGGAGGTAAGTGTCTGTCATACTGTACCAAGTCCAGAATT|No|||||||||||||Few naïve CD4⁺ and CD8⁺ T cells, autoimmunity, 5 fold decrease in DP Tcells and significantly fewer CD4⁺ and CD8⁺ SP cells, partial block in T cell deveolpment at the Pre TCR checkpoint, very low expression of CD5 on DP thymocytes, defect in TCR signalling, mutation intrinsic to thymocytes, reduced expression of Slp76, Defects in positive selection and reduced negative thymocyte selection, hypergammaglobulinemia and hyper-IgE||C57BL/6JSfdAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Excellent||||No|06-Feb-2006|Cryopreserved sperm|142.0|0.0|Unknown||T cell, CD8, hypergammaglobulinaemia, autoimmunity, ENU|Yes| 4743.0||B6.129-Rc3h1 Icos/AnuApb|B6.129-Rc3h1 Icos/AnuApb|Semi-dominant|Ring finger and CCCH-type zinc finger domains 1|Rc3h1|Unknown|Roquin|MGI:2685397|sanroque|Rc3h1|MGI:3581675|1||||||||||Unknown to Unknown||||||Yes|||||||||||||||C57BL/JAnu|Yes|No|Yes|Yes|No|Yes|No|Unknown||1|Rc3h1 x ICOS -/-|No|27-Apr-2009|Cryopreserved sperm|90.0|0.0|Unknown||Systemic lupus erythematosus (SLE), autoimmunity, T cell, ubiquitin ligase, signal transduction, germinal centre|Yes| 4743.0||B6.129-Rc3h1 Icos/AnuApb|B6.129-Rc3h1 Icos/AnuApb|Semi-dominant|inducible T-cell co-stimulator|Icos|Unknown||MGI:1858745|targeted mutation 1, Richard A Flavell|Icos|MGI:2683635|1|||||||||||||||||||||||||||||||C57BL/JAnu|Yes|No|Yes|Yes|No|Yes|No|Unknown||1|Rc3h1 x ICOS -/-|No|27-Apr-2009|Cryopreserved sperm|||Unknown||Systemic lupus erythematosus (SLE), autoimmunity, T cell, ubiquitin ligase, signal transduction, germinal centre|Yes| 122.0|CD28 -/-|B6.129S2-Cd28/ThwAnuApb|B6.129S2-Cd28/ThwAnuApb|Recessive|CD28 antigen|CD28|Nil||MGI:88327|targeted mutation 1, Tak Mak|Cd28|MGI:1857150|1||||||||||||||||Yes|||||||||||||Homozygous mutation of this gene results in impairment of some T cell responses and decreased basal immunoglobulin levels. Mutant animals have reduced T helper cell activity and impaired T cell response to lectins, but cytotoxic T cells can still be induced||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|06-Feb-2006|Cryopreserved sperm|295.0|0.0|No||T cell, immunoglobulin, costimulation, lymphocyte, lectin|Yes| 6955.0|ENU19 WT:040:b:B6:G3|ANU:ENU19WT:040:b:G3||Recessive|Unknown||||||||Unknown||||||||||||||||Unknown|||||||||||||Unknown|Unknown|C57BL/6JAnu|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||1||No|05-Jul-2012|Cryopreserved sperm|10.0|0.0|Unknown||ENU, random, mutagenesis, screen|Yes| 6956.0|ENU20:005:a:B6:G3|ANU:ENU20:005:a:G3||Recessive|Unknown||||||||Unknown||||||||||||||||Unknown|||||||||||||Unknown|Unknown|C57BL/6JAnu|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||1||No|05-Jul-2012|Cryopreserved sperm|30.0|0.0|Unknown||ENU, random, mutagenesis, screen|Yes| 10330.0||C57Bl/6N-Osxp53pRbR26/Apb||Semi-dominant|Osx-Cre p53fl/fl pRbfl/fl R26-Adar1E861A|||||Osx-Cre p53fl/fl pRbfl/fl R26-Adar1E861A|||Unknown|||||||||||||||||Osx-Cre|Sp7|||||||||||Homozygous viable and fertile; stock maintained as Cre negative line with all other alleles homozygous. When crossed to Osx-Cre will develop osteosarcoma|Heterozygous viable and fertile; stock maintained as Cre negative line with all other alleles homozygous. When crossed to Osx-Cre will develop osteosarcoma|C57Bl/6N|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|09-May-2023|Cryopreserved sperm|30.0|0.0|Unknown|||Possibly| 6958.0|ENU20:007:a:B6:G3|ANU:ENU20:007:a:G3||Recessive|Unknown||||||||Unknown||||||||||||||||Unknown|||||||||||||Unknown|Unknown|C57BL/6JAnu|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||1||No|05-Jul-2012|Cryopreserved sperm|30.0|0.0|Unknown||ENU, random, mutagenesis, screen|Yes| 279.0||129-Ifnar/Apb||Recessive|interferon (alpha and beta) receptor 1|Ifnar1|Unknown|CD118, Ifar, Ifrc, INF-a receptor, Infar|MGI:107658|Ifnar1|targeted mutation 1, Michel Aguet|MGI:1930950|16||||||||||||||||Yes|||||||||||||Homozygotes for targeted null mutations exhibit increased susceptibility to viral infection, elevated levels of myeloid lineage cells in the peripheral blood and bone marrow, and reduced immune response to immunostimulatory DNA.||129|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|02-May-2006|Cryopreserved sperm|100.0|0.0|Unknown||interferon, infection, immunity, T cell|Yes| 6879.0|RBC14|FVB/NJ-Hbb-b1/MarpApb||Dominant|hemoglobin, beta adult major chain|Hbb-b1|Reduced|beta maj, beta major globin, beta1, beta-s|MGI:96021|hemoglobin, beta adult major chain; modifier of murine metastable epialleles, D7|Hbb-b1|MGI:3821597|7|||||||||||||||||||||||||||||Lethal at E18.5 or just after (not present at birth). Embryos are normal until E16.5 where they manifest progressive pallor and reduced fetal liver cellularity.|Microcytic, hypochromic anemia with severe reticulocytosis. Compensatory erythropoiesis with splenic extramedullary hematopoiesis due to red cell destruction. |FVB/NJ|No|No|Yes|No|No|Yes|No|Good|||Heterozygote intercrosses |No|26-Apr-2012|Cryopreserved sperm|50.0|0.0|Yes|Beta-thalassemia|Beta-thalassemia, Hbb-b1/beta major globin, ENU-mutagenesis, PolyA-tail|Possibly| 7707.0|Adra1aflx|B6(Cg)-Adra1a/MArpVccrApb||Recessive|adrenergic receptor, alpha 1a|Adra1a||Adra1c|MGI:104773|Adrenergic receptor, alpha 1a; targeted mutation 1c, Helmholtz Zentrum Muenchen GmbH|Adra1a|MGI:6502595|14||||||||||Unknown to Unknown|||||||||||||||||||Unknown|Normal|C57BL/6J|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|25-Jun-2014|Cryopreserved sperm|60.0|0.0|Unknown|||Possibly| 10371.0|Mroh9|C57BL/6J-Mroh9em2MAGEC||Dominant|Maestro Heat-Like Repeat-Containing Protein Family Member 9|Mroh9|Reduced||MGI:1925508||||1|ENSMUSG00000071890 ||||||||||||||||||||||||||||Sub-fertile|Normal|C57Bl/6J|Yes|Yes|Yes|Yes|Yes|Yes|Yes|Good||||No|12-Oct-2023|Cryopreserved sperm|50.0|0.0|Unknown|||Possibly| 7067.0|Gardenia|FVB/NJ-Gardenia Tg(Hba1-Gfp)1Ew||Semi-dominant|modifier of murine metastable epialleles, Gardenia|||||Gardenia|||16|||||||||||||||||Green Fluorescent Protein|human alpha-globin promoter and enhancer region|||||||||||Unknown|Unknown|FVB/NJ|No|No|Yes|No|No|Yes|No|Good|||Gardenia<+/->;Tg(Hba1-Gfp)1Ew x Tg(Hba1-Gfp)1Ew|No|24-Aug-2012||0.0|0.0|Unknown||ENU, epigenetics, suppressor of variegation|Possibly| 6636.0||GALA-Supreme||Dominant||||||||||||||||||||||||||||||||||||||To be determined by screening|||Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|25-Oct-2011|Embryo|0.0|0.0|Unknown||The Gene Mine, The Collaborative Cross|Yes| 9261.0||C57BL/6NCrlAnu-Heatr3/Apb||Semi-dominant|HEAT repeat containing 3 |Heatr3|||MGI:2444491|HEAT repeat containing 3; targeted mutation 1c, Helmholtz Zentrum Muenchen GmbH|Heatr3||8||||||||||Unknown to Unknown|||||||||||||||||||Normal|Normal|C57BL/6NCrlAnu|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Aug-2021|Cryopreserved sperm|59.0|0.0|Unknown|||Possibly| 652.0|Activin Beta C+ FL1|C57BL/6-Tg(ACTIVIN-β{C})1Grb/Apb||Dominant|||||||||Unknown||||||||||||||||No|human activin beta C|CMV|low (2 copies)||||||||||Essentially normal at gross level. male fertility decreases from 10 weeks (decreased sperm production, decreased liter size)|Essentially normal at gross level. male fertility decreases from 16 weeks (decreased sperm production, decreased liter size), evidence of liver disease and prostate hyperplasia|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|Yes|Poor||3|Het x WT or Het x Het|No|25-Apr-2007|Cryopreserved sperm|70.0|0.0|Unknown||activin, inhibin, prostate, testis, liver|No| 7525.0|B6.3R|B6.3R||Recessive||||||||||||||||||||||||||||||||||||||Normal||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|29-Nov-2013|Embryo|0.0|0.0|Unknown|||Yes| 5025.0|Hulett 4(het) Knock-In|C57BL/6J-Hep.516 KI/WT ||Dominant||||||||||||||||||||||||||||||||||||||||10|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|22-Feb-2010|Cryopreserved sperm|100.0|0.0|Unknown|||No| 7709.0|37L1MCM|B6.Cg-Gpr37L1 Tg(Myh6-cre/Esr1*)1Jmk/JVccrApb||Recessive|G protein-coupled receptor 37-like 1|Gpr37l1||CAG-18, D0Kist8|MGI:1928503|G protein-coupled receptor 37-like 1; targeted mutation 1d, Wellcome Trust Sanger Institute|Gpr37l1|MGI:6150820|1||||||||||Unknown to Unknown|||||||transgene insertion 1, Jeffery D Molkentin|mouse cardiac-specific alpha-myosin heavy chain|heart||||||||||Unknown|Unknown|C57BL/6J|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|25-Jun-2014|Cryopreserved sperm|60.0|0.0|Unknown|||Possibly| 4784.0|WT-127|WT Control for hGM-CSF transgenic mutants||Dominant|||||||||Unknown||||||||||||||||No|human GM-CSF|human GM-CSF promoter and enhancer (10.5kb)|||||||||||Express human GM-CSF. hGM-CSF detected in serum by ELISA. Murine GM-CSF used as internal control.|||Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|06-Sep-2009|Cryopreserved sperm|70.0|0.0|No||T cell, lymphocyte, transcription, chromatin remodelling, NF-kappaB|Yes| 6722.0|Sg1|B6.129-Sgca/Ausb||Recessive|sarcoglycan, alpha (dystrophin-associated glycoprotein) |Sgca|Nil|50DAG, adhalin, Asg |MGI:894698|sarcoglycan, alpha (dystrophin-associated glycoprotein); targeted mutation 1, Kevin P Campbell|Sgca|MGI:1934922|11|||||||||||||||||||||||||||||||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|02-Dec-2011||0.0|0.0|Unknown||Limb-girdle muscular dystrophy type 2D (LGMD 2D), Sgca|Yes| 9371.0|Rag1 KO:Ly5a|B6(Cg)-Rag1tm1Mom Ptprca/Anu||Semi-dominant|only for L2 reder|only for L2 reder|||||||Unknown|||||||||||||||||||||||||||||||C57Bl/6N|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|08-Apr-2022||0.0|0.0|Unknown|||Possibly| 1930.0|OT-1|C57BL/6-Tg(TcraTcrb)1100Mjb||Recessive||||||||||||||||||||||||||transgene insertion 1100, Michael J Bevan|H-2Kb promoter|||||||||||Carries a transgenic T cell receptor that recognizes ovalbumin residues 257-264 (SIINFEKL) in the context of H2K||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|23-Aug-2007||0.0|0.0|Unknown||Ovalbumin, receptor, T cell, Lymphocyte|Yes| 4792.0|B6|C57BL/6J||Dominant||||||||||||||||||||||||||||||||||||||Normal.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|06-Sep-2009|Cryopreserved sperm|80.0|0.0|Unknown||C57BL/6|No| 4793.0|CBA|CBA||Dominant||||||||||||||||||||||||||||||||||||||Normal.||CBA|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|06-Sep-2009|Cryopreserved sperm|10.0|0.0|Unknown||CBA|No| 5135.0||ENU14NIH:089:G3b||Recessive|Unknown|Unknown|Unknown||||||Unknown|||||||||||||||||||||||||||||Skin continues to grow over the lifetime of the mouse|Normal|C57BL/6|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|Yes|Unknown||||No|26-May-2010|Cryopreserved sperm|9.0|0.0|Unknown||Coat, skin, dermis, proliferation, ENU|No| 5227.0|129Sv/Ly5.1|129/Sv-Ptprc/Apb||Dominant|||||||||||||||||||||||||||||protein tyrosine phosphatase, receptor type, C|Ptprc||B220, CD45, Ly-5, Lyt-4, T200|MGI:97810|protein tyrosine phosphatase, receptor type, C; a variant|Ptprc|MGI:4819849|1|N/A (homogenous wild type line)|N/A (homogenous wild type line)|129/Sv|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||More than 10|Sibling mating|No|05-Oct-2010|Cryopreserved sperm|45.0|0.0|No||transplantation, complementation, Ptprc|Yes| 4795.0|FVB|FVB/NJ||Dominant||||||||||||||||||||||||||||||||||||||Normal.||FVB/NJ|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|06-Sep-2009|Cryopreserved sperm|45.0|0.0|Unknown||FVB|No| 4788.0||129/SvJ||Dominant||||||||||||||||||||||||||||||||||||||Normal.||129/SvJ|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|06-Sep-2009|Cryopreserved sperm|73.0|0.0|Unknown||129|Yes| 6206.0|vabl40/266Del|STOCK Bcl2l11 Tg(Igh-Abl1)40Sco||Recessive|BCL2-like 11 (apoptosis facilitator)|Bcl2l11|Nil|1500006F24Rik, Bim, Bod|MGI:1197519|BCL2-like 11 (apoptosis facilitator); targeted mutation 1.1, Andreas Strasser|Bcl2l11|MGI:2156498|2|||||||||||||||||transgene insertion 40, Suzanne Cory|SV40 early promoter|||||||||||Low incidences of plasmacytoma. Look out for dragging hind legs, enlarged spleen, enlarged mesenteric lymph nodes - tumours. Visually check. 1-2% will die at 20 weeks of age, 19-20% will die at 1 year. Mice die as a result of plasmacytoma. Mice will bear one of the following tumours: lymphoma, splenomegaly, messentary associated, abdominal, caecal, Peyer's Patches. They may also suffer from small bowel obstruction, intestinal haemorrhage, hind leg paralysis, intussusception, vabl40 mice develop plasmocytoma tumours. Onset may be accelerated in Bim -/- vabl40 T/+ and Bim +/- vabl40 T/+ Bim -/- develop autoimmune kidney disease when older.||Unknown|Yes|Unknown|Yes|Yes|Unknown|Yes|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown||v-abl oncogene, pre-B lymphomas, bcl-2|Yes| 4790.0||BALB/c||Dominant||||||||||||||||||||||||||||||||||||||Normal.||BALB/c|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|06-Sep-2009|Cryopreserved sperm|180.0|0.0|Unknown||BALB/c|No| 6439.0|A2?|B6.129P2-Arnt2/Ausb||Recessive|aryl hydrocarbon receptor nuclear translocator 2|Arnt2|Nil|bHLHe1, mKIAA0307|MGI:107188|aryl hydrocarbon receptor nuclear translocator 2; targeted mutation 1, Yoshiaki Fujii-Kuriyama|Arnt2|MGI:2178831|7|||||||||||||||||||||||||||||Complete postnatal lethality:*No homozygotes survive to 2 weeks after birth.*Homozygotes within 1 day of birth are grossly normal.Abnormal neurohypophysis morphology:*Arginine vasopressin and oxytocin absent in the posterior lobe.*Corticotropin releasing hormone and somatostatin absent in the posterior lobe. Abnormal pituitary secretion:*Arginine vasopressin and oxytocin absent in the posterior lobe.*Corticotropin releasing hormone and somatostatin absent in the posterior lobe .Enlarged third ventricle:*Diameter of third ventricle is increased.Abnormal paraventricular hypothalamic nucleus morphology:*Hypocellular in newborn mice.Abnormal supraoptic nucleus morphology:*Hypocellular in newborn mice.Abnormal pituitary hormone level:*Arginine vasopressin and oxytocin absent in the posterior lobe.*Corticotropin releasing hormone and somatostatin absent in the posterior lobe.||C57BL/6|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown||Arnt2, Transcription regulator, Secretory neurone|Yes| 6449.0|VDRJ?|B6.129S4-Vdr/JAusb||Recessive|vitamin D receptor|Vdr|Nil|Nr1i1|MGI:103076|vitamin D receptor; targeted mutation 1, Marie B Demay|Vdr|MGI:2183404|15|||||||||||||||||||||||||||||Abnormal mineral homeostasis:*hypophosphatemia.Increased width of hypertrophic chondrocyte zone:*Expansion of the growth plate is associated with impaired apoptosis of late hypertrophic chondrocytes.Abnormal chondrocyte morphology:*Impaired hypertrophic chondrocyte apoptosis.*A 'rescue diet' of high-calcium/low-phosphate restores the normal level of apoptosis and the growth plate phenotype.Rickets:*Mutants develop rickets secondary to impaired apoptosis of late hypertrophic chondrocytes.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown||vitamin D-dependent rickets type II (VDDR II), Vitamin D receptor|Yes| 168.0|Elf3 knockout|B6.129S4-Elf3/Apb|B6.129S4-Elf3/Apb|Recessive|E74-like factor 3|Elf3|Nil|ESE-1, ESX, jen|MGI:1101781|targeted mutation 1, Paul J Hertzog|Elf3|MGI:2662485|1||||||||||||||||Yes|Neomycin resistance gene||||||||||||embryonic lethality during organogenesis: only about 71% of expected numbers of homozygotes are still alive at E11.5postnatal lethality: by weaning, only about 27% of expected numbers are still alive.decreased body size: smaller than controls during suckling period although normal in size from E11.5 to birth. After 6 weeks of age, weight gain is normal and mice attain normal sizecachexia: 2-3 days before death, mice begin to display a wasted phenotype, appear malnourished, lethargic, watery diarrhoealethargy: beginning 2-3 days before deathabnormal intestinal epithelium morphology: intestinal endothelium fails to transform from pseudostratified to columnar by E17.5. Formation of villi is delayed and those present are misshapen. Connective tissue under the lamina propria of the villi is disorganized.abnormal enterocyte morphology: absorptive enterocytes are morphologically abnormal. Tightly packed with apical cytoplasmic snouts. Microvilli are short. Increased numbers of mitochondria and ribosomes.abnormal intestinal goblet cells: reduced numbers of goblet cells producing sialomucin.diarrhoea: watery diarrhea in mice that die starting 2-3 days before death. |No over phenotype|C57BL/6|No|No|Yes|No|No|Yes|No|Good|10||Het x Het OR Het male x WT female OR Het female x WT male|No|15-Apr-2006|Cryopreserved sperm|60.0|0.0|Unknown||ETS transcription factor, intestine, TGF, epithelium, differentiation|Yes| 4794.0|CBA x B6|CBA/CaJ x C57BL/6J:F1||Dominant||||||||||||||||||||||||||||||||||||||Normal.||CBA x C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Excellent||||No|06-Sep-2009|Cryopreserved sperm|3939.0|0.0|Unknown||CBA/CaJ x C57BL/6J:F1, hybrid vigour|No| 5398.0|HK1-Shh|B6;CBA-Tg(KRT1-Shh)/Apb||Dominant||||||||||||||||||||||||||rat sonic hedgehog|human keratin 1 |increased||||||||||Unknown|skin anomalies, fore- and hindlimp abnormalities|C57BL/6|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Good|||het x wt|No|27-Jan-2011|Cryopreserved sperm|60.0|0.0|No||Sonic Hedgehog, skin, limb, embryonic development, overexpression|Possibly| 1969.0|available from Animal Resources Centre - www.arc.wa.gov.au|BALB/c Series (H2, H2) ||Dominant|Congenic albino: A, Tyr, Tyrp1, Congenic partner BALB/c.||Unknown||||||Unknown||||||||||||||||Yes|||||||||||||General Information: Note inbred BALB/c except for usage where histocompatibility differences will be noted between strains.|||Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||Yes|04-Sep-2007||0.0|0.0|No|||Yes| 4800.0|Rain ; ENU11B6:226b|C57BL/6JAnu-Ptprc/AnuApb|C57BL/6JAnu-Ptprc/AnuApb|Recessive|protein tyrosine phosphatase, receptor type, C|Ptprc|Unknown|B220, CD45, Ly-5, Lyt-4, T200 |MGI:97810|rain|Ptprc|MGI:4819248|1|ENSMUSG00000026395|ENSMUST00000027645|Ptprc-201||||||||140007727|11|||TGTTATAAATGTGCAGACAGATTTGGGGAGTAAGTATATCGTTTATGTTTATAAAATAAA|Yes|||||||||||||Shifted CD45 expression measured by flow cytometry||C57BL/6JAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|10-Sep-2009|Cryopreserved sperm|75.0|0.0|Unknown||cd45, signal transduction, T cell, ENU, NIH|Yes| 237.0|MLR10|FVB/N-Tg(Cryaa-cre)10Mlr/Apb||Dominant||||||||||||||||||||||||||transgene insertion 10, Mike Robinson|modified alpha A crystallin promoter with an inserted copy of Pax6 consensus binding site|||||||||||Nil. Mice express Cre in lens, vibrissae. Weak expression in maxillary arch at E12.5. ||FVB/N|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|25-Apr-2006|Cryopreserved sperm|70.0|0.0|Unknown||crystallin, lens, eye, epithelial, Pax6|Yes| 246.0|B6.B2m-/-|B6.129S2-B2m/AnuApb|B6.129S2-B2m/AnuApb|Recessive|beta-2 microglobulin|B2m|Nil|beta 2 microglobulin, beta2-m, Ly-m11|MGI:88127|targeted mutation 1, Rudolf Jaenisch|B2m|MGI:1927183|2||||||||||||||||No|||||||||||||Homozygotes lacking B2m appear normal, but have no detectable MHC class I antigen on their cells and are deficient in CD4- CD8+ T cells which mediate cytotoxic T cell function. Mutant mice are also subject to systemic iron loading.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|26-Apr-2006|Cryopreserved sperm|110.0|0.0|Yes||MHC, antigen presentation, cytotoxic, T cell, lymphocyte|Yes| 8478.0|ASD777:TNFRSF13b:C76R|C57BL/6NCrlAnu-Tnfrsf13b/AnuApb||Recessive|tumor necrosis factor receptor superfamily, member 13b|Tnfrsf13b|Unknown|1200009E08Rik, Taci|MGI:1889411|Tnfrsf13b; endonuclease-mediated mutation 1, Australian National University|Tnfrsf13b||11||||||||||Unknown to Unknown|||||||||||||||||||||C57BL/6NCrlAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|30-Apr-2018|Cryopreserved sperm|33.0|0.0|Unknown|||Yes| 6728.0|GFP1|C57BL/6-Tg(CAG-EGFP)1Osb/J/Ausb||Dominant||||||||||||||||||||||||||transgene insertion 1, Research Institute for Microbial Diseases, Osaka University |chicken beta actin promoter|||||||||||Complete prenatal lethality:*Homozygous transgenic mice die in the embryonic stage, putatively due to integration site effect.|No abnormal phenotype detected:*Mice are viable and show no functional or morphological abnormalities of the retina.*All tissues, except for erytrhocytes and hair, are green under excitation light.|C57BL/6|No|No|Yes|No|No|Yes|No|Unknown||||No|02-Dec-2011||0.0|0.0|Unknown||GFP|Yes| 9464.0|TgmiR-146a KO|C57BL/6J-miR146a/Apb||Semi-dominant|microRNA 146|miR146a|||MGI:2676831||||11|||||||||||||||||||||||||||||T-cells: miR-146a-/- mice have been reported to have an increased incidence of T-cell derived lymphomas and exhibit enlarged spleens starting at 6 months of age. Seizure occurrence: Based on routine health monitoring of TgmiR-146a strain, 6 mice with a miR-146a-/- genotype over 11-months of age were observed to have seizure occurrence.Weight loss: 14 out of 120 TgmiR-146a mice that were over 12-month of age exhibited weight loss ranging from 5-15%. Overall, the TgmiR-146a strain over 12-month of age had 11.7% chance of weight loss.Skin irritation and inflammation: 7 out of 90 miR-146a-/- mice that were over 12-months of age were observed with skin irritation and inflammation. Overall, miR-146a-/- mice had a 7.8% chance of skin irritation and inflammation.Hind limb weakness: 10 out of 105 miR-146a-/- mice that were over 6-month of age were observed with hind limb weakness and decreased tail mobility. In total, miR-146a-/- mice had a 9.5% chance of hind limb weakness which potentially leads to hind limb paralysis.|Seizure occurrence: Based on routine health monitoring of TgmiR-146a strain, 2 out of 131 mice with a miR-146a-/+ genotype were observed to have seizure occurrence.Skin irritation and inflammation: 7 out of 90 miR-146a-/+ mice that were over 12-month of age were observed with skin irritation and inflammation. Overall, TgmiR-146a strain with -/+ genotypes had 7.8% chance of skin irritation and inflammation.Hind limb weakness: 10 out of 105 miR-146a-/+ mice that were over 6-month of age were observed with hind limb weakness and decreased tail mobility. In total, TgmiR-146a strain with miR-146a-/+ genotypes had 9.5% chance of hind limb weakness which potentially leads to hind limb paralysis.|C57Bl/6J|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|20-Dec-2022|Cryopreserved sperm|39.0|100.0|Unknown|||Possibly| 5203.0|ENU15 NIH 17|ENU15NIH:017||Dominant|Unknown|Unknown|Unknown||||||Unknown|||||||||||||||||||||||||||||Unknown|Kinked tail. Mice have variable types of kinks, some with a small kink at the end of the tail, and others with either a pronounced or slight zigzag. |C57BL/6JAnu|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Good||3|affected x B6|No|09-Aug-2010|Cryopreserved sperm|50.0|0.0|Unknown||kink tail, ENU|No| 5205.0|theoden ; ENU4AT:050 |B6JAnu(Cg)-Fas/AnuApb|B6JAnu(Cg)-Fas/AnuApb|Recessive|Fas (TNF receptor superfamily member 6)|Fas|Nil|APO-1, CD95, TNFR6, Tnfrsf6|MGI:95484|theoden|Fas|MGI:4455060|19|ENSMUSG00000024778|ENSMUST00000025691|Fas-201|416|422|G to A|ENSMUSE00000144910|4|139|Cysteine to Tyrosine|||||CTACTGCGATTCTCCTGGCTGTGAACACTGTGTTCGCTGCGCCTCGTGTGAACATGGAACC|Yes|||||||||||||Antinuclear autoantibodies, lymphadenopathy.||C57BL/6JAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|10|||No|13-Aug-2010|Cryopreserved sperm|104.0|0.0|Unknown||B cell, T cell, lymphadenopathy, ENU, Wellcome Trust|Yes| 2363.0|uMT|B6.129S2-Ighm/AnuApb|B6.129S2-Ighm/AnuApb|Recessive|immunoglobulin heavy chain 6 (heavy chain of IgM)|Igh-6|Nil|BCR, Ig mu, Igh-M, Igh6, IgM, muH, muMT|MGI:96448|targeted mutation 1, University of Cologne|Igh-6|MGI:1857187|12||||||||||||||||No|||||||||||||Immune system phenotype:* T cell numbers in lymph nodes are normal.* dendritic cells show normal function in mutants.Decreased dendritic cell number: numbers of CD11c+ dendritic cells (DCs) are reduced in mutants.Decreased CD4-positive T cell number:* there are 5- to 40-fold fewer antigen specific CD4 cells producing Il-2 in mutants compared to controls 6 months after keyhole limpet hemocyanin immunization.* numbers are reduced 3-fold in spleen vs wild-type.Decreased CD8-positive T cell number: numbers are reduced 3-fold in spleen vs wild-type.Arrested B cell differentiation: a transitional block in early B cell development in evident in bone marrow; pre-B cells are decreased in number.Abnormal spleen morphology:* in mutants, area of T zone stromal cell network in the spleen is decreased four- to five-fold compared to wild-type* T zone cross sectional area is decreased 2- to 3-foldDecreased spleen weight: spleens are ~50% the weight of wild-type spleens.Abnormal humoral immune response: mice fail to respond to T cell-dependent (OVA) or T cell-independent (dextra) antigenic stimulation and do not produce serum specific antibodies to these antigens.Decreased immunoglobulin level: null mice have almost undetectable serum levels of IgG1, IgG2a, IgG2b, IgG3, IgM and IgA compared to wild-type controls or Fas mice.Decreased IgE level: IgE is not detectable in serum of OVA-treated mutants, but high levels are produced in treated wild-type.Decreased IgG level:* IgG is not detectable in OVA-treated mutants, but high levels are produced in treated wild-type.* IgG levels drop rapidly after birth due to loss of maternal Ig.Decreased IgG1 level: IgG1 is not detected in serum after OVA challenge.Abnormal cytokine secretion: in mutants, Il-2 secretion is diminished from T cells primed in absence of B cells compared to controls 6 months after keyhole limpet hemocyanin immunization.Increased susceptibility to parasitic infection:* mice fail to clear a Giardia muris infectiontwo weeks after Giardia infection, there are 10-fold more Giardia cysts present in the feces of mice.* mice have 10-fold more Giardia trophozoites in the small intestine three weeks after infection and a thousand-fold more 7 weeks after infection compared to controls.* mutant mice still have an active Giardia population in the gut one year after infection while wild-type mice clear Giardia after about 7 weeks.* mice are not protected from Giardia upon a secondary challenge as wild-type mice are.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|13-Dec-2007|Cryopreserved sperm|60.0|0.0|Unknown||Immunoglobulin, B cell, IgM, lymphocyte|Yes| 1603.0|Galnr1-/-|C57BL/6-Galr1||Recessive|galanin receptor 1|Galr1|Nil|Galnr1|MGI:1096364|galanin receptor 1; targeted mutation 1, Tiina Pauline Iismaa|Galr1|MGI:2446477|18||||||||||||||||No|||||||||||||Normal phenotype.Develops spontaneous seizures.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|11-Jul-2007||0.0|0.0|Unknown||GFP, seizure, synapse, hippocampus|Yes| 299.0||C57BL/6J-Lama2||Recessive|laminin, alpha 2|Lama2|Unknown|mer, merosin, nmf417|MGI:99912|dystrophia muscularis|Lama2|MGI:1856026|10||||||||||||||||No|||||||||||||This mutation arose spontaneously in the 129/Re inbred strain at The Jackson Laboratory in 1951. Homozygotes are deficient in merosin (J:18187). Partial restoration of the ability to express Lama2 can be achieved by transplantation of a primary muscle cell culture (J:32227). Lama2dy homozygotes are characterized by progressive weakness and paralysis beginning at about 3 1/2 weeks of age. The hindlimbs are affected first, later the axial and forelimb musculature. Death usually occurs before 6 months of age, and the mice are usually sterile (J:13125). Skeletal muscle shows degenerative changes with proliferation of sarcolemmal nuclei, increase in amount of interstitial tissue, and size variation among individual muscle fibers (J:13125). In the dorsal and ventral roots of the peripheral nerves, both spinal and cranial, Schwann cells fail to separate and ensheathe axons so that groups of closely apposed naked axons, normally seen only in early stages, persist into adulthood (J:5331). At birth there is a deficiency of Schwann cells in the spinal roots, but many undifferentiated cells are present which are probably uncommitted Schwann cells that can differentiate when transplanted to a normal environment (J:12727). In the rest of the peripheral nervous system, the basement membrane of Schwann cells is interrupted by gaps (J:5565), the internodal gap in the nodes of Ranvier is lengthened (J:5866, J:6188), and there is delayed onset of myelination with fewer myelinated axons and shorter internode length (J:12730). There is reduced conduction velocity in spinal roots and peripheral nerves (J:5948) and evidence of defective axonal transport in the sciatic nerve (J:5709, J:5906). It is probable that the myelination defects of the peripheral nerves are due to an intrinsic defect in the dystrophic Schwann cells but the evidence from transplantation experiments, chimeras, and cell cultures is somewhat conflicting (J:30709, J:5580, J:5904, J:7618). There is some evidence for defective myelination in the central nervous system also (J:7911). In culture, myogenic cells from homozygous Lama2dy mice develop muscle properties just as well as cells from control mice (J:5909) and there is no peripheral block of neuromuscular transmission (J:5851, J:5922). Muscle of Lama2dy homozygous mice transplanted into normal hosts is indistinguishable from transplanted control muscle by 100 days (J:8221). There is an extensive literature on morphological and biochemical defects in Lama2dy/Lama2dy muscle.|||Yes|Unknown|Yes|Yes|Unknown|Yes|No|Unknown||||No|03-May-2006||0.0|0.0|Yes||muscular dystrophy, ataxia, degeneration|Yes| 7706.0|Adra1aConR|B6(Cg)-Adra1a/MarpVccrApb||Recessive|adrenergic receptor, alpha 1a|Adra1a|Nil|Adra1c|MGI:104773|adrenergic receptor, alpha 1a; targeted mutation 1a, Helmholtz Zentrum Muenchen GmbH|Adra1a|MGI:4451809|14|||||||||||||||||||||||||||||Unknown|Normal|C57BL/6J|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|25-Jun-2014|Cryopreserved sperm|60.0|0.0|Unknown|||Possibly| 9395.0|Met-K|B10.BR;B6.SJL-Tg(sMt1-H2-KGM)/Apb||Dominant|Major histocompatibility-2, MHC; b variant|H-2Kb|||MGI:3579319||||17|||||||||||||||||Major histocompatibility-2, MHC; b variant|sheep metallothionein promoter|||||||||||These transgenic mice have a normal phenotype but express a transgenic H-2Kb MHC I molecule in hepatocytes under the control of the sheep metallothionein promoter. These transgenic mice were originally generated in (C57BL/6 x SJL) ES cells and bred onto a B10.BR for more than 10 generations. Tg mice express the allogenic H-2Kb molecule mostly in hepatocytes as well as in some bone marrow derived cells in lymph nodes and spleen (low expression).|Same as homozygous mice |B10.BR|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|03-Jun-2022|Cryopreserved sperm|50.0|0.0|Unknown|||Possibly| 6957.0|ENU20:006:a:B6:G3|ANU:ENU20:006:a:G3||Recessive|Unknown||||||||Unknown||||||||||||||||Unknown|||||||||||||Unknown|Unknown|C57BL/6JAnu|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||1||No|05-Jul-2012|Cryopreserved sperm|39.0|0.0|Unknown||ENU, random, mutagenesis, screen|Yes| 5633.0|Backcross B6xCav-1 KO||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 216.0|Nodal floxed|Nodal||Dominant|Nodal|Nodal|Unknown|early embryo mesoderm formation, Tg.413d|MGI:97359|targeted mutation 1, Michael R Kuehn|Nodal|MGI:2158730|10||||||||||||||||Yes|||||||||||||The floxed allele is hypomorphic. Mice homozygote for this floxed allele are viable and fertile. ||C57BL/6 x 129/Sv|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|24-Apr-2006||0.0|0.0|Unknown||nodal, mesoderm, left / right axis, signalling, endodermal|Yes| 7281.0|Sppl2a KO2|C57BL/6N-A Sppl2a/2MarpAnu||Recessive|signal peptide peptidase like 2A|Sppl2a|Unknown|2010106G01Rik, C130089K23Rik|MGI:1913802|signal peptide peptidase like 2A; targeted mutation 1a, Helmholtz Zentrum Muenchen GmbH|Sppl2a|MGI:4887673|2|||||||||||||||||||||||||||||Unknown|Unknown|C57BL/6NCrlAnu|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|15-Feb-2013|Cryopreserved sperm|40.0|0.0|Unknown|||Possibly| 248.0||Stock-TgN(CDX)||Recessive|caudal type homeo box 1|Cdx1|Unknown|Cdx, Cdx-1|MGI:88360||||18||||||||||||||||No|||||||||||||Homozygous mutation of this gene results in abnormalities of the basiocciptal bone, vertebrae, and ribs.|||Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|26-Apr-2006||0.0|0.0|Unknown|||Yes| 4550.0||B6.129-Rnf2/WehiApb||Recessive|ring finger protein 2|Rnf2|Nil|dinG, Ring1B|MGI:1101759|targeted mutation 1, Haruhiko Koseki|Rnf2|MGI:2447529|1||||||||||||||||Yes|||||||||||||Abnormal sternum ossification* additional ossification at the cranial end of the sternumThoracic vertebral transformation * spinous process of thoracic vertebra 2 found on thoracic vertebra 1 in 40% of mice (T1 becomes T2)Cervical vertebral transformation * ectopic ribs are associated with cervical vertebra 7 in about 60% of mice (C7 becomes T1)||C57BL/6|No|No|Yes|No|No|Yes|No|Good|10||Het x WT|No|02-Mar-2009|Cryopreserved sperm|60.0|0.0|Unknown||Polycomb group proteins, polycomb repressive complex 1, skeletal|Yes| 5760.0|EPHA1 KO||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 240.0|MLR37|FVB/N-Tg(Cryaa-cre)37Mlr/Apb||Dominant||||||||||||||||||||||||||transgene insertion 37, Mike Robinson|modified alpha A crystallin promoter with an inserted copy of Pax6 consensus binding site|||||||||||Mice express Cre in lens fibres and retina and ciliary body with weak ectopic expression in skin and CNS.||FVB/N|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|25-Apr-2006|Cryopreserved sperm|40.0|0.0|Unknown||crystallin, lens, eye, epithelial, Pax6|Yes| 249.0||Balb/c-Cd40/Apb||Recessive|CD40 antigen|Cd40|Unknown|Bp50, Cd40, p50, Tnfrsf5|MGI:88336|targeted mutation 1, Hitoshi Kikutani|Cd40|MGI:1857457|2||||||||||||||||Yes|||||||||||||Absence of germinal center formation in response to TI-I antigen stimulation. Defective IgM and IgG response to TI antigen and TD antigen stimulation. Decreased IgG2b||Balb/c|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|26-Apr-2006|Cryopreserved sperm|105.0|0.0|Unknown||B cell, germinal centre, T cell dependent, immunoglobulin class switch|Yes| 6498.0|PKCe?|B6.129P2-Prkce/Ausb||Recessive|protein kinase C, epsilon|Prkce|Nil|5830406C15Rik, PKC[e], Pkce, PKCepsilon|MGI:97599|protein kinase C, epsilon; targeted mutation 1, Michael Leitges|Prkce|MGI:2680163|17|||||||||||||||||||||||||||||Unknown|Unknown|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown||Protein kinase Cepsilon, Diabetes|Yes| 9284.0|Six2TGC|CD1-Tg(Six2-EGFP/cre)1Amc/Apb||Semi-dominant|sine oculis-related homeobox 2|Six2|||MGI:102778 ||||17|||||||||||||||||Six2-EGFP/Cre BAC transgene|Six2|||||||||||Viable homozygous Six2TGC mice are not produced by intercross of heterozygous animals. Homozygous Six2TGC mice are assumed to die during development via an unknown mechanism.|Hemizygous Six2-TGCtg mice are viable and fertile. A slight reduction in kidney size during development, and ~20-30% reduction in nephrons in adults has been identified after detailed phenotypic analysis.|CD1|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|06-Oct-2021|Cryopreserved sperm|50.0|0.0|Unknown|||Possibly| 7708.0|Adra1ackO|B6.Cg-Adra1a Tg(Myh6-cre/Esr1*)1Jmk/JVccrApb||Recessive|adrenergic receptor, alpha 1a|Adra1a||Adra1c|MGI:104773||||14|||||||||||||||||transgene insertion 1, Jeffery D Molkentin|mouse cardiac-specific alpha-myosin heavy chain|heart||||||||||Unknown|Unknown|C57BL/6J|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|25-Jun-2014|Cryopreserved sperm|50.0|0.0|Unknown|||Possibly| 30.0|B-blast|C57BL/6JSfdAnu-Trp53/AnuApb|C57BL/6JSfdAnu-Trp53/AnuApb|Semi-dominant|transformation related protein 53|Trp53|Unknown|p53|MGI:98834|b-blast|Trp53|MGI:3611496|11|ENSMUSG00000059552|ENSMUST00000108658|Trp53-201||1111|T to A|||195|Isoleucine to Asparagine||||||No|||||||||||||Homozygotes develop B cell leukaemia/lymphoma or primitive haemopoietic leukaemia at 4-6 mths. |Heterozygotes develop solid tumours osteosarcoma, lymphoma, haemangiosarcoma, fibrosarcoma, thymic lymphoma, multinodal lymphoma, brain tumour and teratocarcinoma at 8-15mths.|C57BL/6JSfdAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||13||No|06-Feb-2006|Cryopreserved sperm|110.0|0.0|Yes||p53, apoptosis, tumour, cell cycle, ENU|Yes| 4186.0|CD151 KO|FVB.B6(C)-CD151/Apb|FVB.B6(C)-CD151/Apb|Recessive|CD151 antigen|Cd151|Nil|PETA-3, SFA-1, Tspan24|MGI:1096360|targeted mutation 1, Leonie K Ashman|Cd151|MGI:3050539|7||||||||||||||||Yes|||||||||||||Mice have kidney defects and eventually develop kidney failure due to problems with glomerular basement membrane formation and maintenance. Mutation is lethal in all cases, at from 4 months to 6 months of age. ||FVB/N|Yes|Yes|Yes|Yes|Yes|Yes|No|Poor|10|||No|19-Dec-2008|Cryopreserved sperm|150.0|0.0|Unknown||tetraspanin, proteinuria, kidney, integrin, Alport syndrome|Yes| 6500.0|PKCET2?|B6.129T2-Prkce/Ausb||Recessive|protein kinase C, epsilon|Prkce|Nil|5830406C15Rik, PKC[e], Pkce, PKCepsilon|MGI:97599|protein kinase C, epsilon; targeted mutation 1, Michael Leitges|Prkce|MGI:2680163|17|||||||||||||||||||||||||||||Unknown|Unknown|129T2|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown||Protein kinase Cepsilon, Diabetes|Yes| 236.0|LoxP/b-catenin|B6.129-Ctnnb1||Recessive|catenin (cadherin associated protein), beta 1|Ctnnb1|Normal|beta-catenin, cadherin associated protein, Catnb|MGI:88276|targeted mutation 4, Walter Birchmeier|Ctnnb1|MGI:2148594|9||||||||||||||||Yes|||||||||||||Normal||C57BL/6 x 129|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|25-Apr-2006||0.0|0.0|Unknown||Catenin, hair, follicle, stem cell, skin, differentiation|Yes| 7712.0|H2A.Lap1:NM5|FVB/NJArc-H2afb2 H2afb3 Gm14920/AnuApb||X-linked|H2A histone family, member B2|H2afb2|Nil|EG624153, H2A.Bbd4, H2afb2-ps (lap1c)|MGI:3644980||||X|||||||||||||||||||||||||||||Normal. Small percentage dies when reaches the age of 7-9 months. Under investigation|Normal. Small percentage dies when reaches the age of 7-9 months. Under investigation|FVB/NJArc|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|3||het to wt; homo to wt; homo to homo|No|30-Jun-2014||0.0|0.0|Unknown||H2A.Lap1, histone, NM10|Possibly| 7712.0|H2A.Lap1:NM5|FVB/NJArc-H2afb2 H2afb3 Gm14920/AnuApb||X-linked|H2A histone family, member B3|H2afb3|Nil|EG624957, H2A.Bbd3, H2afb3-ps (Lap1a)|MGI:3644875||||X|||||||||||||||||||||||||||||Normal. Small percentage dies when reaches the age of 7-9 months. Under investigation|Normal. Small percentage dies when reaches the age of 7-9 months. Under investigation|FVB/NJArc|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|3||het to wt; homo to wt; homo to homo|No|30-Jun-2014||||Unknown||H2A.Lap1, histone, NM10|Possibly| 7712.0|H2A.Lap1:NM5|FVB/NJArc-H2afb2 H2afb3 Gm14920/AnuApb||X-linked|predicted pseudogene 14920|Gm14920||ENSMUSG00000067441, H2A.Bbd1 (lap1b)|MGI:3642445||||X|||||||||||||||||||||||||||||Normal. Small percentage dies when reaches the age of 7-9 months. Under investigation|Normal. Small percentage dies when reaches the age of 7-9 months. Under investigation|FVB/NJArc|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|3||het to wt; homo to wt; homo to homo|No|30-Jun-2014||||Unknown||H2A.Lap1, histone, NM10|Possibly| 7031.0|APN 235|C57BL/6N-Cdcp1/Marp||Recessive|CUB domain containing protein 1|Cdcp1 |Unknown|9030022E12Rik, E030027H19Rik |MGI:2442010 |CUB domain containing protein 1; targeted mutation 1, Wellcome Trust Sanger Institute |Cdcp1|MGI:4419722|9||||||||||||||||Yes|||||||||||||Unknown - Not bred to homozygocity |Normal |C57BL/6N |Unknown|Unknown|Unknown|Unknown|Unknown|Yes|No|Unknown||||No|30-Jul-2012|Cryopreserved sperm|50.0|0.0|Unknown||ES cell|Possibly| 10317.0|Foxn1-Cre|B6;D2-Tg(Foxn1-cre)8Ghr/Apb||Semi-dominant|forkhead box N1|Foxn1||D11Bhm185e, Hfh11, whn|MGI:102949||||11|||||||||||||||||Cre|Foxn1|||||||||||Mice express Cre under the control of a Foxn1 promoter|Mice express Cre under the control of a Foxn1 promoter|C57Bl/6J|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|22-Mar-2023||0.0|0.0|Unknown|||Possibly| 5499.0|Twist-delBp|B6;129-Twist1/WchriApb||Semi-dominant|twist gene homolog 1 (Drosophila)|Twist1|Nil|charlie chaplin, M-Twist, pdt, Pluridigite, Skam10Jus, Ska10|MGI:98872|targeted mutation 1, Richard R Behringer|Twist1|MGI:1857265|12||||||||||||||||Yes|||||||||||||Homozygous mutant embyros have neural tube defects and die around E11.|Heterozygous mutants are viable and exhibit features of human Saethre-Chotzen syndrome, including hindlimb polydactyly, craniofacial defects, long bone abnormalities, an abnormal gait and a small size.|C57BL/6|No|No|Yes|No|No|Yes|No|Unknown|1|||No|04-May-2011|Cryopreserved sperm|20.0|0.0|Yes||polydactyly, neural tube, mesenchyme, cranial, morphogenesis|Yes| 7711.0|H2A.Lap1:NM10|FVB/NJArc-H2afb2 H2afb3 Gm14920/AnuApb||X-linked|H2A histone family, member B2|H2afb2|Nil|EG624153, H2A.Bbd4, H2afb2-ps (lap1c)|MGI:3644980||||X|||||||||||||||||||||||||||||Normal. Small percentage dies when reaches the age of 7-9 months. Under investigation|Normal. Small percentage dies when reaches the age of 7-9 months. Under investigation|FVB/NJArc|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|3||het to wt; homo to wt; homo to homo|No|30-Jun-2014|Cryopreserved sperm|103.0|0.0|Unknown||H2A.Lap1, histone, NM10|Possibly| 7711.0|H2A.Lap1:NM10|FVB/NJArc-H2afb2 H2afb3 Gm14920/AnuApb||X-linked|H2A histone family, member B3|H2afb3|Nil|EG624957, H2A.Bbd3, H2afb3-ps (Lap1a)|MGI:3644875||||X|||||||||||||||||||||||||||||Normal. Small percentage dies when reaches the age of 7-9 months. Under investigation|Normal. Small percentage dies when reaches the age of 7-9 months. Under investigation|FVB/NJArc|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|3||het to wt; homo to wt; homo to homo|No|30-Jun-2014|Cryopreserved sperm|||Unknown||H2A.Lap1, histone, NM10|Possibly| 7711.0|H2A.Lap1:NM10|FVB/NJArc-H2afb2 H2afb3 Gm14920/AnuApb||X-linked|predicted pseudogene 14920|Gm14920||ENSMUSG00000067441, H2A.Bbd1|MGI:3642445||||X|||||||||||||||||||||||||||||Normal. Small percentage dies when reaches the age of 7-9 months. Under investigation|Normal. Small percentage dies when reaches the age of 7-9 months. Under investigation|FVB/NJArc|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|3||het to wt; homo to wt; homo to homo|No|30-Jun-2014|Cryopreserved sperm|||Unknown||H2A.Lap1, histone, NM10|Possibly| 5466.0|MCP1 KO|B6.129S4-Ccl2/JApb||Recessive|chemokine (C-C motif) ligand 2|Ccl2|Nil|HC11, MCAF, MCP-1, MCP1, monocyte chemoattractant protein-1, monocyte chemotactic protein, Scya2, Sigje, SMC-CF|MGI:98259|chemokine (C-C motif) ligand 2; targeted mutation 1, Barrett J Rollins|Ccl2|MGI:2175911|11||||||||||||||||No|||||||||||||Increased CD4-positive T cell number: in an EAE model, mutants show an increase in proportion of CD4+ cells and reduction in CD11b+CD4- in the CNS leukocyte infiltrates compared to wild-type, although total numbers of T cells are not different.Decreased leukocyte cell number: numbers of leukocytes isolated from CNS tissue during EAE attacks are about 1/3 of those from wild type mice with comparable EAE severity.Decreased macrophage cell number: age-dependent accumulation of macrophages in the choroids is less than in wild-type mice.Increased neutrophil cell number: 1 and 3 days after femoral artery excision, mice exhibit an earlier increase in neutrophil accumulation (measured by MPO activity) than in similarly treated wild-type mice.Increased osteoclast cell number: * at P5 during tooth eruption * peak osteoclast accumulation occurs at P5 instead of at P9 as in wild-type mice.Abnormal chemokine level: * in thioglycollate- or zymosan- induced peritonitis models, no Ccl2 is detected while reduce levels of Ccl7 are present in peritoneal fluid. * 1 day after femoral artery excision, muscles accumulate more chemoattractants (KC and MIP-2) than in similarly treated wild-type mice.Increased IgG level * at 16 months, IgG is present in the retinal pigmented epithelium or choroids unlike in wild-type mice. * IgG light chain deposition in the retinal pigmented epithelium accumulates with age unlike in wild-type mice.Increased IgG1 level: significantly higher levels of anti-MOG35-55 IgG1 antibodies are seen in mutants compared to wild-typeAbnormal macrophage recruitment: * the timing of macrophage recruitment during tooth eruption is different than in wild-type mice with peak numbers occurring earlier than in wild-type mice. * the total number of macrophages recruited is normalImpaired macrophage recruitment: * mutants show impaired macrophage recruitment to the CNS after MOG35-55 induced EAE. * only half the number of macrophages are recruited to the peritoneum in an induced peritonitis model as occurs in wild-type controls. * initially following femoral artery excision.Abnormal neutrophil physiology: the number of neutrophils recruited to the peritoneum in an induced peritonitis model is almost double that controls.Abnormal cytokine secretion: MOG35-55-specific Th1 cytokine responses are diminished in mutants.Abnormal chemokine secretion: * there is no Ccl2 (MCP-1) secretion by peritoneal macrophages activated in vitro compared to controls * secretion of Ccl7 (MCP-3) and Ccl12 (MCP-5) is also dramatically reduced by these activated macrophages.Decreased interferon-gamma secretion: mutants exhibit reduced production of IFN-gamma in response to MOG35-55 induced EAE.Increased interleukin-10 secretion: mutants exhibit enhanced secretion of IL-10 in response to MOG35-55 induced EAE.Decreased susceptibility to experimental autoimmune encephalomyelitis: * homozygotes are resistant to active experimental autoimmune encephalomyelitis (EAE) induction with MOG35-55, with delayed onset of disease, reduced inflammatory reaction including impaired recruitment of macrophages to the central nervous system (CNS), and faster and complete recovery * adoptive transfer of primed T cells from wild-type mice to naive homozygous mutant recipients does not mediate clinical EAE, however wild-type mice receiving mutant T cells do develop clinical EAE.Retinal photoreceptor degeneration: at 16 months.Abnormal retinal pigment epithelium morphology: * after 9 months of age, lipofuscin granules are observed in the swollen and vacuolated retinal pigmented epithelial cells unlike in wild-type mice. * at 16 months, mice exhibit attenuation of the retinal pigmented epithelium unlike in wild-type mice.Abnormal choroid morphology: age-dependent accumulation of macrophages in the choroids is less than in wild-type miceAbnormal choriocapillaris morphology: at 16 months, mice exhibit dilation and attenuation of the choriocapillaris unlike wild-type mice.Choroidal neovascularization: * at 15 to 19 months, mice exhibit intrachoroidal neovascularization with angiographic leakage unlike wild-type mice. * after 18 months, 4 of 15 mice exhibit choroidal neovascularization with angiographic leakage unlike in wild-type mice. * between 18 and 27 months, neovasculatization breaches the Bruch membrane and causes retinal pigmented epithelium and photoreceptor disruptions unlike in wild-type mice.Abnormal Bruch membrane morphology: * the Bruch membrane is thickened compared to in wild-type mice after 9 months of age * at 20 months, the outer Bruch membrane is breached by choriocapillary processes unlike in wild-type mice.Retinal outer nuclear layer degeneration: at 16 months.Retinal degeneration: * at 16 months, mice exhibit progressive outer retinal degeneration and confluent areas of visible atrophy unlike in wild-type mice * at 18 months, mice exhibit geographic atrophy unlike in wild-type mice.Retinal deposits: after 9 months of age, mice exhibit subretinal deposits similar to drusen that increase with age unlike in wild-type mice.Alcohol aversion: in female mice.Alcohol preference: * male mice exhibit a greater ethanol preference compared with wild-type (in post hoc analysis) mice, Ccr2 homozygotes, and Ccl2 Ccr2 double homozygotes * female mice exhibit a greater ethanol preference compared with Ccl2 Ccr2 double homozygotes and Ccr2 homozygotes.Decreased drinking behavior: of an ethanol solution in female mice.Decreased alcohol consumption: in female mice compared with wild-type mice and Ccr2 homozygotes.Increased drinking behavior: * mice exhibit increased drinking of an ethanol solution compared with Ccl2 Ccr2 double homozygotes and Ccr2 homozygotes. * mice exhibit increased drinking of a quinine solution compared with wild-type mice.Increased alcohol consumption: * male mice consume more ethanol than wild-type (in post hoc analysis) mice and Ccl2 Ccr2 double homozygotes. * female mice consume more ethanol than Ccl2 Ccr2 double homozygotes.Abnormal conditioned taste aversion behavior: * mice exhibit a stronger response to ethanol in an ethanol-induced conditioned taste aversion test compared with similarly treated wild-type mice * however, saccharin consumption is normal.Impaired righting response: mice exhibit longer duration of ethanol-induced loss of righting response compared with similarly treated wild-type mice.Abnormal choriocapillaris morphology: at 16 months, mice exhibit dilation and attenuation of the choriocapillaris unlike wild-type mice.Choroidal neovascularization: * at 15 to 19 months, mice exhibit intrachoroidal neovascularization with angiographic leakage unlike wild-type mice. * after 18 months, 4 of 15 mice exhibit choroidal neovascularization with angiographic leakage unlike in wild-type mice. * between 18 and 27 months, neovasculatization breaches the Bruch membrane and causes retinal pigmented epithelium and photoreceptor disruptions unlike in wild-type mice.Abnormal blood circulation: following femoral artery excision, mice exhibit a delay in the restoration of perfusion compared with similarly treated wild-type mice.Retinal photoreceptor degeneration: at 16 months.Abnormal retinal pigment epithelium morphology: * after 9 months of age, lipofuscin granules are observed in the swollen and vacuolated retinal pigmented epithelial cells unlike in wild-type mice. * at 16 months, mice exhibit attenuation of the retinal pigmented epithelium unlike in wild-type mice.Lipofuscinosis: after 9 months of age, lipofuscin granules are observed in the swollen and vacuolated retinal pigmented epithelial cells unlike in wild-type mice.Accelerated tooth eruption: * tooth eruption begins at P14 instead of P16 as in wild-type mice. * from P16 to P18, mice exhibit a 31-fold increase in erupted cusps compared with wild-type mice.Increased osteoclast cell number: at P5 during tooth eruptionpeak osteoclast accumulation occurs at P5 instead of at P9 as in wild-type mice.Increased muscle weight: after 1 and 7 days, mice subjected to femoral artery excision exhibit an extended period of increased ischemic muscle weight compared with similarly treated wild-type mice.Abnormal skeletal muscle morphology: following femoral artery excision, muscles accumulate more adipocytes than in similarly treated wild-type mice.Skeletal muscle necrosis: following femoral artery excisionAbnormal muscle regeneration: muscle regeneration, as measured by LDH and fiber size, is impaired following femoral artery excision.||(129S4/SvJae x C57BL/6)F1|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|22-Mar-2011|Cryopreserved sperm|50.0|0.0|Yes|Macular Degeneration, Age-Related, 2; ARMD2|monocyte, chemokine, cytokines|Possibly| 9419.0|Plag1–/–|129- Plag1/Apb||Dominant|pleiomorphic adenoma gene 1|Plag1|||MGI:1891916|pleiomorphic adenoma gene 1; targeted mutation 1, Wim J M Van de Ven|Plag1|MGI:3580633|4||||||||||Unknown to Unknown||||||||||||||||||| No anatomical differences are obvious at birth, except that the weight of Plag1–/– mice is significantly lower in comparison to control litter mates. This early growth retardation is maintained throughout adult life with proportionally smaller organs except for the disproportionally small seminal vesicles and ventral prostate; however, plasma testosterone levels in males were not affected. Furthermore, fertility of both male and female Plag1–/– is reduced.|Normal|129S1/Sv|Yes|Yes|Yes|Yes|Yes|Yes|Yes|Poor||||No|17-Aug-2022|Cryopreserved sperm|80.0|0.0|Unknown|||Yes| 4813.0|Binda|ENU8BAT:075||Recessive|||||||||Unknown|||||||||||||||||transgene insertion 3, Christopher C Goodnow|Rat insulin promoter|Expression of the inserted sequence specifically to pancreatic islet beta cells||||||||||Mice carrying the ins-HEL gene have a subclinical predisposition to diabetes due to islet cell failure. Mice carrying the insHEL and TCR transgenes have asubclinical predisposition to autoimmune destruction of the beta cell. Screening mice by urine glucose test. High glucose levels indicate diabetes and thus autoimmunity. "Early onset diabetes" definition changed during screen from approx 80 days to 40 days.||C57BL/6 x CBA x C57BL/10BR|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|||Breed diabetic Double transgenic with a non transgenic sib for next generation|No|24-Sep-2009|Cryopreserved sperm|30.0|0.0|Yes|Type I Diabetes|ENU, Singapore, autoimmunity, T cell, B cell, glucose|Possibly| 4813.0|Binda|ENU8BAT:075||Recessive||||||||||||||||||||||||||transgene insertion 1, Mark M Davis||||||||||||Mice carrying the ins-HEL gene have a subclinical predisposition to diabetes due to islet cell failure. Mice carrying the insHEL and TCR transgenes have asubclinical predisposition to autoimmune destruction of the beta cell. Screening mice by urine glucose test. High glucose levels indicate diabetes and thus autoimmunity. "Early onset diabetes" definition changed during screen from approx 80 days to 40 days.||C57BL/6 x CBA x C57BL/10BR|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|||Breed diabetic Double transgenic with a non transgenic sib for next generation|No|24-Sep-2009|Cryopreserved sperm|||Yes|Type I Diabetes|ENU, Singapore, autoimmunity, T cell, B cell, glucose|Possibly| 7523.0|NOD.Beta|NOD-Tg(TcrVβ11)1Gem/ArcApb||Dominant||||||||||||||||||||||||||T cell receptor||||||||||||Normal||NOD/Lt|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|29-Nov-2013|Embryo|0.0|0.0|Unknown||T cell receptor|Yes| 4816.0|Warroo|ENU8BAT:084||Recessive|||||||||Unknown|||||||||||||||||transgene insertion 3, Christopher C Goodnow|Rat insulin promoter|Expression of the inserted sequence specifically to pancreatic islet beta cells||||||||||Mice carrying the ins-HEL gene have a subclinical predisposition to diabetes due to islet cell failure. Mice carrying the insHEL and TCR transgenes have asubclinical predisposition to autoimmune destruction of the beta cell. Screening mice by urine glucose test. High glucose levels indicate diabetes and thus autoimmunity. "Early onset diabetes" definition changed during screen from approx 80 days to 40 days.||C57BL/6 x C57BL/10BR x CBA|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|||Breed diabetic Double transgenic with a non transgenic sib for next generation|No|24-Sep-2009|Cryopreserved sperm|35.0|0.0|Yes|Type I Diabetes|ENU, Singapore, autoimmunity, T cell, B cell, glucose|Possibly| 4816.0|Warroo|ENU8BAT:084||Recessive||||||||||||||||||||||||||transgene insertion 1, Mark M Davis||||||||||||Mice carrying the ins-HEL gene have a subclinical predisposition to diabetes due to islet cell failure. Mice carrying the insHEL and TCR transgenes have asubclinical predisposition to autoimmune destruction of the beta cell. Screening mice by urine glucose test. High glucose levels indicate diabetes and thus autoimmunity. "Early onset diabetes" definition changed during screen from approx 80 days to 40 days.||C57BL/6 x C57BL/10BR x CBA|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|||Breed diabetic Double transgenic with a non transgenic sib for next generation|No|24-Sep-2009|Cryopreserved sperm|||Yes|Type I Diabetes|ENU, Singapore, autoimmunity, T cell, B cell, glucose|Possibly| 4817.0|Apari|ENU8BAT:091||Recessive|||||||||Unknown|||||||||||||||||transgene insertion 3, Christopher C Goodnow|Rat insulin promoter|Expression of the inserted sequence specifically to pancreatic islet beta cells||||||||||Mice carrying the ins-HEL gene have a subclinical predisposition to diabetes due to islet cell failure. Mice carrying the insHEL and TCR transgenes have asubclinical predisposition to autoimmune destruction of the beta cell. Screening mice by urine glucose test. High glucose levels indicate diabetes and thus autoimmunity. "Early onset diabetes" definition changed during screen from approx 80 days to 40 days.||C57BL/6 x C57BL/10BR x CBA|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|||Breed diabetic Double transgenic with a non transgenic sib for next generation|No|24-Sep-2009|Cryopreserved sperm|55.0|0.0|Yes|Type I Diabetes|ENU, Singapore, autoimmunity, T cell, B cell, glucose|Possibly| 4817.0|Apari|ENU8BAT:091||Recessive||||||||||||||||||||||||||transgene insertion 1, Mark M Davis||||||||||||Mice carrying the ins-HEL gene have a subclinical predisposition to diabetes due to islet cell failure. Mice carrying the insHEL and TCR transgenes have asubclinical predisposition to autoimmune destruction of the beta cell. Screening mice by urine glucose test. High glucose levels indicate diabetes and thus autoimmunity. "Early onset diabetes" definition changed during screen from approx 80 days to 40 days.||C57BL/6 x C57BL/10BR x CBA|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|||Breed diabetic Double transgenic with a non transgenic sib for next generation|No|24-Sep-2009|Cryopreserved sperm|||Yes|Type I Diabetes|ENU, Singapore, autoimmunity, T cell, B cell, glucose|Possibly| 7375.0|ENU19:B6:Mlkl|C57BL6NCrlAnu-Mlkl/Anu||Recessive|mixed lineage kinase domain-like|Mlkl||9130019I15Rik|MGI:1921818||Mlkl||8|ENSMUSG00000012519|ENSMUST00000120432|Mlkl-002|949|1305|T to A|ENSMUSE00000214984|7|317|Arginine to STOP|||||ACAGGCTACACCATTCGGAAACACTCCACAGAAACATCAGCAGCTCCAGTTTCCTCGTAGC||||||||||||||||C57BL/6NCrlAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|11-Jul-2013|Cryopreserved sperm|30.0|0.0|Unknown||ENU|Yes| 7713.0|Zdhhc2|C57BL/6N-Zdhhc2/MarpApb||Dominant|zinc finger, DHHC domain containing 2|Zdhhc2|Nil|5730415P04Rik, 6430583A19Rik|MGI:1923452|zinc finger, DHHC domain containing 2; targeted mutation 1a, Wellcome Trust Sanger Institute|Zdhhc2|MGI:4362764|8|||||||||||||||||||||||||||||wildtype|wildtype|C57BL/6N|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|2|4||No|01-Jul-2014|Cryopreserved sperm|50.0|0.0|Unknown||palmitoylation|Possibly| 10316.0|Mr1-K43A|C57BL/6J-Mr1<(tm1K43A)JvUom>/Apb||Semi-dominant|major histocompatibility complex, class I-related|Mr1||H2ls, MR1|MGI:1195463||Mr1||1|||||||||||||||||||||||||||||Normal|Normal|C57Bl/6J|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|15-Mar-2023|Cryopreserved sperm|50.0|0.0|Unknown|||Possibly| 4819.0||ENU8BAT:097||Recessive|||||||||Unknown|||||||||||||||||transgene insertion 3, Christopher C Goodnow|Rat insulin promoter|Expression of the inserted sequence specifically to pancreatic islet beta cells||||||||||Mice carrying the ins-HEL gene have a subclinical predisposition to diabetes due to islet cell failure. Mice carrying the insHEL and TCR transgenes have asubclinical predisposition to autoimmune destruction of the beta cell. Screening mice by urine glucose test. High glucose levels indicate diabetes and thus autoimmunity. "Early onset diabetes" definition changed during screen from approx 80 days to 40 days.||C57BL/6 x C57BL/10BR x CBA|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|||Breed diabetic Double transgenic with a non transgenic sib for next generation|No|24-Sep-2009|Cryopreserved sperm|30.0|0.0|Yes|Type I Diabetes|ENU, Singapore, autoimmunity, T cell, B cell, glucose|No| 4819.0||ENU8BAT:097||Recessive||||||||||||||||||||||||||transgene insertion 1, Mark M Davis||||||||||||Mice carrying the ins-HEL gene have a subclinical predisposition to diabetes due to islet cell failure. Mice carrying the insHEL and TCR transgenes have asubclinical predisposition to autoimmune destruction of the beta cell. Screening mice by urine glucose test. High glucose levels indicate diabetes and thus autoimmunity. "Early onset diabetes" definition changed during screen from approx 80 days to 40 days.||C57BL/6 x C57BL/10BR x CBA|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|||Breed diabetic Double transgenic with a non transgenic sib for next generation|No|24-Sep-2009|Cryopreserved sperm|||Yes|Type I Diabetes|ENU, Singapore, autoimmunity, T cell, B cell, glucose|No| 5761.0|EPHA2 KO||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 3446.0|OT-II / Bim KO|Un-Bcl2l11 Tg(TcraTcrb)425Cbn/Wehi||Recessive|BCL2-like 11 (apoptosis facilitator)|Bcl2l11|Nil|1500006F24Rik, Bim, Bod|MGI:1197519|targeted mutation 1.1, Andreas Strasser|Bcl2l11|MGI:2156498|2||||||||||||||||Yes|transgene insertion 425, Frank Carbone||||||||||||Bim KO clone 266 females may not have vaginal opening. These results demonstrate that TCR/CD3-stimulation-induced killing of semimature CD4+CD8-HSA+ thymocytes in vivo requires the BH3-only protein Bim and can be inhibited by Bcl-2 but occurs independently of Fas-signaling. Data indicate that the deletion of potentially deleterious autoreactive immature CD4+8+ thymocytes as well as semimature CD4+8-HSA+ thymocytes requires the BH3-only protein Bim. The deletion process is largely independent of the Apaf-1/caspase-9 apoptosome and does not require death receptor signaling.|||Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|17-Jul-2008||0.0|0.0|Unknown||T cell, selection, tolerance, CD4 , CD8, ovalbumin|Yes| 4821.0|Myndee|ENU8CAT:017||Recessive|||||||||Unknown|||||||||||||||||transgene insertion 3, Christopher C Goodnow|Rat insulin promoter|Expression of the inserted sequence specifically to pancreatic islet beta cells||||||||||Mice carrying the ins-HEL gene have a subclinical predisposition to diabetes due to islet cell failure. Mice carrying the insHEL and TCR transgenes have asubclinical predisposition to autoimmune destruction of the beta cell. Screening mice by urine glucose test. High glucose levels indicate diabetes and thus autoimmunity. "Early onset diabetes" definition changed during screen from approx 80 days to 40 days.||C57BL/6 x C57BL/10BR x CBA|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|||Breed diabetic Double transgenic with a non transgenic sib for next generation|No|24-Sep-2009|Cryopreserved sperm|45.0|0.0|Yes|Type I Diabetes|ENU, Singapore, autoimmunity, T cell, B cell, glucose|No| 4821.0|Myndee|ENU8CAT:017||Recessive||||||||||||||||||||||||||transgene insertion 1, Mark M Davis||||||||||||Mice carrying the ins-HEL gene have a subclinical predisposition to diabetes due to islet cell failure. Mice carrying the insHEL and TCR transgenes have asubclinical predisposition to autoimmune destruction of the beta cell. Screening mice by urine glucose test. High glucose levels indicate diabetes and thus autoimmunity. "Early onset diabetes" definition changed during screen from approx 80 days to 40 days.||C57BL/6 x C57BL/10BR x CBA|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|||Breed diabetic Double transgenic with a non transgenic sib for next generation|No|24-Sep-2009|Cryopreserved sperm|||Yes|Type I Diabetes|ENU, Singapore, autoimmunity, T cell, B cell, glucose|No| 7524.0|3R.B6|3R.B6||Recessive||||||||||||||||||||||||||||||||||||||Normal||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|29-Nov-2013|Embryo|0.0|0.0|Unknown|||Yes| 6821.0|A/J gp130Y757F|A/J(Cg)-IL6st/LudApb||Dominant|interleukin 6 signal transducer|Il6st|Normal|CD130, D13Ertd699e, gp130|MGI:96560|interleukin 6 signal transducer; targeted mutation 1, Matthias Ernst|Il6st|MGI:2388478|13||||||||||||||||Yes|||||||||||||Gastric tumors; splenomegaly; thrombocytosis; lymphadenopathy; multi-organ inflammation.|Gastric tumors; splenomegaly; thrombocytosis; lymphadenopathy; multi-organ inflammation.|A/J|Yes|Yes|Yes|Yes|Yes|Yes|Yes|Good|4|||No|15-Feb-2012|Cryopreserved sperm|50.0|0.0|Unknown||signal transduction, JAK-STAT, cytokine, interferon, kinase, phosphorylation|Yes| 3419.0|OT-1 / Bim KO|C57BL/6-Bcl2l11 Tg(TcraTcrb)1100Mjb/Wehi||Dominant|BCL2-like 11 (apoptosis facilitator)|Bcl2l11|Nil|1500006F24Rik, Bim, Bod|MGI:1197519|BCL2-like 11 (apoptosis facilitator); targeted mutation 1.1, Andreas Strasser|Bcl2l11|MGI:2156498|2||||||||||||||||Yes|transgene insertion 1100, Michael J Bevan|H-2Kb promoter|||||||||||Cross used to create Bim knockout, OVA specific CD8 T cells.Bim -/- females often lack vaginal opening.||C57BL/6|No|No|Yes|Yes|No|Yes|No|Unknown|10|||No|14-Jul-2008||0.0|0.0|Unknown||T cell, receptor (TCR), ovalbumin, autoimmunity, Bcl-2|Yes| 6489.0|VILcre|B6.SJL-Tg(Vil-cre)997Gum/JAusb||Dominant||||||||||||||||||||||||||transgene insertion 997, Deborah L Gumucio|A 12.4-kb promoter fragment from the villin 1 gene|||||||||||Unknown|Unknown|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown||Villin, Intestine|Yes| 4823.0|Teangi|ENU8CAT:027||Recessive|||||||||Unknown|||||||||||||||||transgene insertion 3, Christopher C Goodnow|Rat insulin promoter|Expression of the inserted sequence specifically to pancreatic islet beta cells||||||||||Mice carrying the ins-HEL gene have a subclinical predisposition to diabetes due to islet cell failure. Mice carrying the insHEL and TCR transgenes have asubclinical predisposition to autoimmune destruction of the beta cell. Screening mice by urine glucose test. High glucose levels indicate diabetes and thus autoimmunity. "Early onset diabetes" definition changed during screen from approx 80 days to 40 days.||C57BL/6 x C57BL/10BR x CBA|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|||Breed diabetic Double transgenic with a non transgenic sib for next generation|No|24-Sep-2009|Cryopreserved sperm|45.0|0.0|Yes|Type I Diabetes|ENU, Singapore, autoimmunity, T cell, B cell, glucose|No| 4823.0|Teangi|ENU8CAT:027||Recessive||||||||||||||||||||||||||transgene insertion 1, Mark M Davis||||||||||||Mice carrying the ins-HEL gene have a subclinical predisposition to diabetes due to islet cell failure. Mice carrying the insHEL and TCR transgenes have asubclinical predisposition to autoimmune destruction of the beta cell. Screening mice by urine glucose test. High glucose levels indicate diabetes and thus autoimmunity. "Early onset diabetes" definition changed during screen from approx 80 days to 40 days.||C57BL/6 x C57BL/10BR x CBA|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|||Breed diabetic Double transgenic with a non transgenic sib for next generation|No|24-Sep-2009|Cryopreserved sperm|||Yes|Type I Diabetes|ENU, Singapore, autoimmunity, T cell, B cell, glucose|No| 4824.0|Lluka|ENU8CAT:029||Recessive|||||||||Unknown|||||||||||||||||transgene insertion 3, Christopher C Goodnow|Rat insulin promoter|Expression of the inserted sequence specifically to pancreatic islet beta cells||||||||||Mice carrying the ins-HEL gene have a subclinical predisposition to diabetes due to islet cell failure. Mice carrying the insHEL and TCR transgenes have asubclinical predisposition to autoimmune destruction of the beta cell. Screening mice by urine glucose test. High glucose levels indicate diabetes and thus autoimmunity. "Early onset diabetes" definition changed during screen from approx 80 days to 40 days.||C57BL/6 x C57BL/10BR x CBA|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|||Breed diabetic Double transgenic with a non transgenic sib for next generation|No|24-Sep-2009|Cryopreserved sperm|35.0|0.0|Yes|Type I Diabetes|ENU, Singapore, autoimmunity, T cell, B cell, glucose|No| 4824.0|Lluka|ENU8CAT:029||Recessive||||||||||||||||||||||||||transgene insertion 1, Mark M Davis||||||||||||Mice carrying the ins-HEL gene have a subclinical predisposition to diabetes due to islet cell failure. Mice carrying the insHEL and TCR transgenes have asubclinical predisposition to autoimmune destruction of the beta cell. Screening mice by urine glucose test. High glucose levels indicate diabetes and thus autoimmunity. "Early onset diabetes" definition changed during screen from approx 80 days to 40 days.||C57BL/6 x C57BL/10BR x CBA|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|||Breed diabetic Double transgenic with a non transgenic sib for next generation|No|24-Sep-2009|Cryopreserved sperm|||Yes|Type I Diabetes|ENU, Singapore, autoimmunity, T cell, B cell, glucose|No| 5912.0|Min Chen Tubbs||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 4825.0|Daku|ENU8CAT:068||Recessive|||||||||Unknown|||||||||||||||||transgene insertion 3, Christopher C Goodnow|Rat insulin promoter|Expression of the inserted sequence specifically to pancreatic islet beta cells||||||||||Mice carrying the ins-HEL gene have a subclinical predisposition to diabetes due to islet cell failure. Mice carrying the insHEL and TCR transgenes have asubclinical predisposition to autoimmune destruction of the beta cell. Screening mice by urine glucose test. High glucose levels indicate diabetes and thus autoimmunity. "Early onset diabetes" definition changed during screen from approx 80 days to 40 days.||C57BL/6 x C57BL/10BR x CBA|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|||Breed diabetic Double transgenic with a non transgenic sib for next generation|No|24-Sep-2009|Cryopreserved sperm|45.0|0.0|Yes|Type I Diabetes|ENU, Singapore, autoimmunity, T cell, B cell, glucose|No| 4825.0|Daku|ENU8CAT:068||Recessive||||||||||||||||||||||||||transgene insertion 1, Mark M Davis||||||||||||Mice carrying the ins-HEL gene have a subclinical predisposition to diabetes due to islet cell failure. Mice carrying the insHEL and TCR transgenes have asubclinical predisposition to autoimmune destruction of the beta cell. Screening mice by urine glucose test. High glucose levels indicate diabetes and thus autoimmunity. "Early onset diabetes" definition changed during screen from approx 80 days to 40 days.||C57BL/6 x C57BL/10BR x CBA|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|||Breed diabetic Double transgenic with a non transgenic sib for next generation|No|24-Sep-2009|Cryopreserved sperm|||Yes|Type I Diabetes|ENU, Singapore, autoimmunity, T cell, B cell, glucose|No| 9206.0||NOD/Lt-Tn(sb-pTrans-SA-IRESLacZ-CAG-GFP-SD:Neo)4Tcb/Apb|Svi|Recessive|solute carrier family 16 (monocarboxylic acid transporters), member 10|Slc16a10|Nil| 2610103N14Rik, Mct10, PRO0813, TAT1|MGI:1919722|Tn(sb-pTrans-SA-IRESLacZ-CAG-GFP-SD:Neo)4Tcb|||10|||||||||||||||||pTrans-SA-IRESLacZ-CAG-GFP-SD:Neo||||||||||||These homozygous congenic mice exhibit an earlier onset and increased diabetes incidence compared to NOD/Lt wildtype mice.|Unknown|NOD/ShiLtJ|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|||backcross and intercross|No|17-Jun-2021|Cryopreserved sperm|50.0|0.0|Yes|type 1 diabetes|type 1 diabetes, amino acid transporter|Possibly| 4828.0|6AT:062|ENU6AT:062||Recessive|||||||||Unknown|||||||||||||||||transgene insertion 3, Christopher C Goodnow|Rat insulin promoter|Expression of the inserted sequence specifically to pancreatic islet beta cells||||||||||Mice carrying the ins-HEL gene have a subclinical predisposition to diabetes due to islet cell failure. Mice carrying the insHEL and TCR transgenes have asubclinical predisposition to autoimmune destruction of the beta cell. Screening mice by urine glucose test. High glucose levels indicate diabetes and thus autoimmunity. "Early onset diabetes" definition changed during screen from approx 80 days to 40 days.||C57BL/6 x C57BL/10BR|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|||Breed diabetic Double transgenic with a non transgenic sib for next generation|No|24-Sep-2009|Cryopreserved sperm|90.0|0.0|Yes|Type I Diabetes|ENU, JDRF, autoimmunity, T cell, B cell, glucose|No| 4828.0|6AT:062|ENU6AT:062||Recessive||||||||||||||||||||||||||transgene insertion 1, Mark M Davis||||||||||||Mice carrying the ins-HEL gene have a subclinical predisposition to diabetes due to islet cell failure. Mice carrying the insHEL and TCR transgenes have asubclinical predisposition to autoimmune destruction of the beta cell. Screening mice by urine glucose test. High glucose levels indicate diabetes and thus autoimmunity. "Early onset diabetes" definition changed during screen from approx 80 days to 40 days.||C57BL/6 x C57BL/10BR|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|||Breed diabetic Double transgenic with a non transgenic sib for next generation|No|24-Sep-2009|Cryopreserved sperm|||Yes|Type I Diabetes|ENU, JDRF, autoimmunity, T cell, B cell, glucose|No| 1857.0|SCL tTA|CD1-Tg(Tal1-tTA)19Dgt ?||Recessive||||||||||||||||||||||||||transgene insertion 19, Daniel G Tenen ??|SV40 minimal promoter, rabbit beta-globin intron 2, and the 3' enhancer sequence from the mouse T-cell acute lymphocytic leukemia gene||||||||||||This mouse model recapitulates many characteristics of human chronic myeloid leukemia (CML) and may help elucidate basic leukemogenic mechanisms in CML stem cells during disease initiation and progression.||Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|10-Aug-2007||0.0|0.0|Unknown||erythrocytes, granulocytes, megakaryocytes, c-kit, tetracycline responsive|Yes| 5635.0|BAX 1 x OCT 4 GFP||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5646.0|C3aR Het||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 254.0||B6,129-Csfgm Csfg||Semi-dominant|colony stimulating factor 2 (granulocyte-macrophage)|Csf2|Nil|Csfgm, Gm-CSf|MGI:1339752|colony stimulating factor 2 (granulocyte-macrophage); targeted mutation 1, Ashley R Dunn|Csf2|MGI:1930997|11||||||||||||||||No|||||||||||||Double knockout ice suffer from osteopetrosis and are toothless because of failure of incisor eruption.They have a characteristic alveolar-proteinosis-like lung pathology, but it is more severe than that of GM-CSF-deficient mice and is often fatal.Survival is reduced.Broncho- or lobar-pneumonia at death.|||Yes|No|Yes|Yes|No|Yes|No|Unknown||||No|28-Apr-2006||0.0|0.0|Unknown||macrophage, osteoporosis, lung, alveolar, cytokine, myeloid|Yes| 254.0||B6,129-Csfgm Csfg||Semi-dominant|colony stimulating factor 3 (granulocyte)|Csf3|Unknown|Csfg, G-CSF|MGI:1339751|targeted mutation 1, Ashley R Dunn|Csf3|MGI:1857155|11||||||||||||||||Yes|||||||||||||Double knockout ice suffer from osteopetrosis and are toothless because of failure of incisor eruption.They have a characteristic alveolar-proteinosis-like lung pathology, but it is more severe than that of GM-CSF-deficient mice and is often fatal.Survival is reduced.Broncho- or lobar-pneumonia at death.|||Yes|No|Yes|Yes|No|Yes|No|Unknown||||No|28-Apr-2006||||Unknown||macrophage, osteoporosis, lung, alveolar, cytokine, myeloid|Yes| 4832.0|6CAT:006|ENU6CAT:006||Recessive|||||||||Unknown|||||||||||||||||transgene insertion 3, Christopher C Goodnow|Rat insulin promoter|Expression of the inserted sequence specifically to pancreatic islet beta cells||||||||||Mice carrying the ins-HEL gene have a subclinical predisposition to diabetes due to islet cell failure. Mice carrying the insHEL and TCR transgenes have asubclinical predisposition to autoimmune destruction of the beta cell. Screening mice by urine glucose test. High glucose levels indicate diabetes and thus autoimmunity. "Early onset diabetes" definition changed during screen from approx 80 days to 40 days.||C57BL/6 x C57BL/10BR x CBA|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|||Breed diabetic Double transgenic with a non transgenic sib for next generation|No|24-Sep-2009|Cryopreserved sperm|75.0|0.0|Yes|Type I Diabetes|ENU, JDRF, autoimmunity, T cell, B cell, glucose|No| 4832.0|6CAT:006|ENU6CAT:006||Recessive||||||||||||||||||||||||||transgene insertion 1, Mark M Davis||||||||||||Mice carrying the ins-HEL gene have a subclinical predisposition to diabetes due to islet cell failure. Mice carrying the insHEL and TCR transgenes have asubclinical predisposition to autoimmune destruction of the beta cell. Screening mice by urine glucose test. High glucose levels indicate diabetes and thus autoimmunity. "Early onset diabetes" definition changed during screen from approx 80 days to 40 days.||C57BL/6 x C57BL/10BR x CBA|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|||Breed diabetic Double transgenic with a non transgenic sib for next generation|No|24-Sep-2009|Cryopreserved sperm|||Yes|Type I Diabetes|ENU, JDRF, autoimmunity, T cell, B cell, glucose|No| 4833.0|6CAT:019|ENU6CAT:019||Recessive|||||||||Unknown|||||||||||||||||transgene insertion 3, Christopher C Goodnow|Rat insulin promoter|Expression of the inserted sequence specifically to pancreatic islet beta cells||||||||||Mice carrying the ins-HEL gene have a subclinical predisposition to diabetes due to islet cell failure. Mice carrying the insHEL and TCR transgenes have asubclinical predisposition to autoimmune destruction of the beta cell. Screening mice by urine glucose test. High glucose levels indicate diabetes and thus autoimmunity. "Early onset diabetes" definition changed during screen from approx 80 days to 40 days.||C57BL/6 x C57BL/10BR x CBA|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|||Breed diabetic Double transgenic with a non transgenic sib for next generation|No|24-Sep-2009|Cryopreserved sperm|60.0|0.0|Yes|Type I Diabetes|ENU, JDRF, autoimmunity, T cell, B cell, glucose|No| 4833.0|6CAT:019|ENU6CAT:019||Recessive||||||||||||||||||||||||||transgene insertion 1, Mark M Davis||||||||||||Mice carrying the ins-HEL gene have a subclinical predisposition to diabetes due to islet cell failure. Mice carrying the insHEL and TCR transgenes have asubclinical predisposition to autoimmune destruction of the beta cell. Screening mice by urine glucose test. High glucose levels indicate diabetes and thus autoimmunity. "Early onset diabetes" definition changed during screen from approx 80 days to 40 days.||C57BL/6 x C57BL/10BR x CBA|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|||Breed diabetic Double transgenic with a non transgenic sib for next generation|No|24-Sep-2009|Cryopreserved sperm|||Yes|Type I Diabetes|ENU, JDRF, autoimmunity, T cell, B cell, glucose|No| 7526.0|B6.IJ|B6.IJ||Recessive|||||||||||||||||||||||||||||Unknown||||||||6|Normal||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|29-Nov-2013|Embryo|0.0|0.0|Unknown|||Yes| 5764.0|EphA4KD||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5763.0|Epha4 Loxp||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 4837.0|Hopscotch|ENU8B6:027:B10||Recessive|Unknown||Unknown||||||13|||||||||||||||||||||||||||||Generalised ataxia usually noted between weaning and 75 days old.|Normal|C57BL/6 x C57BL/10|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|24-Sep-2009|Cryopreserved sperm|75.0|0.0|Unknown||ataxia, ENU|Possibly| 5395.0|KRN|C57BL/6SfdAnu-Tg(TcraR28,TcrbR28)KRNDimAnuApb||Recessive||||||||||||||||||||||||||transgene insertion KRN, Diane Mathis |natural TCR alpha and -beta promoter/enhancer elements.|||||||||||A single founder (KRN) in which TCRalpha and TCRbeta transgenes were cointegrated was identified. These constructs together express a T cell receptor that recognizes the 41-61 peptide of bovine pancreas ribonuclease (RNase) in the context of A. These mice develop spontaneous rheumatoid arthritis (RA) joint disease highly reminiscent of man. The trigger for the murine disorder is chance recognition of a NOD-derived major histocompatibility complex (MHC) class II molecule by the transgenic TCR.||C57BL/6SfdAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|24-Jan-2011|Cryopreserved sperm|24.0|0.0|Yes|Rheumatoid Arthritis; RA|rheumatoid arthritis, autoimmunity, TCR, T cell, CD4, B cell|Yes| 4818.0|Mani|ENU8BAT:092||Recessive|||||||||Unknown|||||||||||||||||transgene insertion 3, Christopher C Goodnow|Rat insulin promoter|Expression of the inserted sequence specifically to pancreatic islet beta cells||||||||||Mice carrying the ins-HEL gene have a subclinical predisposition to diabetes due to islet cell failure. Mice carrying the insHEL and TCR transgenes have asubclinical predisposition to autoimmune destruction of the beta cell. Screening mice by urine glucose test. High glucose levels indicate diabetes and thus autoimmunity. "Early onset diabetes" definition changed during screen from approx 80 days to 40 days.||C57BL/6 x C57BL/10BR|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|||Breed diabetic Double transgenic with a non transgenic sib for next generation|No|24-Sep-2009|Cryopreserved sperm|75.0|0.0|Yes|Type I Diabetes|ENU, Singapore, autoimmunity, T cell, B cell, glucose, JDRF|No| 4818.0|Mani|ENU8BAT:092||Recessive||||||||||||||||||||||||||transgene insertion 1, Mark M Davis||||||||||||Mice carrying the ins-HEL gene have a subclinical predisposition to diabetes due to islet cell failure. Mice carrying the insHEL and TCR transgenes have asubclinical predisposition to autoimmune destruction of the beta cell. Screening mice by urine glucose test. High glucose levels indicate diabetes and thus autoimmunity. "Early onset diabetes" definition changed during screen from approx 80 days to 40 days.||C57BL/6 x C57BL/10BR|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|||Breed diabetic Double transgenic with a non transgenic sib for next generation|No|24-Sep-2009|Cryopreserved sperm|||Yes|Type I Diabetes|ENU, Singapore, autoimmunity, T cell, B cell, glucose, JDRF|No| 6959.0|ENU20:008:a:B6:G3|ANU:ENU20:008:a:G3||Recessive|Unknown||||||||Unknown||||||||||||||||Unknown|||||||||||||Unknown|Unknown|C57BL/6JAnu|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||1||No|05-Jul-2012|Cryopreserved sperm|40.0|0.0|Unknown||ENU, random, mutagenesis, screen|Yes| 4836.0|Hopscotch|ENU8B6:027:B6||Recessive|Unknown||Unknown||||||13|||||||||||||||||||||||||||||Generalised ataxia usually noted between weaning and 75 days old.|Normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|24-Sep-2009|Cryopreserved sperm|35.0|0.0|Unknown||ataxia, ENU|Possibly| 4835.0|TNAP-Cre|BALB/c-Alpl/AnuApb||Recessive|alkaline phosphatase, liver/bone/kidney|Alpl|Nil|Akp-2, Akp2, TNSALP, TNAP|MGI:87983|targeted mutation 1, Andras Nagy|Alpl|MGI:2177588|4||||||||||||||||Yes|Cre recombinase|TNAP|||||||||||Embryonic Lethal||Balb/c|No|No|Yes|No|No|Yes|No|Unknown|8|||No|24-Sep-2009|Cryopreserved sperm|40.0|0.0|Unknown||alkaline phosphatase, primordial germ cell|Yes| 6520.0|2CLY5.1tg|B6.SJL-Ptprc Tg(Tcra2C,Tcrb2C)1Dlo/Ausb||Recessive|protein tyrosine phosphatase, receptor type, C|Ptprc||B220, CD45, Ly-5, Lyt-4, T200|MGI:97810|protein tyrosine phosphatase, receptor type, C; a variant|Ptprc|MGI:4819849|1|||||||||||||||||transgene insertion 1, Dennis Y Loh||||||||||||Abnormal CD8-positive T cell morphology: CD5 levels are reduced, indicating CD8-positive T cells are being activated by self-antigen.||C57BL/6 x SJL|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown||T cell receptor, MHC|Possibly| 5636.0|BAX 1.1||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 7528.0|Zambesi|B6.Cg-Tg(Col1a1*2.3-GFP)1Rowe/Ausb|B6.Cg-Tg(Col1a1*2.3-GFP)1Rowe/Ausb|Dominant||||||||||||||||||||||||||transgene insertion 1, David Rowe|rat type I collagen (Col1a1) promoter|bone and tail tendon||||||||||Expression of GFP restricted to vertebral bone tissue.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|04-Dec-2013||0.0|0.0|Unknown||collagen, GFP, osteoblast|Yes| 5108.0|Plt20|B6.C-Bcl2l1/WehiAnuApb||Recessive|BCL2-like 1|Bcl2l1|Reduced|Bcl(X)L, bcl-x, Bcl-XL, Bcl-Xs, BclX|MGI:88139|BCL2-like 1; platelet 20|Bcl2l1|MGI:3847887|2|ENSMUSG00000007659|ENSMUST00000109820|Bcl2l1-201|44|437|A to G|ENSMUSE00001233620|2|15|Tyrosine to Cysteine|||||CCGGGAGCTGGTGGTCGACTTTCTCTCCTACAAGCTTTCCCAGAAAGGATACAGCTGGAGT|No|||||||||||||Decreased platelet cell number: * platelet counts are 25% of normal * splenectomy only partially restored platelet cell countExtramedullary hematopoiesis: there is a slight increase in splenic erythropoiesis.Increased megakaryocyte cell number: megakaryocyte numbers are significantly elevated compared to controls.Abnormal platelet physiology: platelet half-life is reduced to under 12 hours compared to 57 hours for controls.|Decreased platelet cell number: platelet counts are significantly lower than controls (598x10<3>/microliter vs 1100x10<3>/microliter).Increased megakaryocyte cell number: megakaryocyte numbers are marginally elevated compared to controls.Abnormal platelet physiology: platelet half-life is reduced by 50% compared to controls (57 hours to 24 hours).|BALB/c x C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|04-May-2010|Cryopreserved sperm|40.0|0.0|Unknown||Bcl2, ENU, platelet, thrombocytopenia, Bak|Yes| 5777.0|FGF2 KO||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5776.0|FCG||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 7717.0|KstC57|B6.129P2-Frem2/MarpApb||Dominant|Fras1 related extracellular matrix protein 2|Frem2|Unknown|6030440P17Rik, 8430406N05Rik, b2b1562Clo, my, ne|MGI:2444465|Fras1 related extracellular matrix protein 2; gene trap KST252, BayGenomics|Frem2|MGI:3578640|3|||||||||||||||||||||||||||||Embryonic lethal |wildtype|C57BL/6|No|No|Yes|No|No|Yes|No|Good|13|3||No|02-Jul-2014|Cryopreserved sperm|50.0|0.0|Yes|Fraser Syndrome an autosomal recessive congenic disorder affecting development|Fraser Syndrome|Possibly| 10322.0|ENU59:G2|ANU:ENU59:G2||Recessive|Unknown||||||||Unknown||||||||||||||||||||||||||||| | |C57Bl/6N|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|01-Apr-2023|Cryopreserved sperm|6128.0|0.0|Unknown|||Possibly| 4856.0|T-Bird|STOCK Dsg4/AnuApb|STOCK Dsg4/AnuApb|Recessive|desmoglein 4|Dsg4|Unknown|CDHF13, lah|MGI:2661061|T-Bird|Dsg4|MGI:5007752|18|ENSMUSG00000001804|ENSMUST00000019426|Dsg4-001|643|777|A to C|ENSMUSE00000445469|6|215|Threonine to Proline|||||GTGCACCCATGTTCATGGTGAACAGGTACACTGGAGAAGTCCGCACGATGTCCAATTTCCT|Unknown|||||||||||||Greasy Coat. Affected mice develop a dull, sparse and greasy coat at about ~40 days of age. ||C57BL/6 x C57BL/10 x CBA|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|2|||No|24-Sep-2009|Cryopreserved sperm|7.0|0.0|Unknown||Coat, greasy, hair, ENU|Yes| 4858.0|Jersey|ENU8CAT:049||Dominant|2'-5' oligoadenylate synthetase 2|Oas2|Unknown|2'-5' oligoadenylate synthetase-like 11, Oasl11|MGI:2180852||||5|ENSMUSG00000032690|ENSMUST00000081491|Oas2-002|1214|1294|T to A|ENSMUSE00000490404|6|405|Isoleucine to Asparagine|||||CCAGCCCAACAAGCTCTTCCTAAAGCAGATCAAGGAAGCTGTTGACATTATATGTTCCTTC|Yes|||||||||||||Females fail to lactate between days 1 and 4 (after birth of pups).Pups can be maintained by adding lactating foster mother.|Females fail to lactate by day 8 (after birth of pups).|C57BL/6 x CBA/CaJ|Yes|No|No|Yes|Yes|Yes|No|Unknown||||No|24-Sep-2009|Cryopreserved sperm|80.0|0.0|Unknown||lactation, milk, ENU, infertility, fostering, mammary gland|Yes| 4858.0|Jersey|ENU8CAT:049||Dominant|two pore channel 1|Tpcn1|Unknown||MGI:2182472||||5|ENSMUSG00000032741|ENSMUST00000046426|Tpcn1-201||||||||120989697|23|||TTTATCATGCTCTAGTGGAAGCCTCCCTGTGCCCCCTGACAGGCTCTGGGTATCTGACTA|Yes|||||||||||||Females fail to lactate between days 1 and 4 (after birth of pups).Pups can be maintained by adding lactating foster mother.|Females fail to lactate by day 8 (after birth of pups).|C57BL/6 x CBA/CaJ|Yes|No|No|Yes|Yes|Yes|No|Unknown||||No|24-Sep-2009|Cryopreserved sperm|||Unknown||lactation, milk, ENU, infertility, fostering, mammary gland|Yes| 7718.0|MUL1|MULAN|MUL1|Dominant|mitochondrial ubiquitin ligase activator of NFKB 1|Mul1||0610009K11Rik|MGI:1915600||||4|||||||||||||||||||||||||||||Mice are slightly smaller in size but appear healthy and behave normally|Normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Poor||||No|18-Jul-2014|Cryopreserved sperm|60.0|0.0|Unknown|||No| 2376.0|Piaf|ENU7B6:022||Recessive|||||||||Unknown||||||||||||||||Yes|||||||||||||Ataxia||C57BL/6|Yes|No|Yes|Yes|No|Yes|No|Unknown||||No|14-Dec-2007|Cryopreserved sperm|60.0|0.0|Unknown||ataxia, ENU|Yes| 4993.0|Ring Finger TCR InsHel 129>B10.BR|STOCK H2 Cbl Tg(TcrHEL3A9)Mmd/AnuApb||Recessive|Casitas B-lineage lymphoma|Cbl|Unknown|c-Cbl, cbl, Cbl-2|MGI:88279|targeted mutation 2, Wallace Y Langdon|Cbl|MGI:3610727|9||||||||||||||||Yes|transgene insertion 1, Mark M Davis||||||||||||Mutants are embryonic lethal|Unknown|B10.BR-H2 x C57BL/6 x 129|No|No|Yes|No|No|Yes|No|Good||||No|28-Jan-2010|Cryopreserved sperm|30.0|0.0|No||cbl, thymocyte, T cell, ring finger, ubiquitin ligase|Yes| 4857.0||ENU6PH:058:BALB||Recessive|Unknown||||||||Unknown||||||||||||||||Yes|||||||||||||Hypo IgE response following allergic challenge.||C57BL/6 x C57BL/10 x BALB/b|Yes|Yes|Yes|Yes|Yes|Yes|No|Poor||||No|24-Sep-2009|Cryopreserved sperm|60.0|0.0|Unknown||allergic challenge, ENU, Immunoglobulin, IgE|No| 6382.0|GREENtg|C57BL/6-Tg(UBC-GFP)30Scha/JAusb||Dominant||||||||||||||||||||||||||transgene insertion 30, Brian Schaefer|human ubiquitin C promoter|||||||||||Unknown|Unknown|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown||GFP, Dendritic cells|Yes| 4886.0||129X1/Sv||Dominant||||||||||||||||||||||||||||||||||||||Normal.Strain cryopreserved as control for APB #4887, 4888, 4889.Light Bellied, Black Agouti||129X1/Sv|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|28-Sep-2009||0.0|0.0|Unknown|||Yes| 6960.0|ENU20:009:b:B6:G3|ANU:ENU20:009:b:G3||Recessive|Unknown||||||||Unknown||||||||||||||||Unknown|||||||||||||Unknown|Unknown|C57BL/6JAnu|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||1||No|05-Jul-2012|Cryopreserved sperm|18.0|0.0|Unknown||ENU, random, mutagenesis, screen|Yes| 6961.0|ENU20:010:b:B6:G3|ANU:ENU20:010:b:G3||Recessive|Unknown||||||||Unknown||||||||||||||||Unknown|||||||||||||Unknown|Unknown|C57BL/6JAnu|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||1||No|05-Jul-2012|Cryopreserved sperm|30.0|0.0|Unknown||ENU, random, mutagenesis, screen|Yes| 7052.0|ENU14:C3H007 G2|ENU14:C3H:007:G2||Semi-dominant|Unknown|||||mutation 10, The Australian National University|m10Anu|MGI:5510772|Unknown|||||||||||||||||||||||||||||Abnormal kidney morphology:* abnormal kidney morphology ( J:199856 )• renal anomalies more prevalent in male than female mice• abnormal kidney position in 3 of 7 miceHydronephrosis ( J:199856 )• in 3 of 7 miceAbnormal kidney size ( J:199856 )• in 3 of 7 miceAbsent kidney ( J:199856 )• in 1 of 7 miceAbnormal ureter morphology:Double ureter ( J:199856 )• in 1 of 7 miceHydroureter ( J:199856 )• in 1 of 7 mice||C3H/HeH * C57BL/6JAnu|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|21-Aug-2012|Cryopreserved sperm|10.0|0.0|Unknown||ENU, kidney|Possibly| 6338.0|TLR9|C57BL/6-Tlr9||Recessive|toll-like receptor 9|Tlr9|Nil||MGI:1932389|toll-like receptor 9; targeted mutation 1, Shizuo Akira|Tlr9|MGI:2660562|9|||||||||||||||||||||||||||||Abnormal immune system physiology:*Response to LPS and CpG is completely abrogated. Impaired NK cell cytolysis: *No NK cell activation is observed following infection with L. infantum. Decreased interferon-alpha secretion: *Following infection with Leishmania baziliensis. *However, secretion could be restored by treatment with GU-rich ssRNA, a TLR7 ligand. Decreased interferon-beta secretion: *Following infection with Leishmania baziliensis. *However, secretion could be restored by treatment with GU-rich ssRNA, a TLR7 ligand. Decreased interleukin-12b secretion: *Following infection with attenuated yellow fever vaccine 17D (YF-17D), dendritic cells produce less IL-12p40 relative to wild-type mice. *Unlike in wild-type mice, IL-12p40 production from dendritic cells following infection with Leishmania infantum is indetectable. Decreased tumor necrosis factor secretion: *Following treatment with PbA(Plasmodium bergbei ANKA)-parasitized erythrocytes or LPS-stimulation, TNF secretion is reduced. Decreased susceptibility to experimental autoimmune encephalomyelitis: *Myelin oligodendrocyte glycoprotein injection results in delayed onset of disease, 17.9 days after injection rather than 15.9 days as in controls. *Fewer infiltrating foci in the spinal cord. Abnormal response to infection: *Following treatment with PbA (Plasmodium bergbei ANKA)-parasitized erythrocytes, mice have a partially decreased immune response in terms of TNF secretion and response to CpG. Decreased susceptibility to parasitic infection: *Resistant to cerebral malaria. *Reduced accumulation of hemozoin. *Less upregulation of TNF-alpha in Plasmodium infection.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown||TLR9|Yes| 6962.0|ENU20:011:a:B6:G3|ANU:ENU20:011:a:G3||Recessive|Unknown||||||||Unknown||||||||||||||||Unknown|||||||||||||Unknown|Unknown|C57BL/6JAnu|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||1||No|05-Jul-2012|Cryopreserved sperm|20.0|0.0|Unknown||ENU, random, mutagenesis, screen|Yes| 5027.0|MTKneo|Outbred ICR M-TKneo2||Dominant||||||||||||||||||||||||||||||||||||||||10|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|22-Feb-2010|Cryopreserved sperm|100.0|0.0|Unknown|||No| 6963.0|ENU20:013:b:B6:G3|ANU:ENU20:013:b:G3||Recessive|Unknown||||||||Unknown||||||||||||||||Unknown|||||||||||||Unknown|Unknown|C57BL/6JAnu|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||1||No|05-Jul-2012|Cryopreserved sperm|48.0|0.0|Unknown||ENU, random, mutagenesis, screen|Yes| 6964.0|ENU20:015:a:B6:G3|ANU:ENU20:015:a:G3||Recessive|Unknown||||||||Unknown||||||||||||||||Unknown|||||||||||||Unknown|Unknown|C57BL/6JAnu|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||1||No|05-Jul-2012|Cryopreserved sperm|59.0|0.0|Unknown||ENU, random, mutagenesis, screen|Yes| 4884.0|NODlpr|NOD-Fas||Recessive|Fas (TNF receptor superfamily member 6)|Fas|Unknown|APO-1, CD95, TNFR6, Tnfrsf6|MGI:95484|lymphoproliferation|Fas|MGI:1856334|19|||||||||||||||||||||||||||||NODlpr homozygotes have lymphadenopathy similar to the NOD.MRL(C3)-Faslpr/LtJ parental strain. This strain also has autoimmune characteristics similar to that seen on the MRL background (eg: immune complex glomerulonephritis).Unlike NOD/Lt mice, NOD.lpr mice do not develop diabetes. By 15 weeks of age lymphadenopathy is severe and mice need to be euthanased.|NODlpr heterozygotes are similar to NOD/LtJ (but there is a possibly reduced incidence of diabetes though not formerly tested).|NOD/Lt|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|10|15||No|28-Sep-2009||0.0|0.0|Yes|Insulin-dependent diabetes mellitus|autoimmunity, lymphadenopathy, glomerulonephritis, lymph node architecture, cytotoxic, T cell|Yes| 6965.0|ENU20:017:b:B6:G3|ANU:ENU20:017:b:G3||Recessive|Unknown||||||||Unknown||||||||||||||||Unknown|||||||||||||Unknown|Unknown|C57BL/6JAnu|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||1||No|05-Jul-2012|Cryopreserved sperm|36.0|0.0|Unknown||ENU, random, mutagenesis, screen|Yes| 6211.0|B6/bcl-x flox|B6.129S6-Bcl2l1/Wehi||Recessive|BCL2-like 1 |Bcl2l1|Reduced|Bcl(X)L, bcl-x, Bcl-XL, Bcl-Xs, BclX |MGI:88139|BCL2-like 1; targeted mutation 1.1, Lothar Hennighausen|Bcl2l1|MGI:2176700|2|||||||||||||||||||||||||||||Normal||C57BL/6|Yes|Unknown|Yes|Yes|No|Yes|No|Unknown|6|||No|13-Sep-2011||0.0|0.0|Unknown||Bcl-x, Bax, Bcl2|Yes| 6968.0|ENU20:022:a:B6:G3|ANU:ENU20:022:a:G3||Recessive|Unknown||||||||Unknown||||||||||||||||Unknown|||||||||||||Unknown|Unknown|C57BL/6JAnu|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||1||No|05-Jul-2012|Cryopreserved sperm|40.0|0.0|Unknown||ENU, random, mutagenesis, screen|Yes| 6970.0|ENU20:025:a:B6:G3|ANU:ENU20:025:a:G3||Recessive|Unknown||||||||Unknown||||||||||||||||Unknown|||||||||||||Unknown|Unknown|C57BL/6JAnu|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||1||No|05-Jul-2012|Cryopreserved sperm|47.0|0.0|Unknown||ENU, random, mutagenesis, screen|Yes| 5001.0|aF11 aa278|FVB/N-Tg(Prm1-Pebp1)11Mkob/MarpApb||Dominant||||||||||||||||||||||||||phosphatidylethanolamine binding protein 1|Protamine 1|low level expression||||||||||||FVB/N|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown|0|0||No|22-Feb-2010|Cryopreserved sperm|60.0|0.0|Unknown||fertility, sperm|No| 4839.0|Kenny ; ENU9CAT:040|STOCK Muc2/AnuApb|STOCK Muc2/AnuApb|Recessive|mucin 2|Muc2|Unknown||MGI:1339364|kenny|Muc2|MGI:4820425|7|ENSMUSG00000025515|ENSMUST00000026590|Muc2-202|4187|4192|C to A|ENSMUSE00000519387|31|1396|Serine to STOP|||||AATGGAATACTGTACTCCTTCAACTATCTCACCTACAACTTCAACAACAACCTTGTCTACC|No|||||||||||||Diarrhoea.Multiple plaques on GIT and lymphomegaly.Other mutants homozygote for a point mutation have soft feces at weaning and develop diarrhea associated with malapsorption syndrome. Homozygous null mutants pass blood in their feces at 6 months, and 65% of null mutants have intestinal tumors at 1 year.||C57BL/6 x CB10.BR x CBA|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|24-Sep-2009|Cryopreserved sperm|69.0|0.0|Unknown||malabsorption, colon, goblet cells, diarrhoea, ENU|Yes| 4880.0|B6.Rag1/Gal KO|C57BL/6-Rag1 Ggta1/Apb||Recessive|recombination activating gene 1|Rag1|Nil|Rag-1|MGI:97848|targeted mutation 1, Peter Mombaerts|Rag1|MGI:1857241|2||||||||||||||||No|||||||||||||Homozygotes for targeted null mutations exhibit arrested development of T and B cell maturation at the CD4-8- thymocyte or B220+/CD43+pro-B cell stage due to inability to undergo V(D)J recombination.All blood/tissue samples lack Gal expression.Cortical cataracts developed in all GalT-/- mice at 4-6 weeks of age.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|28-Sep-2009|Cryopreserved sperm|70.0|0.0|Unknown||T cell, B cell, eosinophil, inflammation, interferon, Xenotransplantation, antibody, transferase, galactose|Yes| 4880.0|B6.Rag1/Gal KO|C57BL/6-Rag1 Ggta1/Apb||Recessive|glycoprotein galactosyltransferase alpha 1, 3|Ggta1|Nil|alpha Gal, alpha3GalT, Gal, GALT, Ggta, Ggta-1, glycoprotein alpha galactosyl transferase 1|MGI:95704||||2|||||||||||||||||||||||||||||Homozygotes for targeted null mutations exhibit arrested development of T and B cell maturation at the CD4-8- thymocyte or B220+/CD43+pro-B cell stage due to inability to undergo V(D)J recombination.All blood/tissue samples lack Gal expression.Cortical cataracts developed in all GalT-/- mice at 4-6 weeks of age.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|28-Sep-2009|Cryopreserved sperm|||Unknown||T cell, B cell, eosinophil, inflammation, interferon, Xenotransplantation, antibody, transferase, galactose|Yes| 6966.0|ENU20:019:b:B6:G3|ANU:ENU20:019:b:G3||Recessive|Unknown||||||||Unknown||||||||||||||||Unknown|||||||||||||Unknown|Unknown|C57BL/6JAnu|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||1||No|05-Jul-2012|Cryopreserved sperm|80.0|0.0|Unknown||ENU, random, mutagenesis, screen|Yes| 6967.0|ENU20:021:b:B6:G3|ANU:ENU20:021:b:G3||Recessive|Unknown||||||||Unknown||||||||||||||||Unknown|||||||||||||Unknown|Unknown|C57BL/6JAnu|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||1||No|05-Jul-2012|Cryopreserved sperm|63.0|0.0|Unknown||ENU, random, mutagenesis, screen|Yes| 6969.0|ENU20:023:b:B6:G3|ANU:ENU20:023:b:G3||Recessive|Unknown||||||||Unknown||||||||||||||||Unknown|||||||||||||Unknown|Unknown|C57BL/6JAnu|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||1||No|05-Jul-2012|Cryopreserved sperm|40.0|0.0|Unknown||ENU, random, mutagenesis, screen|Yes| 4892.0||Infertility Project||Recessive|Unknown||Unknown||||||Unknown|||||||||||||||||||||||||||||Unknown|Unknown|C57BL/6 x CBA|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|30-Sep-2009|Cryopreserved sperm|395.0|0.0|Unknown||ENU, sperm, lactation, milk|Possibly| 7719.0|gp130Y757F x Aim2|B6.129/Sv-Aim2 Il6st/MarpApb||Dominant|interleukin 6 signal transducer|Il6st|Unknown|CD130, D13Ertd699e, gp130|MGI:96560|interleukin 6 signal transducer; targeted mutation 1, Matthias Ernst|Il6st|MGI:2388478|13||||||||||||||||Yes|||||||||||||Mice develop gastric tumours and splenomegaly.|If the mice are heterozygous for the gp130 knock-in mutation (F+) then the mice appear normal. |C57BL/6 x 129Sv|Yes|No|Yes|Yes|Yes|Yes|No|Good|10||heterozogous x homozygous|No|23-Jul-2014|Cryopreserved sperm|50.0|0.0|Yes|Gastric cancer|gastric, cancer, gp130|No| 7719.0|gp130Y757F x Aim2|B6.129/Sv-Aim2 Il6st/MarpApb||Dominant|absent in melanoma 2|Aim2|Nil||MGI:2686159|absent in melanoma 2; targeted mutation 1.1, Vishva M Dixit|Aim2|MGI:5428935|1||||||||||||||||No|||||||||||||Mice develop gastric tumours and splenomegaly.|If the mice are heterozygous for the gp130 knock-in mutation (F+) then the mice appear normal. |C57BL/6 x 129Sv|Yes|No|Yes|Yes|Yes|Yes|No|Good|10||heterozogous x homozygous|No|23-Jul-2014|Cryopreserved sperm|||Yes|Gastric cancer|gastric, cancer, gp130|No| 4903.0||BALB/c-IL13/MelbApb||Recessive|interleukin 13|Il13|Nil|Il-13|MGI:96541|targeted mutation 2, Andrew NJ McKenzie|Il13|MGI:1931804|11|||||||||||||||||||||||||||||Decreased T-helper 2 cell number.Abnormal T-helper 2 cell differentiaion.Increase immunoglobulin levels.Increase susceptibility to parasitic infection.Impaired eosinophil response to parasitic infection||BALB/c|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|10|||No|09-Oct-2009|Cryopreserved sperm|150.0|0.0|Unknown||interleukin, IL10, IL5, Th2, T cell, parasite|Yes| 4894.0|Ifngr1<441F>|C57BL/6-Ifngr1/Apb||Recessive|interferon gamma receptor 1|Ifngr1|Normal|CD119, Ifgr, IFN-gamma R, IFN-gammaR, Ifngr, Nktar|MGI:107655|interferon gamma receptor 1; targeted mutation 1.1, Robyn Starr|Ifngr1|MGI:4361521|10||||||||||Unknown to Unknown||||||Yes|||||||||||||Homozygous Ifngr1<441F> mice were born in the expected Mendelian ratios and showed no signs of illness or obvious pathological abnormalities to at least 6 mo of age (data not shown). Similarly, the cellularity of lymphoid organs and activation state of lymphocytes was comparable to that of wt mice. the IFNGR1 Y441F mutation had significant effects on IFN-γ sensitivity and tumor resistance in vivo. We have shown improved anti-metastatic activity of GalCer in Ifngr1441F mice, and further that these mice have a subtle but significantly increased innate resistance to tumor formation.|Normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|09-Oct-2009|Cryopreserved sperm|100.0|0.0|Unknown||signal transduction, tumour, SOCS, STAT1, cytokine receptor, Jak|Yes| 5013.0|ASD078|B6.Cg-H2||Dominant||||||||||||||||||||||||||||||||||||||||7|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|22-Feb-2010|Cryopreserved sperm|139.0|0.0|Unknown|||Possibly| 7720.0|killer -/-|B6.129S6-Tnfrsf10b/Anu||Recessive|tumor necrosis factor receptor superfamily, member 10b|Tnfrsf10b|Nil|DR5, KILLER, Killer/Dr5, Ly98, TRAILR2, TRAIL-R2, Trail Receptor, TRICK2A, TRICK2B, TRICKB|MGI:1341090|tumor necrosis factor receptor superfamily, member 10b; targeted mutation 1, Astar Winoto|Tnfrsf10b|MGI:3522001|14|||||||||||||||||||||||||||||decreased susceptibility to viral infection induced morbidity/mortality ( J:94681 )• after encephalomyocarditis virus infection, homozygotes had a slightly enhanced survival rate than controls but not when a 10-fold higher viral dose was usedimmune systemincreased NK cell number ( J:94681 )• observed a slight increase in CD69+ natural killer cells in MCMV-infected homozygotes indicating that NK cells were slightly more activated, however lytic activity of NK cells was normalincreased circulating interleukin-12b level ( J:94681 )• 10-fold increase in serum levels of the IL-12 p40 subunit 24 hours after MCMV infection compared to controlsabnormal interferon level ( J:94681 )• elevated levels of interferon-alpha and interferon-beta in spleen of MCMV-infected homozygotes compared to wild-typeincreased circulating interferon-gamma level ( J:94681 )• serum levels of interferon-gamma at 36 hours postinfection with MCMV were greatly elevated compared to wild-typeincreased interleukin-12 secretion ( J:94681 )• spleen derived dendritic cells of MCMV-infected mutants produced 8-fold more IL-12 than infected wild-type• bone marrow derived dendritic cells stimulated with E.coli LPS had higher levels of IL-12 than controls• peritoneal macrophages stimulated with E.coli or Salmonella LPS, lipoteichoic acid, or poly (I:C) had higher levels of IL-12 than controlsincreased tumor necrosis factor secretion ( J:94681 )• peritoneal macrophages stimulated with E.coli or Salmonella LPS had higher levels of TNF-alpha than controlsabnormal innate immunity ( J:94681 )• enhanced innate immune responses to encephalomyocarditis virus and murine cytomegalovirus (MCMV) infection but not to Salmonella typhimurium or Listeria monocytogenes infectiondecreased susceptibility to viral infection ( J:94681 )• 3 days after murine cytomegalovirus infection, viral titers in the spleen, but not the liver or lung, were decreased by 40-fold compared to wild-type, indicating enhanced clearance of MCMVdecreased susceptibility to viral infection induced morbidity/mortality ( J:94681 )• after encephalomyocarditis virus infection, homozygotes had a slightly enhanced survival rate than controls but not when a 10-fold higher viral dose was used||C57BL/6|Yes|Yes|Yes|Yes|Yes|Unknown|No|Unknown||||No|23-Jul-2014|Cryopreserved sperm|54.0|0.0|Unknown||infection, receptor, Toll like|Yes| 1355.0|MSH2C delta|B6.129-Msh2/Apb||Recessive|mutS homolog 2 (E. coli)|Msh2|Unknown||MGI:101816|targeted mutation 1, H te Riele|Msh2|MGI:1858055|17||||||||||||||||Yes|||||||||||||T cell derived lymphoma: 30% of homozygous animals developed metastasizing lymphomas of T cell origin, peaking at 2 months of age.Msh2-deficient cells have lost mismatch binding and have acquired microsatellite instability, a mutator phenotype, and tolerance to methylating agents. Moreover, in these cells, homologous recombination has lost dependence on complete identity between interacting DNA sequences, suggesting that Msh2 is involved in safeguarding the genome from promiscuous recombination.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|22-Jun-2007|Cryopreserved sperm|50.0|0.0|Unknown||Lymphoma, genome stability, mismatch repair|Yes| 3685.0|Storm ; ENU9B6:023a|C57BL/6JAnu-Ptprc/AnuApb|C57BL/6JAnu-Ptprc/AnuApb|Recessive|protein tyrosine phosphatase, receptor type, C|Ptprc|Unknown|B220, CD45, Cd45, Ly-5, Lyt-4, T200|MGI:97810|storm|Ptprc|MGI:4819159|1|ENSMUSG00000026395|ENSMUST00000027645|Ptprc-201|1393|1491|T to C|ENSMUSE00000595908|13|465|Cysteine to Arginine|||||AGATTCAAAGAAATGGGACTGCTGAGAAGTGCAATTTTCACACAAAAGCAGATCGTCCGGA|Yes|||||||||||||Low B and T cell numbers||C57BL/6JAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||4|affected x littermate or affected by B6|No|26-Aug-2008|Cryopreserved sperm|110.0|0.0|Unknown||T cell, B cell, signal transduction, receptor, ENU, NIH, Wellcome Trust, Phosphorylation|Yes| 5471.0|APN 78|C57BL/6N-Zdhhc2/Marp||Recessive|zinc finger, DHHC domain containing 2|Zdhhc2|||MGI:1923452|zinc finger, DHHC domain containing 2; targeted mutation 1a, Wellcome Trust Sanger Institute|Zdhhc2|MGI:4362764|8||||||||||||||||Yes|||||||||||||Unknown - Not bred to homozygocity |Normal |C57Bl/6N|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|25-Mar-2011|Cryopreserved sperm|50.0|0.0|Unknown||ES cell|Yes| 9236.0|ENU51:058|ANU:ENU51:058||Recessive|Not known yet||||||||Unknown||||||||||||||||||||||||||||| | |C57BL/6NcrlAnu|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|26-Jul-2021|Cryopreserved sperm|12.0|0.0|Unknown|||Possibly| 4904.0|IL2 KO TCR Arjuna|C57BL/6-IL2 Tg(ILK3mHEL)3Ccg Tg(TcrHEL3A9)1Mmd/AnuApb||Recessive|interleukin 2|IL2|Nil|Il-2|MGI:96548|targeted mutation 1, Ivan Horak|Il2|MGI:1857191|3|||||||||||||||||transgene insertion 3, Christopher C Goodnow|Rat insulin promoter|||||||||||Increased T cell numbers and prolonged T cell response to antigen.Heightened susceptibility to autoimmune diabetes on the transgenically sensitized TCR x insHEL background. Phenotype Screen: Urine glucose|Normal|C57BL/6|Yes|No|Yes|Yes|No|Yes|No|Unknown||||No|09-Oct-2009|Cryopreserved sperm|120.0|0.0|Yes|Type I Diabetes|CD4, HEL, T cell, autoimmunity, T cell receptor|Yes| 4904.0|IL2 KO TCR Arjuna|C57BL/6-IL2 Tg(ILK3mHEL)3Ccg Tg(TcrHEL3A9)1Mmd/AnuApb||Recessive||||||||||||||||||||||||||transgene insertion 1, Mark M Davis||||||||||||Increased T cell numbers and prolonged T cell response to antigen.Heightened susceptibility to autoimmune diabetes on the transgenically sensitized TCR x insHEL background. Phenotype Screen: Urine glucose|Normal|C57BL/6|Yes|No|Yes|Yes|No|Yes|No|Unknown||||No|09-Oct-2009|Cryopreserved sperm|||Yes|Type I Diabetes|CD4, HEL, T cell, autoimmunity, T cell receptor|Yes| 5780.0|FGF8FloxC57||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6971.0|ENU20:026:b:B6:G3|ANU:ENU20:026:b:G3||Recessive|Unknown||||||||Unknown||||||||||||||||Unknown|||||||||||||Unknown|Unknown|C57BL/6JAnu|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||1||No|05-Jul-2012|Cryopreserved sperm|40.0|0.0|Unknown||ENU, random, mutagenesis, screen|Yes| 69.0|Sweaty|C57BL/6JStdAnu-Scd2/AnuApb|C57BL/6JStdAnu-Scd2/AnuApb|Recessive|stearoyl-Coenzyme A desaturase 2|Scd2|Unknown|Scd-2|MGI:98240|stearoyl-Coenzyme A desaturase 2; sweaty|Scd2|MGI:4888575|19|ENSMUSG00000025203|ENSMUST00000026221|Scd2-201|330|1042|C to T|ENSMUSE00000148829|3|109|Serine to Serine|||||CTCTTCGCGTATTTGTACTATGTAATCAGCGCCCTGGGCATCACAGCCGGGGCTCATCGCC|Unknown|||||||||||||Sweaty/oily thin coat; hyperplasia of sebacious glands, periocular inflammation, homozygote females breed poorly, males OK||C57BL/6JSfdAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||G15|Het x Het|No|06-Feb-2006|Cryopreserved sperm|25.0|0.0|Unknown||Sweat, oily, coat, ENU|Yes| 5782.0|FGF8FloxC57/Rosa26EGFP/Emx1Cre||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 7655.0||SJL/ASAM/Apb||Dominant|Unknown|Unknown|Reduced||||||Unknown|||||||||||||||||||||||||||||Unknown|The mice displays a slight growth retardation phenotype.|SJL/J|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Good||||No|09-Apr-2014|Cryopreserved sperm|53.0|0.0|Unknown||ENU|Yes| 7530.0|Park9|C57BL/6N-Atp13a2/MarpAusb|C57BL/6N-Atp13a2/MarpAusb|Recessive|ATPase type 13A2|Atp13a2|||MGI:1922022|ATPase type 13A2; targeted mutation 1e, Wellcome Trust Sanger Institute|Atp13a2|ATPase type 13A2; targeted mutation 1e, Wellcome Trust Sanger Institute|4|||||||||||||||||||||||||||||Elderly mice might show weak to mild signs of neurodegeneration.||C57BL/6N|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|04-Dec-2013||0.0|0.0|Unknown|||Yes| 4908.0|DeltaEF1|C57BL/6-Zeb1/AnuApb||Recessive|zinc finger E-box binding homeobox 1|Zeb1|Normal|[delta]EF1, 3110032K11Rik, AREB6, MEB1, Nil2, Tcf18, Tcf8, ZEB, Zfhep, Zfhx1a, Zfx1a|MGI:1344313|targeted mutation 1, Yujiro Higashi|Zeb1|MGI:1857515|18|||||||||||||||||||||||||||||Postnatal lethality.Decreased T cell number and abnormal T cell differentiation.Abnormal thymus development.Abnormal corneal morphology.||C57BL/6|No|No|Yes|No|No|Yes|No|Unknown||||No|09-Oct-2009|Cryopreserved sperm|150.0|0.0|Unknown||Corneal Dystrophy, Posterior Polymorphous, 3; PPCD3, T cell, differentiation, thymus, spleen, lymph node|Possibly| 4910.0|MommeR1|FVB-Foxo3/Apb||Recessive|forkhead box O3|Foxo3|Unknown|Fkhr2, FKHRL1, Foxo3a|MGI:1890081|modifier of murine metastable epialleles, R1|Foxo3||10||||||||||||||||Yes|Green Fluorescent Protein|human alpha-globin promoter and enhancer region|||||||||||Percentage of cells expressing the Line3 GFP transgene is decreased (enhancer of variegation).||FVB/NJ|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Poor|||MommeD5<+/->;Tg(α-Globin-GFP)3EWh x Tg(α-Globin-GFP)3EWh|No|09-Oct-2009|Cryopreserved sperm|120.0|0.0|No||epigenetics, histone modification|Yes| 89.0||Wavy||Recessive|||Unknown||||||3||||||||||||||||Yes|||||||||||||Rough coat with slightly wavy hair most visible at weaning, adults have only subtle coat changes, normal vibrissae; no overt hematological abnormality based on complete blood counts.Phenotype unique to this chromosome location, approx 65 genes in this region.||C57BL/6 x NOD|Yes|Yes|Yes|Yes|Yes|Yes|No|Poor||||No|06-Feb-2006|Cryopreserved sperm|75.0|0.0|Unknown||coat, hair, follicle, ENU|Yes| 5785.0|FGFR2||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 4927.0|Chloe|DBA-Acan||Recessive|aggrecan|Acan|Normal|Agc1, Cspg1|MGI:99602|aggrecan; targeted mutation 1, Amanda J Fosang|Acan|MGI:3577026|7||||||||||||||||Yes|||||||||||||Mutants develop normally with no skeletal abnormalities but do not accumulate aggregan in cartilage even though Agc1 is not cleaved by matrix metalloproteases||DBA|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|12-Nov-2009||0.0|0.0|Unknown||Cartilage, Skeletal, metalloproteinase (MMP), collagen, cleavage|Yes| 7721.0|Trail -/-|B6.129-Tnfsf10/AnuApb||Recessive|tumor necrosis factor (ligand) superfamily, member 10|Tnfsf10||A330042I21Rik, APO-2L, Trail|MGI:107414|tumor necrosis factor (ligand) superfamily, member 10; targeted mutation 1, Lisa M Sedger|Tnfsf10|MGI:2388390|3|||||||||||||||||||||||||||||Tumorigenesis:Normal • Background Sensitivity: unlike mice on a BALB/c congenic background, mice on a C57BL/6 congenic background show no difference from controls in the rate of A20 lymphoma tumor progression.Immune system phenotype:Normal• despite the potential contribution of genetic epistatic factors to autoimmune disease, no signs of lymphoproliferative disease are detected. • all lymphoid tissues and cell numbers of myeloid, lymphoid, and immature erythroid cell subpopulations are similar to controls.Skeleton phenotype:Normal:• despite the fact that this protein binds to osteoprotegrin, bone biology is normal and mice are not osteopetrotic (J:79085)||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|23-Jul-2014|Cryopreserved sperm|49.0|0.0|Unknown||Trail, Toll, infection, lymphoid|Yes| 7656.0|ENU25:007:Wdfy3:B6|C57BL/6NCrlAnu-Wdfy3/AnuApb|C57BL/6NCrlAnu-Wdfy3/AnuApb|Recessive|WD repeat and FYVE domain containing 3|Wdfy3|Unknown|2610509D04Rik, Bchs, Bwf1, D5Ertd66e, Ggtb3, mKIAA0993|MGI:1096875|WD repeat and FYVE domain containing 3; mutation 1, The Australian National University|Wdfy3|MGI:5648436|5|ENSMUSG00000043940|ENSMUST00000053177|Wdfy3-001|1501|2046|A to T|ENSMUSE00000326146|11|501|Arginine to Tryptophan|||||GGCACGACTACATATTTAAAGATGTCTTCAGGGAGGTGGGCCTGCTGGAGGTCATGGTAAA||||||||||||||Unknown||C7BL/6NCrlAnu|Yes|Unknown|Yes|Yes|Unknown|Yes|No|Unknown||||No|09-Apr-2014|Cryopreserved sperm|16.0|0.0|Unknown||ENU|Yes| 5647.0|C3aR KO ||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 192.0|CD26 -/-|C57BL/6-Dpp||Recessive|dipeptidylpeptidase 4|Dpp4|Nil|Cd26, Dpp-4, THAM|MGI:94919|targeted mutation 1, Nicolai Wagtmann|Dpp4|MGI:2150161|2||||||||||||||||Yes|||||||||||||Reduced type II diabetes symptoms in diabetes models. Reduced insulin resistance when fed high fat diet.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|17-Apr-2006||0.0|0.0|Unknown||diabetes, insulin, glucose tolerance, CD26|Yes| 1639.0|Jaffa|C57BL/6-Acan||Recessive|aggrecan|Acan|Normal|Agc1, Cspg1|MGI:99602|targeted mutation 2, Amanda J Fosang|Acan|MGI:3713763|7||||||||||||||||Yes|||||||||||||Mice are phenotypically normal. Mice show part protection against aggrecanolysis and cartilage erosion in models of experimentally induced arthritis.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|17-Jul-2007||0.0|0.0|Unknown||Cartilage, ADAMTS, arthritis, aggrecanase|Yes| 7722.0|Id4GFPB6|C57BL/6-Id4||Dominant|inhibitor of DNA binding 4|Id4||bHLHb27, Id4, Idb4|MGI:99414||||13|||||||||||||||||||||||||||||GFP at Id4 locus|GFP at Id4 locus|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|4||Pairs|No|24-Jul-2014|Cryopreserved sperm|50.0|0.0|Unknown|||Yes| 4928.0|Jaffa|DBA1-Acan||Recessive|aggrecan|Acan|Normal|Agc1, Cspg1|MGI:99602|targeted mutation 2, Amanda J Fosang|Acan|MGI:3713763|7||||||||||||||||Yes|||||||||||||Mice are phenotypically normal. Mice show part protection against aggrecanolysis and cartilage erosion in models of experimentally induced arthritis.||DBA1|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|12-Nov-2009||0.0|0.0|Unknown||Cartilage, ADAMTS, arthritis, aggrecanase|Yes| 1727.0|Eu-bcl2-25|B6.SJLWehi-Tg(BCL2)25Wehi||Dominant||||||||||||||||||||||||||transgene insertion 25, Walter and Eliza Hall Institute of Medical Research|Emu immunoglobulin heavy chain enhancer and SV40 promoter.|||||||||||Excess B cells throughout life. Develop glomerulonephritis, lymphoma and plasmacytoma Enlarged spleens lymphadenopathy (more white blood cells), larger (2-3fold) spleen and lymph nodes .|||Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|01-Aug-2007||0.0|0.0|Unknown||T cell, B cell, lymphocyte, bcl-2|Yes| 6368.0|PKCD?|B6.129P2-Prkcd/Ausb||Recessive|protein kinase C, delta|Prkcd|Nil|D14Ertd420e, PKC[d], Pkcd, PKCdelta|MGI:97598 |protein kinase C, delta; targeted mutation 1, Qingbo Xu|Prkcd|MGI:2385756|14|||||||||||||||||||||||||||||Premature deathImproved glucose toleranceIncreased insulin sensitivity:*Whole-body and in the liverDecreased liver triglyceride levelDecreased body weight:*Slightly at 20 weeks when mice are fed standard chowDecreased liver triglyceride level ||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown||Smooth muscle cell, Atherosclerosis|Yes| 7723.0|SoloxMed AR2|B6;CBA-Ifnar2 Tg(sIfnar2)2Pjh/MarpApb||Recessive|interferon (alpha and beta) receptor 2|Ifnar2|Increased|Ifnar-2 |MGI:1098243 |interferon (alpha and beta) receptor 2; targeted mutation 1, Paul J Hertzog|Ifnar2|MGI:2680693|16|||||||||||||||||interferon (alpha and beta) soluble receptor 2 |mouse Ifnar2|medium expression ||||||||||Normal. Increased expression of soluble IFNAR2 receptor.|Normal. |CBA|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|30-Jul-2014|Cryopreserved sperm|50.0|0.0|Unknown||septic shock, proinflammatory cytokine, agonist|Possibly| 2372.0||ENU8B6:061||Recessive|||||||||Unknown||||||||||||||||Yes|||||||||||||Defective antibody response to immunization: failure to mount a normal Th2 polarized IgG1 antibody response to chicken gammaglobulin (CGG). ||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|14-Dec-2007|Cryopreserved sperm|10.0|0.0|Unknown||B cell, antibody, immunization, ENU, Wellcome Trust|Yes| 6972.0|ENU20:027:a:B6:G3|ANU:ENU20:027:a:G3||Recessive|Unknown||||||||Unknown||||||||||||||||Unknown|||||||||||||Unknown|Unknown|C57BL/6JAnu|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||1||No|05-Jul-2012|Cryopreserved sperm|27.0|0.0|Unknown||ENU, random, mutagenesis, screen|Yes| 6191.0|Axin2/TOM|FVB-Tg(Axin2-d2EGFP)5Cos Tg(tetO-MYC)1Lach/Wehi||Recessive||||||||||||||||||||||||||transgene insertion 5, Frank Costantini|Axin2|||||||||||This strain carries the human c-myc gene and the rttA3-IRES-GFP cassette which are controlled by the Tet/O and the Axin2 promoter respectively. This stain should not have any obvious phenotype without treatment of doxycycline. DOX - The phenotypes of this strain with treatment of doxycycline remain unknown. But this strain may potentially develop tumors in certain tissues upon treatment with doxycycline.||FVB|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown||mammary, tumourigenesis, tetracycline responsive, signal transduction, phosphorylation, wnt|Possibly| 6191.0|Axin2/TOM|FVB-Tg(Axin2-d2EGFP)5Cos Tg(tetO-MYC)1Lach/Wehi||Recessive||||||||||||||||||||||||||transgene insertion 1, Lewis A Chodosh|bacterial tetracycline-resistance operon|||||||||||This strain carries the human c-myc gene and the rttA3-IRES-GFP cassette which are controlled by the Tet/O and the Axin2 promoter respectively. This stain should not have any obvious phenotype without treatment of doxycycline. DOX - The phenotypes of this strain with treatment of doxycycline remain unknown. But this strain may potentially develop tumors in certain tissues upon treatment with doxycycline.||FVB|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|13-Sep-2011||||Unknown||mammary, tumourigenesis, tetracycline responsive, signal transduction, phosphorylation, wnt|Possibly| 285.0||Balb/c.B6-IL13/Apb||Recessive|interleukin 13|Il13|Unknown|Il13|MGI:96541|targeted mutation 2, Andrew NJ McKenzie|Il13|MGI:1931804|11||||||||||||||||No|||||||||||||abnormal T helper 2 physiology: homozygotes display impaired pulmonary granuloma formation in response to schistosome egg immunizationeosinophil infiltration is impaired in response to schistosome egg immunizationincreased susceptibility to parasitic infection:the expulsion of parasitic worms from the gut is delayedA neomycin cassette was inserted into exon 3.||Balb/c|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|03-May-2006|Cryopreserved sperm|125.0|0.0|Unknown||IL4, IL5, T cell, infection|Yes| 4562.0|Krüppel-like Factor 3 (KLF3/BKLF) Knockout |FVB/NJ.129-Klf3/Apb||Recessive|Kruppel-like factor 3 (basic)|Klf3|Nil|BKLF, Bklf, Tef-2|MGI:1342773|targeted mutation 1, Merlin Crossley|Klf3|MGI:3799368|5||||||||||||||||Yes|||||||||||||Postnatal lethality, only 17% survive to weaning. Decreased adipose tissue, mice appear leaner, abnormal fat pads. Similar in size to wildtype at birth but significantly smaller than littermate controls from 3 to 12 weeks of age.|||Yes|No|Yes|Yes|No|Yes|Yes|Unknown||||No|05-Mar-2009|Cryopreserved sperm|100.0|0.0|Unknown||Kruppel-like Factor 3, Basic Kruppel-like Factor, KLF, Obesity, adipose|Yes| 3437.0|common beta chain KO|C57BL/6-Csf2rb/Wehi||Recessive|colony stimulating factor 2 receptor, beta, low-affinity (granulocyte-macrophage)|Csf2rb|Nil|AIC2B, Bc, beta c, CDw131, common beta chain, Csf2rb1, Il3r, Il3rb1, Il5rb|MGI:1339759|targeted mutation 1, C Glenn Begley|Csf2rb|MGI:2181245|15||||||||||||||||No|||||||||||||Homozygotes for targeted null mutations exhibit lung pathology including lymphocytic infiltration, alveolar proteinosis-like areas, and increased saturated phosphatidylcholine pool sizes. Mutants also have low peripheral eosinophil numbers.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|16-Jul-2008||0.0|0.0|Unknown||GM-CSF , IL-3 , IL-5, Receptor , signal transduction, lymphocyte infiltration, lung|Yes| 6973.0|ENU20:027:b:B6:G3|ANU:ENU20:027:b:G3||Recessive|Unknown||||||||Unknown||||||||||||||||Unknown|||||||||||||Unknown|Unknown|C57BL/6JAnu|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||1||No|05-Jul-2012|Cryopreserved sperm|40.0|0.0|Unknown||ENU, random, mutagenesis, screen|Yes| 4915.0|IL-13 -/- IL-4Ra -/-|BALB/c-IL13 IL4ra/AnuApb||Recessive|interleukin 13|Il13|Nil|Il-13|MGI:96541|targeted mutation 2, Andrew NJ McKenzie|Il13|MGI:1931804|11|||||||||||||||||||||||||||||Unknown||BALB/c|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|10|||No|16-Oct-2009|Cryopreserved sperm|100.0|0.0|Unknown||interleukin, IL10, IL5, Th2, T cell, parasite|Yes| 4915.0|IL-13 -/- IL-4Ra -/-|BALB/c-IL13 IL4ra/AnuApb||Recessive|interleukin 4 receptor, alpha|Il4ra|Unknown|D124, IL-4 receptor alpha chain, Il4r|MGI:105367|targeted mutation 1, Leonard Shultz|Il4ra|MGI:1861951|7|||||||||||||||||||||||||||||Unknown||BALB/c|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|10|||No|16-Oct-2009|Cryopreserved sperm|||Unknown||interleukin, IL10, IL5, Th2, T cell, parasite|Yes| 6646.0|HOM.NOD.FADD51|NOD-Tg(RIP2-dnFADD)51Wehi/WehiStvApb||Dominant||||||||||||||||||||||||||human dominant negative FADD|rat insulin promoter 2 (RIP)|||||||||||NOD.FADD.51 homozygous mice have reduced incidence of diabetes compared to NOD/Lt mice. They are healthy and breed well.|Mice have a slightly reduced incidence of diabetes when compared to NOD/Lt mice|NOD/Lt|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|10+|20+|Sister x Brother (hom x hom)|No|15-Nov-2011|Cryopreserved sperm|50.0|0.0|Yes|Type 1 diabetes|Pancreatic Beta cell, Type 1 diabetes, apoptosis, fas, cytikines|No| 273.0||BALB/c-H2-DMa||Recessive|histocompatibility 2, class II, locus DMa|H2-DMa|Unknown|H-2Ma, H2-Ma|MGI:95921||||17||||||||||||||||No|||||||||||||Homozygotes for targeted null mutations exhibit impaired antigen presenting cell function, poor IgG responses to T-dependent antigens, reduced numbers of mature CD4+ T cells, and increased susceptibility to Leishmania major infection.||BALB/c|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|01-May-2006|Cryopreserved sperm|125.0|0.0|Unknown||T cell, CD4, antigen presentation, IgG, infection|Yes| 4906.0|Stiliom; ENU4AT:032|B6;NODAnu-Tomm40/AnuApb||Semi-dominant|translocase of outer mitochondrial membrane 40 homolog (yeast)|Tomm40|Unknown|Tom40|MGI:1858259|Stiliom|Stil||7|ENSMUSG00000002984|ENSMUST00000093552|Tomm40-202|977|1048|C to T|ENSMUSE00000582554|10|326|Alanine to Valine|||||CTCTGTGAACAGTAACTGGATCGTGGGCGCCACGCTGGAGAAGAAGCTTCCGCCCTTGCCC|Yes|||||||||||||Lethal lung haemorrhage at 4 – 6 weeks, blood vessel fragility may be caused by suspected transdifferentiation of smooth muscle cells into skeletal muscle (a physiological process in the oesophagus) occurring throughout the body.TOM complex is absent in Blue-native PAGE analysis|Blue-native PAGE shows reduced levels of TOM complex in mitochondria in HETs; Monomeric Tomm40 is detected, but the mutant version of the protein migrates faster on SDS-PAGE than the wild-type protein (data from Diana Stojanovski and Mike Ryan at Latrobe.|C57BL/6JSfdAnu x NODk|Yes|No|Yes|Yes|No|Yes|No|Unknown||||No|09-Oct-2009|Cryopreserved sperm|30.0|0.0|Unknown||lung, haemorrhage, smooth muscle, mitochondrial myopathy, skeletal muscle, differentiation, blood vessel, transdifferentiation, JDRF|Yes| 6647.0|APN 89|C57BL/6N-ATP13a2/Marp||Recessive|ATPase type 13A2 |Atp13a2 |Unknown|1110012E06Rik |MGI:1922022 |ATPase type 13A2; targeted mutation 1e, Wellcome Trust Sanger Institute |Atp13a2|MGI:4433545|4||||||||||||||||Yes|||||||||||||Unknown - Not bred to homozygocity |Normal |C57BL/6N|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|15-Nov-2011|Cryopreserved sperm|50.0|0.0|Unknown||ES cell|Yes| 10336.0|Lats1 fl:Lats2 fl:K5-creERT2 |STOCK Lats1 Lats2 Tg(KRT5-cre/ERT2)2Ipc||Recessive|large tumor suppressor|Lats1|||MGI:1333883|large tumor suppressor; targeted mutation 1.1, James F Martin|Lats1|MGI:5568586|10|ENSMUSG00000040021 ||||||||||||||||transgene insertion 2, I Pierre Chambon|transgene insertion 2, I Pierre Chambon|||||||||||Normal|Normal||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|30-May-2023|Cryopreserved sperm|40.0|0.0|Unknown|||Possibly| 10336.0|Lats1 fl:Lats2 fl:K5-creERT2 |STOCK Lats1 Lats2 Tg(KRT5-cre/ERT2)2Ipc||Recessive|large tumor suppressor 2|Lats2|||MGI:1354386|large tumor suppressor 2; targeted mutation 1.1, James F Martin|Lats2|MGI:5568589|14|ENSMUSG00000021959 ||||||||||||||||||||||||||||Normal|Normal||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|30-May-2023|Cryopreserved sperm|||Unknown|||Possibly| 4549.0||B6.129-Ring1/WehiApb||Recessive|ring finger protein 1|Ring1|Nil||MGI:1101770|targeted mutation 1, Miguel Vidal|Ring1|MGI:1926913|17||||||||||||||||Yes|||||||||||||Increased rib number* 42% had 8 vertebrosternal ribs instead of 7Abnormal vertebrae morphology * 100% exhibited vertebrae abnormalities with abnormal C1 and C2Abnormal cervical atlas morphology Anormal cervical axis morphology Vertebral transformation * anterior transformations||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|10|||No|02-Mar-2009|Cryopreserved sperm|100.0|0.0|No||Polycomb group proteins, polycomb repressive complex 1, skeletal, anterior|Yes| 5019.0|B6 Lac I|B6.FVB/n-Lac I (USA) Tg1||Dominant||||||||||||||||||||||||||||||||||||||||10|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|22-Feb-2010|Cryopreserved sperm|150.0|0.0|Unknown|||No| 6974.0|ENU20:028:a:B6:G3|ANU:ENU20:028:a:G3||Recessive|Unknown||||||||Unknown||||||||||||||||Unknown|||||||||||||Unknown|Unknown|C57BL/6JAnu|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||1||No|05-Jul-2012|Cryopreserved sperm|20.0|0.0|Unknown||ENU, random, mutagenesis, screen|Yes| 287.0|Tune|BALB/c-Il4/AnuApb||Recessive|interleukin 4|Il4|Unknown|IgG1, Il-4|MGI:96556|targeted mutation 2, Nancy Noben-Trauth|Il4|MGI:1857195|11||||||||||||||||No|||||||||||||abnormal dendritic cell differentiation:numbers of MHCII/CD86-positive dendritic cells found in inflamed lungs are reduced by two-thirdsdecreased IgE level:reduced serum concentrations of IgE, however lymphocyte composition and function comparable to wild-type controlsdecreased IgG1 level:reduced serum concentrations of IgG1, however lymphocyte composition and function comparable to wild-type controlsabnormal dendritic cell antigen presentation:memory CD4 T cells activated by mutant DCs from inflamed lungs secrete low levels of Th2 cytokinesincreased interferon-gamma secretion:T cells from mice sensitized and challenged with OVA produce more IFN-gamma than controlsdecreased interleukin-13 secretion:lymphocytes from mice sensitized and challenged with OVA produce less IL-13 than controlsdecreased interleukin-5 secretion:lymphocytes from mice sensitized and challenged with OVA produce less IL-5 than controlsdecreased susceptibility to autoimmune disorder:mice fail to develop blood eosinophilia after being sensitized and challenged with OVA peptideairway hyperresponsiveness still occurs in these mice though less mucosal cells are found in the inflamed airwayhematopoietic systemabnormal dendritic cell differentiation:numbers of MHCII/CD86-positive dendritic cells found in inflamed lungs are reduced by two-thirds||BALB/c|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|03-May-2006|Cryopreserved sperm|100.0|0.0|Unknown||infection, inflammation, immunoglobulin, lymphocyte|Yes| 5567.0|ENU14Ch:048b|C57BL/6JAnu-Prkdc/AnuApb|C57BL/6JAnu-Prkdc/AnuApb|Recessive|protein kinase, DNA activated, catalytic polypeptide|Prkdc|Unknown|DNA-PK, DNA-PKcs, DNAPDcs, DOXNPH, dxnph, slip, XRCC7|MGI:104779|protein kinase, DNA activated, catalytic polypeptide; mutation 1, The Australian National University|Prkdc|MGI:5563438|16|ENSMUSG00000022672|ENSMUST00000023352|prkdc-201||||||||15714375|34|||GTTTCTCTCATGTTATATCACCATCTCAGGTAACTATGATCAGTTTGTTTTAACATATCT||||||||||||||Decreased % of T and B cells|Decreased % of T and B cells|C57BL/6JAnu|Yes|Unknown|Yes|Yes|Unknown|Yes|No|Good|4-6|5|Sib x sib|No|24-Aug-2011|Cryopreserved sperm|46.0|0.0|Unknown||ENU, T cell, B cell, lymphocyte|Possibly| 2777.0|C57BL/6.hK14-FLII 18|C57BL/6-Tg(hK14-FLII)18 ||Dominant|||||||||Unknown||||||||||||||||Yes|Human Flightless|Human Keratin 14|||||||||||Not bred to Homozygous state|Normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|5||Het FLII transgenic x WT C57BL/6|No|16-Feb-2008|Cryopreserved sperm|95.0|0.0|Unknown||human, skin, enhancer, keratin|Yes| 10335.0|R26-YAP5SA:K5-creERT|STOCK Gt(ROSA)26Sor(CAGGS-Yap5SA,LacZ)Mao Tg(KRT5-cre/ERT2)2Ipc/Anu||Recessive|gene trap ROSA 26, Philippe Soriano|Gt(ROSA)26Sor||Gtrosa26, R26, ROSA26|MGI:104735|gene trap ROSA 26, Philippe Soriano; targeted mutation 3, Junhao Mao|Gt(ROSA)26Sor|MGI:6763056|6|ENSMUSG00000086429 |||||||||Unknown to Unknown|||||||transgene insertion 2, I Pierre Chambon|K5-Cre |||||||||||Normal|Normal|C57Bl/6J|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|28-May-2023|Cryopreserved sperm|55.0|0.0|Unknown|||Possibly| 5529.0|Joey-SCO CBA|CBA.B6-Etv5/MarpApb|CBA.B6-Etv5/MarpApb|Recessive|ets variant gene 5|Etv5|Unknown|ERM|MGI:1096867|ets variant gene 5; sco|Etv5|MGI:5563470|16|ENSMUSG00000013089|ENSMUST00000079601|Etv5-202|1234|1414|A to T|ENSMUSE00000560895|12|412|Lysine to STOP|||||AAGAGGTTGCTCGCCGTTGGGGTATCCAGAAGAATCGGCCAGCCATGAACTATGACAAGCT|No|||||||||||||Sertoli cells only.Male infertility.Progressive loss of germ cells following the first wave of spermatogenesis.Germ cells appeared to be preferentially lost in a basal to apical direction from the seminiferous epithelium as detected in 7 week old testis.Reduced testis size, compared to WT, at 8 weeks of age.Etv5 mRNA levels 95% reduced compared to WT males.Etv5 mRNA is unstable.Reduced expression of Etv5 target genes Cxcr4 and Ccl9.Increased incidence of embryonic and perinatal lethality.Reduced body weight.Renal asymmetry.Polydactyly.||CBA|Yes|Yes|Yes|Yes|No|Yes|No|Unknown|7|||No|04-Jul-2011|Cryopreserved sperm|50.0|0.0|Unknown||infertility, sperm, arrest, ENU, sertoli|Yes| 4830.0|6CAT:002|ENU6CAT:002||Recessive|||||||||Unknown|||||||||||||||||transgene insertion 3, Christopher C Goodnow|Rat insulin promoter|Expression of the inserted sequence specifically to pancreatic islet beta cells||||||||||Mice carrying the ins-HEL gene have a subclinical predisposition to diabetes due to islet cell failure. Mice carrying the insHEL and TCR transgenes have asubclinical predisposition to autoimmune destruction of the beta cell. Screening mice by urine glucose test. High glucose levels indicate diabetes and thus autoimmunity. "Early onset diabetes" definition changed during screen from approx 80 days to 40 days.||C57BL/6 x C57BL/10BR x CBA|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|||Breed diabetic Double transgenic with a non transgenic sib for next generation|No|24-Sep-2009|Cryopreserved sperm|75.0|0.0|Yes|Type I Diabetes|ENU, JDRF, autoimmunity, T cell, B cell, glucose|No| 4830.0|6CAT:002|ENU6CAT:002||Recessive||||||||||||||||||||||||||transgene insertion 1, Mark M Davis||||||||||||Mice carrying the ins-HEL gene have a subclinical predisposition to diabetes due to islet cell failure. Mice carrying the insHEL and TCR transgenes have asubclinical predisposition to autoimmune destruction of the beta cell. Screening mice by urine glucose test. High glucose levels indicate diabetes and thus autoimmunity. "Early onset diabetes" definition changed during screen from approx 80 days to 40 days.||C57BL/6 x C57BL/10BR x CBA|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|||Breed diabetic Double transgenic with a non transgenic sib for next generation|No|24-Sep-2009|Cryopreserved sperm|||Yes|Type I Diabetes|ENU, JDRF, autoimmunity, T cell, B cell, glucose|No| 6771.0|Cryo expt|ENU23B6:G1||Recessive|Unknown||||||||Unknown|||||||||||||||||||||||||||||Normal|||Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|20-Dec-2011|Cryopreserved sperm|97.0|0.0|Unknown|||No| 4895.0||C57BL/6-Lyn/Apb||Recessive|Yamaguchi sarcoma viral (v-yes-1) oncogene homolog|Lyn|Normal|Hck-2|MGI:96892|Yamaguchi sarcoma viral (v-yes-1) oncogene homolog; multilineage defect 4 |Lyn|MGI:3832561|4|||||||||||||||||||||||||||||Peritneal inflammation.Increased T cell number: there is a bout a doubling in the number of T cells found in the peritoneum.Slight increase of macrophages in peripheral lymph tissues.Abnormal B cell morphology.Abnormal myelopoiesis.Glomerulonephritis||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|09-Oct-2009|Cryopreserved sperm|100.0|0.0|Unknown||signal transduction, kinase, receptor, B cell, autoimmunity, proinflammatory, signalling, myeloid, splenomegaly, autoantibody|Yes| 6796.0|MIN75tg|MIN 075||Recessive||||||||||||||||||||||||||||||||||||||Normal.Gene expressed in macrophages.|Normal|C57BL6|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|19-Jan-2012||0.0|0.0|Unknown|||Yes| 7724.0|Nasp KO|C57BL/6N-Nasp/MarpApb||Recessive|nuclear autoantigenic sperm protein (histone-binding)|Nasp||5033430J04Rik, D4Ertd767e, Epcs32, Nasp-T|MGI:1355328|nuclear autoantigenic sperm protein (histone-binding); targeted mutation 1a, Wellcome Trust Sanger Institute|Nasp|MGI:5006782|4|||||||||||||||||||||||||||||Unknown||C57BL/6N|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|20-Aug-2014|Cryopreserved sperm|55.0|0.0|Unknown|||Yes| 4471.0|cc10-rtTA|BALB/c-Tg(Scgb1a1-rtTA)/AnuApb||Dominant||||||||||||||||||||||||||reverse tetracycline response element (rtTA)|secretoglobin, family 1A, member 1 gene (Scgb1a1) or cc10|||||||||||Mice express reverse tetracycline response element under control of the promoter from the rat secretoglobin, family 1A, member 1 gene, which directs expression in Clara cells of the pulmonary epithelium. ||BALB/c|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|22-Feb-2009|Cryopreserved sperm|40.0|0.0|Unknown||inducible, tetracycline, inflammation, asthma|Yes| 7680.0|ENU7PMH:130:RagKO ; Krusty:Rag1 KO|B6.Cg-Ndfip1 Rag1/AnuApb||Recessive|Nedd4 family interacting protein 1|Ndfip1||0610010M22Rik|MGI:1929601|krusty|Ndfip1||18|ENSMUSG00000024425|ENSMUST00000025293|Ndfip1-201||||||||38612084|5|||TCTCTAATTAAGTGGATCCTTATTGTCAGGGTAAGTTGCATAGCAGAGAACAGATTGTGA||||||||||||||Autoimmune disease||C57BL/6JAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|13-May-2014|Cryopreserved sperm|30.0|0.0|Unknown||T cell, autoimmunity, CD4, ENU|Yes| 7680.0|ENU7PMH:130:RagKO ; Krusty:Rag1 KO|B6.Cg-Ndfip1 Rag1/AnuApb||Recessive|recombination activating gene 1|Rag1||Rag-1|MGI:97848|recombination activating gene 1; targeted mutation 1, Peter Mombaerts|Rag1|MGI:1857241|2|||||||||||||||||||||||||||||Autoimmune disease||C57BL/6JAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|13-May-2014|Cryopreserved sperm|||Unknown||T cell, autoimmunity, CD4, ENU|Yes| 4470.0|eotaxin -/-|C57BL/6-Ccl11/AnuApb||Recessive|small chemokine (C-C motif) ligand 11|Ccl11|Nil|eotaxin, Scya11|MGI:103576|targeted mutation 1, Marc E Rothenberg|Ccl11|MGI:2384435|11||||||||||||||||Yes|||||||||||||Abnormal immune system physiology * mutant mice have markedly fewer eosinophils in the jejunum than do wild-type controls||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|22-Feb-2009|Cryopreserved sperm|150.0|0.0|Unknown||chemokine, asthma, eosinophil|Yes| 7725.0|Solox Low AR|B6;CBA-Ifnar2 Tg(sIfnar2)1Pjh/MarpApb||Recessive|interferon (alpha and beta) receptor 2|Ifnar2|Increased|Ifnar-2 |MGI:1098243 |interferon (alpha and beta) receptor 2; targeted mutation 1, Paul J Hertzog|Ifnar2|MGI:2680693|16|||||||||||||||||interferon (alpha and beta) soluble receptor 2 |mouse Ifnar2|Low expression ||||||||||Normal. Increased expression of soluble IFNAR2 receptor.|Normal. |CBA|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|21-Aug-2014|Cryopreserved sperm|50.0|0.0|Unknown||septic shock, proinflammatory cytokine, agonist|Possibly| 5211.0|Gpc1 knockout|B6;CD-1-Gpc1/Apb||Dominant|glypican 1|gpc1|Nil||MGI:1194891|glypican 1; targeted mutation 1.1, Arthur Lander|Gpc1|MGI:3774029|1|||||||||||||||||||||||||||||Lifespan, fertility and health are normal. Occasional malocclusions. Brain may be slightly smaller than normal.|Unknown|C57BL/6 x CD-1|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|25-Aug-2010|Cryopreserved sperm|45.0|0.0|Unknown||growth plate, angiogenesis, heparan sulfate proteoglycans, fibroblast growth factor (FGF) signaling, glypican family|Possibly| 4476.0||C.B6-TLR2 TLR4/AnuApb||Recessive|toll-like receptor 2|Tlr2|Unknown|Ly105|MGI:1346060|toll-like receptor 2; targeted mutation 1, Shizuo Akira|Tlr2|MGI:2178675|3||||||||||||||||Yes|||||||||||||Homozygous null mice demonstrate abnormal responses to bacterial and viral infections.||Balb/c X C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|22-Feb-2009|Cryopreserved sperm|110.0|0.0|Unknown||Infection, lipopolysaccharide (LPS), MyD88, signal transduction|Yes| 4476.0||C.B6-TLR2 TLR4/AnuApb||Recessive|toll-like receptor 4|Tlr4|Unknown|lipopolysaccharide response, Lps, Rasl2-8|MGI:96824|toll-like receptor 4; targeted mutation 1, Shizuo Akira |Tlr4|MGI:1860885|4|||||||||||||||||||||||||||||Homozygous null mice demonstrate abnormal responses to bacterial and viral infections.||Balb/c X C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|22-Feb-2009|Cryopreserved sperm|||Unknown||Infection, lipopolysaccharide (LPS), MyD88, signal transduction|Yes| 4453.0|Johnson|BALB/c-Tlr2/AnuApb||Recessive|toll-like receptor 2|Tlr2|Nil|Ly105|MGI:1346060|toll-like receptor 2; targeted mutation 1, Shizuo Akira|Tlr2|MGI:2178675|3||||||||||||||||Yes|||||||||||||Homozygous null mice demonstrate abnormal responses to bacterial and viral infections.||BALB/c|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|20-Feb-2009|Cryopreserved sperm|120.0|0.0|Unknown||infection, bacterial, viral infection, macrophage|Yes| 2432.0|B7h knockout (ICOS ligand)|B6;129P2-Icosl/AnuApb|B6;129P2-Icosl/AnuApb|Recessive|icos ligand|Icosl|Nil|B7-H2, B7h, B7RP-1, GL50, GL50-B, ICOS-L, LICOS|MGI:1354701|targeted mutation 1, Kong-Peng Lam|Icosl|MGI:2673557|10||||||||||||||||No|||||||||||||Mice homozygous for disruptions in this gene exhibit defects in the humoral immune response associated with an impaired interactions between T and B cells. impaired germinal center formation. impaired interaction between T and B cellswhile normal repsonses are mounted against both type I and type II Tcell-independent antigens, the response to T-cell-dependent antigen was attenuated||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|||Het x Het ; Hom x Hom|No|13-Jan-2008|Cryopreserved sperm|80.0|0.0|No||B cell, T cell, lymphocyte, Germinal centre, costimulation|Yes| 5795.0|Gad 67 x C57||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 4465.0||C57BL/6-IL5 Eotaxin/AnuApb||Recessive|interleukin 5|Il5|Unknown|Il-5|MGI:96557|targeted mutation 1, Manfred A Kopf|Il5|MGI:1861948|11||||||||||||||||Yes|||||||||||||||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|10|||No|22-Feb-2009|Cryopreserved sperm|160.0|0.0|Unknown||eosinophil, chemokine, asthma, B cell, infection|Yes| 4465.0||C57BL/6-IL5 Eotaxin/AnuApb||Recessive|chemokine (C-C motif) ligand 11|Ccl11|Unknown|eotaxin, Scya11|MGI:103576|targeted mutation 1, Marc E Rothenberg|Ccl11|MGI:2384435|11|||||||||||||||||||||||||||||||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|10|||No|22-Feb-2009|Cryopreserved sperm|||Unknown||eosinophil, chemokine, asthma, B cell, infection|Yes| 6396.0|PTPcnLPRHLtg|B6.Cg-Fas Igh Pepc Ptprc Tg(IgkHyHEL10)1Rbr>/Ausb||Dominant|immunoglobulin heavy chain complex|Igh|Normal||MGI:96442|immunoglobulin heavy chain complex; targeted mutation 1, Robert Brink|Igh|MGI:3800383|Unknown|||||||||||||||||transgene insertion 1, Robert Brink||||||||||||Unknown|Unknown|C57BL/6|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Yes| 6396.0|PTPcnLPRHLtg|B6.Cg-Fas Igh Pepc Ptprc Tg(IgkHyHEL10)1Rbr>/Ausb||Dominant|peptidase C|Pepc|Normal|Dip-1, Pep-3, Pep3|MGI:97541|peptidase C; b variant|Pepc|MGI:4819861|Unknown|||||||||||||||||||||||||||||Unknown|Unknown|C57BL/6|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|13-Sep-2011||||Unknown|||Yes| 6396.0|PTPcnLPRHLtg|B6.Cg-Fas Igh Pepc Ptprc Tg(IgkHyHEL10)1Rbr>/Ausb||Dominant|Fas (TNF receptor superfamily member 6)|Fas|Normal|APO-1, CD95, TNFR6, Tnfrsf6|MGI:95484|Fas (TNF receptor superfamily member 6); lymphoproliferation|Fas|MGI:1856334|19|||||||||||||||||||||||||||||Unknown|Unknown|C57BL/6|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|13-Sep-2011||||Unknown|||Yes| 6396.0|PTPcnLPRHLtg|B6.Cg-Fas Igh Pepc Ptprc Tg(IgkHyHEL10)1Rbr>/Ausb||Dominant|protein tyrosine phosphatase, receptor type, C|Ptprc|Normal|B220, CD45, Ly-5, Lyt-4, T200|MGI:97810|protein tyrosine phosphatase, receptor type, C; a variant|Ptprc|MGI:4819849|1|||||||||||||||||||||||||||||Unknown|Unknown|C57BL/6|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|13-Sep-2011||||Unknown|||Yes| 6587.0|MLR34|FVB/N-Tg(Cryaa-cre)34Mlr/Apb||Dominant||||||||||||||||||||||||||transgene insertion 34, Mike Robinson|modified alpha A crystallin promoter with an inserted copy of Pax6 consensus binding site|||||||||||Nil. Mice express Cre in lens fibres, and retina and various embryonic structures|Normal|FVB/N|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|unkown||inbred|No|23-Sep-2011|Cryopreserved sperm|40.0|0.0|Unknown||crystallin, lens, eye, epithelial, Pax6|Yes| 343.0|B7C kk|B10.Cg-Tg(SERPINC1-CD86)/Apb||Dominant||||||||||||||||||||||||||murine CD86|human anti-thrombin III (SERPINC1) + regulatory intronic sequences of MHC class II|low on 15% of hepatocytes||||||||||Express CD86 on 15% of hepatocytes. Expression elsewhere has not been reported.|Express CD86 on 15% of hepatocytes. Expression elsewhere has not been reported.|C57BL/10.BR|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|10|15|B7Ckk X B7Ckk|No|22-Sep-2006|Cryopreserved sperm|30.0|0.0|No||costimulation, hepatocytes, T cells, liver, T cell activation, Hepatitis C (HCV), hepatocellular carcinoma|Yes| 5024.0|ASD201|B6.129-H2/J||Recessive||||||||||||||||||||||||||||||||||||||||10|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|22-Feb-2010|Cryopreserved sperm|100.0|0.0|Unknown|||No| 5796.0|Gal4 Robin (Balb/C)||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6864.0|ENU16Ch:085a reln|C57BL/6JAnu-Reln/AnuApb|C57BL/6JAnu-Reln/AnuApb|Recessive|reelin|Reln|Unknown||MGI:103022|reelin; mutation 1, The Australian National University|Reln|MGI:5563426|5|ENSMUSG00000042453|ENSMUST00000161356|Reln-001||||||||21408594|59|||ATCCAGCTCCCAGACCACGTCTCGTCAAGGTGGGTTGTCTACAGAGGTAAGCCTAGTGGG||||||||||||||Pups are uncoordinated and runted|Normal|C57BL/6JAnu|Yes|Yes|Yes|Yes|Unknown|Yes|No|Good||G6|het x het|No|23-Mar-2012|Cryopreserved sperm|36.0|0.0|Unknown||runted, uncoordinated, small, ENU|Yes| 3577.0|C57BL/6-Tg TCR F5|C57BL/6-Tg(CD2-TcraF5,CD2-TcrbF5)1Kio/Wehi||Dominant||||||||||||||||||||||||||transgene insertion 1, Dimitris Kioussis|||||||||||||This clone is CD8+ and recognises amino acids 366-374 of the nucleoprotein (NP 366-374) of influenza virus (A/NT/60/68), in the context of Class I MHC Db (Townsend et al., 1986). The usage of V beta 11 makes this TcR reactive to Class II IE molecules and an endogenous ligand recently identified as a product of the endogenous mammary tumour viruses (Mtv) 8, 9, and 11. Report the development of F5 transgenic T cells and their function in mice of the appropriate MHC (C57BL/10 H-2b, IE-) or in mice expressing Class II MHC IE (e.g., CBA/Ca H-2k and BALB/c H-2d) and the endogenous Mtv ligands. Positive selection of CD8+ T cells expressing the V beta 11 is seen in C57BL/10 transgenic mice (H-2b). Peripheral T cells from these mice are capable of killing target cells in an antigen-dependent manner after a period of in vitro culture with IL-2. In the presence of Class II MHC IE molecules and the endogenous Mtv ligand, most of the single-positive cells carrying the transgenic T-cell receptor are absent in the thymus. Unexpectedly, CD8+ peripheral T-cells in these (H-2k or H-2d) F5 mice are predominantly V beta 11 positive and also have the capacity to kill targets in an antigen-dependent manner. This is true even following backcrossing of the F5 TcR transgene to H-2d scid/scid mice, in which functional rearrangement of endogenous TcR alpha- and beta-chain genes is impaired.|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|04-Aug-2008||0.0|0.0|Unknown||T cell receptor (TCR), T cell, influenza, cytotoxic, CD8|Yes| 1507.0||C57BL/6-IL12b IL18/Apb||Recessive|interleukin 12b|Il12b|Unknown|IL-12 p40, Il-12b, Il-12p40, IL-23 subunit p40|MGI:96540|targeted mutation 1, Jeanne Magram|Il12b|MGI:1857201|11||||||||||||||||Yes|||||||||||||Homozygous mutants have reduced ability to produce IFN-γ, reduced NK cell activity, impaired T helper cell response and increased susceptibility to bacterial growth and tuberculosis. NK activity lower than seen in either single gene knockout.||C57BL/6 x 129|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|04-Jul-2007|Cryopreserved sperm|100.0|0.0|No||T cell, Natural Killer cell, interferon, infection|Yes| 1507.0||C57BL/6-IL12b IL18/Apb||Recessive|interleukin 18|Il18|Nil|Igif, Il-18|MGI:107936|targeted mutation 1, Shizuo Akira|Il18|MGI:2136769|9|||||||||||||||||||||||||||||Homozygous mutants have reduced ability to produce IFN-γ, reduced NK cell activity, impaired T helper cell response and increased susceptibility to bacterial growth and tuberculosis. NK activity lower than seen in either single gene knockout.||C57BL/6 x 129|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|04-Jul-2007|Cryopreserved sperm|||No||T cell, Natural Killer cell, interferon, infection|Yes| 4992.0|c-cbl KO|STOCK H2 Cbl/AnuApb ||Recessive|Casitas B-lineage lymphoma|Cbl|Nil|c-Cbl, cbl, Cbl-2|MGI:88279|targeted mutation 1, David D L Bowtell|Cbl|MGI:2180578|9||||||||||||||||Yes|||||||||||||Homozygotes for targeted null mutations exhibit increased thymic CD3 and CD4 expression and tyrosine-phosphorylation, lymphoid hyperplasia, and altered splenic hemopoiesis. Females show increased ductal density and branching in mammary fat pads.Abnormal spleen red pulp morphology- expandedenlarged spleen. Spleen is enlarged about 1.2- to 2-fold compared to wild type mice due to expansion of the red pulpspleen hyperplasia.Increase in the number of megakaryocytes, megakaryoblasts, and myelocytes but no increase in the number of lymphocytes is seen in the spleen.Abnormal adipocyte morphology- adipocyte volume is reduced by about 64% compared to wild type mice.Decreased adipose tissue amount- despite increased caloric intake, a 40-50% decrease in the size of the adipose tissue depots (including both white and brown fat) is seenthis phenotype is more pronounced in males than in females.Increased lean body mass- balances the decrease in adipose tissue resulting in no significant difference in total body weight.Polyphagia.Hyperactivity- about a 4-fold increase in ambulatory activity is seen, especially during the dark phase.Increased body temperature- rectal temperature is increased by 1 degree C independent of time of day or if the mice are fed or fasted overnight. However, circulating levels of triiodothyronine or thyroxine are similar to wild type in both the fed and fasted states.Decreased circulating leptin level- leptin levels are decreased by 66%; however adiponectin levels are similar to wild type.Abnormal gas homeostasis- increased oxygen consumption:whole body oxygen consumption corrected for the difference in lean mass is increased by 22% compared to wild type mice.Abnormal respiratory quotient- reduced respiratory quotientAbnormal glucose homeostasis- decreased circulating insulin level, after an overnight fast insulin levels are decreased relative to wild type but glucose levels are similar to wild type.Improved glucose tolerance- improved glucose tolerance despite decreased insulin levels throughout the test.Increased insulin sensitivity.Abnormal lipid homeostasis- decreased circulating free fatty acid level.Decreased triglyceride level- triglyceride levels in the liver are decreased but those in the quadriceps muscle are similar to wild type muscleAbnormal muscle physiology- glucose clearance in to glycogen is increased in the soleus and extensor digitorum longus muscles but not in the liver.Abnormal muscle cell glucose uptake- glucose uptake into skeletal muscle is increased about 2-fold; however glucose uptake into white and brown adipose tissue is not different from wild type. Basal and insulin-stimulated glucose uptake are increased in soleus muscle explants by 65% and 30%, respectively; however, glucose uptake is not increased in fat explants basal, but not insulin-stimulated, glucose uptake is increased by 30% in extensor digitorum longus muscle explantscellular.Abnormal mitochondrial morphology- a 2-fold increase in the average size of subsarcolemmal mitochondria is seen; however, no increase in mitochondrial area or cristae density is seen in the subsarcolemmal region.Spleen hyperplasia- increase in the number of megakaryocytes, megakaryoblasts, and myelocytes but no increase in the number of lymphocytes is seen in the spleen.||129/1SV x C57BL/6 x C57BL/10.BR-H2|Yes|Yes|Yes|Yes|Yes|Yes|No|Poor||||No|28-Jan-2010|Cryopreserved sperm|45.0|0.0|No||Cbl, tyrosine kinase, TKB, Zap-70, adipose|Yes| 10338.0|Igh2A10-GFP|C57BL/6JAnu-Itgal Tg(IgH2A10)1Anu/Anu||Dominant|IgH|||||Tg:IgH2A10|||Unknown|||||||||||||||||2A10|||for L2 reder||||||||Unknown|Normal|normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|31-May-2023||0.0|0.0|Unknown||Infection|Yes| 1556.0|P47phox-/-|NOD/Lt-Ncf1/AnuApb||Recessive|neutrophil cytosolic factor 1|Ncf1|Unknown|NADPH oxidase subunit (47kDa), Ncf-1, NOXO2, p47phox, p47phox|MGI:97283||||5||||||||||||||||Yes|||||||||||||Abnormal neutrophil physiology. Granulomatous inflammation. Crystal in lungs and bile ducts. Skin abscess||NOD/Lt|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|06-Jul-2007|Cryopreserved sperm|150.0|0.0|Unknown||neutrophil, granulocytes|Yes| 5354.0|rbp4 KO|B6;129/Sv-Rbp4/Apb||Recessive|retinol binding protein, plasma|Rbp4|Nil|Rbp-4, retinol binding protein 4, cellular|MGI:97879|retinol binding protein 4, plasma; targeted mutation 1, Max E Gottesman|Rbp4 |MGI:2445721|19||||||||||||||||No|||||||||||||Mutant mice fed a vitA-enriched diet are healthy and fertile. They exhibit impaired retinal function during the first few months of life but acquire normal vision on a vitA sufficient diet.Pups bred from dams maintained on vitA deficient diet for extended periods develop severe developmental deformities and die in utero.|Unknown but probably same as normal.|Mixed 129/Sv-C57BL/6 genetic background|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|Unknown|1|Inbred|No|20-Dec-2010|Cryopreserved sperm|70.0|0.0|Unknown||retinol, vitamin A, knockout, retinol binding protein, plasma|Yes| 641.0|c-Cbl (G304E)|STOCK Cbl/Apb|STOCK Cbl/Apb|Recessive|Casitas B-lineage lymphoma|Cbl|Normal|4732447J05Rik, c-Cbl, cbl, Cbl-2|MGI:88279|targeted mutation 1, Wallace Langdon|Cbl|MGI:2451336|9||||||||||||||||Yes|||||||||||||Mice have a physically normal outward appearance and are generally healthy. Up to ~40% homozygous females have blockages in the uterine horns and fallopian tubes, while ~25% of homozygous males appear infertile. All homozygous mice show slight splenomegaly (~50% larger than wildtype control).|Appear normal and healthy|129S1/SvJ x C57BL/6J|Yes|Yes|Yes|Yes|Yes|Yes|Yes|Good|||Hom x Het|No|25-Apr-2007|Cryopreserved sperm|100.0|0.0|Unknown||Cbl, tyrosine kinase binding domain, TKB, Zap-70|Yes| 1524.0||C.Cg-Myd88 Tg(CD2-IL5)5C2Ldt/Apb|C.Cg-Myd88 Tg(CD2-IL5)5C2Ldt/Apb|Recessive|myeloid differentiation primary response gene 88|Myd88|Nil||MGI:108005|targeted mutation 1, Shizuo Akira|Myd88|MGI:2385681|9||||||||||||||||Yes|transgene insertion 5C2, Lindsay A Dent |The dominant control region (DCR) of the gene encoding human CD2|High - 49 Copies||||||||||Provide a source of Myd88 deficient eosinophils||BALB/c|Yes|No|Yes|Yes|No|Yes|No|Unknown||||No|05-Jul-2007|Cryopreserved sperm|80.0|0.0|Unknown||eosinophils, infection, virus clearance, TLR, interferon|Yes| 5028.0||Ym2 Tg(+/+) Balb/c X CC10/rtTA Tg(+/-) Balb/c||Dominant||||||||||||||||||||||||||||||||||||||||6|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|22-Feb-2010|Cryopreserved sperm|60.0|0.0|Unknown|||No| 4528.0||B6.CBA-Tg(hGMCSF-CK1m)397/AnuApb||Dominant||||||||||||||||||||||||||human GMCSF (GM-CSF)|human GM-CSF promoter and enhancer (10.5kb)|||||||||||Express human GM-CSF. hGM-CSF detected in serum by ELISA. Murine GM-CSF used as internal control.|||Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|27-Feb-2009|Cryopreserved sperm|40.0|0.0|Unknown||T cell, lymphocyte, transcription, chromatin remodelling, NF-kappaB|Yes| 4969.0|Beta Tg|C.129/Sv-Tg(hGM-CSFRb) Csf2rb Csf2rb2/Apb||Dominant|colony stimulating factor 2 receptor, beta, low-affinity (granulocyte-macrophage)|Csf2rb|Unknown|AIC2B, Bc, beta c, CDw131, common beta chain, Csf2rb1, Il3r, Il3rb1, Il5rb|MGI:1339759|targeted mutation 1, Clare L Scott|Csf2rb|MGI:3653883|15||||||||||||||||Yes|human beta common chain receptor for GM-CSF/IL-3/IL-5|human ubiquitin C promoter|low||||||||||Normal|Normal|BALB/c|Yes|Yes|Yes|Yes|Yes|Yes|No|Excellent|10|0|Purchased BALB/c mated with transgenic mouse from colony to maintain colony|No|15-Jan-2010|Cryopreserved sperm|100.0|0.0|Unknown||growth factor, interleukin, signal transduction, receptor|Yes| 4969.0|Beta Tg|C.129/Sv-Tg(hGM-CSFRb) Csf2rb Csf2rb2/Apb||Dominant|colony stimulating factor 2 receptor, beta 2, low-affinity (granulocyte-macrophage)|Csf2rb2|Unknown|AIC2A, BetaIl3, Bil3, Il3r, Il3rb2|MGI:1339760|targeted mutation 1, C Glenn Begley|Csf2rb2|MGI:3652583|15|||||||||||||||||||||||||||||Normal|Normal|BALB/c|Yes|Yes|Yes|Yes|Yes|Yes|No|Excellent|10|0|Purchased BALB/c mated with transgenic mouse from colony to maintain colony|No|15-Jan-2010|Cryopreserved sperm|||Unknown||growth factor, interleukin, signal transduction, receptor|Yes| 6975.0|ENU20:028:b:B6:G3|ANU:ENU20:028:b:G3||Recessive|Unknown||||||||Unknown||||||||||||||||Unknown|||||||||||||Unknown|Unknown|C57BL/6JAnu|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||1||No|05-Jul-2012|Cryopreserved sperm|45.0|0.0|Unknown||ENU, random, mutagenesis, screen|Yes| 6979.0|ENU20:034:a:B6:G3|ANU:ENU20:034:a:G3||Recessive|Unknown||||||||Unknown||||||||||||||||Unknown|||||||||||||Unknown|Unknown|C57BL/6JAnu|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||1||No|05-Jul-2012|Cryopreserved sperm|28.0|0.0|Unknown||ENU, random, mutagenesis, screen|Yes| 7726.0|ShhTg|C57BL/6-Tg(CAG)LSL(eGFP/mShh)Dnw||Dominant||||||||||||||||||||||||||sonic hedgehog|chicken beta-actin|||||||||||Unknown|Normal in the absence of Cre recombinase.|C57BL/6|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Excellent||||No|25-Aug-2014|Cryopreserved sperm|36.0|0.0|Unknown||signal transduction|Yes| 4527.0||B6.CBA-Tg(hGMCSF-CK1m)418/AnuApb||Dominant|||||||||Unknown||||||||||||||||Yes|human GMCSF (GM-CSF)|human GM-CSF promoter and enhancer (10.5kb)|||||||||||Express human GM-CSF. hGM-CSF detected in serum by ELISA. Murine GM-CSF used as internal control.|||Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|27-Feb-2009|Cryopreserved sperm|50.0|0.0|Unknown||T cell, lymphocyte, transcription, chromatin remodelling, NF-kappaB|Yes| 7535.0|P14|B6;D2-tg(TcrLMCV)327Sdz/JDvsJWehiAusb|B6;D2-tg(TcrLMCV)327Sdz/JDvsJWehi|Dominant||||||||||||||||||||||||||transgene insertion 327, Birgit Ledermann||10-20||||||||||||(C57BL/6 x DBA/2)F2|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|12-Dec-2013||0.0|0.0|Unknown||T cell, MHC, lymphocytic choriomeningitis virus, TCR|Yes| 4965.0||FVB/N.129-Gt(ROSA)26Sor/AusbApb||Dominant|gene trap ROSA 26, Philippe Soriano|Gt(ROSA)26Sor|Unknown|beta geo, Gtrgeo26, Gtrosa26, R26, ROSA26|MGI:104735|gene trap ROSA 26, Philippe Soriano|Gt(ROSA)26Sor|MGI:1890203|6|||||||||||||||||||||||||||||Normal|Expresses Beta-galactosidase in cells where Cre recombinase is expressed|FVB/N|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|15-Jan-2010|Cryopreserved sperm|90.0|0.0|Unknown||Cre recombinase, LacZ, ROSA26|Yes| 5171.0|Thin Coat|ENU16WT:006a||Recessive|Unknown|Unknown|||||||Unknown|||||||||||||||||||||||||||||Mice have "thin coats" at weaning. This develops into a "fluffy" coat as they get older||C57BL/6JAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||1|Random sib x sib intercross|No|01-Jul-2010|Cryopreserved sperm|36.0|0.0|Unknown||hair, coat, keratin, ENU, Wellcome Trust|Possibly| 6976.0|ENU20:029:a:B6:G3|ANU:ENU20:029:a:G3||Recessive|Unknown||||||||Unknown||||||||||||||||Unknown|||||||||||||Unknown|Unknown|C57BL/6JAnu|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||1||No|05-Jul-2012|Cryopreserved sperm|70.0|0.0|Unknown||ENU, random, mutagenesis, screen|Yes| 4777.0|CCR +/+|B6.129-Ccr(WT)||Dominant||||||||||||||||||||||||||||||||||||||Normal.Control for experiments with Ccr5 knockouts. A control strain in which the CCR gene cluster is derived from the 129/Ola strain was developed by crossing wild-type F1 progeny of 129/Ola × C57BL/6J matings (40). A BglII restriction fragment length polymorphism was found that distinguishes the CCR5 allele in 129/Ola and C57BL/6J; a probe made from a 1.5-kb XbaI fragment located about 1.8 kb upstream of the CCR5 coding exon detects a 3.3-kb BglII fragment in 129/Ola and a 3.6-kb BglII fragment in C57BL/6J genomic DNA.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|06-Sep-2009|Cryopreserved sperm|150.0|0.0|No||chemokine, Ccr2, Ccr5, Ccr1, control|Yes| 5034.0||FVB/N-Tg(MMTV-PyVT)634Mul/JAusbApb||Dominant||||||||||||||||||||||||||transgene insertion 634, William Muller|mouse mammary tumor virus LTR|High|||||||||||Mammary gland tumor: * average onset of tumor development is 66 days. * tumor nodules are present throughout the entire mammary gland. * extensive adenomas are found.|FVB/N|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Good||||No|22-Feb-2010|Cryopreserved sperm|88.0|0.0|Unknown||Mammary, oncogene, metastasis, transformation, epithelium|Yes| 5638.0|BDNFFlox||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5639.0|BKLF/B||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5640.0|BOO||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 10340.0|Rpl41 cKO (5)|C57BL/6NCrl-Rpl41/Anu||Recessive|ribosomal protein L41|Rpl41|||MGI:1915195 ||||10|ENSMUSG00000093674||||||||||||||||||||||||||||Unknown|Unknown|C57Bl/6N|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Good||||No|19-Jun-2023|Cryopreserved sperm|57.0|0.0|Unknown|||Possibly| 65.0||Rockstar||Recessive|||Unknown||||||2||||||||||||||||Yes|||||||||||||Microphthalmia or no eyes, weepy eyes; clumpy fur, chocolate coat and some hair loss in older mice|||Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|06-Feb-2006|Cryopreserved sperm|35.0|0.0|Unknown||eye, microphthalmia, ENU|Yes| 7727.0|ENU32:G1|ANU:ENU32:G1||Recessive|Unknown||||||||Unknown||||||||||||||||Unknown|||||||||||||Unknown|Unknown|C57BL/6NCrlAnu|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||1||No|26-Aug-2014|Cryopreserved sperm|2197.0|0.0|Unknown||ENU, random, mutagenesis, screen|Yes| 3564.0||C57BL/6.CBA-Sfpi1 Tg(CAG-cre/Esr1)5Amc||Semi-dominant|SFFV proviral integration 1|Sfpi1|Unknown|Dis-1, PU.1, Sfpi-1, Spi-1, Tcfpu1, Tfpu.1|MGI:98282|SFFV proviral integration 1; targeted mutation 1.2, Stephen L Nutt |Sfpi1|MGI:3578011|2||||||||||||||||Yes|transgene insertion 5, Andrew P McMahon|chicken beta actin promoter/enhancer coupled with the cytomegalovirus (CMV) immediate-early enhancer|||||||||||cre-ER fertility - sterile|Heterozygous mutant mice are viable, fertile, normal in size and do not display any gross physical or behavioural abnormalities.|C57BL/6 x CBA|Yes|No|Yes|Yes|No|Yes|No|Unknown||||No|01-Aug-2008||0.0|0.0|Unknown||inducible, lymphoid, myeloid, granulocyte, bone marrow|Yes| 7287.0|B6/JAnu-redev - Red G20|C57BL/6JAnu-redev-RedG20||Dominant||||||||||||||||||||||||||||||||||||||||C57BL/6JAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|12-Mar-2013|Cryopreserved sperm|19.0|0.0|Unknown|||No| 5518.0|Partial Rescue|ENU18PiDTau_164||Dominant|Unknown|Unknown|||||||Unknown|||||||||||||||||||||||||||||Unknown|Rescue of Parkinsonism PiDTau phenotype ie: reduced tremors, clasping, gait and weight scores.|PiDTau balb/B6|No|Yes|Yes|No|Yes|Yes|No|Good||||No|03-Jun-2011|Cryopreserved sperm|8.0|0.0|Unknown|||No| 1971.0|available from Animal Resources Centre - www.arc.wa.gov.au|C.C3-H2k/LilMcdJArc (BALB.K)||Dominant|Congenic albino: A, Tyr, Tyrp1, Congenic partner BALB/c.||Unknown||||||Unknown||||||||||||||||No||||||||||||||||Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||Yes|04-Sep-2007||0.0|0.0|No|||Yes| 4791.0|C3H|C3H/HeH||Dominant||||||||||||||||||||||||||||||||||||||Normal.||C3H/HeH|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|06-Sep-2009|Cryopreserved sperm|40.0|0.0|Unknown||C3H|No| 4532.0|Cat-1-eGFP|C57BL/6-Tg(Tie2-Slc7a1/eGFP)/Apb||X-linked||||||||||||||||||||||||||solute carrier family 7 (cationic amino acid transporter, y+ system), member 1 fused to eGFP (Atrc-1, Atrc1, Cat1, mCAT-1, Rec-1, Rev-1)|endothelial-specific receptor tyrosine kinase (Tek, Tie2)|||||||||||||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|27-Feb-2009|Cryopreserved sperm|95.0|0.0|Yes||endothelial arginine transport, nitric oxide (NOS), hypertension|Yes| 7728.0|ENU32:G2|ANU:ENU32:G2||Recessive|Unknown||||||||Unknown||||||||||||||||Unknown|||||||||||||Unknown|Unknown|C57BL/6NCrlAnu|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||1||No|26-Aug-2014|Cryopreserved sperm|3631.0|0.0|Unknown||ENU, random, mutagenesis, screen|Yes| 5801.0|Genia (ko) x Teague (ko)||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5031.0|C3H|C3H||Dominant||||||||||||||||||||||||||||||||||||||||1|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|22-Feb-2010|Cryopreserved sperm|10.0|0.0|Unknown|||No| 5033.0||ENU11B6:007b||Recessive|||||||||Unknown||||||||||||||||Unknown|||||||||||||||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|22-Feb-2010|Cryopreserved sperm|10.0|0.0|Unknown||ENU|Yes| 5032.0||Control||Dominant||||||||||||||||||||||||||||||||||||||||1|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|22-Feb-2010|Cryopreserved sperm|940.0|0.0|Unknown|||No| 7537.0|Smarta|C57BL/6-Tg(TcrLCMV)Aox/WehiAnuApb|C57BL/6-Tg(TcrLCMV)Aox/WehiAnuApb|Dominant||||||||||||||||||||||||||transgene insertion, Annette Oxenius|Tcr|||||||||||||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|12-Dec-2013|Cryopreserved sperm|36.0|0.0|Unknown||TCR, MHC, CD4, lymphocytic choriomeningitis virus|Yes| 5067.0|ED1f|EDD1 KO||Recessive||||||||||||||||||||||||||||||||||||||Unknown|||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown|10|||No|25-Mar-2010|Cryopreserved sperm|100.0|0.0|Unknown|||Yes| 5022.0|B6.H2k:B6xB6H2k|B6(Cg).AK-H2/JAnuApb||Dominant|||||||||||||||||||||||||||||histocompatibility-2, MHC|H2||H-2, MHC-II|MGI:95894|histocompatibility-2, MHC; k variant|H2|MGI:3579322|17|||C57BL/6SfdAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|22-Feb-2010|Cryopreserved sperm|150.0|0.0|No||MHC, H2, C57BL/6J|No| 5005.0||EGFP tg||Dominant||||||||||||||||||||||||||||||||||||||||4|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|22-Feb-2010|Cryopreserved sperm|40.0|0.0|Unknown|||No| 5026.0|Bertolino|Bertolino||Recessive||||||||||||||||||||||||||||||||||||||||1|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|22-Feb-2010|Cryopreserved sperm|10.0|0.0|Unknown|||No| 5009.0|Yastrzemski|B6.129-Ryr pTar 4E6 tg1||Dominant||||||||||||||||||||||||||||||||||||||||12|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|22-Feb-2010|Cryopreserved sperm|145.0|0.0|Unknown|||Possibly| 5012.0|ED2Delta|EDD1 KO Clone 2||Recessive||||||||||||||||||||||||||||||||||||||||11|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|22-Feb-2010|Cryopreserved sperm|165.0|0.0|Unknown|||No| 5018.0|BALB/cLac I|BALB/c.FVB/n-Lac I (USA) Tg1||Dominant||||||||||||||||||||||||||||||||||||||||10|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|22-Feb-2010|Cryopreserved sperm|150.0|0.0|Unknown|||No| 5023.0|Waugh|BALB/c-Homo Rosa EGFP||Dominant||||||||||||||||||||||||||||||||||||||||9|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|22-Feb-2010|Cryopreserved sperm|120.0|0.0|Unknown|||No| 10339.0||C57BL/6J-mACE2-hACE2/Apb||Semi-dominant|hACE2 transgene||||||||Unknown|||||||||||||||||hACE2|mACE2|||||||||||hACE2 is expressed from a transgene under control of the mACE2 promoter - providing authentic gene expression. This hACE2 expression allows for SARS-CoV-2 infection of mouse lungs and nasal turbinates, with ensuing histopathology and inflammatory responses comparable to human disease. Please see the attached publication for more information and discussion. Homozygotes are viable and fertile (normal litter sizes etc.).|Same as homozygous|C57Bl/6J|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|08-Jun-2023||0.0|0.0|Unknown|||Possibly| 5807.0|GH-GFP||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 4985.0|FATSO ; ENU6AT:055|C57BL/6JSfdAnu-Ints10/AnuApb||Recessive|integrator complex subunit 10|Ints10|Unknown||MGI:1918135||||8|ENSMUSG00000031864|ENSMUST00000070713|Ints10-006|859|865|C to T|ENSMUSE00000214077|8|287|Arginine to Tryptophan|||||GGAGACGAAGCTGCAGTGACCTGCTGCACCGGATGAAGGAGCTCTGCAGATACATGAACAG|Yes|||||||||||||Obesity.|Normal|C57BL/6JSfdAnu|Yes|Unknown|Yes|Yes|Unknown|Yes|No|Unknown||||No|22-Jan-2010|Cryopreserved sperm|45.0|0.0|Unknown||Obese, glucose|Yes| 9463.0||FVB/N-Ywhaz/Apb||Semi-dominant|tyrosine 3-monooxygenase/tryptophan 5-monooxygenase activation protein, zeta polypeptide|Ywhaz||14-3-3zeta|MGI:109484|14-3-3ζGt(OST062)Lex |||15||||||||||Unknown to Unknown|||||||||||||||||||Viable to adulthood, but exhibit multi-organ dysfunction.|Normal|FVB/n|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|14-Dec-2022|Cryopreserved sperm|100.0|0.0|Unknown|||Possibly| 10334.0||C57Bl/6-STOCK Gt(ROSA)26Sor(CAGGS-Yap5SA,LacZ)Mao Tg(KRT5-cre/ERT2)2Ipc/AnuApb||Semi-dominant|gene trap ROSA 26, Philippe Soriano|Gt(ROSA)26Sor||Gtrosa26, R26, ROSA26|MGI:104735|gene trap ROSA 26, Philippe Soriano; targeted mutation 3, Junhao Mao|Gt(ROSA)26Sor|MGI:6763056|6|ENSMUSG00000086429 |||||||||Unknown to Unknown|||||||transgene insertion 2, I Pierre Chambon|K5-Cre |||||||||||Normal|Normal|C57Bl/6J|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|26-May-2023||0.0|0.0|Unknown|||Possibly| 5006.0|O'Driscoll ; C57BL/6-IL-13 tg|C57BL/6-Tg(IL13)||Dominant||||||||||||||||||||||||||||||||||||||||10|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|22-Feb-2010|Cryopreserved sperm|100.0|0.0|Unknown|||Possibly| 5014.0|Anne|FVB/n-LAC 1 Tg1 (USA) (ASD068)||Dominant||||||||||||||||||||||||||||||||||||||||10|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|22-Feb-2010|Cryopreserved sperm|140.0|0.0|Unknown|||Possibly| 233.0|TNAP-Cre|B6.129-Alpl/Apb||Recessive|alkaline phosphatase, liver/bone/kidney|Alpl|Nil|Akp-2, Akp2, TNSALP, TNAP|MGI:87983|targeted mutation 1, Andras Nagy|alpl|MGI:2177588|4||||||||||||||||Yes|||||||||||||Perinatal lethal|Normal|C57BL/6 x 129|No|No|Yes|No|No|Yes|No|Unknown|10|||No|25-Apr-2006|Cryopreserved sperm|150.0|0.0|Unknown||alkaline phosphatase, primordial germ cell, Cre|Yes| 8481.0|Tcrd KO|B6.129-Tcrd/JAnu||Recessive|T cell receptor delta chain|Tcrd|Nil|Tcrdelta, Tcr delta|MGI:98611|T cell receptor delta chain; targeted mutation 1, Peter Mombaerts|Tcrd|MGI:1857257|14|||||||||||||||||||||||||||||Normal||C57BL/6J|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|10-May-2018||0.0|0.0|Unknown||T cell, receptor|Yes| 6977.0|ENU20:030:a:B6:G3|ANU:ENU20:030:a:G3||Recessive|Unknown||||||||Unknown||||||||||||||||Unknown|||||||||||||Unknown|Unknown|C57BL/6JAnu|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||1||No|05-Jul-2012|Cryopreserved sperm|28.0|0.0|Unknown||ENU, random, mutagenesis, screen|Yes| 5806.0|GFAPCre x Epha4Loxp||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5808.0|GHR 391||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 4870.0|Bc.HTF1.Tg|BALB/c-Tg(H2-K-huFUT1)1/Apb||Dominant||||||||||||||||||||||||||human fucosyltransferase 1|H2-K|All blood/tissue samples express human fucosyltransferase 1||||||||||Attempts to breed homozygous animals failed. Unknown if homozygous transgene expression is embryonic lethal.|Normal.All blood/tissue samples express human fucosyltransferase.|BALB/c|No|No|Yes|No|No|Yes|No|Unknown|15|||No|28-Sep-2009|Cryopreserved sperm|80.0|0.0|Unknown||glycosylation, xenotransplantation, transplantation, transferase, lectins, H transferase, antibody|Yes| 234.0||In(X)1H||Dominant|inversion, Chr X, Harwell 1|In(X)1H||In1H|MGI:104238||||Unknown||||||||||||||||Yes|||||||||||||Inverted fragment of X-chromosome, producting oocytes without X-chromosome due to meiotic non-disjunction, leading to production of XO embryos|||No|No|Yes|No|No|Yes|No|Unknown||||No|25-Apr-2006||0.0|0.0|Unknown||X-chromosome, embryo, imprinting, inversion|Yes| 3476.0|Querkopf|129-Myst4/Wehi||Recessive|MYST histone acetyltransferase monocytic leukemia 4|Myst4|Reduced|B130044K16Rik, KAT6B, monocytic leukemia, Morf, qkf, querkopf|MGI:1858746|MYST histone acetyltransferase monocytic leukemia 4; gene trap 1, Peter Gruss|Myst4|MGI:2679726|14||||||||||||||||Yes|||||||||||||Reduced expression of this gene results in developmental defects of the skeleton and brain, particularly the cerebral cortex.||129|Yes|No|Yes|Yes|No|Yes|No|Unknown||||No|22-Jul-2008||0.0|0.0|Unknown||MORF, DNA binding transcription factors, histone acetyltransferase, telencephalon, cerebral cortex|Yes| 5068.0||ENU8C:032||Recessive|Unknown||Unknown||||||Unknown||||||||||||||||Unknown|||||||||||||Subclinical autoimmune susceptibility. Antinuclear autoantibodies: homogeneous nuclear.||C57BL/6 x CBA|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|25-Mar-2010|Cryopreserved sperm|53.0|0.0|Unknown||Autoimmune disease, autoimmunity, ANA, ENU|Yes| 7729.0||ENU20:016a||Recessive|caspase recruitment domain family, member 1|Card11|Unknown|0610008L17Rik, 2410011D02Rik, BIMP3, CARMA1|MGI:1916978||||5|||||||||||||||||||||||||||||Unknown||C57BL/6NCrlAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|27-Aug-2014|Cryopreserved sperm|20.0|0.0|Unknown|||Yes| 6978.0|ENU20:033:a:B6:G3|ANU:ENU20:033:a:G3||Recessive|Unknown||||||||Unknown||||||||||||||||Unknown|||||||||||||Unknown|Unknown|C57BL/6JAnu|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||1||No|05-Jul-2012|Cryopreserved sperm|20.0|0.0|Unknown||ENU, random, mutagenesis, screen|Yes| 7730.0||ENU27:027:Arhgef12||Recessive|Rho guanine nucleotide exchange factor (GEF) 12|Arhgef12|Unknown|2310014B11Rik, LARG, mKIAA0382|MGI:1916882||||9|||||||||||||||||||||||||||||Unknown||C57BL/6NCrlAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|27-Aug-2014|Cryopreserved sperm|52.0|0.0|Unknown|||Yes| 4942.0|osterix-cre|B6.Cg-Tg(Sp7-tTA,tetO-EGFP/cre)1Amc/Apb||Dominant||||||||||||||||||||||||||transgene insertion 1, Andrew P McMahon| tetracycline-regulated transactivator (tTA) cassette upstream of a tetracycline-responsive element (tetO)||||||||||||Hemizygous mice are viable and fertile. The Sp7 promoter limits EGFP-Cre fusion protein expression to the osteoblast lineage during embryonic/early postnatal development. Expression can be stopped by tetracycline/doxycycline addition. Fusion protein activity is largely absent from chondrocytes.|C57BL/6|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|04-Dec-2009|Cryopreserved sperm|88.0|38.0|Unknown||Cre recombinase, GFP, tTA|Yes| 6218.0|B6del478|C57BL/6-Fasl||Dominant|Fas ligand (TNF superfamily, member 6)|Fasl|Normal|APT1LG1, CD178, CD95L, Fas-L, Tnfsf6|MGI:99255|Fas ligand (TNF superfamily, member 6); targeted mutation 1.1, Andreas Strasser|Fasl|MGI:4366050|1|||||||||||||||||||||||||||||Premature death:*Compared with wild-type mice and Fasl homozygotes.Immune system phenotype:*Mice mount a normal immune response to influenza. Enlarged spleen Increased circulating tumor necrosis factor level *At 12 to 20 weeks. Enlarged lymph nodes Increased immunoglobulin level Increased IgA level Increased IgE level Increased IgG level Increased IgG1 level Increased IgG2a level Increased IgG2b level Increased IgM level Defective cytotoxic T cell cytolysis: *T cells are less efficient than wild-type cells at killing CH1 cells. Increased susceptibility to systemic lupus erythematosus *62% of terminally ill mice exhibit systemic lupus erythematosus-like (SLE) autoimmune disease with cellular crescents, protein casts, and compliment in renal glomeruli unlike wild-type mice. *Mice develop more severe SLE-like disease than Fasl homozygotes. *By 57 weeks, 50% of mice develop fatal SLE-like autoimmune kidney disease compared with 15% of Faslgld homozygotes. Increased anti-nuclear antigen antibody level: *Higher than in wild-type mice and Fasl homozygotes. Increased anti-double stranded DNA antibody level: *Higher than in wild-type mice and Fasl homozygotes. Glomerulonephritis *Mice develop SLE-like glomerulonephritis unlike wild-type mice and more frequently than Faslgld homozygotes. Dermatitis: *30% of mice develop severe dermatitis with lesions on the ears and necks unlike wild-type mice.Increased histiocytic sarcoma incidence:*By 78 weeks, 27% of mice develop hepatic tumors with characteristics of histiocytic sarcoma with deposits in the spleen and lungs.Increased liver tumor incidence:*By 78 weeks, 27% of mice develop hepatic tumors with characteristics of histiocytic sarcoma with deposits in the spleen and lungs.Increased circulating tumor necrosis factor level:*At 12 to 20 weeks.||C57BL/6|Yes|Unknown|Yes|Yes|Unknown|Yes|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown||Fas ligand (FasL), Lymphadenopathy, Autoimmune disease|Yes| 10331.0||C57Bl/6-Osx(Cre p53fl/fl) pRb< R26-Adar1p110/Apb||Semi-dominant|Osx-Cre p53fl/fl pRbfl/fl R26-Adar1p110|||||Osx-Cre p53fl/fl pRbfl/fl R26-Adar1p110|||Unknown|||||||||||||||||Osx-Cre|Sp7|||||||||||Homozygous viable and fertile; stock maintained as Cre negative line with all other alleles homozygous. When crossed to Osx-Cre will develop osteosarcoma.|Heterozygous viable and fertile; stock maintained as Cre negative line with all other alleles homozygous. When crossed to Osx-Cre will develop osteosarcoma.|C57Bl/6N|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|09-May-2023|Cryopreserved sperm|40.0|0.0|Unknown|||Possibly| 7731.0|MPEG1 targeted KO clone 1B|C57BL/6J-Mpeg1/Pib||Dominant|macrophage expressed gene 1|Mpeg1||Mpg-1, MPS1|MGI:1333743|macrophage expressed gene 1; targeted mutation 1, Phillip I Bird|Mpeg1|MGI:7545676|19||||||||||Unknown to Unknown|||||||||||||||||||Unknown|Unknown|C57BL/6J|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|01-Sep-2014|Cryopreserved sperm|100.0|0.0|Unknown|||Yes| 6980.0|ENU20:034:b:B6:G3|ANU:ENU20:034:b:G3||Recessive|Unknown||||||||Unknown||||||||||||||||Unknown|||||||||||||Unknown|Unknown|C57BL/6JAnu|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||1||No|05-Jul-2012|Cryopreserved sperm|40.0|0.0|Unknown||ENU, random, mutagenesis, screen|Yes| 6982.0|ENU20:038:a:B6:G3|ANU:ENU20:038:a:G3||Recessive|Unknown||||||||Unknown||||||||||||||||Unknown|||||||||||||Unknown|Unknown|C57BL/6JAnu|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||1||No|05-Jul-2012|Cryopreserved sperm|10.0|0.0|Unknown||ENU, random, mutagenesis, screen|Yes| 6822.0|MTf knockout|B6.129X1-Mfi2/Apb|B6.129X1-Mfi2|Recessive|antigen p97 (melanoma associated) identified by monoclonal antibodies 133.2 and 96.5|Mfi2|Nil|CD228, melanotransferrin, MTf|MGI:1353421|antigen p97 (melanoma associated) identified by monoclonal antibodies 133.2 and 96.5; targeted mutation 1, Des R Richardson|Mfi2|MGI:3691276|16|||||||||||||||||||||||||||||Normal|Normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||20+||No|24-Feb-2012|Cryopreserved sperm|50.0|0.0|Unknown||melanoma, melanotransferrin, iron|Yes| 4982.0||ENU11B6:G1||Recessive||||||||||||||||||||||||||||||||||||||Matings with B6 females resulted in embryos with skeletal defects to head possible mesenchymal defects in lung.|Normal||No|No|Yes|No|No|Yes|No|Unknown||||No|22-Jan-2010|Cryopreserved sperm|10.0|0.0|Unknown||Lung, skeleton, ENU|Yes| 5080.0|APPyen|B6.D2-Tg(Thy1-APPswyen)1Jgo||Dominant||||||||||||||||||||||||||human Amyloid Precusor Protein|murine Thy1.2|3 fold higher levels of APP in neurons of transgenic mice compared to WT||||||||||Not fully characterised|Not fully characterised|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|Yes|Poor||||No|25-Mar-2010|Cryopreserved sperm|100.0|0.0|Yes|Alzhiemer’s disease|amyloid, Alzhiemer’s disease, overexpression, APP, plaque|Possibly| 6987.0|ENU20:046:b:B6:G3|ANU:ENU20:046:b:G3||Recessive|Unknown||||||||Unknown||||||||||||||||Unknown|||||||||||||Unknown|Unknown|C57BL/6JAnu|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||1||No|05-Jul-2012|Cryopreserved sperm|49.0|0.0|Unknown||ENU, random, mutagenesis, screen|Yes| 6988.0|ENU20:047:a:B6:G3|ANU:ENU20:047:a:G3||Recessive|Unknown||||||||Unknown||||||||||||||||Unknown|||||||||||||Unknown|Unknown|C57BL/6JAnu|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||1||No|05-Jul-2012|Cryopreserved sperm|45.0|0.0|Unknown||ENU, random, mutagenesis, screen|Yes| 6990.0|ENU20:053:a:B6:G3|ANU:ENU20:053:a:G3||Recessive|Unknown||||||||Unknown||||||||||||||||Unknown|||||||||||||Unknown|Unknown|C57BL/6JAnu|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||1||No|05-Jul-2012|Cryopreserved sperm|30.0|0.0|Unknown||ENU, random, mutagenesis, screen|Yes| 6992.0|ENU20:055:a:B6:G3|ANU:ENU20:055:a:G3||Recessive|Unknown||||||||Unknown||||||||||||||||Unknown|||||||||||||Unknown|Unknown|C57BL/6JAnu|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||1||No|05-Jul-2012|Cryopreserved sperm|60.0|0.0|Unknown||ENU, random, mutagenesis, screen|Yes| 6981.0|ENU20:036:a:B6:G3|ANU:ENU20:036:a:G3||Recessive|Unknown||||||||Unknown||||||||||||||||Unknown|||||||||||||Unknown|Unknown|C57BL/6JAnu|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||1||No|05-Jul-2012|Cryopreserved sperm|10.0|0.0|Unknown||ENU, random, mutagenesis, screen|Yes| 6983.0|ENU20:039:b:B6:G3|ANU:ENU20:039:b:G3||Recessive|Unknown||||||||Unknown||||||||||||||||Unknown|||||||||||||Unknown|Unknown|C57BL/6JAnu|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||1||No|05-Jul-2012|Cryopreserved sperm|60.0|0.0|Unknown||ENU, random, mutagenesis, screen|Yes| 6985.0|ENU20:043:a:B6:G3|ANU:ENU20:043:a:G3||Recessive|Unknown||||||||Unknown||||||||||||||||Unknown|||||||||||||Unknown|Unknown|C57BL/6JAnu|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||1||No|05-Jul-2012|Cryopreserved sperm|36.0|0.0|Unknown||ENU, random, mutagenesis, screen|Yes| 6986.0|ENU20:045:b:B6:G3|ANU:ENU20:045:b:G3||Recessive|Unknown||||||||Unknown||||||||||||||||Unknown|||||||||||||Unknown|Unknown|C57BL/6JAnu|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||1||No|05-Jul-2012|Cryopreserved sperm|48.0|0.0|Unknown||ENU, random, mutagenesis, screen|Yes| 6989.0|ENU20:051:b:B6:G3|ANU:ENU20:051:b:G3||Recessive|Unknown||||||||Unknown||||||||||||||||Unknown|||||||||||||Unknown|Unknown|C57BL/6JAnu|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||1||No|05-Jul-2012|Cryopreserved sperm|40.0|0.0|Unknown||ENU, random, mutagenesis, screen|Yes| 6995.0|ENU21:001:a:B6:G3|ANU:ENU21:001:a:G3||Recessive|Unknown||||||||Unknown||||||||||||||||Unknown|||||||||||||Unknown|Unknown|C57BL/6NCrlAnu|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||1||No|05-Jul-2012|Cryopreserved sperm|40.0|0.0|Unknown||ENU, random, mutagenesis, screen|Yes| 7026.0|MommeD14|FVB/NJ-MommeD14 Tg(Hba1-Gfp)1Ew||Semi-dominant|DNA methyltransferase 3B|Dnmt3b|||MGI:1261819|DNA methyltransferase 3B; modifier of murine metastable epialleles, D14|Dnmt3b|MGI:5515362|2||||||||||Unknown to Unknown|||||||transgene insertion 1, Emma Whitelaw|human alpha-globin promoter and enhancer region|11 copies||||||||||Some homozygous viable at 3 weeks.Transgene expressed in red blood cells. Percentage of cells expressing GFP transgene is increased in Momme D14. |Transgene expressed in red blood cells. Percentage of cells expressing GFP transgene is increased in Momme D14. |FVBNJ|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|||MommeD14<+/->;Tg(Hba1-Gfp)1Ew x Tg(Hba1-Gfp)1Ew|No|23-Jul-2012|Cryopreserved sperm|39.0|0.0|Unknown||DNA methylation, epigenetics|Possibly| 5063.0|Montu|C.C3H-Rps7/AnuApb||Semi-dominant|ribosomal protein S7|Rps7|Unknown|S7|MGI:1333818|Montu|Rps7|MGI:3043039|12||||||||||||||||Yes|||||||||||||Unkown. Assumed lethal.|Phenotype may include variable ventral spotting, tail kinks and small size compared to littermates.|BALB/c x C3H/HeH|No|No|Yes|No|No|Yes|No|Good||||No|02-May-2007|Cryopreserved sperm|38.0|0.0|Unknown||organogenesis, ENU, Diamond-Blackfan anemia|Yes| 6400.0|SHHtgSHLtg|B6.Cg-Igh Tg(IgkHyHEL10)1Rbr>/Ausb||Dominant|immunoglobulin heavy chain complex|Igh|Normal||MGI:96442|immunoglobulin heavy chain complex; targeted mutation 1, Robert Brink|Igh|MGI:3800383|Unknown|||||||||||||||||transgene insertion 1, Robert Brink||||||||||||Unknown|Abnormal B cell morphology:*40-60% of B cells in the spleen produce immunoglobulins that bind hen egg lysozyme antigen (HEL) with high affinity. Increased immature B cell number: *The splenic B cells that bind HEL antigen are immature as indicated by the IgM IgD surface markers. Abnormal B-2 B cell morphology: *All of the B cells found in the peritoneal cavity that bind HEL antigen are of the B-2 lineage as determined by B220 CD5expression.Increased immunoglobulin level: Increased IgA level: *There are low levels of anti-HEL IgA in the sera of unimmunized mice. Increased IgG1 level: *There are low levels of anti-HEL IgG1 in the sera of unimmunized mice. Increased IgG2a level: *There are low levels of anti-HEL IgG2a in the sera of unimmunized mice. Increased IgG2b level: *There are low levels of anti-HEL IgG2b in the sera of unimmunized mice. Increased IgG3 level: *There are low levels of anti-HEL IgG3 in the sera of unimmunized mice. Increased IgM level: *There are high levels of anti-HEL IgM in the sera of unimmunized mice.|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown||IgG, Autoantibody-mediated diseases|Yes| 6993.0|ENU20:058:b:B6:G3|ANU:ENU20:058:b:G3||Recessive|Unknown||||||||Unknown||||||||||||||||Unknown|||||||||||||Unknown|Unknown|C57BL/6JAnu|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||1||No|05-Jul-2012|Cryopreserved sperm|40.0|0.0|Unknown||ENU, random, mutagenesis, screen|Yes| 5233.0|Cid|C57BL/6-Tigd3||Recessive|tigger transposable element derived 3|Tigd3|||MGI:2681860||||19||||||||||||||||Yes|||||||||||||Normal|Normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|08-Oct-2010|Cryopreserved sperm|50.0|0.0|Unknown||chromosomal, epigenetics|Possibly| 5642.0|Bre-LacZ x C57 ||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5643.0|Bre-LacZ x CD1||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 4937.0|BALB/c. Socs2 KO|BALB/c-Socs2/Wehi||Recessive|suppressor of cytokine signaling 2|Socs2|Nil|CIS2, Cish2, cytokine-inducible SH2 protein 2, D130043N08Rik, JAB, SOCS-2, SSI-2, STAT-induced STAT inhibitor 2|MGI:1201787|targeted mutation 1, Walter and Eliza Hall Institute of Medical Research|Socs2|MGI:1934557|10||||||||||||||||Yes|||||||||||||SOCS-2(-/-) mice grew significantly larger than their wild-type littermates. Increased body weight became evident after weaning and was associated with significantly increased long bone lengths and the proportionate enlargement of most organs. Characteristics of deregulated growth hormone and insulin-like growth factor-I (IGF-I) signalling, including decreased production of major urinary protein, increased local IGF-I production, and collagen accumulation in the dermis, were observed in SOCS-2-deficient mice, indicating that SOCS-2 may have an essential negative regulatory role in the growth hormone/IGF-I pathway. ||BALB/c|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|24-Nov-2009||0.0|0.0|Unknown||Growth, weight, growth hormone, STAT, JAK, gigantism|Yes| 6994.0|ENU20:059:a:B6:G3|ANU:ENU20:059:a:G3||Recessive|Unknown||||||||Unknown||||||||||||||||Unknown|||||||||||||Unknown|Unknown|C57BL/6JAnu|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||1||No|05-Jul-2012|Cryopreserved sperm|20.0|0.0|Unknown||ENU, random, mutagenesis, screen|Yes| 5815.0|GOAT KO||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 7538.0|Rag2|B6N.129S6-Rag2/FwaAusb|B6N.129S6-Rag2/FwaAusb|Recessive|recombination activating gene 2|Rag2|Normal|Rag-2|MGI:97849|recombination activating gene 2; targeted mutation 1, Frederick W Alt|Rag2|MGI:1858556|2|||||||||||||||||||||||||||||Homozygous mice exhibit total inability to initiate V(D)J rearrangement and fail to generate mature T or B lymphocytes.||C57BL/6NTac|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|12|||No|13-Dec-2013||0.0|0.0|Unknown||GFP, B cell, T cell, IgM|Yes| 6790.0|2D2tg|C57BL/6-Tg(Tcra2D2,Tcra2D2)1Kuch/Ausb||Semi-dominant||||||||||||||||||||||||||transgene insertion 1, Vijay Kuchroo ||||||||||||Homozygous lethal|Expanded T cells population.Spontaneus cases of paralysis might occur.Altered inmunoregulation in brain.Spontaneus optic neuritis.|C57BL/6|No|No|Yes|No|No|Yes|No|Unknown|||+/+ sibling x Hemizygote (Female x Male) |No|18-Jan-2012||0.0|0.0|Unknown||T cells, Experimental autoimmune encephalomyelitis, CNS, Optic Nerve, multiple sclerosis |Yes| 6789.0|TK3|B6.129-Nrg1/Ausb||Recessive|neuregulin 1|Nrg1 ||6030402G23Rik, ARIA, D230005F13Rik, GGF, GGFII, heregulin, HGL, Hgl, HRG, HRGalpha, NDF, SMDF |MGI:96083 |neuregulin 1; targeted mutation 1, Lorna W Role |Nrg1tm1Lwr|MGI:1928831|8|ENSMUSG00000062991|ENSMUST00000073884|Nrg1-201 ||||||||||||||||||||||||||complete neonatal lethality, limp posture, no spontaneous movement, unresponsive to tactile stimuli, cyanosis, centrally nucleated skeletal muscle fibers, thin diaphragm muscle, abnormal intercostal muscle morphology, respiratory failure, decreased Schwann cell number, abnormal motor neuron innervation, abnormal sensory neuron projections, decreased motor neuron number, decreased sensory neuron number, abnormal cranial ganglia morphology, abnormal cranial nerve morphology, small dorsal root ganglion, abnormal spinal nerve morphology, |Unknown|C57BL6|No|No|Yes|No|No|Yes|No|Unknown||||No|18-Jan-2012||0.0|0.0|Unknown||nervous system, peripheral synapses, spinal nerve|Yes| 5007.0|ED2f|EDD1 KO||Recessive||||||||||||||||||||||||||||||||||||||Unknown|||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown|10|||No|22-Feb-2010|Cryopreserved sperm|60.0|0.0|Unknown|||Yes| 2378.0|ENU8F:030 , Hipster|B6Apb;CB-Adamts20/Apb|B6Apb;CB-Adamts20/Apb|Recessive|a disintegrin-like and metallopeptidase (reprolysin type) with thrombospondin type 1 motif, 20|Adamts20|Normal|ADAMTS-20, bt|MGI:2660628|a disintegrin-like and metallopeptidase (reprolysin type) with thrombospondin type 1 motif, 20; hipster|Adamts20|MGI:3847117|15|ENSMUSG00000022449|ENSMUST00000035342|Adamts20-001|3664|3833|G to A|ENSMUSE00000646542|26|1221|Glycine to Arginine|||||GGTCACCATGTTCAGCCTCCTGTGGACATGGGAAAACCACCCGACGTGTTTTATGCGTGAA|No|||||||||||||Coat abnormality. Belted, White spotting.Affected mice develop a white stripe transverse across abdomen or a large white spot in the same location.||C57BL/6 x CBA|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|14-Dec-2007|Cryopreserved sperm|150.0|0.0|Unknown||Migration, pigment, melanocyte, stripe, white belly patch, ENU|Yes| 5073.0|Syrup|FVB/N-MommeD7||Semi-dominant|modifier of murine metastable epialleles, D7|MommeD7|Unknown||MGI:3821590|modifier of murine metastable epialleles, D7|MommeD7|MGI:3821597|7||||||||||Unknown to Unknown||||||Yes|Green Fluorescent Protein (GFP)|human alpha-globin promoter and enhancer region|||||||||||Mice homozygous for a mutation at this locus display semidominant lethality and are never seen at weaning.Postnatal lethality: * semidominant homozygous lethal * never seen at weaning * death occurs within a few days of birthPallor: about 1/4 of mice are pale in color at E17.5Decreased erythrocyte cell number: at E17.5|Percentage of cells expressing the GFP transgene (Line3) is increased (suppressor of variegation). Reticulocytosis: a 3 fold increase in the number of circulating reticulocytes.Enlarged spleen: severe|FVB/NJ|No|No|Yes|No|No|Yes|No|Good|||MommeD7<+/->;Tg(Hba1-Gfp)3Ew x Tg(Hba1-Gfp)3Ew|No|25-Mar-2010|Cryopreserved sperm|30.0|0.0|Unknown||epigenetics, suppressor of variegation|Yes| 5076.0|Nutmeg|FVB/N-MommeD16||Semi-dominant|||Unknown||||||Unknown||||||||||Unknown to Unknown||||||Yes|Green Fluorescent Protein (GFP)|human alpha-globin promoter and enhancer region|||||||||||Unknown|Unknown|FVB/NJ|No|No|Yes|No|No|Yes|No|Good|||MommeD16<+/->;Tg(Hba1-Gfp)3Ew x Tg(Hba1-Gfp)3Ew|No|25-Mar-2010|Cryopreserved sperm|30.0|0.0|Unknown||epigenetics, suppressor of variegation|Yes| 5077.0|Charlie|FVB/N-MommeR2||Semi-dominant|||Unknown||||||Unknown||||||||||Unknown to Unknown||||||Yes|Green Fluorescent Protein (GFP)|human alpha-globin promoter and enhancer region|||||||||||Unknown|Percentage of cells expressing the GFP transgene (Line3) is decreased (enhancer of variegation). |FVB/NJ|No|No|Yes|No|No|Yes|No|Good|||MommeR2<+/->;Tg(Hba1-Gfp)3Ew x Tg(Hba1-Gfp)3Ew|No|25-Mar-2010|Cryopreserved sperm|40.0|0.0|Unknown||epigenetics, suppressor of variegation|Yes| 5074.0|Rocky|FVB/N-MommeD8||Semi-dominant|modifier of murine metastable epialleles, D8|MommeD8|Unknown||MGI:3821592|modifier of murine metastable epialleles, D8|MommeD8|MGI:3821599|4||||||||||Unknown to Unknown||||||Yes|Green Fluorescent Protein (GFP)|human alpha-globin promoter and enhancer region|||||||||||Mutant mice show a reduction in survival past weaning. Survivors at weaning are smaller than controls.Postnatal lethality: * few animals survive to weaning * normal litter size at birthDecreased body size: at weaning||FVB/NJ|No|No|Yes|No|No|Yes|No|Good|||MommeD8<+/->;Tg(Hba1-Gfp)3Ew x Tg(Hba1-Gfp)3Ew|No|25-Mar-2010|Cryopreserved sperm|40.0|0.0|Unknown||epigenetics, suppressor of variegation|Yes| 6930.0|ENU21:G1|ANU:ENU21:G1||Recessive|Unknown||||||||Unknown||||||||||||||||Unknown|||||||||||||Unknown|Unknown|C57BL/6NCrlAnu|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||1||No|02-Jul-2012|Cryopreserved sperm|744.0|0.0|Unknown||ENU, random, mutagenesis, screen|Yes| 7060.0|Momme D12|FVB/NJ-MommeD12 Tg(Hba1-Gfp)1Ew||Semi-dominant|eukaryotic translation initiation factor 3, subunit H|Eif3h|||MGI:1915385|eukaryotic translation initiation factor 3, subunit H; modifier of murine metastable epialleles, D12|Eif3h|MGI:5514383|15||||||||||Unknown to Unknown|||||||Green Fluorescent Protein|human alpha-globin promoter and enhancer region|||||||||||Homozygous lethality (before E9.5 dpc)|Unknown|FVB/NJ|No|No|Yes|No|No|Yes|No|Good|||MommeD12<+/->;Tg(Hba1-Gfp)1Ew x Tg(Hba1-Gfp)1Ew|No|24-Aug-2012|Cryopreserved sperm|27.0|0.0|Unknown||ENU, epigenetics, suppressor of variegation|Possibly| 5075.0|Sarah|FVB/N-MommeD9||Semi-dominant|modifier of murine metastable epialleles, D9|MommeD9|Unknown||MGI:3821594|modifier of murine metastable epialleles, D9|MommeD9|MGI:3821600|7||||||||||Unknown to Unknown||||||Yes|Green Fluorescent Protein (GFP)|human alpha-globin promoter and enhancer region|||||||||||Homozygotes usually die as embryos. Abnormal sex ratios are seen among heterozygotes.Embryonic growth arrest: * semidominant homozygous lethality * developmental arrest before E9.5 * reduced litter size at birth|Abnormal sex determination: there is a paternal affect on sex ratio|FVB/NJ|No|No|Yes|No|No|Yes|No|Good|||MommeD9<+/->;Tg(Hba1-Gfp)3Ew x Tg(Hba1-Gfp)3Ew|No|25-Mar-2010|Cryopreserved sperm|37.0|0.0|Unknown||epigenetics, suppressor of variegation|Yes| 5071.0|BALB/c-CMV1r|BALB/c.B6-Klra8||Dominant|killer cell lectin-like receptor, subfamily A, member 8|Klra8|Normal|Cmv-1, Cmv1, Ly49H, Ly49h, Ly49u<129>|MGI:102968|||MGI:2387148|6||||||||||||||||Yes|||||||||||||Mice expressing Klra8 are resistant to CMV infection compared to Balb/c and Balb/b controls||BALB/c|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|25-Mar-2010||0.0|0.0|No||cytomegalovirus, lymphocyte, natural killer cell, resistance, infection|Yes| 5071.0|BALB/c-CMV1r|BALB/c.B6-Klra8||Dominant|||Unknown|||||MGI:3579319|Unknown|||||||||||||||||||||||||||||Mice expressing Klra8 are resistant to CMV infection compared to Balb/c and Balb/b controls||BALB/c|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|25-Mar-2010||||No||cytomegalovirus, lymphocyte, natural killer cell, resistance, infection|Yes| 6996.0|ENU21:004:b:B6:G3|ANU:ENU21:004:b:G3||Recessive|Unknown||||||||Unknown||||||||||||||||Unknown|||||||||||||Unknown|Unknown|C57BL/6NCrlAnu|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||1||No|06-Jul-2012|Cryopreserved sperm|27.0|0.0|Unknown||ENU, random, mutagenesis, screen|Yes| 6997.0|ENU21:007:a:B6:G3|ANU:ENU21:007:a:G3||Recessive|Unknown||||||||Unknown||||||||||||||||Unknown|||||||||||||Unknown|Unknown|C57BL/6NCrlAnu|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||1||No|06-Jul-2012|Cryopreserved sperm|10.0|0.0|Unknown||ENU, random, mutagenesis, screen|Yes| 5141.0|Nodal Δ600|129;iCR-Nodal||Recessive|nodal|Nodal|Unknown|Tg.413d|MGI:97359|nodal; targeted mutation 2, Elizabeth J Robertson|Nodal|MGI:2181583|Unknown|||||||||||||||||||||||||||||Embryonic lethal||129|No|No|Yes|No|No|Yes|No|Unknown||||No|27-May-2010||0.0|0.0|Unknown||TGF, anterior-posterior, visceral endoderm, enhancer, transcription|Yes| 6998.0|ENU21:007:b:B6:G3|ANU:ENU21:007:b:G3||Recessive|Unknown||||||||Unknown||||||||||||||||Unknown|||||||||||||Unknown|Unknown|C57BL/6NCrlAnu|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||1||No|06-Jul-2012|Cryopreserved sperm|18.0|0.0|Unknown||ENU, random, mutagenesis, screen|Yes| 6406.0|TYRcn|B6(Cg)-Tyr/JAusb||Recessive|tyrosinase|Tyr|Nil|skc35|MGI:98880|tyrosinase; albino 2 Jackson|Tyr|MGI:1855985|7|||||||||||||||||||||||||||||Absent hair follicle melanin granules:*Forskolin treatment does not protect mice from UV effects; numbers of apoptotic epidermal keratinocytes are similar to those in vehicle-treated mutants.Absent coat pigmentation:*Albino coat.Absent skin pigmentationOcular albinism:*Total iris albinismAbnormal aqueous drainage system morphology:*Had mild focal angle developmental defects, whereas pigmented mice had no observed defects.Abnormal retina morphology:*Increased total number of cells in temporal retina during E11-13.*Sustained, early production of ipsilateral retinal ganglion cells up to E14.*Increased surface area of temporal retina, as well as additional sectors during E11-13. Abnormal retinal photoreceptor morphology: *Background Sensitivity: mean synaptic ribbon length is decreased in comparison to C57BL/6J. Decreased retinal photoreceptor cell number: *Increased apoptosis in outer nuclear layer during adulthood (2-12 months), then decreasing to control levels. Abnormal retinal ganglion layer morphology: *Beginning at E11 through E16, cells exhibit smaller size and abnormal packing and organization. Retinal degeneration:Abnormal eye physiology:*Resistant to light damage as compared to albino BALB/cByJ Abnormal eye electrophysiology: *Reduction in a-wave and b-wave amplitude in young adults as demonstrated by electroretinogram. Abnormal intraocular pressure: *Increased pressure as compared to pigmented C57BL/6J. Abnormal vision: *Dark-adapted threshold s are elevated (decreased sensitivity) in comparison to C57BL/6J.Increased cellular sensitivity to ionizing radiation:*Mice show dose-dependent DNA lesion formation (cyclobutane dimers) from UV-B exposure, but wild-type or forskolin-treated Mc1r mutants show little damage.Abnormal keratinocyte apoptosis||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown||c-locus mutations, Pigment mutations|Yes| 4720.0|TGFbRIII KO|129S1(B6)-Tgfbr3/Apb|129S1(B6)-Tgfbr3/Apb|Recessive|transforming growth factor, beta receptor III|Tgfbr3|Nil|betaglycan, TBRIII|MGI:104637|targeted mutation 1, Kaye Stenvers|Tgfbr3|MGI:2664514|5||||||||||||||||Yes|||||||||||||Mice homozygous for disruptions in this gene usually die as embryos. The very few individuals that survive are poorly fertile with abnormalities of the spleen, liver, heart, and skeletal system. Embryonic lethal E16.5-E18.5 of heart and liver defects||129S1/Sv|No|No|Yes|No|No|Yes|No|Unknown||||No|08-Apr-2009|Cryopreserved sperm|60.0|0.0|Unknown||Heart, Liver, embryonic lethal|Yes| 6999.0|ENU21:009:a:B6:G3|ANU:ENU21:009:a:G3||Recessive|Unknown||||||||Unknown||||||||||||||||Unknown|||||||||||||Unknown|Unknown|C57BL/6NCrlAnu|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||1||No|06-Jul-2012|Cryopreserved sperm|60.0|0.0|Unknown||ENU, random, mutagenesis, screen|Yes| 7133.0|Larry|B6129S5-Tpsb2/TAC/Ausb||||mMCP6,mMCP7|||MGI:96942|||||||||||||||||||||||||||||||||||C57BL6|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|02-Nov-2012||0.0|0.0|Unknown|||Possibly| 4998.0|Wanchi ; ENU8B6:053|C57BL/6JAnu-Cdk4/AnuApb|C57BL/6JAnu-Cdk4/AnuApb|Recessive|cyclin-dependent kinase 4|Cdk4||Crk3, p34/cdk4|MGI:88357|Wanchi|Cdk4|MGI:5009264|10|ENSMUSG00000006728|ENSMUST00000006911|Cdk4-001|910|1152|T to A|ENSMUSE00000796826|8|304|STOP to Arginine|||||ACCTGCACAAGGAGGAAAGCGACGCAGAGTGA|Yes|||||||||||||Diabetic as measured by glucose - diastix test.Diabetes independent of el/TCR transgenes.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|28-Jan-2010|Cryopreserved sperm|54.0|0.0|Unknown||T cell, glucose, ENU, Wellcome Trust, JDRF|Yes| 7542.0|ENU22::PAN2:B6|C57BL/6NCrlAnu-Pan2/AnuApb|C57BL/6NCrlAnu-Pan2/AnuApb|Recessive|PAN2 polyA specific ribonuclease subunit homolog (S. cerevisiae)|Pan2|Unknown|1200014O24Rik, Usp52|MGI:1918984|PAN2 polyA specific ribonuclease subunit homolog (S. cerevisiae); mutation 1, The Australian National University|Pan2|MGI:5563441|10|ENSMUSG00000005682|ENSMUST00000005825|Pan2-201|1408|1662|C to T|ENSMUSE00000271028|9|470|Glutamine to STOP|||||AGTCAGACCATGAATTTGACAACTTCAGCCAAGTCACGGAGTCACCGACAGGGCGAGAAGA||||||||||||||Embryonic Lethal||C57BL/6NCrlAnu|No|No|Yes|No|No|Yes|No|Unknown||G5||No|13-Dec-2013|Cryopreserved sperm|36.0|0.0|Unknown||ENU, embryonic lethal|Yes| 7109.0|Rd1|B6(Cg)-Pde6b||Recessive|phosphodiesterase 6B, cGMP, rod receptor, beta polypeptide|Pde6b|Unknown|nmf137, Pdeb, r, rd, rd1, rd10|MGI:97525|phosphodiesterase 6B, cGMP, rod receptor, beta polypeptide; retinal degeneration 1|Pde6b|MGI:1856373|5|||||||||||||||||||||||||||||Mice undergo rapid retinal degeneration leading to blindness. Rod photoreceptor death peaks at P14 and this is followed by a secondary cone degeneration.Due to a murine viral insert in the Pde6b gene. The Xmv-28 provirus is integrated into intron I of the rd gene 1511 bp downstream of the exon-intron boundary (Bowes C et al, 1993, PNAS 90(7):2955-9). Mutations in the gene encoding the β subunit of cGMP-PDE have been found in human patients suffering from autosomal recessive retinitis pigmentosa (OMM 180072), a disorder bearing phenotypic resemblance to the mouse Pde6brd1 phenotype.|Unknown|C57BL/6J|Yes|Yes|Yes|Yes|Yes|Yes|No|Poor|unknown - at least 2 in our hands in last 2 years|unknwon||No|17-Oct-2012||0.0|0.0|Yes|Mutations in the gene encoding the β subunit of cGMP-PDE have been found in human patients suffering from autosomal recessive retinitis pigmentosa (OMM 180072), a disorder bearing phenotypic resemblance to the mouse Pde6brd1 phenotype.|eye, vision, rod|Possibly| 7543.0|ENU28:008:Ndst3|C57BL/6NCrlAnu-Ndst3/AnuApb|C57BL/6NCrlAnu-Ndst3/Apb|Recessive|N-deacetylase/N-sulfotransferase (heparan glucosaminyl) 3|Ndst3||4921531K01Rik, 4930511P15Rik|MGI:1932544|N-deacetylase/N-sulfotransferase (heparan glucosaminyl) 3; mutation 1, The Australian National University|Ndst3|MGI:5571271|3|ENSMUSG00000027977|ENSMUST00000154668|Ndst3-001|2351|2620|T to C|ENSMUSE00001216254|12|784|Glutamine to Arginine|||||TACCCCTGCGACAGTGATGGATGAAGTCCAGAAGTTTCTAGGAGTCTCACCTCATTATAAT||||||||||||||Unknown||C57BL/6NCrlAnu|Unknown|Unknown|Yes|Yes|Unknown|Yes|No|Unknown||G3||No|13-Dec-2013|Cryopreserved sperm|66.0|0.0|Unknown||ENU|Yes| 814.0|Grb10 KO|B6.CBA-Grb10||Dominant|growth factor receptor bound protein 10|Grb10|Nil|5730571D09Rik, maternally expressed gene 1, Meg1, mKIAA0207|MGI:103232|gene trap 1, Andrew Ward|Grb10|MGI:2668436|11||||||||||||||||Yes|||||||||||||Maternal transmission of a mutant allele results in both fetal and placental overgrowth. Disproportionate overgrowth of the liver is observed.|Maternal transmission of a mutant allele results in both fetal and placental overgrowth. Disproportionate overgrowth of the liver is observed.|C57BL/6 x CBA|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|21-May-2007||0.0|0.0|Unknown||embryonic, placenta, liver, maternal, adapter, tyrosine kinase, phosphotase|Yes| 5821.0|HB9-EGFP||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6825.0|MT-1/II KO|B6.129-Mt1 Mt2/Apb||Recessive|metallothionein 1|Mt1|Reduced|Mt-1, MT-I|MGI:97171|metallothionein 1; targeted mutation 1, Anna E Michalska|Mt1|MGI:2668454|8|||||||||||||||||||||||||||||Increased circulating alanine transaminase level: in acetaminophen-treated miceAbnormal ion homeostasis: * increased cadmium sensitivity * take up a hunched back posture, ruffed coat and display general lethargyAbnormal lipid homeostasis: acetaminophen-induced lipid peroxidation is increased compared to in similarly treated wild-type mice.Increased sensitivity to xenobiotic induced morbidity/mortality: mice are more sensitive to acetaminophen-induced lethality compared with similarly treated wild-type mice.Increased physiological sensitivity to xenobiotic: * mice exhibit increased susceptibility to acetaminophen-induced hepatotoxicity, alanine aminotransferase, hepatic necrosis, lipid peroxidation, and lethality compared with similarly treated wild-type mice * acetaminophen-induced injuries are not ameliorated by pretreatment with zinc unlike in similarly treated wild-type mice * hepatocytes are more sensitive to acetaminophen and NAPQI-induced oxidative stress compared with similarly treated wild-type cells * however, acetaminophen metabolism is normalIncreased incidence of chemically-induced tumors: increased sensitivity to DMBA/TPA treatment; 100% of treated mice have tumors by 19 weeks, and only 10% of wild-type mice have tumors at 20 weeks, and the average tumor size of treated mice is 2X larger.Abnormal hepatocyte morphology: hepatocytes are more sensitive to acetaminophen and NAPQI-induced oxidative stress indicated by lactate dehydrogenase leakage compared with similarly treated wild-type cells.Hepatic necrosis: in acetaminophen-treated micetumorigenesis.Increased tumor incidence: 90% of mice with tumors by 13 weeks (earliest tumors by 9 weeks).Increased incidence of chemically-induced tumors: increased sensitivity to DMBA/TPA treatment; 100% of treated mice have tumors by 19 weeks, and only 10% of wild-type mice have tumors at 20 weeks, and the average tumor size of treated mice is 2X larger.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|10|||No|27-Feb-2012|Cryopreserved sperm|50.0|0.0|Unknown||Zinc, cadmium, diet|Yes| 6825.0|MT-1/II KO|B6.129-Mt1 Mt2/Apb||Recessive|metallothionein 2|Mt2|Nil|Mt-2, MT-II|MGI:97172|metallothionein 2; targeted mutation 1, Anna E Michalska|Mt2|MGI:2668455|8||||||||||Unknown to Unknown|||||||||||||||||||Increased circulating alanine transaminase level: in acetaminophen-treated miceAbnormal ion homeostasis: * increased cadmium sensitivity * take up a hunched back posture, ruffed coat and display general lethargyAbnormal lipid homeostasis: acetaminophen-induced lipid peroxidation is increased compared to in similarly treated wild-type mice.Increased sensitivity to xenobiotic induced morbidity/mortality: mice are more sensitive to acetaminophen-induced lethality compared with similarly treated wild-type mice.Increased physiological sensitivity to xenobiotic: * mice exhibit increased susceptibility to acetaminophen-induced hepatotoxicity, alanine aminotransferase, hepatic necrosis, lipid peroxidation, and lethality compared with similarly treated wild-type mice * acetaminophen-induced injuries are not ameliorated by pretreatment with zinc unlike in similarly treated wild-type mice * hepatocytes are more sensitive to acetaminophen and NAPQI-induced oxidative stress compared with similarly treated wild-type cells * however, acetaminophen metabolism is normalIncreased incidence of chemically-induced tumors: increased sensitivity to DMBA/TPA treatment; 100% of treated mice have tumors by 19 weeks, and only 10% of wild-type mice have tumors at 20 weeks, and the average tumor size of treated mice is 2X larger.Abnormal hepatocyte morphology: hepatocytes are more sensitive to acetaminophen and NAPQI-induced oxidative stress indicated by lactate dehydrogenase leakage compared with similarly treated wild-type cells.Hepatic necrosis: in acetaminophen-treated micetumorigenesis.Increased tumor incidence: 90% of mice with tumors by 13 weeks (earliest tumors by 9 weeks).Increased incidence of chemically-induced tumors: increased sensitivity to DMBA/TPA treatment; 100% of treated mice have tumors by 19 weeks, and only 10% of wild-type mice have tumors at 20 weeks, and the average tumor size of treated mice is 2X larger.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|10|||No|27-Feb-2012|Cryopreserved sperm|||Unknown||Zinc, cadmium, diet|Yes| 5823.0|HDAC Short||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5648.0|C3H/HeJ||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6799.0|TGFbr2f|B6.129S6-Tgfbr2/Ausb||Recessive|transforming growth factor, beta receptor II |Tgfbr2||1110020H15Rik, TbetaR-II, TbetaRII, TBR-II |MGI:98729 |transforming growth factor, beta receptor II; targeted mutation 1, Harold L Moses |Tgfbr2tm1Hlm |MGI:2384511|9|ENSMUSG00000032440||||||||||||||||||||||||||||Homozygous mice are fertile and phenotypically normal. Preweaning mortality 8.4%|Normal|B6.129S6 |Yes|Yes|Yes|Yes|Yes|Yes|No|Good|||Homozygous breeding|No|19-Jan-2012||0.0|0.0|No||yolk sac hematopoiesis , vasculogenesis, mortality, aging|Yes| 7000.0|ENU21:011:a:B6:G3|ANU:ENU21:011:a:G3||Recessive|Unknown||||||||Unknown||||||||||||||||Unknown|||||||||||||Unknown|Unknown|C57BL/6NCrlAnu|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||1||No|06-Jul-2012|Cryopreserved sperm|29.0|0.0|Unknown||ENU, random, mutagenesis, screen|Yes| 7001.0|ENU21:013:b:B6:G3|ANU:ENU21:013:b:G3||Recessive|Unknown||||||||Unknown||||||||||||||||Unknown|||||||||||||Unknown|Unknown|C57BL/6NCrlAnu|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||1||No|06-Jul-2012|Cryopreserved sperm|10.0|0.0|Unknown||ENU, random, mutagenesis, screen|Yes| 4107.0||KRN:069||Recessive|||||||||Unknown||||||||||||||||Yes|transgene insertion KRN, Diane Mathis|Natural TCR alpha and -beta promoter/enhancer elements.|||||||||||No arthritis in KRN/H2g7 model||C57BL/6 x NODk x C57BL/10 x Balb/b|Yes|Yes|Yes|Yes|Yes|Yes|No|Poor||||No|05-Dec-2008|Cryopreserved sperm|20.0|0.0|Yes||Autoimmunity, Arthritis, KRN, ENU|No| 7002.0|ENU21:015:b:B6:G3|ANU:ENU21:015:b:G3||Recessive|Unknown||||||||Unknown||||||||||||||||Unknown|||||||||||||Unknown|Unknown|C57BL/6NCrlAnu|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||1||No|06-Jul-2012|Cryopreserved sperm|10.0|0.0|Unknown||ENU, random, mutagenesis, screen|Yes| 6800.0|MIC1B6X^|MIC1B6^N10||Recessive|growth differentiation factor 15 |Gdf15||macrophage inhibiting cytokine-1, MIC-1, NAG-1 |MGI:1346047 ||||8|||||||||||||||||||||||||||||Normal|Normal|C57BL6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|20-Jan-2012||0.0|0.0|Unknown|||Yes| 7922.0|Id2|C57BL/6-Id2/WehiAnu||Dominant|inhibitor of DNA binding 2|Id2|Normal|bHLHb26, C78922, Idb2, inhibitor of differentiation 2|MGI:96397|inhibitor of DNA binding 2; targeted mutation 1, Gabrielle T Belz|Id2|MGI:5486127|12|||||||||||||||||||||||||||||The targeted reporter allele, Id2, resulted in the transcription of a bicistronic mRNA that produced wild‐type Id2 protein and GFP. This targeting strategy predicted that the IRES‐GFP cassette would not affect the upstream Id2 mRNA transcript. To confirm this, homozygous Id2 mice were generated (Figure 1B). Id2 mice were indistinguishable in survival, haematopoietic cellularity and lineage composition from C57BL/6 controls ||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|19-Jun-2015||0.0|0.0|Unknown||GFP, dendritic cell|Yes| 7003.0|ENU21:017:a:B6:G3|ANU:ENU21:017:a:G3||Recessive|Unknown||||||||Unknown||||||||||||||||Unknown|||||||||||||Unknown|Unknown|C57BL/6NCrlAnu|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||1||No|06-Jul-2012|Cryopreserved sperm|38.0|0.0|Unknown||ENU, random, mutagenesis, screen|Yes| 7004.0|ENU21:017:b:B6:G3|ANU:ENU21:017:b:G3||Recessive|Unknown||||||||Unknown||||||||||||||||Unknown|||||||||||||Unknown|Unknown|C57BL/6NCrlAnu|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||1||No|06-Jul-2012|Cryopreserved sperm|9.0|0.0|Unknown||ENU, random, mutagenesis, screen|Yes| 7007.0|ENU21:022:b:B6:G3|ANU:ENU21:022:b:G3||Recessive|Unknown||||||||Unknown||||||||||||||||Unknown|||||||||||||Unknown|Unknown|C57BL/6NCrlAnu|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||1||No|06-Jul-2012|Cryopreserved sperm|60.0|0.0|Unknown||ENU, random, mutagenesis, screen|Yes| 7011.0|ENU21:029:a:B6:G3|ANU:ENU21:029:a:G3||Recessive|Unknown||||||||Unknown||||||||||||||||Unknown|||||||||||||Unknown|Unknown|C57BL/6NCrlAnu|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||1||No|06-Jul-2012|Cryopreserved sperm|10.0|0.0|Unknown||ENU, random, mutagenesis, screen|Yes| 7005.0|ENU21:020:a:B6:G3|ANU:ENU21:020:a:G3||Recessive|Unknown||||||||Unknown||||||||||||||||Unknown|||||||||||||Unknown|Unknown|C57BL/6NCrlAnu|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||1||No|06-Jul-2012|Cryopreserved sperm|30.0|0.0|Unknown||ENU, random, mutagenesis, screen|Yes| 6418.0|A20|B6.Cg-Tnfaip3/AnuAusb?||Recessive|tumor necrosis factor, alpha-induced protein 3|Tnfaip3|Nil|A20, Tnfip3, zinc finger protein A20|MGI:1196377|tumor necrosis factor, alpha-induced protein 3; targeted mutation 1, Averil Ma|Tnfaip3|MGI:3055173|10|||||||||||||||||||||||||||||Abnormal cytokine secretion:*Bone marrow derived macrophages produce more TNF, IL-6, and nitric oxide in response to LPS treatment compared to wild-type macrophages.Abnormal inflammatory response:*The absolute number and percentage of myeloid cells is increased in multiple tissues.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown||Nuclear factor kappaB (NF-kappaB), Tumor necrosis factor (TNF)|Yes| 5324.0|Gin; col2a1Cre|C57BL/6-Tg(Col2a1-cre)1Asz||Dominant||||||||||||||||||||||||||transgene insertion 1, Attila Aszodi|Col2a1|7 copies||||||||||Normal|Normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Excellent||||No|17-Nov-2010||0.0|0.0|No||Arthritis |Yes| 5824.0|Hes 1||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 88.0|Vibes|C57BL/6JSfdAnu-Kcnv1/AnuApb|C57BL/6JSfdAnu-Kcnv1/AnuApb|Recessive|potassium channel, subfamily V, member 1|Kcnv1|Nil||MGI:1914748|vibes|Kcnv1|MGI:3614803|15|ENSMUSG00000022342|ENSMUST00000022967|Kcnv1-201||2612|T to C|ENSMUSE00000258359|3||Unknown to Unknown||||||No|||||||||||||Tetanic ataxia at weaning, shaking. Video available. Please contact APB Curator for the video. It is too large to post here.||C57BL/6JSfdAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Poor||||No|06-Feb-2006|Cryopreserved sperm|117.0|0.0|Unknown||Ataxia, Shaking, Weakness, ENU|Yes| 3942.0||B6-Tg(Cyp19a1-cre)5912Gle/Apb||Dominant||||||||||||||||||||||||||transgene insertion 5912, Gustavo Leone|cytochrome P450, family 19, subfamily a, polypeptide 1|Limited to Placenta||||||||||||FVB x C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|1|9|Backcross to C57BL/6 (CYP19-Cre/+ X +/+)|No|17-Oct-2008|Cryopreserved sperm|69.0|0.0|No||Trophoblast giant cells, placenta, Tpbpa, GFP|Yes| 4917.0|eed3354|B6.C-Eed<17Rn5-3354SB>/WehiApb||Recessive|embryonic ectoderm development|Eed|Unknown|l(7)5Rn, l7Rn5|MGI:95286|lethal, Chr 7, Rinchik 5, 3354SB|Eed<17Rn5-3354SB>|MGI:1856856|7|||||||||||||||||||||||||||||Gastrulation defects.The amnion and chorion are formed.The head process and notochord are absent and somites fail to organise.Unlike eed deletion mutants, Eed<3354SB> embryos develop characteristic folds in the anterior embryonic ectoderm.|||No|No|Yes|No|No|Yes|No|Unknown||||No|16-Oct-2009|Cryopreserved sperm|100.0|0.0|Unknown||embryonic, anterior, axial, gastrulation|Yes| 7009.0|ENU21:026:b:B6:G3|ANU:ENU21:026:b:G3||Recessive|Unknown||||||||Unknown||||||||||||||||Unknown|||||||||||||Unknown|Unknown|C57BL/6NCrlAnu|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||1||No|06-Jul-2012|Cryopreserved sperm|30.0|0.0|Unknown||ENU, random, mutagenesis, screen|Yes| 5016.0|nZEGs|BALB/c.B6-nZeg EGFP||Dominant||||||||||||||||||||||||||||||||||||||||7|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|22-Feb-2010|Cryopreserved sperm|105.0|0.0|Unknown||EGFP|Possibly| 5356.0|NOD.303|NOD-Tg(HLA DR3-DQ2)303/Apb||Dominant||||||||||||||||||||||||||human leukocyte antigen class II||||||||||||Expression of HLA DR and DQ evident on B cells, dendritic cells and a proportion of macrophages.Evaluation of HLA DR3-DQ2 haplotype-transgenic mice indicates regulated HLA gene expression, T cell selection and functional antigen presentation mediated by the DR and DQ genes encoded within the YAC transgene.Histological examination of tissues in transgenic mice including pancreatic B-islets did not reveal any evidence of spontaneous pathology.||NOD|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|22|7||No|20-Dec-2010|Cryopreserved sperm|50.0|0.0|Unknown||MHC, B cell, selection, autoimmunity|Yes| 8057.0|Masp2 KO|B6.129P2-Masp2/WjscAdel||Recessive|mannan-binding lectin serine peptidase 2|Masp2|Nil|MAp19, MASP-2|MGI:1330832|mannan-binding lectin serine peptidase 2; targeted mutation 1, Wilhelm J Schwaeble|Masp2|MGI:5007776|4|||||||||||||||||||||||||||||Decreased myocardial infarction size:• significant reduction in myocardial ischemia/reperfusion injury-induced myocardial damageDecreased susceptibility to injury:• significant protection from gastrointestinal ischemia/reperfusion injuryImpaired lectin complement pathway:• total absence of lectin pathway-dependent C4 cleavage on mannan- and zymosan-coated surfaces||C57BL/6J|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|07-Jun-2016||0.0|0.0|Unknown||postischemic reperfusion injury, complement, lectin|Yes| 6652.0|NOD.HJ12D-18|NOD/Lt-Tg(IL12B)HJ18Gem/Arc||Dominant||||||||||||||||||||||||||human interleukin 12b||||||||||||Mice express human interleukin 12B||NOD/Lt|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|10||Hom x Hom|No|29-Nov-2011|Embryo|0.0|0.0|Unknown||cyttokine, interleukin, autoimmunity|Yes| 4511.0|fluoro ; ENU8B6:058|C57BL/10JAnu-Prdx1/AnuApb||Recessive|peroxiredoxin 1|Prdx1|Unknown|macrophage 23kDa stress protein, macrophase stress protein 22kDa, MSP23, OSF-3, osteoblast specific factor 3, PAG, Paga, Prx I, PrxI, Tdpx2, TDX2, thioredoxin dependent peroxide reductase 2, Trx dependent peroxide reductase 2|MGI:99523|fluoro|Prdx1|MGI:4819263|4|ENSMUSG00000005161|ENSMUST00000005292|Prdx2-001|236|301|C to G|ENSMUSE00000499125|3|79|Serine to Cysteine|||||CTGCGAGGTGCTGGGAGTGTCTGTGGACTCTCAGTTCACCCACCTGGCGTGGATCAATACC|Yes|||||||||||||Autofluorescence, multiple wavelengths, in flow cytometry of all lymphocyte subsets and erythrocytes.||C57BL/10|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|26-Feb-2009|Cryopreserved sperm|107.0|0.0|Unknown||lymphocyte, erythrocyte, red blood cell, ENU, Wellcome Trust|Yes| 7008.0|ENU21:024:b:B6:G3|ANU:ENU21:024:b:G3||Recessive|Unknown||||||||Unknown||||||||||||||||Unknown|||||||||||||Unknown|Unknown|C57BL/6NCrlAnu|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||1||No|06-Jul-2012|Cryopreserved sperm|40.0|0.0|Unknown||ENU, random, mutagenesis, screen|Yes| 7010.0|ENU21:027:a:B6:G3|ANU:ENU21:027:a:G3||Recessive|Unknown||||||||Unknown||||||||||||||||Unknown|||||||||||||Unknown|Unknown|C57BL/6NCrlAnu|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||1||No|06-Jul-2012|Cryopreserved sperm|40.0|0.0|Unknown||ENU, random, mutagenesis, screen|Yes| 7013.0|ENU21:032:b:B6:G3|ANU:ENU21:032:b:G3||Recessive|Unknown||||||||Unknown||||||||||||||||Unknown|||||||||||||Unknown|Unknown|C57BL/6NCrlAnu|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||1||No|06-Jul-2012|Cryopreserved sperm|30.0|0.0|Unknown||ENU, random, mutagenesis, screen|Yes| 6829.0|APN 142|C57Bl/6NTac-Gpr18/Marp||Recessive|G protein-coupled receptor 18|Gpr18|Unknown||MGI:107859 |G protein-coupled receptor 18; targeted mutation 1, Velocigene|Gpr18 |MGI:3812675|14|||||||||||||||||||||||||||||Unknown|Normal|C57Bl/6N|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|01-Mar-2012|Cryopreserved sperm|50.0|0.0|Unknown|||Possibly| 2433.0|CD22-/-:Hamlet|B6;129P2-Cd22 Tg(IghelMD4)4Ccg/AnuApb|B6;129P2-Cd22 Tg(IghelMD4)4Ccg/AnuApb|Recessive|CD22 antigen|Cd22|Nil|Lyb-8, Lyb8|MGI:88322|CD22 antigen; targeted mutation 1, Edward A Clark|Cd22|MGI:2180680|7||||||||||||||||Yes|transgene insertion 4, Christopher C Goodnow|||||||||||||Abnormal mature B cell morphology:* expression of CD22 on the surface of cells is half that of controls* surface expression of IgM is about 70-80% of controls|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|||Cd22-/- x Ig+|No|13-Jan-2008|Cryopreserved sperm|110.0|0.0|No||B cell, T cell, lymphocyte, signalling, B cell antigen receptor, autoimmunity|Yes| 8163.0|Nlrp3 KO|B6.129S6-Nlrp3/J||Recessive|NLR family, pyrin domain containing 3|Nlrp3||Cias1, cryopyrin, Mmig1, NALP3, Pypaf1|MGI:2653833|NLR family, pyrin domain containing 3; targeted mutation 1, Beverly H Koller|Nlrp3|MGI:5465108|11|||||||||||||||||||||||||||||Immune system phenotype:N • macrophages exhibit normal response to anthrax lethal toxin• bone marrow derived macrophages are not sensitive to the challenge by the bacteria peptidoglycan motif of muramyl dipeptide (MDP).Decreased interleukin-1 beta secretion: • in macrophages exposed to titanium oxide with or without muramyl dipeptide or peptidoglycan• in macrophages exposed to L18-muramyl dipeptideDecreased lactate dehydrogenase level: • in the bronchoalveolar lavage (BAL) fluids||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|23-Jan-2017||0.0|0.0|Unknown||inflammasome, Caspase1|Yes| 1736.0|B6.EµSV-v-abl 1|C57BL/6-Tg(Igh-Abl1)1Sco/Wehi||Dominant|||||||||Unknown||||||||||||||||No|transgene insertion 1, Suzanne Cory |mouse Igh enhancer and the SV40 early promoter||||||||||||Low incidences of plasmacytoma. Look out for dragging hind legs, enlarged spleen, enlarged menteric lymph nodes - tumours. Visually check daily.1-2% will die at 20 weeks of age, 19-20% will die at 1 year. Mice die as a result of plasmcytoma. Mice will bear one of the following tumours: lymphoma, splenomegaly, messentary associated, abdominal, caecal, Peyer's Patches. They may also suffer from small bowel obstruction, intestinal haemorrhage, hind leg paralysis, intussusception.|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|01-Aug-2007||0.0|0.0|Unknown||plasmacytoma, B cell, oncogene, lymphoma, Abelson virus|Yes| 7012.0|ENU21:031:a:B6:G3|ANU:ENU21:031:a:G3||Recessive|Unknown||||||||Unknown||||||||||||||||Unknown|||||||||||||Unknown|Unknown|C57BL/6NCrlAnu|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||1||No|06-Jul-2012|Cryopreserved sperm|60.0|0.0|Unknown||ENU, random, mutagenesis, screen|Yes| 8246.0|Aim2 KO|C57BL/6N-Aim2/VmdAnu||Recessive|absent in melanoma 2|Aim2|Nil|Ifi210, LOC383619|MGI:2686159|absent in melanoma 2; targeted mutation 1.1, Vishva M Dixit|Aim2|MGI:5428935|1|||||||||||||||||||||||||||||Abnormal macrophage physiology:• improved cell viability following transfection with poly(dA:dT) or pcDNA3• improved bone marrow derived macrophage viability following infection with F. tularensisAbnormal cytokine secretion.Increased interferon-beta secretion:• in bone marrow derived macrophages stimulated by poly(dA:dT) or pcDNA3Decreased interleukin-1 beta secretion:• in LPS-primed bone marrow derived macrophages or peritoneal macrophages stimulated by dsDNA• bone marrow derived macrophages do not secrete IL1B in response to F. tularensisDecreased interleukin-18 secretion:• in LPS-primed bone marrow derived macrophages stimulated by dsDNAIncreased tumor necrosis factor secretion:• in bone marrow derived macrophages stimulated by poly(dA:dT) or pcDNA3Increased susceptibility to bacterial infection:• fail to control F. tularensis infection||C57BL/6NCrlAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|20-Apr-2017||0.0|0.0|Unknown||Caspase 1, inflammasome, DNA|Yes| 6791.0|D3a/min (ME-98)|B6.129-Apc Tg(Gpa33-Dnmt3a)1Ern/Lud||Recessive|adenomatosis polyposis coli|Apc|Unknown|CC1, Min|MGI:88039|adenomatosis polyposis coli; multiple intestinal neoplasia|Apc|MGI:1856318|18|||||||||||||||||transgenic insertion 1, Matthias Ernst|glycoprotein A33 (transmembrane)|||||||||||Lesions in B6.129-Apc Tg(Gpa33-Dnmt3a)1Ern/Lud mice frequently retain the wild-type Apc allele. However, epithelia from normal mucosa and polyps of B6.129-Apc Tg(Gpa33-Dnmt3a)1Ern/Lud mice show hypermethylation-mediated transcriptional silencing of the Wnt antagonists Sfrp5, and to a lesser extent, Sfrp1 and increased nuclear beta-catenin alongside activation of the Wnt-target gene Axin2/Conductin. Min homozygotes are not viable and are embryonic lethal.Mice develop increased intestinal polyposis(cp to Apc min mice) with a prevalence of colonic polyps due to epigenetic silencing of wnt antagonists (Sfrp5).|Unknown|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|18-Jan-2012||0.0|0.0|Unknown||signal transduction, polyp, Wnt, hypermethylation|Yes| 2435.0|Louise2 ; TLK-2|C57BL/6JSfdAnu-Tg(TLK2mHEL)2Ccg/AnuApb|C57BL/6JSfdAnu-Tg(TLK2mHEL)2Ccg/AnuApb|Dominant||||||||||||||||||||||||||transgene insertion 2, Christopher C Goodnow|rat thyroglobulin|expression limited to thyroid||||||||||Express low levels of membrane bound HEL in thyroid. Low serum levels of HEL detected.||C57BL/6JStdAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||5|sib x sib|No|13-Jan-2008|Cryopreserved sperm|130.0|0.0|Unknown||autoimmunity, B cell, tolerance, Hen egg lysozyme (HEL), T cell|Yes| 7288.0|ENU12B6:020:G3|ANU:ENU12B6:020:G3||Recessive|Unknown|Unknown|||||||Unknown|||||||||||||||||||||||||||||Unknown|Unknown|C57BL/6JSfdAnu|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Good||||No|14-Mar-2013|Cryopreserved sperm|27.0|0.0|Unknown|||Possibly| 6654.0|TUQIRI|BALB/c-Tnfsf10/Ausb||Recessive|tumor necrosis factor (ligand) superfamily, member 10|Tnfsf10|Nil|A330042I21Rik, APO-2L, Trail |MGI:107414|tumor necrosis factor (ligand) superfamily, member 10; targeted mutation 1, Mark J Smyth|Tnfsf10|MGI:2179709|3|||||||||||||||||||||||||||||||BALB/c|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|02-Dec-2011||0.0|0.0|Unknown||TNF-related apoptosis-inducing ligand (TRAIL), toxicity, metastasis, T-helper 2, Asthma|Yes| 5329.0||129T2/SvK-Ryk/Apb||Recessive|Receptor-like tyrosine kinase|Ryk|Nil|ERK-3, Vik|MGI:101766|receptor-like tyrosine kinase; targeted mutation 1, Steven A Stacker|Ryk|MGI:2667542|9||||||||||||||||Yes|||||||||||||Homozygotes die on the day of birth. Approx. 90% of E18.5 embryos have heart defects, the probable cause of neonatal death. They also have a cleft palate, craniofacial defects, shortened limbs and body axis, inner ear defects and abnormal corpus callosum (brain).Abnormal gait: mice surviving to adulthood dragged their hindlimbs.Short mandible.Abnormal maxilla morphology: in conjunction with shortened nasal bone, resulting in flattened midface.Abnormal neurocranium morphology: slightly smaller and rounder than that of wild-type or heterozygous mutant mice.Short nasal bone: shortened nasal bone, resulting in flattened midface.Cleft secondary palate: * cleft secondary palate observed in 88% of mice * consequence of abnormally high positioning and enlargement of the tongue.Increased tongue size: enlargement observed around E14, resulting in the disruption of the development of the palatal shelf.Short snout.Microcephaly: exhibited by mice that survived to adulthood.Cachexia.Postnatal growth retardation: growth was severely impaired in mice surviving past the first day of life.Cyanosis: mice were largely unable to suckle, became dehydrated, cyanotic, and exhibited gasping respirations.Short ulna: reduced in length.Abnormal hindlimb morphology: hindlimbs were splayed laterally.Short fibula.Short limbs: 18% to 25% reduction in the length of the long bones.Microphthalmia: bilateral microphthalmia was observed in mice that survived to adulthood.||129T2/Sv/K|No|No|Yes|No|No|Yes|No|Unknown||||No|19-Nov-2010|Cryopreserved sperm|50.0|0.0|Unknown||craniofacial, Eph receptor, TGF, receptor protein tyrosine kinases (RTKs), Wnt signalling, axon guidance|Yes| 7546.0|APN 354|C57BL/6N-A Wars/MarpApb||Recessive|tryptophanyl-tRNA synthetase 1|Wars1 |||MGI:104630 |tryptophanyl-tRNA synthetase1; targeted mutation 1a, Helmholtz Zentrum Muenchen GmbH12|Wars1|MGI:4435065|12||||||||||Unknown to Unknown|||||||||||||||||||Unknown|Normal|C57Bl/6N|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|18-Dec-2013|Cryopreserved sperm|40.0|0.0|Unknown|||Possibly| 9189.0||B6.129S7-FoxP3(KO)-Rag1/Apb||Dominant|FoxP3ko||||||||Unknown|||||||||||||||||||||||||||||normal|normal|rag1|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|20-May-2021||0.0|76.0|Unknown|||Possibly| 9189.0||B6.129S7-FoxP3(KO)-Rag1/Apb||Dominant|Rag1(tm1Mom)||||||||Unknown|||||||||||||||||||||||||||||normal|normal|rag1|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|20-May-2021||||Unknown|||Possibly| 7014.0|ENU21:034:a:B6:G3|ANU:ENU21:034:a:G3||Recessive|Unknown||||||||Unknown||||||||||||||||Unknown|||||||||||||Unknown|Unknown|C57BL/6NCrlAnu|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||1||No|06-Jul-2012|Cryopreserved sperm|60.0|0.0|Unknown||ENU, random, mutagenesis, screen|Yes| 219.0||C57BL/6-Gt(ROSA)26Sor/WehiAnuApb||Dominant||||||||||||||||||||||||||gene trap ROSA 26, Philippe Soriano|unknown endogenous|||||||||||Viable and fertile. Mice carrying this mutation are considered to be reporter strains, with successful Cre excision indicated by beta-gal expression in Cre-expressing tissues. There is no phenotype and mice appear normal.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|25-Apr-2006|Cryopreserved sperm|43.0|0.0|Unknown||Lac Z, genetrap, beta-galactosidase, reporter|Yes| 309.0|Nude|B6.Cg-Foxn1||Recessive|forkhead box N1|Foxn1|Unknown|D11Bhm185e, Hfh11, whn|MGI:102949|nude|Foxn1|MGI:1856108|11||||||||||||||||Yes|||||||||||||Postnatal lethality:some mice die within 1 week of birth55% mortality within 2 weeksPremature death:100% mortality by 25 weeksDecreased body size and weight.Postnatal growth retardation.Abnormal T cell differentiation.Athymia.Abnormal cell-mediated immunity.Abnormal liver morphology:liver lobes were atrophied and covered with red scarsvariable degrees of severity, typically increasing with age at time of death.Small ovaryCoiled sperm flagellum: many sperm had coiled tailsAbnormal estrous cycle: many females exhibited continuous dioestrus and metaoestrus phasesFemale infertility: severely reduced fertilityReduced male fertility.Asthenozoospermia.Nude: sparse hair growth around 5 weeks of agein some mice, cephalo-caudal migration of an irregular band of short sparse hairThin skin:reduction in skin thickness at 3 weeks of age, corresponding to the catagen stage of normal skinAbsent vibrissae: absent at birthShort and wavy vibrissae: older mice show repeated growth and loss of short and wavy vibrissae.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|03-May-2006||0.0|0.0|Unknown||hair loss, T cell, thymus, body size / mass, growth retardation, alopecia, keratin|Yes| 6656.0|Vasa-cre|FVB-Tg(Ddx4-cre)1Dcas/J/Ausb||Semi-dominant||||||||||||||||||||||||||transgene insertion 1, Diego Castrillon||||||||||||||FVB/N|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|02-Dec-2011||0.0|0.0|Unknown||Vasa promoter, Gametogenesis|Yes| 8378.0|NOD.Nkrp1b.Nkt2b|NOD-Klrb1b Nktcn2b/Bax||Recessive|||||||||||||||||||||||||||||killer cell lectin-like receptor subfamily B member 1B|Klrb1b||Klrb1d, Ly55b, Ly55d, Nkrp1-b, NKR-P1B, Nkrp1d, NKR-P1D|MGI:107539||||6|Mice that are homozygous for this allele are viable, fertile and normal in size.Congenic Nk Cell Marker. Congenic Marker for NKT2 region. Increased Nkt cell numbers.||NOD/Lt|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|10|||No|11-Dec-2017||0.0|0.0|Unknown||Nk1.1, TCR, NK cell, autoimmunity|Yes| 8378.0|NOD.Nkrp1b.Nkt2b|NOD-Klrb1b Nktcn2b/Bax||Recessive|||||||||||||||||||||||||||||natural killer T cell numbers 2|Nktcn2||Nkt2b|MGI:2681137||||2|Mice that are homozygous for this allele are viable, fertile and normal in size.Congenic Nk Cell Marker. Congenic Marker for NKT2 region. Increased Nkt cell numbers.||NOD/Lt|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|10|||No|11-Dec-2017||||Unknown||Nk1.1, TCR, NK cell, autoimmunity|Yes| 5408.0|Gp130Y757f / Stat3+/- / Stat1-/-|STOCK Il6st Stat3 Stat1/LudApb||Recessive|interleukin 6 signal transducer|Il6st|Unknown|CD130, D13Ertd699e, gp130|MGI:96560|interleukin 6 signal transducer; targeted mutation 1, Matthias Ernst|Il6st|MGI:2388478|13||||||||||||||||Yes|||||||||||||Unknown|Unknown|C57BL/6 x 129/Sv|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|03-Feb-2011|Cryopreserved sperm|50.0|0.0|Unknown||signal transduction, kinase, acute peritoneal inflammation, neutrophil|Yes| 5408.0|Gp130Y757f / Stat3+/- / Stat1-/-|STOCK Il6st Stat3 Stat1/LudApb||Recessive|signal transducer and activator of transcription 3|Stat3|Unknown|Aprf|MGI:103038|signal transducer and activator of transcription 3; targeted mutation 1, Shizuo Akira|Stat3|MGI:1926814|11||||||||||||||||Yes|||||||||||||Unknown|Unknown|C57BL/6 x 129/Sv|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|03-Feb-2011|Cryopreserved sperm|||Unknown||signal transduction, kinase, acute peritoneal inflammation, neutrophil|Yes| 5408.0|Gp130Y757f / Stat3+/- / Stat1-/-|STOCK Il6st Stat3 Stat1/LudApb||Recessive|signal transducer and activator of transcription 1|Stat1|||MGI:103063|signal transducer and activator of transcription 1; targeted mutation 1, Robert D Schreiber|Stat1|MGI:1861949|1||||||||||||||||No|||||||||||||Unknown|Unknown|C57BL/6 x 129/Sv|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|03-Feb-2011|Cryopreserved sperm|||Unknown||signal transduction, kinase, acute peritoneal inflammation, neutrophil|Yes| 335.0||B6,129-Lyn||Recessive|Yamaguchi sarcoma viral (v-yes-1) oncogene homolog|Lyn|Nil|Hck-2|MGI:96892|targeted mutation 1, Ashley R Dunn|Lyn|MGI:2157129|4||||||||||||||||Yes|||||||||||||Peritoneal inflammation: there is about a doubling in the number of T cells found in the peritoneumIncreased T cell number: there is about a doubling in the number of T cells found in the peritoneumAbnormal B cell morphology: B cells express lower levels of CD21 and higher levels of CD23 on the cell surface compared to controls.Decreased transitional stage B cell number: profound reduction in transitional stage-2 B cells.Decreased follicular B cell number: about a five-fold reduction in follicular B cellsDecreased marginal zone B cell number: profound reduction in marginal zone B cells.Abnormal B cell activation: significant expression of MHCII complexes by circulating B cells suggest these B cells are in an activated state. B cells have enhanced calcium flux upon activationAbnormal myelopoiesis: myelopoiesis is greatly enhanced in these mice.there is a significant increase in the number of colonies generated by bone marrow cells or splenocytes in response to in vitro culturing with GM-CSF, M-CSF, or IL-3.Spleen hypoplasia: spleen cellularity is reduced by more than half due to B cell lymphopenia.Increased anti-nuclear antigen antibody level: auto-antibodies of the IgA, IgG IgM classes develop as the mice age.Increased anti-double stranded DNA antibody level: mice develop anti-DS DNA IgG antibodies as they age with high levels detectable in all mice by 20 weeks of age.Glomerulonephritis: all mice have immunoglobulin complex deposition in the kidney by 8 weeks of age.83% of mice also have C3 complement deposition in the kidneysevere glomerulonephritis occurs in these mice by one year of age.||C57BL/6 x 129|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|05-May-2006||0.0|0.0|Unknown||splenomegaly, autoimmunity, B cell, glomerulonephritis, myelomonocytic|Yes| 1739.0|B6. Eµ-myc 292-1|C57BL/6-Tg(Tg(IghMyc)22Bri/Wehi||Dominant||||||||||||||||||||||||||transgene insertion 22, Ralph L Brinster|Igh (E mu) enhancer and Myc promoter|High|||||||||||Premature death:* mice die at 6 to 15 weeks of age with 94% of mice dying by 4 months of age.Increased tumor incidence:* mice occasionally develop thyoma without involvement of peripheral lymphoid organs.Leukemia:* mice develop multicentric lymphosarcoma associated with leukemia.Lymphoma:* 13 of 15 mice develop lymphomas* mice develop multicentric lymphosarcoma associated with leukemia.B cell derived lymphoma:* lymphomas develop from single B-lymphoid clones at different stages of differentiation.Sarcoma: mice develop multicentric lymphosarcoma associated with leukemia.Abnormal lymphopoiesis:* mice exhibit an increased in the number of lymphoblasts in lymph tissues and the blood compared to wild-type miceEnlarged spleen: two-fold.Enlarged thymus.Enlarged lymph nodes.|C57BL/6|Yes|No|Yes|Yes|No|Yes|No|Unknown||||No|01-Aug-2007||0.0|0.0|Unknown||B cell, Lymphoma, immunoglobulin enhancer, lymphocyte, myc|Yes| 1752.0|Hepsin KO|129-Hpn/Wehi||Semi-dominant|hepsin|Hpn|Nil||MGI:1196620|targeted mutation 1, Qingyu Wu|Hpn|MGI:3639336|7||||||||||||||||Yes|||||||||||||Mice develop normally and are viable and fertile.Mice are deaf. Mice homozygous for a null mutation are hypothyroidic and develop profound hearing loss associated with structural changes in the tectorial membrane and a myelination defect affecting the compaction of spiral ganglion neurons.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|02-Aug-2007||0.0|0.0|Unknown||deafness, serine protease, transmembrane, TMPRSS1, cochlear|Yes| 8479.0|ENU22::ANAPC1|C57BL/6NCrlAnu-Ighm/AnuApb||Recessive|immunoglobulin heavy constant mu|Ighm|Unknown|BCR, Igh6, Igh-M, IgM, Ig mu, muH, muMT|MGI:96448|Ighm; endonuclease-mediated mutation 1, Australian National University|Ighm||12||||||||||Unknown to Unknown|||||||||||||||||||||C57BL/6NCrlAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|01-May-2018|Cryopreserved sperm|66.0|0.0|Unknown||immunoglobulin|Yes| 1728.0|Pkd1 KO|C57BL/6-Pkd1||Recessive|polycystic kidney disease 1 homolog|Pkd1|Normal|PC-1, PC1, polycystin-1|MGI:97603|targeted mutation 1, Jing Zhou|Pkd1|MGI:1857562|17||||||||||||||||No|||||||||||||Perinatal lethality:* after E18.5, most mutant embryos are dead, partly absorbed or misshapen.* few homozygotes survive to term but die, on average, 4 hours after birth.Postnatal lethality:* only 1 out of 400 homozygotes survived the neonatal period and died at P8 with pale cystic kidneys and a cystic pancreas.Decreased pancreatic islet number:* homozygotes contain fewer islets of Langerhans than wild-type mice; in contrast, acini appear to develop normally.Dilated pancreatic duct:* homozygotes show early and massive dilatation of pancreatic ducts.Pancreas cysts:* homozygotes exhibit cysts in major pancreatic ducts as early as E13.5, before renal cysts develop.* newborn (and P8) pancreases contain massive yellow fluid-filled cysts that enlarge with age.Disproportionate dwarf:* at P8, the sole mutant survivor is significantly smaller relative to wild-type.* newborn homozygotess exhibit dwarfism relative to newborn wild-type mice.Distended abdomen:* homozygotes that die perinatally display distended abdomens.Hydrops fetalis:* exhibit mild hydrops fetalis at late stages of fetal developmentSkin edema:* histologically, mutant fetuses exhibit a mild subcutaneous edema.Polyhydramnios:* exhibit mild polyhydramnios at late stages of fetal development.Liver/biliary system phenotype:* unlike patients with ADPKD, homozygotes display no liver cyst formation.Renal/urinary system phenotype:* in mutants, the initial stages of lumen formation and tubule differentiation proceed normally as late as E15.5.Abnormal kidney epithelium morphology:* by P8, renal parencyma in the sole survivor is almost completely replaced by cysts; cuboidal tubular epithelia are replaced by flattened cyst-lining epithelia.Abnormal kidney medulla morphology:* at E15.5, tubular and periglomerular cysts are scattered throughout the outer medulla; nephrogenesis at the rim of the kidney remains unaffected.* cyst formation is subsequently noted in collecting tubules of the inner medulla.* in newborn homozygotes, epithelial cysts occupy the entire medulla.Enlarged kidney:* homozygotes that die perinatally exhibit massive kidney enlargement.Dilated proximal convoluted tubules:* at E15.5, homozygotes display progressive multifocal microdilatation of tubules in proximal tubules of the outer medulla.* in newborn homozygotes, tubule dilatation is more extensive, affecting most of the kidney.Kidney cysts:* homozygotes that die perinatally first exhibit tubular and periglomerular cysts at E15.5; no histological abnormalities are noted until E14.5.* the number and size of cysts increase with age.Kidney cortex cysts:* after E15.5, progressive tubule dilatation and cyst formation is noted in mutant cortex.* in newborn homozygotes, epithelial cysts occupy most of the cortex.Abnormal kidney physiology:* in culture, kidney epithelial cells isolated from E15.5 (pre-cystic) mutant mice form primary cilia but fail to increase Ca2+ influx in response to physiological fluid flow at low levels of fluid shear stress (0.75 dyne cm-2).* no Ca2+ signaling is detected in wild-type or mutant cells at higher levels of fluid shear stress (15 dyne cm-2).* both wild-type and mutant cells respond to thrombin by increasing cytosolic Ca2+ concentrations, indicating that mutant cells retain the ability to conduct Ca2+ but lose the ability to sense fluid flow.* notably, the Ca2+ response to thrombin is enhanced in mutant cells relative to wild-type cells, either in the presence of extracellular Ca2+.Abnormal thyroid cartilage morphology:* a number of newborn homozygotes exhibit thyroid cartilage malformation.Small lung:* homozygotes that die perinatally have small lungs relative to wild-type mice.Pulmonary hypoplasia:* homozygotes that die perinatally have hypoplastic lungs.Respiratory distress:* homozygotes that survive to term but die perinatally exhibit difficulty in breathing and fail to turn pink.Spina bifida occulta:* 8 out of 11 (73%) homozygotes develop mild spina bifida occulta in the lumbar region at late embryonic or newborn stages.Abnormal thyroid cartilage morphology:* a number of newborn homozygotes exhibit thyroid cartilage malformation.Chondrodystrophy:* newborn homozygotes display osteochondrodysplasiaAbnormal bone mineralization:* newborn homozygotes display a delay in bone mineralization of vertebrae, long bones and skull relative to wild-type mice.Skin edema:* histologically, mutant fetuses exhibit a mild subcutaneous edema.|Decreased pancreatic islet number:* at >20 months, few islets are present; in areas of pancreatic lipomatosis, islets appear isolated, and surrounded by mature adipocytes.Abnormal exocrine pancreas morphology:* at >20 months, heterozygotes show multiple cystic structures lined by cuboidal cyst epithelium.Abnormal pancreatic acinus morphology:* at >20 months, few acini are present; in areas of pancreatic lipomatosis, acini appear atrophic, isolated, and surrounded by mature adipocytes.Dilated pancreatic duct:* at >20 months, heterozygotes show dilatation of pancreatic ducts.Pancreas cysts:* at >20 months, 10% of heterozygotes display macroscopic pancreatic cysts; no cysts are observed at 9-20 months.* some cysts with small lumens also contain cuboidal epithelium, with a large portion of eosinophilic cytoplasm suggesting an acinar origin.Pancreas fibrosis:* at >20 months, pancreatic cystic lesions are surrounded by interstitial fibrosis.Pancreas lipomatosis:* at >20 months, the pancreas is massively replaced by adipose tissue.Abnormal bile duct morphology:* heterozygotes exhibit ductal plate malformation with occasional biliary microhamartomas.Bile duct inflammation:* in heterozygotes, impaired liver function correlates with cyst volume and cholangitis; increased cyst volume is due to increased secretion from the cystic epithelia.Dissociated hepatocytes:* heterozygotes with multiple liver cysts exhibit little residual parenchyma relative to wild-type mice.Liver cysts:* at 9-14 months of age, 4 out of 15 heterozygotes (27%) display liver cysts; notably, no liver cysts are found in perinatal homozygotes.* after 14 months of age, 7 of 8 (87%) heterozygotes have liver cysts filled with clear or dark-brown fluid (up to 10 ml in volume) occupying one- to two-thirds of the liver.* most liver cysts are lined by cuboidal or squamous biliary-like epithelium positive for cytokeratin 19 (a biliary-specific epithelial marker) and show focal hyperplasia.Decreased liver function:* in heterozygotes, cyst number and impaired liver function are associated with a significant rise in ALT, AST and LDH enzyme levels with progressive age.Renal/urinary system phenotype:* heterozygotes show no differences in kidney anatomy or histology up to 7 months of age; no renal cysts are observed at 220 days.Kidney inflammation:* in heterozygotes, large renal cysts are often surrounded by atrophic parenchyma with inflammation.Dilated renal tubules:* at 9-14 months of age, heterozygotes with renal cysts show a greater than 5-fold dilatation in tubule diameter relative to wild-type.Kidney cysts:* at 9-14 months of age, 12 out of 15 heterozygotes (80%) display 1-7 renal cysts per mouse; 5 of these mutants show bilateral cysts.* after 16 months, 100% of heterozygotes have renal cysts (2-50 per mouse); 6 of 8 heterozygotes show bilateral cysts.* most cysts fail to stain with lotus tetragonolobus lectin, a proximal tubule marker, and dolichos biflorus agglutinin, a collecting tubule marker; in contrast, glomerular cysts are common.* notably, some cysts show loss of polycystin-1 expression; in addition, EGFR is improperly localized to apical membranes in cysts and some slightly dilated tubules.* in heterozygotes, large cysts contain epithelia that range from columnar to cuboidal to squamous.Renal interstitial fibrosis:* in heterozygotes, large renal cysts are often surrounded by atrophic parenchyma with interstitial fibrosis.|C57BL/6|No|No|Yes|No|No|Yes|No|Unknown||||No|01-Aug-2007||0.0|0.0|Yes|Polycystic Kidneys|polycystic kidney disease, cyst, renal, pancreas|Yes| 1732.0|EµSV-NRAS-18|B6.129-Tg(SV40-NRAS*G12D)1Sco/Wehi||Dominant||||||||||||||||||||||||||transgene insertion 1, Suzanne Cory|SV40 early region promoter with the immunoglobulin heavy chain enhancer (Emu)||||||||||||T cell derived lymphoma.Sarcoma.|C57BL/6 x 129|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|01-Aug-2007||0.0|0.0|Unknown||T cell, Lymphoma, oncogene, tumorigenesis, myc|Yes| 1741.0|Dnmt3l KO|C57BL/6-Dnmt3l/Wehi||Recessive|DNA (cytosine-5-)-methyltransferase 3-like|Dnmt3l|Unknown|D6Ertd14e, ecat7|MGI:1859287|targeted mutation 1, Hamish S Scott|Dnmt3l|MGI:3574947|10||||||||||||||||Yes|||||||||||||Abnormal seminiferous epithelium morphology:* the epithelium has a vacuolated appearanceAzoospermia:* germ cells are lost through apoptosis and sloughing with many tubules containing only Sertoli cells.Arrest of male meiosis:* at P14 in first spermatogenic wave a build up of leptotene and zygotene spermatocytes is seen with no cells progressing beyond stage IV.* at P70 only leptotene spermatocytes and spermatogonia are present.* the pachytene synaptonemal complex is not seen.Small gonad:* adults display severe hypogonadismInfertility.||C57BL/6|Yes|Yes|No|Yes|No|Yes|Yes|Unknown||||No|01-Aug-2007||0.0|0.0|Unknown||Spermatogenesis, Sterility, DNA methylation, epigenetic, Meiotic|Yes| 8480.0|KRN TCR transgenic/B10.Br|B10.BR-Tg(TcraR28,TcrbR28)KRNDim/Apb||Dominant||||||||||||||||||||||||||transgene insertion KRN, Diane Mathis||||||||||||Normal|Normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|03-May-2018|Cryopreserved sperm|40.0|0.0|Unknown||TCR, Rheumatoid arthritis|Yes| 8584.0|ASD538:Mrd:MrTless|B6(Cg)-Zap70 Zap70/AnuApb|B6(Cg)-Zap70 Zap70/AnuApb|Recessive|Zap70, zeta-chain (TCR) associated protein kinase|Zap70|Reduced|Zap-70, Srk, TZK|MGI:99613|Mr T-Less|Zap70|MGI:3614790|1|ENSMUSG00000026117|ENSMUST00000027291|Zap70-201|1510|1601|T to C|ENSMUSE00000230099|11|504|Tryptophan to Arginine|||||CCCGGTCTGCAGGGAAGTGGCCTCTGAAGTGGTACGCGCCAGAGTGCATCAACTTTCGGAA|No|||||||||||||Identified by severe reduction in T cell numbers in blood.B cells are normalBoth CD4⁺ and CD8⁺ T cell populations were almost completely absent in peripheral blood. Therefore, no αβ T cells but have increase in γδ T cellsNormal numbers of DN and DP T cells. Implies that have block at DP stage and mice unable to perform positive thymocyte selection.Intrinsic to T cells not microenvirnment.Cells unable to pass thymic selection steps.Cells unable to up-regulate TCRReduced signalling through TCR.Zap70 protein expression of mrt/mrt thymocytes was 25% of wildtype thymocytes.Kinase domain affected by mutation, kinase assays not performedHeterozygous mice, mrt/+ have normal levels of CD4⁺ and CD8⁺ thymocytes but Zap70 protein expression is 2 fold lower.Unlike cells devoid of ZAP-70, mrtless thymocytes showed partial induction of CD5 and CD69, and were sensitive to TCR stimulation with a dose-response shifted approximately 10-fold. However, essentially no T cells were able to compensate for the mrtless mutation and mature beyond the CD4⁺ CD8⁺ stage.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|04-Oct-2018|Cryopreserved sperm|69.0|0.0|Unknown||T cell, zap70, B cell, TCR, lymphocyte , ENU|Yes| 8584.0|ASD538:Mrd:MrTless|B6(Cg)-Zap70 Zap70/AnuApb|B6(Cg)-Zap70 Zap70/AnuApb|Recessive|Zap70, zeta-chain (TCR) associated protein kinase|Zap70|Unknown|Zap-70, Srk, TZK|MGI:99613|Murdoch|Zap70|MGI:3614796|1|ENSMUSG00000026117|ENSMUST00000027291|Zap70-201|1099|1190|A to T|ENSMUSE00000448670|9|366|Isoleucine to Phenylalanine|||||GCATGCGCAAGAAGCAGATTGACGTGGCCATCAAGGTGCTGAAGCAGGGCACAGAGAAGGC||||||||||||||Identified by severe reduction in T cell numbers in blood.B cells are normalBoth CD4⁺ and CD8⁺ T cell populations were almost completely absent in peripheral blood. Therefore, no αβ T cells but have increase in γδ T cellsNormal numbers of DN and DP T cells. Implies that have block at DP stage and mice unable to perform positive thymocyte selection.Intrinsic to T cells not microenvirnment.Cells unable to pass thymic selection steps.Cells unable to up-regulate TCRReduced signalling through TCR.Zap70 protein expression of mrt/mrt thymocytes was 25% of wildtype thymocytes.Kinase domain affected by mutation, kinase assays not performedHeterozygous mice, mrt/+ have normal levels of CD4⁺ and CD8⁺ thymocytes but Zap70 protein expression is 2 fold lower.Unlike cells devoid of ZAP-70, mrtless thymocytes showed partial induction of CD5 and CD69, and were sensitive to TCR stimulation with a dose-response shifted approximately 10-fold. However, essentially no T cells were able to compensate for the mrtless mutation and mature beyond the CD4⁺ CD8⁺ stage.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|04-Oct-2018|Cryopreserved sperm|||Unknown||T cell, zap70, B cell, TCR, lymphocyte , ENU|Yes| 1756.0|Bmf 376|C57BL/6-Bmf/Wehi||Recessive|Bcl2 modifying factor|Bmf|Normal||MGI:2176433|BCL2 modifying factor; targeted mutation 1, Andreas Villunger|Bmf|MGI:3778609|2||||||||||||||||Yes|||||||||||||Normal||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|02-Aug-2007||0.0|0.0|Unknown||Bcl-2, BH3 only, B cell, cell death, stress|Yes| 1769.0|Scl knockout 221|C57BL/6-Tal1/Wehi||Recessive|T-cell acute lymphocytic leukemia 1|Tal1|Nil|Scl, SCL/tal-1|MGI:98480|targeted mutation 1, Walter and Eliza Hall Institute of Medical Research|Tal1|MGI:1857566|4||||||||||||||||Yes|||||||||||||Homozygous targeted null mutants show retarded growth, edema, lack yolk sac hematopoiesis and die at embryonic day 9.5-10.5. Embryonic lethality during organogenesis: homozygotes die by E10.5; only resorption sites with small embryonic remnants are detected at E11.5.Incomplete embryo turning: ~1/3 of homozygotes fail to complete axial rotation.Abnormal embryonic hematopoiesis:*homozygotes exhibit failure of yolk sac hematopoiesis, with no erythrocytes found in embryonic vessels.* in vitro, cultures of E8.5-E9.5 mutant yolk sacs display absence of all hematopoietic colony types.Absent vitelline blood vessels: at E8.75-E9.0, mutant yolk sacs show absence of major vitelline vessels.Absent blood islands: at E8.75-E9.0, mutant yolk sacs show absence of blood islands.Pale yolk sac: by E8.75-E9.0, mutant yolk sacs are significantly pale.Embryonic growth arrest: only a few mutant embryos develop beyond 18 somites (range 8-20).Embryonic growth retardation: homozygotes become increasingly retarded after E8.75.Distended pericardium: at E8.75-E9.0, mutant embryos exhibit dilated pericardial sacs but normal cardiac contraction.Skin edema: by E8.75-E9.0, mutant embryos are edematous.||C57BL/6|No|No|Yes|No|No|Yes|No|Unknown||||No|03-Aug-2007||0.0|0.0|Unknown||T cell leukaemia, yolk sac, GATA-1 , GATA1, progenitor, embryogenesis|Yes| 1737.0|VavP-BCL2-69|C57BL/6-Tg(Vav-BCL2)1Jad/Wehi||Dominant||||||||||||||||||||||||||transgene insertion 1, Jerry M Adams|mouse Vav promoter|High, haemopoietic cells|||||||||||Abnormal lymphocyte cell number:* the ratio of CD4 cells per B cell is 25% to 50% lower than in wild-type mice.Increased B cell number: 5-fold higher in the spleen at 18 weeksIncreased T cell number:* mice exhibit higher splenic T cell numbers than in wild-type and Tg(BCL2)22Wehi or Tg(BCL2)36Wehi mice.Increased CD4-positive T cell number:* the increase in CD4+ T cells is greater than the increase in CD8+ T cells.Increased CD8-positive T cell number:* the increase in CD4+ T cells is greater than the increase in CD8+ T cells.Abnormal class switch recombination:* the total number of B cells that undergo class switching is 50-fold higher than in wild-type mice.Abnormal somatic hypermutation frequency:* 22 of 23 clones isolated from class-switching cells harbor on average about 6 somatic mutations compared to in wild-type cells where no mutations are found.Enlarged spleen:Abnormal spleen germinal center morphology:* mice exhibit a larger pool of cycling B cells with a germinal center phenotype than in wild-type mice.* at 18 weeks, mice exhibit an increased in germinal center size and number compared to in wild-type mice.* however, expansion of germinal centers is dependent on CD4 T cell help.Increased spleen germinal center number: at 18 weeks.Increased spleen germinal center size: at 18 weeks.Enlarged lymph nodes.Glomerulonephritis:* at 40 weeks, 15% to 25% of mice develop autoimmune glomerulonephritis.Increased tumor incidence:* 12% of mice develop plasma cell tumorsLymphoma: less than 10% of mice develop lymphoblastic lymphomas.B cell derived lymphoma:* less than 10% of mice develop large cell B lymphomasFollicular lymphoma:* at 18 months, 37% to 50% of mice develop monoclonal follicular lymphoma.Thymic lymphoma: in less than 10% of miceHistiocytic sarcoma: in less than 10% of mice.|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|01-Aug-2007||0.0|0.0|Unknown||B cell, bcl-2, vav, Progenitor, lymphoma, germinal centre|Yes| 1748.0|SOCS1/IfNg Knockout|B6.129-Socs1 Ifng/Wehi||Recessive|suppressor of cytokine signaling 1|Socs1|Nil|Cish1, Cish7, JAB, JAK-binding protein, JAK2-binding protein, SOCS-1, SSI-1, STAT-induced STAT inhibitor 1|MGI:1354910|targeted mutation 1, Walter and Eliza Hall Institute of Medical Research|Socs1|MGI:1934607|16||||||||||||||||No|||||||||||||May show signs of Inflamatory diseases over 6 months of age. ||C57BL/6 x 129|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|02-Aug-2007||0.0|0.0|Unknown||inflammation, cytokine, signal transduction, T cell, phosphorylation|Yes| 1748.0|SOCS1/IfNg Knockout|B6.129-Socs1 Ifng/Wehi||Recessive|interferon gamma|Ifng|Nil|Ifg, IFN-gamma|MGI:107656|targeted mutation 1, Timothy Stewart|Ifng|MGI:1857184|10||||||||||||||||No|||||||||||||May show signs of Inflamatory diseases over 6 months of age. ||C57BL/6 x 129|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|02-Aug-2007||||Unknown||inflammation, cytokine, signal transduction, T cell, phosphorylation|Yes| 1754.0|Bmf Del/372|C57BL/6-Bmf/Wehi||Recessive|Bcl2 modifying factor|Bmf|Nil||MGI:2176433|BCL2 modifying factor; targeted mutation 1.1, Andreas Villunger|Bmf|MGI:3778610|2||||||||||||||||Yes|||||||||||||Abnormal spleen morphology.Enlarged spleen: significantly enlarged at 12 months.Spleen hyperplasia: increased by more than 50%.Abnormal immune system cell morphology.Abnormal B cell morphology: increased immature B cell number.Increased pre-B cell number: significantly elevated numbers in bone marrow while pro-B cell numbers are normal.Increased transitional stage B cell number:* both T1 and T2 transitional B cells are elevated* increased T1 transitional B cells in inguinal lymph nodesIncreased mature B cell number: * mature B cell numbers are elevated.* increased numbers in inguinal lymph nodes* increased numbers in peripheral bloodIncreased follicular B cell number: elevated while marginal B cell numbers are normal.Decreased B cell apoptosis: highly resistant to apoptosis caused by dexamethasone.Increased immunoglobulin level: total serum levels elevated at 8-10 weeks but not at 1 year of age.Decreased T cell apoptosis:* double positive T cells with increased resistance to the apoptotic effects of dexamethasone* thymocytes and double positive T cells resistant to the apoptotic effects of suberoylanilide hydroxamic acidTumorigenesis: no B cell neoplasia through 18 months of ageThymic lymphoma: increased susceptibility to gamma irradiation induced thymic lymphomas made up of double positive or CD8 single positive cells.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|02-Aug-2007||0.0|0.0|Unknown||Bcl-2, BH3 only, B cell, cell death, stress|Yes| 7378.0|Yellow|SJL-ASAM||Dominant|Unknown|Unknown|||||||Unknown|||||||||||||||||||||||||||||Yellow coat colour on a white coat colour background without other associated abnormalities.|Yellow coat colour on a white coat colour background without other associated abnormalities.|SJL/J|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|18-Jul-2013|Cryopreserved sperm|47.0|0.0|Unknown||Dermatology, Coat colour, yellow, ENU|Yes| 1766.0||GATA4 KO||Recessive|GATA binding protein 4|Gata4|Unknown|Gata-4|MGI:95664||||14||||||||||||||||No|||||||||||||Homozygotes for targeted null mutations exhibit defects in ventral morphogenesis, lack a primitive heart tube and foregut, develop partially outside the yolk sac, and die by midgestation.||C57BL/6|No|No|Yes|No|No|Yes|No|Unknown||||No|03-Aug-2007||0.0|0.0|Unknown||ventral morphogenesis, heart tube, midgestation, yolk sac|Yes| 8482.0|IL10 KO|B6.129-Il10/LudAnuApb||Recessive|interleukin 10|Il10||cytokine synthesis inhibitory factor, IL-10|MGI:96537|interleukin 10; targeted mutation 1, University of Cologne|Il10|MGI:1857199|1|||||||||||||||||||||||||||||Large intestinal inflammation: • mutants develop severe inflammation in the colon leading to inflammatory bowel disease Abnormal regulatory T cell physiology: • CD25-positive CD4 T cells from these mice fail to protect against the wasting disease induced by transferring nave CD4 T cells into immunodeficient hosts|Unknown|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|11-May-2018|Cryopreserved sperm|55.0|0.0|Unknown||il10, colitis, T cell|Possibly| 4925.0||B6;129-Gfpt2/Apb||Recessive|glutamine fructose-6-phosphate transaminase 2|Gfpt2|Unknown|GFAT2|MGI:1338883|glutamine fructose-6-phosphate transaminase 2; gene trap 352F9, Centre for Modeling Human Disease|Gfpt2|MGI:4965721|11||||||||||||||||No|||||||||||||Normal|Normal|C57BL/6 x 129|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|11-Nov-2009|Cryopreserved sperm|99.0|0.0|Unknown||glucosamine, hexosamine|Yes| 1764.0|EµMyc/Apaf-1 knockout|C57BL/6-Tg(IghMyc)22Bri Apaf/Wehi||Dominant|apoptotic peptidase activating factor 1|Apaf1|Unknown|6230400I06Rik, Apaf1l|MGI:1306796|gene trap XIX18, Peter Gruss|Apaf1|MGI:1857868|10||||||||||||||||No|transgene insertion 22, Ralph L Brinster|Igh (E mu) enhancer and Myc promoter|B cell lineage||||||||||Due to perinatal lethality, Emu-myc transgenic Apaf-1(-/-) or caspase-9(-/-) fetal liver cells were used to reconstitute lethally irradiated recipient mice. Surprisingly, no differences were seen in rate, incidence, or severity of lymphoma with loss of Apaf-1 or caspase-9, and Apaf-1 was not a critical determinant of anticancer drug sensitivity of c-myc-induced lymphomas. Moreover, loss of Apaf-1 did not promote oncogene-induced transformation of mouse embryo fibroblasts. Thus, Apaf-1 and caspase-9 do not suppress c-myc-induced lymphomagenesis and embryo fibroblast transformation.||C57BL/6|No|No|Yes|No|No|Yes|No|Unknown||||No|03-Aug-2007||0.0|0.0|Unknown||B cell, Lymphoma, Lymphocyte, Caspase, myc, apoptosome, cell death|Yes| 7736.0|P110-Tg|B6(Cg)-Gt(ROSA)26Sor/JAnuApb||Dominant|gene trap ROSA 26, Philippe Soriano|Gt(ROSA)26Sor||beta geo, Gtrgeo26, Gtrosa26, R26, ROSA26|MGI:104735|gene trap ROSA 26, Philippe Soriano; targeted mutation 7, Klaus Rajewsky|Gt(ROSA)26Sor|MGI:4430527|6|||||||||||||||||||||||||||||Unknown||C57BL/6NCrlAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|2|||No|07-Sep-2014|Cryopreserved sperm|10.0|0.0|Unknown||B cell|Yes| 6433.0|RIcre|B6.Cg-Tg(Ins2-cre)25Mgn/J||Dominant||||||||||||||||||||||||||transgene insertion 25, Mark A Magnuson|rat insulin promoter (Ins2)|||||||||||Abnormal insulin secretion:*Transgenic mice appear to show impaired glucose-stimulated insulin secretion compared to wild-type controls after receiving a glucose injection; this is observed on a mixed and on a 95% B6 backgrounds.*The first phase of insulin secretion by 4 minutes after intraperitoneal injection of glucose appears to be absent in transgenic mice.Abnormal circulating insulin level:*Following intraperitoneal injection of glucose (3g/kg body weight), insulin levels in fasted transgenic mice (on mixed B6) background do not increase until 30 minutes after injection, whereas control mice show an immediate spike (>2-3 fold higher levels 2 minutes after injection) with elevated insulin levels persisting for over 30 minutes.*On a 95% B6 background, 36 week-old mice show no increase in serum insulin levels for about 60 minutes following intraperitoneal injection of glucose.*Results indicated a loss of the first phase of insulin secretion by 4 minutes after intraperitoneal injection of glucose.Impaired glucose tolerance:*At 2 months, mice show impaired glucose tolerance after intraperitoneal injection of glucose (2g/kg body weight) relative to control C57BL/6 (B6) mice but no difference in fasting blood glucose levels are seen; blood glucose (mg/dl) remains higher than levels in injected controls during the full 2 hour post-injection period.*Glucose intolerance is more profound in females than males.*This is observed on a congenic (or 'pure') C57BL/6 background or on a mixed B6 background.*Similar findings are observed independently in other labs where transgenic mice are on mixed (undetermined B6 contribution) or primarily C57BL/6 (95% B6) backgrounds; blood glucose levels remain elevated relative to controls for at least 30-60 minutes after glucose injection in transgenic mice at 6 or 18 weeks of age on a highly (95%) B6 background.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown||Glucokinase, Diabetes, MODY-2|Yes| 1788.0|HRIpClg|B6.C-H2 Tg(Ins-CTLA4/IgFc)/Wehi||Dominant||||||||||||||||||||||||||Mouse CTLA4 was fused to the Fc of mouse IgG2c|rat insulin promoter|High and Low clones||||||||||No Phenotype, except continue to excrete rotovirus longer than usual. No diabetes developes. IMMUNOCOMPROMISED||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|03-Aug-2007||0.0|0.0|Unknown||graft survival, islet, CD4 T cell|Yes| 1767.0||CD3e chain knockout mice||Recessive|CD3 antigen, epsilon polypeptide|Cd3e|Unknown|CD3, CD3epsilon, T3e|MGI:88332||||9||||||||||||||||Yes|||||||||||||No Mature T cells. No CD4+ or CD8+ cells in thymus or spleen.Arrested T cell development at double negative stage.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|03-Aug-2007||0.0|0.0|Unknown||T cell, Lymphocyte, TCR, CD4 , CD8, differentiation|Yes| 1774.0|Bim Knockout clone 266 del|C57BL/6-Bcl2l11/Wehi||Recessive|BCL2-like 11 (apoptosis facilitator)|Bcl2l11|Nil|1500006F24Rik, Bim, Bod|MGI:1197519|BCL2-like 11 (apoptosis facilitator); targeted mutation 1.1, Andreas Strasser|Bcl2l11|MGI:2156498|2||||||||||||||||Yes|||||||||||||Increased numbers of lymphoid and myeloid cells. Spleen and lymph nodes are 2-3-fold bigger than in wt. Sternum is sticking out. Bim-/- females are bad mothers and should not be used for breeding unless necessary. Bim -/-: blood - increased lymphocytes (B + T cells), granulocytes & monocytes. - decreased platelets - Increased serum Ig. Thymus - fewer pre T cells. Age 1 year - lymphadenopathy - 55% -/-, 35% +/- mice sick with kidney disease or cardiac infarction/vasculitis. Fewer -/- females born. When born, often have poorly formed reproductive organs. -/- have protruding sternum. ||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|10|||No|03-Aug-2007||0.0|0.0|Unknown||T cell, B cell, Lymphoid, Myeloid, Sternum|Yes| 311.0|obese|C57BL/6-Lep||Recessive|leptin|Lep|Nil||MGI:104663|obese|Lep|MGI:1856424|6||||||||||||||||No|||||||||||||Homozygotes are obese, hyperphagic, have low activity, high metabolic efficiency, impaired thermogenesis, infertility and short lifespan. Strain background greatly affects severity and course of diabetes.|Heterozygotes survive fasting longer than control mice.|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|03-May-2006||0.0|0.0|Yes||obesity, glucose, adipose, fat|Yes| 1775.0|IL-7r|C57BL/6-Il7r/Wehi||Recessive|interleukin 7 receptor|Il7r|Unknown|CD127, IL-7 receptor alpha chain, IL-7Ralpha|MGI:96562|targeted mutation 1, Immunex|Il7r|MGI:1857198|15||||||||||||||||Yes|||||||||||||Decreased thymocyte number:* thymic cellularity is severely decreased* at all double negative stages, reduction in thymocytes is more severe than in Il7r homozygotes.Abnormal T cell differentiation:* thymic progenitor cell number is decreased by 20-fold compared to wild-type mice.* double negative cell development is blocked at stage IV* CD4+ and CD8+ T cell development is severely disrupted.Decreased double-positive T cell number: mice have less double positive thymocytes than Il7rtm1Abra homozygotes.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|12|||No|03-Aug-2007||0.0|0.0|Unknown||B cell, differentiation, hypoplasia|Yes| 1789.0|CD137 knockout|C57BL/6-Tnfrsf9||Recessive|tumor necrosis factor receptor superfamily, member 9|Tnfrsf9|Nil|4-1BB, A930040I11Rik, Cd137, CDw137, ILA, Ly63|MGI:1101059|targeted mutation 1, Byoung Kwon|Tnfrsf9|MGI:2664914|4||||||||||||||||Yes|||||||||||||Homozygous mutation of this gene results in enhanced T cell proliferation, decreased B cell IgG production, decreased cytotoxic T cell activity, and increased numbers of erythrocytes, granulocyte macrophages, and multipotential progenitor cells in the bone marrow, blood, and spleen.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|03-Aug-2007||0.0|0.0|Unknown||Progenitor cell, T cell, cytotoxic, hyperplasia, myelopoiesis|Yes| 1832.0|ICSBP / Blimp-1 knockout|Un-Prdm1 Irf8/Wehi||Recessive|PR domain containing 1, with ZNF domain|Prdm1|Unknown|Blimp-1, Blimp1, PRDI-BF1|MGI:99655|PR domain containing 1, with ZNF domain; targeted mutation 1, Stephen L Nutt|Prdm1|MGI:3510704|10||||||||||||||||Yes|Green fluorescent protein (GFP)||||||||||||Blimp-1 homozygous mice die late gestation - after fetal liver reconstitution are immunocompromised.ICSBP KO - Immune deficient leukaemia with age.|||No|No|Yes|No|No|Yes|No|Unknown||||No|08-Aug-2007||0.0|0.0|Unknown||B cell, T cell, transcription, DNA binding domain, differentiation|Yes| 1832.0|ICSBP / Blimp-1 knockout|Un-Prdm1 Irf8/Wehi||Recessive|interferon regulatory factor 8|Irf8|Unknown|ICSBP, Icsbp1, IRF-8, Myls|MGI:96395||||8|||||||||||||||||||||||||||||Blimp-1 homozygous mice die late gestation - after fetal liver reconstitution are immunocompromised.ICSBP KO - Immune deficient leukaemia with age.|||No|No|Yes|No|No|Yes|No|Unknown||||No|08-Aug-2007||||Unknown||B cell, T cell, transcription, DNA binding domain, differentiation|Yes| 1834.0|Pax5 knockout|C57BL/6-Pax5/Wehi||Recessive|paired box gene 5|Pax5|Nil|EBB-1, Pax-5|MGI:97489|paired box gene 5; targeted mutation 1, Meinrad Bussinger|Pax5|MGI:1926938|4||||||||||||||||Yes|||||||||||||Null mutants exhibit impaired development of the midbrain resulting in a reduced inferior colliculus and an altered cerebellar folial pattern, failure of B cell differentiation, runting, and high postnatal mortality with few survivors. Leg clasping phenotype when held up by the tail.||C57BL/6|Yes|No|Yes|Yes|No|Yes|No|Unknown||||No|08-Aug-2007||0.0|0.0|Unknown||NK cell (Natural Killer), T cell, progenitor, transcription factor|Yes| 1856.0||C57BL/6-Tg(CIITA)||Recessive||||||||||||||||||||||||||class II transactivator (CIITA)||||||||||||Normal||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|10-Aug-2007||0.0|0.0|No||MHC, H2, T cell|Yes| 4841.0|ENU12NIH:030a|C57BL/6JAnu-Kcnq1/AnuApb|C57BL/6JAnu-Kcnq1/AnuApb|Recessive|potassium voltage-gated channel, subfamily Q, member 1|Kcnq1|Unknown||MGI:108083|mutation 1, The Australian National University|Kcnq1|MGI:5490247|7|ENSMUSG00000009545|ENSMUST00000009689|Kcnq1-201|1303|1408|A to T|ENSMUSE00000426955|10|435|Lysine to STOP|||||ATAAGGATAATGGGATGAGTCCTGGAGAGAAGATGTTCAATGTTCCTCACATCACTTATGA|Yes|||||||||||||Continuous tremors and circling in both directions.Abnormal motor capabilities/coordination/movement:• under high stress, mice occasionally fall and circle around the cage in very fast movements unlike wild-type miceOpisthotonus: • some miceTremors: • constantlyJerky movement: • under mild stressHead tossing: • oftenCircling: • under high stress|None|C57BL/6JAnu|Yes|Unknown|Yes|Yes|Unknown|Yes|No|Unknown||7||No|24-Sep-2009|Cryopreserved sperm|34.0|0.0|Unknown||tremors, circling, ENU|Yes| 1822.0|RelA knockout Bcl-2 transgenic|C57BL/6-Rela Tg(Vav-BCL2)1Jad/Wehi||Recessive|v-rel reticuloendotheliosis viral oncogene homolog A (avian)|Rela|Nil|p65, p65 NF kappaB|MGI:103290|targeted mutation 1, David Baltimore|Rela|MGI:1857270|19||||||||||||||||Yes|transgene insertion 1, Jerry M Adams|hemopoiesis-specific vav promoter|||||||||||Strain may be partially immunocompromised, due to the P65 strain. P65 homozygous knockouts are embryonic lethal at day 15 gestation||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|06-Aug-2007||0.0|0.0|Unknown||Lymphocyte, T cell, B cell, transcription factor, NF-kappa B|Yes| 6662.0|BILLY|BALB/c-Tlr4/ANU/Ausb||Recessive|toll-like receptor 4|Tlr4|Nil|lipopolysaccharide response, Lps, Rasl2-8|MGI:96824|toll-like receptor 4; targeted mutation 1, Shizuo Akira|Tlr4|MGI:1860885|4|||||||||||||||||||||||||||||||BALB/c|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|02-Dec-2011||0.0|0.0|Unknown||Toll-like receptor 4 (TLR4), LPS response|Yes| 1820.0|Oct-2 knockout|C57BL/6-Oct2/Wehi||Recessive|POU domain, class 2, transcription factor 2|Pou2f2|Unknown|Oct-2, Oct2a, Oct2b, Otf-2, Otf2|MGI:101897|POU domain, class 2, transcription factor 2; targeted mutation 1, David Baltimore|Pou2f2|MGI:3028896|7||||||||||||||||Yes|||||||||||||Neonatal lethality: homozygous mice die shortly after birth.Decreased B cell number: in adult Rag-1 deficient mice in which the immune system has been reconstituted with fetal liver stem cells from mutants the proportion of B cells is significantly reduced.Arrested B cell differentiation: in adult Rag-1 deficient mice in which the immune system has been reconstituted with fetal liver stem cells from mutants peripheral B cells appear immature with high heat stable antigen levels.Decreased immunoglobulin level: in adult Rag-1 deficient mice in which the immune system has been reconstituted with fetal liver stem cells from mutants an 8 - 10 fold reduction in immunoglobulin concentrations is seen.|Decreased mature B cell number: levels reduced compared to wild-type control.Decreased IgG1 and IgM levels: cultured liver and spleen cells produce less antibody than wild-type cells but more than homozygous knockout cells.|C57BL/6|No|No|Yes|No|No|Yes|No|Unknown||||No|06-Aug-2007||0.0|0.0|Unknown||B cell, immunoglobulin, lymphocyte, POU domain, transcription factor|Yes| 1819.0|Col 2a1-cre transgenic|C57BL/6-Tg(Col2a1-cre)1Asz||Dominant||||||||||||||||||||||||||transgene insertion 1, Attila Aszodi|Cartilage specific Col2a1 gene promoter|||||||||||Normal||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|10+|||No|06-Aug-2007|Cryopreserved sperm|30.0|0.0|Unknown||Collagen, Cartilage, Cre recombinase|Yes| 7737.0|Ikk2ca-Tg|B6(Cg)-Gt(ROSA)26Sor/JAnuApb||Dominant|gene trap ROSA 26, Philippe Soriano|Gt(ROSA)26Sor||beta geo, Gtrgeo26, Gtrosa26, R26, ROSA26|MGI:104735|gene trap ROSA 26, Philippe Soriano; targeted mutation 4, Klaus Rajewsky|Gt(ROSA)26Sor|MGI:3687199|6|||||||||||||||||||||||||||||Unknown||C57BL/6NCrlAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|2|||No|07-Sep-2014|Cryopreserved sperm|10.0|0.0|Unknown||B cell|Yes| 1844.0|Matriptase knockout|NIH Black Swiss-St14/Wehi||Recessive|suppression of tumorigenicity 14 (colon carcinoma)|St14|Nil|Epithin, matriptase, MT-SP1, Prss14|MGI:1338881|targeted mutation 1, Thomas H Bugge|St14|MGI:2683707|9||||||||||||||||No|||||||||||||Homozygous inactivation of this locus results in pleiotropic defects affecting the development of the epidermis, hair follicles, and immune system. Mutant mice become dehydrated due to impaired epidermal barrier function and die within 48hrs of birth.||Black Swiss|No|No|Yes|No|No|Yes|No|Unknown||||No|10-Aug-2007||0.0|0.0|Unknown||Thymocyte, Hair follicle, wrinkled skin, dehydration, epidermal|Yes| 1862.0|B6.CD19Cre/PU.1|C57BL/6-Cd19 Sfpi1/Wehi||Recessive|SFFV proviral integration 1|Sfpi1|Unknown|Dis-1, PU.1, Sfpi-1, Spi-1, Tcfpu1, Tfpu.1|MGI:98282|SFFV proviral integration 1; targeted mutation 1.2, Stephen L Nutt|Sfpi1|MGI:3578011|2||||||||||||||||Yes|||||||||||||Mice develop B cells leukemia after > 1/2 year. Only in 15% of all mice, only in aged mice.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|10-Aug-2007||0.0|0.0|Unknown||B cell, lymphoma, transcription factor, development|Yes| 1862.0|B6.CD19Cre/PU.1|C57BL/6-Cd19 Sfpi1/Wehi||Recessive|CD19 antigen|Cd19|Nil||MGI:88319|CD19 antigen; targeted mutation 1, University of Cologne|Cd19|MGI:1931143|7|||||||||||||||||||||||||||||Mice develop B cells leukemia after > 1/2 year. Only in 15% of all mice, only in aged mice.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|10-Aug-2007||||Unknown||B cell, lymphoma, transcription factor, development|Yes| 3402.0|Tssc6 genetrap|B6.129-Tspan32/Wehi||Recessive|tetraspanin 32|Tspan32|Nil|Art-1, D7Wsu37e, Phemx, Tspan32, Tssc6|MGI:1350360|gene trap 1, Jacqueline M Tarrant|Tspan32|MGI:2183564|7||||||||||||||||Yes|||||||||||||Increased T cell proliferation: in vitro proliferative responses of T cells were increased upon concanavalin A, anti-CD3 antibody or anti-CD28 antibody stimulation.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|13-Jul-2008||0.0|0.0|Unknown||T cell, IL2, IL-2, proliferation, receptor|Yes| 9213.0|ASD1106:Bsn KO 83|C57Bl/6N-Bsn/Apb||Semi-dominant|bassoon|Bsn|||MGI:1277955||||9|||||||||||||||||||||||||||||unknown|unknown|C57BL6/NCrl|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|07-Jul-2021|Cryopreserved sperm|12.0|0.0|Unknown|||Possibly| 5836.0|Hugo||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 7016.0|ENU21:035:b:B6:G3|ANU:ENU21:035:b:G3||Recessive|Unknown||||||||Unknown||||||||||||||||Unknown|||||||||||||Unknown|Unknown|C57BL/6NCrlAnu|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||1||No|06-Jul-2012|Cryopreserved sperm|10.0|0.0|Unknown||ENU, random, mutagenesis, screen|Yes| 6448.0|ST5?|B6.129S6-Stat5a/Stat5b/Ausb?||Recessive|signal transducer and activator of transcription 5A|Stat5a|Nil|STAT5|MGI:103036|signal transducer and activator of transcription 5A; targeted mutation 2.1, Lothar Hennighausen|Stat5a/Stat5b|MGI:3055320|11|||||||||||||||||||||||||||||Partial perinatal lethality:*Most of the mice die perinatally.Premature death:*Approximately 1% of the mice reach weaning age, and die within the first 6 weeks after birth.Decreased body size:*Mice surviving to weaning age are smaller than their littermates. Decreased body weight: *Reduced body weight in survivor mice at the age of 4 weeks.Decreased total lung capacity:*Reduced lung capacity.Decreased B cell number:*No early and late pro-B cells in the bone marrow (22-fold and 40-fold reduction, respectively).*Reduced numbers of mature B cells in spleen and lymph nodes(6.4-fold and 2.2-fold, respectively).*Few mature B-lymphoid cells are present in the periphery.Decreased CD8-positive T cell number:*Reduction of CD8+ T cells (2.5-fold) in the thymus.*Reduction of CD8+ T cells (12-fold) in the lymph nodes.Absent gamma-delta T cells:*Absent CD4- CD8- gamma-delta TCR+ cells in the thymic cell suspension.Arrested B cell differentiation:*B-cell development is arrested at the pre-pro-B-cell stage in survivor mice and in fetal liver-derived cultures.*No pro-B, immature, and mature B cells in cultures derived from fetal livers.*No early and late pro-B cells in the bone marrow (22-fold and 40-fold reduction, respectively).*Reduced numbers of mature B cells in spleen and lymph nodes(6.4-fold and 2.2-fold, respectively).*Few mature B-lymphoid cells are present in the periphery.Small spleen:*Smaller spleen than that would be expected from the body size of the mice.Small thymus:*Smaller thymus than that would be expected from the body size and age of the mice.Small lymph nodes:*Smaller lymph nodes than that would be expected from the body size of the mice.Decreased tumor incidence:*No growth factor-independent colonies in cultured fetal livers and bone marrow cells transformed by Abelson oncogene or a murine stem-cell virus.*Abelson-transformed cells fail to induce leukemia in vivo.Anemia:*Severe anemia.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown||Signal transducer, Stat5|Yes| 6448.0|ST5?|B6.129S6-Stat5a/Stat5b/Ausb?||Recessive|signal transducer and activator of transcription 5B|Stat5b|Nil||MGI:103035|signal transducer and activator of transcription 5B; targeted mutation 2.1, Lothar Hennighausen |Stat5a/Stat5b|MGI:3055321|11|||||||||||||||||||||||||||||Partial perinatal lethality:*Most of the mice die perinatally.Premature death:*Approximately 1% of the mice reach weaning age, and die within the first 6 weeks after birth.Decreased body size:*Mice surviving to weaning age are smaller than their littermates. Decreased body weight: *Reduced body weight in survivor mice at the age of 4 weeks.Decreased total lung capacity:*Reduced lung capacity.Decreased B cell number:*No early and late pro-B cells in the bone marrow (22-fold and 40-fold reduction, respectively).*Reduced numbers of mature B cells in spleen and lymph nodes(6.4-fold and 2.2-fold, respectively).*Few mature B-lymphoid cells are present in the periphery.Decreased CD8-positive T cell number:*Reduction of CD8+ T cells (2.5-fold) in the thymus.*Reduction of CD8+ T cells (12-fold) in the lymph nodes.Absent gamma-delta T cells:*Absent CD4- CD8- gamma-delta TCR+ cells in the thymic cell suspension.Arrested B cell differentiation:*B-cell development is arrested at the pre-pro-B-cell stage in survivor mice and in fetal liver-derived cultures.*No pro-B, immature, and mature B cells in cultures derived from fetal livers.*No early and late pro-B cells in the bone marrow (22-fold and 40-fold reduction, respectively).*Reduced numbers of mature B cells in spleen and lymph nodes(6.4-fold and 2.2-fold, respectively).*Few mature B-lymphoid cells are present in the periphery.Small spleen:*Smaller spleen than that would be expected from the body size of the mice.Small thymus:*Smaller thymus than that would be expected from the body size and age of the mice.Small lymph nodes:*Smaller lymph nodes than that would be expected from the body size of the mice.Decreased tumor incidence:*No growth factor-independent colonies in cultured fetal livers and bone marrow cells transformed by Abelson oncogene or a murine stem-cell virus.*Abelson-transformed cells fail to induce leukemia in vivo.Anemia:*Severe anemia.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|13-Sep-2011||||Unknown||Signal transducer, Stat5|Yes| 8489.0|NOD.Nkrp1b.Art2b|NOD-Klrb1b Art2b/BaxApb||Recessive|ADP-ribosyltransferase 2b|Art2b||ART2.2, Rt6, Rt-6, Rt6-2|MGI:107545|ADP-ribosyltransferase 2b; targeted mutation 1, Friedrich Koch-Nolte|Art2b|MGI:2388827|7||||||||||||||||||||killer cell lectin-like receptor subfamily B member 1B|Klrb1b||Klrb1d, Ly55b, Ly55d, Nkrp1-b, NKR-P1B, Nkrp1d, NKR-P1D|MGI:107539||||6|Mice that are homozygous for this allele are viable, fertile, normal in size.||NOD/Lt|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|10|||No|31-May-2018|Cryopreserved sperm|50.0|0.0|Unknown||Nk1.1, TCR, NK cell|Yes| 1836.0||B6.CBA-Tg(CAG-cre/Esr1)5Amc||Recessive||||||||||||||||||||||||||transgene insertion 5, Andrew P McMahon|chicken beta actin promoter/enhancer coupled with the cytomegalovirus (CMV) immediate-early enhancer|tamoxifen inducible||||||||||Embryonic lethal|Normal|C57BL/6 x CBA|No|No|Yes|No|No|Yes|No|Unknown||||No|08-Aug-2007||0.0|0.0|Unknown||inducible, tamoxifen, estrogen receptor, temporal, Cre recombinase|Yes| 10323.0|Rpl41 (7) 34 bp insertion|C57BL/6NCrl-Rpl41/AnuApb||Semi-dominant|ribosomal protein L41|Rpl41|||MGI:1915195||||10|||||||||||||||||||||||||||||Unknown|Unknown|C57Bl/6N|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Good||||No|12-Apr-2023|Cryopreserved sperm|22.0|0.0|Unknown|||Possibly| 9226.0|ASD917::Kofta|C57Bl/6N-Zic2/Apb||Semi-dominant|zinc finger protein of the cerebellum 2|Zic2|||MGI:106679|Kofta|||14|||||||||||||||||||||||||||||The homozygous state is embryonic lethal, with embryos non-viable at approximately 13 dpc. Prior to this, HPE phenotypes and cardiac defects are observed. |Heterozygous animals are viable and present with belly spots and curly tails (incompletely penetrant). In addition to this, males are aggressive. |C57BL.6N|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|15-Jul-2021|Cryopreserved sperm|60.0|0.0|Unknown|||Possibly| 2800.0|BPLT1|C57BL/6-C1galt1/Wehi||Recessive|core 1 synthase, glycoprotein-N-acetylgalactosamine 3-beta-galactosyltransferase, 1|C1galt1|Unknown|core 1 beta3-Gal-T, T-synthase|MGI:2151071|ptl1|C1galt1|MGI:3693890|6||||||||||||||||Yes|||||||||||||Premature death: by 10 weeks of age, mice become ill; 90% are moribund by 200 days.Decreased body weight: young adults (males - 15.4 grams, females - 14.4 grams) are smaller than controls (males - 24 grams, females - 18 grams).Increased blood urea nitrogen level: serum has excessive levels of urea compared to controls (169 mmol/l vs 9 mmol/l).Increased circulating creatinine level: serum has excessive levels of creatinine compared to controls( 200 mol/l vs 47 mmol/l).Proteinuria.Albuminuria: mice have high levels of albumin in urine from early ages.Kidney inflammation: kidneys show inflammatory infiltration.Glomerulonephritis: affected foci show infiltrating inflammatory cells.Abnormal renal glomerular capsule: structure is 2-4 cell layers thick compared to 1 layer in wild-type.Abnormal renal glomerulus morphology: kidneys display lesions affecting clusters of glomeruli and their proximal tubules.Cortical renal glomerulopathies: kidneys display cortical atrophy.Decreased renal glomerulus number: kidneys show glomerular loss.Abnormal proximal convoluted tubule morphology:* kidneys display lesions affecting clusters of glomeruli and their proximal tubules.* these show fatty degeneration and contain protein casts.Abnormal thrombopoiesis: generation of platelets in mutants is slower than in wild-type.Increased mean platelet volume: volume is 10.0 fl for mutant platelets compared to 8.4 fl for wild-type.Decreased platelet cell number: homozygotes have platelet counts only 40% of those in wild-type.||C57BL/6|Yes|No|Yes|Yes|No|Yes|No|Unknown||||No|22-Feb-2008||0.0|0.0|Unknown||ENU, Platelet, thrombocytopenia, mucin, kidney|Yes| 3403.0|NP2 KO|B6.129-Nrp2|MGI:3712239|1||||||||||||||||No|||||||||||||Overall body size is reduced compared to wild-type. Increased perinatal lethality is observed compared to wild-type.||129 x C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|13-Jul-2008||0.0|0.0|Unknown||neuronal, neural crest, gut|Yes| 3415.0|RIP-OVA|C57BL/6-Tg(Ins2-OVA)307Wehi/Wehi||Dominant|||Unknown||||||Unknown||||||||||||||||No|transgene insertion 307, Walter and Eliza Hall Institute of Medical Research|rat insulin 2|low||||||||||This transgene expresses a secreted form of ovalbumin from the full-length chicken ovalbumin cDNA under control of the rat insulin 2 promoter.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|14-Jul-2008||0.0|0.0|Unknown||ovalbumin, T cell, autoimmunity, CD8|Yes| 3412.0|Conditional SOCS3 knockout|C57BL/6-Socs3/Wehi||Recessive|suppressor of cytokine signaling 3|Socs3|Normal|CIS3, Cish3, cytokine-inducible SH2 protein 3, E2a-Pbx1 target gene in fibroblasts 10, EF-10, SOCS-3, SSI-3, STAT-induced STAT inhibitor 3|MGI:1201791|suppressor of cytokine signaling 3; targeted mutation 2, Warren S Alexander|Socs3|MGI:2663917|11||||||||||||||||No|||||||||||||Normal||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|14-Jul-2008||0.0|0.0|Unknown||flox, conditional, Cre, signal transduction|Yes| 3445.0|TCR transgenic - HNT|BALB/c-Tg(Tcra,Tcrb)1Mcd/Wehi||Recessive||||||||||||||||||||||||||transgene insertion 1, Hugh O McDevitt||||||||||||HNT-TCR mice express an I-A-restricted TCR specific for the HA peptide 126–138 (HNTngvtaacshe). TCR transgenics immunocompromised by having mono-specific TCR however in a clean environment mice do not show a phenotype different to B6.||BALB/c|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|17-Jul-2008||0.0|0.0|Unknown||T cell, receptor (TCR), selection, tolerance, haemaglutanin|Yes| 3468.0|Socs6 KO|C57BL/6-Socs6/Wehi||Recessive|suppressor of cytokine signaling 6|Socs6|Nil|1500012M23Rik, 5830401B18Rik, CIS4, Cish4, HSPC060, SOCS-4, SOCS-6, Socs4, SSI4, STAI4, STAT4, STATI4|MGI:1924885|targeted mutation 1, Danielle L Krebs|Socs6|MGI:2429394|18||||||||||||||||Yes|||||||||||||Mice homozygous for a targeted null mutation exhibit reduced body weight, but normal hematopoiesis and glucose homeostasis.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|22-Jul-2008||0.0|0.0|Unknown||Sh2 domain, signal transduction, E3 ubiquitin ligase, weight, growth retardation|Yes| 6835.0|Tie2cre|B6.Cg-Tg(Tek-cre)1Ywa/WEHIAusb||Dominant||||||||||||||||||||||||||transgene insertion 1, Masashi Yanagisawa |mouse Tek promoter |This promoter is active in endothelial cells||||||||||None|None|C67BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|02-Mar-2012||0.0|0.0|Unknown||Cre-lox System, endothelial cells , embryogenesis|Yes| 6666.0|T286|C57BL6-Camk2a/Ausb||Dominant|calcium/calmodulin-dependent protein kinase II alpha|Camk2a|Normal|alpha-CaMKII, CaMKII, mKIAA0968|MGI:88256|calcium/calmodulin-dependent protein kinase II alpha; targeted mutation 2, Alcino Silva|Camk2a|MGI:2158733|18|||||||||||||||||||||||||||||||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|02-Dec-2011||0.0|0.0|Unknown||Calcium-calmodulin-dependent kinase II (CaMKII), Autophosphorylation|Yes| 2329.0|Shewag|C57BL/6-Gzma Gzmb Prf1 Tg(TcraTcrb)1100Mjb/AnuApb||Recessive|granzyme A|Gzma|Nil|BLT esterase, Ctla-3, Ctla3, H factor, Hanukah factor, Hf, SE1, serine esterase 1, TSP-1, TSP1|MGI:109266|targeted mutation 1, Markus M Simon|Gzma|MGI:2449926|13||||||||||||||||Yes|transgene insertion 1100, Michael J Bevan|H-2Kb promoter|||||||||||||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|04-Dec-2007|Cryopreserved sperm|106.0|0.0|No||T cell, Natural Killer Cell, cytotoxicity, receptor, ovalbumin|Yes| 2329.0|Shewag|C57BL/6-Gzma Gzmb Prf1 Tg(TcraTcrb)1100Mjb/AnuApb||Recessive|granzyme B|Gzmb|Unknown|CCP-1/C11, CCP1, Ctla-1, Ctla1|MGI:109267|targeted mutation 1, Timothy J Ley|Gzmb|MGI:1857156|14|||||||||||||||||||||||||||||||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|04-Dec-2007|Cryopreserved sperm|||No||T cell, Natural Killer Cell, cytotoxicity, receptor, ovalbumin|Yes| 2329.0|Shewag|C57BL/6-Gzma Gzmb Prf1 Tg(TcraTcrb)1100Mjb/AnuApb||Recessive|perforin 1 (pore forming protein)|Prf1|Nil|perforin, Pfp, Prf-1|MGI:97551|targeted mutation 1, Sandoz Pharmaceutical|Prf1|MGI:1857235|10|||||||||||||||||||||||||||||||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|04-Dec-2007|Cryopreserved sperm|||No||T cell, Natural Killer Cell, cytotoxicity, receptor, ovalbumin|Yes| 3417.0|OT-II / CD154 KO|C57BL/6-Tg(TcraTcrb)425Cbn Cd40lg/Wehi||Recessive|CD40 ligand|Cd40lg|Nil|CD154, Cd40L, gp39, HIGM1, IMD3, Ly-62, T-BAM, Tnfsf5|MGI:88337|CD40 ligand; targeted mutation 1, Richard A Flavell|Cd40lg|MGI:2182733|X||||||||||||||||Yes|transgene insertion 425, Frank Carbone||||||||||||Transgenic mice express the mouse alpha-chain and beta-chain T-cell receptor that pairs with the CD4 coreceptor and is specific for chicken ovalbumin 323-339 in the context of I-A b. TCR transgenics are immunocompromised by having a mono-specific T cell receptor however, in a clean envirnoment, mice show no difference in phenoptype from wild-type B6 mice. ||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|8|||No|14-Jul-2008||0.0|0.0|Unknown||T cell, receptor (TCR), ovalbumin, autoimmunity, CD4|Yes| 5649.0|C57 x Mafia ||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 3598.0|B6.129-Tg(FoxP3-GFP)|B6.129-Foxp3/AnuApb||Dominant|forkhead box P3|Foxp3|Normal|JM2, scurfin|MGI:1891436|targeted mutation 2, Alexander Y Rudensky|Foxp3|MGI:3574964|X||||||||||||||||No|||||||||||||Normal. Cells expressing FoxP3 fluoresce green, predominantly T cells||129 x C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|06-Aug-2008|Cryopreserved sperm|176.0|0.0|Unknown||T cell, IL-2, GFP, transcription factor|Yes| 3427.0|GK5 transgenic|C57BL/6-Tg(TcraCD4,TcrbCD4)||Dominant||||||||||||||||||||||||||Chimeric anti-mouse CD4 antibody|human cytomegalovirus immediate-early promoter|||||||||||No peripheral CD4 cells||C57BL/6-H2-K|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|15-Jul-2008||0.0|0.0|Unknown||T cell, selection, CD4, allograft rejection|Yes| 3428.0|Socs5 KO|C57BL/6-Socs5/Wehi||Recessive|suppressor of cytokine signaling 5|Socs5|Nil|1810018L08Rik, Cish5, SOCS-5|MGI:2385459|suppressor of cytokine signaling 5; targeted mutation 1, Warren S Alexander|Socs5|MGI:3050577|17||||||||||||||||Yes|||||||||||||Homozygous null mutants are viable and fertile with normal immune system morphology and function.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|15-Jul-2008||0.0|0.0|Unknown||signal transduction, cytokine, stat, T cell, Lymphocyte|Yes| 3422.0|Ot-1 / SOCS1 KO / Rag1 KO|B6.129-Rag1 Socs1 Tg(TcraTcrb)1100Mjb/Wehi||Recessive|suppressor of cytokine signaling 1|socs1|Nil|cish1, Cish7, JAB, JAK-binding protein, JAK2-binding protein, SOCS-1, SSI-1, STAT-induced STAT inhibitor 1|MGI:1354910|targeted mutation 1, Walter and Eliza Hall|Socs1|MGI:1934607|16||||||||||||||||Yes|transgene insertion 1100, Michael J Bevan|H-2Kb promoter|||||||||||These mice are moribund form 4-10 weeks of age as a result of generalised lymphocytic infiltrates of various tissues including heart, eye and muscle.OT strain carries a transgenic T cell receptor that recognizes ovalbumin residues 257-264 (SIINFEKL) in the context of H2Kb||129/1SVJ x C57BL/6|Yes|No|Yes|Yes|No|Yes|No|Unknown||||No|15-Jul-2008||0.0|0.0|Unknown||T cell, Autoimmunity, CD8, ovalbumin, receptor (TCR)|Yes| 3422.0|Ot-1 / SOCS1 KO / Rag1 KO|B6.129-Rag1 Socs1 Tg(TcraTcrb)1100Mjb/Wehi||Recessive|recombination activating gene 1|Rag1|Unknown|Rag-1|MGI:97848|targeted mutation 1, David Baltimore|Rag1|MGI:2448994|2|||||||||||||||||||||||||||||These mice are moribund form 4-10 weeks of age as a result of generalised lymphocytic infiltrates of various tissues including heart, eye and muscle.OT strain carries a transgenic T cell receptor that recognizes ovalbumin residues 257-264 (SIINFEKL) in the context of H2Kb||129/1SVJ x C57BL/6|Yes|No|Yes|Yes|No|Yes|No|Unknown||||No|15-Jul-2008||||Unknown||T cell, Autoimmunity, CD8, ovalbumin, receptor (TCR)|Yes| 6463.0|G4?|B6.Cg-Slc2a4/Ausb?||Recessive|solute carrier family 2 (facilitated glucose transporter), member 4|Slc2a4|Nil|Glut-4, Glut4|MGI:95758|solute carrier family 2 (facilitated glucose transporter), member 4; targeted mutation 1, Maureen J Charron|Slc2a4|MGI:2149725|11|||||||||||||||||||||||||||||Abnormal glucose homeostasis:*Mutant adipocytes, cardiac and skeletal muscles show abnormal subcellular distribution and impaired insulin-stimulated translocation of leucyl/cystinyl aminopeptidase (LNPEP; an insulin-regulated membrane aminopeptidase sharing the same trafficking route with SLC2A4) from an intracellular compartment to the plasma membrane.*As a result, LNPEP is redistributed to the plasma membrane under basal conditions and no translocation of the enzyme is observed in response to insulin.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown||GLUT4|Yes| 3436.0|relB KO (Line 272)|C57BL/6-Relb/Wehi||Recessive|avian reticuloendotheliosis viral (v-rel) oncogene related B|Relb|Nil||MGI:103289|avian reticuloendotheliosis viral (v-rel) oncogene related B; transgene insertion 106, Ralph L Brinster|Relb|MGI:2179544|7||||||||||||||||Yes|||||||||||||Homozygotes for targeted and insertional null mutations exhibit inflammatory cell infiltration of organs, myeloid hyperplasia, splenomegaly, reduction in thymic dendritic cells, impaired cellular immunity, hyperkeratosis, and epidermal hyperplasia. Runted, swollen abdomens. Scaly feet, ears and tails. Tight skin, hard to scruff.||C57BL/6|Yes|No|Yes|Yes|No|Yes|No|Unknown||||No|16-Jul-2008||0.0|0.0|Unknown||T cell, B cell, inflammation, macrophage, antigen presentation|Yes| 3470.0|Taube nuss Genetrap|129-Taf8/Wehi||Recessive|TAF8 RNA polymerase II, TATA box binding protein (TBP)-associated factorq|Taf8|Nil|Taf8, Tbn|MGI:1926879|gene trap 9, Peter Gruss|Taf8|MGI:3033758|17||||||||||||||||Yes|||||||||||||Embryos homozygous for a gene trap mutation die at E4.0 and exhibit apoptosis of inner mass cells.|Normal|129/SvPas|No|No|Yes|No|No|Yes|No|Unknown||||No|22-Jul-2008||0.0|0.0|Unknown||inner cell mass, embryonic lethal, trophoblast|Yes| 8484.0|IL-4 -/-|B6(Cg).129-Il4/AnuApb||Recessive|interleukin 4|Il4|Unknown|Il-4|MGI:96556|interleukin 4; targeted mutation 1, Manfred Kopf|Il4|MGI:2176268|11|||||||||||||||||||||||||||||Decreased IgE level: unlike in wild-type mice, IgE levels are undetectable prior to and following immunization.Decreased IgG1 level:* IgG1 levels are reduced 20-fold compared to in wild-type mice and following immunization IgG1 levels are 12-fold lower than in immunized wild-type mice.* following immunization with DNP-ovalbumin, IgG1 antibodies are 10-fold lower than in wild-type mice.Increased IgG level:* following infection with N. brasiliensis, IgG2 and IgG3 levels are slightly higher than in wild-type mice.* following immunization with DNP-ovalbumin, IgG2 and IgG3 levels are 100- to 500-fold higher than in wild-type mice.Decreased interleukin-10 secretion: stimulated CD4+ T cells in vitro fail to produce IL-10.Decreased interleukin-3 secretion: in stimulated CD4+ T cells, the production of IL-3 is reduced more than 70% of wild-type value.Decreased interleukin-4 secretion: stimulated CD4+ T cells in vitro fail to produce IL-4.Decreased interleukin-5 secretion: stimulated CD4+ T cells in vitro fail to produce IL-5.Abnormal response to infection: * following infection with N. brasiliensis, CD4+ T cells produce reduced levels of Th2 cytokines, increased levels of interferon-gamma, and reduced blood eosinophilia levels compared to infected wild-type mice.* however, CD8+ T cells do produce IL-5 following infection with N. brasiliensis.||C57BL/6NCrlAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|5|||No|18-May-2018|Cryopreserved sperm|48.0|0.0|Unknown||T cell, infection, asthma, hyperresponsiveness, eosinophil, IFN, IL2|Yes| 5355.0|B6.303|C57BL/6-Tg(HLA DR3-DQ2)303/Apb||Dominant||||||||||||||||||||||||||human leukocyte antigen class II||||||||||||Expression of HLA DR and DQ evident on B cells, dendritic cells and a proportion of macrophages.Evaluation of HLA DR3-DQ2 haplotype-transgenic mice indicates regulated HLA gene expression, T cell selection and functional antigen presentation mediated by the DR and DQ genes encoded within the YAC transgene.Histological examination of tissues in transgenic mice including pancreatic B-islets did not reveal any evidence of spontaneous pathology.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|1|4||No|20-Dec-2010|Cryopreserved sperm|40.0|0.0|Unknown||MHC, B cell, selection, autoimmunity|Yes| 5840.0|Hugo/ChatCreERT2||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 9163.0|GABRB3E77K|C57Bl/6J-Gabrb3/Apb||Semi-dominant|gamma-aminobutyric acid (GABA) A receptor, subunit beta 3|Gabrb3|||MGI:95621||||7|||||||||||||||||||||||||||||Unknown|Seizure phenotype|C57Bl/6J|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|25-Mar-2021|Cryopreserved sperm|28.0|0.0|Unknown|||Possibly| 7745.0|ENU23:017:Pyhin1:G6:G3|C57BL/6NCrlAnu-Pyhin1/AnuApb||Recessive|pyrin and HIN domain family, member 1|Pyhin1|Unknown|Ifi209, Ifix|MGI:2138243|Pyhin1; mutation 1, the Australian National University|Pyhin1||1||||||||||Unknown to Unknown|||||||||||||||||||Embryonic Lethal|Unknown|C57BL/6NCrlAnu x 129|No|No|Yes|No|No|Yes|No|Good||||No|23-Sep-2014|Cryopreserved sperm|11.0|0.0|Unknown||ENU|Possibly| 3480.0|Bm1.RIP-CD5LIg|C57BL/6-Tg(ins2-CD5lIg)/Wehi||Dominant||||||||||||||||||||||||||CD5 leader sequence (control=CD5LIg) fused to the Fc of mouse IgG2c|Rat insulin 2|||||||||||Normal||C57BL/6-H2-K|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|23-Jul-2008||0.0|0.0|Unknown||graft survival, islet, CD4 T cell, transplantation|Yes| 3486.0|MMTVneu|FVB-Tg(MMTVneu)/Wehi||Dominant||||||||||||||||||||||||||transgene insertion 202, William Muller|MMTV (mouse mammary tumor virus)|||||||||||These mice develop tumours at approximately 6 - 8 months. Mammary adenocarcinoma.Metastatic potential.||FVB|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|23-Jul-2008||0.0|0.0|Yes||Her2, breast cancer, signal transduction, c-erbB2, tyrosine kinase, adenocarcinoma|Yes| 8485.0|Gpr37l1 KO B6|B6(Cg).129S1-Gpr37l1/Apb||Recessive|G protein-coupled receptor 37-like 1|Gpr37l1||CAG-18, D0Kist8|MGI:1928503||||1|||||||||||||||||||||||||||||Reported elevated blood pressure|unknown|C57BL/6J|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|10|||No|23-May-2018|Cryopreserved sperm|39.0|0.0|Unknown|||Yes| 5258.0|DMP1.gp130fl/fl|C57BL/6-Il6st Tg(Dmp1-cre)1Jqfe||Recessive|interleukin 6 signal transducer|Il6st|Normal|CD130, gp130|MGI:96560|interleukin 6 signal transducer; targeted mutation 1, Werner Mueller|Il6st|MGI:1931239|13||||||||||||||||Yes|transgene insertion 1, Jian Q Feng|dentin matrix protein 1 (Dmp1)|Cre expression restricted to dontoblasts and osteocytes||||||||||Unknown|Unknown|C57BL/6|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|21-Oct-2010|Cryopreserved sperm|20.0|0.0|Unknown||osteocytes, signal transduction, dentin, Odontoblasts|Possibly| 5256.0|OsMR KO|C57BL/6-Osmr||Recessive|oncostatin M receptor|Osmr|Nil|OSMRB|MGI:1330819|oncostatin M receptor; targeted mutation 1, Minoru Tanaka|Osmr|MGI:2680723|15||||||||||||||||No|||||||||||||Hematopoietic system phenotype: * homozygotes display normal kinetics of erythrocyte recovery after acute hemolysis induced by phenylhydrazine, as determined by measuring peripheral red cells, reticulocytes, and CFU-Es in bone marrow (BM) and spleen. * in addition, homozygotes show normal kinetics of recovery of BM progenitors after 5-fluorouracil-induced myelosuppression.Abnormal hematopoiesis: homozygotes exhibit impaired hematopoiesis in the bone marrow, and increased hematopoiesis in the spleen.Abnormal common myeloid progenitor cell morphology:* in clonal culture assays, homozygotes show a significant reduction in the number of CFU-GEMMs, CFU-MEs, and BFU-Es in the bone marrow (BM) relative to wild-type mice. * in contrast to the BM, the number of CFU-GEMMs, CFU-MEs, and BFU-Es in mutant spleen is elevated relative to that observed in wild-type mice. * whereas no significant differences are observed in the number of granulocyte-macrophage colony-forming cells (GM-CFCs), including granulocyte CFUs (CFU-Gs), macrophage CFUs (CFU-Ms), and granulocyte-macrophage CFUs (CFU-GMs) in the mutant BM, the numbers of all types of GM-CFCs in mutant spleen are elevated relative to wild-type mice, indicating an opposite effect on hematopoiesis in BM and spleen. * in BM transplantation experiments, neonatal homozygotes engrafted with wild-type BM cells fail to produce erythrocytic and megakaryocytic progenitors to the levels observed in wild-type mice, indicating an effect on the hematopoietic microenvironment. * conversely, wild-type mice reconstituted with homozygous mutant BM cells exhibit a reduction in erythrocytic and megakaryocytic progenitors in the BM, whereas the GM-CFC number remains unchanged. * interestingly, hematopoietic progenitors in spleen are increased in homozygotes engrafted with either wild-type or homozygoys mutant BM cells, whereas they are not increased in wild-type mice that receive either wild-type or mutant BM cells.Abnormal erythroid progenitor cell morphology: * in clonal culture assays, homozygotes show a significant reduction in the number of CFU-Es in the BM relative to wild-type mice. * in contrast to the BM, the number of CFU-Es in mutant spleen is significantly increased relative to that observed in wild-type mice.Decreased erythrocyte cell number: * homozygotes show a significant reduction in the mean number of peripheral erythrocytes relative to wild-type mice (894 ± 64 x 104/mL vs 1028 ± 52 x 104/mL, respectively). * in contrast, the mean number of peripheral white blood cells remains relatively unaffected.Decreased hematocrit: homozygotes display a reduced hematocrit relative to wild-type mice.Anemia: homozygotes are slightly anemic relative to wild-type mice.Decreased platelet cell number: homozygotes show a significant reduction in the mean number of peripheral platelets relative to wild-type mice (82 ± 10 x 104/mL vs 106 ± 15 x 104/mL, respectively).Abnormal megakaryocyte progenitor cell morphology: homozygotes show a significant reduction in the number of megakaryocyte progenitors, as determined in liquid cultures of BM cells.Decreased megakaryocyte cell number: homozygotes show a significant reduction in the number of mature megakaryocytes in the BM relative to wild-type mice, as measured in H&E stained femoral sections.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|21-Oct-2010||0.0|0.0|Unknown||OSM, osteoporosis, osteoblasts, cytokine, progenitor stem cell, bone marrow, megakaryocyte, erythrocyte|Possibly| 7017.0|ENU21:036:a:B6:G3|ANU:ENU21:036:a:G3||Recessive|Unknown||||||||Unknown||||||||||||||||Unknown|||||||||||||Unknown|Unknown|C57BL/6NCrlAnu|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||1||No|06-Jul-2012|Cryopreserved sperm|38.0|0.0|Unknown||ENU, random, mutagenesis, screen|Yes| 2762.0|BALB/c.Flii 1.4A|BALB/c-Flii/2AnuApb|BALB/c-Flii/2AnuApb|Recessive|flightless I homolog (Drosophila)|Flii|Nil|Fli1, Fliih|MGI:1342286|targeted mutation 1, Hugh D Campbell|Flii|MGI:2179825|11||||||||||||||||Yes|||||||||||||Embryonic lethality at implantation: no embryos are recovered after E5.5; embryos develop normally until cellularization, the development arrests before completion of gastrulation blastocysts initiate uterine implantation but embryos fail to develop. embryonic growth arrest: development arrests during gastrulation|Enhanced wound healing: 3 days after a 1 cm full-thickness incision was made in the dorsal skin, surface wound area measurements show smaller, more contracted wounds than in wild-type mice. Length of neoepidermis is significantly greater in mutant animals, and percentage or re-epithelialization of wounds is greater at 5 days after wounding. By day 7, healing is comparable in mutants and wild-type|BALB/c|No|No|Yes|No|No|Yes|No|Poor|10|11|Het male x WT female|No|14-Feb-2008|Cryopreserved sperm|150.0|0.0|Unknown||gelsolin, embryonic lethal, wound repair, gastrulation, cell migration|Yes| 5438.0|Rap1b KO|B6.129-Rap1b/Apb||Semi-dominant|RAS related protein 1b|Rap1b|||MGI:894315||||10|||||||||||||||||||||||||||||Perinatal lethality: about 55% of homozygous embryos die perinatally.Embryonic lethality during organogenesis: * in heterozygous crosses only 4.4% of pups at weaning are homozygous. * 40% of homozygous embryos begin to die around E13.5.Hemorrhage: 40% of homozygous embryos had abdominal, cranial, and hepatic bleeding.Decreased body size: surviving homozygotes are smaller than their littermates.Decreased platelet aggregation: platelet aggregation in response to collagen, convulxin (snake venom), an F2RL3 activating peptide, or a calcium ionophore (A23187) is reducedhowever, similar to wild-type, P2RY1 and P2RY12 antagonists can block aggregation.Decreased litter size: crosses between surviving homozygotes produce 45% smaller litters at weaning; however more homozygous pups survive compared to heterozygous crosses.Increased bleeding time.Thrombosis: homozygotes begin to form thrombi in a platelet-dependent carotid artery thrombosis model however vessel occlusion is not seen.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|7|||No|16-Feb-2011|Cryopreserved sperm|50.0|0.0|Unknown||platelet, aggregation, thrombosis|Yes| 7548.0|APN 388|C57BL/6N-A Gprc6a/MarpApb||Recessive| G protein-coupled receptor, family C, group 6, member A|Gprc6a |||MGI:2429498 |G protein-coupled receptor, family C, group 6, member A; targeted mutation 1a, Wellcome Trust Sanger Institute|Gprc6atm1a(EUCOMM)Wtsi|MGI:4461735|10|||||||||||||||||||||||||||||Unknown|Normal|C57Bl/6N|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|19-Dec-2013|Cryopreserved sperm|46.0|0.0|Unknown|||Possibly| 6837.0|Gpc1 knockout|B6;CD-1-Gpc1/Apb||Dominant|glypican 1|Gpc1|Nil||MGI:1194891|glypican 1; targeted mutation 1.1, Arthur Lander|Gpc1|MGI:3774029|1|||||||||||||||||||||||||||||Lifespan, fertility and health are normal. Occasional malocclusions. Brain may be slightly smaller than normal.|Unknown|C57BL/6 x CD-1|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|06-Mar-2012|Cryopreserved sperm|50.0|0.0|Unknown||growth plate, angiogenesis, heparan sulfate proteoglycans, fibroblast growth factor (FGF) signaling, glypican family|Possibly| 5846.0|Ifng||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5847.0|IFNg-/-||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5848.0|IFNGR||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 7018.0|ENU21:037:b:B6:G3|ANU:ENU21:037:b:G3||Recessive|Unknown||||||||Unknown||||||||||||||||Unknown|||||||||||||Unknown|Unknown|C57BL/6NCrlAnu|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||1||No|06-Jul-2012|Cryopreserved sperm|40.0|0.0|Unknown||ENU, random, mutagenesis, screen|Yes| 5263.0|RARgamma|C57BL/6-Rarg/StvApb||Recessive|retinoic acid receptor, gamma|Rarg|Nil|MGC:11555, MGC:18523, RAR gamma 2, RARgamma2|MGI:97858|retinoic acid receptor, gamma; targeted mutation 1, Pierre Chambon|Rarg|MGI:1931079|15||||||||||||||||No|||||||||||||Homozygotes for targeted null mutations exhibit stunted growth, homeotic transformations of the rostral axial skeleton and tracheal cartilage, Harderian gland agenesis, high postnatal mortality, and male sterility.||C57BL/6|Yes|Unknown|Yes|Yes|Unknown|Yes|No|Unknown||||No|21-Oct-2010|Cryopreserved sperm|63.0|0.0|Unknown||bone marrow, progenitor, Myeloproliferative syndromes, Harderian gland agenesis, skeleton|Yes| 3526.0||NOD.B6 Idd9/11||Recessive|||Unknown|||insulin dependent diabetes susceptibility 9; C57BL/6J|Idd9|MGI:3036801|4||||||||||||||||Yes|||||||||||||Non obese diabetic (NOD) mice exhibit a susceptibility to Spontaneous development of type 1 diabetes.||NOD|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|28-Jul-2008||0.0|0.0|Unknown||Diabetic, insulin, T cell, autoimmunity|Yes| 3526.0||NOD.B6 Idd9/11||Recessive|||Unknown|||insulin dependent diabetes susceptibility 11|Idd11|MGI:3036811|4|||||||||||||||||||||||||||||Non obese diabetic (NOD) mice exhibit a susceptibility to Spontaneous development of type 1 diabetes.||NOD|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|28-Jul-2008||||Unknown||Diabetic, insulin, T cell, autoimmunity|Yes| 5267.0|MxCre/RARgamma|C57BL/6-Rarg Tg(Mx1-cre)1Cgn||Recessive|retinoic acid receptor, gamma|Rarg|Normal|RAR gamma 2, RARgamma2|MGI:97858|retinoic acid receptor, gamma; targeted mutation 3, Pierre Chambon|Rarg|MGI:2386111|15||||||||||||||||Yes|transgene insertion 1, University of Cologne|inducible Mx1|||||||||||Unknown|Unknown|C57BL/6|Yes|Unknown|Yes|Yes|Unknown|Yes|No|Unknown|10|||No|21-Oct-2010||0.0|0.0|Unknown||Cre Recombinase|Possibly| 5266.0|OsxCre/RARalphaRARgamma|C57BL/6-Rara Rarg Tg(Sp7-tTA,tetO-EGFP/cre)1Amc||Recessive|retinoic acid receptor, alpha|Rara|Normal|RAR alpha 1, RARalpha1|MGI:97856|retinoic acid receptor, alpha; targeted mutation 3, Pierre Chambon|Rara|MGI:2386106|11||||||||||||||||Yes|transgene insertion 1, Andrew P McMahon|Sp7|||||||||||Unknown|Unknown|C57BL/6|Yes|Unknown|Yes|Yes|Unknown|Yes|No|Unknown|10|||No|21-Oct-2010||0.0|0.0|Unknown||osteoblast, Cre recombinase|Possibly| 5266.0|OsxCre/RARalphaRARgamma|C57BL/6-Rara Rarg Tg(Sp7-tTA,tetO-EGFP/cre)1Amc||Recessive|retinoic acid receptor, gamma|Rarg|Normal|RAR gamma 2, RARgamma2|MGI:97858|retinoic acid receptor, gamma; targeted mutation 3, Pierre Chambon|Rarg|MGI:2386111|15||||||||||||||||Yes|||||||||||||Unknown|Unknown|C57BL/6|Yes|Unknown|Yes|Yes|Unknown|Yes|No|Unknown|10|||No|21-Oct-2010||||Unknown||osteoblast, Cre recombinase|Possibly| 8488.0|NOD.Nkrp1b|NOD-Klrb1b/Bax||Recessive|||||||||||||||||||||||||||||killer cell lectin-like receptor subfamily B member 1B|Klrb1b||Klrb1d, Ly55b, Ly55d, Nkrp1-b, NKR-P1B, Nkrp1d, NKR-P1D|MGI:107539||||6|Mice that are homozygous for this allele are viable, fertile, normal in size.||NOD/Lt|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|10|||No|31-May-2018|Cryopreserved sperm|50.0|0.0|Unknown||Nk1.1, TCR, NK cell, autoimmunity|Yes| 6669.0|ROBB|BALB/c-Il3/Ausb||Recessive|interleukin 3 |Il3|Nil|BPA, Csfmu, HCGF, Il-3, MCGF, PSF |MGI:96552|interleukin 3; targeted mutation 1, Stephen J Galli |Il3|MGI:2446538|11|||||||||||||||||||||||||||||||BALB/c|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|02-Dec-2011||0.0|0.0|Unknown||IL3|Yes| 3550.0||BALB/c-LMO4/Wehi||Recessive|LIM domain only 4|Lmo4|Unknown|A730077C12Rik, Crp3, Etohi4|MGI:109360|targeted mutation 2, Stuart Orkin|Lmo4|MGI:3035914|3||||||||||||||||Yes|||||||||||||Homozygous null mice die embryonically and exhibit a failure of neural tube closure and exencephaly, which is associated with abnormal patterns of cell proliferation and with high levels of apoptosis within the neuroepithelium.||BALB/c|No|No|Yes|No|No|Yes|No|Unknown||||No|30-Jul-2008||0.0|0.0|Unknown||perinatal lethality, neural tube, exencephaly, hindbrain, zinc finger|Yes| 5268.0|LLD KO|C57BL/6-Thdb||Recessive|thrombomodulin|Thbd|Nil|CD141, TM|MGI:98736|thrombomodulin; targeted mutation 2, Edward M Conway|Thbd|MGI:3712468|2||||||||||||||||No|||||||||||||Increased sensitivity to induced morbidity/mortality: during hypoxia 7 of 18 mice die with diffuse lung fibrin depositions compared to only one wild-type mouse.Abnormal leukocyte physiology: leukocyte accumulation in the lung is increased.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|24-Oct-2010||0.0|0.0|Yes|Thrombomodulin; THBD|neutrophil, lectin, adhesion, MAPk, kinase|Yes| 3554.0||C57BL/6-Tg(UBC-GFP)30Scha/JWehi||Semi-dominant||||||||||||||||||||||||||transgene insertion 30, Brian Schaefer|human ubiquitin C promoter|||||||||||Homozygous transgenic mice are viable, fertile, normal in size, and do not display any gross physical or behavioral abnormalities. These mice express GFP in all tissues examined. Expression levels vary between certain hematapoetic cell types. GFP expression is uniform within a cell type lineage and remains constant throughout development. T cells have a 2-fold higher GFP expression than CD19+B220+ B cells or peripheral blood cells. Leukocytes and red blood cells from homozygous transgenic mice fluoresce at approximately twice the level of cells from hemizygous mice.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|31-Jul-2008||0.0|0.0|Unknown||ubiquitous, GFP|Yes| 8494.0|NOD.BDC2.5|NOD.Cg-Tg(TcraBDC2.5,TcrbBDC2.5)1Doi/BaxApb||Recessive||||||||||||||||||||||||||transgene insertion 1, Christophe Benoist||||||||||||These transgenic mice carry both rearranged TCR alpha and beta genes from the cytotoxic CD4+ T cell clone BDC-2.5. On the NOD background, mice carrying the transgenes have a reduced incidence of diabetes relative to NOD/ShiLtJ controls (12% incidence at age 30 weeks).||NOD|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|31-May-2018|Cryopreserved sperm|50.0|0.0|Unknown||Insulitis|Yes| 10337.0|K5-creERt :R26-YAP5SA|C57Bl/6-K5(creERt)-R26(YAP5SA)Anu/Apb||Semi-dominant|yes-associated protein 1|Yap|||MGI:103262||||9|||||||||||||||||K5 |K5 Cre |||||||||||Normal|Normal|C57Bl/6J|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|30-May-2023|Cryopreserved sperm|55.0|0.0|Unknown|||Possibly| 5379.0|TS1|C.Cg-Tg(Tcra/Tcrb)1Vbo||Dominant||||||||||||||||||||||||||transgene insertion 1, Harald von Boehmer||||||||||||Normal|Normal|BALB/c|Yes|Yes|Yes|Yes|Yes|Yes|No|Excellent|||Hom x Hom|Yes|06-Jan-2011|Cryopreserved sperm|90.0|0.0|No||TCR transgenic, CD4, influenza|Possibly| 6840.0|Captain Morgan, ENU4AT:038 |C57BL/6JAnu-Dock8/TacAnuApb|C57BL/6JAnu-Dock8/TacAnuApb|Recessive|dedicator of cytokinesis 8|Dock8|Nil||MGI:1921396|dedicator of cytokinesis 8; captain morgan|Dock8|MGI:3835422|19|ENSMUSG00000052085|ENSMUST00000025831|Dock8-201||||||||25202202|20|||GCAGCCCATGGTCATTGCTGGCCAAACAGGTAGAGGCCTGTGGGTAGGGAGGAGGCATGG|Yes|||||||||||||Defective antibody response to immunization: failure to sustain antibody formation, undergo affinity maturation or to mount heightened recall (memory) response upon booster immunization. DOCK8-mutant B cells were unable to form marginal zone B cells or to persist in germinal centers and undergo affinity maturation. Dock8 mutations disrupted accumulation of the integrin ligand ICAM-1 in the B cell immunological synapse but did not alter other aspects of B cell antigen receptor signaling.||C57BL/6JAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|8|3||No|08-Mar-2012|Cryopreserved sperm|92.0|0.0|Unknown||gammaglobulin, immunization, antibody, ENU, Wellcome Trust, memory, B cell, GTP|Yes| 7740.0|SB12|STOCK Gt(ROSA)26Sor TgTn(sb-T2/Onc3)12775Njen/Nci||Dominant|gene trap ROSA 26, Philippe Soriano|Gt(ROSA)26Sor||beta geo, Gtrgeo26, Gtrosa26, R26, ROSA26|MGI:104735|gene trap ROSA 26, Philippe Soriano; targeted mutation 2, Nancy A Jenkins|Gt(ROSA)26Sor|MGI:3839796|6|||||||||||||||||transgenic transposon concatemer 12775, Nancy A Jenkins|CAG promoter |||||||||||Normal|Normal|C57BL/6|Yes|Yes|Unknown|Yes|Yes|Unknown|No|Poor||||No|15-Sep-2014|Cryopreserved sperm|60.0|0.0|Unknown|||Yes| 5264.0|RARgamma/TNFalpha|C57BL/6-Rarg Tnf||Recessive|retinoic acid receptor, gamma|Rarg|Nil|MGC:11555, MGC:18523, RAR gamma 2, RARgamma2|MGI:97858|retinoic acid receptor, gamma; targeted mutation 1, Pierre Chambon|Rarg|MGI:1931079|15||||||||||||||||No|||||||||||||Unknown|Unknown|C57BL/6|Yes|Unknown|Yes|Yes|Unknown|Yes|No|Unknown||||No|21-Oct-2010||0.0|0.0|Unknown||bone marrow, progenitor, infection, immunity, B cell|Yes| 5264.0|RARgamma/TNFalpha|C57BL/6-Rarg Tnf||Recessive|tumor necrosis factor|Tnf|Nil|DIF, TNF alpha, TNF-alpha, Tnfa, TNFalpha, Tnfsf1a, tumor necrosis factor-alpha|MGI:104798|tumor necrosis factor; targeted mutation 1, George Kollias|Tnf|MGI:2149024|17||||||||||||||||No|||||||||||||Unknown|Unknown|C57BL/6|Yes|Unknown|Yes|Yes|Unknown|Yes|No|Unknown||||No|21-Oct-2010||||Unknown||bone marrow, progenitor, infection, immunity, B cell|Yes| 6839.0|APN 222|C57Bl/6N-mir-196a-1/MarpApb||Recessive|microRNA 196a-1|Mir196a-1|Unknown|Mirn196, Mirn196a-1, mmu-mir-196a-1|MGI:2676860||||11|||||||||||||||||||||||||||||Unknown|Normal|C57Bl/6N|Unknown|Unknown|Unknown|Unknown|Unknown|Yes|No|Unknown||||No|08-Mar-2012|Cryopreserved sperm|50.0|0.0|Unknown|||Possibly| 4934.0|Cathepsin-S Knockout|SJL-Ctss/Wehi||Recessive|cathepsin S|Ctss|Nil|Cat S|MGI:107341|cathepsin S; targeted mutation 1, Harold A Chapman|Ctss|MGI:2182133|3||||||||||||||||Yes|||||||||||||Defective CD4 T cell response and humoral responses, but no overt immunodeficiency. Homozygous null mice are resistant to the development of experimental autoimmune myasthenia gravis and showed reduced T and B cell responses to acetylcholine receptor.||SJL|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|24-Nov-2009||0.0|0.0|Unknown||T cell, MHC class II, cysteine proteinase, Humoral resposne, arthritis, germinal centre|Yes| 8492.0|BALB.cCrslc|BALB/cCrSlcBax||Dominant||||||||||||||||||||||||||||||||||||||Subline of BALB/c||BALB/c|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|31-May-2018|Cryopreserved sperm|50.0|0.0|Unknown|||Yes| 10333.0|B10.BR CI/PB|B10.BR CI/PB||Recessive|NA|||||NA|||Unknown||||||||||||||||||||||||||||| B10.BR mouse line originally imported from ARC (Perth) in 1998. It has been used to backcross all Tg mouse lines under the B10.BR background at Centenary Institute (P. Bertolino group). Mice have a normal phenotype.|Normal|B10.BR|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|15-May-2023|Cryopreserved sperm|40.0|0.0|Unknown|||Possibly| 3556.0|Traube|CBA.129-Aatf||Recessive|apoptosis antagonizing transcription factor|Aatf|Nil|Che-1, MGC:35916, Trb, traube|MGI:1929608|gene trap 3, Peter Gruss|Aatf|MGI:2176283|11||||||||||||||||Yes|||||||||||||Embryonic lethality before implantation * embryos die after failing to undergo compactionEmbryogenesisDecreased embryo size * 50% reduction in total cell numberAbnormal blastocyst morphology * E1.5 embryos cultured in vitro do not form blastocysts as wild type and instead start to decompact and die after 72 hours of cultureFailure to form blastocele * embryos have not formed a blastocoel cavity by E3.5Embryonic growth arrest * development is arrested at the compacted morula stage at E2.5Growth/SizeDecreased embryo size * 50% reduction in total cell numbercellularAbnormal cell content/ morphology* embryos have few ribosomes, polyribosomes, and rough endoplasmic reticulum* greatly enlarged secretory vesicles are seen in embryosDecreased cell proliferation* embryos exhibit severe reduction in cell proliferation before blastocyst formation||CBA|No|No|Yes|No|No|Yes|No|Unknown||||No|31-Jul-2008||0.0|0.0|Unknown||leucine zipper, pre-implantation, nuclear localisation signal, morula|Yes| 1959.0|available from Animal Resources Centre - www.arc.wa.gov.au|C3H/HeJ||Dominant|Inbred agouti: A, Pde6b, H-2||Unknown||||||Unknown||||||||||||||||No|||||||||||||General Information: Typically C3H/HeJ are unresponsive to lipopolysaccharide due to a B-cell deficit. (Anderson and Ostermann (1980). LPS responsiveness of C3H substrains. Acta virol. 24:294-296).|||Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||Yes|04-Sep-2007||0.0|0.0|No|||Yes| 3560.0||C57BL/6-Tg(TcraTcrb)425Cbn Dnmt3l||Recessive|DNA (cytosine-5-)-methyltransferase 3-like|Dnmt3l|Unknown||MGI:1859287|DNA (cytosine-5-)-methyltransferase 3-like; targeted mutation 1, Hamish S Scott |Dnmt3l|MGI:3574947|10||||||||||||||||Yes|transgene insertion 425, Frank Carbone |endogenous TCR|||||||||||TCR transgenics are immunocompromised by having a mono-specific T cell receptor however, in a clean envirnoment, mice show no difference in phenoptype from wild-type B6 mice. Dnmt3l -/- mice have fertility defects and it is not possible to breed mice as a homozygous line.||C57BL/6|Yes|No|Yes|Yes|No|Yes|No|Unknown||||No|01-Aug-2008||0.0|0.0|Unknown||T cell, CD4, receptor (TCR), ovalbumin, thymic selection|Yes| 8493.0|BALB.Gasa1|BALB/c-Gasa1/BaxApb||Recessive|||||||||||||||||||||||||||||gastritis type A susceptibility locus 1|Gasa1|||MGI:1346075|gastritis type A susceptibility locus 1; C57BL/6|Gasa1|MGI:2155785|4|This allele confers resistance to autoimmune gastritis compared to BALB/cCrSlc. ||BALB/c|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|31-May-2018|Cryopreserved sperm|49.0|0.0|Unknown||Gastritis|Yes| 5366.0|RIP7-Socs1|C57BL/6-Tg(Ins2-Socs1)21Wehi||Dominant||||||||||||||||||||||||||suppressor of cytokine signaling-1|rat insulin promoter 2 (RIP7)|||||||||||SOCS-1 overexpression inhibits β cell responsiveness to IFNs.SOCS-1 overexpression in β cells prevents progression to diabetes in CD8<+>TCR transgenic NOD8.3 mice.Transgenic mice develop massive insulitis.SOCS-1 overexpression prevents the induction of Fas expression on β cells in NOD8.3 mice and in response to TNF and IFN-γ.Cells isolated from transgenic mice have a reduced ability to stimulate 8.3 T cell proliferation and IFN-γ production.SOCS-1 overexpression suppresses islet expression of IL-15 in response to TNF and IFN-γ.β cell up-regulation of Fas and class I MHC expression in mice adoptively transferred with diabetogenic splenocytes is also prevented by SOCS-1 overexpression.||C57BL/6|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|21-Dec-2010||0.0|0.0|Unknown||JAK, Janus kinase, signal transduction, islets, T cell|Yes| 5365.0|NOD.hCD4.IAE.427-3 ; triple 427|NOD-H2 Tg(Cd4-CD4)2362Litt Tg(HLA DR4-DQ8)427/Apb||Dominant|histocompatibility-2, MHC|H2|Nil|H-2, MHC-II|MGI:95894|histocompatibility-2, MHC; targeted deletion, H2 complex|H2|MGI:2658725|17||||||||||||||||No|human leukocyte antigen class II||||||||||||HLA DR4 and DQ3 expression was evident on B cell but not T cells, dendritic cells and a proportion of macrophages.DR4-DQ3 mice develop protective immunity following infectious challenge with S. typhimurium.||NOD|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|21-Dec-2010|Cryopreserved sperm|50.0|0.0|Unknown||MHC, B cell, selection, autoimmunity, celiac disease|Yes| 5365.0|NOD.hCD4.IAE.427-3 ; triple 427|NOD-H2 Tg(Cd4-CD4)2362Litt Tg(HLA DR4-DQ8)427/Apb||Dominant||||||||||||||||||||||||||transgene insertion 2362, Dan R Littman|murine Cd4 and human CD4|equivalent to human CD4+ cells||||||||||HLA DR4 and DQ3 expression was evident on B cell but not T cells, dendritic cells and a proportion of macrophages.DR4-DQ3 mice develop protective immunity following infectious challenge with S. typhimurium.||NOD|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|21-Dec-2010|Cryopreserved sperm|||Unknown||MHC, B cell, selection, autoimmunity, celiac disease|Yes| 7097.0|DMP-cre|C57BL/6-Tg(Dmp1-cre)1Jqfe/Apb||Dominant||||||||||||||||||||||||||transgene insertion 1, Jian Q Feng|dentin matrix protein 1 (Dmp1)|Cre expression restricted to dontoblasts and osteocytes||||||||||Normal.Cre expression in odontoblasts and osteocytes|Normal.Cre expression in odontoblasts and osteocytes|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|28-Sep-2012|Cryopreserved sperm|50.0|0.0|Unknown||Cre recombinase|Possibly| 8487.0|C57BL/6.Myd88-/-|B6.129P2-Myd88/BaxApb||Recessive|myeloid differentiation primary response gene 88|Myd88|Nil||MGI:108005|myeloid differentiation primary response gene 88; targeted mutation 1, Shizuo Akira|Myd88|MGI:2385681|9|||||||||||||||||||||||||||||Increased apoptosis:*5 days after lung injury, mutants show significantly increased numbers of apoptotic lung epithelial and inflammatory cells.Increased physiological sensitivity to xenobiotic:*Knockout mice are more susceptible to bleomycin-induced lung injury.Increased dendritic cell number:*Increased numbers of dendritic cells in brains of mice infected with Plasmodium.Abnormal dendritic cell differentiation:*Dendritic cell maturation fails to occur in vivo upon exposure to TLR9 agonists.Abnormal immune system physiology:*Response to LPS and CpG is completely abrogated. Abnormal dendritic cell physiology: *Cytokine secretion elicited by zymosan or LPS is impaired. *Following infection with attenuated yellow fever vaccine 17D (YF-17D), dendritic cells produce less IL-12p40, IL-6 and interferon-gamma relative to wild-type mice. Abnormal macrophage physiology: *TNF production is impaired in thioglycollate-elicited macrophages treated with intact zymosan. *Cytokine production by macrophages cultured with P. carinii cysts is reduced compared to wild-type. Abnormal NK cell physiology: *NK cells fail to make IFN-gamma in response to injections of TLR9 agonists. Abnormal T cell physiology: *Induction of the antigen-specific CD8+ T-cell response by immunizing with soluble ovalbumin and TLR9 agonists, but not TLR2 and TLR6 agonists, was severely impaired. Abnormal cytokine secretion: *LPS-induced cytokine production by BMDCs is almost abolished compared to controls and Myd88-sufficient mutants. Abnormal chemokine secretion: *Hyaluronan fragment-induced expression of chemokines by peritoneal macrophages is completely abolished in double knockout mice. Decreased interferon-alpha secretion: *CpG-A or RNA polyuridylic acid induced production of interferon-alpha was abolished in plasmacytoid dendritic cells. Decreased interferon-gamma secretion: *Less up regulation of INF-gamma in Plasmodium infection. *Following infection with attenuated yellow fever vaccine 17D (YF-17D), dendritic cells produce less interferon-gamma. Decreased interleukin-12 secretion: *After stimulation with zymosan, TNF production is significantly reduced in Myd88-deficient animals. Decreased interleukin-12b secretion: *Less upregulation of IL-12b in Plasmodium infection. *Following infection with attenuated yellow fever vaccine 17D (YF-17D), dendritic cells produce less IL-12p40 relative to wild-type mice. Decreased interleukin-6 secretion: *Following treatment with PbA(Plasmodium bergbei ANKA)-parasitized erythrocytes or LPS-stimulation, IL-6 secretion is reduced. *Following infection with attenuated yellow fever vaccine 17D (YF-17D), dendritic cells produce less IL-6 relative to wild-type mice. Decreased tumor necrosis factor secretion: *Less upregulation of TNF-alpha in Plasmodium infection. *Following treatment with PbA(Plasmodium bergbei ANKA)-parasitized erythrocytes or LPS-stimulation, TNF secretion is reduced. *After stimulation with zymosan, TNF production is significantly reduced in Myd88-deficient animals. Decreased inflammatory response: *In a model of induced pneumococcal meningitis-associated labyrinthitis, homozygotes exhibit a significantly lower granulocytic infiltration of the labyrinth and increased bacterial density in the cochlea at 24 hrs post-infection relative to wild-type control mice. Abnormal response to infection: *Following treatment with PbA (Plasmodium bergbei ANKA)-parasitized erythrocytes, mice have a decreased immune response in terms of TNF and IL-6 secretion and response to CpG. Decreased susceptibility to parasitic infection: *Resistant to cerebral malaria but eventually die of extremely high parasitemia. Increased susceptibility to viral infection: *Increased susceptibility to encephalomyocarditis virus (EMCV) infection compared to wildtype.Abnormal susceptibility to hearing loss:*In a model of induced pneumococcal meningitis-associated labyrinthitis, homozygotes exhibit significantly less hearing impairment at 24 hrs post-infection in response to click, 1- or 10-kHz stimuli relative to wild-type control mice.Abnormal neuron differentiation:*Improved differentiation of progenitor cells into neurons.*Survival of newly formed neurons is reduced.Abnormal nervous system physiology:*After cold induced cortical injury, recruitment of neutrophiles to lesion site is reduced by 85% in comparison to controls.*Cold induced cortical lesion volume is reduced by 25% compared to controls.*Fewer cortical cells have damaged DNA compared to controls after cold induced cortical injury.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|31-May-2018|Cryopreserved sperm|49.0|0.0|Unknown||MyD88, IL-1, IL-18, NF-kappaB, c-Jun N-terminal kinase (JNK)|Yes| 1543.0|C57BL/6.gZA-/- OT-1 ; Pathans|C57BL/6-Gzma Tg(TcraTcrb)1100Mjb/AnuApb||Recessive|granzyme A|Gzma|Unknown|BLT esterase, Ctla-3, Ctla3, H factor, Hanukah factor, Hf, SE1, serine esterase 1, TSP-1, TSP1|MGI:109266|targeted mutation 1, Markus M Simon|Gzma|MGI:2449926|13||||||||||||||||Yes|transgene insertion 1100, Michael J Bevan ||||||||||||||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|06-Jul-2007|Cryopreserved sperm|50.0|0.0|Unknown||T cell, Natural Killer cell, cytotoxicity, receptor, ovalbumin|Yes| 10342.0|Tcf3 A513X (46)|C57BL/6NCrlAnu-Tcf3Anu/46Anu||Dominant|transcription factor 3|Tcf3|||MGI:98510|Tcf3; endonuclease mutation 4, Australian National University|Tcf3||10||||||||||Unknown to Unknown|||||||||||||||||||Most likely embryonic lethal (so far not enough offspring tested to be certain)|Mild reduction of B cells.|C57Bl/6N|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|20-Jun-2023|Cryopreserved sperm|43.0|0.0|Unknown|||Possibly| 632.0|T3DKO|B6;129-Tlr3 Eif2ak2|B6;129-Tlr3 Eif2ak2|Dominant|toll-like receptor 3|Tlr3|Unknown||MGI:2156367|targeted mutation 1, Richard A Flavell|Tlr3|MGI:2653138|8||||||||||||||||Yes|||||||||||||Comparable spleen and bone marrow cell populations in tlr3(-/)-, pkr(-/-), and tlr3(-/-)pkr(-/-) mice to wild-type controls. Splenomegaly developing between 8 and 10 weeks of age was observed in tlr3(-/-) and tlr3(-/-)pkr(-/-) mice but not in wild-type or pkr(-/-) mice.These data also suggest that PKR may have a role in preventing progression from splenomegaly to lymphadenopathy in these mice.||C57BL/6 x 129|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|25-Apr-2007||0.0|0.0|Unknown||splenomegaly, lymphadenopathy, lymphocyte, lymph node|Yes| 8496.0|NOD.Il10-/-|NOD.Cg-Il10/BaxApb||Recessive|interleukin 10|Il10||cytokine synthesis inhibitory factor, IL-10|MGI:96537|interleukin 10; targeted mutation 1, University of Cologne|Il10|MGI:1857199|1|||||||||||||||||||||||||||||This mutant develops type 1 diabetes at the same rate as the NOD/Lt parental strain. The Il10 tm1Cgn mutation also renders this NOD/Lt stock susceptible to colitis (although not as severe as other strains of Il10 deficient mice) when maintained under standard housing conditions.Large intestinal inflammation: • mutants develop severe inflammation in the colon leading to inflammatory bowel disease Abnormal regulatory T cell physiology: • CD25-positive CD4 T cells from these mice fail to protect against the wasting disease induced by transferring nave CD4 T cells into immunodeficient hosts|Unknown|NOD|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|31-May-2018|Cryopreserved sperm|50.0|0.0|Unknown||il10, colitis, T cell|Possibly| 7741.0|ENU23:B6:016:TACO1|C57BL/6NCrlAnu-Taco1/AnuApb||Recessive|translational activator of mitochondrially encoded cytochrome c oxidase I|Taco1 |Unknown| 2310066I18Rik, Ccdc44 |MGI:1917457 |Taco1; mutation 1, the Australian National University|Taco1||11|ENSMUSG00000001983|ENSMUST00000002048|Taco1-001|491|678|T to A|ENSMUSE00000108220|3|164|Isoleucine to Asparagine|||||||||||||||||||Unknown|Normal|C57BL/6NCrlAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||7|Het x Het|No|22-Sep-2014|Cryopreserved sperm|20.0|0.0|Yes|Leigh syndrome with cardiomyopathy|Mitochondrion, Translation, Molecular|Yes| 4933.0|SOCS-1 KO|129-SOCS1/Wehi||Recessive|suppressor of cytokine signaling 1|Socs1|Nil|Cish1, Cish7, JAB, JAK-binding protein, JAK2-binding protein, SOCS-1, SSI-1, STAT-induced STAT inhibitor 1|MGI:1354910|targeted mutation 1, Walter and Eliza Hall Institute of Medical Research|Socs1|MGI:1934607|16||||||||||||||||No|||||||||||||Postnatal lethality:* homozygotes become ill and die before reaching 3 weeks of age.* mice die from inflammatory disease before weaning.Decreased body weight:* homozygotes become smaller within 10 days after birthPostnatal growth retardation.Pancreas inflammation: monocytic infiltration.Decreased hematocrit.Decreased lymphocyte cell number.Decreased B cell number:* progressive loss of maturing B lymphocytes in the marrow, spleen, and peripheral blood.Decreased pre-B cell number:* pre-B cells are depleted significantly in the marrow.Decreased eosinophil cell number:* moderate reduction in eosinophil numbersAbnormal mature B cell morphology:* number of mature B cells expressing surface Ig in the bone marrow is reduced.Abnormal follicular B cell morphology:* lymphoid follicles of the spleen are either completely absent or are composed of immature cells.Increased spleen red pulp amount:* most spleens show expanded areas of red pulp with nucleated erythroid cells as the main cell population.Thymus cortex hypoplasia:* the cortex becomes progressively depleted of lymphoid cellsSmall thymus.Abnormal Peyer's patch morphology:* Peyer's patches are present but contain few lymphocytes.Abnormal lymph node B cell domain:* lymph nodes show absence of lymphoid follicle formation.Increased inflammatory response:* mice die from massive generalized inflammation that affects multiple organs.Heart inflammation: monocytic, and less frequently, granulocytic infiltration.Pancreas inflammation: monocytic infiltration.Liver inflammation: livers exhibit both focal and generalized infiltration, predominantly by immature and mature monocytic and granulocytic cells, and less frequently, megakaryocytes and eosinophils.Hepatic steatosis: parenchymal cells contain an accumulation of lipid-containing vacuoles.Liver degeneration: fatty degeneration either involves local areas not related to portal vessels or is generalized to the entire liver.Abnormal respiratory alveoli morphology: increase in cellularity of alveolar walls in the lung, often associated with macrophage cuffing around major vessels.||129|No|No|Yes|No|No|Yes|No|Unknown||||No|20-Nov-2009||0.0|0.0|Unknown||Cytokine signalling, phosphorylation, signal transduction, IL-6 receptor, growth retardation|Yes| 5255.0|LIF-KO|C57BL/6-Lif||Recessive|leukemia inhibitory factor|Lif|Nil||MGI:96787|leukemia inhibitory factor; targeted mutation 1, Philippe Brulet|Lif|MGI:2181618|11||||||||||||||||No|||||||||||||Hematopoietic system phenotype: * homozygotes exhibit normal circulating numbers of mature red and white blood cells and platelets relative to wild-type controls. * no significant differences in thymus cellularity or thymocyte subsets are observed. * B-cell subsets in the bone marrow, spleen and peritoneum are normal. * both spleens and thymuses are of normal size.Decreased common myeloid progenitor cell number: granulocyte-macrophage (GM-colony forming capacity) progenitors are reduced by 73% in spleen but are less affected in the bone marrow.Decreased erythroid progenitor cell number: committed erythroid (BFU-E) progenitors are reduced by 85% in spleen but are less affected in the bone marrow.Decreased T cell proliferation: * at 6-8 weeks of age, homozygotes display a severely reduced thymic T-cell proliferation in response to concanavalin A and allogeneic stimulation relative to wild-type controls. * however, when lethally irradiated wild-type mice are reconstituted with mutant bone marrow or spleen cells, normal thymic T-cell stimulation is observed, suggesting a defect in the hematopoietic microenvironment. * peripheral T-cell responses remain normal.Decreased hematopoietic stem cell number: * pluripotent hematopoietic stem cells (CFU-S) are reduced by 88% in spleen and by 59% in the bone marrow. * however, total nucleated cell numbers and the subset of hematopoietic progenitors defined by markers Sca+Thyl+Lin- in spleen and bone marrow are normal. * injection of mutant spleen and bone marrow cells promotes long-term survival of lethally irradiated wild-type mice, indicating that mutant stem cells remain pluripotent. * the diminished CFU-S pool can be restored by exogenous LIF (10<3> IU).Decreased body size: homozygotes are overtly normal but somewhat smaller than wild-type controls.Abnormal embryo apposition: * no uterine expression of the heparin-binding EGF-like growth factor (HB-EGF) is detected in the luminal epithelium at the site of blastocyst apposition at the anticipated time prior to the attachment reaction on day 4 or even on the morning of day 5 of pregnancy, unlike in wild-type controls. * however, HB-EGF expression in brain or in the luminal epithelium on day 1 of pregnancy is equivalent to that in wild-type controls.Abnormal embryo attachment: * epiregulin, which is normally expressed in the luminal epithelium and underlying stroma adjacent to the implanting blastocyst at the time of the attachment reaction on day 4 and then on day 5, is not induced on day 5 of pregnancy in mutant uteri. * uterine expression of prostaglandin-endoperoxide synthase 2 (Ptgs2) is normally present in the luminal epithelium but absent in underlying stromal cells surrounding the blastocyst during the attachment reaction on day 5 of pregnancy, unlike in wild-type controls.Failure of embryo implantation: * blastocysts fail to implant partly due to loss or aberrant expression of specific members of the EGF family of growth factors in mutant uteri before and during the expected time of implantation, although EGF receptor family members are properly expressed. * however, uterine cell-specific proliferation and differentation, responsiveness to ovarian steroids, and expression of angiogenic factors remain normal during the preimplantation period in mutant uteri.Abnormal uterine receptivity: * amphiregulin, which is normally expressed in the luminal and glandular epithelia of wild-type uteri, is undetectable in mutant uteri on day 4 of pregnancy, suggesting that uterine preparation is impaired despite normal plasma progesterone levels. * however, amphiregulin is induced in ovariectomized mutant uteri after progesterone (P4) treatment, though at reduced levels.Female infertility: * female, but not male, homozygotes are sterile. * female homozygotes are infertile due to uterine defects that affect embryo implantation.|Decreased erythroid progenitor cell number: in spleen, the numbers of committed erythroid (BFU-E) progenitors are intermediate between those of wild-type and homozygous mutant mice.Decreased T cell proliferation: at 6-8 weeks of age, heterozygotes display a severe reduction in thymic T-cell response to concanavalin A and allogeneic stimulation relative to wild-type controls.Decreased hematopoietic stem cell number: in spleen, the numbers of pluripotent hematopoietic stem cells (CFU-S) are intermediate between those of wild-type and homozygous mutant mice.|C57BL/6|Yes|No|Yes|Yes|Yes|Yes|No|Unknown||||No|21-Oct-2010||0.0|0.0|Unknown||growth factor, embryonic stem cell, proliferation, spleen|Yes| 10332.0||C57Bl/6-Osx(Cre> p53 pRb R26-Adar1p150/AnuApb||Dominant|Osx-Cre p53fl/fl pRbfl/fl R26-Adar1p150|||||Osx-Cre p53fl/fl pRbfl/fl R26-Adar1p150|||Unknown|||||||||||||||||Osx-Cre|Sp7|||||||||||Homozygous viable and fertile; stock maintained as Cre negative line with all other alleles homozygous. When crossed to Osx-Cre will develop osteosarcoma|Heterozygous viable and fertile; stock maintained as Cre negative line with all other alleles homozygous. When crossed to Osx-Cre will develop osteosarcoma|C57Bl/6N|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|09-May-2023|Cryopreserved sperm|30.0|0.0|Unknown|||Possibly| 7098.0|APN193|Neo1/Marp||Recessive|neogenin|Neo1 |Unknown|2610028H22Rik, D930014N22Rik, Igdcc2 |MGI:1097159 |neogenin; targeted mutation 1a, Helmholtz Zentrum Muenchen GmbH |Neo1tm1a(EUCOMM)Hmgu|MGI:4435562|9|||||||||||||||||||||||||||||Unknown|Normal|C57BL/6N|Unknown|Unknown|Unknown|Unknown|Unknown|Yes|No|Unknown||||No|01-Oct-2012|Cryopreserved sperm|50.0|0.0|Unknown||ES cell clone|Possibly| 4820.0|Jiba|ENU8CAT:009||Recessive|||||||||Unknown|||||||||||||||||transgene insertion 3, Christopher C Goodnow|Rat insulin promoter|Expression of the inserted sequence specifically to pancreatic islet beta cells||||||||||Mice carrying the ins-HEL gene have a subclinical predisposition to diabetes due to islet cell failure. Mice carrying the insHEL and TCR transgenes have asubclinical predisposition to autoimmune destruction of the beta cell. Screening mice by urine glucose test. High glucose levels indicate diabetes and thus autoimmunity. "Early onset diabetes" definition changed during screen from approx 80 days to 40 days.||C57BL/6 x C57BL/10BR x CBA|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|||Breed diabetic Double transgenic with a non transgenic sib for next generation|No|24-Sep-2009|Cryopreserved sperm|100.0|0.0|Yes|Type I Diabetes|ENU, Singapore, autoimmunity, T cell, B cell, glucose|No| 4820.0|Jiba|ENU8CAT:009||Recessive||||||||||||||||||||||||||transgene insertion 1, Mark M Davis||||||||||||Mice carrying the ins-HEL gene have a subclinical predisposition to diabetes due to islet cell failure. Mice carrying the insHEL and TCR transgenes have asubclinical predisposition to autoimmune destruction of the beta cell. Screening mice by urine glucose test. High glucose levels indicate diabetes and thus autoimmunity. "Early onset diabetes" definition changed during screen from approx 80 days to 40 days.||C57BL/6 x C57BL/10BR x CBA|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|||Breed diabetic Double transgenic with a non transgenic sib for next generation|No|24-Sep-2009|Cryopreserved sperm|||Yes|Type I Diabetes|ENU, Singapore, autoimmunity, T cell, B cell, glucose|No| 7742.0|ENU19:B6:MRPS34|C57BL/6JAnu-Mrps34/AnuApb||Recessive|mitochondrial ribosomal protein S34|Mrps34|Unknown|0610007F04Rik, 5330430D13Rik, Tce2 |MGI:1930188 |Mrps34; mutation 1, the Australian National University|Mrps34||17|ENSMUSG00000038880|ENSMUST00000043907|Mrps34-001|203|252|T to C|ENSMUSE00000747863|1|68|Leucine to Proline|||||||||||||||||||Unknown|Normal|C57BL/6NCrlAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||5|mut x mut|No|23-Sep-2014|Cryopreserved sperm|22.0|0.0|Unknown||mitochondrion, ribonucleoprotein complex, Molecular function|Yes| 4938.0|Crlf1 KO|C57BL/6-Crlf1/Wehi||Recessive|cytokine receptor-like factor 1|Crlf1|Nil|CLF-1, CRLM3, cytokine receptor like molecule 3, NR6.1|MGI:1340030|targeted mutation 1, Warren S Alexander|Crlf1|MGI:2387956|8||||||||||||||||Yes|||||||||||||Mice homozygous for a targeted mutation fail to suckle effectively and do not survive beyond 24 hrs after birth. Newborns exhibit reduced numbers of hematopoietic progenitor cells as well as a significant reduction in the number of motoneurons in the lumbar spinal cord and facial nucleus.Neonatal lethality: at birth, homozygotes are present at the expected Mendelian frequency; however, no homozygotes survive beyond 24 hrs after birth.Absent gastric milk in neonates: newborn homozygotes contain no milk in their stomachs.Abnormal suckling behavior: newborn homozygotes open and close their mouths but fail to suckle effectively, despite the absence of gross or histologic abnormalities in brain (i.e. cortex and hippocampus), olfactory bulb, as well as facial or mouth tissues.Decreased motor neuron number:* newborn homozygotes display a significantly reduced number of motoneurons in the lumbar spinal cord, with no apparent change in the brachial or thoracic cord.* newborn homozygotes also exhibit a significant decrease in the number of motoneurons in the facial but not hypoglossal nucleus; sensory neurons of the dorsal root ganglia remain unaffected.Impaired hematopoiesis:* newborn homozygotes display reduced numbers of hemopoietic progenitor cells in the bone marrow and spleen* no differences in the numbers and lineage commitment of progenitor cells are observed in neonatal liver.||C57BL/6|Yes|No|Yes|Yes|No|Yes|No|Poor||||No|01-Dec-2009||0.0|0.0|Unknown||cytokine signalling, haemopoietic progenitor, soluble receptor, suckling|Yes| 1512.0|DmTNF|C57BL/6-Tnf||Recessive|tumor necrosis factor|Tnf|Normal|DIF, TNF alpha, TNF-alpha, Tnfa, TNFalpha, Tnfsf1a, tumor necrosis factor-alpha|MGI:104798|targeted mutation 2, Jonathon D Sedgwick|Tnf|MGI:3578747|17||||||||||||||||Yes|||||||||||||Abnormal spleen white pulp morphology:* some loss of B and T cell area segregation, however less than seen in homozygous Tnf mice.Abnormal metallophillic macrophage morphology:* the MOMA-1+ marginal zone metallophilic macrophages did not form a completely continuous cell layer.Abnormal spleen follicular dendritic cell network:* follicular dendritic cell networks were undetectable in unimmunized homozygous mutant mice.* size and frequency of the formation CR1+ follicular dendritic networks upon immunization was substantially less than in wild-type.Abnormal spleen primary B follicle morphology:* absent primary B cell folliclesDecreased spleen germinal center number:* frequency of the formation of PNA+ germinal centers upon immunization was substantially less than in wild-type.Decreased spleen germinal center size:* size of PNA+ germinal centers upon immunization was substantially less than in wild-type.Abnormal Peyer's patch follicle morphology:* imperfect primary B cell follicles, however separation of T and B cell regions was fairly normal.Abnormal lymph node primary follicle.Abnormal immune system physiology:Decreased susceptibility to experimental autoimmune encephalomyelitis:* reduced severity of experimental autoimmune encephalomyelitis (EAE) under suboptimal immunization conditions relative to wild-type, with less inflammation in the spinal cord and the majority of homozygous mutant mice recovering rapidly.Decreased susceptibility to endotoxin shock:* resistant to endotoxic shock induced by low doses of LPS, however at high doses, started to show signs of shock and 2/5 mice succumbed to shock, however with a delayed time of death compared to wild-type.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|04-Jul-2007||0.0|0.0|Unknown||T cell, membrane bound, B cell, marginal zone|Yes| 251.0||129-Ccr1/Apb|129-Ccr1/Apb|Recessive|chemokine (C-C motif) receptor 1|Ccr1|Nil|Cmkbr1, MIP-1 alphaR, Mip-1a-R|MGI:104618|targeted mutation 1, Craig Gerard|Ccr1|MGI:1931849|9||||||||||||||||No|||||||||||||Homozygotes for targeted null mutations exhibit altered trafficking and proliferation of myeloid progenitor cells, and impairments in granulomatous inflammation of the lung and neutrophil associated host defense.||129|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|28-Apr-2006|Cryopreserved sperm|50.0|0.0|Unknown||chemokine, RANTES, neutrophil, inflammation|Yes| 4822.0|Leena|ENU8CAT:025||Recessive|||||||||Unknown|||||||||||||||||transgene insertion 3, Christopher C Goodnow|Rat insulin promoter|Expression of the inserted sequence specifically to pancreatic islet beta cells||||||||||Mice carrying the ins-HEL gene have a subclinical predisposition to diabetes due to islet cell failure. Mice carrying the insHEL and TCR transgenes have asubclinical predisposition to autoimmune destruction of the beta cell. Screening mice by urine glucose test. High glucose levels indicate diabetes and thus autoimmunity. "Early onset diabetes" definition changed during screen from approx 80 days to 40 days.||C57BL/6 x C57BL/10BR x CBA|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|||Breed diabetic Double transgenic with a non transgenic sib for next generation|No|24-Sep-2009|Cryopreserved sperm|120.0|0.0|Yes|Type I Diabetes|ENU, Singapore, autoimmunity, T cell, B cell, glucose, JDRF|No| 4822.0|Leena|ENU8CAT:025||Recessive||||||||||||||||||||||||||transgene insertion 1, Mark M Davis||||||||||||Mice carrying the ins-HEL gene have a subclinical predisposition to diabetes due to islet cell failure. Mice carrying the insHEL and TCR transgenes have asubclinical predisposition to autoimmune destruction of the beta cell. Screening mice by urine glucose test. High glucose levels indicate diabetes and thus autoimmunity. "Early onset diabetes" definition changed during screen from approx 80 days to 40 days.||C57BL/6 x C57BL/10BR x CBA|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|||Breed diabetic Double transgenic with a non transgenic sib for next generation|No|24-Sep-2009|Cryopreserved sperm|||Yes|Type I Diabetes|ENU, Singapore, autoimmunity, T cell, B cell, glucose, JDRF|No| 7743.0|ENU23:005:MRPL44|C57BL/6NCrlAnu-Mrpl44/AnuApb||Recessive|mitochondrial ribosomal protein L44|Mrpl44 |Unknown|1810030E18Rik, 5730593H20Rik|MGI:1916413 |Mrpl44; mutation 1, the Australian National University|Mrpl44||1|ENSMUSG00000026248|ENSMUST00000027464|Mrpl44-001|868|983|C to T|ENSMUSE00000356749|4|290|Leucine to Phenylalanine|||||||||||||||||||Unknown|Normal|C57BL/6NCrlAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||7|het x het|No|23-Sep-2014|Cryopreserved sperm|21.0|0.0|Unknown||mitochondrial translational elongation, RNA processing, ribonucleoprotein complex, bidentate ribonuclease III , endonuclease activity|Yes| 7905.0|SGTA KO|C57BL/6-Sgta/DrmcrApb|DRMCR|Recessive|Small Glutamine-Rich Tetratricopeptide Repeat (TPR)-Containing, Alpha|Sgta|Nil|5330427H01Rik, D10Ertd190e, MGC:6336, Sgt|MGI:1098703|small glutamine-rich tetratricopeptide repeat (TPR)-containing, alpha; targeted mutation 1.1, Dame Roma Mitchell Cancer Research|Sgta|MGI:5788683|10||||||||||||||||Yes|||||||||||||Increased heart weight.Abnormal intestine morphology: • increased intestine weightAbnormal testis development: • increased testis descent (AGD)Decreased body size: • small body size observed in both males and females beginning at P19• feed intake, adiposity, lean and skeletal mass, when corrected for body weight, are similar to controlsDecreased body weight.Decreased body length.Decreased circulating insulin-like growth factor I level: • decreased serum IGF-1 levelsLethality, incomplete penetrance: • heterozygote x heterozygote matings produced fewer female homozygotes than expected (18.80% versus 25%)Neonatal lethality, incomplete penetrance: • high neonatal death rate (30.77%) day 2 to 21Increased brain weight.Large penis: • increased penis length and weightDecreased litter size: • litter size trends smaller for homozygote x homozygote matingsReduced fertility.|Small stomach: • reduced stomach weightAbnormal male preputial gland morphology:• increased preputial gland weightDecreased circulating insulin-like growth factor I level: • decreased serum IGF-1 levels in femalesLarge penis: • increased penis weight|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|12-Jun-2015|Cryopreserved sperm|50.0|0.0|Unknown||SGTA, AR, small glutamine-rich tetratricopeptide repeat-containing protein alpha, SGT|Possibly| 8499.0||A2(T172A) KI||Recessive|AMPK Alpha 2|a2|||||||4|||||||||||||||||||||||||||||Normal|Normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|05-Jun-2018|Cryopreserved sperm|50.0|0.0|Unknown|||Possibly| 6582.0|B6129-P2-GSK|B6.129P2-Gsk3b/MarpApb||Semi-dominant|glycogen synthase kinase 3 beta|Gsk3b|Nil|7330414F15Rik, 8430431H08Rik, GSK-3, GSK-3beta, GSK3|MGI:1861437||||16|||||||||||||||||||||||||||||Complete preweaning lethality. No homozygotes are found at weaning.|No abnormal phenotype detected. Heterozygotes are viable and fertile with no gross abnormalities.|C57BL/6|No|No|Yes|No|No|Yes|No|Good|||wildtype x heterozygote|No|13-Sep-2011|Cryopreserved sperm|50.0|0.0|No|||No| 7555.0|ENU25:041:Casd1:B6|C57BL/6NCrlAnu-Casd1/Apb|C57BL/6NCrlAnu-Casd1/Apb|Recessive|CAS1 domain containing 1|Casd1|Unknown|Cast1, MGC:6840|MGI:2384865||||6|ENSMUSG00000015189|ENSMUST00000015333|Casd1-001||||||||4557979|1|||CTAATATTTACACTACCGTGCTTTACTGTTATAGGCAATGATTCGTGTGAATACCTTCTC||||||||||||||Unknown||C57BL/6NCrlAnu|Yes|Unknown|Yes|Yes|Unknown|Yes|No|Unknown||||No|19-Dec-2013||0.0|0.0|Unknown||ENU|Yes| 2773.0|BALB/c.Flii<-/-> FLII ; FITR|BALB/c-Flii Tg(FLII)2Hdc/AnuApb|BALB/c-Flii Tg(FLII)2Hdc|Recessive|flightless I homolog (Drosophila)|Flii|Unknown|Fli1, Fliih|MGI:1342286|targeted mutation 1, Hugh D Campbell|Flii|MGI:2179825|11||||||||||||||||Yes|Human Flightless gene|Human Flightless|||||||||||Embryonic lethal phenotype of FLii knockout is rescued by human FLII transgene. ||BALB/c|Yes|Yes|Yes|Yes|Yes|Yes|No|Poor|1||Flii<-/-> FLII x Flii<-/-> FLII|No|16-Feb-2008|Cryopreserved sperm|150.0|0.0|No||human flightless, wound repair, cellular proliferation, cell migration, gelsolin|Yes| 7744.0|ENU26:048:Ptcd1|C57BL/6NCrlAnu-Ptcd1/AnuApb||Recessive|pentatricopeptide repeat domain 1|Ptcd1 |Unknown|1110069M14Rik |MGI:1919049 |Ptcd1; mutation 1, the Australian National University|Ptcd1||5|ENSMUSG00000029624|ENSMUST00000031628|Ptcd1-001||||||||145151282|8|||GCCGAGTACCCTCCCACCTTTGACCGGGTATGTGCACCAAGTTTACTGTCAGTGCTGATG||||||||||||||Unknown|Normal|C57BL/6NCrlAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||6|mut x mut|No|23-Sep-2014|Cryopreserved sperm|20.0|0.0|Unknown||tRNA processing, mitochondrion, molecular function|Yes| 5260.0|OsxCregp130|C57BL/6-Il6st Tg(Sp7-tTA,tetO-EGFP/cre)1Amc||Recessive|interleukin 6 signal transducer|Il6st|Normal|CD130, gp130|MGI:96560|interleukin 6 signal transducer; targeted mutation 1, Werner Mueller|Il6st|MGI:1931239|13||||||||||||||||Yes|transgene insertion 1, Andrew P McMahon|Sp7 transcription factor 7 (Sp7) (osterix, Osx)|Cre expression restricted to bone||||||||||Unknown|Unknown|C57BL/6|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|21-Oct-2010||0.0|0.0|Unknown||osterix, signal transduction, Cre recombinase|Possibly| 4697.0|NOD260/260|NOD.Cg-Socs1/WehiApb||Recessive|suppressor of cytokine signaling 1|Socs1|Unknown|Cish1, Cish7, JAB, JAK-binding protein, JAK2-binding protein, SOCS-1, SSI-1, STAT-induced STAT inhibitor 1|MGI:1354910|targeted mutation 1, Walter and Eliza Hall Institute of Medical Research|Socs1|MGI:1934607|16||||||||||||||||No|||||||||||||postnatal lethality (J:51281) mice die prior to weaning digestive/alimentary system pancreas inflammation (J:51281) monocytic infiltration postnatal growth retardation (J:51281) hematopoietic system decreased B cell number (J:51281) progressive loss of maturing B lymphocytes in the marrow, spleen, and peripheral blood small thymus (J:51281) thymus hypoplasia (J:51281) fatty liver||NOD|Yes|No|Yes|Yes|No|Yes|No|Unknown||||No|07-Apr-2009|Cryopreserved sperm|110.0|0.0|Unknown||Cytokine signalling, Phosphorylation, Signal transduction, IL-6 receptor, Growth retardation|Yes| 5259.0|SOST-luciferase|C57BL/6-Tg(Sost-luc)Kne||Dominant||||||||||||||||||||||||||Luciferase|Sclerostin (Sost)|Osteocyte specific|||||||||||Phenotype does not differ from a wildtype of the same genetic background. Luciferase expression under control of the SOST promoter (osteocyte specific)|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|21-Oct-2010|Cryopreserved sperm|50.0|0.0|Unknown||osteocyte, expression|Possibly| 5865.0|K14E7.FVB||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5866.0|K14E7.hgh||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 1509.0|H2-Bf|B6;129-Cfb/Apb|B6;129-Cfb/Apb|Recessive|complement factor B|Cfb|Nil|alternative-complement pathway C3/C5 convertase, B, Bf, Bf, Factor B, FB, H2-Bf, properdin|MGI:105975|targeted mutation 1, Harvey R Colten|Cfb|MGI:1861129|17||||||||||||||||No|||||||||||||Homozygotes for targeted null mutations lack the alternative complement pathway, and have reduced overall complement activity.Abnormal complement cascade:total hemolytic complement activation was reduced 50% in mutant sera.Impaired complement alternative pathway:* serum from mutant mice showed no evidence of C3 deposition on zymosan.* serum from mutant mice did not support in vitro cleavage of C3 by cobra venom factor.* alternative pathway-dependent hemolytic activity was undetectable in mutant serum.||C57BL/6 x 129|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|||Brother x Sister|No|04-Jul-2007|Cryopreserved sperm|148.0|0.0|Unknown||complement, C3, alternative pathway|Yes| 8585.0|ENU42:108:P2rx7:G3|C57BL/6NCrlAnu-P2rx7/AnuApb||Recessive|purinergic receptor P2X, ligand-gated ion channel, 7|P2rx7||P2X(7), P2X7R, P2X7 receptor|MGI:1339957||||5|||||||||||||||||||||||||||||||C57BL/6NCrlAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|05-Oct-2018|Cryopreserved sperm|33.0|0.0|Unknown||ENU|Yes| 120.0|Cblb KO|B6.129P2-Cblb/AnuApb|B6.129P2-Cblb/AnuApb|Recessive|Casitas B-lineage lymphoma b|Cblb|Nil|Cbl-b|MGI:2146430|targeted mutation 1, Josef M Penninger|Cblb|MGI:2180570|16||||||||||||||||Yes|||||||||||||Homozygotes for targeted null mutations exhibit elevated IL2 production by T cells, develop spontaneous autoimmunity, and are highly susceptible to experimental autoimmune encephalomyelitis.||B6/129 intercross, bred with wild type B10.BR|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|1|2||No|06-Feb-2006|Cryopreserved sperm|63.0|0.0|No||IL-2, T cell, encephalomyelitis, autoimmune, signal transduction|Yes| 4826.0|Huon|ENU8CAT:069||Recessive|||||||||Unknown|||||||||||||||||transgene insertion 3, Christopher C Goodnow|Rat insulin promoter|Expression of the inserted sequence specifically to pancreatic islet beta cells||||||||||Mice carrying the ins-HEL gene have a subclinical predisposition to diabetes due to islet cell failure. Mice carrying the insHEL and TCR transgenes have asubclinical predisposition to autoimmune destruction of the beta cell. Screening mice by urine glucose test. High glucose levels indicate diabetes and thus autoimmunity. "Early onset diabetes" definition changed during screen from approx 80 days to 40 days.||C57BL/6 x C57BL/10BR x CBA|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|||Breed diabetic Double transgenic with a non transgenic sib for next generation|No|24-Sep-2009|Cryopreserved sperm|15.0|0.0|Yes|Type I Diabetes|ENU, Singapore, autoimmunity, T cell, B cell, glucose|No| 4826.0|Huon|ENU8CAT:069||Recessive||||||||||||||||||||||||||transgene insertion 1, Mark M Davis||||||||||||Mice carrying the ins-HEL gene have a subclinical predisposition to diabetes due to islet cell failure. Mice carrying the insHEL and TCR transgenes have asubclinical predisposition to autoimmune destruction of the beta cell. Screening mice by urine glucose test. High glucose levels indicate diabetes and thus autoimmunity. "Early onset diabetes" definition changed during screen from approx 80 days to 40 days.||C57BL/6 x C57BL/10BR x CBA|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|||Breed diabetic Double transgenic with a non transgenic sib for next generation|No|24-Sep-2009|Cryopreserved sperm|||Yes|Type I Diabetes|ENU, Singapore, autoimmunity, T cell, B cell, glucose|No| 5870.0|K5Cre;Ptc1/Ptc2||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5871.0|K5mOVA||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 1528.0|B6.TNF-/-|C57BL/6-Tnf/AnuApb||Recessive|tumor necrosis factor|Tnf|Nil|DIF, TNF alpha, TNF-alpha, Tnfa, TNFalpha, Tnfsf1a, tumor necrosis factor-alpha|MGI:104798|targeted mutation 1, Johnathon D Sedgwick|Tnf|MGI:1860953|17||||||||||||||||No|||||||||||||Tnf–/– mice developed normally apart from absence of Peyer’s patches and abnormal microarchitectural lymphoid structure in secondary lymphoid tissues. Although the T and B cell number was not affected, T and B cell regions in lymphoid follicles were disorganized and primary B cell follicles and germinal centers were absent.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|05-Jul-2007|Cryopreserved sperm|225.0|0.0|Unknown||B cell, T cell, peyer's patches, infection, germinal centre|Yes| 5272.0|MA (p523) ; B6-TgN(MsLLD-MUSMH2Kb)XMZ|C57BL/6-Tg(H2-K-Thdb)Xmz||Dominant||||||||||||||||||||||||||Mouse soluble lectin-like domain of thrombomodulin with FLAG tag|H2-K|||||||||||Strong expression of mouse soluble lectin-like domain in lymphocytes and endothelial cells and secretion into circulating blood; no deleterious effect Phenotype does not differ from a wildtype of the same genetic background.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|26-Oct-2010||0.0|0.0|Unknown||mitogen activated protein kinase (MAP), NFkB, neutrophil, adhesion|Possibly| 83.0|Tipsy|NOD;B6JSfdAnu-Arhgap10/AnuApb|NOD;B6JSfdAnu-Arhgap10/AnuApb|Recessive|Rho GTPase activating protein 10|Arhgap10|Unknown|PSGAP-m, PSGAP-s|MGI:1925764|Rho GTPase activating protein 10; mutation 1, The Australian National University|Arhgap10|MGI:5563425|8|ENSMUSG00000037148|ENSMUST00000076316|Arhgap10-202|2094|2218|C to A|ENSMUSE00000249793|21|698|Serine to Serine|||||AATATGCAGTCTCCAACCACACCAAGCTCCAACCCAGCTGGAACACCTCCTTCACCCAGAA|Yes|||||||||||||Weak and ataxic hindlimbs evident after 100 days of age, splayed hindlimbs. Those animals displaying weaker phenotype can be detected with rotor-rod technique. Full histology requested by APN. Video available. Severely affected cannot breed. Phenotype unique to this chromosomal location. There is a QTL associated with engailed.||C57BL/6 x NODk|Yes|No|Yes|Yes|No|Yes|No|Poor||||No|06-Feb-2006|Cryopreserved sperm|175.0|0.0|Unknown||Ataxia, Hindlimb, Weakness, ENU|Yes| 3943.0|TPBcreC2B6Δ|B6.CD1-Tg(Tpbpa-Cre-GFP)5 Cited2/Apb||Dominant|Cbp/p300-interacting transactivator, with Glu/Asp-rich carboxy-terminal domain, 2|Cited2|Unknown|Mrg1, Msg2, p35srj|MGI:1306784|targeted mutation 1, Sally L Dunwoodie|Cited2|MGI:3696061|10||||||||||||||||Yes|Cre recombinase|5.4 kb of the trophoblast specific protein alpha (Tpbpa) promoter|||||||||||Not examined|Normal|C57BL/6 x CD1|No|No|Yes|No|No|Yes|No|Good|||This allele is kept with another one ie the TPB/+;+/+ X +/+;C2B6/+|No|17-Oct-2008|Cryopreserved sperm|57.0|0.0|Unknown||Trophoblast giant cells, placenta, GFP, transcription factor, embryonic lethal|Yes| 7746.0|ENU33:G1|ANU:ENU33:G1||Recessive|Unknown||||||||Unknown||||||||||||||||Unknown|||||||||||||Unknown|Unknown|C57BL/6NCrlAnu|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||1||No|02-Oct-2014|Cryopreserved sperm|1509.0|0.0|Unknown||ENU, random, mutagenesis, screen|Yes| 8561.0|Cav1|BALB/c-Cav1/OnjcriApb||Recessive|caveolin 1, caveolae protein|Cav1|Unknown|Cav-1, caveolin-1|MGI:102709||||6|||||||||||||||||||||||||||||Null mutant females do not breed well and pups may be unable to feed due abnormal mammary gland development during pregnancy and abnormal lactation in the mother and/or low levels of fat tissue.|Normal|BALB/c|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|18-Sep-2018|Cryopreserved sperm|50.0|0.0|Unknown|||Yes| 4744.0|ICOS KO|C57BL/6-Icos/AnuApb||Recessive|inducible T-cell co-stimulator|Icos|Nil||MGI:1858745|Name: targeted mutation 1, Richard A Flavell|Icos|MGI:2683635|1||||||||||||||||No|||||||||||||Immune system phenotype: T lymphocyte development normal in the thymus.Abnormal interferon level: Ifn-gamma levels were normal to slightly increasedAbnormal interleukin level: Il-2 production defective, Il-4 production very low, Il-10 levels normal, Il-13 levels reduced.Small lymph nodes: lymph nodes were small in immunized miceabout 1/2 as many cells/node as in wild-type miceAbnormal immunoglobulin level: decreased IgE level, decreased IgG1 level.Abnormal T-helper 2 physiology: defect indicated by low Il-4 levels and low IgG1 and IgE levels, Th2 differentiation normal but function disruptedIncreased susceptibility to experimental autoimmune encephalomyelitis.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|27-Apr-2009|Cryopreserved sperm|38.0|0.0|Unknown||CD28, T cell, germinal centre, IgG, humoral immunity|Yes| 5368.0|NOD.Bid|NOD;129S1(B6)-Bid||Recessive|BH3 interacting domain death agonist|Bid|Nil||MGI:108093|BH3 interacting domain death agonist; targeted mutation 1.1, Andreas Strasser|Bid|MGI:4440571|6||||||||||||||||No|||||||||||||Decreased sensitivity to induced morbidity/mortality: * unlike wild-type mice that die from fatal hepatitis within 3?4 hr of anti-Fas antibody treatment, all mutants survive. * homozygous mice develop and age normally and have no increased incidence of tumor development. * cell subset composition and total cellularity of thymus, spleen, and lymph nodes were normal.Cellular phenotype: unlike other reports, hematopoietic cell and fibroblasts from homozygous mice are normally sensitive to apoptotic stimuli including DNA damage and gamma-irradiation or treatment with etoposide.||NOD|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|21-Dec-2010||0.0|0.0|Unknown||apoptosis, Bcl2, Islet, DNA damage, cell cycle|Yes| 5574.0|Shmu|C.C3H-Shamu/AnuApb||Semi-dominant|shamu|Shmu|||MGI:3047697|shamu|Shmu|MGI:3047738|9|||||||||||||||||||||||||||||Embryonic lethal, possibly at or before gastrulation|White ventral spotting, a head spot, a mild distal tail kink, and white feet|C3H/HeH|No|No|Yes|No|No|Yes|No|Good|19|0|Heterozygous carrier aniamals are paired with C3H/HeH animals|No|01-Sep-2011|Cryopreserved sperm|50.0|0.0|Unknown||ENU, neural crest|Yes| 5448.0|Idd14 R11|NOD.B6-Idd14 R11||Recessive||||||||||||||||||||||||||||||||||||||Unknown|Unknown|NOD/Lt|Yes|Yes|Unknown|Yes|Yes|Unknown|No|Unknown||||Yes|01-Mar-2011|Cryopreserved sperm|50.0|0.0|Unknown|||No| 5372.0|B6 gR/GP|B6.Cg-Tg(Ins2-dnIfngr1)10Wehi Tg(ins2-GP)34-20Olds||Dominant||||||||||||||||||||||||||dominant negative interferon gamma receptor|rat insulin promoter (Ins2) (RIP)|||||||||||These mice were still capable of upregulatingMHC class I on islets, similarly to other cytokine-deficientmice, which was sufficient to render RIP-R/glycoprotein+ islets susceptible to perforin-mediated lysis in vitro. Surprisingly, such double transgenic mice did not develop type 1 diabetes to a significant degree (<10%, 1 of 12 mice F3 or 0 of 5 mice F4, compared with a >50% type 1 diabetes incidence in RIP-glycoprotein single transgenic controls.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|21-Dec-2010||0.0|0.0|Unknown||CTL, cytotoxic, perforin, interferon, islet, MHC|Yes| 5372.0|B6 gR/GP|B6.Cg-Tg(Ins2-dnIfngr1)10Wehi Tg(ins2-GP)34-20Olds||Dominant||||||||||||||||||||||||||transgene insertion 34-20, Michael BA Oldstone, MD|rat insulin promoter (RIP) (Ins2)|||||||||||These mice were still capable of upregulatingMHC class I on islets, similarly to other cytokine-deficientmice, which was sufficient to render RIP-R/glycoprotein+ islets susceptible to perforin-mediated lysis in vitro. Surprisingly, such double transgenic mice did not develop type 1 diabetes to a significant degree (<10%, 1 of 12 mice F3 or 0 of 5 mice F4, compared with a >50% type 1 diabetes incidence in RIP-glycoprotein single transgenic controls.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|21-Dec-2010||||Unknown||CTL, cytotoxic, perforin, interferon, islet, MHC|Yes| 8505.0|NOD.Nkrplb.CD45.2|NOD.Nkrplb.CD45.2||Recessive|CD45.2||||||||Unknown||||||||||||||||||||killer cell lectin-like receptor subfamily B member 1B|Klrb1b||Klrb1d, Ly55b, Ly55d, Nkrp1-b, NKR-P1B, Nkrp1d, NKR-P1D|MGI:107539||||6|Mice that are homozygous for this allele are viable, fertile, normal in size.||NOD/Lt|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|10|||No|08-Jun-2018|Cryopreserved sperm|49.0|0.0|Unknown||Nk1.1, TCR, NK cell, autoimmunity|Yes| 8511.0|NOD.CD45.2|NOD.CD45.2||Recessive|CD45.2||||||||Unknown|||||||||||||||||||||||||||||Mice that are homozygous for this allele are viable, fertile, normal in size.||NOD/Lt|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|10|||No|08-Jun-2018|Cryopreserved sperm|49.0|0.0|Unknown||Nk1.1, TCR, NK cell, autoimmunity|Yes| 7747.0|ENU33:G2|ANU:ENU33:G2||Recessive|Unknown||||||||Unknown||||||||||||||||Unknown|||||||||||||Unknown|Unknown|C57BL/6NCrlAnu|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||1||No|02-Oct-2014|Cryopreserved sperm|1995.0|0.0|Unknown||ENU, random, mutagenesis, screen|Yes| 6674.0|NORIEGAS|BALB/c.B6-Stat6/ANU/Ausb||Recessive|signal transducer and activator of transcription 6|Stat6|Nil||MGI:103034|signal transducer and activator of transcription 6; targeted mutation 1, Shizuo Akira|Stat6|MGI:2386746|10|||||||||||||||||||||||||||||||BALB/c|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|02-Dec-2011||0.0|0.0|Unknown||Stat6, IL4|Yes| 8508.0|NOD.Nkrplb.Slam1A|NOD.Nkrplb.Slam1A||Recessive|||||||||||||||||||||||||||||killer cell lectin-like receptor subfamily B member 1B|Klrb1b||Klrb1d, Ly55b, Ly55d, Nkrp1-b, NKR-P1B, Nkrp1d, NKR-P1D|MGI:107539||||6|Mice that are homozygous for this allele are viable, fertile and normal in size.Congenic Nk Cell Marker. Congenic Marker for NKT1 region. Congenic Marker for Slam1d region. Increased Nkt cell numbers.||NOD/Lt|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|10|||No|08-Jun-2018|Cryopreserved sperm|49.0|0.0|Unknown||Nk1.1, TCR, NK cell, autoimmunity|Yes| 8508.0|NOD.Nkrplb.Slam1A|NOD.Nkrplb.Slam1A||Recessive|||||||||||||||||||||||||||||slam1a||||||||Unknown|Mice that are homozygous for this allele are viable, fertile and normal in size.Congenic Nk Cell Marker. Congenic Marker for NKT1 region. Congenic Marker for Slam1d region. Increased Nkt cell numbers.||NOD/Lt|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|10|||No|08-Jun-2018|Cryopreserved sperm|||Unknown||Nk1.1, TCR, NK cell, autoimmunity|Yes| 4834.0|6CAT:040|ENU6CAT:040||Recessive|||||||||Unknown|||||||||||||||||transgene insertion 3, Christopher C Goodnow|Rat insulin promoter|Expression of the inserted sequence specifically to pancreatic islet beta cells||||||||||Mice carrying the ins-HEL gene have a subclinical predisposition to diabetes due to islet cell failure. Mice carrying the insHEL and TCR transgenes have asubclinical predisposition to autoimmune destruction of the beta cell. Screening mice by urine glucose test. High glucose levels indicate diabetes and thus autoimmunity. "Early onset diabetes" definition changed during screen from approx 80 days to 40 days.||C57BL/6 x C57BL/10BR x CBA|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|||Breed diabetic Double transgenic with a non transgenic sib for next generation|No|24-Sep-2009|Cryopreserved sperm|45.0|0.0|Yes|Type I Diabetes|ENU, JDRF, autoimmunity, T cell, B cell, glucose|No| 4834.0|6CAT:040|ENU6CAT:040||Recessive||||||||||||||||||||||||||transgene insertion 1, Mark M Davis||||||||||||Mice carrying the ins-HEL gene have a subclinical predisposition to diabetes due to islet cell failure. Mice carrying the insHEL and TCR transgenes have asubclinical predisposition to autoimmune destruction of the beta cell. Screening mice by urine glucose test. High glucose levels indicate diabetes and thus autoimmunity. "Early onset diabetes" definition changed during screen from approx 80 days to 40 days.||C57BL/6 x C57BL/10BR x CBA|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|||Breed diabetic Double transgenic with a non transgenic sib for next generation|No|24-Sep-2009|Cryopreserved sperm|||Yes|Type I Diabetes|ENU, JDRF, autoimmunity, T cell, B cell, glucose|No| 5886.0|Lifeact-RFP||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 7560.0||SJL/Mrit-MRI28562|SJL/Mrit-MRI28562|Dominant|unknown||Unknown||||||Unknown|||||||||||||||||||||||||||||Unknown|Heterozygous mice display a slight decrease growth phenotype|SJL/J|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Good||||No|07-Jan-2014|Cryopreserved sperm|60.0|0.0|Unknown||growth, ENU|Yes| 7561.0||B6/Mrit-106370|B6/Mrit-106370|Dominant|unknown||Unknown||||||Unknown|||||||||||||||||||||||||||||Unknown|Heterozygous mice display an harmonious and transient growth increase|C57BL/6|No|No|Yes|No|No|Yes|No|Good||||No|07-Jan-2014|Cryopreserved sperm|30.0|0.0|Unknown||growth , ENU|Yes| 6673.0|HOMER|FVB/N-Cd151/Ausb||Recessive|CD151 antigen|Cd151|Nil|PETA-3, SFA-1, Tspan24|MGI:1096360|CD151 antigen; targeted mutation 1, Arnoud Sonnenberg|Cd151|MGI:3691076|7|||||||||||||||||||||||||||||Weight loss:*Exhibit substantial loss of body weight before 9 months of age.Increased urine protein level:*Develop proteinuria before 3 weeks of age which progresses to massive proteinuria with age. AlbuminuriaTubulointerstitial nephritis:*Focal interstitial inflammation in close proximity to interlobular blood vessels.Abnormal kidney morphology:*Mice exhbit renal abnormalities that are seen in patients with nephropathy with pretibial epidermolysis bullosa and deafness, however do no develop the typical skin or hearing abnormalities.*Severely affected kidneys are contracted. Abnormal renal glomerular capsule morphology: *Capsules are granulated because of cortical degeneration in severely affected kidneys. Absent podocyte foot process: *Exhibit loss of podocyte foot processes. Podocyte foot process effacement: *Foot processes in contact with the abnormal GBM are effaced. Absent podocyte slit diaphragm: *Exhibit complete loss of glomerular epithelial slit diaphragm architecture. *Glomerulosclerosis precedes the loss of glomerular epithelial slit diaphragm components. Abnormal renal glomerulus basement membrane morphology: *Glomerular basement membrane (GBM) of some capillary loops is disorganized, laminated, abnormally thick and forms extensive spikes. Increased renal glomerulus basement membrane thickness: *GBM of some capillary loops is abnormally thick. Abnormal renal glomerulus morphology: Abnormal glomerular capillary endothelium morphology: *The capillary endothelium is swollen. Abnormal glomerular endothelium fenestra morphology: *Fenestrations are occasionally lost. Expanded mesangial matrix: *Show expansion of the mesangial matrix. Glomerulosclerosis: *Exhibit focal glomerulosclerosis; glomeruli are segmentally or globally sclerosed with extensive deposits of basement membrane components. Renal glomerular synechia: *Tuft adhesions to Bowman's capsule with extracapillary cell proliferation and fibrosis are observed. Renal interstitial fibrosis: *Exhibit interstitial and periglomerular fibrosis. Abnormal proximal convoluted tubule morphology: *Proximal tubules either show degeneration of varying severity or are dilated. Dilated proximal convoluted tubules: *Proximal tubules are either dilated or show degeneration of varying severity. Renal cast: *In severe cases, proximal tubules exhibit protein casts indicative of proteinuria.Kidney failure:*Develop severe renal failure, caused by progressive abnormalities of the glomerular basement membrane, loss of podocyte foot processes, glomeruloscelrosis, and cystic tubular dilation.Abnormal glomerular capillary endothelium morphology:*The capillary endothelium is swollen. Abnormal glomerular endothelium fenestra morphology: *Fenestrations are occasionally lost.Hearing/vestibular/ear phenotype:*Do not exhibit a hearing impairment.Integument phenotype:*Skin integrity is not impaired.||FVB/N|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|02-Dec-2011||0.0|0.0|Unknown||CD151, Kidney failure, alpha3beta1, podocyte|Yes| 8506.0|NOD.Nkrplb.CD45.2.A8Ca|NOD.Nkrplb.CD45.2.A8Ca||Recessive|CD45.2||||||||Unknown||||||||||||||||||||killer cell lectin-like receptor subfamily B member 1B|Klrb1b||Klrb1d, Ly55b, Ly55d, Nkrp1-b, NKR-P1B, Nkrp1d, NKR-P1D|MGI:107539||||6|Mice that are homozygous for this allele are viable, fertile, normal in size.||NOD/Lt|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|10|||No|08-Jun-2018|Cryopreserved sperm|49.0|0.0|Unknown||Nk1.1, TCR, NK cell, autoimmunity|Yes| 4188.0|(SOCS1/RIP)|B6.Cg-Socs1 Socs1 Tg(Ins2-cre)25Mgn/Apb||Recessive|suppressor of cytokine signaling 1|Socs1|Nil|Cish1, Cish7, JAB, JAK-binding protein, JAK2-binding protein, SOCS-1, SSI-1, STAT-induced STAT inhibitor 1|MGI:1354910|suppressor of cytokine signaling 1|Socs1|MGI:1934607|16||||||||||||||||Yes|transgene insertion 25, Mark A Magnuson |rat insulin promoter 2|||||||||||Mice with SOCS1 targeted mutation in beta cells develop normally.|Normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Poor||12|Heterozygous For Cre transgene (T/+) and for SOCS1c with SOCS1 KO (fl/-)|No|19-Dec-2008|Cryopreserved sperm|50.0|0.0|Unknown||cytokine signalling, beta cells, phosphorylation, Glucose|Yes| 4188.0|(SOCS1/RIP)|B6.Cg-Socs1 Socs1 Tg(Ins2-cre)25Mgn/Apb||Recessive|suppressor of cytokine signaling 1|Socs1|Unknown|Cish1, Cish7, JAB, JAK-binding protein, JAK2-binding protein, SOCS-1, SSI-1, STAT-induced STAT inhibitor 1|MGI:1354910|targeted mutation 3, Walter and Eliza Hall Institute of Medical Research|Socs1|MGI:2656917|16||||||||||||||||No|||||||||||||Mice with SOCS1 targeted mutation in beta cells develop normally.|Normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Poor||12|Heterozygous For Cre transgene (T/+) and for SOCS1c with SOCS1 KO (fl/-)|No|19-Dec-2008|Cryopreserved sperm|||Unknown||cytokine signalling, beta cells, phosphorylation, Glucose|Yes| 5085.0|APN24|B6.129Ola-Setdb1/MIMR||Recessive|SET domain, bifurcated 1|Setdb1|Unknown|ESET, KMT1E, mKIAA0067||gene trap RRK370, BayGenomics|Gt(RRK370)Byg||3||||||||||||||||Yes|||||||||||||Unknown for this mutation.Homozygous inactivation of this locus results in peri-implantation lethality. Inner cell mass growth is impaired in null blastocysts.||C57BL/6 x 129|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|09-Apr-2010|Cryopreserved sperm|72.0|0.0|Unknown||Genetrap, APN, ES cell|No| 4850.0||ENU6CAT:09||Recessive|Unknown||||||||Unknown|||||||||||||||||transgene insertion 3, Christopher C Goodnow|Rat insulin promoter|Expression of the inserted sequence specifically to pancreatic islet beta cells||||||||||Male infertility. Mutant found in HEL:TCR ENU library.HEL:TCR transgenes not required for mutant phenotype||C57BL/6 x CBA x C57BL/10BR|Yes|Yes|Yes|Yes|No|Yes|No|Poor||||No|24-Sep-2009|Cryopreserved sperm|15.0|0.0|Yes|Male Infertility|ENU, fertility, sperm|No| 4850.0||ENU6CAT:09||Recessive||||||||||||||||||||||||||transgene insertion 1, Mark M Davis||||||||||||Male infertility. Mutant found in HEL:TCR ENU library.HEL:TCR transgenes not required for mutant phenotype||C57BL/6 x CBA x C57BL/10BR|Yes|Yes|Yes|Yes|No|Yes|No|Poor||||No|24-Sep-2009|Cryopreserved sperm|||Yes|Male Infertility|ENU, fertility, sperm|No| 7381.0|Dicer|B6.129-Dicer1/WehiAnuApb||Recessive|dicer 1, ribonuclease type III|Dicer1|||MGI:2177178|dicer 1, ribonuclease type III; targeted mutation 1, Brian D Harfe|Dicer1|MGI:3589208|12|||||||||||||||||||||||||||||Normal||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|25-Jul-2013|Cryopreserved sperm|59.0|0.0|Unknown||microRNA, Cre|Yes| 7748.0|DBC3-cre|C57BL/6-Brinp3/MarpApb||Recessive|bone morphogenetic protein/retinoic acid inducible neural specific 3|Brinp3|Nil|B830045N13Rik, Fam5c|MGI:2443035||||1|||||||||||||||||||||||||||||Normal|Normal|C57BL/6|Yes|Yes|Yes|Unknown|Unknown|Unknown|No|Good|10||From hetrozygous breeding|No|02-Oct-2014||0.0|0.0|Unknown|||Yes| 8507.0|NOD.Nkrplb.CD45.2.CD-1|NOD.Nkrplb.CD45.2.CD-1||Recessive|||||||||||||||||||||||||||||killer cell lectin-like receptor subfamily B member 1B|Klrb1b||Klrb1d, Ly55b, Ly55d, Nkrp1-b, NKR-P1B, Nkrp1d, NKR-P1D|MGI:107539||||6|Mice that are homozygous for this allele are viable, fertile, normal in size.||NOD/Lt|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|10|||No|08-Jun-2018|Cryopreserved sperm|49.0|0.0|Unknown||Nk1.1, TCR, NK cell, autoimmunity|Yes| 6845.0|Dhfr|SJL/Mrit-Dhfr/MritApb||Dominant|Dihydrofolate reductase|Dhfr|Unknown|8430436I03Rik|MGI:94890|Dhfr;MRI32666R|Dhfr||13||||||||||||||||||||||||||||||Normal red blood cells parameters.Normal susceptibility to P. chabaudi infection.|SJL|No|No|Yes|No|No|Yes|No|Good||||No|12-Mar-2012|Cryopreserved sperm|50.0|0.0|Yes|Maturity onset diabetes of the young 2|Dihydrofolate reductase, ENU|Yes| 4855.0|Piaf|ENU7B6:022:B10BR||Recessive|||||||||Unknown||||||||||||||||Yes|||||||||||||Ataxia||C57BL/6 x C57BL/10BR|Yes|No|Yes|Yes|No|Yes|No|Unknown||||No|24-Sep-2009|Cryopreserved sperm|75.0|0.0|Unknown||ataxia, ENU|Yes| 6843.0|Lepr|B6.Cg-Dock7 Lepr/++/JAusb||Recessive|dedicator of cytokinesis 7|Dock7|Normal|3110056M06Rik, LOC242555, m, mKIAA1771|MGI:1914549|dedicator of cytokinesis 7; misty|Dock7|MGI:1856946|4|||||||||||||||||||||||||||||Displays a mellitus diabetes at 3-4 weeks of age|The phenotype is normal|C57BL/6|Yes|No|Yes|Yes|No|Yes|No|Good||||No|12-Mar-2012|Cryopreserved sperm|50.0|0.0|Yes|Diabetes|Obesity, Leptin receptor gene, melanocyte|No| 6843.0|Lepr|B6.Cg-Dock7 Lepr/++/JAusb||Recessive|leptin receptor|Lepr|Normal|Leprb, LEPROT, leptin receptor gene-related protein, Modb1, OB-RGRP, obese-like, obl, Obr|MGI:104993|leptin receptor; diabetes|Lepr|MGI:1856009|4|||||||||||||||||||||||||||||Displays a mellitus diabetes at 3-4 weeks of age|The phenotype is normal|C57BL/6|Yes|No|Yes|Yes|No|Yes|No|Good||||No|12-Mar-2012|Cryopreserved sperm|||Yes|Diabetes|Obesity, Leptin receptor gene, melanocyte|No| 5568.0|Klf3-LoxP|B6;129-Klf3||Dominant|Kruppel-like factor 3 (basic)|Klf3||BKLF, Bklf, Tef-2|MGI:1342773||||5|||||||||||||||||||||||||||||Unknown|Unknown|C57BL/6 x 129|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|26-Aug-2011|Cryopreserved sperm|50.0|0.0|Unknown||Cre recombinase, conditional|No| 5273.0|MB (p535) ; B6-TgN(MsLLD-MUSMAlbumin)XMZ|C57BL/6-Tg(Alb-Thdb)Xmz||Dominant||||||||||||||||||||||||||Mouse soluble lectin-like domain of thrombomodulin with FLAG tag|albumin|Strong||||||||||Strong expression of mouse soluble lectin-like domain in liver and secretion into circulating blood; no deleterious effects Phenotype does not differ from a wildtype of the same genetic background.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|26-Oct-2010||0.0|0.0|Unknown||mitogen activated protein kinase (MAP), NFkB, neutrophil, adhesion|Possibly| 8509.0|NOD.Nkrplb.Slam1B|NOD.Nkrplb.Slam1B||Recessive|||||||||||||||||||||||||||||killer cell lectin-like receptor subfamily B member 1B|Klrb1b||Klrb1d, Ly55b, Ly55d, Nkrp1-b, NKR-P1B, Nkrp1d, NKR-P1D|MGI:107539||||6|Mice that are homozygous for this allele are viable, fertile and normal in size.Congenic Nk Cell Marker. Congenic Marker for NKT1 region. Congenic Marker for Slam1d region. Increased Nkt cell numbers.||NOD/Lt|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|10|||No|08-Jun-2018|Cryopreserved sperm|49.0|0.0|Unknown||Nk1.1, TCR, NK cell, autoimmunity|Yes| 8509.0|NOD.Nkrplb.Slam1B|NOD.Nkrplb.Slam1B||Recessive|||||||||||||||||||||||||||||slam1b||||||||Unknown|Mice that are homozygous for this allele are viable, fertile and normal in size.Congenic Nk Cell Marker. Congenic Marker for NKT1 region. Congenic Marker for Slam1d region. Increased Nkt cell numbers.||NOD/Lt|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|10|||No|08-Jun-2018|Cryopreserved sperm|||Unknown||Nk1.1, TCR, NK cell, autoimmunity|Yes| 8562.0|MMP-12|BALB/c-Mmp12/OnjcriApb||Recessive|matrix metallopeptidase 12|Mmp12|Unknown|macrophage elastase, Mmel, MMP12|MGI:97005||||9|||||||||||||||||||||||||||||The MMP-12 null mice look normal and are viable and fertile. They are less susceptible to stress/smoke-induced inflammation and emphysema. They have smaller litter sizes (~60% or wild type) due to placental abnormalities. MMP12 null macrophages lack degrading activity and are unable to invade through the basement membrane.|Normal|BALB/c|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|18-Sep-2018|Cryopreserved sperm|40.0|0.0|Unknown||Macrophage|Yes| 4893.0|Phenomix|Phx||Recessive|Unknown||||||||Unknown|||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|30-Sep-2009|Cryopreserved sperm|710.0|0.0|Unknown||ENU, Phenomix, screen|Possibly| 6946.0|ENU19 WT:022:a|ENU19 WT:022:a||Recessive|Unknown||||||||Unknown||||||||||||||||Unknown|||||||||||||Unknown|Unknown|C57BL/6JAnu|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||1||No|05-Jul-2012|Cryopreserved sperm|58.0|0.0|Unknown||ENU, random, mutagenesis, screen|Yes| 6844.0|Dudley 2|SJL/Mrit-Gck/MritApb||Dominant|Glucokinase|Gck|Unknown|Gk, hexokinase 4, HK4, MODY2|MGI:1270854|Glucokinase;MRI30862|Gck||11||||||||||||||||||||||||||||||HyperglycemiaHyperinsulinemiaGlucose intolerant|SJL|No|No|Yes|No|No|Yes|No|Good||||No|12-Mar-2012|Cryopreserved sperm|60.0|0.0|Yes|Maturity onset diabetes of the young 2|Diabetes, Glucokinase, ENU|Yes| 8510.0|NOD.H2b.Nkrplb.CD-1|NOD.H2b.Nkrplb.CD-1||Recessive|CD1 antigen complex|Cd1|Nil||MGI:102561|CD1 antigen complex; targeted mutation 1, Michael Grusby|Cd1|MGI:1857482|3||||||||||||||||||||killer cell lectin-like receptor subfamily B member 1B|Klrb1b||Klrb1d, Ly55b, Ly55d, Nkrp1-b, NKR-P1B, Nkrp1d, NKR-P1D|MGI:107539||||6|Difficult breeders. Have had to restart the breeding, multiple times due to the difficulty in getting them homozygous. Seems homozygous mice do not breed. Congenic Nk Cell Marker. Congenic Marker for NKT2 region. Increased Nkt cell numbers.Knockout lacking the CD1 antigen complex gene||NOD/Lt|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|10|||No|08-Jun-2018|Cryopreserved sperm|49.0|0.0|Unknown||Nk1.1, TCR, NK cell, autoimmunity|Yes| 8510.0|NOD.H2b.Nkrplb.CD-1|NOD.H2b.Nkrplb.CD-1||Recessive|||||||||||||||||||||||||||||H2b||||||||Unknown|Difficult breeders. Have had to restart the breeding, multiple times due to the difficulty in getting them homozygous. Seems homozygous mice do not breed. Congenic Nk Cell Marker. Congenic Marker for NKT2 region. Increased Nkt cell numbers.Knockout lacking the CD1 antigen complex gene||NOD/Lt|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|10|||No|08-Jun-2018|Cryopreserved sperm|||Unknown||Nk1.1, TCR, NK cell, autoimmunity|Yes| 9162.0|ASD1012:PB:2|ASD1012:PB:2||Semi-dominant|guanylate binding protein 2|Gbp2|||MGI:102772||||3|||||||||||||||||||||||||||||Normal|Normal|C57Bl/6N|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|12-Mar-2021|Cryopreserved sperm|56.0|0.0|Unknown|||Possibly| 6812.0|B/c.CD39.Tg.1079-4|C.Cg-Tg(H2-K-ENTPI)/SvhmApb||Dominant||||||||||||||||||||||||||Human ectonucleoside triphosphate diphosphohydrolase 1|H2-K|moderate/high||||||||||Unknown|Normal|BALB/c|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Good|18|||No|08-Feb-2012|Cryopreserved sperm|50.0|0.0|Unknown||Cd39|Possibly| 8563.0|MMP-9|BALB/c-Mmp9/OnjcriApb||Recessive|matrix metallopeptidase 9|Mmp9|Unknown|B/MMP9, Clg4b, gelatinase B, Gelatinase B, Gel B, MMP-9|MGI:97011||||2|||||||||||||||||||||||||||||MMP-9 null mice have a very mild bone phenotype (lengthening of the growth plates) that tends to normalize with age. |Normal|BALB/c|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|18-Sep-2018|Cryopreserved sperm|50.0|0.0|Unknown|||Yes| 5046.0|KRN14|KRN:014||Recessive|glutamate receptor, ionotropic, kainate 4|Grik4|Unknown|GluRgamma1, KA-1, KA1|MGI:95817||||9||||||||||||||||Yes|transgene insertion KRN, Diane Mathis|Natural TCR alpha and -beta promoter/enhancer elements.|||||||||||No arthritis, no GPI autoantibodies in KRN/H2g7 model.||C57BL/6 x NODk x C57BL/10 x Balb/b|Yes|Yes|Yes|Yes|Yes|Yes|No|Poor||||No|26-Feb-2010|Cryopreserved sperm|107.0|0.0|Yes||Autoimmunity, Arthritis, KRN, ENU|No| 5274.0|MC (p528) ; B6-TgN(LLD-CD4-MUSMH2Kb)XMZ|C57BL/6-Tg(H2-K-Thdb/CD4)Xmz||Dominant||||||||||||||||||||||||||Mouse lectin-like domain of thrombomodulin fused to human CD4|H2-K|Strong||||||||||Phenotype does not differ from a wildtype of the same genetic background. No deleterious phenotype: Strong expression of mouse lectin-like domain + human CD4 in lymphocytes and endothelial cells.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|26-Oct-2010||0.0|0.0|Unknown||mitogen activated protein kinase (MAP), NFkB, neutrophil, adhesion|Possibly| 5040.0|APN21|129/Ola-Rab10/MAS||Recessive|RAB10, member RAS oncogene family|Rab10|Unknown||MGI:105066|RAB10, member RAS oncogene family; gene trap XC820, BayGenomics|Rab10|MGI:4125038|12|||||||||||||||||||||||||||||Unknown|Unknown|C57BL/6 x 129/OlaHsd|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Good||||No|22-Feb-2010|Cryopreserved sperm|80.0|0.0|Unknown||ES cell|Yes| 7751.0|DBC3 knockout|C57BL/6-Brinp3/MarpApb||Recessive|bone morphogenetic protein/retinoic acid inducible neural specific 3|Brinp3|Nil|B830045N13Rik, Fam5c|MGI:2443035||||1|||||||||||||||||||||||||||||Normal|Normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|10||From hetrozygous breeding|No|02-Oct-2014|Cryopreserved sperm|50.0|0.0|Unknown|||Yes| 7752.0|DBC1 knockout|C57BL/6-Brinp1/MarpApb||Recessive|bone morphogenic protein/retinoic acid inducible neural specific 1|Brinp1|Nil|Dbc1, Dbccr1, Fam5a|MGI:1928478||||4|||||||||||||||||||||||||||||Behavioural phenotypes|Normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Poor|10||From hetrozygous breeding|No|02-Oct-2014|Cryopreserved sperm|50.0|0.0|Unknown|||Yes| 9173.0|ASD1118:Kif13a G318R:F0|C57Bl/6NCrlAnu-Kif13a/Apb||Semi-dominant|kinesin family member 13A|Kif13a|||MGI:1098264|Kif13a:endonuclease-mediated mutation 1, Australian National University|Kif13a||13|||||||||||||||||||||||||||||Mouse #14|unknown|C57Bl/6NCrl|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|08-Apr-2021|Cryopreserved sperm|12.0|0.0|Unknown|||Possibly| 5276.0|NOD-NGL|NOD-Tg(NFkB-eGFP/Luc)Het||Dominant||||||||||||||||||||||||||enhanced green fluorescent protein + luciferase|nuclear factor of kappa light polypeptide gene enhancer in B-cells 1, p105 ; NFkB|||||||||||Unknown||NOD/Lt x C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|28-Oct-2010||0.0|0.0|Unknown||Luciferase, NFkB|Possibly| 5280.0|NODBID/8.3|NOD.Cg-Bid Tg(TcraTcrbNy8.3)1Pesa||Recessive|BH3 interacting domain death agonist|Bid|Nil||MGI:108093|BH3 interacting domain death agonist; targeted mutation 1.1, Andreas Strasser|Bid|MGI:4440571|6||||||||||||||||No|transgene insertion 1, Pere Santamaria|TCR alpha and beta enhancers|||||||||||Mice may develop diabetes faster than wildtype.||NOD/Lt|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|28-Oct-2010||0.0|0.0|Yes|insulin-dependent diabetes mellitus (IDDM)|apoptosis, pancreas, islet, T cell|Possibly| 8512.0|NOD.Nkrplb.CD-1|NOD.Nkrplb.CD-1||Recessive|CD1 antigen complex|Cd1|Nil||MGI:102561|CD1 antigen complex; targeted mutation 1, Michael Grusby|Cd1|MGI:1857482|3||||||||||||||||||||killer cell lectin-like receptor subfamily B member 1B|Klrb1b||Klrb1d, Ly55b, Ly55d, Nkrp1-b, NKR-P1B, Nkrp1d, NKR-P1D|MGI:107539||||6|Difficult breeders. Have had to restart the breeding, multiple times due to the difficulty in getting them homozygous. Seems homozygous mice do not breed. Congenic Nk Cell Marker. Congenic Marker for NKT2 region. Increased Nkt cell numbers.Knockout lacking the CD1 antigen complex gene||NOD/Lt|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|10|||No|08-Jun-2018|Cryopreserved sperm|49.0|0.0|Unknown||Nk1.1, TCR, NK cell, autoimmunity|Yes| 7069.0|Momme D19|FVB/NJ-Smarcc1 Tg(Hba1-Gfp)1Ew/QimrApb||Semi-dominant|SWI/SNF related, matrix associated, actin dependent regulator of chromatin, subfamily c, member 1|Smarcc1|Unknown|BAF155, SRG3|MGI:1203524|SWI/SNF related BAF chromatin remodeling complex subunit C1; modifier of murine metastable epialleles, D19|Smarcc1|MGI:5515368|9||||||||||Unknown to Unknown|||||||transgene insertion 1, Emma Whitelaw|human alpha-globin promoter and enhancer region|11 copies||||||||||Lethal|HET LOSS|FVB/NJ|No|No|Yes|No|No|Yes|No|Good|||MommeD19<+/->;Tg(Hba1-Gfp)1Ew x Tg(Hba1-Gfp)1Ew|No|29-Aug-2012|Cryopreserved sperm|10.0|0.0|Unknown||ENU, epigenetics, suppressor of variegation|Possibly| 5275.0|NODTG950 ; NOD.B6-TgN(HUSOD1-HUSOD3-HUGPX-MUSMHH2KB)1Lt/J|NOD;B6-Tg(H2-K-GPX1,-SOD1,-SOD3/CD55)CCpj||Dominant||||||||||||||||||||||||||human CuZn superoxide dismutase (SOD1) tagged with a hemagglutinin epitope tag|H2-K|||||||||||Expression of all three enzymes was the only combination protective against hypoxia/reoxygenation. In contrast to single- and double-transgenic grafts, triple-transgenic grafts significantly improved control of blood glucose compared with wild type. ||NOD/Lt x C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|26-Oct-2010||0.0|0.0|Unknown||reactive oxygen species (ROS) , transplantation, islet, antioxidant, graft|Possibly| 5275.0|NODTG950 ; NOD.B6-TgN(HUSOD1-HUSOD3-HUGPX-MUSMHH2KB)1Lt/J|NOD;B6-Tg(H2-K-GPX1,-SOD1,-SOD3/CD55)CCpj||Dominant||||||||||||||||||||||||||human extracellular superoxide dismutase (SOD3) modified to include a glycosyl phosphatidylinositol (GPI) membrane linkage signal & tagged with a FLAG epitope tag|H2-K|||||||||||Expression of all three enzymes was the only combination protective against hypoxia/reoxygenation. In contrast to single- and double-transgenic grafts, triple-transgenic grafts significantly improved control of blood glucose compared with wild type. ||NOD/Lt x C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|26-Oct-2010||||Unknown||reactive oxygen species (ROS) , transplantation, islet, antioxidant, graft|Possibly| 5275.0|NODTG950 ; NOD.B6-TgN(HUSOD1-HUSOD3-HUGPX-MUSMHH2KB)1Lt/J|NOD;B6-Tg(H2-K-GPX1,-SOD1,-SOD3/CD55)CCpj||Dominant||||||||||||||||||||||||||human cellular glutathione peroxidase (Gpx-1) tagged with a histidine (6xHis) tag|H2-K|||||||||||Expression of all three enzymes was the only combination protective against hypoxia/reoxygenation. In contrast to single- and double-transgenic grafts, triple-transgenic grafts significantly improved control of blood glucose compared with wild type. ||NOD/Lt x C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|26-Oct-2010||||Unknown||reactive oxygen species (ROS) , transplantation, islet, antioxidant, graft|Possibly| 5890.0|LP/J||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5891.0|LUCIFERASE||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 712.0|NR4MD4|NOD.NOR-(D4Mit31-D4Mit310) Tg(IghelMD4)4Ccg||Dominant||||||||||||||||||||||||||transgene insertion 4, Christopher C Goodnow||High||||||||||||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|03-May-2007||0.0|0.0|Unknown||Immunoglobulin, diabetes, autoimmunity, hen egg lysozyme (HEL)|Yes| 712.0|NR4MD4|NOD.NOR-(D4Mit31-D4Mit310) Tg(IghelMD4)4Ccg||Dominant||||||||||||||||||||||||||Tg(ILK3mHEL)3Ccg|rat insulin promoter|||||||||||||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|03-May-2007||||Unknown||Immunoglobulin, diabetes, autoimmunity, hen egg lysozyme (HEL)|Yes| 818.0|Grb14 KO|B6.129-Grb14||Recessive|growth factor receptor bound protein 14|Grb14|Nil||MGI:1355324|targeted mutation 1, Roger J Daly|Grb14|MGI:3029164|2||||||||||||||||Yes|||||||||||||Improved glucose tolerance, lower circulating insulin levels, and increased incorporation of glucose into glycogen in the liver and skeletal muscle.||C57BL/6 x 129|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|21-May-2007||0.0|0.0|Unknown||insulin, kinase, phosphorylation, receptor, liver|Yes| 8565.0|ASD948:PKR 1bp ins:EIF2AK2|C57BL/6NCrlAnu-Eif2ak2/AnuApb||Recessive|eukaryotic translation initiation factor 2-alpha kinase 2|Eif2ak2|Unknown|2310047A08Rik, 4732414G15Rik, dsRNA-activated kinase, eIF-2 alpha, eIF-2 alpha, IFN-induced and double-stranded RNA-activated kinase, IFN- type I-induced and dsRNA-activated kinase, Pkr, Prkr, Tik|MGI:1353449|Eif2ak2, endonuclease-mediated mutation 1, Australian National University |Eif2ak2||17||||||||||Unknown to Unknown|||||||||||||||||||Normal|Normal|C57BL/6NCrlAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|20-Sep-2018|Cryopreserved sperm|33.0|0.0|Unknown|||Yes| 6823.0|MTf Tg #1|B6.129-Tg(UBC-Mfi2)43Drrn/Apb||Dominant||||||||||||||||||||||||||murin melanotransferrin|human unbiquitin c|ubiquitous||||||||||Normal.Mild but significant decrease of erythrocyte number in both male and female MTf Tg mice compared to the wildtype counterparts||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|24-Feb-2012|Cryopreserved sperm|30.0|0.0|Unknown||melanoma, melanotransferrin, iron, erythrocyte|Yes| 8513.0|ENU41:G2|ANU:ENU41:G2||Recessive|Unknown||||||||Unknown||||||||||||||||Unknown|||||||||||||Unknown|Unknown|C57BL/6NCrlAnu|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||1||No|12-Jun-2018|Cryopreserved sperm|145.0|0.0|Unknown||ENU, random, mutagenesis, screen|Yes| 5895.0|Ly6E||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 7070.0|Momme D4|FVB/NJ-Smarca5 Tg(Hba1-Gfp)1Ew/QimrApb||Semi-dominant|SWI/SNF related, matrix associated, actin dependent regulator of chromatin, subfamily a, member 5|Smarca5|Unknown|4933427E24Rik, D030040M08Rik, D330027N15Rik, MommeD4, Snf2h|MGI:1935129|SWI/SNF related, matrix associated, actin dependent regulator of chromatin, subfamily a, member 5; modifiers of murine metastable epiallele D4|Smarca5|MGI:3586551|8|ENSMUSG00000031715|ENSMUST00000043359|Smarca5-001|1558|1959|T to A|ENSMUSE00001218842|12|520|Tryptophan to Arginine|||||TATTAGACATTTTGGAAGATTATTGCATGTGGAGAAATTATGAGTACTGCAGGTTGGATGG||transgene insertion 1, Emma Whitelaw|human alpha-globin promoter and enhancer region|||||||||||Homozygous lethality E17|Normal|FVB/NJ|No|No|Yes|No|No|Yes|No|Good|||MommeD4<+/->;Tg(Hba1-Gfp)1Ew x Tg(Hba1-Gfp)1Ew|No|29-Aug-2012|Cryopreserved sperm|49.0|0.0|Unknown||ENU, epigenetics|Possibly| 1960.0|available from Animal Resources Centre - www.arc.wa.gov.au|C57BL/6JArc||Dominant|Inbred black: a, Cdh23, H-2||Unknown||||||Unknown||||||||||||||||No|||||||||||||Good breeding performance 0.56 young/female/wk., average litter 6.5. Active, long lived mouse (male and females 2+ years). Very low incidence of mammary tumours. Resistant to toxic effects of chloroform. High rate of spontaneous mutations at the agouti and W loci. Used commonly as the background for various mutant genes (eg. nude, beige, etc). Used in alcohol tolerance studies. Susceptible to the development of atheromatous lesions after 20 weeks on high fat diets. Develops non-insulin dependent diabetes mellitus and hypertension when fed high fat, high simple carbohydrate diet. Congenital abnormalities include microphthalmia and anophthalmia (8-20%) and hydrocephalus (1-3%) (Smith, R.S., Roderick, T.H. and Sundberg, J.P. (1994) Microphthalmia and associated abnormalities in inbred black mice. Laboratory Animal Science 44:551-560). Normal C5.|||Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||Yes|04-Sep-2007||0.0|0.0|Unknown|||Yes| 8515.0|ENU43:G2|ANU:ENU43:G2||Recessive|Unknown||||||||Unknown||||||||||||||||Unknown|||||||||||||Unknown|Unknown|C57BL/6NCrlAnu|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||1||No|12-Jun-2018|Cryopreserved sperm|8459.0|0.0|Unknown||ENU, random, mutagenesis, screen|Yes| 7564.0|ENU25:048:P2ry10:B6|C57BL/6NCrlAnu-P2ry10/AnuApb|C57BL/6NCrlAnu-P2ry10/AnuApb|X-linked|purinergic receptor P2Y, G-protein coupled 10|P2ry10|Unknown|5830408N17Rik, P2Y10|MGI:1926076|purinergic receptor P2Y, G-protein coupled 10; mutation 1, The Australian National University|P2ry10|MGI:5648450|X|ENSMUSG00000050921|ENSMUST00000053375|P2ry10-001|123|497|T to A|ENSMUSE00000710686|3|41|Serine to Arginine|||||ATATTCATCCCGGGTCTCCTGGCTAACAGTGCAGCCCTGTGGGTTCTGTGCCGCTTCATCA||||||||||||||Unknown|Unknown|C57BL/6NCrlAnu|Yes|Unknown|Yes|Yes|Unknown|Yes|No|Unknown||G4||No|14-Jan-2014|Cryopreserved sperm|60.0|0.0|Unknown||ENU, missense, mutation, MMP|Possibly| 7756.0|Confetti|B6.129P2-Gt(ROSA)26Sor/J||Dominant|gene trap ROSA 26, Philippe Soriano|Gt(ROSA)26Sor||beta geo, Gtrgeo26, Gtrosa26, R26, ROSA26|MGI:104735|targeted mutation 1, Hans Clevers|Gt(ROSA)26Sor||6|||||||||||||||||||||||||||||Mice homozygous for the R26R-Confetti conditional allele are viable and fertile, with a CAG promoter, loxP site, and STOP cassette preventing transcription of the downstream Brainbow 2.1 sequences.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|09-Oct-2014||0.0|0.0|Unknown||Fluorescent proteins|Yes| 1963.0|available from Animal Resources Centre - www.arc.wa.gov.au|CBA/CaHArc||Dominant|Inbred agouti: A, H-2||Unknown||||||Unknown||||||||||||||||No|||||||||||||Good breeders, 0.75 young/female/wk., average litter 5.5. Life span 17 months male, 24 months female. Shorter male life span has been attributed to a vitamin k deficiency in SPF animals. Low activity and docile. High overall tumour incidence (29% male and 55% female). Hepatomas 23.5% male 0% in female; mammary tumours 33% in female, 0% in male. Resistant to the induction of atherosclerosis by high fat diet. Widely distributed as a general purpose strain. Considerable variation between sublines, thus care must be exercised in comparing CBA subline data. High rate of spontaneous mutations. Normal C5.|||Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||Yes|04-Sep-2007||0.0|0.0|No|||Yes| 1975.0|available from Animal Resources Centre - www.arc.wa.gov.au|HRA/Skh-hr/Arc (Hairless)||Recessive||||||||||||||||||||||||||||||||||||||Born with hair and euthymic. Lose hair before weaning. Thymic atrophy by 6 months.||HRA/Skh|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|04-Sep-2007||0.0|0.0|Unknown||Hairless, coat, skin|Yes| 8514.0|ENU42:G2|ANU:ENU42:G2||Recessive|Unknown||||||||Unknown||||||||||||||||Unknown|||||||||||||Unknown|Unknown|C57BL/6NCrlAnu|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||1||No|12-Jun-2018|Cryopreserved sperm|3469.0|0.0|Unknown||ENU, random, mutagenesis, screen|Yes| 1958.0|available from Animal Resources Centre - www.arc.wa.gov.au|BALB/cArc||Dominant|Inbred albino: Tyrc, Tyrp1b, A, H-2d||Unknown||||||Unknown||||||||||||||||No|||||||||||||Good breeding performance, 0.75 young/female/wk., average litter 5.5. Long breeding life. Relatively robust and moderate life span (males and females 20 months). Low incidence of mammary tumours. Amyloidosis (40%) in older males. BALB/c mice can have high blood pressure; left auricular thrombosis and mineralisation common (66%) in older breeding females. Slightly aggressive. High social dominance exhibited by males in presence of females resulting in high aggression. Commonly used for ascites fluid production. Injection of mineral oil IP induces high incidence of transplantable plasmacytomas. Low mortality after neonatal thymectomy. Normal C5.|||Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||Yes|04-Sep-2007||0.0|0.0|No|||Yes| 8567.0|PKR 8bp del:EIF2AK2|C57BL/6NCrlAnu-Eif2ak2/AnuApb||Recessive|eukaryotic translation initiation factor 2-alpha kinase 2|Eif2ak2|Unknown|2310047A08Rik, 4732414G15Rik, dsRNA-activated kinase, eIF-2 alpha, eIF-2 alpha, IFN-induced and double-stranded RNA-activated kinase, IFN- type I-induced and dsRNA-activated kinase, Pkr, Prkr, Tik|MGI:1353449|Eif2ak2, endonuclease-mediated mutation 3, Australian National University |Eif2ak2||17||||||||||Unknown to Unknown|||||||||||||||||||Normal|Normal|C57BL/6NCrlAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|21-Sep-2018|Cryopreserved sperm|55.0|0.0|Unknown|||Yes| 6522.0|2MHC?|B6.129S2-H2/JAusb||Recessive|histocompatibility-2, MHC|H2|Nil|H-2, MHC-II|MGI:95894|histocompatibility-2, MHC; targeted deletion, H2 complex|H2|MGI:2658725|Unknown|||||||||||||||||||||||||||||Increased sensitivity to induced morbidity/mortality:*Following infection with either a low or high dose of IOE, mice succumb to the infection at 11 to 15 days and 7 to 9 days, respectively, compared to wild-type mice, which succumb at 14 to 17 days and 8 to 12 days, respectively.Increased susceptibility to bacterial infection:*Mice are more susceptible to infection with a monocytotropic Ehrlichia bacteria from Ixodes ovatrus ticks (IOE) than wild-type mice.*Following infection with either a low or high dose of IOE, mice succumb to the infection at 11 to 15 days and 7 to 9 days, respectively, compared to wild-type mice, which succumb at 14 to 17 days and 8 to 12 days, respectively.*Mice have higher burdens of Ehrlichia bacteria in all organs following infection than do wild-type mice.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown||MHC-II, Autoimmune disorders|Yes| 5411.0|NOD.HJ20-5|NOD/Lt-Tg(IL12B)HJ20-5Gem/ArcApb||Dominant||||||||||||||||||||||||||human interleukin 12b||||||||||||Mice express human interleukin 12B||NOD/Lt|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|10||Hom x Hom|No|03-Feb-2011|Embryo|0.0|0.0|Unknown||cytokine, interleukin, autoimmunity|Yes| 8516.0|MR1-tom|C57BL/6-Mr1||Recessive|major histocompatibility complex, class I-related|Mr1|Nil|H2ls, MR1|MGI:1195463||||1|||||||||||||||||||||||||||||Essentially normal but lacks a T cell known as a MAIT cell. |Normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|14-Jun-2018|Cryopreserved sperm|50.0|0.0|Unknown||T cell, MAIT|Yes| 8568.0|ASD801:TgPKR|B6(Cg)-Tg(Vav1-EIF2AK2)#Wsmay/AnuApb||Dominant||||||||||||||||||||||||||transgene insertion, W May|vav1||||||||||||peripheral blood counts from TgPKR mice decrease with age in association with dysplastic marrow changes. TgPKR mice have reduced colony-forming capacity and the colonies also are more sensitive to hematopoietic stresses. Furthermore, TgPKR mice have fewer hematopoietic stem/progenitor cells (HSPCs), and the percentage of quiescent (G0) HSPCs is increased. Importantly, treatment of TgPKR bone marrow (BM) with a PKR inhibitor specifically rescues sensitivity to growth factor deprivation. In contrast, marrow from PKR knockout (PKRKO) mice has increased potential for colony formation and HSPCs are more actively proliferating and resistant to stress. Significantly, TgPKR HSPCs have increased expression of p21 and IFN regulatory factor, whereas cells from PKRKO mice display mechanisms indicative of proliferation such as reduced eukaryotic initiation factor 2α phosphorylation, increased extracellular signal-regulated protein kinases 1 and 2 phosphorylation, and increased CDK2 expression.|C57BL/6J|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|21-Sep-2018||0.0|0.0|Unknown||Bone Marrow, Haemopoiesis|Yes| 322.0|C.B-17/IcrHanHsd-scid|C.B-17-Igh-1-Prkdc||Recessive|protein kinase, DNA activated, catalytic polypeptide|Prkdc|Unknown|DNA-PK, DNA-PKcs, DNAPDcs, DNPK1, HYRC1, slip, XRCC7|MGI:104779|severe combined immunodeficiency|Prkdc|MGI:1857113|16||||||||||||||||Yes|||||||||||||Mutations at this locus effect genome stability, radiation sensitivity and DNA repair. Nonsense (scid) and null homozygotes have severe combined immunodeficiency. Homozygotes have little or no immunoglobulin in serum. Lymphoid organs consist of vascular connective tissue and macrophages and are devoid of lymphocytes. Bone marrow lacks plasma cells and lymphocytes and skin lacks dendritic Thy-1+ epidermal cells. Although B and T-cells and pre-B and pre-T cells are absent early B and T-cells are present. A variable percentage (2-20%) of young adults develop low numbers of functional B and T-cells. This is not genetically determined. Macrophage activation and antigen presentation, NK cell activity and myeloid cell differentiation is normal.||CB17|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|05-May-2006||0.0|0.0|Yes||scid, T cell, B cell, lymphocyte, immunoglobulin|Yes| 7757.0|MMTV/cre|STOCK Tg(MMTV-cre)1Mam/JAusb||Dominant||||||||||||||||||||||||||transgene insertion, Lothar Hennighausen|mouse mammary tumor virus (MMTV) long terminal repeat|secretory epithelium of the mammary gland, the salivary gland and in the female germline||||||||||This transgenic strain expresses P1 Cre recombinase under the control of the MMTV LTR promoter. The MMTV LTR promoter directs a widespread pattern of expression including the female germline.|||Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|09-Oct-2014||0.0|0.0|Unknown||Mammary, Cre recombinase, striated ductal, epithelial|Yes| 1968.0|available from Animal Resources Centre - www.arc.wa.gov.au|SJL/JArc||Dominant|Inbred albino: Tyr, p, Pde6b, H-2, homozygous for SJL/J type Myo-D1 allele||Unknown||||||Unknown||||||||||||||||Yes|||||||||||||General Information: Moderate breeding performance 0.5 young/female/wk., average litter 6.5 but about 50% mortality from birth to weaning. Short life span (males 16 months, females 13 months). High incidence of type B reticulum cell sarcomas (90% in males and females > 12 months). Primary tumours arise in germinal centres in Peyer's patches and mesenteric lymph nodes. Secondary increase in thymus weight between 6 to 12 months due to influx of surface immunoglobulin-positive B cells. High incidence of spontaneous amyloidosis. Produce low levels of 1gE due to a strong tendency to develop 1gE-specific suppressor cells. Sensitive to immune tolerance induction at birth but by 2 months becomes resistant to tolerance induction. Susceptible to demyelination due to Theiler's murine encephalomyelitis virus and highly susceptible to induction of EAE. High sensitivity to vasoactive amines and exhibit blood-organ barrier leakiness. Very high heart rate compared to most strains. Used as a model to study Hodgkin's disease. High resistance to whole-body X -irradiation. Normal C5. The Myod1 gene is able to initiate the complete sequence of genetic events required for formation of skeletal muscle. In mice there are at least 3 different structural forms of Myod1, one of, which is unique to SJL/J mice. SJL mice regenerate skeletal muscle much more efficiently than most other strains of inbred mice and it is believed that the unique form of Myod1 is involved with this.|||Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||Yes|04-Sep-2007||0.0|0.0|No|||Yes| 8569.0|Cd47 KO|B6.129-Cd47/AnuApb||Recessive|CD47 antigen (Rh-related antigen, integrin-associated signal transducer)|Cd47||9130415E20Rik, B430305P08Rik, IAP, integrin-associated protein, Itgp|MGI:96617||||16|||||||||||||||||||||||||||||||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|24-Sep-2018|Cryopreserved sperm|55.0|0.0|Unknown|||Yes| 3565.0||C57BL/6-Tg(TcraTcrb)1100Mjb H2-K||Recessive||||||||||||||||||||||||||transgene insertion 1100, Michael J Bevan||||||||||||TCR transgenics are immunocompromised by having a mono-specific T cell receptor however, in a clean envirnoment, mice show no difference in phenoptype from wild-type B6 mice. OT-I mice have a higher incidence of thymoma from 4 months of age. OT-I/bm1 CD8 T cells are reduced in number compared to OT-I/B6 mice.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|01-Aug-2008||0.0|0.0|Unknown||T cell, receptor (TCR), ovalbumin, CD8, major histocompatibility class (MHC)|Yes| 3591.0|Phc1 Phc2 KO|Un-Phc1 Phc2||Recessive|polyhomeotic-like 1 (Drosophila)|Phc1|Reduced|Edr1, Mph1, Rae-28, rae28|MGI:103248|targeted mutation 1, Osaka University Medical School|Phc1|MGI:1857629|6||||||||||||||||Yes|||||||||||||Embryonic lethality during organogenesis - double homozygotes are lost in a progressive manner starting around E9.5. At E9.5 the first and second branchial arches are poorly developed. At E9.5 only about 20 somites are present compared to 25 in littermates. After E8.5 double homozygous embryos become progressively growth retarded. The tail bud is smaller.|||No|No|Yes|No|No|Yes|No|Unknown||||No|06-Aug-2008||0.0|0.0|Unknown||Pharangeal arch, embryonic lethal, Hox, anterior-posterior , mesoderm, neural crest|Yes| 3591.0|Phc1 Phc2 KO|Un-Phc1 Phc2||Recessive|polyhomeotic-like 2 (Drosophila)|Phc2|Unknown|D130050K19Rik, D4Ertd810e, Edr2, Mph2|MGI:1860454|targeted mutation 1, Haruhiko Koseki|Phc2|MGI:3586989|4|||||||||||||||||||||||||||||Embryonic lethality during organogenesis - double homozygotes are lost in a progressive manner starting around E9.5. At E9.5 the first and second branchial arches are poorly developed. At E9.5 only about 20 somites are present compared to 25 in littermates. After E8.5 double homozygous embryos become progressively growth retarded. The tail bud is smaller.|||No|No|Yes|No|No|Yes|No|Unknown||||No|06-Aug-2008||||Unknown||Pharangeal arch, embryonic lethal, Hox, anterior-posterior , mesoderm, neural crest|Yes| 8518.0|Rab32.3|C57BL/6-Rab32||Recessive|RAB32, member RAS oncogene family|Rab32|Nil|2810011A17Rik|MGI:1915094||||10|||||||||||||||||||||||||||||Normal|Normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|14-Jun-2018||0.0|0.0|Unknown|||Yes| 7758.0|ERIN|C57BL/6-Tg(rtTA2-IRES-Cre/ERT2)/Ausb||Dominant||||||||||||||||||||||||||||||||||||||Inducible model designed for lineage tracing experiment.|||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|09-Oct-2014||0.0|0.0|Unknown||Cre recombinase, inducible|Yes| 1826.0|Blimp1 knockout|C57BL/6-Prdm1/Wehi||Recessive|PR domain containing 1, with ZNF domain|Prdm1|Unknown|Blimp1, PRDI-BF1|MGI:99655|targeted mutation 1, Stephen L Nutt|Prdm1|MGI:3510704|10||||||||||||||||Yes|||||||||||||Prenatal lethality: homozygotes die late in gestation.||C57BL/6|No|No|Yes|No|No|Yes|No|Unknown||||No|06-Aug-2007||0.0|0.0|Unknown||T cell, lymphocyte, transcription factor, expression, maturation|Yes| 3490.0||NOR/LtJWehi||Dominant||||||||||||||||||||||||||||||||||||||This strain is homozygous for Cdh23, the age related hearing loss 1 mutation, which on this background results in progressive hearing loss with onset prior to 3 months of age. NOR/LtJ mice are insulitis resistant and diabetes free. NOR/LtJ mice still exhibit peripheral T-lymphocyte accumulation and defective peritoneal macrophage responses characteristic of NOD/LtJ mice. NOR/LtJ mice are matched at the diabetogenic H2g7 complex to NOD/LtJ. NOR/LtJ is a recombinant congenic strain in which limited regions of the NOD/LtJ genome have been replaced by genome from the C57BLKS/J strain.|||Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|23-Jul-2008||0.0|0.0|Unknown||insulitis, hearing / deafness, T cell, macrophage|Yes| 3599.0||C57BL/6-Tg(Wnt1-Cre)||Dominant||||||||||||||||||||||||||Cre recombinase|wingless-related MMTV integration site 1 (Wnt1), The Wnt1 promoter preceded the cre recombinase coding sequence which was followed downstream by the Wnt1 enhancer.|||||||||||The Wnt1 regulatory sequences initially direct expression of Cre recombinase in the midbrain. After neural tube closure, expression occurs in the dorsal and ventral midlines of the midbrain and caudal diencephalon, the midbrain-hindbrain junction and in the dorsal spinal cord.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|06-Aug-2008||0.0|0.0|Unknown||wnt1, Cre recombinase, midbrain, dorsal and ventral midlines, audal diencephalon|Yes| 3518.0||C57BL/6.Balb/c-Lmr1Lmr2||Recessive|leishmaniasis resistance 1|Lmr1|Unknown||MGI:1277203|leishmaniasis resistance 1; C57BL/6J |Lmr1C57BL/6J|MGI:2446909|17||||||||||||||||Yes|||||||||||||These mice are more susceptible to leishmaniasis infection than C57BL/6.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|28-Jul-2008||0.0|0.0|Unknown||T cell, infection, IL-4, helper T cell response|Yes| 3518.0||C57BL/6.Balb/c-Lmr1Lmr2||Recessive|leishmaniasis resistance 2|Lmr2|Unknown||MGI:1277141|leishmaniasis resistance 2; C57BL/6J |Lmr2|MGI:2446907|9|||||||||||||||||||||||||||||These mice are more susceptible to leishmaniasis infection than C57BL/6.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|28-Jul-2008||||Unknown||T cell, infection, IL-4, helper T cell response|Yes| 3519.0||Balb/c.C57BL/6-Lmr1 Lmr2||Recessive|leishmaniasis resistance 1 |Lmr1|Normal||MGI:1277203 |Lmr1|Lmr1|MGI:2446908|17||||||||||||||||Yes|||||||||||||These mice are more resistant to leishmaniasis infection than BALB/c.||Balb/c|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|28-Jul-2008||0.0|0.0|Unknown||T cell, infection, IL-4, helper T cell response|Yes| 3519.0||Balb/c.C57BL/6-Lmr1 Lmr2||Recessive|leishmaniasis resistance 2|Lmr2|Unknown||MGI:1277141|leishmaniasis resistance 2; BALB/c |Lmr2|MGI:2446906|9|||||||||||||||||||||||||||||These mice are more resistant to leishmaniasis infection than BALB/c.||Balb/c|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|28-Jul-2008||||Unknown||T cell, infection, IL-4, helper T cell response|Yes| 8519.0|Ankrd13A.4|C57BL/6-Ankrd13a||Recessive|ankyrin repeat domain 13a|Ankrd13a|Nil|1100001D10Rik|MGI:1915670||||5|||||||||||||||||||||||||||||Normal|Normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|14-Jun-2018|Cryopreserved sperm|50.0|0.0|Unknown|||Yes| 8520.0|OGT-flox|B6.129-Ogt/J||Recessive|O-linked N-acetylglucosamine (GlcNAc) transferase (UDP-N-acetylglucosamine:polypeptide-N-acetylglucosaminyl transferase)|Ogt|Unknown|1110038P24Rik, 4831420N21Rik, OGT, Ogtl|MGI:1339639|O-linked N-acetylglucosamine (GlcNAc) transferase (UDP-N-acetylglucosamine:polypeptide-N-acetylglucosaminyl transferase); targeted mutation 1, Gerald W Hart|Ogt|MGI:2387867|X|||||||||||||||||||||||||||||Normal|Normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|14-Jun-2018|Cryopreserved sperm|50.0|0.0|Unknown|||Yes| 3503.0|Balb/c.LMO4 transgenic clone 36|BALB/c-Tg(MMTV-Lmo4)36/Wehi||Dominant||||||||||||||||||||||||||LIM domain only 4 (Lmo4) + rabbit β-globin and SV40 intronic sequences to augment mRNA stability, as well as a polyadenylation sequence|MMTV long-terminal repeat|3 fold higher than endogenous||||||||||No overt phenotypic abnormalities were detected in the mammary glands of nulliparous mice or mice during their first pregnancy by whole-mount and histological analyses. Furthermore, transgenic mice were capable of lactation and their glands were histologically indistinguishable from wild-type mice. After three pregnancies four of five transgenic, multiparous female mice developed multifocal acinar hyperplasia, with a mean latency of 16 months (range, 14–20) and one of these mice also exhibited an adenosquamous carcinoma at 18 months. In contrast, mammary glands from 13 nontransgenic littermate mice that underwent three pregnancies did not develop hyperplasia or tumors during a similar follow-up period of 14–19 months.||BALB/c|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||6||No|25-Jul-2008||0.0|0.0|Unknown||oncogene, breast cancer, mammary, intraepithelial neoplasia or adenosquamous carcinoma, proliferation|Yes| 6526.0|CD25?|B6.129S4-Il2ra/JScrAusb||Recessive|interleukin 2 receptor, alpha chain|Il2ra|Nil|CD25, IL-2R alpha chain, Il2r, Ly-43|MGI:96549|interleukin 2 receptor, alpha chain; targeted mutation 1, Dennis M Willerford|Il2ra|MGI:1857192|2|||||||||||||||||||||||||||||Abnormal induced morbidity/mortalityAbnormal T cell activation:*Over 80% of the T cells from bone marrow chimeras (mutant bone marrow in Rag2-deficient hosts) exhibit an activated phenotype.Lymphoid hyperplasia:*Some bone marrow chimeras (mutant bone marrow in Rag2-deficient hosts) have enlarged lymph nodes containing up to 3 x 10<8> lymphocytes.Abnormal regulatory T cell physiology:*Bone marrow chimeras (mutant bone marrow in Rag2-deficient hosts) die within 40-50 days of autoimmune disorders.*However, when bone marrow chimeras receive 10<5> CD25-positive CD4-positive wild-type T cells two weeks after reconstitution they live past six months of age without any symptoms of autoimmune disorder.*Premature death can also be prevented by including 50% normal or Il2 bone marrow during reconstitution.Anemia:*Bone marrow chimeras (mutant bone marrow in Rag2-deficient hosts) exhibit anemia.Decreased body size:*Bone marrow chimeras (mutant bone marrow in Rag2-deficient hosts) exhibit decreased body weight due to an autoimmune disorder.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown||IL-2R alpha, Autoimmune disorders|Yes| 7759.0|NUR77H-Ferra|STOCK Tg(MMTV-Nur77)H/Ausb||Dominant||||||||||||||||||||||||||neurological 77|mouse mammary tumor virus (MMTV) long terminal repeat||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|09-Oct-2014||0.0|0.0|Unknown||Mammary|Yes| 8522.0|MARCH 1|B6.129-March1||Recessive|membrane-associated ring finger (C3HC4) 1|March1|Nil|2900024D24Rik|MGI:1920175|membrane-associated ring finger (C3HC4) 1; targeted mutation 1.1, Satoshi Ishido|March1|MGI:3706321|8|||||||||||||||||||||||||||||MARCH1 K.O. mice have enriched surface expression in professional antigen presenting cells (i.e. dendritic cells and B cells) compared to WT miceMARCH1 K.O. mice show reduced numbers of CD4+ T cells (i.e. regulatory T cells) in the thymus compared to WT mice.|The same as homozygous K.O. but to a lesser extent|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|14-Jun-2018|Cryopreserved sperm|50.0|0.0|Unknown||T cell, B cell, E3 ubiquitin ligase, MHC, dendritic cells|Yes| 7293.0|B6/J - Blue G18|C57BL/6JAnu-redev-BlueG18||Dominant||||||||||||||||||||||||||||||||||||||||C57BL/6JAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|21-Mar-2013|Cryopreserved sperm|20.0|0.0|Unknown|||No| 5662.0|Casp1-/- x K14E7.C57||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 3579.0||CBA-Tg(CIITA)||Recessive||||||||||||||||||||||||||class II transactivator (CIITA)||||||||||||||CBA|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|04-Aug-2008||0.0|0.0|Unknown||MHC, class II, H2, histocompatability 2, T cell|Yes| 5334.0|NODβ2M-/- flβ2Ma 8.3TCRαβ|NOD-B2m Tg(B2m)1Rms Tg(TcraTcrbNY8.3)1Pesa/MarpApb||Recessive|beta-2 microglobulin|B2m|Unknown|beta 2 microglobulin, beta2-m, Ly-m11|MGI:88127|targeted mutation 1, Rudolf Jaenisch|B2m|MGI:1927183|2||||||||||||||||Yes|transgene insertion 1, Robyn M Slattery|B2m|||||||||||Unknown|TCR transgenic mouse with accelerated diabetes.|NOD|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Good||||No|01-Dec-2010|Cryopreserved sperm|50.0|0.0|Unknown||Autoimmunity, insulin, MHC I, beta cell|Possibly| 5334.0|NODβ2M-/- flβ2Ma 8.3TCRαβ|NOD-B2m Tg(B2m)1Rms Tg(TcraTcrbNY8.3)1Pesa/MarpApb||Recessive|||||||||Unknown|||||||||||||||||transgene insertion 1, Pere Santamaria|TCR|||||||||||Unknown|TCR transgenic mouse with accelerated diabetes.|NOD|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Good||||No|01-Dec-2010|Cryopreserved sperm|||Unknown||Autoimmunity, insulin, MHC I, beta cell|Possibly| 7112.0|ENU22:Stxbp2|C57BL/6NCrlAnu-Stxbp2/AnuApb|C57BL/6NCrlAnu-Stxbp2/AnuApb|Recessive|syntaxin binding protein 2|Stxbp2|Unknown|C79054, Munc-18-2, Munc18b, Munc-18b, muSec1, Sxtp2 |MGI:107370|syntaxin binding protein 2; mutation 1, The Australian National University|Stxbp2|MGI:5563406|8|ENSMUSG00000004626|ENSMUST00000160708|Stxbp2-001||||||||3636354|11|||ACGATCTCTACCCTCTCCTACCATTACCTCAGGCCAACATCAAAGACCTGTCCCACATCC||||||||||||||Reduced fusion of cytolytic granules with cell membrane|Unknown|C57BL/6NCrlAnu|Yes|Unknown|Yes|Yes|Unknown|Yes|No|Good|none|3|het x het|No|24-Oct-2012|Cryopreserved sperm|32.0|0.0|Yes|HLH or hemophagocytic lymphohistiocytosis type 5|ENU|Yes| 8595.0|mm1286del|C57Bl/6J-Grhl/Apb||Dominant|grainyhead like transcription factor 2|Grhl2|||MGI:2182543||||15|||||||||||||||||||||||||||||Normal|Heterozygous adults which completely lack Grhl2 (Grhl2+/-) present with no phenotypes. As the mm1286del line has only an enhancer element deleted, there is no possibility of heterozygosity leading to phenotypes; we have already observed that heterozygous adults present with no phenotype. We predict that nullizygous(-/-) embryos will have slight alterations to craniofacial morphology|C57Bl/6J|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|02-Nov-2018|Cryopreserved sperm|30.0|0.0|Unknown|||Possibly| 6530.0|IL12?|B6.129S1-Il12b/ScrAusb?||Recessive|interleukin 12b |Il12b|Nil|IL-12 p40, Il-12b, Il-12p40, IL-23 subunit p40|MGI:96540|interleukin 12b; targeted mutation 1, Jeanne Magram|Il12b|MGI:1857201|11|||||||||||||||||||||||||||||Increased sensitivity to xenobiotic induced morbidity/mortality:*Increase in mortality following a single dose of N-methyl-N-nitrosourea (MNU) compared to similarly treated wild-type controls.Decreased circulating interferon-gamma level:*Serum levels of IFNG in LPS-injected mice are only 17 +/- 5% of LPS-induced controls.Abnormal macrophage physiology:*Fewer than expected macrophages in the dermis of carcinogen treated skin.Abnormal granulocyte physiology:*Fewer than expected granulocytes in the dermis of carcinogen treated skin.Abnormal lymphocyte physiology:*Lymph node cells from keyhole limpet hemocyanin (KLH) immunized mice are severely impaired in their ability to produce IFNG when cultured with KLH; however, their production of IL4 is increased. Abnormal NK cell physiology: *Mean NK lytic activity is about 66% of controls; however when cultured with IL2 lytic activity is similar to controls. Abnormal CD8-positive T cell physiology: *Dramatic increase in the number of cytotoxic CD8+ cells in the dermis and epidermis of carcinogen treated skin.Decreased susceptibility to type IV hypersensitivity reaction:*Specific foot pad swelling 48 hours after challenge with methylated bovine serum albumin is inhibited by 47 +/- 3% compared to wild-type mice; however, cytotoxic T lymphocyte responses are similar to wild-type.Decreased interleukin-17 secretion:*Barely detectable levels of IL17 in the skin after carcinogen treatment unlike wild-type mice which express high levels of IL17.Increased susceptibility to bacterial infection:*Vaccination does not produce a protective response to M. tuberculosis.Decreased incidence of chemically-induced tumors:*Resistant to induction of papillomas compared to wild-type mice after treatment with DMBA and TPA in a 2 step skin carcinogenesis protocol.*However, there is an increase in the incidence of tumors following intradermal challenge with PDV squamous carcinoma cells.Abnormal alveolar process:*3 fold increase in alveolar bone loss at 30 weeks relative to mice at 6 and 16 weeks.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown||IL-12, IFN gamma, DTH responses|Yes| 3587.0||CBA.129-Rapgef1||Recessive|Rap guanine nucleotide exchange factor (GEF) 1|Rapgef1|Nil|4932418O06Rik, C3G, Grf2|MGI:104580|gene trap 5, Peter Gruss|Rapgef1|MGI:2445403|2||||||||||||||||Yes|||||||||||||Mice homozygous for a gene trap allele exhibit embryonic lethality, altered neuroepithelium morphology, embryonic and extra-embryonic vascular defects, and reduced cell migration and adhesion.||CBA|No|No|Yes|No|No|Yes|No|Unknown||||No|05-Aug-2008||0.0|0.0|Unknown||cerebral cortex, nucleotide exchange factor, embryonic lethal, Akt/PKB, Ras signalling|Yes| 691.0|SPA/SPA 456|C57BL/6-Glrb Tg(rNSE-rGlyR)456||Semi-dominant|glycine receptor, beta subunit|Glrb|Reduced||MGI:95751|spastic|Glrb|MGI:1856363|3||||||||||||||||Yes|rat glycine receptor beta subunit|rat neuron-specific enolase (NSE)|||||||||||This transgene can modify by partial rescue the phenotype of the spastic mutation in a gene dosage-dependent manner. It revealed that the rescue of the different behavioural and motor deficits showed distinct transgene dosage requirements. In TG456 homozygotes male fertility and righting response were completely rescued, whereas tremor induction and hind feet clasping behaviour were only partially improved. Data also show that the different deficiencies appeared independently of each other, e.g. hind feet clasping did not require a defective righting response or tremor proneness. |In spa/spa-TG456/+ heterozygotes, no rescue was seen with respect to tremor inducibility, whereas male fertility, hind feet clasping and righting response were clearly improved.|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|30-Apr-2007||0.0|0.0|Yes||glycine recptor, spa, Startle, axatia, tremor|Yes| 7286.0|B6NCrl redev - Green G7|C57BL/6NCrlAnu-redev - GreenG7||Dominant||||||||||||||||||||||||||||||||||||||Normal||C57BL/6NCrlAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|12-Mar-2013|Cryopreserved sperm|5.0|242.0|Unknown|||No| 274.0||FVB-TgN(AHPV16E6/E7)19||Dominant||||||||||||||||||||||||||Human Papilloma Virus 16 E6 and E7||||||||||||||FVB|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|01-May-2006||0.0|0.0|Unknown||Vaccine, occular, cataract, cervical carcinoma|Yes| 7383.0|ENU28:G2|ANU:ENU28:G2||Recessive||||||||||||||||||||||||||||||||||||||Unknown|Unknown|C57BL/6NCrlAnu|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown|1|||No|26-Jul-2013|Cryopreserved sperm|1808.0|0.0|Unknown||ENU, mutagenesis, screen, random|Yes| 8523.0|primurus BALB/c|C.B6J-Dock8/AnuApb||Recessive|dedicator of cytokinesis 8|Dock8|Unknown||MGI:1921396|primurus|Dock8|MGI:3835421|19|ENSMUSG00000052085|ENSMUST00000025831|Dock8-201|5479|5601|T to C|ENSMUSE00000145941|42|1827|Serine to Proline|||||AACCCGCAATCACGAAGCTCCCGGAGATCTCACATAGACTAGAGGGATTTTATGGCCAGTG|Yes|||||||||||||Defective antibody response to immunization: failure to sustain antibody formation, undergo affinity maturation or to mount heightened recall (memory) response upon booster immunization. DOCK8-mutant B cells were unable to form marginal zone B cells or to persist in germinal centers and undergo affinity maturation. Dock8 mutations disrupted accumulation of the integrin ligand ICAM-1 in the B cell immunological synapse but did not alter other aspects of B cell antigen receptor signaling.||BALB/c|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|9|5||No|15-Jun-2018|Cryopreserved sperm|84.0|0.0|Unknown||memory, antibody, immunization, ENU, Wellcome Trust, B cell, GTP|Yes| 7566.0|ENU24:042:Usp15:B6|C57BL/6NCrlAnu-Usp15/AnuApb|C57BL/6NCrlAnu-Usp15/AnuApb|Recessive|Ubiquitin specific peptidase 15|Usp15|Unknown|4921514G19Rik, E430033I05Rik, Gcap18, mKIAA0529|MGI:101857|Ubiquitin specific peptidase 15; mutation 1, The Australian National University|Usp15|MGI:5648448|10|ENSMUSG00000020124|ENSMUST00000020334|Usp15-201|2855|2875|G to A|ENSMUSE00000403753|22|952|Serine to Leucine|||||CCCTCTTGACCGAGAAACTAAAGGTGCTTCAGCTGCCACAGGTATCCCCCTGGAAAGTGAC||||||||||||||Unknown|Unknown|C57BL/6NCrlAnu|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|14-Jan-2014|Cryopreserved sperm|48.0|0.0|Unknown||ENU, missense, mutation, MMP|Possibly| 5296.0|B6.EPCR.Tg ; CBA/B6-Tg(HUEPCR)|CBA;B6-Tg(H2-K-EPCR)||Recessive||||||||||||||||||||||||||human protein C receptor, endothelial|H2-K|Strong, endothelial cells and neutrophils||||||||||Unknown||C57BL/6|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|29-Oct-2010|Cryopreserved sperm|50.0|0.0|Unknown||transplantation, thrombin, inflammation, receptor|Possibly| 5644.0|BTBRT||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 7760.0|NUR77L-Florenzi|STOCK Tg(MMTV-Nur77)L/Ausb||Dominant||||||||||||||||||||||||||neurological 77|mouse mammary tumor virus (MMTV) long terminal repeat||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|09-Oct-2014||0.0|0.0|Unknown||Mammary|Yes| 6533.0|IL7?|B6.129P2-Il7/ScrAusb?||Recessive|interleukin 7|Il7|Nil|A630026I06Rik, hlb368, Il-7|MGI:96561|interleukin 7; targeted mutation 1, DNAX Research Institute of Cellular and Molecular Biology|Il7|MGI:1857652|3|||||||||||||||||||||||||||||Decreased lymphocyte cell number:*Lymphopenia.*Retention of normal CD4 to CD8 ratioArrested B cell differentiation:*Lymphopoiesis blocked at pro-B to pre-B cell stage.Abnormal CD8-positive T cell morphology:*CD8 expression on T cells is reduced by 60%.Small spleen:*Spleen reduced in size and weight, but retains the normal structure. Decreased spleen weight Spleen hypoplasia: *Reduced absolute numbers of both mature B and T cells in spleen.Small thymus:*Thymus reduced in size and weight, but normal structure. Decreased thymus weight. Thymus hypoplasia: *Reduced cellularity.Absent Peyer's patches:*Peyer's patches undetected.Absent lymph nodes:*Lymph nodes undetected.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown||IL-7|Yes| 5179.0|16FOX 004 B6.129-Tg(FoxP3-GFP)|ENU16FOX:004 Foxp3||Recessive|forkhead box P3|Foxp3|Normal|JM2, scurfin|MGI:1891436|||MGI:3574964|X||||||||||||||||No|||||||||||||Malocclusion with secondary immune phenotypeCells from the Foxp3-gfp background strain that express FoxP3 fluoresce green, predominantly T cells|Normal |129 x C57BL/6|Yes|No|Yes|Yes|No|Yes|Yes|Good|||unaffected sib intercross|No|19-Jul-2010|Cryopreserved sperm|40.0|0.0|Unknown||malocclusion, hyper IgE, immunology, immune phenotype, ENU|Possibly| 5179.0|16FOX 004 B6.129-Tg(FoxP3-GFP)|ENU16FOX:004 Foxp3||Recessive|Unknown|Unknown|||||||Unknown||||||||||||||||Unknown|||||||||||||Malocclusion with secondary immune phenotypeCells from the Foxp3-gfp background strain that express FoxP3 fluoresce green, predominantly T cells|Normal |129 x C57BL/6|Yes|No|Yes|Yes|No|Yes|Yes|Good|||unaffected sib intercross|No|19-Jul-2010|Cryopreserved sperm|||Unknown||malocclusion, hyper IgE, immunology, immune phenotype, ENU|Possibly| 7765.0|UBCcre/J|B6.Cg-Tg(UBC-cre/ERT2)1Ejb/JAusb||Dominant||||||||||||||||||||||||||transgene insertion 1, Eric J Brown|human ubiquitin C (UBC) promoter|||||||||||Normal|Normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|12-Oct-2014||0.0|0.0|Unknown||DNA damage response, ATR|Yes| 3592.0|Fasl-gld|B6.C3-Fasl/AnuApb|B6.C3-Fasl|Recessive|Fas ligand (TNF superfamily, member 6)|Fasl|Unknown|APT1LG1, CD178, CD95L, Fas-L, Tnfsf6|MGI:99255|generalized lymphoproliferative disease|Fasl|MGI:1856384|1||||||||||||||||Yes|||||||||||||Increased peripheral blood lymphocyte number. Increased T cell number. Increased neutrophil number. Abnormal T cell differentiation. Decreased B cell numbers. Anemia. Premature death - animals die around 60 weeks. Splenomegaly, lymphoadenopathy.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|06-Aug-2008|Cryopreserved sperm|144.0|0.0|Unknown||T cell, lymphocyte, splenomegaly , lymphoadenopathy, autoimmunity, antinuclear antibodies|Yes| 7103.0|ENU23:015:SOST:B6|C57BL/6NCrlAnu-Sost/AnuApb||Recessive|sclerostin|SOST|Unknown|5430411E23Rik|MGI:1921749||||11|ENSMUSG00000001494|ENSMUST00000001534|Sost-001|95|125|T to C|ENSMUSE00000113103|1|32|Aspartic acid to Glycine|||||GGGCCAGGGGTGGCAAGCCTTCAGGAATGATGCCACAGAGGTCATCCCAGGGCTTGGAGAG||||||||||||||Unknown|Unknown|C57BL/6NCrlAnu|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|05-Oct-2012||0.0|0.0|Unknown||ENU|Possibly| 7102.0|ENU23:008:P2RX5:B6|C57BL/6NCrlAnu-P2rx5/AnuApb||Recessive|purinergic receptor P2X, ligand-gated ion channel, 5|P2rx5|Unknown|P2X5|MGI:2137026||||11|ENSMUSG00000005950|ENSMUST00000006104|P2rx5-001||||||||73167492|7|||ACTCTAGCATTCATCCTGTCTTATGTATCAAGGGCGGTGTGATAGGAATCCACATTGAAT||||||||||||||Unknown|Unknown|C57BL/6NCrlAnu|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|05-Oct-2012||0.0|0.0|Unknown||ENU|Possibly| 3316.0|FATT-C57|C57BL/6-Lepr/Apb||Recessive|Leptin Receptor|LepR|Unknown|Leprb, LEPROT, leptin receptor gene-related protein, Modb1, OB-RGRP, obese-like, obl, Obr|MGI:104993|FATT|Lepr||4||||||||||||||||Yes|||||||||||||The homozygote mutant has juvenile obesity, florid diabetes. The adult is hypogonadal and does not breed, and had an increased body length (10-20%).|There is a slight change in adipose tissue distribution and liver weight but no other significant changes. |129Sv/EvTac x C57BL/6|Yes|No|Yes|Yes|No|Yes|Yes|Good|4||Heterozygous FATT-C57/BL6 mice crossed with C57/BL6 working towards a C57/BL6 background. Homozygous mutants are not fertile/do not breed. |No|09-Jun-2008|Cryopreserved sperm|130.0|0.0|Yes||Obesity, Diabetes, leptin, receptor|Yes| 5645.0|C-Ski - Incomplete||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6684.0|DALLAGLIO-10|Balb/c-Tlr7/Ausb||||TLR7||||||||||||||||||||||||||||||||||||||BALBc|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|02-Dec-2011||0.0|0.0|Unknown|||Possibly| 5310.0|ENU15 CHINA 075c B6 G3|ENU15China:075c||Recessive|Unknown|Unknown|||||||Unknown||||||||||||||||Unknown|||||||||||||Reduced B cell population. May possibly be fertility defects too because affecteds don't breed. Phenotyping via peripheral blood FACS.|||Yes|Unknown|Yes|Yes|Unknown|Yes|No|Unknown||||No|08-Nov-2010|Cryopreserved sperm|20.0|0.0|Unknown||B cell, ENU|Possibly| 7372.0|ENU26:047:Trpv4:B6:G2|C57BL/6NCrlAnu-Trpv4/AnuApb||Recessive|transient receptor potential cation channel, subfamily V, member 4|Trpv4|Unknown|0610033B08Rik, OTRPC4, Trp12, VRL-2, VROAC, VR-OAC|MGI:1926945|mutation 1, The Australian National University|Trpv4||5|ENSMUSG00000014158|ENSMUST00000071968|Trpv4-001|1859|1970|A to G|ENSMUSE00001210261|12|620|Valine to Alanine|||||CTTCAAAGACCTCTTCCGCTTCCTGCTTGTGTACCTGCTCTTCATGATCGGCTATGCCTCA||||||||||||||Unknown||C57BL/6NCrlAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|05-Jul-2013||0.0|0.0|Unknown||ENU|Yes| 5902.0|Mafia||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5449.0|Idd14 R12|NOD.B6-Idd14 R12||Recessive||||||||||||||||||||||||||||||||||||||Unknown|Unknown|NOD/Lt|Yes|Yes|Unknown|Yes|Yes|Unknown|No|Unknown||||Yes|01-Mar-2011|Cryopreserved sperm|50.0|0.0|Unknown|||No| 8525.0|CMV-cre|B6.Cg-Tg(CMV-cre)1Cgn/AnuApb||Dominant||||||||||||||||||||||||||transgene insertion 1, University of Cologne|human cytomegalovirus (CMV) promoter||||||||||||Cre recombinase under the control of a human cytomegalovirus (CMV) promoter, active in most cells and tissues.|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|26-Jun-2018|Cryopreserved sperm|36.0|0.0|Unknown||CMV, Cre recombinase, ubiquitous, deleter|Yes| 4473.0|George|C(Cg)-Gstp1/Gstp2/AnuApb||Recessive|glutathione S-transferase, pi 1|Gstp1|Nil|Gst p-1, GstpiB|MGI:95865|targeted mutation 1, C Roland Wolf|Gstp1/Gstp2|MGI:3046099|19||||||||||||||||Yes|||||||||||||Mutant mice with null mutations in both Gstp1 and Gstp2 exhibit an increased susceptibility to DMBA and TPA induced skin papillomas. Male mutant mice exhibit an increased body weight with age. Studying allergic airway disease compared with allergic WT mice, eosinophilia, goblet cell hyperplasia, airway remodeling, lung resistance, and IL-5 were enhanced in allergic Gstp-null mice.||BALB/c x 129|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|6|||No|22-Feb-2009|Cryopreserved sperm|135.0|0.0|Unknown||asthma, eosinophil, signal transduction, IL-5, phosphorylation, papilloma|Yes| 4473.0|George|C(Cg)-Gstp1/Gstp2/AnuApb||Recessive|glutathione S-transferase, pi 2|Gstp2|Nil|Gst p-2, Gst-3, Gst3, GSTpiA|MGI:95864|glutathione S-transferase, pi 2; targeted mutation 1, C Roland Wolf|Gstp1/Gstp2|MGI:3046101|19|||||||||||||||||||||||||||||Mutant mice with null mutations in both Gstp1 and Gstp2 exhibit an increased susceptibility to DMBA and TPA induced skin papillomas. Male mutant mice exhibit an increased body weight with age. Studying allergic airway disease compared with allergic WT mice, eosinophilia, goblet cell hyperplasia, airway remodeling, lung resistance, and IL-5 were enhanced in allergic Gstp-null mice.||BALB/c x 129|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|6|||No|22-Feb-2009|Cryopreserved sperm|||Unknown||asthma, eosinophil, signal transduction, IL-5, phosphorylation, papilloma|Yes| 4190.0||NOD.B6-Prf1/J||Recessive|perforin 1 (pore forming protein)|Prf1|Unknown|perforin, Pfn, Pfp, Prf-1|MGI:97551|targeted mutation 1, Sandoz Pharmaceutical|Prf1|MGI:1857235|10||||||||||||||||No|||||||||||||Type 1 diabetes incidence was decreased from 77% in wildtype females to 16% in homozygotes. The onset of disease was also delayed from a median of 19 weeks to 39.5 weeks of age.|Mice develop Type 1 diabetes with reduced incidence compared to NOD/Lt control or littermate control mice. Phenotype is intermediate.|NOD/Lt|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|9||Sib x Sib|No|19-Dec-2008||0.0|0.0|Unknown||Cytotoxic T cell, CD8, Perforin|Yes| 269.0||C57BL/6-Gzma Prf1||Recessive|granzyme A|Gzma|Unknown|BLT esterase, Ctla-3, Ctla3, H factor, Hanukah factor, Hf, SE1, serine esterase 1, TSP-1, TSP1|MGI:109266|targeted mutation 1, Markus M Simon|Gzma|MGI:2449926|13||||||||||||||||Yes|||||||||||||||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|30-Apr-2006||0.0|0.0|Unknown||cytotoxic T cell, virus, infection, CD8|Yes| 269.0||C57BL/6-Gzma Prf1||Recessive|perforin 1 (pore forming protein)|Prf1|Nil|perforin, Pfp, Prf-1|MGI:97551|targeted mutation 1, Sandoz Pharmaceutical|Prf1|MGI:1857235|10|||||||||||||||||||||||||||||||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|30-Apr-2006||||Unknown||cytotoxic T cell, virus, infection, CD8|Yes| 7296.0||SJL/Mrit||Dominant|unknown|unknown|||||||Unknown|||||||||||||||||||||||||||||Prenatal mortality (E15) with severe anaemia and fragmented red blood cells|Heterozygous mice display a microcytic anaemia with decrease osmotic fragility.|SJL/J|No|No|Yes|No|No|Yes|No|Good|6|||No|22-Mar-2013|Cryopreserved sperm|50.0|0.0|Yes|thalassaemia|red blood cells, microcytosis, anaemia, thalassaemia, ENU|Yes| 7928.0|S6 Mx1-Cre|B6(Cg).129-Rps6 Tg(Mx1-Cre)1Cgn/JAnu||Recessive|ribosomal protein S6|Rps6|Normal|S6R|MGI:98159|ribosomal protein S6; targeted mutation 1, George Thomas|Rps6|MGI:2387471|4|||||||||||||||||transgene insertion 1, University of Cologne|Mx1|||||||||||Abnormal cell morphology:• mice induced with interferon gamma exhibited similar responses to starvation as controls, although it was noted that 40S ribosomes were absent and 60S ribosomes were increased in number in mutant liver recovering from starvationAbnormal cell cycle• xpression of cell cycle markers such as cyclin E and cyclin A were not seen in mutant hepatocytes suggesting a block in cell cycle progressionDecreased liver regeneration:• after partial hepatectomy, mutant liver failed to regenerate after 10 days; histopathology revealed no evidence of regenerative or pathological processes in mutant liver; expression of cell cycle markers such as cyclin E and cyclin A were not seen in mutants suggesting a block in cell cycle progression||C57BL/6J|Yes|Unknown|Yes|Yes|Unknown|Yes|No|Unknown||||No|19-Jun-2015|Cryopreserved sperm|55.0|0.0|Unknown||Liver|Yes| 6856.0|AID KO|B6.CBA-Aicda/OlaAnu|B6.CBA-Aicda/OlaAnu|Dominant|activation-induced cytidine deaminase|Aicda|Nil|Aid|MGI:1342279|activation-induced cytidine deaminase; targeted mutation 1, Tasuku Honjo|Aicda|MGI:2156156|6|||||||||||||||||||||||||||||Increased susceptibility to bacterial infection induced morbidity/mortality: following administration of 15 ug cholera toxin.Abnormal class switch recombination: * absent class switching in B cells * class switching recombination (CSR)-induced Smu internal deletion is impaired * B cells cultured with LPS and IL-4 fail to switch immunoglobulin expression to IgG1 * similar defects in IgG3 switching are also observed.Abnormal somatic hypermutation frequency: * mice exhibit an increase in somatic hypermutation rates compared to in wild-type mice * the somatic mutation rates of the upstream region of the S-mu switch is severely reduced.Increased germinal center B cell number: * in Peyer's patches and spleen. * in the lamina propria and Peyer's patches.Decreased IgA level: serum and faecal.Decreased IgG level: faecal.Decreased IgG1 level: levels are less than one tenth of those in controls.Decreased IgG2a level: levels are less than one tenth of those in controls.Decreased IgG2b level.Decreased IgG3 level.Increased IgM level: * 2-3 fold elevation in IgM level. * faecal.|Abnormal class switch recombination: * absent class switching in B cells * class switching recombination (CSR)-induced Smu internal deletion is impaired * B cells cultured with LPS and IL-4 fail to switch immunoglobulin expression to IgG1 * similar defects in IgG3 switching are also observed.Abnormal somatic hypermutation frequency: * mice exhibit an increase in somatic hypermutation rates compared to in wild-type mice * the somatic mutation rates of the upstream region of the S-mu switch is severely reduced.Increased germinal center B cell number: * in Peyer's patches and spleen * in the lamina propria and Peyer's patches|C57BL/6JOla|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|8|||No|15-Mar-2012|Cryopreserved sperm|30.0|0.0|Unknown||immunoglobulin, class switch, germinal centre, B cell|Possibly| 7297.0||SJL/Mrit||Dominant|unknown|unknown|||||||Unknown|||||||||||||||||||||||||||||Pre and Perinatal mortality with Jaundice, enlarge spleen and fragmented red blood cells|Heterozygous mice display a microcytic anaemia with decrease osmotic fragility.|SJL/J|No|No|Yes|No|No|Yes|No|Good|4|||No|22-Mar-2013|Cryopreserved sperm|50.0|0.0|Yes|thalassaemia|red blood cells, microcytosis, anaemia, thalassaemia, ENU|Yes| 5543.0|ENU14Yaa:032b|B6.SB-Lyn/AnuApb|B6.SB-Lyn/AnuApb|Recessive|Yamaguchi sarcoma viral (v-yes-1) oncogene homolog|Lyn||Hck-2|MGI:96892|Yamaguchi sarcoma viral (v-yes-1) oncogene homolog; mutation 2, The Australian National University|Lyn|MGI:5563397|4|ENSMUSG00000042228|ENSMUST00000041377|Lyn-001||||||||3683632|9|||CTACATCATCACCGAGTTCATGGCTAAGGGTGAGTGGCATCACGAGTCTGTACCCCTAAA||||||||||||||Increased % immature B cells, and reduced % mature B cells (Almost no Mature B cells)||C57BL/6JAnu|Yes|Unknown|Yes|Yes|Unknown|Yes|No|Unknown||||No|27-Jul-2011|Cryopreserved sperm|45.0|0.0|Unknown||ENU, B cell, signal transduction|Possibly| 5522.0|Idd14 R10|NOD.B6-Idd14/R10Apb||Recessive|||||||||||||||||||||||||||||insulin dependent diabetes susceptibility 14|Idd14|||MGI:99416||||13|Unknown|Unknown|NOD/Lt|Yes|Yes|Unknown|Yes|Yes|Unknown|No|Unknown||||Yes|10-Jun-2011|Cryopreserved sperm|50.0|0.0|Unknown|||No| 7763.0|B6-H2k|B6.AK-H2/FlaEgJAusb|B6.AK-H2/FlaEgJAusb|Recessive|||||||||||||||||||||||||||||histocompatibility-2, MHC|H2||H-2, MHC-II|MGI:95894|histocompatibility-2, MHC; k variant|H2|MGI:3579322|17|The H2 complex contains 3 major classes of highly polymorphic gene sets: class I (H2-K, H2-D, Q, H2-T18 genes), class II (H2-I genes), and class III (H2-S genes). These genes are involved in many processes, including graft rejection, immune response, antigen presentation and complement component.||C57BL/6JFlaEg|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|12-Oct-2014||0.0|0.0|No||MHC, T cell, antigen presentation, H2|Yes| 5900.0|MacGreen||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6855.0|Apobec3 KO|B6.129P2-Apobec3/OlaAnu|B6.129P2-Apobec3/OlaAnu|Recessive|apolipoprotein B mRNA editing enzyme, catalytic polypeptide 3|Apobec3|Nil|CEM15, Gm20117, MGC:7002, Rfv-3, Rfv3|MGI:1933111|apolipoprotein B mRNA editing enzyme, catalytic polypeptide 3; targeted mutation 1, Michael S Neuberger|Apobec3|MGI:3701836|15|||||||||||||||||||||||||||||Normal but potentially susceptible to viral infection.||C57BL/6J|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|18|||No|15-Mar-2012|Cryopreserved sperm|42.0|0.0|Unknown||infection, retrovirus, replication|Possibly| 9364.0|C3TAC (CX3CR1-CreERT2 x Ai9 x CSF1Ffl/fl)|B6.129P2(C)-Cx3cr1/J, Gt(ROSA)26Sortm9(CAG-tdTomato)Hze/J, Csf1r/J|MGI:3813511, MGI:5568569, MGI:5780867|Semi-dominant|colony stimulating factor 1 receptor|Csf1r|||MGI:1339758|colony stimulating factor 1 receptor; targeted mutation 1.2, Jeffrey W Pollard|Csf1r|MGI:5780867|18|||||||||||||||||||||||||||||Mice in which tamoxifen treatment induces Cre expression in all CX3CR1+ cells, leading them to express Tomato and disrupt CSF1R expression in all CX3CR1+ cells. This mouse line results from the cross of 3 mouse lines imported from Jackson labs:Ai9 (B6.Cg-Gt(ROSA)26Sortm9(CAG-tdTomato)Hze/J): a Tamoxifen inducible CreERT2 reporter tool strain designed to have a loxP-flanked STOP cassette preventing transcription of a CAG promoter-driven red fluorescent protein variant (tdTomato) - all inserted into the Gt(ROSA)26Sor locus. Ai9 mice express robust tdTomato fluorescence following Cre-mediated recombination. This strain is congenic on the C57BL/6J genetic background. CX3CR1-CreERT2 (B6.129P2(C)-Cx3cr1tm2.1(cre/ERT2)Jung/J) : Cx3cr1CreER knock-in/knock-out mice express tamoxifen-inducible Cre recombinase under the direction of the Cx3cr1 promoter in the mononuclear phagocyte system making them useful for fate-mapping studies of the monocyte and macrophage compartment, as well as microglia.CSF1R fl/fl (B6.Cg-Csf1rtm1.2Jwp/J): a floxed mutant mice possess loxP sites flanking exon 5 of the colony stimulating factor 1 receptor (Csf1r) gene and may be useful in studying the role of CSF1R in development.Mice homozygous for the 3 mutations are CX3CR-1 deficient. While in untreated mice, all cells do not express Tomato and are CSF1R sufficient, Tamoxifen treatment induces Tomato exppression and CSF1R deficiency in all CX3CR1+ cells |Mice heterozygous for the 3 mutations are hemizygous for CX3CR1 Untreated mice have a normal phenotype with no Tomato expression and CSF1R deficiency. Tamoxifen treatment induces Tomato expression and disruption of one CSF1 gene. Their phenotype looks normal otherwise. |C57Bl/6N|Yes|Yes|Yes|Yes|Yes|Yes|No|Excellent|more than 10|||No|21-Mar-2022|Cryopreserved sperm|50.0|0.0|Unknown|||Possibly| 9364.0|C3TAC (CX3CR1-CreERT2 x Ai9 x CSF1Ffl/fl)|B6.129P2(C)-Cx3cr1/J, Gt(ROSA)26Sortm9(CAG-tdTomato)Hze/J, Csf1r/J|MGI:3813511, MGI:5568569, MGI:5780867|Semi-dominant|chemokine (C-X3-C motif) receptor 1|Cx3cr1||| MGI:1333815|C-X3-C motif chemokine receptor 1; targeted mutation 2.1, Steffen Jung|Cx3cr1|MGI:5467985|9|||||||||||||||||||||||||||||Mice in which tamoxifen treatment induces Cre expression in all CX3CR1+ cells, leading them to express Tomato and disrupt CSF1R expression in all CX3CR1+ cells. This mouse line results from the cross of 3 mouse lines imported from Jackson labs:Ai9 (B6.Cg-Gt(ROSA)26Sortm9(CAG-tdTomato)Hze/J): a Tamoxifen inducible CreERT2 reporter tool strain designed to have a loxP-flanked STOP cassette preventing transcription of a CAG promoter-driven red fluorescent protein variant (tdTomato) - all inserted into the Gt(ROSA)26Sor locus. Ai9 mice express robust tdTomato fluorescence following Cre-mediated recombination. This strain is congenic on the C57BL/6J genetic background. CX3CR1-CreERT2 (B6.129P2(C)-Cx3cr1tm2.1(cre/ERT2)Jung/J) : Cx3cr1CreER knock-in/knock-out mice express tamoxifen-inducible Cre recombinase under the direction of the Cx3cr1 promoter in the mononuclear phagocyte system making them useful for fate-mapping studies of the monocyte and macrophage compartment, as well as microglia.CSF1R fl/fl (B6.Cg-Csf1rtm1.2Jwp/J): a floxed mutant mice possess loxP sites flanking exon 5 of the colony stimulating factor 1 receptor (Csf1r) gene and may be useful in studying the role of CSF1R in development.Mice homozygous for the 3 mutations are CX3CR-1 deficient. While in untreated mice, all cells do not express Tomato and are CSF1R sufficient, Tamoxifen treatment induces Tomato exppression and CSF1R deficiency in all CX3CR1+ cells |Mice heterozygous for the 3 mutations are hemizygous for CX3CR1 Untreated mice have a normal phenotype with no Tomato expression and CSF1R deficiency. Tamoxifen treatment induces Tomato expression and disruption of one CSF1 gene. Their phenotype looks normal otherwise. |C57Bl/6N|Yes|Yes|Yes|Yes|Yes|Yes|No|Excellent|more than 10|||No|21-Mar-2022|Cryopreserved sperm|||Unknown|||Possibly| 9364.0|C3TAC (CX3CR1-CreERT2 x Ai9 x CSF1Ffl/fl)|B6.129P2(C)-Cx3cr1/J, Gt(ROSA)26Sortm9(CAG-tdTomato)Hze/J, Csf1r/J|MGI:3813511, MGI:5568569, MGI:5780867|Semi-dominant|gene trap ROSA 26, Philippe Soriano|Gt(ROSA)26Sor|||MGI:104735|gene trap ROSA 26, Philippe Soriano; targeted mutation 9, Hongkui Zeng|Gt(ROSA)26Sor|MGI:3809523|6|||||||||||||||||||||||||||||Mice in which tamoxifen treatment induces Cre expression in all CX3CR1+ cells, leading them to express Tomato and disrupt CSF1R expression in all CX3CR1+ cells. This mouse line results from the cross of 3 mouse lines imported from Jackson labs:Ai9 (B6.Cg-Gt(ROSA)26Sortm9(CAG-tdTomato)Hze/J): a Tamoxifen inducible CreERT2 reporter tool strain designed to have a loxP-flanked STOP cassette preventing transcription of a CAG promoter-driven red fluorescent protein variant (tdTomato) - all inserted into the Gt(ROSA)26Sor locus. Ai9 mice express robust tdTomato fluorescence following Cre-mediated recombination. This strain is congenic on the C57BL/6J genetic background. CX3CR1-CreERT2 (B6.129P2(C)-Cx3cr1tm2.1(cre/ERT2)Jung/J) : Cx3cr1CreER knock-in/knock-out mice express tamoxifen-inducible Cre recombinase under the direction of the Cx3cr1 promoter in the mononuclear phagocyte system making them useful for fate-mapping studies of the monocyte and macrophage compartment, as well as microglia.CSF1R fl/fl (B6.Cg-Csf1rtm1.2Jwp/J): a floxed mutant mice possess loxP sites flanking exon 5 of the colony stimulating factor 1 receptor (Csf1r) gene and may be useful in studying the role of CSF1R in development.Mice homozygous for the 3 mutations are CX3CR-1 deficient. While in untreated mice, all cells do not express Tomato and are CSF1R sufficient, Tamoxifen treatment induces Tomato exppression and CSF1R deficiency in all CX3CR1+ cells |Mice heterozygous for the 3 mutations are hemizygous for CX3CR1 Untreated mice have a normal phenotype with no Tomato expression and CSF1R deficiency. Tamoxifen treatment induces Tomato expression and disruption of one CSF1 gene. Their phenotype looks normal otherwise. |C57Bl/6N|Yes|Yes|Yes|Yes|Yes|Yes|No|Excellent|more than 10|||No|21-Mar-2022|Cryopreserved sperm|||Unknown|||Possibly| 7570.0|Grey macro|B6/Mrit-MRI114908|B6/Mrit-MRI114908|Recessive|unknown||Unknown||||||Unknown|||||||||||||||||||||||||||||Grey coat color in a C57BL/6 mice associated with macrocytosis. The females are infertile.|The heterozygous are normal.|C57BL/6|Yes|No|Yes|Yes|Yes|Yes|No|Good||||No|20-Jan-2014|Cryopreserved sperm|70.0|0.0|Unknown||Macrocytosis, coat-color, ENU|Yes| 7764.0|LeptinRfloxed|B6.129P2-Lepr/JAusb||Recessive|leptin receptor|Lepr||Leprb, LEPROT, leptin receptor gene-related protein, Modb1, obese-like, obl, Obr, OB-RGRP|MGI:104993|leptin receptor; targeted mutation 1, Jeffrey M Friedman|Lepr|MGI:2176774|4|||||||||||||||||||||||||||||Normal phenotype||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|12-Oct-2014||0.0|0.0|Unknown||receptor, ob/ob|Yes| 7298.0|Il7Tg:Thy1.1|B6.Cg-Thy1 Tg(H2-Ea-Il7)10Rhdr/ScrAusbAnu||Recessive|thymus cell antigen 1, theta|Thy1||CD90, T25, theta, Thy-1, Thy1.1, Thy 1.2, Thy-1.2, Thy1.2|MGI:98747|thymus cell antigen 1, theta; a variant|Thy1|MGI:3579311|9|||||||||||||||||transgene insertion 10, Rhodri Ceredig|H2-Ea promoter|||||||||||No B cells||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|22-Mar-2013|Cryopreserved sperm|44.0|0.0|Unknown||ENU, B cell, ATPase|Yes| 1784.0|Cathepsin- B X OT-1|C57BL/6-Ctsb Tg(TcraTcrb)1100Mjb/Wehi||Recessive|cathepsin B|Ctsb|Nil||MGI:88561|cathepsin B; targeted mutation 1, Jan Deussing|Ctsb|MGI:2182129|14||||||||||||||||Yes|transgene insertion 1100, Michael J Bevan||||||||||||Purified CD8+ cytotoxic T lymphocytes of cathepsin B-null gene-targeted mice were able to induce normal death of target cells both in vitro and in vivo and to survive the encounter with target cells as efficiently as cathepsin B-expressing killer cells. We conclude that cathepsin B is not essential for protection of cytotoxic lymphocytes from the toxic effects of their secreted perforin.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|03-Aug-2007||0.0|0.0|Unknown||T cell, protease, CD8, cytotoxic, perforin|Yes| 5091.0|APP23/Tau KO|C57BL/6-Tg(Thy1-APP)3Somm Mapt||Recessive|microtubule-associated protein tau|Mapt|Nil|Mtapt, Tau|MGI:97180|microtubule-associated protein tau; targeted mutation 1, Kerry Lee Tucker|Mapt|MGI:2670768|11|||||||||||||||||transgene insertion 3, Bernd Sommer|mouse Thy1|Highest levels of transgene expression in the neocortex and hippocampus||||||||||Unknown|Unknown|C57BL/6|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|15-Apr-2010||0.0|0.0|Yes|Alzheimer disease (AD)|Alzheimer disease (AD), amyloid precursor protein, Swedish double mutation, tau, human APP751, congophilic plaques, dystrophic cholinergic fibers|No| 1843.0|PU.1|C57BL/6-Sfpi1/Wehi||Dominant|SFFV proviral integration 1|Sfpi1|Normal|Dis-1, PU.1, Sfpi-1, Spi-1, Tcfpu1, Tfpu.1|MGI:98282|targeted mutation 1, Stephen L Nutt|Sfpi1|MGI:3528071|2||||||||||||||||Yes|Green Fluorescent Protein|Sfpi1|||||||||||Normal. Mice express GFP||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|10-Aug-2007||0.0|0.0|Unknown||Ets transcription factor, haemopoietic progenitor, Stem Cell, Myeloid Progenitor|Yes| 3474.0|Moz KO|BALB/c;FVB-Myst3/Wehi||Recessive|MYST histone acetyltransferase (monocytic leukemia) 3|Myst3|Nil|9930021N24Rik, KAT6A, MOZ, Zfp220|MGI:2442415|MYST histone acetyltransferase (monocytic leukemia) 3; targeted mutation 1, Anne K Voss MGI ID: |Myst3|MGI:3626344|8||||||||||||||||No|||||||||||||Homozygous null mice display perinatal lethality, cyanosis, decreased hematopoietic progenitor cell numbers, and severely impaired spleen and thymus development, but are not anemic. |Subfertile. Heterozygotes display strain background dependent reductions in fertility.|FVB x BALB/c|No|No|Yes|No|No|Yes|No|Unknown||||No|22-Jul-2008||0.0|0.0|Unknown||Thymus, perinatal lethality, craniofacial, heart, absent spleen|Yes| 8587.0|F2rl1 fl|C57BL/6N-F2rl1/MarpApb||Recessive|coagulation factor II (thrombin) receptor-like 1|F2rl1||Gpcr11, Par2, PAR-2, Protease-activated receptor-2, proteinase-activated receptor-2|MGI:101910|coagulation factor II (thrombin) receptor-like 1; targeted mutation 1c, Wellcome Trust Sanger Institute|F2rl1|MGI:6151132|12|||||||||||||||||||||||||||||Normal||C57BL/6N|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|17-Oct-2018|Cryopreserved sperm|30.0|0.0|Unknown||T cell, periodontitis, thymic and splenic hypoplasia|Yes| 7766.0|Scl-flox|C57BL/6-Sost/Ausb||Recessive|sclerostin|Sost|Unknown|5430411E23Rik|MGI:1921749||||11|||||||||||||||||||||||||||||Normal||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|12-Oct-2014||0.0|0.0|Unknown|||Yes| 3489.0||129/Sv-gp130||Recessive|interleukin 6 signal transducer|Il6st|Normal|5133400A03Rik, CD130, D13Ertd699e, gp130|MGI:96560|interleukin 6 signal transducer; targeted mutation 1, Ashley R Dunn |Il6st|MGI:2388476|13||||||||||||||||No|||||||||||||Degenerative joint disease, gastrointestinal ulceration, and failure of uterine implantation. Mice develop a different gait. Stiff joints beginning at 2 weeks of age.||129/Sv|Yes|No|Yes|Yes|Yes|Yes|No|Unknown||||No|23-Jul-2008||0.0|0.0|Unknown||signal transduction, src, kinase, receptor, IL-6|Yes| 3496.0||BALB/c-H2||Recessive|histocompatibility-2, MHC|H2|Unknown|H-2, MHC-II|MGI:95894|b variant|H2|MGI:3579319|17||||||||||||||||Yes|||||||||||||Balb/c is usually H2. The H2 complex contains 3 major classes of highly polymorphic gene sets: class I (H2-K, H2-D, Q, H2-T18 genes), class II (H2-I genes), and class III (H2-S genes). These genes are involved in many processes, including graft rejection, immune response, antigen presentation and complement component.||BALB/c|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|24-Jul-2008||0.0|0.0|Unknown||haplotype, presentation, antigen presentation, T cell|Yes| 7767.0|OncCre|B6N.FVB-Tg(BGLAP-cre)1Clem/JAusb||Dominant||||||||||||||||||||||||||transgene insertion 1, Thomas L Clemens|human osteocalcin (BGLAP) promoter|Osteoblasts|||||||||||Normal.Cre recombinase expression restricted to osteoblasts.|C57BL/6N|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|12-Oct-2014||0.0|0.0|Unknown||osteoblast, osteocalcin, Cre recombinase, IGF, mineralization|Yes| 8588.0|MDX:PAR2|B6.B10-Dmd F2rl1/Apb||Recessive|dystrophin, muscular dystrophy|Dmd||Dp427, Dp71, Duchenne muscular dystrophy, dys, mdx, pke, X-linked muscular dystrophy|MGI:94909|mdx & F2rl1|dystrophin, muscular dystrophy; X linked muscular dystrophy|Dmd|X|||||||||||||||||||||||||||||Dystrophic (mdx)PAR2 deficiency|Normal|C57BL/6 ; C57BL/10|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|17-Oct-2018|Cryopreserved sperm|40.0|0.0|Unknown|||Yes| 8588.0|MDX:PAR2|B6.B10-Dmd F2rl1/Apb||Recessive|coagulation factor II (thrombin) receptor-like 1|F2rl1||Gpcr11, Par2, PAR-2, Protease-activated receptor-2, proteinase-activated receptor-2|MGI:101910|coagulation factor II (thrombin) receptor-like 1; targeted mutation 1, Shaun R Coughlin|F2rl1|MGI:2179844|13|||||||||||||||||||||||||||||Dystrophic (mdx)PAR2 deficiency|Normal|C57BL/6 ; C57BL/10|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|17-Oct-2018|Cryopreserved sperm|||Unknown|||Yes| 3521.0||Oct-1 Knockout||Recessive|POU domain, class 2, transcription factor 1 |Pou2f1|Nil|2810482H01Rik, oct-1, Oct-1A, Oct-1B, Oct-1C, Oct-1z, Otf-1, Otf1|MGI:101898|POU domain, class 2, transcription factor 1; targeted mutation 1, Phillip A Sharp |Pou2f<1tm1Shrp>|MGI:3028868|1||||||||||Unknown to Unknown||||||Yes|||||||||||||Prenatal lethality - on mixed background involving 129S4/SvJae and C57BL/6 genetic background, death occurs during a window spanning from approximately E12 through birth. Decreased erythropoiesis in embryos. Vision/eye phenotype - lens placode induction and subsequent lens morphogenesis appears normal, with some embryos having morphologically normal,small lens pits. Small lens - some embryos at E10.5 have small lenses.||129 x C57BL/6|No|No|Yes|No|No|Yes|No|Unknown||||No|28-Jul-2008||0.0|0.0|Unknown||embryonic lethality, erythropoiesis, DNA binding transcription factor, Oct-2, anemic|Yes| 3546.0||B6.D2-Kitl/JWehi||Semi-dominant|kit ligand|Kitl|Normal|Gb, grizzle-belly, Mgf, SF, Sl, SLF, Steel, Steel factor, stem cell factor|MGI:96974|kit ligand; steel Dickie |Kitl|MGI:1856164|10||||||||||||||||No|||||||||||||Anaemic, Light Coat, White Spotting Maximal severity of phenotype according to age (pre-weaning): E13 - wean Homozygotes will be black-eyed whites and die between E13 and Weaning. Although homozygous Kitl/Kitl have been described as being viable, Dr. Jane Barker of The Jackson Laboratory has found that in her colony B6.D2-Kitl homozygotes die at birth or soon thereafter. ||C57BL/6 x DBA/2|Yes|No|Yes|Yes|No|Yes|No|Unknown||||No|30-Jul-2008||0.0|0.0|Unknown||c-kit, melanocyte, progenitor stem cell, mast cell, pigment|Yes| 3537.0||OBF-1 knockout||Recessive|POU domain, class 2, associating factor 1|Pou2af1|Nil|Bob-1, BOB.1, Bob1, OBF-1, OBF.1, OCA-B, OCAB|MGI:105086|targeted mutation 1, Patrick Matthias|Pou2af1|MGI:2388055|9||||||||||||||||Yes|||||||||||||Homozygotes for targeted null mutations exhibit reduced numbers of mature B cells, absence of germinal centers, and low serum levels of non-IgM immunoglobulins.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|29-Jul-2008||0.0|0.0|Unknown||B cell, immunoglobulin, antibody, germinal centre|Yes| 7768.0|ONCtgN|C57BL/6-Tg(Bglap)/Ausb||Dominant||||||||||||||||||||||||||bone gamma carboxyglutamate protein||||||||||||Normal||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|12-Oct-2014||0.0|0.0|Unknown|||Yes| 5911.0|Min Chen C57||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 3516.0|Aiolos Knockout|129-Ikzf3/Wehi||Recessive|IKAROS family zinc finger 3|Ikzf3|Nil|5830411O07Rik, Aiolos, Zfpn1a3|MGI:1342542|targeted mutation 1, Katia Georgopoulos|Ikzf3|MGI:2388132|11||||||||||||||||Yes|||||||||||||Homozygous mutants exhibit greatly reduced B cell populations in the peritoneum, marginal zone and recirculating bone marrow. Aging mutants express autoantibodies, frequently develop B cell lymphomas, and display symptoms characteristic of SLE||129/Sv|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|28-Jul-2008||0.0|0.0|Yes||autoimmunity, systemic lupus erythromatosis, B cell, autoantibodies, lymphoma|Yes| 3533.0||C57BL/6.129-Pou2f2Tg(IL5rα)1Ktk||Recessive|POU domain, class 2, transcription factor 2|Pou2f2|Normal|Oct-2, Oct2a, Oct2b, Otf-2, Otf2|MGI:101897|POU domain, class 2, transcription factor 2; targeted mutation 1, Lynn M Corcoran |Pou2f2|MGI:3037094|7||||||||||||||||Yes|interleukin 5 receptor alpha (IL5Rα)||||||||||||Oct2 -/- mice die shortly after birth. B cell fail to mature.||C57BL/6|No|No|Yes|No|No|Yes|No|Unknown||||No|29-Jul-2008||0.0|0.0|Unknown||transcription, B cell, antibody secreting cells, IL5 receptor, differentiation|Yes| 3517.0|Ikaros Knockout|129-Ikzf1/Wehi||Recessive|IKAROS family zinc finger 1|Ikzf1|Nil|5832432G11Rik, hlk-1, Ikaros, LyF-1, Zfpn1a1|MGI:1342540|targeted mutation 2, Katia Georgopoulos|Ikzf1|MGI:2158690|11||||||||||||||||No|||||||||||||Homozygous mutants have a variety of T, B, and hematopoeitic cell maturation defects.||129/Sv|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|28-Jul-2008||0.0|0.0|Unknown||T cell, B cell , Natural killer cell ; NK cell, differentiation, progenitor|Yes| 3527.0||C57BL/6-Socs3/Socs3 Tg(Vav1-cre)1Awr/0||Recessive|suppressor of cytokine signaling 3|Socs3|Unknown|CIS3, Cish3, cytokine-inducible SH2 protein 3, E2a-Pbx1 target gene in fibroblasts 10, EF-10, SOCS-3, SSI-3, STAT-induced STAT inhibitor 3|MGI:1201791|suppressor of cytokine signaling 3; targeted mutation 1, Warren S Alexander |Socs3|MGI:2180861|11||||||||||||||||Yes|transgene insertion 1, Andrew W Roberts |Vav1|||||||||||Deletion of Socs3 in all haemopoietic cells and endothelial cells. Increased neutrophil cell number - enhanced by injection with CSF3 (G-CSF), which also induced progenitor cell mobilization, splenomegaly, and inflammatory neutrophil infiltration into multiple tissues resulting in partial hind leg paralysis. Increased inflammatory response - evident by 17 weeks of age and characterized by inflammation in the pleural and peritoneal cavities and infiltration of hematopoietic cells into the liver and lungs.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|28-Jul-2008||0.0|0.0|Unknown||granulopoiesis, inflammation, neutrophil, G-CSF|Yes| 3527.0||C57BL/6-Socs3/Socs3 Tg(Vav1-cre)1Awr/0||Recessive|suppressor of cytokine signaling 3 |Socs3 |Unknown|CIS3, Cish3, cytokine-inducible SH2 protein 3, E2a-Pbx1 target gene in fibroblasts 10, EF-10, SOCS-3, SSI-3, STAT-induced STAT inhibitor 3|MGI:1201791 |suppressor of cytokine signaling 3; targeted mutation 2, Warren S Alexander |Socs3|MGI:2663917|11|||||||||||||||||||||||||||||Deletion of Socs3 in all haemopoietic cells and endothelial cells. Increased neutrophil cell number - enhanced by injection with CSF3 (G-CSF), which also induced progenitor cell mobilization, splenomegaly, and inflammatory neutrophil infiltration into multiple tissues resulting in partial hind leg paralysis. Increased inflammatory response - evident by 17 weeks of age and characterized by inflammation in the pleural and peritoneal cavities and infiltration of hematopoietic cells into the liver and lungs.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|28-Jul-2008||||Unknown||granulopoiesis, inflammation, neutrophil, G-CSF|Yes| 8532.0|ENU41:G3|ANU:ENU41:G3||Recessive|Unknown||||||||Unknown||||||||||||||||Unknown|||||||||||||Unknown|Unknown|C57BL/6NCrlAnu|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||1||No|10-Jul-2018||0.0|0.0|Unknown||ENU, random, mutagenesis, screen|Yes| 3547.0||K5-mOVA.bm1||Recessive||||||||||||||||||||||||||membrane bound chicken ovalbumin|Keratin 5 (K5)|||||||||||Mice express membrane bound ovalbumin in the skin and thymus. In bm1 mice the MHC I K molecule cannot present the OVA peptide as can K in wild-type C57BL/6 mice and recognised by the OT-1 TCR. ||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|30-Jul-2008||0.0|0.0|Unknown||autoimmunity, T cell, presentation, selection, major histocompatibility class (MHC)|Yes| 9377.0|SEPS1 global knockout (GKO)|C57Bl/6-Selenos/Apb||Semi-dominant|selenoprotein S|Selenos||1500011E07Rik, C78786, H4, H-4, H47, H-47, Seps1, Vimp|MGI:95994||||7|||||||||||||||||||||||||||||Young Seps1 GKO knockout mice present with a reduction in muscle strength and exercise capacity, and there is a blood vessel phenotype characterised by increased vascular reactivity. The mice are otherwise healthy.|Young Seps1 GKO heterozygous mice present with a reduction in muscle strength and exercise capacity, and there is a blood vessel phenotype characterised by increased vascular reactivity. The mice are otherwise healthy, fertility and breeding performance are not compromised in the heterozygous male and female mice.|C57Bl/6J|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|22-Apr-2022|Cryopreserved sperm|50.0|0.0|Unknown|||Yes| 3578.0||C57BL/6-Tg(RIP-Ova) Bcl2l11||Recessive|BCL2-like 11 (apoptosis facilitator)|Bcl2l11|Unknown|1500006F24Rik, Bim, Bod|MGI:1197519|targeted mutation 1.1, Andreas Strasser|Bcl2l11|MGI:2156498|2||||||||||||||||Yes|Chicken Ovalbumin|rat insulin 2|Low||||||||||||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|04-Aug-2008||0.0|0.0|Unknown||T cell, B cell, myeloid, ovalbumin, T cell receptor (TCR)|Yes| 8533.0|ENU42:G3|ANU:ENU42:G3||Recessive|Unknown||||||||Unknown||||||||||||||||Unknown|||||||||||||Unknown|Unknown|C57BL/6NCrlAnu|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||1||No|10-Jul-2018|Cryopreserved sperm|286.0|0.0|Unknown||ENU, random, mutagenesis, screen|Yes| 3588.0||C57BL/6-IL7rTg(TcraTcrb)1100Mjb||Recessive|interleukin 7 receptor|Il7r|Nil|CD127, IL-7 receptor alpha chain, IL-7Ralpha|MGI:96562|targeted mutation 1, Immunex|Il7r|MGI:1857198|1||||||||||||||||Yes|transgene insertion 1100, Michael J Bevan||||||||||||Transgenic mice on a C57BL/6 background are somewhat immunodeficient, and may be used to study the role of peptides in positive selection and the response of CD8+ T cells to antigen. Carry OVA-specific, H-2Kb-restricted T cell receptor.IL-7r KO mice: - arrested B cell differentiation (J:21135) development arrested at the pro-B cell stage decreased B cell number (J:21135) reduced numbers of B cells arrested T cell differentiation (J:21135) development arrested before T cell receptor beta chain rearrangement and before CD4 and CD8 surface expression decreased T cell number (J:21135) reduced numbers of T cells spleen hypoplasia (J:21135) thymus hypoplasia (J:21135)||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|05-Aug-2008||0.0|0.0|Unknown||T cell, B cell, ovalbumin, differentiation, hypoplasia|Yes| 3600.0||C57BL/6-Tg(CAG-Bgeo/GFP)21Lbe/JWehi||Dominant||||||||||||||||||||||||||transgene insertion 21, Corrinne Lobe|CMV enhancer/chicken beta actin|||||||||||Mice that are homozygous for the transgenic insert are viable, fertile, normal in size and do not display any gross physical or behavioural abnormalities. Expression of lacZ in transgenic mice is widespread, with notable exceptions being liver and lung tissue. This expression is observed throughout all embryonic and adult stages Expresses enhanced GFP upon Cre-mediated excision.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|06-Aug-2008||0.0|0.0|Unknown||LacZ, Green Fluorescent Protein (GFP), embryonic development|Yes| 3580.0||BALB/c-Tg(CIITA)||Recessive||||||||||||||||||||||||||class II transactivator (CIITA)||||||||||||||BALB/c|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|04-Aug-2008||0.0|0.0|Unknown||MHC, class II, H2, histocompatability 2, T cell|Yes| 8534.0|ENU43:G3|ANU:ENU43:G3||Recessive|Unknown||||||||Unknown||||||||||||||||Unknown|||||||||||||Unknown|Unknown|C57BL/6NCrlAnu|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||1||No|10-Jul-2018|Cryopreserved sperm|452.0|0.0|Unknown||ENU, random, mutagenesis, screen|Yes| 6693.0|129R|R1-129/Ausb||||||||||||||||||||||||||||||||||||||||None||R1-129|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|02-Dec-2011||0.0|0.0|Unknown|||Possibly| 1548.0|WB6|C57BL/6-Tyr/AnuApb||Recessive|tyrosinase|Tyr|Nil|skc35|MGI:98880|tyrosinase; albino 2 Jackson|Tyr|MGI:1855985|7||||||||||||||||No|||||||||||||Absent skin pigmentation:* mice lack pigmentation in the skin and eyes* mice lack detectable amounts of melanin in the hairbulbs||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|06-Jul-2007|Cryopreserved sperm|150.0|0.0|Unknown||albino, hypopigmentation, melanin, retina|Yes| 5906.0|MC4R||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 7573.0|37L1lacZ|C57BL/6N-A Gpr37L1/Apb||Dominant|G protein-coupled receptor 37-like 1|Gpr37l1|Unknown|CAG-18, D0Kist8|MGI:1928503|G protein-coupled receptor 37-like 1; targeted mutation 1b, Wellcome Trust Sanger Institute|Gpr37L1||1||||||||||Unknown to Unknown|||||||||||||||||||Unknown. Reporter mouse with gene deletion.|Unknown. Reporter mouse with gene deletion.|C57BL/6N|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown|Pure background||het x het|No|20-Jan-2014|Cryopreserved sperm|70.0|0.0|No|||Possibly| 4198.0|NOD-Tg(IE-Igrp)69Wehi/J|NOD-Tg(H2-Ea-G6pc2)69Tkay/Apb ||Dominant|||Unknown||||||Unknown||||||||||||||||No|transgene insertion 69, Thomas Kay|1.8-kb fragment encoding nucleotides -1,903 through -39 of the 5' flanking sequence of the MHC Class II gene, H2-Ea (k allele)|Low||||||||||Insulitis: * mice develop insulitis with similar incidence and severity as non-transgenic controlsDecreased T cell proliferation: * G6pc2206-214-specific CD8+ T cells transferred from Tg(TcraTcrbNY8.3)1Pesa NOD mice proliferate extensively in peripheral and other lymph nodesAbnormal CD8-positive T cell morphology:* T cells specific for IGRP206-214 (G6pc2206-214) are not detected in peripheral blood* a complete absence of G6pc2206-214-specific CD8+ T cells is observed in expanded, cultured islet-infiltrating T cells compared to 40% of cultured T cells from control littermatesAbnormal CD4-positive T cell physiology:* no spontaneous CD4+ T cell response by cultured splenocytes exposed to G6pc24-22 peptide is detected in contrast to wild-type NOD miceAbnormal immune tolerance:* expanded T cells from pancreatic islets demonstrate tolerance to MHC class I and II-restricted G6pc2 peptidesIncreased susceptibility to autoimmune diabetes:* mice develop Type I diabetes at rate similar to wild-type NOD controlsIncreased anti-insulin autoantibody level:* insulin autoantibodies are elevated in 12-week old transgenic animals, similar to control wild-type NOD mice.Decreased T cell proliferation:* G6pc2206-214-specific CD8+ T cells transferred from Tg(TcraTcrbNY8.3)1Pesa NOD mice proliferate extensively in peripheral and other lymph nodes.Abnormal CD8-positive T cell morphology:* T cells specific for IGRP206-214 (G6pc2206-214) are not detected in peripheral blood.* a complete absence of G6pc2206-214-specific CD8+ T cells is observed in expanded, cultured islet-infiltrating T cells compared to 40% of cultured T cells from control littermates.Insulitis:* mice develop insulitis with similar incidence and severity as non-transgenic controls.|Type 1 Diabetes with same incidence as NOD/Lt control or littermate control mice. Mice do not develop T cell responses to the beta cell autoantigen G6pc2.|NOD/Lt|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|20-Dec-2008|Cryopreserved sperm|130.0|0.0|Yes||Tolerance, Autoimmunity, Autoantigen|Yes| 7769.0|RANK|B6.129P2-Tnfrsf11a/Ausb||Recessive|tumor necrosis factor receptor superfamily, member 11a, NFKB activator|Tnfrsf11a|Normal|Rank, TRANCE-R|MGI:1314891|tumor necrosis factor receptor superfamily, member 11a, NFKB activator; targeted mutation 1.1, Josef M Penninger|Tnfrsf11a|MGI:4415800|1|||||||||||||||||||||||||||||Normal|Normal|129P2/OlaHsd x C57BL/6J|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|12-Oct-2014||0.0|0.0|Unknown||receptor, signal transduction|Yes| 2434.0|Laxman:Hamlet|C57BL/6-Tg(H2-sHELdimer)/Apb Tg(IghelMD4)4Ccg/AnuApb||Recessive||||||||||||||||||||||||||soluble Hen Egg Lysozyme dimeric molecule|H-2K promoter|High|||||||||||High serum expression of dimeric soluble HEL.B cells express immunoglobulin that has a high affinity for hen egg lysozyme antigen (HEL).|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|13-Jan-2008|Cryopreserved sperm|75.0|0.0|No||Hen Egg Lysozyme HEL, dimeric, immunoglobulin, B cell, lymphocyte|Yes| 2434.0|Laxman:Hamlet|C57BL/6-Tg(H2-sHELdimer)/Apb Tg(IghelMD4)4Ccg/AnuApb||Recessive||||||||||||||||||||||||||transgene insertion 4, Christopher C Goodnow|||||||||||||High serum expression of dimeric soluble HEL.B cells express immunoglobulin that has a high affinity for hen egg lysozyme antigen (HEL).|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|13-Jan-2008|Cryopreserved sperm|||No||Hen Egg Lysozyme HEL, dimeric, immunoglobulin, B cell, lymphocyte|Yes| 7574.0|37L1KO|C57BL/6-Gpr37L1/NsmitApb||Recessive|G protein-coupled receptor 37-like 1|Gpr37l1|Reduced|CAG-18, D0Kist8|MGI:1928503|G protein-coupled receptor 37-like 1; targeted mutation 1d, Wellcome Trust Sanger Institute|Gpr37L1||1||||||||||Unknown to Unknown|||||||||||||||||||deletion of GPR37L1 causes a female-specific increase in systolic, diastolic, and mean arterial pressures.When challenged with short-term AngII infusion, only male GPR37L1 KO/KO mice developed exacerbated left ventricular hypertrophy and evidence of heart failure, while the female GPR37L1 KO/KO mice were protected from cardiac fibrosis.||C57BL/6J|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|6||het x het|No|20-Jan-2014|Cryopreserved sperm|54.0|0.0|No|||Possibly| 4781.0|T-Bird|B10.B6JAnu-Dsg4/AnuApb|B10.B6JAnu-Dsg4/AnuApb|Recessive|desmoglein 4|Dsg4|Unknown|CDHF13, lah|MGI:2661061|desmoglein 4; t-bird|Dsg4|MGI:5007752|18|ENSMUSG00000001804|ENSMUST00000019426|Dsg4-001|643|777|A to C|ENSMUSE00000445469|6|215|Threonine to Proline|||||GTGCACCCATGTTCATGGTGAACAGGTACACTGGAGAAGTCCGCACGATGTCCAATTTCCT|Unknown|||||||||||||Greasy Coat. Affected mice develop a dull, sparse and greasy coat at about ~40 days of age. ||C57BL/6 x C57BL10|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|5|||No|06-Sep-2009|Cryopreserved sperm|114.0|0.0|Unknown||Coat, greasy, hair, ENU|Yes| 93.0|Xander|C57BL/6JSfdAnu-Nfkb2/AnuApb|C57BL/6JSfdAnu-Nfkb2/AnuApb|Recessive|nuclear factor of kappa light polypeptide gene enhancer in B-cells 2, p49/p100|NFkb2|Nil|lyt, NF-kappaB2, p49, p49/p100, p50B, p52|MGI:1099800|xander|Nfkb2|MGI:2667230|19|ENSMUSG00000025225|ENSMUST00000073116|Nfkb2-201||||||||46381842|6|||TCATGGTCAAAGAGGACAAAGCCTCCTCCTTGTCCTCTCCAGATTTAATAATCTGGGTGT|No|||||||||||||Normal Thy1.2⁺ cellsReduced B220⁺ cellsDecrease numbers of peripheral B cells, normal numbers of BM B cellsNormal T cell numbersDecreased mature B2 cells in spleenSeven fold decrease in B1 cells in peritoneal cavitySmall peripheral lymph nodesDisturbed splenic microarchitectureLack of follicular dendritic cell clusters in spleen.Intrinsic to B cells||C57BL/6JSfdAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|06-Feb-2006|Cryopreserved sperm|20.0|0.0|Unknown||B cell, follicular dendritic cell, spleen, lymphocyte|Yes| 4474.0|SPC-rtTA|C.FVB/N-Tg(SFTPC-rtTA)5Jaw/AnuApb||Dominant||||||||||||||||||||||||||transgene insertion 5, Jeffrey A Whitsett|human SFTPC (SPC) (surfactant protein-C)|respiratory epithelial cells|||||||||||The human SFTPC promoter is active in respiratory epithelial cells.|BALB/c x FVB/N|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|10|||No|22-Feb-2009|Cryopreserved sperm|165.0|0.0|Unknown||epithelium, asthma, eosinophil, IgE, lung|No| 4521.0|blonde ; ENU8C:032|B6;CBA-Erp44/AnuApb|B6;CBA-Erp44/AnuApb|Recessive|endoplasmic reticulum protein 44|Erp44||1110001E24Rik, Txndc4|MGI:1923549|endoplasmic reticulum protein 44; mutation 1, The Australian National University|Erp44|MGI:5563471|4|ENSMUSG00000028343|ENSMUST00000030028|Erp44-001||||||||48231077|5|||TTTATATGTTGCAAAATAATTGGATGCTTTATTTTACAGCGCAGTAAGAGAAATATCATT|Yes|||||||||||||Light coat colour, small stature, scaly tail.Positive for anti-nuclear antibodies?||C57BL/6JSfdAnu x CBA/H|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|26-Feb-2009|Cryopreserved sperm|160.0|0.0|Unknown||Coat colour, dwarf, ENU, Wellcome Trust, ANAphylaxis|Yes| 8589.0|F2rl1tm1c:K14-cre|B6.129-F2rl1 Krt14/Apb||Recessive|coagulation factor II (thrombin) receptor-like 1|F2rl1||Gpcr11, Par2, PAR-2, Protease-activated receptor-2, proteinase-activated receptor-2|MGI:101910|coagulation factor II (thrombin) receptor-like 1; targeted mutation 1c, Wellcome Trust Sanger Institute|F2rl1|MGI:6151132|13|||||||||||||||||||||||||||||These mice were subjected to a model of periodontitis involving placement of a ligature around a tooth, combined with P. gingivalis infection ("Lig + Inf"). The intervention caused a significant 44% decrease in alveolar bone volume (assessed by microcomputed tomography) in wildtype (K14-Cre:F2rl1wt/wt ), but not littermate keratinocyte-specific PAR2 -null (K14-Cre:F2rl1fl/fl ) mice. Keratinocyte-specific ablation of PAR2 prevented the significant Lig + Inf-induced increase (2.8-fold) in the number of osteoclasts in alveolar bone and the significant up-regulation (2.4-4-fold) of the inflammatory markers IL-6, IL-1β, interferon-γ, myeloperoxidase, and CD11b in gingival tissue.|Normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|17-Oct-2018|Cryopreserved sperm|20.0|0.0|Unknown||Periodontal disease, infection|Yes| 8589.0|F2rl1tm1c:K14-cre|B6.129-F2rl1 Krt14/Apb||Recessive|keratin 14|Krt14||Cytokeratin 14, epidermolysis bullosa simplex, Dowling-Meara, Koebner, K14, Krt-1.14, Krt1-14|MGI:96688|keratin 14; targeted mutation 1.1, Walter Birchmeier|Krt14|MGI:2148597|11|||||||||||||||||||||||||||||These mice were subjected to a model of periodontitis involving placement of a ligature around a tooth, combined with P. gingivalis infection ("Lig + Inf"). The intervention caused a significant 44% decrease in alveolar bone volume (assessed by microcomputed tomography) in wildtype (K14-Cre:F2rl1wt/wt ), but not littermate keratinocyte-specific PAR2 -null (K14-Cre:F2rl1fl/fl ) mice. Keratinocyte-specific ablation of PAR2 prevented the significant Lig + Inf-induced increase (2.8-fold) in the number of osteoclasts in alveolar bone and the significant up-regulation (2.4-4-fold) of the inflammatory markers IL-6, IL-1β, interferon-γ, myeloperoxidase, and CD11b in gingival tissue.|Normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|17-Oct-2018|Cryopreserved sperm|||Unknown||Periodontal disease, infection|Yes| 5910.0|MID1KO||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 7575.0|37L1null|B6;129S1/SvImJ-Gpr37l1/Apb||Dominant|G protein-coupled receptor 37-like 1|Gpr37l1|Nil|CAG-18, D0Kist8|MGI:1928503||||1|||||||||||||||||||||||||||||Elevated blood pressure|Unknown. Potentially elevated blood pressure.|C57BL/6J|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|unknown|unknown|hom x hom|No|20-Jan-2014|Cryopreserved sperm|50.0|0.0|No||Heart, myocardium|Possibly| 7350.0|ST2 knockout|C.Cg-Il1rl1/Apb||Recessive|interleukin 1 receptor-like 1|Il1rl1|Nil|DER4, Fit-1, Ly84, St2, ST2, ST2L, St2-rs1, T1, T1 gene, T1/ST2|MGI:98427|interleukin 1 receptor-like 1; targeted mutation 1, Andrew NJ McKenzie|Il1rl1|MGI:2386675|1|||||||||||||||||||||||||||||Mice lack ST2 and ST2L proteins (these arise from splice variants of transcripts) that are respectively the soluble decoy receptot and membrane bound high affinity receptor for interleukin-33 (IL33). This results in resistance to chronic inflammatory conditions and some defects in Th2-dependent immunity, although the mice in an unchallenged condition can be considered as almost same as WT.|Normal|BALB/c|Yes|Yes|Yes|Yes|Yes|Yes|No|Excellent|many, >10 years||KO x KO with backcrossing on BALB/c every 2 generations or so.|No|06-Jun-2013|Cryopreserved sperm|45.0|0.0|No||Inflammation, Th2 cell, Bone, Mast cells|Yes| 7576.0|37L1cTg|C57BL/6-Tg(αMHC-Gpr37L1)/Apb||Dominant||||||||||||||||||||||||||G protein-coupled receptor 37-like 1|alpha-myosin heavy chain|||||||||||Unknown.|Unknown. |C57BL/6J|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|Pure background||hom x hom|No|20-Jan-2014|Cryopreserved sperm|65.0|0.0|No||Heart, myocardium|Possibly| 5208.0|Line:TF23|FVB/NJ-Tg(Prm1-Fgfr1*)4-9/MarpApb||Dominant||||||||||||||||||||||||||mutant fibroblast growth factor receptor 1|Prm1|restricted to sperm|||||||||||Mating of transgenic mice showed a significant reduction in pups per litter compared with wild-type littermates. Further analysis demonstrated that this subfertility was driven by a combination of reduced daily sperm output and a severely compromised ability of those sperm that were produced to undergo capacitation prior to fertilization. An analysis of key signal transduction proteins indicated that FGFR-1 is functional on wild-type sperm and probably signals via the phosphatidylinositol 3-kinase pathway. FGFR-1 activation also resulted in the downstream suppression of mitogen activated protein kinase signaling. These data demonstrate the FGFR-1 is required for quantitatively and qualitatively normal spermatogenesis and has a key role in the regulation of the global tyrosine phosphorylation events associated with sperm capacitation.|FVB/NJ|Yes|Yes|Yes|Yes|No|Yes|Yes|Unknown||||No|23-Aug-2010|Cryopreserved sperm|30.0|0.0|Unknown||signal transduction, Capacitation, Spermatogenesis, FGFR-1, Sperm|Yes| 6538.0|JAK3?|B6;129S4-Jak3/JAusb||Recessive|Janus kinase 3|Jak3|Nil||MGI:99928|Janus kinase 3; targeted mutation 1, Leslie J Berg|Jak3|MGI:1857276|8|||||||||||||||||||||||||||||Decreased CD4-positive T cell number:*Decrease in the proportion and absolute number of CD4+ cells in the spleen.Decreased CD8-positive T cell number:*Decrease in the proportion and absolute number of CD8+ cells in the spleen.Abnormal dendritic cell morphology Decreased myeloid dendritic cell number: *The proportion and absolute number of CD11c+ dendritic cells is decreased in the spleen. *However, the frequency plasmacytoid dendritic cells in the spleen is not significantly different from wild-type controls. Abnormal dendritic cell differentiation: *Splenic dendritic cells express higher levels of activation markers compared to cells from wild-type controls. *However, bone marrow precursors in vitro show a similar capacity to generate immature dendritic cells compared to wild-type controls.Abnormal splenic cell ratio:*Reduced numbers of splenocytes.*Decrease in the proportion and absolute number of CD11c+ dendritic, CD4+, and CD8+ cells in the spleen.*However, the frequency plasmacytoid dendritic cells is not significantly different from wild-type controls.Abnormal dendritic cell physiology:*In culture, dendritic cells are resistant to cytokine withdrawal-induced apoptosis.*Bone marrow-derived dendritic cells overproduce IL12 and IL10.*When bone marrow-derived dendritic cells are used in an adoptive transfer model the proportion of IFNG-producing cells is increased compared to when wild-type cells are used.|Abnormal leukocyte morphology:*Slight increase in the number of cells classified as myeloid or premonocytic. Decreased lymphocyte cell number: *Lymphopenia is seen in peripheral and bone marrow smears. *At 6-12 months of age, lymphocyte numbers in whole blood suspensions are decreased. Increased leukocyte cell number: *At 6-12 months of age, a profound increase in large granular cells is seen in the peripheral blood and spleen. *These large granular cells consist of 2 populations; cells of the neutrophilic lineage and cells of the monocytic lineage. Increased neutrophil cell number: *Significantly higher numbers of both segmented and band neutrophils. Increased monocyte cell number: *At 6 - 12 months of age in the bone marrow and spleen.|Mixed mice|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown||Jak3, IL-2 receptor|Yes| 5207.0|Line:TF14|FVB/NJ-Tg(Prm1-Fgfr1*)4-9/MarpApb||Dominant||||||||||||||||||||||||||mutant fibroblast growth factor receptor 1|Prm1|restricted to sperm|||||||||||Mating of transgenic mice showed a significant reduction in pups per litter compared with wild-type littermates. Further analysis demonstrated that this subfertility was driven by a combination of reduced daily sperm output and a severely compromised ability of those sperm that were produced to undergo capacitation prior to fertilization. An analysis of key signal transduction proteins indicated that FGFR-1 is functional on wild-type sperm and probably signals via the phosphatidylinositol 3-kinase pathway. FGFR-1 activation also resulted in the downstream suppression of mitogen activated protein kinase signaling. These data demonstrate the FGFR-1 is required for quantitatively and qualitatively normal spermatogenesis and has a key role in the regulation of the global tyrosine phosphorylation events associated with sperm capacitation.|FVB/NJ|Yes|Yes|Yes|Yes|No|Yes|Yes|Unknown||||No|23-Aug-2010|Cryopreserved sperm|30.0|0.0|Unknown||signal transduction, Capacitation, Spermatogenesis, FGFR-1, Sperm|Yes| 6858.0|UNC CF null mouse |B6.129P2-Cftr/J||Recessive|cystic fibrosis transmembrane conductance regulator homolog|Cftr|Nil|Abcc7|MGI:88388|cystic fibrosis transmembrane conductance regulator homolog; targeted mutation 1, University of North Carolina|Cftr|MGI:1856709|6|||||||||||||||||||||||||||||Poor body weight gain, females have low fertility; early death unless high fat diet with mild diahoreal agent to prevent gut obstruction. Poor survival. Upper incisors white chalky and weaker than normal. |Normal|C57BL/6J (inbred since 1992)|Yes|No|Yes|Yes|Yes|Yes|No|Poor|10|Extensive - colony est 1992, no new stock added since then|Male homozygous for CF with Het female|No|16-Mar-2012||0.0|0.0|Yes|Cystic fibrosis: multi-organ early fatal disease, primary channel defect is Cl-|cystic fibrosis, nasal airway, lung, CFTR, chloride, sodium|Possibly| 3552.0|KRN|C57BL/6-Tg(TcraR28,TcrbR28)KRNDim||Recessive||||||||||||||||||||||||||transgene insertion KRN, Diane Mathis |natural TCR alpha and -beta promoter/enhancer elements.|||||||||||A single founder (KRN) in which TCRalpha and Tcrbeta transgenes were cointegrated was identified. These constructs together express a T cell receptor that recognizes the 41-61 peptide of bovine pancreas ribonuclease (RNase) in the context of A. These mice develop spontaneous rheumatoid arthritis (RA) joint disease highly reminiscent of man. The trigger for the murine disorder is chance recognition of a NOD-derived major histocompatibility complex (MHC) class II molecule by the transgenic TCR.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|31-Jul-2008||0.0|0.0|Yes|Rheumatoid Arthritis; RA|rheumatoid arthritis, autoimmunity, TCR, T cell, CD4, B cell|Yes| 7577.0|AKBbm1|STOCK H2-K Tg(Alb-H2-K)/Apb||Dominant|histocompatibility 2, K region|H2-K|Unknown||MGI:3040519|histocompatibility 2, K region; b haplotype mutation 1|H2-K|MGI:3618114|17|||||||||||||||||mouse H2-K (MHC class I)|Mouse albumin promoter|similar to wild type H2-K expression||||||||||Normal|Normal|B10.BR|Yes|Yes|Yes|Yes|Yes|Yes|No|Excellent|more than 10|||No|21-Jan-2014|Cryopreserved sperm|50.0|0.0|No||tolerance, liver, CD8 T cells, MHC class I, autoimmunity|Possibly| 7753.0|Y20A; (kls/kls)|BALB/c-Atp4b/Apb||Recessive|ATPase, H+/K+ exchanging, beta polypeptide|Atp4b|Nil|H+,K+-ATPase, H+/K+-ATPase beta, H,K-ATPase-Beta|MGI:88114|ATPase, H+/K+ exchanging, beta polypeptide; targeted mutation 1, Ian R van Driel|Atp4b|MGI:2158258|8||||||||||||||||||||||||||||| The stomachs of H+,K+-ATPase beta subunit-deficient mice were achlorhydric. Histological and immunocytochemical analyses with antibodies to the H+,K+-ATPase alpha subunit revealed that parietal cell development during ontogeny was retarded in H+,K+-ATPase beta subunit-deficient mice. In 15-day-old mice, cells with secretory canaliculi were observed in wild-type but not in H+,K+-ATPase beta subunit-deficient mice. Parietal cells of H+,K+-ATPase beta subunit-deficient mice 17 days and older contained an abnormal canaliculus that was dilated and contained fewer and shorter microvilli than normal. In older parietal cells, the abnormal canaliculus was massive (25 mu m in diameter) and contained few microvilli. We did not observe typical tubulovesicular membranes in any parietal cell from H+,K+-ATPase beta subunit-deficient mice. Histopathologic alterations were only observed in the stomach.|normal|BALB/c|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|>10|||No|03-Oct-2014|Cryopreserved sperm|50.0|0.0|Unknown||gastric acid, gastric proton pump, stomach, endocytosis|Possibly| 4762.0|Fxy Mid|B6.A/J-Mid1/MarpApb ||Semi-dominant|midline 1|Mid1|Nil||MGI:1100537|midline 1; targeted mutation 1, Alan Ashworth|Mid1|MGI:5562687|X||||||||||||||||Yes|||||||||||||Viable. Reduced / delayed fertility. Litter size may be slightly reduced. No other phenpotype described as yet.Abnormal axon morphology:• axon length and branch number are increased in cultured cortical neurons• callosal axons grow further into the contralateral hemisphere at P4• at P14, axon distribution in the corpus callosum is disturbed with a greater number of axon terminals, with a wider distribution in both the S1 and S2 regions• broader distribution of the contralateral axon projection pattern in the corpus callosumEmbryogenesis phenotype:• no obvious midline defects, unlike in Opitz Syndrome patients|Breeder pairs often only litter down after 3 months together, if they litter down at all. Around 1 in 3 produce litters.|A/J ; C57BL6/J|Yes|Yes|Yes|No|No|Yes|Yes|Poor||||No|01-May-2009|Cryopreserved sperm|88.0|0.0|Yes||Reporter, X-linked, craniofacial, cleft lip|Yes| 6859.0|18YAA024a|ENU18Yaa:024a||Recessive|accelerated autoimmunity and lymphoproliferation transposition|Yaa|Unknown|Tp(X;Y)1Ekw|MGI:99140|||MGI:1856277|Y||||||||||||||||Yes|||||||||||||Low B cell numbers||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|20-Mar-2012|Cryopreserved sperm|49.0|0.0|Unknown||Monocytes, T cell, lymphoma, autoantibody, ENU, B cell|Yes| 6859.0|18YAA024a|ENU18Yaa:024a||Recessive|Unknown|Unknown|Unknown||||||Unknown||||||||||||||||Yes|||||||||||||Low B cell numbers||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|20-Mar-2012|Cryopreserved sperm|||Unknown||Monocytes, T cell, lymphoma, autoantibody, ENU, B cell|Yes| 4529.0|B6.129-163C KI Tg1|B6.129-Ryr1/AnuApb||Recessive|ryanodine receptor 1, skeletal muscle|Ryr1|Normal|calcium release channel isoform 1, Ryr, skrr|MGI:99659|ryanodine receptor 1, skeletal muscle; targeted mutation 2, Paul D Allen|Ryr1||7||||||||||||||||Yes|||||||||||||Embryonic Lethal E17-18.|Fulminant malignant hyperthermia episodes inR163C heterozygous mice after exposure to 1.25–1.75% halothaneor an ambient temperature of 42°C characterized by increasedrectal temperature, respiratory rate, and inspiratoryeffort, with significant blood biochemical changes indicatingmetabolic acidosis, ending in death and hyperacute rigor mortis;(3) intraperitoneal pretreatment with dantrolene provided100% protection from the halothane-triggered fulminant malignanthyperthermia episode; (4) significantly increased sensitivity(decreased effective concentration causing 50% of the maximalresponse) of R163C heterozygous and homozygousmyotubes to caffeine, 4-chloro-m-cresol, and K-induced depolarization;(5) R163C heterozygous and homozygous myotubeshave a significantly increased resting intracellular Ca2 concentrationcompared with wild type; (6) R163C heterozygous sarcoplasmicreticulum membranes have a twofold higher affinity(Kd =35.4 nM) for [3H]ryanodine binding compared with wild type (Kd= 80.1 nM) and a diminished inhibitory regulation byMg2.|C57BL/6|No|No|Yes|No|No|Yes|No|Unknown|4|||No|27-Feb-2009|Cryopreserved sperm|50.0|0.0|Yes||hyperthermia, muscle, sarcoplasmic reticulum, myotubules, MALIGNANT hyperthermia|Yes| 8537.0|Tle2|C57BL/6NCrlAnu-Tle2/AnuApb||Recessive|transducin-like enhancer of split 2|Tle2|Unknown|Grg2|MGI:104635||||10|||||||||||||||||||||||||||||Normal||C57BL/6NCrlAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|13-Jul-2018|Cryopreserved sperm|58.0|0.0|Unknown||CRISPR|Yes| 5528.0|LylKI ; Scl Lyl1 knockin|B6;129S1/Sv-Tal1/MarpApb||Dominant|T-cell acute lymphocytic leukemia 1|Tal1|Reduced|bHLHa17, Scl, SCL/tal-1|MGI:98480|T-cell acute lymphocytic leukemia 1; targeted mutation 2, Walter and Eliza Hall, Institute of Medical Research|Tal1|MGI:1858004|4||||||||||||||||Yes|||||||||||||Embryonic lethal.Complete embryonic lethality during organogenesis: homozygotes die by about E9.5 due to absolute anemia.Absent vitelline blood vessels: at E9.5, mutant yolk sacs lack large branching vitelline vessels.Disorganized yolk sac vascular plexus: by E8, mutant yolk sacs exhibit a disorganized network of fine vascular channels.Abnormal embryonic hematopoiesis: homozygotes exhibit failure of yolk sac hematopoiesis, with no erythrocytes found in embryonic vessels.Absent blood islands: at E8.5, mutant yolk sacs display bloodless channels; PECAM-1 staining is restricted to the endothelium.Embryonic growth arrest: at E9.5, preterminal homozygotes are severely growth-retarded.Abnormal blood vessel morphology: * at E8.5, homozygotes display reduced cerebral vasculature with dilated intraembryonic vessels. * at E9.0, incomplete somitic vessels appear to undergo apoptosis resulting in loss of vascular architecture by E9.5.Dilated dorsal aorta: at E8.5, homozygotes exhibit dilated dorsal aortae.Abnormal vein morphology: at E8.5, homozygotes display dilated cardinal and perineural veins.Abnormal heart development.Delayed heart looping: at E8.5, the mutant heart is still a straight tube as a result of delayed cardiac looping.Distended pericardium: at E8.5, homozygotes exhibit dilated pericardial sacs.Pericardial edema: at E8.5, homozygotes display significant pericardial edema.Anemia: at E8.5-E9, homozygotes exhibit absolute anemia leading to hypoxia.Hypoxia: by E9.0, homozygotes display widespread intraembryonic hypoxic cell death.Increased neuron apoptosis: at E8.5, homozygotes display an increased number of apoptotic cells in the neural tube, probably secondary to hypoxia.|Normal|C57BL/6J|No|No|Yes|No|No|Yes|No|Good|||Maintain on C57BL/6 background|No|24-Jun-2011|Cryopreserved sperm|50.0|0.0|No||TAL-1, Lyl-1, hematopoiesis, bHLH, stem cells|Yes| 7770.0|SB 9|STOCK Gt(ROSA)26Sor TgTn(sb-T2/Onc3)12740Njen/NciApb||Dominant|gene trap ROSA 26, Philippe Soriano|Gt(ROSA)26Sor||beta geo, Gtrgeo26, Gtrosa26, R26, ROSA26|MGI:104735|gene trap ROSA 26, Philippe Soriano; targeted mutation 2, Nancy A Jenkins|Gt(ROSA)26Sor|MGI:3839796|6|||||||||||||||||transgenic transposon concatemer 12740, Nancy A Jenkins||||||||||||Normal|Normal|C57BL/6|Yes|Yes|Unknown|Yes|Yes|Unknown|No|Good||||No|13-Oct-2014|Cryopreserved sperm|50.0|0.0|Unknown||sleeping beauty|Possibly| 6697.0|CRE3|B6-Tg(ACTA1-cre/ERT2)97.16Mtz|B6-Tg(ACTA1-cre/ERT2)97.16Mtz/MtzAusb|Semi-dominant||||||||||||||||||||||||||transgene insertion 97.16, Daniel Metzger|human skeletal alpha-actin|||||||||||Normal||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|02-Dec-2011|Embryo|0.0|0.0|Unknown||inducible, skeletal, tamoxifen|Yes| 5494.0|APN 106|C57BL/6N-Socs4/Marp||Recessive|suppressor of cytokine signaling 4 |Socs4|Unknown|Socs7|MGI:1914546 |suppressor of cytokine signaling 4; targeted mutation 1a, Wellcome Trust Sanger Institute|Socs4|MGI:4434370|14||||||||||||||||Yes|||||||||||||Unknown - Not bred to homozygocity |Normal |C57BL/6N|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|02-May-2011|Cryopreserved sperm|50.0|0.0|Unknown||ES cell|Yes| 5495.0|APN 43|Egfl6/Marp||Recessive|EGF-like-domain, multiple 6 |Egfl6 |Unknown|Maeg |MGI:1858599 |EGF-like-domain, multiple 6; gene trap CMHD-GT_485H8-5S, Centre for Modeling Human Disease|Egfl6|MGI:3923078|X||||||||||||||||No|||||||||||||Not bred to homozygosity - unknown.|Normal|C57BL/6J|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|02-May-2011|Cryopreserved sperm|50.0|0.0|Unknown||ES cell|Possibly| 7771.0|Ptcd3|C57BL/6NCrlAnu-Ptcd3/AnuApb||Recessive|pentatricopeptide repeat domain 3|Ptcd3|Unknown|2610034F17Rik, 2810422B04Rik |MGI:1917206 |Ptcd3; mutation 1, the Australian National University|Ptcd3||6|ENSMUSG00000063884|ENSMUST00000082094|Ptcd3-201|289|311|A to T|ENSMUSE00000432359|5|97|Isoleucine to Lysine|||||CTTATGTATTTCACGATGATCCTTACCTCATACCAACCTCTGCTCTGGAGTCTCGTTCATT||||||||||||||Unknown|Normal|C57BL/6NCrlAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||5|Het x Het|No|13-Oct-2014|Cryopreserved sperm|22.0|0.0|Unknown||Mitochondion, Translation, RNA binding, ENU|Yes| 6860.0|RNAi-17|C57Bl/6J-HDAC6/Apb||X-linked|histone deacetylase 6|Hdac6|Unknown|mHDA2, Sfc6|MGI:1333752||||X|||||||||||||||||||||||||||||Unknown|Normal|C57Bl/6N|Unknown|Unknown|Unknown|Unknown|Unknown|Yes|No|Good||||No|21-Mar-2012|Cryopreserved sperm|50.0|0.0|Unknown|||Possibly| 8540.0|MARCH 8 KO|C57BL/6-March8/Apb||Recessive|membrane-associated ring finger (C3HC4) 8|March8||1300017E09Rik, Mir|MGI:1919029||||6|||||||||||||||||||||||||||||Absence of MARCH 8Increase MHCII at surface of cortical thyme epithet cells and autoimmune regulator medullary thyme epithelial cells|Unknown|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|29-Jul-2018|Cryopreserved sperm|50.0|0.0|Unknown||MHC II, T cell|Yes| 1491.0|Inos-/-|B6;129-Nos2/Apb|B6;129-Nos2|Recessive|nitric oxide synthase 2, inducible, macrophage|Nos2|Nil|iNOS, Nos-2, NOS-II, Nos2, Nos2a|MGI:97361|targeted mutation 1, John S Mudgett|Nos2|MGI:2158791|11||||||||||||||||No|||||||||||||Abnormal artery morphology:* the large arteries of the uterus during pregnancy have thickened arterial walls and smaller lumina.Abnormal circulating estradiol level:* the cyclic changes in estradiol level are abnormal in homozygous mutant females with the peak in estradiol concentration coming later than in 129/SvEv wild-type females.Abnormal uterus morphology:* the lining of the uterus during pregnancy shows a distinct lack of cellularity in homozygous female mutants compared to wild-type females.Abnormal oestrous cycle:* diestrus length is increased in homozygous mutant females compared to 129/SvEv wild-type mice without an increase in total oestrus cycle lengthDecreased litter size:* by mid-gestation homozygous female mutants have significantly fewer viable embryos compared to wild-type females.||C57BL/6 x 129|Yes|Yes|Yes|Yes|Yes|Yes|No|Poor||||No|03-Jul-2007|Cryopreserved sperm|235.0|0.0|Unknown||viral infection, uterus, interferon, influenza, estradiol|Yes| 6831.0|APN 138|C57Bl/6N-Inpp4a/MarpApb||Recessive|inositol polyphosphate-4-phosphatase, type I |Inpp4a|Unknown|107kDa |MGI:1931123|inositol polyphosphate-4-phosphatase, type I; targeted mutation 1a, Helmholtz Zentrum Muenchen GmbH|Inpp4a |MGI:4434756|1|||||||||||||||||||||||||||||Unknown|Normal|C57Bl/6N|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|01-Mar-2012|Cryopreserved sperm|50.0|0.0|Unknown|||Possibly| 6871.0|APN206|C57Bl/6NTac-Gpr183/MarpApb||Recessive|G protein-coupled receptor 183|Gpr183|Unknown|Ebi2|MGI:2442034|G protein-coupled receptor 183; targeted mutation 1, Velocigene |Gpr183|MGI:3808449|14|||||||||||||||||||||||||||||Unknown|Normal|C57Bl/6N|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|05-Apr-2012|Cryopreserved sperm|50.0|0.0|Unknown|||Possibly| 7074.0|APN 196|C57BL/6N-Scmh1Mu||Dominant|sex comb on midleg homolog 1|Scmh1 ||Scml3 |MGI:1352762 |sex comb on midleg homolog 1; targeted mutation 1a, Helmholtz Zentrum Muenchen GmbH|Scmh1tm1a(EUCOMM)Hmgu|MGI:4456695|4|||||||||||||||||||||||||||||Unknown|Normal|C57Bl/6N|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|04-Sep-2012|Cryopreserved sperm|50.0|0.0|Unknown|||Possibly| 9254.0|OT-1 bm1 Ly5.1 RAG-/-|OT-1 bm1 Ly5.1 RAG-/-/Apb||Semi-dominant|Ly5.1 , TCR, MHC I allele, RAG allele|||||ptprca, TCRa, TCRb, H-2a, RAG |||Unknown|||||||||||||||||TCR promoter driving Transgenic TCR expression|na|||||||||||Mice lacks B cells and CD4T cells as well as NKT cells and its CD8 T cells are monospecific. Mice that are homozygous for Ly5.1, bm1 and RAG-deficient are immunodeficient but otherwise do not display any anomaly. |same as homozygous mice.|bm1 background|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|11-Aug-2021|Cryopreserved sperm|50.0|0.0|Unknown|||Possibly| 7773.0|Dynll-KO|C57BL/6-Dynll1/StvApb||Dominant|dynein light chain LC8-type 1|Dynll1|Normal|8kDa LC, DLC8, Dnclc1, Pin|MGI:1861457|dynein light chain LC8-type 1; targeted mutation 1.2, Jorg Heierhorst|Dynll1|MGI:5463937|5||||||||||||||||Yes|||||||||||||Unknown|Normal|C57BL/6|No|No|Yes|No|No|Yes|No|Excellent||||No|16-Oct-2014||0.0|0.0|Unknown||Dynll-1, ASCIZ|Possibly| 5.0|Buffy|C57BL/6JSfdAnu-Jak3/AnuApb|C57BL/6JSfdAnu-Jak3/AnuApb|Recessive|Janus kinase 3|Jak3|Normal||MGI:99928|buffy|Jak3|MGI:3611885|8|ENSMUSG00000031805|ENSMUST00000051995|Jak3-001|1193|1490|T to C|ENSMUSE00000329342|9|398|Leucine to Proline|||||CGCTGGCTCCCTCCCAGGCACCTACATTCTCCGCCGCAGCCCGCAGGACTATGACAGCTTT|No|||||||||||||Pan-Lymphopenia with hyperactivated CD4⁺ cellsObstructed B cell maturationReduced B cell numbers in peripheryB220⁺CD19⁺cells, IgM⁺IgD⁺ cells or CD21⁺IgD⁺ cells were reduced in the spleen by factor of 3.Peritoneal cavity: reduced IgM⁺IgD⁻ cells and only partially reduced IgM⁺IgD⁺ cell numbersReduced numbers of thymocytes at all stages of T cell maturation.Thymi are smaller than aged-matched controls.50% of CD4⁺ cells compared to controls4 fold lower levels of CD8⁺ cells compared to controlsMutation intrinsic to B and T cells, exaggerated under competitive reconstitution with wild-type cells, SCID mouse. Develop diarrhoea||C57BL/6JSfdAnu|Yes|Yes|Unknown|Yes|Yes|Yes|No|Good||||No|28-Nov-2005|Cryopreserved sperm|25.0|0.0|Unknown||T cell, B cell, IL-2, Thymus, ENU|Yes| 34.0|Captain Morgan, ENU4AT:038 |C57BL/6JSfdAnu-Dock8/AnuApb|C57BL/6JSfdAnu-Dock8/AnuApb|Recessive|dedicator of cytokinesis 8|Dock8|Nil||MGI:1921396|dedicator of cytokinesis 8; captain morgan|Dock8|MGI:3835422|19|ENSMUSG00000052085|ENSMUST00000025831|Dock8-201||||||||25202202|20|||GCAGCCCATGGTCATTGCTGGCCAAACAGGTAGAGGCCTGTGGGTAGGGAGGAGGCATGG|Yes|||||||||||||Defective antibody response to immunization: failure to sustain antibody formation, undergo affinity maturation or to mount heightened recall (memory) response upon booster immunization. DOCK8-mutant B cells were unable to form marginal zone B cells or to persist in germinal centers and undergo affinity maturation. Dock8 mutations disrupted accumulation of the integrin ligand ICAM-1 in the B cell immunological synapse but did not alter other aspects of B cell antigen receptor signaling.||C57BL/6JSfdAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|20-Apr-2004|Cryopreserved sperm|26.0|0.0|Unknown||gammaglobulin, immunization, antibody, ENU, Wellcome Trust, memory, B cell, GTP|Yes| 5922.0|Mycbp2-15mttMb||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 1485.0|B6.OT-1|C57BL/6-Tg(TcraTcrb)1100Mjb/AnuApb||Dominant||||||||||||||||||||||||||transgene insertion 1100, Michael J Bevan|H-2K promoter|||||||||||Transgenic mice on a C57BL/6 background are somewhat immunodeficient, and may be used to study the role of peptides in positive selection and the response of CD8+ T cells to antigen.Carry OVA-specific, H-2K-restricted T cell receptor|||Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|02-Jul-2007|Cryopreserved sperm|150.0|0.0|No||T cell, receptor, ovalbumin, CD8|Yes| 6869.0||Porthos:kk||Dominant||||||||||||||||||||||||||Genomic IgG anti-HEL H + L||low copy|histocompatibility-2, MHC|H2||H-2, MHC-II|MGI:95894|histocompatibility-2, MHC; k variant |H2|MGI:3579322|17|||C57BL/6 x B10.BR|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|04-Apr-2012|Cryopreserved sperm|68.0|0.0|No||Hen Egg Lysozyme, autoimmunity, T cell, B cell|Yes| 6861.0|APN 144|C57Bl/6NTac-Gpr18/MarpApb||Recessive|G protein-coupled receptor 18 |Gpr18|Unknown||MGI:107859|G protein-coupled receptor 18; targeted mutation 1, Velocigene |Gpr18 |MGI:3812675|14|||||||||||||||||||||||||||||Unknown|Normal|C57Bl/6N|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|21-Mar-2012|Cryopreserved sperm|50.0|0.0|Unknown|||Possibly| 6830.0|APN 128|C57Bl/6N-Pxmp4/MarpApb||Recessive|peroxisomal membrane protein 4|Pxmp4 |Unknown|3010018P03Rik |MGI:1891701 |peroxisomal membrane protein 4; targeted mutation 1, Wellcome Trust Sanger Institute |Pxmp4 |MGI:4419659|2|||||||||||||||||||||||||||||Unknown|Normal|C57Bl/6N|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|01-Mar-2012|Cryopreserved sperm|50.0|0.0|Unknown|||Possibly| 8541.0|MHCII KR |B6.129-H2-Ab1/SishApb||Recessive|histocompatibility 2, class II antigen A, beta 1|H2-Ab1||Abeta, A beta, H-2Ab, H2-Ab, Ia2, Ia-2, IAb, I-A, I-Abeta, Rmcs1|MGI:103070|histocompatibility 2, class II antigen A, beta 1; targeted mutation 1.1, Satoshi Ishido|H2-Ab1|MGI:4436864|17|||||||||||||||||||||||||||||MHCII cytoplasmic lysine residue replaced by arginine residue.MHCII unable to be modified by ubiquitinationIncreased MHCII surface levels on haematopoietic antigen presenting cells including dendritic cells. Higher levels of antigen presentation by thyme dendritic cells. Impaired abiliity of dendritic cells to differentiate immature thymocytes into T regulatory cells. Reduced frequency & number of regulatory T cells.|Unknown|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|30-Jul-2018|Cryopreserved sperm|50.0|0.0|Unknown||E3 ubiquitin ligase, MHCII|Yes| 8318.0|CIB1 Knockout|B6.129S6-Cib1/Apb||Recessive|calcium and integrin binding 1 (calmyrin)|Cib1|Nil|Kip|MGI:1344418|calcium and integrin binding 1 (calmyrin); targeted mutation 1, Leslie V Parise|Cib1|MGI:3690129|7|||||||||||||||||||||||||||||Female, normalDecreased testis weight:• weight of testis at 3-4 months of age is about 47.5% that of controlsAbnormal spermatogenesis: • spermatogonia, spematocytes, and round spermatids are present in the testis; however, seminiferous tubules lack advanced spermatids, have multinucleated spermatids near the tubule lumen and no sperm are found in the epididymis• increase in spermatid apoptosis in the testisAzoospermia: • sperm production is undetectable in the epididymisAbnormal spermiogenesis.• disruption of the haploid phase of germ cell differentiationarrest of spermatogenesis.• spermatogenic cells complete both mitotic and meiotic divisions, however postmeiotic spermatids do not develop normally and sperm are not producedMale infertility: • males are sterile due to disruption of the haploid phase of spermatogenesis|Both female and male are normal|C57BL/6|Yes|Yes|Yes|Yes|No|Yes|No|Unknown||||No|03-Oct-2017|Cryopreserved sperm|50.0|0.0|Unknown||Sperm|Yes| 5928.0|Neogenin 129||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 51.0|LeukSkywalker, ENU3strain:004 |B6JSfdAnu;NODAnu-Eed/AnuApb|B6SfdAnu;NODAnu-Eed/AnuApb|Recessive|embryonic ectoderm development|Eed|Nil|l(7)5Rn, l7Rn5|MGI:95286|LeukSkywalker|Eed|MGI:3611895|7|ENSMUSG00000030619|ENSMUST00000107234|Eed-001||||||||97120003|4|||GTTTTTATAGCCCTGGTTTAAGAAATTTGATAAGTACATCAGAACTTTGAAAACGAATTC|No|||||||||||||Dwarf, dilute coat, possible leukemia ||C57BL/6JSfdAnu x NOD|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||7||No|06-Feb-2006|Cryopreserved sperm|121.0|0.0|Unknown||leukaemia, dwarfism, ENU|Yes| 5069.0|Elektra|C57BL/6J-Slfn2/BltrAnuApb|C57BL/6J-Slfn2/BltrAnuApb|Recessive|schlafen 2|Slfn2|Unknown|Shlf2|MGI:1313258|schlafen 2; mutation 1, Bruce Beutler|Slfn2|MGI:3850348|11||||||||||||||||Yes|||||||||||||CD8 deficiency, decreased CD8 response, hematopoietic system, immune system, mouse cytomegalovirus (MCMV) susceptibility, NKT cell deficiency.Elektra mice died six to eight days after infection with 2x10 5 PFU of MCMV, whereas nearly all wild type mice survived.Elektra homozygotes were also highly susceptible to infection with Listeria monocytogenes, exhibiting increased bacterial loads in the liver 2 days post-infection relative to those of wild type mice. Elektra mice displayed normal cellularity of the spleen, thymus, lymph nodes, and peripheral blood. B cells from elektra mice proliferated normally in response to BCR stimulation or CpG treatment. However, antibody production in response to MCMV infection was delayed. Elektra mice lacked NKT (CD3+NK1.1+) cells in the thymus and spleen, and had reduced numbers in the liver. When elektra NKT cells were stimulated with α-galactosylceramide tetramer, they produced greatly reduced levels of IFN-γ and IL-4 compared to wild type cells. Elektra mice displayed a 50% reduction in Foxp3+ regulatory T cells.Elektra CD8+ T cells failed to proliferate upon stimulation with CD3ε and CD28 antibodies, with PMA and ionomycin, or with IL-12 in vitro.||C57BL/6J|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|25-Mar-2010|Cryopreserved sperm|49.0|0.0|Unknown||CD8, MCMV, interferon, T cell, infection, NKT, ENU|Yes| 8590.0|mm1286del|C57BL/6-Grh2/Apb||Recessive|grainyhead like transcription factor 2|Grhl2|Unknown|0610015A08Rik, BOM, clft3, grainyheadlike, Tcfcp2l3|MGI:2182543||||15|||||||||||||||||||||||||||||We predict that nullizygous (-/-) embryos will have slight alterations to craniofacial morphology.|Normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|25-Oct-2018||0.0|0.0|Unknown|||Yes| 7075.0|ENU24:006:5730590G19RIK|C57BL/6NCrlAnu-Ticrr/AnuApb|C57BL/6NCrlAnu-Ticrr/AnuApb|Recessive|TOPBP1-interacting checkpoint and replication regulator|Ticrr||5730590G19Rik|MGI:1924261|TOPBP1-interacting checkpoint and replication regulator; mutation 1, The Australian National University|Ticrr|MGI:5563404|7|ENSMUSG00000046591|ENSMUST00000035977|Ticrr-201|1748|1892|A to C|ENSMUSE00000592184|7|583|Asparagine to Threonine|||||TACCATGTCCCGCTCCTTGAAGATGTTGAATGTGGCAAGGCTAAATGTAAAGGCTCAGAAA||||||||||||||Homozygous mice are mostly hairless, with only a light patch of hair around the face and tail. |Normal|C57BL/6NCrlAnu|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|05-Sep-2012|Cryopreserved sperm|6.0|0.0|Unknown||ENU, coat, hair|Yes| 7088.0|SOCS-1 KO Des Rag|B10.BR.Cg-H2 SOCS1/Wehi Tag1 Tg(TcraKB5.C20,TcrbKB5.C20)10395Arnd/Apb||Recessive|suppressor of cytokine signaling 1|Socs1|Nil|Cish1, Cish7, JAB, JAK-binding protein, JAK2-binding protein, SOCS-1, SSI-1, STAT-induced STAT inhibitor 1|MGI:1354910|targeted mutation 1, Walter and Eliza Hall Institute of Medical Research|Socs1|MGI:1934607|16||||||||||||||||No|transgene insertion 10395, Bernd Arnold|||histocompatibility-2, MHC|H2||H-2, MHC-II|MGI:95894|histocompatibility-2, MHC; k variant|H2|MGI:3579322|17|Postnatal lethality:* homozygotes become ill and die before reaching 3 weeks of age.* mice die from inflammatory disease before weaning.Decreased body weight:* homozygotes become smaller within 10 days after birthPostnatal growth retardation.Pancreas inflammation: monocytic infiltration.Decreased hematocrit.Decreased lymphocyte cell number.Decreased B cell number:* progressive loss of maturing B lymphocytes in the marrow, spleen, and peripheral blood.Decreased pre-B cell number:* pre-B cells are depleted significantly in the marrow.Decreased eosinophil cell number:* moderate reduction in eosinophil numbersAbnormal mature B cell morphology:* number of mature B cells expressing surface Ig in the bone marrow is reduced.Abnormal follicular B cell morphology:* lymphoid follicles of the spleen are either completely absent or are composed of immature cells.Increased spleen red pulp amount:* most spleens show expanded areas of red pulp with nucleated erythroid cells as the main cell population.Thymus cortex hypoplasia:* the cortex becomes progressively depleted of lymphoid cellsSmall thymus.Abnormal Peyer's patch morphology:* Peyer's patches are present but contain few lymphocytes.Abnormal lymph node B cell domain:* lymph nodes show absence of lymphoid follicle formation.Increased inflammatory response:* mice die from massive generalized inflammation that affects multiple organs.Heart inflammation: monocytic, and less frequently, granulocytic infiltration.Pancreas inflammation: monocytic infiltration.Liver inflammation: livers exhibit both focal and generalized infiltration, predominantly by immature and mature monocytic and granulocytic cells, and less frequently, megakaryocytes and eosinophils.Hepatic steatosis: parenchymal cells contain an accumulation of lipid-containing vacuoles.Liver degeneration: fatty degeneration either involves local areas not related to portal vessels or is generalized to the entire liver.Abnormal respiratory alveoli morphology: increase in cellularity of alveolar walls in the lung, often associated with macrophage cuffing around major vessels.||B10.BR|No|No|Yes|No|No|Yes|No|Unknown||||No|20-Sep-2012|Cryopreserved sperm|50.0|0.0|Unknown||Cytokine signalling, phosphorylation, signal transduction, IL-6 receptor, growth retardation|Yes| 7088.0|SOCS-1 KO Des Rag|B10.BR.Cg-H2 SOCS1/Wehi Tag1 Tg(TcraKB5.C20,TcrbKB5.C20)10395Arnd/Apb||Recessive|Recombination activating gene 1|Rag1||Rag-1|MGI:97848||||2|||||||||||||||||||||||||||||Postnatal lethality:* homozygotes become ill and die before reaching 3 weeks of age.* mice die from inflammatory disease before weaning.Decreased body weight:* homozygotes become smaller within 10 days after birthPostnatal growth retardation.Pancreas inflammation: monocytic infiltration.Decreased hematocrit.Decreased lymphocyte cell number.Decreased B cell number:* progressive loss of maturing B lymphocytes in the marrow, spleen, and peripheral blood.Decreased pre-B cell number:* pre-B cells are depleted significantly in the marrow.Decreased eosinophil cell number:* moderate reduction in eosinophil numbersAbnormal mature B cell morphology:* number of mature B cells expressing surface Ig in the bone marrow is reduced.Abnormal follicular B cell morphology:* lymphoid follicles of the spleen are either completely absent or are composed of immature cells.Increased spleen red pulp amount:* most spleens show expanded areas of red pulp with nucleated erythroid cells as the main cell population.Thymus cortex hypoplasia:* the cortex becomes progressively depleted of lymphoid cellsSmall thymus.Abnormal Peyer's patch morphology:* Peyer's patches are present but contain few lymphocytes.Abnormal lymph node B cell domain:* lymph nodes show absence of lymphoid follicle formation.Increased inflammatory response:* mice die from massive generalized inflammation that affects multiple organs.Heart inflammation: monocytic, and less frequently, granulocytic infiltration.Pancreas inflammation: monocytic infiltration.Liver inflammation: livers exhibit both focal and generalized infiltration, predominantly by immature and mature monocytic and granulocytic cells, and less frequently, megakaryocytes and eosinophils.Hepatic steatosis: parenchymal cells contain an accumulation of lipid-containing vacuoles.Liver degeneration: fatty degeneration either involves local areas not related to portal vessels or is generalized to the entire liver.Abnormal respiratory alveoli morphology: increase in cellularity of alveolar walls in the lung, often associated with macrophage cuffing around major vessels.||B10.BR|No|No|Yes|No|No|Yes|No|Unknown||||No|20-Sep-2012|Cryopreserved sperm|||Unknown||Cytokine signalling, phosphorylation, signal transduction, IL-6 receptor, growth retardation|Yes| 6862.0||ENU18NIH21a||Recessive|Unknown|Unknown|||||||Unknown|||||||||||||||||||||||||||||few mature B cells|unknown|C57BL/6JAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|21-Mar-2012|Cryopreserved sperm|40.0|0.0|Unknown||ENU, B cell|No| 5929.0|Neogenin B6||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5931.0|NesCreERT2Line4 x IDTR||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 7089.0|178.3|B10.BR.Cg-Tg(H2-K)178.3/Apb||Dominant||||||||||||||||||||||||||transgene insertion|H-2Kb|||||||||||Normal|Normal|B10.BR|Yes|Yes|Yes|Yes|Yes|Yes|No|Excellent|more than 10|||No|20-Sep-2012|Cryopreserved sperm|50.0|0.0|No||MHC class II|Yes| 110.0|Arjuna ; ILK3|C57BL/6JSfdAnu-Tg(ILK3mHEL)3Ccg/AnuApb|C57BL/6JSfdAnu-Tg(ILK3mHEL)3Ccg/AnuApb|Dominant||||||||||||||||||||||||||transgene insertion 3, Christopher C Goodnow|Rat insulin promoter|Expression of the inserted sequence specifically to pancreatic islet beta cells||||||||||||C57BL/6JSfdAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||6|sib x sib|No|06-Feb-2006|Cryopreserved sperm|150.0|0.0|No||Hen egg Lysozyme, tolerance, immunity, T cell, B cell|Yes| 7772.0|Hic1-lacz|B6.129S4-Hic1/AusbApb||Dominant|hypermethylated in cancer 1|Hic1|Nil|HIC-1|MGI:1338010|hypermethylated in cancer 1; targeted mutation 1, Stephen B Baylin|Hic1|MGI:2386879|11|||||||||||||||||||||||||||||Homozygotes die perinatally and exhibit varying combinations of gross developmental defects throughout the second half of development, including acrania, exenchephaly, cleft palate, limb abnormalities and omphalocele. |Develop many different spontaneous malignant tumours, including the predominance of epithelial tumours in males and lymphomas and sarcomas in females.|C57BL/6|No|No|Yes|No|No|Yes|No|Good||||No|14-Oct-2014|Cryopreserved sperm|50.0|0.0|Unknown||zinc-finger transcription factor, epithelial, lymphoma, sarcoma, epigenetic|Yes| 5663.0|Caspase11 KO||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 10346.0|RnaseH1 fl/fl|C57BL/6NCrlAnu-RnaseH1/67Apb||Dominant|ribonuclease H1|RnaseH1|||MGI:1335073|Rnaseh1: endonuclease-mediated mutation 1, ANU|||12|||||||||||||||||||||||||||||Lethal|Normal|C57BL/6NCrlAnu|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|26-Jun-2023|Cryopreserved sperm|65.0|0.0|Unknown|||Possibly| 7567.0|Alpha 2 mice|B6.129-Gabra2/J||Recessive|gamma-aminobutyric acid (GABA) A receptor, subunit alpha 2|Gabra2|Nil|C630048P16Rik, Gabra-2|MGI:95614|gamma-aminobutyric acid (GABA) A receptor, subunit alpha 2; targeted mutation 1.1, Gregg E Homanics|Gabra2|MGI:5000434|5|||||||||||||||||||||||||||||Homozygotes are under represented at birth. They respond differently to alcohol and anaesthetics |Normal|C57BL/6|Yes|Yes|Unknown|Yes|Yes|Yes|No|Good||||No|15-Jan-2014||0.0|0.0|Unknown|||No| 4787.0||129/SvApb||Dominant||||||||||||||||||||||||||||||||||||||Normal.||129/SvApb|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|06-Sep-2009|Cryopreserved sperm|30.0|0.0|Unknown||129|No| 7090.0|AKbDes|B10.BR(Cg)-Tg(Alb-H2-K) Tg(TcraKB5.C20,TcrbKB5.C20)10395Arnd/Apb||Dominant||||||||||||||||||||||||||mouse H2-Kb (MHC class I)|Mouse albumin promoter|similar to wild type H2-K expression||||||||||Normal|Normal|B10.BR|Yes|Yes|Yes|Yes|Yes|Yes|No|Excellent|10|||No|20-Sep-2012|Cryopreserved sperm|40.0|0.0|Unknown||CD8 , T cells, MHC Class I, Liver, hepatocyte|Yes| 7090.0|AKbDes|B10.BR(Cg)-Tg(Alb-H2-K) Tg(TcraKB5.C20,TcrbKB5.C20)10395Arnd/Apb||Dominant||||||||||||||||||||||||||transgene insertion 10395, Bernd Arnold||||||||||||Normal|Normal|B10.BR|Yes|Yes|Yes|Yes|Yes|Yes|No|Excellent|10|||No|20-Sep-2012|Cryopreserved sperm|||Unknown||CD8 , T cells, MHC Class I, Liver, hepatocyte|Yes| 5517.0|P selectin|B6,129-Selp/JAnuApb||Recessive|selectin, platelet|Selp|Nil|CD62P, Grmp, P-selectin|MGI:98280|selectin, platelet; targeted mutation 1, Baylor College of Medicine|Selp|MGI:1857244|1||||||||||||||||No|||||||||||||Increased leukocyte cell number: systemic leukocyte counts are ~9800/ul (~61% neutrophils, ~37% lymphocytes) compared to wild-type counts of ~5660/ul (53% neutrophils, 46% lymphocytes).Abnormal leukocyte tethering or rolling: * after surgery to exteriorize cremaster muscle, mice do not display leukocyte rolling for the first hour, but a significant amount of rolling is detected after 2 hours (~8% rolling leukocyte flux). * leukocytes show intermittent interactions with endothelium causing an increase in rolling velocity to ~129 um/second (~35 um/second in wild-type). * treatment with Tnfa (tumor necrosis factor alpha) reduces rolling velocity to ~5 um/second.||Unknown|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|03-Jun-2011|Cryopreserved sperm|35.0|0.0|Unknown||rolling, adhesion, inflammation, endothelium|Yes| 10344.0|Cisd2(1)|C57BL/6NCrl-Cisd2/Anu||Dominant|CDGSH iron sulfur domain 2|Cisd2|||MGI:1914256|Cisd2 |||3|ENSMUSG00000028165 ||||||||||||||||||||||||||||Unknown |Unknown|C57Bl/6N|Yes|Unknown|Yes|Yes|Unknown|Yes|No|Good||||No|26-Jun-2023|Cryopreserved sperm|52.0|0.0|Unknown|||Possibly| 10353.0|Adidias|C57BL/6NCrlAnu-Nfkb2/Anu||Recessive|nuclear factor of kappa light polypeptide gene enhancer in B cells 2|Nfkb2 |||MGI:1099800 |nuclear factor of kappa light polypeptide gene enhancer in B cells 2, p49/p100; endonuclease-mediated mutation 1, Matthew C Cook|Nfkb2Macc|MGI:6835770|19|||||||||||||||||||||||||||||thymic medullary hypoplasia|thymic medullary hypoplasia|C57Bl/6N|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|18-Aug-2023|Cryopreserved sperm|33.0|0.0|Unknown|||Possibly| 10352.0|Mettl3 LysMcre|B6.129P2-Lifr Lyz2 Mettl3JAusbAnu||Recessive|methyltransferase 3, N6-adenosine-methyltransferase complex catalytic subunit|Mettl3 ||M6A, Spo8 |MGI:1927165|methyltransferase 3, N6-adenosine-methyltransferase complex catalytic subunit; targeted mutation 1.1, Jacob Hanna|Mettl3tm1.1Jhha|MGI:6491677|14|||||||||||||||||||||||||||||Normal|Normal||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|21-Jul-2023||0.0|0.0|Unknown|||Possibly| 10352.0|Mettl3 LysMcre|B6.129P2-Lifr Lyz2 Mettl3JAusbAnu||Recessive|lysozyme 2|Lyz2|||MGI:96897 |lysozyme 2; targeted mutation 1, Irmgard Forster|Lyz2tm1(cre)Ifo|MGI:1934631|10|||||||||||||||||||||||||||||Normal|Normal||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|21-Jul-2023||||Unknown|||Possibly| 6698.0|Fh2|F-Tg(ACTA1-Fh/1)12Hrd/Ausb||Dominant||||||||||||||||||||||||||||||||||||||Mild muscle hypertrophy||FVBn|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|02-Dec-2011||0.0|0.0|Unknown|||Possibly| 7019.0||ENU22:Bcl2:022:b:B6||Recessive||||||||||||||||||||||||||||||||||||||The strain has a possible low lymphocyte phenotype.|||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|12-Jul-2012|Cryopreserved sperm|10.0|0.0|Unknown||ENU|No| 6863.0|ENU18NIH57a vav1|C57BL/6JAnu-Vav1/AnuApb|C57BL/6JAnu-Vav1/AnuApb|Recessive|vav1 oncogene|Vav1|Unknown||MGI:98923|vav1 oncogene; mutation 1, The Australian National University|Vav1|MGI:5563399|17|ENSMUSG00000034116|ENSMUST00000169220|Vav1-004|607|705|T to C|ENSMUSE00000139022|8|203|Phenylalanine to Serine|||||AGCAGCACTTCATGAAGCCTCTGCAGCGATTCCTTAAGCCTCAAGACATGGAGACCATCTT||||||||||||||Increased Klrg1<+> CD8<+> T cells following immunisation|Normal|C57BL/6JAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||G5|homozygous x homozygous|No|23-Mar-2012|Cryopreserved sperm|46.0|0.0|Unknown||lymphocyte, T cell, KLRG1, CD8, immunisation, ENU|Yes| 5491.0|WWP2|WWP2||Recessive|Unknown|Unknown|||||||Unknown||||||||||Unknown to Unknown|||||||||||||||||||Unknown||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|02-May-2011|Cryopreserved sperm|60.0|0.0|Unknown|||Possibly| 7265.0|B6.D2-CHR1|B6.D2-(D1Mit124-D1Mit291)||Semi-dominant|||||||||||||||||||||||||||||Unknown||||||||1|Anxious, low exploratary behaviour in open field, memory defict for contextaul fear memory|unknown|C57BL/6J|Yes|Yes|Yes|Yes|Yes|Yes|No|Excellent|>10|>2|standrad breeding to maintain homozygosity, sib-mating not required|Yes|22-Jan-2013||0.0|0.0|Yes|anxiety trait, neuroticism|Anxiety, Neuroticsm, Fear memory, memory, stress, responsiveness|No| 6701.0|Gt1|B6D2-T2(ACTA1-GTF2IRD1.1alfa1)22Hrd/Ausb||Recessive||Gt1||||||||||||||||||||||||||||||||||||None||B6D2|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|02-Dec-2011||0.0|0.0|Unknown|||Possibly| 67.0|Listerin, Senseless|STOCK Ltn1/AnuApb|STOCK Ltn1/AnuApb|Recessive|listerin E3 ubiquitin protein ligase 1|Ltn1|Normal|Listerin, Rnf160, Zfp294|MGI:1926163|listerin E3 ubiquitin protein ligase 1; lister|Ltn1|MGI:3838105|16|ENSMUSG00000052299|ENSMUST00000039449|Rnf160-201||||||||87415397|11|||GGAGTTCTCTTCTTCAGGTCATTGAAAAGGTATTTTAGCCCCCTCTCCCCTTTCCCTTTC|Yes|||||||||||||Late onset spastic paralysis & appear to have sensory defects, progresses to seizures and death||C57BL/6JSfdAnu x NOD|Yes|Yes|Yes|Yes|Yes|Yes|No|Poor||||No|06-Feb-2006|Cryopreserved sperm|127.0|0.0|Unknown||paralysis, seizures, ataxia, ENU|Yes| 6707.0|Tie2cre|B6.Cg-Tg(Tek-cre)1Ywa/Ausb||Semi-dominant|||||||||||||||||||||||||||mouse endothelial-specific receptor tyrosine kinase promoter/enhancer|||||||||||Reduced fertility:*Mice mated to Tg(Tek-cre)12Flv mice produce litters that exhibit high lethality.||C57BL/6|Yes|No|Yes|Yes|No|Yes|No|Unknown||||No|02-Dec-2011||0.0|0.0|Unknown||Vascular cell adhesion molecule (VCAM)-1, B cell|Yes| 7077.0|APN173|C57Bl/6N-A-Map3k5/Marp||Recessive|mitogen-activated protein kinase kinase kinase 5|Map3k5|Unknown|7420452D20Rik, ASK, ASK1, Mekk5|MGI:1346876|mitogen-activated protein kinase kinase kinase 5; targeted mutation 1a, Helmholtz Zentrum Muenchen GmbH |Map3k5|MGI:4434801|10||||||||||Unknown to Unknown|||||||||||||||||||Unknown|Normal|C57Bl/6N|Unknown|Unknown|Unknown|Unknown|Unknown|Yes|No|Good||||No|05-Sep-2012|Cryopreserved sperm|50.0|0.0|Unknown|||Possibly| 3934.0|RRFU|BALB/c-Gt(ROSA)26Sor/AnuApb||Recessive|gene trap ROSA 26, Philippe Soriano|Gt(ROSA)26Sor||beta geo, Gtrgeo26, Gtrosa26, R26, ROSA26|MGI:104735|gene trap ROSA 26, Philippe Soriano; targeted mutation 1.1, Hugh D Campbell|Gt(ROSA)26Sor|MGI:4939371|6|||||||||||||||||||||||||||||Normal.impaired wound healing|Normal|BALB/c|Yes|Yes|Yes|Yes|Yes|Yes|No|Excellent|4||Hom x Hom|No|16-Oct-2008|Cryopreserved sperm|80.0|0.0|Unknown||ROSA, flightless, wound healing|Yes| 6546.0|ID1GFP|B6.129X1-Id1/Ausb||Dominant|inhibitor of DNA binding 1|Id1|Normal|bHLHb24, D2Wsu140e, Idb1 |MGI:96396|inhibitor of DNA binding 1; targeted mutation 1, Xiao-Hong Sun|Id1|MGI:3831561|2|||||||||||||||||||||||||||||Decreased hematopoietic stem cell number:*There is a 45% reduction in the number of long-term HSC in whole bone marrow cells based on the ability to generate multilineage engraftment after serial transplantation in irradiated hosts.*Similar results are observed when fractions of bone marrow cells enriched in stem cells are used in serial transplantation of irradiated hosts.*Multilineage engraftment in the primary bone marrow transplant is the same when mutant or wild-type mice are the donors, indicating short term HSC cells are unaffected.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown||E-protein, Helix-loop-helix (HLH) transcription factors, GFP|Yes| 201.0|TGFbRIII KO|B6;129S1-Tgfbr3/Apb|B6;129S1-Tgfbr3/Apb|Recessive|transforming growth factor, beta receptor III|Tgfbr3|Nil|betaglycan, TBRIII|MGI:104637|targeted mutation 1, Kaye Stenvers|Tgfbr3|MGI:2664514|5||||||||||||||||No|||||||||||||Mice homozygous for disruptions in this gene usually die as embryos. The very few individuals that survive are poorly fertile with abnormalities of the spleen, liver, heart, and skeletal system.Embryonic lethal E16.5-E18.5 of heart and liver defects||C57BL/6 x 129|No|No|Yes|No|No|Yes|Yes|Unknown||||No|18-Apr-2006|Cryopreserved sperm|210.0|0.0|Unknown||heart, liver, embryonic lethal, growth factor|Yes| 91.0|Winnie|C57BL/6JSfdAnu-Muc2/AnuApb|C57BL/6JSfdAnu-Muc2/AnuApb|Recessive|mucin 2|Muc2|Nil||MGI:1339364|Winnie|Muc2|MGI:3614806|7|ENSMUSG00000025515|ENSMUST00000026590|Muc2-202|2963|2968|G to A|ENSMUSE00000467940|25|988|Cysteine to Tyrosine|||||GCTGGACCCCTCTTACAAGGGCACTGTATGTGGTCTGTGTGGGAACTTTGATGACCAGACC|Yes|||||||||||||Diarrhoea, soft feces at weaning, some develop rectal prolapse. GIT does not appear inflamed, goblet cell hyperplasia and developmental or functional deficiency - malabsorption syndrome||C57BL/6JSfdAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Poor||||No|06-Feb-2006|Cryopreserved sperm|34.0|0.0|Unknown||diarrhoea, malabsorption, goblet cell, ENU|Yes| 8597.0|Grhl2+/-;Noggin+/-|B6(Cg).129-Grhl2 Nog/Apb||Recessive|grainyhead like transcription factor 2|Grhl2|Nil|061001|MGI:2182543|grainyhead like transcription factor 2; targeted mutation 1.1, Stephen M Jane|Grhl2|MGI:4836381|15|||||||||||||||||||||||||||||Embryos resulting from intercrosses, and which are genetically null for both Grhl2 and Noggin will be expected to have neural tube, skeletal and/or craniofacial defects.|Grhl2+/-;Noggin+/- adult mice appear to have no discernible phenotype|C57BL/6|No|No|Yes|No|No|Yes|No|Unknown||||No|02-Nov-2018|Cryopreserved sperm|40.0|26.0|Unknown|||Yes| 8597.0|Grhl2+/-;Noggin+/-|B6(Cg).129-Grhl2 Nog/Apb||Recessive|noggin|Nog|||MGI:104327|noggin; targeted mutation 1, Andrew P McMahon|Nog|MGI:1862000|11|||||||||||||||||||||||||||||Embryos resulting from intercrosses, and which are genetically null for both Grhl2 and Noggin will be expected to have neural tube, skeletal and/or craniofacial defects.|Grhl2+/-;Noggin+/- adult mice appear to have no discernible phenotype|C57BL/6|No|No|Yes|No|No|Yes|No|Unknown||||No|02-Nov-2018|Cryopreserved sperm|||Unknown|||Yes| 5596.0|Adrb3||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5527.0|Hif delta/+|STOCK Hif1a Tg(CMV-Cre)1Cgn/JApb||Recessive|hypoxia inducible factor 1, alpha subunit|Hif1a|Unknown|bHLHe78, HIF-1alpha, HIF1alpha, MOP1|MGI:106918|hypoxia inducible factor 1, alpha subunit; targeted mutation 3, Randall S Johnson|Hif1a|MGI:2386679|12||||||||||||||||No|transgene insertion 1, University of Cologne|human cytomegalovirus (CMV)|||||||||||||C57BL/6|No|No|Yes|No|No|Yes|No|Unknown|Several||Het x Het|No|22-Jun-2011|Cryopreserved sperm|50.0|0.0|Unknown||hypoxic, VEGF|Yes| 5520.0|p47phox knockout|B6.129S2-Ncf1/MarpApb||Recessive|neutrophil cytosolic factor 1|Ncf1|Nil|NADPH oxidase subunit (47kDa), Ncf-1, NOXO2, p47, p47phox|MGI:97283|neutrophil cytosolic factor 1; targeted mutation 1, Steven M Holland|Ncf1|MGI:1934143|5||||||||||||||||No|||||||||||||Animals are immunocompromised and hence highly susceptible to bacterial infection.|Animals are immunocompromised and hence highly susceptible to bacterial infection.|C57BL/6J|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|09-Jun-2011|Cryopreserved sperm|50.0|0.0|Yes|Chronic granulomatous disease (CGD)|bacterial infection, Chronic granulomatous disease (CGD), nicotinamide dinucleotide phosphate (NADPH) oxidase, granuloma|Yes| 107.0|Albert ; KLK4|C57BL/6JSfdAnu-Tg(KLK4mHEL)6Ccg/AnuApb|C57BL/6JSfdAnu-Tg(KLK4mHEL)6Ccg/AnuApb|Dominant||||||||||||||||||||||||||transgene insertion 6, Christopher C Goodnow|H2-K|Ubiquitous||||||||||Express membrane bound HEL under control of H2-K promoter. Transmembrane domain cloned from H2-K molecule.||C57BL/6JSfdAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Poor||21|hom x hom|No|06-Feb-2006|Cryopreserved sperm|122.0|0.0|Unknown||Hen egg lysozyme (HEL), membrane bound, H2, autoimmunity|Yes| 6708.0|R26EYFP|R26EYFP (B6)/Ausb||||R26EYFP||||||||||||||||||||||||||||||||||||None||C57BL6|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|02-Dec-2011||0.0|0.0|Unknown|||Possibly| 6711.0|ApoEKO|B6.129P2-Apoe/J/Ausb||Recessive|apolipoprotein E |Apoe|Nil||MGI:88057|apolipoprotein E; targeted mutation 1, University of North Carolina|Apoe|MGI:1857129|7|||||||||||||||||||||||||||||Increased CD4-positive T cell number:*Mice maintained on a high fat diet and infect with Leishmania major generate more IL-4 and IL-5 producing CD4+ T cells compared to wild-type mice.Abnormal cell-mediated immunity:*The immune response of mice fed a high fat diet to Leishmania major infection is skewed towards a Th2-type response.*In an adoptive transfer experiment, the proliferation of Tg(TcrLCMV)2Aox CD45.2+ cell in mice fed a high fat diet and receiving then immunized with GP61-80 peptide with CpG is reduced compared to in wild-type mice similarly treated. Abnormal dendritic cell physiology: *Dendrictic cells mount reduced IL-12p40 and TNF-alpha responses to stimulation with zymosan, poly(I:C), LPS, imiquimod, and a combination of anti-CD40 antibodies and CpG compared to wild-type mice but similar to wild-type mice fed a high fat diet. *In mice fed a high fat diet, dendritic cell production of IL-12p40, IL-6 and TNF-alpha after 35 to 40 weeks, but not after 6 to 10 weeks, is severely impaired compared to wild-type cells in response to CpG/anti-CD-40 stimulation. *CD8alpha-, but not CD8alpha+, dendritic cells are defective in their ability to produce IL-12p40. *Dendritic cells from mice on a high fat diet are severely impaired in their ability to produce Il-12p40, -12p70, -6, and TNF-alpha compared to dendritic cells from wild-type mice on a high fat diet. *Mice fed a high fat diet and co-stimulated with CpG or LPS have fewer IL-12p40-producing CD8alpha- dendritic cells (4.6+/-1.1%) than wild-type mice fed a high fat diet (15.3+/-2.4%). *However, CD8alpha+ dendritic cells produce normal amounts of Il-12p70 and -12p40. *However, the immune responses of bone marrow derived dendritic cells from mice fed a high fat diet or splenic dendritic cells from mice fed a regular diet are normal.Increased susceptibility to parasitic infection:*Mice maintained on a high fat diet and infect with Leishmania major produce more IL-4 and IL-5 producing CD4+ T cells compared to wild-type mice.*The immune response of mice fed a high fat diet to Leishmania major infection is skewed towards a Th2-type response.*Mice maintained on a high fat diet or regular chow and infect with Leishmania major exhibit an increased swelling and parasitic burden at the site of infection (footpad).Decreased circulating leptin level:*Plasma leptin levels are low at both 6 and 18 months.Abnormal lipid level:*Mice have increased levels of circulating oxidized lipids compared to wild-type mice. Increased circulating cholesterol level: *Mice develop severe cholesterolemia when receiving a high fat diet from 6 to 30 weeks (elevated levels are detected at 6, 15, and 30 weeks).Abnormal eating/drinking behavior Increased drinking behavior: *Increased water intake at 18 months. Increased eating behavior: *Increased food intake at 12 and 18 months but not earlier.Increased anxiety-related response:*At 6 months as measured in an elevated plus maze.Abnormal response to new environment:*Mice consume food slower in a new environment than Tg(GFAP-APOE_i4)#Hol Apoe/Apoe and wild-type mice.*Mice require more time to habituate to a novel environment compared to wild-type mice.*Mice are less reluctant than wild-type mice to move into an open area. Decreased exploration in new environment: *Reduced exploratory behavior in an open field test by 12 months although normal earlier. *Exploratory behavior remains constant over several days whereas controls show higher initial exploratory behavior which drops off quickly.Abnormal spatial learning:*At 14 to 17 months of age, mice perform better than Tg(GFAP-APOE_i4)#Hol Apoe/Apoe and wild-type mice in a rotating holeboard test.Decreased startle reflexAbnormal locomotor behavior:*Mice spend more time than Tg(GFAP-APOE_i4)#Hol Apoe/Apoe in the center of an open field.Abnormal thermal nociception:*41% increase in foot withdrawal latency from painful thermal stimuli.*100% slower tail withdrawal latency.Abnormal kindling response:*After-discharge duration is significantly prolonged by the sixth trial.*Delayed rekindling after 3-4 weeks.Hypopituitarism:*Restraint stress at 6 months results in disproportionately low ACTH levels as compared to plasma corticosterone levels.Abnormal myelin sheath morphology:*Very little Schwann cell cytoplasm.*Blurring of lipid membrane border between axons and Schwann cells.Abnormal synaptic vesicle morphology:*Synaptophysin levels are somewhat more reduced than in controls after entorhinal cortex lesion.Abnormal sciatic nerve:*Cross-section of unmyelinated axons is irregular.*Very little Schwann cell cytoplasm.*Blurring of lipid membrane border between axons and Schwann cells.*Reduced number of unmyelinated axons.*Ratio of unmyelinated to myelinated axons is reduced.Abnormal adrenal gland morphology Abnormal adrenal cortex morphology: *Increased lipid droplets seen at six months. Abnormal adrenal medulla morphology: *Increased lipid droplets seen at six months.Abnormal gland physiology Hypersecretion of corticosterone: *After 10 min of restraint stress plasma levels are elevated at six months but not at three months. *Elevated adrenal levels at six months but not earlier. Hypopituitarism: *Restraint stress at 6 months results in disproportionately low ACTH levels as compared to plasma corticosterone levels.Decreased brown adipose tissue amount:*Decreased interscapular brown fat at 18 but not at 6 months.Decreased white adipose tissue amount:*Epididymal white fat reduced at both 6 and 18 months.Atherosclerotic lesions:*Cellular composition of lesions is similar among Serpine1-deficient or transgenic, Apoe-deficient genotypes, or Apoe-deficient only mice; at early time points, a greater foam cell content is observed, with more prominent cholesterol clefts and necrotic areas evident with increasing age.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|02-Dec-2011||0.0|0.0|Unknown||apolipoprotein E (apoE), ES cell|Yes| 7572.0|37L1flx|C57BL/6N-A Gpr37L1/Apb||Dominant|G protein-coupled receptor 37-like 1|Gpr37l1|Unknown|CAG-18, D0Kist8|MGI:1928503|G protein-coupled receptor 37-like 1; targeted mutation 1c, Wellcome Trust Sanger Institute|Gpr37l1||1|||||||||||||||||||||||||||||Unknown. Predicted wild type expression.|Unknown. Predicted wild type expression.|C57BL/6N|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown|Pure background||het x het|No|20-Jan-2014|Cryopreserved sperm|50.0|0.0|No|||Possibly| 7092.0|Mekk2: ENU7PMH 130 B10:B6 (no ndfip1) |C57Bl/6N-Map3k2/Anu||Recessive|mitogen-activated protein kinase kinase kinase 2|Map3k2|Unknown|9630061B06Rik, Mekk2, MEK kinase 2|MGI:1346873||||18|||||||||||||||||||||||||||||Unknown |Unknown|C57BL/6SfdAnu|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Good|unknown|unknown|het x het|No|21-Sep-2012|Cryopreserved sperm|36.0|0.0|Unknown||ENU|Possibly| 10356.0|Irf4K123R14 |C57BL/6NCrlAnu-Irf4/Anu||Recessive|interferon regulatory factor 4|Irf4 |||MGI:1096873 |Irf4:endonuclease-mediated mutation 3, Australian National University|Irf4||13|ENSMUSG00000021356 |ENSMUST00000021784|||||||||||||||||||||||||||Reduced GC responses, other phenotypes unknown|Reduced GC responses, other phenotypes unknown||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|07-Sep-2023|Cryopreserved sperm|44.0|0.0|Unknown|||Possibly| 161.0|D3∆|B6.129P2-Dll3/Apb|B6.129P2-Dll3/Apb|Recessive|delta-like 3|Dll3|Nil||MGI:1096877|Dll3 targetted mutation 1, Rosa Beddington|Dll3|MGI:2178443|7||||||||||||||||No|||||||||||||Homozygous mutants have shortened tail and trunk, with disorganised vertebrae and costal defects resulting from defective segmentation in the embryo and delayed and irregular somite formation.|None|C57BL/6|No|No|No|No|No|Yes|No|Good|10|11|+/Dll3 x C57BL/6. This was found to produce larger litters than +/Dll3 sib-matings|No|09-Mar-2006|Cryopreserved sperm|140.0|0.0|Yes||Dll3, somitogenesis, spondylocostal dysostosis, abnormal vertbral segmentation|Yes| 346.0|NODlprT° (2004)|NOD.Cg-Tnfrsf1a Fas/Apb|NOD.Cg-Tnfrsf1a Fas/Apb|Recessive|Fas (TNF receptor superfamily member)|Fas|Reduced|APO-1, APT1, CD95, Fas, TNFR6, Tnfrsf6|MGI:95484|lymphoproliferation|Fas|MGI:1856334|19||||||||||||||||Yes|||||||||||||NODlprT°(2004) homozygotes have lymphadenopathy similar to the NOD.MRL(C3)-Fas/LtJ parental strain (see http://jaxmice.jax.org/strain/004519.html for complete details of duplicate stran called NOD.MRL(c3)-Fas/DoiJ). This strain also has autoimmune characteristics similar to that seen on the MRL background (e.g. immune complex glomerulonephritis). Thee mice do not develop islet infiltrates. Older mice (>20weeks) develop larger livers. (This is possibly a consequence of liver infiltrates blocking vessels)|Similar to NOD/LtJ but there is a possible reduced incidence of diabetes though not formerly tested.|NOD/LtJ|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|10|8|sib x sib or random within a generation|No|25-Sep-2006|Cryopreserved sperm|40.0|0.0|Unknown||autoimmunity, lymphadenopathy, glomerulonephritis, lymph node architechture|Yes| 346.0|NODlprT° (2004)|NOD.Cg-Tnfrsf1a Fas/Apb|NOD.Cg-Tnfrsf1a Fas/Apb|Recessive|Tumor necrosis family receptor superfamily, member 1a|Tnfrsf1a|Unknown|CD120a, p55, p55-R, TNF receptor alpha chain, TNF-R-I, TNF-R1, TNF-R55, TNFAR, Tnfr-2, Tnfr1, TNFR60, TNFRp55|MGI:1314884|targeted mutation 1, Horst Bluethmann|Tnfrsf1a|MGI:1861040|Unknown|||||||||||||||||||||||||||||NODlprT°(2004) homozygotes have lymphadenopathy similar to the NOD.MRL(C3)-Fas/LtJ parental strain (see http://jaxmice.jax.org/strain/004519.html for complete details of duplicate stran called NOD.MRL(c3)-Fas/DoiJ). This strain also has autoimmune characteristics similar to that seen on the MRL background (e.g. immune complex glomerulonephritis). Thee mice do not develop islet infiltrates. Older mice (>20weeks) develop larger livers. (This is possibly a consequence of liver infiltrates blocking vessels)|Similar to NOD/LtJ but there is a possible reduced incidence of diabetes though not formerly tested.|NOD/LtJ|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|10|8|sib x sib or random within a generation|No|25-Sep-2006|Cryopreserved sperm|||Unknown||autoimmunity, lymphadenopathy, glomerulonephritis, lymph node architechture|Yes| 629.0|Elf5 KO|B6;129S4-Elf5/Apb|B6;129S4-Elf5/Apb|Semi-dominant|E74-like factor 5|Elf5|Nil|ESE-5|MGI:1335079|targeted mutation 1, Melanie A Pritchard|Elf5|MGI:3573855|2||||||||||||||||No|||||||||||||Homozygous embryos die between E3.5 and E7.5|Background Sensitivity: all heterozygous females resulting from backcrosses to 129T2/SvEms failed to lactate even after multiple pregnancies.Initial development of the mammary gland is normal however development stalls during the proliferation phase resulting in retarded alveolar genesis.About 84% of heterozygous females fail to support any pups and about 6% were able to support a reduced number of pups.No overt phenotype, mammary gland defect in females upon pregnancy resulting in a failure to nurse offspring.|129Sv|No|No|Yes|Yes|No|Yes|No|Good|10||Het x Het or Het male x WT female|No|25-Apr-2007|Cryopreserved sperm|70.0|0.0|Unknown||Mammary gland defect, embryonic lethal, prolactin receptor, pregnancy|No| 694.0|Galn KO|129-Gal/Apb|129-Gal/Apb|Recessive|Galanin|Gal|Nil|Galn|MGI:95637|targeted mutation 1, David Wynick|Gal|MGI:2183172|19||||||||||||||||Yes|||||||||||||abnormal branching of the mammary ductal tree -reduced ductal branching in the mammary glands of 8 week old virgin femalesreduced numbers of lactotrophsdecreased insulin secretion abnormal lactation - females unable to lactate resulting in death of all pups within 48 hours of birth unless fostered outinability to lactate is absolute for first pregnancies but pup survival improves to 20% after later pregnanciesabnormal pituitary secretion - prolactin levels in the hypophysis of randomly cycling females reduced about 40%, plasma levels of prolactin are generally normallevels of both prolactin message and peptide reduced in the pituitary 7 days postpartum, serum prolactin also reduced in serum 7 days postpartumestradiol-17beta induces increased prolactin mRNA but not proteinabnormal circulating insulin level - 2-deoxy-glucose has less effect on the initial drop in plasma insulin levels but a causes a greater increase in subsequent insulin levelsabnormal adenophysis morphologyreduced numbers of lactotrophshippocampal neuron degeneration - kainic acid injection induces significantly increased CA1 (62.9%) and CA2 (44.8%) apoptosis, staurosporine and glutamate both cause increased cell death of hippocampal neurons in culturedecreased sensory neuron number, abnormal dorsal root ganglia morphology - dorsal root ganglia of L4 and L5 are reduced 13% relative to controlssmall peptidergic neurons preferentially lostshort period of apoptosis occurs around 3-4 days of ageabnormal nervous system regeneration - nerve regeneration reduced by 30-40%sciatic nerve regeneration after injury incomplete until some time between 4 and 5 weeks whereas complete recovery only takes 2 weeks in controlsabnormal object recognition memory - increased exploration of objects placed in a familiar settingfailure to discriminate familiar objects in a changed location.||Sv129|Yes|No|Yes|Yes|Yes|Yes|No|Poor||||No|01-May-2007|Cryopreserved sperm|100.0|0.0|Unknown||lactation, prolactin, hormone, mammary gland|Yes| 7266.0|ASP ; B6.D2-CHR7/12|B6.D2-(D7Mit267-D7Mit40/12Wehi2-D12Mit144)||Semi-dominant|||||||||||||||||||||||||||||unknown||||||||7|Anxious, low exploratary behaviour in open field,juvenile seizures(audiogenic seizure prone) |Unknown|C57BL/6J|Yes|Yes|Yes|Yes|Yes|Yes|No|Excellent|>10|>2|Standrad breeding to maintain homozygosity, sib-mating not required|Yes|24-Jan-2013||0.0|0.0|Yes|anxiety trait, neuroticism, seizure, epilepsy|Anxiety, neuroticism, fear memory, stress, responsiveness, juvenile seizure, depression|No| 7266.0|ASP ; B6.D2-CHR7/12|B6.D2-(D7Mit267-D7Mit40/12Wehi2-D12Mit144)||Semi-dominant|||||||||||||||||||||||||||||unknown||||||||12|Anxious, low exploratary behaviour in open field,juvenile seizures(audiogenic seizure prone) |Unknown|C57BL/6J|Yes|Yes|Yes|Yes|Yes|Yes|No|Excellent|>10|>2|Standrad breeding to maintain homozygosity, sib-mating not required|Yes|24-Jan-2013||||Yes|anxiety trait, neuroticism, seizure, epilepsy|Anxiety, neuroticism, fear memory, stress, responsiveness, juvenile seizure, depression|No| 8548.0|Foz:Tlr9 KO|C57BL/6-Alms1 Tlr9/AnuApb||Recessive|Alstrom syndrome 1 homolog (human)|Alms1|Unknown||MGI:1934606|Alstrom syndrome 1 homolog (human); fat aussie|Alms1|MGI:3621984|6||||||||||||||||Yes|||||||||||||Foz mice are hyperphagic leading to obesity. Males are sterile. High fat feeding accelerates obesity development, and leads to nonalcoholic steatohepatitis which progresses to liver fibrosis. Steatohepatitis also develops in chow-fed animals.Hyperglycemia: female mice are diabetic by 200 days of age.Increased circulating insulin level: female mice develop insulinemia (20ng/mL insulin vs. 2-5ng/mL in wild-type).Insulin resistance: female mice develop insulin resistance by 200 days of age.Increased eating behavior: mutants eat more than wild-type.Abnormal hepatocyte morphology: mutant livers show many hepatocytes with ballooning degeneration and extensive lobular inflammation with polymorphs and mononuclear cells.Enlarged liver: mice fed high-fat diet show hepatomegaly compared to wild-type (8.9g vs. 2g).Increased liver weight: liver weights in mutant are twice that of wild-type (3.4g vs. 1.6g).Liver fibrosis: mutant livers show pericellular and pericentral fibrosis.Hepatic steatosis: chow-fed mutants develop steatosis; mutants fed the high-fat diet develop severe steatohepatitis.Tlr9 KO mice have:Abnormal immune system physiology:*Response to LPS and CpG is completely abrogated. Impaired NK cell cytolysis: *No NK cell activation is observed following infection with L. infantum. Decreased interferon-alpha secretion: *Following infection with Leishmania baziliensis. *However, secretion could be restored by treatment with GU-rich ssRNA, a TLR7 ligand. Decreased interferon-beta secretion: *Following infection with Leishmania baziliensis. *However, secretion could be restored by treatment with GU-rich ssRNA, a TLR7 ligand. Decreased interleukin-12b secretion: *Following infection with attenuated yellow fever vaccine 17D (YF-17D), dendritic cells produce less IL-12p40 relative to wild-type mice. *Unlike in wild-type mice, IL-12p40 production from dendritic cells following infection with Leishmania infantum is indetectable. Decreased tumor necrosis factor secretion: *Following treatment with PbA(Plasmodium bergbei ANKA)-parasitized erythrocytes or LPS-stimulation, TNF secretion is reduced. Decreased susceptibility to experimental autoimmune encephalomyelitis: *Myelin oligodendrocyte glycoprotein injection results in delayed onset of disease, 17.9 days after injection rather than 15.9 days as in controls. *Fewer infiltrating foci in the spinal cord. Abnormal response to infection: *Following treatment with PbA (Plasmodium bergbei ANKA)-parasitized erythrocytes, mice have a partially decreased immune response in terms of TNF secretion and response to CpG. Decreased susceptibility to parasitic infection: *Resistant to cerebral malaria. *Reduced accumulation of hemozoin. *Less upregulation of TNF-alpha in Plasmodium infection.|Normal|C57BL/6|Yes|Unknown|Yes|Yes|No|Yes|Yes|Good|>10||heterozygote mating|No|06-Aug-2018|Cryopreserved sperm|72.0|0.0|Yes|Alstrom syndrome is a disorder of childhood obesity, diabetes development and infertility.|obesity, diabetes, nonalcoholic fatty liver disease, alstrom syndrome, cilia|Yes| 8548.0|Foz:Tlr9 KO|C57BL/6-Alms1 Tlr9/AnuApb||Recessive|toll-like receptor 9|Tlr9|Nil||MGI:1932389|toll-like receptor 9; targeted mutation 1, Shizuo Akira|Tlr9|MGI:2660562|9|||||||||||||||||||||||||||||Foz mice are hyperphagic leading to obesity. Males are sterile. High fat feeding accelerates obesity development, and leads to nonalcoholic steatohepatitis which progresses to liver fibrosis. Steatohepatitis also develops in chow-fed animals.Hyperglycemia: female mice are diabetic by 200 days of age.Increased circulating insulin level: female mice develop insulinemia (20ng/mL insulin vs. 2-5ng/mL in wild-type).Insulin resistance: female mice develop insulin resistance by 200 days of age.Increased eating behavior: mutants eat more than wild-type.Abnormal hepatocyte morphology: mutant livers show many hepatocytes with ballooning degeneration and extensive lobular inflammation with polymorphs and mononuclear cells.Enlarged liver: mice fed high-fat diet show hepatomegaly compared to wild-type (8.9g vs. 2g).Increased liver weight: liver weights in mutant are twice that of wild-type (3.4g vs. 1.6g).Liver fibrosis: mutant livers show pericellular and pericentral fibrosis.Hepatic steatosis: chow-fed mutants develop steatosis; mutants fed the high-fat diet develop severe steatohepatitis.Tlr9 KO mice have:Abnormal immune system physiology:*Response to LPS and CpG is completely abrogated. Impaired NK cell cytolysis: *No NK cell activation is observed following infection with L. infantum. Decreased interferon-alpha secretion: *Following infection with Leishmania baziliensis. *However, secretion could be restored by treatment with GU-rich ssRNA, a TLR7 ligand. Decreased interferon-beta secretion: *Following infection with Leishmania baziliensis. *However, secretion could be restored by treatment with GU-rich ssRNA, a TLR7 ligand. Decreased interleukin-12b secretion: *Following infection with attenuated yellow fever vaccine 17D (YF-17D), dendritic cells produce less IL-12p40 relative to wild-type mice. *Unlike in wild-type mice, IL-12p40 production from dendritic cells following infection with Leishmania infantum is indetectable. Decreased tumor necrosis factor secretion: *Following treatment with PbA(Plasmodium bergbei ANKA)-parasitized erythrocytes or LPS-stimulation, TNF secretion is reduced. Decreased susceptibility to experimental autoimmune encephalomyelitis: *Myelin oligodendrocyte glycoprotein injection results in delayed onset of disease, 17.9 days after injection rather than 15.9 days as in controls. *Fewer infiltrating foci in the spinal cord. Abnormal response to infection: *Following treatment with PbA (Plasmodium bergbei ANKA)-parasitized erythrocytes, mice have a partially decreased immune response in terms of TNF secretion and response to CpG. Decreased susceptibility to parasitic infection: *Resistant to cerebral malaria. *Reduced accumulation of hemozoin. *Less upregulation of TNF-alpha in Plasmodium infection.|Normal|C57BL/6|Yes|Unknown|Yes|Yes|No|Yes|Yes|Good|>10||heterozygote mating|No|06-Aug-2018|Cryopreserved sperm|||Yes|Alstrom syndrome is a disorder of childhood obesity, diabetes development and infertility.|obesity, diabetes, nonalcoholic fatty liver disease, alstrom syndrome, cilia|Yes| 319.0|B6.Prf -/-|C57BL/6-Prf1/AnuApb|C57BL/6-Prf1/Anu|Recessive|perforin 1 (pore forming protein)|Prf1|Nil|perforin, Pfn, Pfp, Prf-1|MGI:97551|targeted mutation 1, Sandoz Pharmaceutical|Prf1|MGI:1857235|10|||||||||||||||||||||||||||||Homozygous null mice exhibit increased susceptibility to viral infection and defective cytotoxic T cell cytolysis and NK cell cytolysis.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|19|||No|04-May-2006|Cryopreserved sperm|100.0|0.0|Unknown||cytotoxic T cell, CD8, Natural Killer cell, cytolysis, infection|Yes| 8545.0|Foz:Tlr4 |C57BL/6-Alms1 Tlr4/AnuApb||Recessive|Alstrom syndrome 1 homolog (human)|Alms1|Unknown||MGI:1934606|Alstrom syndrome 1 homolog (human); fat aussie|Alms1|MGI:3621984|6||||||||||||||||Yes|||||||||||||Foz mice are hyperphagic leading to obesity. Males are sterile. High fat feeding accelerates obesity development, and leads to nonalcoholic steatohepatitis which progresses to liver fibrosis. Steatohepatitis also develops in chow-fed animals.Hyperglycemia: female mice are diabetic by 200 days of age.Increased circulating insulin level: female mice develop insulinemia (20ng/mL insulin vs. 2-5ng/mL in wild-type).Insulin resistance: female mice develop insulin resistance by 200 days of age.Increased eating behavior: mutants eat more than wild-type.Abnormal hepatocyte morphology: mutant livers show many hepatocytes with ballooning degeneration and extensive lobular inflammation with polymorphs and mononuclear cells.Enlarged liver: mice fed high-fat diet show hepatomegaly compared to wild-type (8.9g vs. 2g).Increased liver weight: liver weights in mutant are twice that of wild-type (3.4g vs. 1.6g).Liver fibrosis: mutant livers show pericellular and pericentral fibrosis.Hepatic steatosis: chow-fed mutants develop steatosis; mutants fed the high-fat diet develop severe steatohepatitis.Tlr4 KO mice are hyporesponsive to bacterial lipopolysaccharide and more susceptible to infection by gram negative bacteria.|Normal|C57BL/6|Yes|Unknown|Yes|Yes|No|Yes|Yes|Good|>10||heterozygote mating|No|06-Aug-2018||0.0|0.0|Yes|Alstrom syndrome is a disorder of childhood obesity, diabetes development and infertility.|obesity, diabetes, nonalcoholic fatty liver disease, alstrom syndrome, cilia, LPS, macrophage|Yes| 8545.0|Foz:Tlr4 |C57BL/6-Alms1 Tlr4/AnuApb||Recessive|toll-like receptor 4|Tlr4|Nil|lipopolysaccharide response, Lps, Rasl2-8|MGI:96824|toll-like receptor 4; targeted mutation 1, Shizuo Akira|Tlr4|MGI:1860885|4|||||||||||||||||||||||||||||Foz mice are hyperphagic leading to obesity. Males are sterile. High fat feeding accelerates obesity development, and leads to nonalcoholic steatohepatitis which progresses to liver fibrosis. Steatohepatitis also develops in chow-fed animals.Hyperglycemia: female mice are diabetic by 200 days of age.Increased circulating insulin level: female mice develop insulinemia (20ng/mL insulin vs. 2-5ng/mL in wild-type).Insulin resistance: female mice develop insulin resistance by 200 days of age.Increased eating behavior: mutants eat more than wild-type.Abnormal hepatocyte morphology: mutant livers show many hepatocytes with ballooning degeneration and extensive lobular inflammation with polymorphs and mononuclear cells.Enlarged liver: mice fed high-fat diet show hepatomegaly compared to wild-type (8.9g vs. 2g).Increased liver weight: liver weights in mutant are twice that of wild-type (3.4g vs. 1.6g).Liver fibrosis: mutant livers show pericellular and pericentral fibrosis.Hepatic steatosis: chow-fed mutants develop steatosis; mutants fed the high-fat diet develop severe steatohepatitis.Tlr4 KO mice are hyporesponsive to bacterial lipopolysaccharide and more susceptible to infection by gram negative bacteria.|Normal|C57BL/6|Yes|Unknown|Yes|Yes|No|Yes|Yes|Good|>10||heterozygote mating|No|06-Aug-2018||||Yes|Alstrom syndrome is a disorder of childhood obesity, diabetes development and infertility.|obesity, diabetes, nonalcoholic fatty liver disease, alstrom syndrome, cilia, LPS, macrophage|Yes| 1634.0|Itsn1Total KO +/- 129Sv|129/Sv-Itsn1/Apb|129/Sv-Itsn1/Apb|Recessive|intersectin 1 (SH3 domain protein 1A)|Itsn1|Nil|Eh domain, SH3 domain regulator of endocytosis 1, EHSH1, Ese1, Intersectin-L, Sh3p17|MGI:1338069|intersectin 1 (SH3 domain protein 1A); targeted mutation 1.1, Melanie A Pritchard|Itsn1|MGI:3812034|16||||||||||||||||Yes|||||||||||||Some homozygotes are runty after birth compared to the wildtype and die before weaning age. Otherwise they can catch up with the wildtype. |No overt phenotype|129Sv|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|||Het x Het|No|17-Jul-2007|Cryopreserved sperm|45.0|0.0|Yes|Alzheimer’s disease; Down syndrome|Alzheimer's disease, Down Syndrome, endocytosis, endosome, neuron|Yes| 868.0|C3H.OH|C3H.OH-H2/AnuApb|C3H.OH-H2/AnuApb|Dominant|histocompatibility-2, MHC|H2|Normal|H-2|MGI:95894||||17||||||||||||||||Yes|||||||||||||||C3H/HeSf x DBA/2|Yes|Yes|Yes|Yes|Yes|Yes|No|Poor|||brother x sister|No|25-May-2007|Cryopreserved sperm|100.0|0.0|Unknown||MHC|Yes| 8600.0|B6-Cpa3Cre;ELKSfl/fl|B6-Elks Tg(Cpa3-cre)3Glli/Apb||Recessive|ELKS||||||||Unknown|||||||||||||||||transgene insertion 3, Stephen J Galli|Carboxypeptidase A3 (Cpa3)|||||||||||It is anticipated that B6-Cpa3Cre;ELKSfl/fl mice will have a defect in mast cell degranulation. Mice should otherwise resemble wildtype mice|Unknown|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|07-Nov-2018|Cryopreserved sperm|50.0|0.0|Unknown||Mast cell|Yes| 1521.0||C.129S1(B6)-Gata1/AnuApb|C.129S1(B6)-Gata1/AnuApb|X-linked|GATA binding protein 1|Gata1|Nil|Gata-1, Gf-1|MGI:95661|targeted mutation 6, Stuart Orkin|Gata1|MGI:3037864|X||||||||||||||||Yes|||||||||||||No eosinophils||BALB/c|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|05-Jul-2007|Cryopreserved sperm|130.0|0.0|Unknown||eosinophil, promoter, inflammation, allergic|Yes| 6566.0|J20BV|B6.Cg-Tg(PDGFB-APPSwInd)20Lms/2JAusb||Semi-dominant||||||||||||||||||||||||||transgene insertion 20, Lennart Mucke|human platelet derived growth factor, B polypeptide (PDGFB) promoter|||||||||||Abnormal cerebral cortex pyramidal cell morphology:*At 6 months and 12 to 16 months of age, 30% fewer pyramidal cells in the entorhinal cortex express Reelin than in wild-type mice.*However, no neuron loss is observed.||C57BL6/DBA/2|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown||Alzheimer's disease, Abeta(1-42)|Yes| 8547.0|Foz:Ppara|C57BL/6-Alms1 Ppara/AnuApb||Recessive|Alstrom syndrome 1 homolog (human)|Alms1|Unknown||MGI:1934606|Alstrom syndrome 1 homolog (human); fat aussie|Alms1|MGI:3621984|6||||||||||||||||Yes|||||||||||||Foz are hyperphagic leading to obesity. Males are sterile. High fat feeding accelerates obesity development, and leads to nonalcoholic steatohepatitis which progresses to liver fibrosis. Steatohepatitis also develops in chow-fed animals.Hyperglycemia: female mice are diabetic by 200 days of age.Increased circulating insulin level: female mice develop insulinemia (20ng/mL insulin vs. 2-5ng/mL in wild-type).Insulin resistance: female mice develop insulin resistance by 200 days of age.Increased eating behavior: mutants eat more than wild-type.Abnormal hepatocyte morphology: mutant livers show many hepatocytes with ballooning degeneration and extensive lobular inflammation with polymorphs and mononuclear cells.Enlarged liver: mice fed high-fat diet show hepatomegaly compared to wild-type (8.9g vs. 2g).Increased liver weight: liver weights in mutant are twice that of wild-type (3.4g vs. 1.6g).Liver fibrosis: mutant livers show pericellular and pericentral fibrosis.Hepatic steatosis: chow-fed mutants develop steatosis; mutants fed the high-fat diet develop severe steatohepatitis.|Normal|C57BL/6|Yes|Unknown|Yes|Yes|No|Yes|Yes|Good|>10||heterozygote mating|No|06-Aug-2018|Cryopreserved sperm|60.0|0.0|Yes|Alstrom syndrome is a disorder of childhood obesity, diabetes development and infertility.|obesity, diabetes, nonalcoholic fatty liver disease, alstrom syndrome, cilia|Yes| 8547.0|Foz:Ppara|C57BL/6-Alms1 Ppara/AnuApb||Recessive|peroxisome proliferator activated receptor alpha|Ppara|Unknown|4933429D07Rik, Nr1c1, Ppar, PPARalpha, PPAR-alpha|MGI:104740||||15|||||||||||||||||||||||||||||Foz are hyperphagic leading to obesity. Males are sterile. High fat feeding accelerates obesity development, and leads to nonalcoholic steatohepatitis which progresses to liver fibrosis. Steatohepatitis also develops in chow-fed animals.Hyperglycemia: female mice are diabetic by 200 days of age.Increased circulating insulin level: female mice develop insulinemia (20ng/mL insulin vs. 2-5ng/mL in wild-type).Insulin resistance: female mice develop insulin resistance by 200 days of age.Increased eating behavior: mutants eat more than wild-type.Abnormal hepatocyte morphology: mutant livers show many hepatocytes with ballooning degeneration and extensive lobular inflammation with polymorphs and mononuclear cells.Enlarged liver: mice fed high-fat diet show hepatomegaly compared to wild-type (8.9g vs. 2g).Increased liver weight: liver weights in mutant are twice that of wild-type (3.4g vs. 1.6g).Liver fibrosis: mutant livers show pericellular and pericentral fibrosis.Hepatic steatosis: chow-fed mutants develop steatosis; mutants fed the high-fat diet develop severe steatohepatitis.|Normal|C57BL/6|Yes|Unknown|Yes|Yes|No|Yes|Yes|Good|>10||heterozygote mating|No|06-Aug-2018|Cryopreserved sperm|||Yes|Alstrom syndrome is a disorder of childhood obesity, diabetes development and infertility.|obesity, diabetes, nonalcoholic fatty liver disease, alstrom syndrome, cilia|Yes| 6721.0|MG1|B6-Tg(EEF1A-MGMT(P140K)Pgun/Ausb||||MG1||||||||||||||||||||||||||||||||||||None||C57BL6|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|02-Dec-2011||0.0|0.0|Unknown|||Possibly| 858.0|B10.HTG|B10.HTG-H2/HarAnuApb|B10.HTG-H2/HarAnuApb|Dominant|histocompatibility-2, MHC|H2|Normal|H-2, MHC-II|MGI:95894||||17||||||||||||||||No|||||||||||||||C57BL/10|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|||sib x sib|No|24-May-2007|Cryopreserved sperm|100.0|0.0|Unknown||Major Histocompability, haplotype, MHC, T cell|Yes| 845.0|SW{HEL}-HL|C57BL/6-Igh Tg(IgkHyHEL10)1Rbr/AnuApb|C57BL/6-Igh Tg(IgkHyHEL10)1Rbr/AnuApb|Dominant|immunoglobulin heavy chain complex|Igh|||MGI:96442|immunoglobulin heavy chain complex; targeted mutation 1, Robert Brink|Igh|MGI:3800383|12||||||||||||||||Yes|transgene insertion 1, Robert Brink||||||||||||B cells express Immunoglobulin specific for hen egg lysozyme and are capable of undergoing class switch.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|23-May-2007|Cryopreserved sperm|68.0|0.0|Unknown||Immunoglobulin, Hen Egg lysozyme (HEL), self-tolerance, autoimmunity, B cell|Yes| 8601.0|ENU44:G2|ANU:ENU44:G2||Recessive|Unknown||||||||Unknown||||||||||||||||Unknown|||||||||||||Unknown|Unknown|C57BL/6NCrlAnu|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||1||No|07-Nov-2018|Cryopreserved sperm|1188.0|0.0|Unknown||ENU, random, mutagenesis, screen|Yes| 5613.0|B Arrestin WT||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6724.0|Tp2|F-Tg(ACTB-Tpm1.Tm3)70Pgun/Ausb||Dominant||Tp2||||||||||||||||||||||||||||||||||||NoneMild dytrsophic features in some skeletal muscles.||FVBn|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|02-Dec-2011||0.0|0.0|Unknown|||Possibly| 5650.0|C57 x Super16TOPFLASH||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 7270.0||SJL/Mrit-MRI96570|SJL/Mrit-MRI96570|Dominant|unknown||Unknown||||||Unknown|||||||||||||||||||||||||||||Perinatal lethality with jaundice|Heterozygous mice display a microcytic anaemia with increase osmotic fragility.|SJL/J|No|No|Yes|No|No|Yes|No|Good||||No|05-Feb-2013|Cryopreserved sperm|50.0|0.0|Yes|Hereditary spherocytosis|Hereditary spherocytosis, microcytosis, ENU|Yes| 5445.0|Servalan ; ENU11B6:025b|C57BL/6JAnu-Ebf1/AnuApb|C57BL/6JAnu-Ebf1/AnuApb|Dominant|early B-cell factor 1 |Ebf1|Reduced|O/E-1, Olf-1, Olf1 |MGI:95275|early B-cell factor 1; Servalan|Ebf1|MGI:5007783|11|ENSMUSG00000057098|ENSMUST00000081265|Ebf1-001|||||||||||||Yes|||||||||||||Low B cell numbers in the peripheral blood.|FACs phenotype - Low B cells|C57BL/6JAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|N/A|5|Sib x sib|No|28-Feb-2011|Cryopreserved sperm|28.0|0.0|Unknown||B cell, NIH, ENU|Yes| 2010.0|Stat3 heterozygous knockout|B6;129P2-Stat3/Apb|B6;129P2-Stat3|Recessive|Signal transducer and activator of transcription 3|Stat3|Nil|Aprf|MGI:103038|targeted mutation 1, Shizuo Akira|Stat3|MGI:1926814|11||||||||||||||||Yes|||||||||||||Embryonic lethal (E7.5)|Viable, fertile - no apparent abnormalities.|129Sv x C57BL/6|No|No|Yes|No|No|Yes|No|Good|||heterozygous x heterozygous|No|17-Sep-2007|Cryopreserved sperm|115.0|0.0|No||STAT, cytokine, transcription, interleukin|Yes| 8602.0|ENU44:G3|ANU:ENU44:G3||Recessive|Unknown||||||||Unknown||||||||||||||||Unknown|||||||||||||Unknown|Unknown|C57BL/6NCrlAnu|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||1||No|07-Nov-2018|Cryopreserved sperm|157.0|0.0|Unknown||ENU, random, mutagenesis, screen|Yes| 5487.0|A33:Lgp130YFKQ.B6 (Line 6). |B6(Cg)-Tg(Gpa33-Il6*)6Ern/Lud||Dominant||||||||||||||||||||||||||transgene insertion 6 Matthias Ernst|glycoprotein A33 (transmembrane)|||||||||||Unknown|Unknown|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|12|||No|19-Apr-2011|Cryopreserved sperm|50.0|0.0|Unknown||signal transduction, dimerization|Yes| 7283.0|Spi6 x Granzyme B double knockout|B6.129-Gzmb Serpin9/MarpApb|B6.129-Gzmb Serpin9|Dominant|granzyme B|Gzmb||CCP1, CCP-1/C11, Ctla1, Ctla-1, GZB|MGI:109267|granzyme B; targeted mutation 1, Timothy J Ley|Gzmb|MGI:1857156|14|||||||||||||||||||||||||||||Immunocompromised|Normal|C57BL/6J|Yes|Yes|Yes|Yes|Yes|Yes|No|Excellent||||No|06-Mar-2013|Cryopreserved sperm|40.0|0.0|Unknown||T cell, CD8, dendritic cell, MHC I, cross-priming|Possibly| 7283.0|Spi6 x Granzyme B double knockout|B6.129-Gzmb Serpin9/MarpApb|B6.129-Gzmb Serpin9|Dominant|serine (or cysteine) peptidase inhibitor, clade B, member 9|Serpinb9||ovalbumin, PI-9, Spi6|MGI:106603|serine (or cysteine) peptidase inhibitor, clade B, member 9; targeted mutation 1.1, Phil Bird|Serpinb9|MGI:5140012|13||||||||||Unknown to Unknown|||||||||||||||||||Immunocompromised|Normal|C57BL/6J|Yes|Yes|Yes|Yes|Yes|Yes|No|Excellent||||No|06-Mar-2013|Cryopreserved sperm|||Unknown||T cell, CD8, dendritic cell, MHC I, cross-priming|Possibly| 5178.0|ENU18FOX:008 B6.129-Tg(FoxP3-GFP)|B6.129-Dclre1c Foxp3/AnuApb||Recessive|DNA cross-link repair 1C, PSO2 homolog (S. cerevisiae)|Dclre1c||Art, Artemis|MGI:2441769||||2|ENSMUSG00000026648|ENSMUST00000061852|Dclre1c-001|656|743|T to C|ENSMUSE00000319676|8|219|Leucine to Proline|||||TTATGGCTACGAGTATTTATTCACCAACCTAAGCGAGGAGCTGGGAGTTCAGGTTCATGTG|Unknown|||||||||||||Reduced lymphocyte population / lymphopenia, with a secondary hyper-IgE phenotype in some cases. Phenotype detected by peripheral blood FACS.Cells from the Foxp3-gfp background strain that express FoxP3 fluoresce green, predominantly T cells|Normal |129 x C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|||Affected x affected|No|19-Jul-2010|Cryopreserved sperm|70.0|0.0|Unknown||lyphopenia, lymphocytopenia, lymphocyte, immunology, hyper IgE|Possibly| 5178.0|ENU18FOX:008 B6.129-Tg(FoxP3-GFP)|B6.129-Dclre1c Foxp3/AnuApb||Recessive|forkhead box P3|Foxp3|Normal|JM2, scurfin|MGI:1891436|forkhead box P3; targeted mutation 2, Alexander Y Rudensky|Foxp3|MGI:3574964|X|||||||||||||||||||||||||||||Reduced lymphocyte population / lymphopenia, with a secondary hyper-IgE phenotype in some cases. Phenotype detected by peripheral blood FACS.Cells from the Foxp3-gfp background strain that express FoxP3 fluoresce green, predominantly T cells|Normal |129 x C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|||Affected x affected|No|19-Jul-2010|Cryopreserved sperm|||Unknown||lyphopenia, lymphocytopenia, lymphocyte, immunology, hyper IgE|Possibly| 6725.0|Tp3|F-Tg(ACTB-TPM3.Tm5NM1)52Pgun/Ausb||Dominant||Tp3||||||||||||||||||||||||||||||||||||NoneHomozygous mice may have reduced lifespan due to convulsive fits. A high proportion of female mice have convulsive fits starting at 4-6 months of age. Males are less affected.||FVBn|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|02-Dec-2011||0.0|0.0|Unknown|||Possibly| 8603.0||FVB/N-Tg(Nos1-EGFP)DP185Gsat/Apb||Dominant||||||||||||||||||||||||||transgene insertion DP185, GENSAT Project at Rockefeller University|Nos1|||||||||||Normal. EGFP expression under control of Nos1 promoter region in modified BAC construct. NOTE: some aberrant expression in the enteric nervous system at different developmental ages. Haven't checked other parts of the nervous system.|Normal. EGFP expression under control of Nos1 promoter region in modified BAC construct. NOTE: some aberrant expression in the enteric nervous system at different developmental ages. Haven't checked other parts of the nervous system.|FVB/N|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|08-Nov-2018|Cryopreserved sperm|50.0|0.0|Unknown|||Yes| 6726.0|Tp7|B6-Tpm3tm2(^9d)Pgun/Ausb||Dominant||Tp7|||||||Unknown|||||||||||||||||||||||||||||Nonehomozygous are poor breeders (partial embryonic lethality.||C57BL6|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|02-Dec-2011|Embryo|0.0|0.0|Unknown|||Possibly| 6727.0|TP8|B6.F-Tg(ACTB-TPM3.tm5NM1)52Pgun/Ausb||Dominant||TP8||||||||||||||||||||||||||||||||||||NoneSome early postnatant deaths.||C57BL6|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|02-Dec-2011|Embryo|0.0|0.0|Unknown|||Possibly| 8543.0|CREB-lox|B6.129-Creb1/GscApb||Recessive|cAMP responsive element binding protein 1|Creb1||2310001E10Rik, 3526402H21Rik, Creb, Creb-1|MGI:88494|cAMP responsive element binding protein 1; targeted mutation 3, Gunther Schutz|Creb1|MGI:2181395|1|||||||||||||||||||||||||||||Normal phenotype until crossed with a Cre-transgenic mouse|Normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|03-Aug-2018|Cryopreserved sperm|50.0|0.0|Unknown|||Yes| 5106.0|Tesk2 KO|C57BL/6-Tesk2/MarpApb||Recessive|testis-specific kinase 2|Tesk2|Unknown||MGI:2385204||||4||||||||||||||||Yes|||||||||||||No apparent phenotype. (No significant differences in weights of i) whole body, testis, reproductive tract, spleen, liver, pancreas, kidney, heart, lungs)|No apparent phenotype. (No significant differences in weights of i) whole body, testis, reproductive tract, spleen, liver, pancreas, kidney, heart, lungs)|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|30-Apr-2010|Cryopreserved sperm|63.0|0.0|Unknown||testis, kinase, spermatid|Possibly| 5933.0|NestinCre||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5934.0|Netrin 1||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5308.0|ENU17FOX:019 B6.129-Tg(FoxP3-GFP)|B6.129-Nup210 Foxp3/AnuApb||Recessive|nucleoporin 210|Nup210||gp190, gp210, Pom210|MGI:1859555||||6|ENSMUSG00000030091|ENSMUST000000032179|Nup210-002|1427|1472|T to C|ENSMUSE00000195087|11|476|Isoleucine to Threonine|||||ACCAAAGACAGGCGCCTATCAGTATACCATAAAGGCCCATGGGGGCAGTGGGAACTTCAGC|Unknown|||||||||||||CD4 T cell: CD8 T cell ratio skew.Cells from the Foxp3-gfp background strain that express FoxP3 fluoresce green, predominantly T cells|Normal |129 x C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|||Affected x affected|No|08-Nov-2010|Cryopreserved sperm|80.0|0.0|Unknown||lymphopenia, lymphocytopenia, lymphocyte, T cell, hyper IgE, ENU|Possibly| 5308.0|ENU17FOX:019 B6.129-Tg(FoxP3-GFP)|B6.129-Nup210 Foxp3/AnuApb||Recessive|forkhead box P3|Foxp3|Normal|JM2, scurfin|MGI:1891436|forkhead box P3; targeted mutation 2, Alexander Y Rudensky|Foxp3|MGI:3574964|X|||||||||||||||||||||||||||||CD4 T cell: CD8 T cell ratio skew.Cells from the Foxp3-gfp background strain that express FoxP3 fluoresce green, predominantly T cells|Normal |129 x C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|||Affected x affected|No|08-Nov-2010|Cryopreserved sperm|||Unknown||lymphopenia, lymphocytopenia, lymphocyte, T cell, hyper IgE, ENU|Possibly| 8551.0|Ddit3 tm1c|C57BL/6N-Ddit3||Recessive|DNA-damage inducible transcript 3|Ddit3||C/EBP homoologous protein 10, chop, CHOP10, CHOP-10, gadd153|MGI:109247|DNA-damage inducible transcript 3; targeted mutation 1c, Helmholtz Zentrum Muenchen GmbH|Ddit3|MGI:5520283|10||||||||||Unknown to Unknown|||||||||||||||||||Normal||C57BL/6N|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|16-Aug-2018|Cryopreserved sperm|23.0|0.0|Unknown|||Yes| 6866.0|Perlecan ; Hspg2 3-/3- exon 3 null|B6.129P2-Hspg2/Apb||Dominant|perlecan (heparan sulfate proteoglycan 2)|Hspg2|Unknown|Pcn, per, Plc|MGI:96257|perlecan (heparan sulfate proteoglycan 2); targeted mutation 1, Raija Soininen|Hspg2|MGI:2449915|4|||||||||||||||||||||||||||||Normal with small eyes|Normal with small eyes|C57BL/6|Yes|Yes|Unknown|Yes|Yes|Unknown|No|Good||||No|03-Apr-2012|Cryopreserved sperm|50.0|0.0|Unknown||Heparan sulfate, proteoglycan, perlecan|Possibly| 5950.0|NodIL1R1||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5951.0|Nrp2tm1.1Mom/MomJ||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5952.0|NtrK-1||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6580.0|GPR43?|B6.Cg-Ffar2/CrlAusb||Dominant|free fatty acid receptor 2|Ffar2|Normal|Gpr43|MGI:2441731|free fatty acid receptor 2; targeted mutation 1, Deltagen|Ffar2|MGI:4367910|7|||||||||||||||||||||||||||||Increased sensitivity to xenobiotic induced morbidity/mortality:*In DSS-treated mice.Increased susceptibility to induced colitis:*During the acute phase after DSS treatment, mice exhibit increased inflammatory response with increased mortality, increased weight loss, reduced colon length, and increased daily activity index compared with similarly treated wild-type mice.*Mice exhibit no protection from DSS-induced colitis when treated with acetate unlike similarly treated wild-type mice.*TNBS (trinitrobenzoic sulphonic acid)-treated mice exhibit increased colitis with decreased colon length and increased colonic damage and CD44+IL17+ T cells accumulation compared with similarly treated wild-type mice.*Transplantation of bone marrow confers increased susceptibility to DSS-induced colitis to wild-type mice.Increased T cell number:*CD44+IL17+ T cells are increased in the mesenteric lymph nodes of TNBS-treated mice.Abnormal granulocyte physiology:*Granulocytes produce more reactive oxygen species and myeloperoxidase activity compared with wild-type cells. Abnormal neutrophil physiology: *Neutrophils fail to exhibit a robust calcium flux when treated with acetate unlike similarly treated wild-type mice. *Neutrophils exhibit increased chemotaxis in response to fMLP and C5a compared with similarly treated wild-type cells. *Recruitment of neutrophils from Staphylococcus aureus injected mice exhibit greater recruitment compared with cells from similarly treated wild-type mice. Impaired neutrophil chemotaxis: *Neutrophils exhibit a low chemotactic index in response to very high concentrations of acetate unlike similarly treated wild-type mice. Impaired neutrophil phagocytosis: *Neutrophils stimulated with short chain fatty acids exhibit reduced release of reactive oxygen species and phagocytic activity compared with similarly treated wild-type mice.Increased susceptibility to induced arthritis:*While mice exhibit a slight delay in the development of induced arthritis, by day 11 mice develop more severe arthritis compared with similarly treated wild-type mice.Lung inflammation:*Mice exhibit increased response to ovalbumin-induced asthma with increased number of inflammatory cells in the bronchoalveolar lavage and lung tissue compared with wild-type mice.||Mixed - mice|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown||GPR43, TLRs, SCFAs|Yes| 6732.0|RFP1|C57BL/6-Tg(CAG-mRuby)#Rows/Ausb||Dominant||||||||||||||||||||||||||transgene insertion, Roland Wedlich-Soldner|CAG promoter|||||||||||||C57BL/6|Yes|Unknown|Yes|Yes|Unknown|Yes|No|Unknown||||No|02-Dec-2011||0.0|0.0|Unknown||mRFPruby, F-actin dynamics|Yes| 6729.0|Tp12^|F-Tpm3tm12(^9d)Pgun/Ausb||Recessive||Tp12||||||||||||||||||||||||||||||||||||Partial embryonic lethality in B6 background, not known on FVB/N background.||FVBn|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|02-Dec-2011|Embryo|0.0|0.0|Unknown|||Possibly| 6731.0|GFP2|C57BL/6-Tg(CAG-EGFP)#Rows/Ausb||Dominant||||||||||||||||||||||||||transgene insertion, Roland Wedlich-Soldner|CAG promoter|||||||||||||C57BL/6|Yes|Unknown|Yes|Yes|Unknown|Yes|No|Unknown||||No|02-Dec-2011||0.0|0.0|Unknown||EGFP, F-actin dynamics|Yes| 4877.0|B6.B-cell deficient/Gal KO|C57BL/6-Igh-6 Ggta/Apb||Recessive|immunoglobulin heavy chain 6 (heavy chain of IgM)|Igh-6|Nil|BCR, Ig mu, Igh-M, Igh6, IgM, muH, muMT|MGI:96448|targeted mutation 1, University of Cologne|Igh-6|MGI:1857187|12||||||||||||||||No|||||||||||||Mice lack mature B cells.All blood / tissue samples lack Gal expression.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|28-Sep-2009|Cryopreserved sperm|88.0|0.0|Unknown||Immunoglobulin, B cell, IgM, lymphocyte, Xenotransplantation, antibody, transferase, galactose|Yes| 4877.0|B6.B-cell deficient/Gal KO|C57BL/6-Igh-6 Ggta/Apb||Recessive|glycoprotein galactosyltransferase alpha 1, 3|Ggta1|Nil|alpha Gal, alpha3GalT, Gal, GALT, Ggta, Ggta-1, glycoprotein alpha galactosyl transferase 1|MGI:95704||||2|||||||||||||||||||||||||||||Mice lack mature B cells.All blood / tissue samples lack Gal expression.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|28-Sep-2009|Cryopreserved sperm|||Unknown||Immunoglobulin, B cell, IgM, lymphocyte, Xenotransplantation, antibody, transferase, galactose|Yes| 4882.0||C.B6-Socs1 Tg(Lck-cre)I57Jxm/Apb||Recessive|suppressor of cytokine signaling 1|socs1|Nil|Cish1, Cish7, JAB, JAK-binding protein, JAK2-binding protein, SOCS-1, SSI-1, STAT-induced STAT inhibitor 1|MGI:1354910|targeted mutation 3, Walter and Eliza Hall Institute of Medical Research|Socs1|MGI:2656917|16||||||||||||||||Yes|transgene insertion I57, Jamey Marth|lymphocyte protein tyrosine kinase (Lck)|||||||||||Enhanced differentiation of thymocytes toward CD8+ T cells. Thymus hyperplasia.Enlarged lymph nodes||BALB/c|Yes|No|Yes|Yes|No|Yes|No|Poor|10|2||No|28-Sep-2009|Cryopreserved sperm|20.0|0.0|Unknown||cytokine signalling, T cell, thymus, hyperplasia|Yes| 4875.0|B6.Gal KO|C57BL/6-Ggta1/Apb||Recessive|glycoprotein galactosyltransferase alpha 1, 3|Ggta1||alpha Gal, alpha3GalT, Gal, GALT, Ggta, Ggta-1, glycoprotein alpha galactosyl transferase 1|MGI:95704||||2|||||||||||||||||||||||||||||Matings between mice heterozygous for the inactivated GalT gene produced genotype ratios that deviated significantly from the predicted Mendelian 1:2:1 (wild type:heterozygote:homozygote) ratio. Cortical cataracts developed in all GalT-/- mice at 4-6 weeks of age.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|28-Sep-2009|Cryopreserved sperm|87.0|0.0|Unknown||Xenotransplantation, Transplantation, antibody, transferase, galactose|Yes| 8598.0|Beta-common chain KO BALB/c (BALB/c.Csf2rb-/-Csf2rb2-/-)|C.129-Csf2rb Csfrb2/CgbApb||Recessive|colony stimulating factor 2 receptor, beta, low-affinity (granulocyte-macrophage)|Csf2rb||AIC2B, Bc, beta c, CDw131, common beta chain, Csf2rb1, Il3r, Il3rb1, Il5rb|MGI:1339759|colony stimulating factor 2 receptor, beta, low-affinity (granulocyte-macrophage); targeted mutation 1, Clare L Scott|Csf2rb|MGI:3653883|15|||||||||||||||||||||||||||||In the steady-state, mice appear normal. Mice may develop pulmonary alveolar proteinosis (PAP) around 6-8 months of age. This is a build-up of fluid in the lungs that would otherwise be removed by alveolar macrophages that are absent in homozygous KO mice. This generally demonstrates no phenotype in mice but can result in breathing difficulty, thus mice will require additional monitoring if housed until this age.mice exhibit eosinopenia, increased surfactant accumulation in lung tissue, infection resistance and attenuated tissue repair after injury.|Normal|BALB/c|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|07-Nov-2018|Cryopreserved sperm|50.0|0.0|Unknown||IL3, beta common chain, signal transduction, GM-CSF|Yes| 8598.0|Beta-common chain KO BALB/c (BALB/c.Csf2rb-/-Csf2rb2-/-)|C.129-Csf2rb Csfrb2/CgbApb||Recessive|colony stimulating factor 2 receptor, beta 2, low-affinity (granulocyte-macrophage)|Csf2rb2|Nil|AIC2A, BetaIl3, Bil3, Il3r, Il3rb2|MGI:1339760|colony stimulating factor 2 receptor, beta 2, low-affinity (granulocyte-macrophage); targeted mutation 1, C Glenn Begley|Csf2rb2|MGI:3652583|15|||||||||||||||||||||||||||||In the steady-state, mice appear normal. Mice may develop pulmonary alveolar proteinosis (PAP) around 6-8 months of age. This is a build-up of fluid in the lungs that would otherwise be removed by alveolar macrophages that are absent in homozygous KO mice. This generally demonstrates no phenotype in mice but can result in breathing difficulty, thus mice will require additional monitoring if housed until this age.mice exhibit eosinopenia, increased surfactant accumulation in lung tissue, infection resistance and attenuated tissue repair after injury.|Normal|BALB/c|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|07-Nov-2018|Cryopreserved sperm|||Unknown||IL3, beta common chain, signal transduction, GM-CSF|Yes| 2369.0|Tilcara ; ENU6WT:121|C57BL/6JSfdAnu-Prkcb/AnuApb|C57BL/6JSfdAnu-Prkcb/AnuApb|Semi-dominant|protein kinase C, beta 1|Prkcb1|Unknown|PKC-Beta, Pkcb, Prkcb2|MGI:97596|tilcara|Prkcb|MGI:4819152|7|ENSMUSG00000052889|ENSMUST00000064989|Prkcb-001|1654|1874|T to C|ENSMUSE00000439236|15|552|Serine to Proline|||||AAGGGGAGGATGAGGATGAACTCTTCCAGTCAATCATGGAACACAATGTGGCGTATCCCAA|Yes|||||||||||||Defective T-cell independent type 2 antibody response to NP-Ficoll.||C57BL/6JSfdAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|14-Dec-2007|Cryopreserved sperm|56.0|0.0|Unknown||B cell, protein kinase, signal transduction, ENU, Wellcome Trust|Yes| 4887.0|129-Elane|129-Elane/Apb||Dominant|elastase, neutrophil expressed|Elane||Ela2, F430011M15Rik, NE, neutrophil elastase|MGI:2679229|targeted mutation 1, Jurgen Roes|Elane|MGI:2182177|10|||||||||||||||||Cre recombinase||myeloid precursor cells||||||||||Decreased susceptibility to bacterial infection:median survival time is increased to 477 +/- 88 min compared to 435 +/- 8 min in wild-type miceIncreased susceptibility to fungal infection:after infection with 500,000 A. fumigatus spores only 60% of homozygotes survived more than 21 days compared to all wild-type mice surviving6 days after infection kidney fungal load (304 mean CFU) is higher than in wild-type (16 mean CFU) but lower than in Ctsg and Ela double homozygotes (1009 mean CFU)||129X1/Sv|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|28-Sep-2009|Cryopreserved sperm|90.0|0.0|Unknown||neutrophil, serine protease, reactive oxygen intermediates, endotoxin, LPS, TNF alpha, elastase|Yes| 4113.0|Helpless, ENU9B6:035|C57BL/6JAnu-Zbtb7b/AnuApb|C57BL/6JAnu-Zbtb7b/AnuApb|Recessive|zinc finger and BTB domain containing 7B|Zbtb7b|Unknown|c-Krox, Th-POK, Thpok, Zfp67|MGI:102755|zinc finger and BTB domain containing 7B; helpless|Zbtb7b|MGI:3838356|3|ENSMUSG00000028042|ENSMUST00000029677|Zbtb7b-001|305|480|T to G|ENSMUSE00000175423|2|101|Leucine to Arginine|||||CTTTGTAGGGCCAGAGGCCCTAGGTGCCCTGCTCGAGTTTGCTTACACAGCCACACTGACC|No|||||||||||||Defective antibody response to immunization: failure to mount a normal primary T cell dependent antibody response. Very few CD4 T cells in peripheral blood or in thymus.||C57BL/6JAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|>8||Affected Male x C57BL/6JAnu|No|05-Dec-2008|Cryopreserved sperm|51.0|0.0|Unknown||B cell, T cell, CD4, antibody, ENU, Wellcome Trust|Yes| 7580.0|Spi6 x Pfp KO|C57BL/6J-SerpinB9 Prf1/MarpApb||Dominant|serine (or cysteine) peptidase inhibitor, clade B, member 9|Serpinb9|Nil|PI-9, Spi6|MGI:106603||||13|||||||||||||||||||||||||||||Immunocompromised|Unknown|C57BL/6J|Yes|Yes|Yes|Yes|Yes|Yes|No|Excellent||||No|28-Jan-2014|Cryopreserved sperm|50.0|0.0|Unknown|||Possibly| 7580.0|Spi6 x Pfp KO|C57BL/6J-SerpinB9 Prf1/MarpApb||Dominant|perforin 1 (pore forming protein)|Prf1|Nil|perforin, Pfn, Pfp, Prf-1|MGI:97551|perforin 1 (pore forming protein); targeted mutation 1, Sandoz Pharmaceuticals|Prf1|MGI:1857235|10|||||||||||||||||||||||||||||Immunocompromised|Unknown|C57BL/6J|Yes|Yes|Yes|Yes|Yes|Yes|No|Excellent||||No|28-Jan-2014|Cryopreserved sperm|||Unknown|||Possibly| 7581.0||B6/Mrit-135080|B6/Mrit-135080|Dominant|unknown||Unknown||||||Unknown|||||||||||||||||||||||||||||Unknown|Heterozygous mice display an harmonious and transient growth decrease|C57BL/6|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Good||||No|03-Feb-2014|Cryopreserved sperm|50.0|0.0|Unknown||growth , ENU|Yes| 6896.0|APN219|C57Bl/6N-mir-196b/MarpApb||Recessive|microRNA 196b|Mir196b |Unknown|mir 196b, Mirn196b, mmu-mir-196b |MGI:3618741 ||Mir196b ||6|||||||||||||||||||||||||||||Unknown|Normal|C57Bl/6N|Unknown|Unknown|Yes|Unknown|Unknown|Unknown|No|Good||||No|17-May-2012|Cryopreserved sperm|50.0|0.0|Unknown|||Possibly| 6232.0|CD1.1|BALB/c-Cd1d1/Cd1d2||Recessive|CD1d1 antigen|Cd1d1|Nil|CD1.1, Cd1a, Cd1d, Ly-38|MGI:107674|CD1d1 antigen; targeted mutation 2.1, Albert Bendelac|Cd1d1/Cd1d2|MGI:5085993|3|||||||||||||||||||||||||||||||BALB/c|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown||IL-4, Type 2 T helper cell, CD1|Yes| 10359.0|Ubc-CreER R26-Adar1E861A|C57BL/6J-Gt(ROSA)26Sor Ndor1||Dominant|gene trap ROSA 26, Philippe Soriano|Gt(ROSA)26Sor||Ubc-CreER R26-Adar1E861A|MGI:104735|Gt(ROSA)26Sor; Endonuclease-mediated mutation 1.1, Melbourne Advanced Gene Editing Centre|Gt(ROSA)26Sor||6|||||||||||||||||NADPH dependent diflavin oxidoreductase 1; transgene insertion 1, Eric J Brown ||||||||||||No phenotype in homozygous state. Require tamoxifen treatment to induce overexpression of Adar1 E861A (editing dead mutation of ADAR1 both p110 and p150) from the R26 locus. |No phenotype in heterozygous state. Require tamoxifen treatment to induce overexpression of Adar1 E861A (editing dead mutation of ADAR1 both p110 and p150) from the R26 locus. |C57Bl/6N|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|20-Sep-2023|Cryopreserved sperm|40.0|0.0|Unknown|||No| 158.0|Mr T-Less|C57BL/6SfdAnu-Zap70/AnuApb|C57BL/6SfdAnu-Zap70/AnuApb|Recessive|Zap70, zeta-chain (TCR) associated protein kinase|Zap70|Reduced|Zap-70, Srk, TZK|MGI:99613|Mr T-Less|Zap70|MGI:3614790|1|ENSMUSG00000026117|ENSMUST00000027291|Zap70-201|1510|1601|T to C|ENSMUSE00000230099|11|504|Tryptophan to Arginine|||||CCCGGTCTGCAGGGAAGTGGCCTCTGAAGTGGTACGCGCCAGAGTGCATCAACTTTCGGAA|No|||||||||||||Identified by severe reduction in T cell numbers in blood.B cells are normalBoth CD4⁺ and CD8⁺ T cell populations were almost completely absent in peripheral blood. Therefore, no αβ T cells but have increase in γδ T cellsNormal numbers of DN and DP T cells. Implies that have block at DP stage and mice unable to perform positive thymocyte selection.Intrinsic to T cells not microenvirnment.Cells unable to pass thymic selection steps.Cells unable to up-regulate TCRReduced signalling through TCR.Zap70 protein expression of mrt/mrt thymocytes was 25% of wildtype thymocytes.Kinase domain affected by mutation, kinase assays not performedHeterozygous mice, mrt/+ have normal levels of CD4⁺ and CD8⁺ thymocytes but Zap70 protein expression is 2 fold lower.Unlike cells devoid of ZAP-70, mrtless thymocytes showed partial induction of CD5 and CD69, and were sensitive to TCR stimulation with a dose-response shifted approximately 10-fold. However, essentially no T cells were able to compensate for the mrtless mutation and mature beyond the CD4⁺ CD8⁺ stage.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|07-Mar-2006|Cryopreserved sperm|36.0|0.0|Unknown||T cell, zap70, B cell, TCR, lymphocyte , ENU|Yes| 7606.0|Joey-RSA|B6(Cg)-Rbm5/MarpApb||Recessive|RNA binding motif protein 5|Rbm5|Unknown||MGI:1933204|Joey|||9|ENSMUSG00000032580|ENSMUST00000035199|Rbm5-201|788|940|G to C|ENSMUSE00000251397|10|63|Arginine to Proline|||||CTATGCTTCCTTAGCTGTCAATAACATTCGCCTCATAAAAGACAAACAGACACAACAGAAC|Yes|||||||||||||Round spermatid arrest||C57BL/6JMarp|Yes|Yes|Yes|Yes|No|Yes|No|Unknown|14|||No|27-Feb-2014||0.0|0.0|Unknown||infertility, sperm, arrest, ENU|Yes| 4589.0|Collins ; ENU12NIH:065b|C57BL/6JAnu-Rag1/AnuApb||Recessive|recombination activating gene 1|Rag1|Unknown|Rag-1|MGI:97848|collins|Rag1|MGI:4819232|2|ENSMUSG00000061311|ENSMUST00000078494|Rag1-001|985|1079|C to T|ENSMUSE00000471535|2|328|Arginine to STOP|||||AAGTCATGGGCAGCTATTGTCCCTCTTGCCGATATCCGTGCTTCCCTACTGACCTGGAGAG|No|||||||||||||No B or T cells||C57BL/6JAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|11-Mar-2009|Cryopreserved sperm|67.0|0.0|Unknown||T cell, B cell, maturation, ENU, NIH|Yes| 3689.0|Rose ; ENU11B6:058b|C57BL/6JAnu-Tap1/AnuApb|C57BL/6JAnu-Tap1/AnuApb|Recessive|transporter 1, ATP-binding cassette, sub-family B (MDR/TAP)|Tap1|Unknown|Abcb2, Ham-1, Ham1, MTP1, PSF-1, RING4, TAP, Tap-1|MGI:98483|Rose|Tap1|MGI:3797750|17|ENSMUSG00000037321|ENSMUST00000041633|Tap1-201|1928|2074|A to T|ENSMUSE00000296635|10|643|Aspartic acid to Valine|||||GATCCGGAAGCCACTCCTGCTTATCTTGGATGATGCCACCAGTGCCCTGGATGCTGGCAAC|No|||||||||||||Very low CD8<+> T cell numbers.Mice homozygous for targeted mutations that inactivate the gene are deficient in antigen presentation, surface class I antigens, and CD4-8+ T cells.||C57BL/6jAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||4|affected x B6|No|26-Aug-2008|Cryopreserved sperm|100.0|0.0|Unknown||T cell, CD8, presentation, ENU, NIH|Yes| 4980.0|Vila ; ENU12NIH:028|C57BL/6JAnu-Btk/AnuApb|C57BL/6JAnu-Btk/AnuApb|Recessive|Bruton agammaglobulinemia tyrosine kinase|Btk|Unknown|Bruton's tyrosine kinase, X-linked immune deficiency, xid|MGI:88216|vila|Btk|MGI:4820731|X|ENSMUSG00000031264|ENSMUST00000113214|Btk-201|586|722|C to T|ENSMUSE00000277322|7|196|Glutamine to STOP|||||AGCCTCTTCCCCCTACCCCAGAGGAAGATCAGATCTTGAAAAAACCGCTTCCCCCGGAGCC|Unknown|||||||||||||Low peripheral blood B cell numbers. Decreased CD45 expression.Lower IgD expression.Higher IgG expression.Hyper IgE.|Normal|C57BL/6JAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|22-Jan-2010|Cryopreserved sperm|57.0|0.0|Unknown||B cell, immunoglobulin, IgE, IgD, NIH|Yes| 1508.0|FAS.AB|B6.Cg-Gzma Gzmb Fas/Apb|B6.Cg-Gzma Gzmb Fas/Apb|Dominant|Fas (TNF receptor superfamily member)|Fas|Nil|APO-1, CD95, TNFR6, Tnfrsf6|MGI:95484|targeted mutation 1, Osaka University Medical School|Fas|MGI:1861923|19||||||||||||||||Yes|||||||||||||Increased susceptibility to parasitic infection:decreased clearance and survival after infection with Trypanosoma cruzi.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|04-Jul-2007|Cryopreserved sperm|117.0|0.0|Unknown||infection, T cell, Natural Killer Cell, cytolysis|Yes| 1508.0|FAS.AB|B6.Cg-Gzma Gzmb Fas/Apb|B6.Cg-Gzma Gzmb Fas/Apb|Dominant|granzyme A|Gzma|Nil|BLT esterase, Ctla-3, Ctla3, H factor, Hanukah factor, Hf, SE1, serine esterase 1, TSP-1, TSP1|MGI:109266|targeted mutation 1, Markus M Simon|Gzma|MGI:2449926|13|||||||||||||||||||||||||||||Increased susceptibility to parasitic infection:decreased clearance and survival after infection with Trypanosoma cruzi.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|04-Jul-2007|Cryopreserved sperm|||Unknown||infection, T cell, Natural Killer Cell, cytolysis|Yes| 1508.0|FAS.AB|B6.Cg-Gzma Gzmb Fas/Apb|B6.Cg-Gzma Gzmb Fas/Apb|Dominant|granzyme B|Gzmb|Unknown|CCP-1/C11, CCP1, Ctla-1, Ctla1|MGI:109267|targeted mutation 1, Timothy J Ley|Gzmb|MGI:1857156|14|||||||||||||||||||||||||||||Increased susceptibility to parasitic infection:decreased clearance and survival after infection with Trypanosoma cruzi.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|04-Jul-2007|Cryopreserved sperm|||Unknown||infection, T cell, Natural Killer Cell, cytolysis|Yes| 10360.0|Tcf3 KO|C57BL/6NCrlAnu-Tcf3/9Anu||Dominant|transcription factor 3|Tcf3||A1, ALF2, bHLHb21, E12, E2A, E47, Pan1, Pan2, Tcfe2a |MGI:98510|Tcf3: endonuclease-mediated mutation 3, Australian National University|Tcf3||10|ENSMUSG00000020167|ENSMUST00000105342|||||||||||||||||||||||||||embryonic lethal |Mild reduction of B cells.|C57Bl/6N|Unknown|Unknown|Unknown|Unknown|Unknown|Yes|No|Unknown||||No|20-Sep-2023|Cryopreserved sperm|55.0|0.0|Unknown|||Possibly| 7370.0|ENU25:011:Zmym2:B6:G5|C57BL/6NCrlAnu-Zmym2/AnuApb|C57BL/6NCrlAnu-Zmym2/AnuApb|Recessive|zinc finger, MYM-type 2|Zmym2|Unknown|FIM, MGC:51607, MYM, RAMP, SCLL, Zfp198|MGI:1923257|zinc finger, MYM-type 2, mutation 1, The Australian National University|Zmym2|MGI:5648435|14|ENSMUSG00000021945|ENSMUST00000022511|Zmym2-201|3774|3847|T to A|ENSMUSE00000122336|22|1258|Cysteine to STOP|||||AATCCTTTAACAATGGAAAATAAAGCATGTCTTCGCTATCAGGTGTCTTCCTTATGTGGAA||||||||||||||No homozygous animals born. Presume embryonic lethal|Normal|C57BL/6NCrlAnu|No|No|Yes|No|No|Yes|No|Unknown||5||No|05-Jul-2013|Cryopreserved sperm|46.0|0.0|Unknown||ENU, embryonic lethal|Yes| 6019.0|Red 47 Rainbow||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 8608.0|ENU43:005:Relb|C57BL/6NCrlAnu-Relb/AnuApb||Recessive|avian reticuloendotheliosis viral (v-rel) oncogene related B|Relb|Unknown|shep|MGI:103289||||7|||||||||||||||||||||||||||||||C57BL/6NCrlAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|21-Nov-2018||0.0|0.0|Unknown|||Yes| 8606.0|NODHepse|NOD-Hpse/AnuApb||Recessive|heparanase|Hpse|Nil|Hpa|MGI:1343124|heparanase; targeted mutation 1, Jin-Ping Li|Hpse|MGI:3844469|5||||||||||||||||||||||||||||||Normal.|NOD|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|16-Nov-2018|Cryopreserved sperm|60.0|0.0|Yes|Type 1 Diabetes|Heparan sulphate, MMP2, T1D|Yes| 6848.0|ENU24FoxRag G1|ENu24FoxRag:G1||Dominant|Unknown|Unknown|Unknown||||||Unknown|||||||||||||||||||||||||||||Foxp3 KO x Rag1 KO quickly develop lymphoproliferative disease.ENU induced mutation of unknown gene results in delayed onset of lymphoproliferative disease||C57BL/6NCrl|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|Yes|Poor|0|0||No|13-Mar-2012|Cryopreserved sperm|10.0|0.0|Unknown||ENU, B cell, proliferation|No| 6848.0|ENU24FoxRag G1|ENu24FoxRag:G1||Dominant|forkhead box P3|Foxp3|Nil|JM2, scurfin|MGI:1891436|forkhead box P3; targeted mutation 1.1, Alexander Y Rudensky|Foxp3|MGI:2654936|X|||||||||||||||||||||||||||||Foxp3 KO x Rag1 KO quickly develop lymphoproliferative disease.ENU induced mutation of unknown gene results in delayed onset of lymphoproliferative disease||C57BL/6NCrl|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|Yes|Poor|0|0||No|13-Mar-2012|Cryopreserved sperm|||Unknown||ENU, B cell, proliferation|No| 6848.0|ENU24FoxRag G1|ENu24FoxRag:G1||Dominant|recombination activating gene 1|Rag1|Unknown|Rag-1|MGI:97848|recombination activating gene 1; targeted mutation 1, Peter Mombaerts|Rag1|MGI:1857241|2|||||||||||||||||||||||||||||Foxp3 KO x Rag1 KO quickly develop lymphoproliferative disease.ENU induced mutation of unknown gene results in delayed onset of lymphoproliferative disease||C57BL/6NCrl|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|Yes|Poor|0|0||No|13-Mar-2012|Cryopreserved sperm|||Unknown||ENU, B cell, proliferation|No| 4751.0|B-down|C57BL/6-Bach2/AnuApb|C57BL/6-Bach2/AnuApb|Recessive|BTB and CNC homology 2|Bach2|Unknown||MGI:894679|BTB and CNC homology 2; mutation 1, Christopher C Goodnow|Bach2|MGI:5056539|4|ENSMUSG00000040270|ENSMUST00000108180|Bach2-001|46|454|T to C|ENSMUSE00000361532|4|16|Serine to Proline|||||AGCCTGGCTCCCCCATGTATGTATATGAGTCCACAGTCCACTGTGCCAACATCCTCCTGGG|No|||||||||||||Mild myeloid expansion (or low lymphoctes), low numbers B220+ cells, elevated CD44 staining on B and T cells in the blood. Reduced marginal zone B cells (CD21bright CD23intermediate-low) in spleen. |Slightly reduced blood B cells.|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||7||No|29-Apr-2009|Cryopreserved sperm|39.0|0.0|Unknown||T cell, ENU, B cell, Cd44, marginal zone|Yes| 4979.0|Avon ; ENU11B6:178a|C57BL/6JAnu-Xrcc6/AnuApb|C57BL/6JAnu-Xrcc6/AnuApb|Recessive|X-ray repair complementing defective repair in Chinese hamster cells 6|Xrcc6||G22p1, Ku p70, Ku70|MGI:95606|avon|Xrcc6|MGI:4458398|15|ENSMUSG00000022471|ENSMUST00000069530|Xrcc6-201|1400|1494|T to C|ENSMUSE00000127289|10|467|Leucine to Proline|||||AGACAAGATGAAGGCCATTGTTCAAAAGCTCCGCTTCACATACAGGAGCGACAGTTTTGAG|Yes|||||||||||||Very low B and T cell numbers in peripheral blood and spleen.Phenotype similar to Rag1 KO.|Normal|C57BL/6JAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|22-Jan-2010|Cryopreserved sperm|75.0|0.0|Unknown||B cell, T cell, immunocompromise, differentiation, NIH|Yes| 4780.0|Tg5C2 ; Young|C.CBA-Tg(CD2-IL5)5C2Ldt/AnuApb|C.CBA-Tg(CD2-IL5)5C2Ldt/AnuApb|Dominant||||||||||||||||||||||||||transgene insertion 5C2, Lindsay A Dent|the dominant control region (DCR) of the gene encoding human CD2|High - 49 Copies||||||||||Constitutive expression of the IL5 gene is sufficient to induce lifelong high-level eosinophilia. Northern blotanalysis identified 11,5 mRNA in the thymus, Peyer's patches, and subcutaneous (pooled inguinal and axillary) lymph nodes. No IL5 mRNA was detected in liver, heart, brain, or skeletal muscle tissues from transgenics, nor in any tissues from normal littermates. Do not maintain as homozygotes. While this is apparently possible, survival of homozygotes likely to be lower.|Appear normal with peripheral blood eosinophilia and increased numbers of eosinophils in the spleen (with splenomegaly), bone marrow. Heterozygous BALB/c and C57BL/6 IL-5 Tg2 mice are resistant to methylcholanthrene-induced carcinogenesis - see Simson, L, et al., 2007, Regulation of carcinogenesis by IL-5 and CCL11: a potential role for eosinophils in tumor immune surveillance. J. Immunol., 178:4222-4229.|BALB/c|No|No|Yes|No|No|Yes|No|Excellent|20||Transgenic male with wild type female|No|06-Sep-2009|Cryopreserved sperm|50.0|0.0|Yes||eosinophil, immune surveillance, resistance to helminthic parasites, asthma, allergy|Yes| 8607.0|DMP1Cre.Socs3|B6-Socs3 Tg(Dmp1-cre)1Jqfe/StVApb||Recessive|suppressor of cytokine signaling 3|Socs3|Unknown|CIS3, Cish3, cytokine-inducible SH2 protein 3, E2a-Pbx1 target gene in fibroblasts 10, EF-10, SOCS-3, SSI-3, STAT-induced STAT inhibitor 3|MGI:1201791|suppressor of cytokine signaling 3; targeted mutation 2, Warren S Alexander|Socs3|MGI:2663917|11|||||||||||||||||transgene insertion 1, Jian Q Feng|Dmp1|odontoblast-specific expression||||||||||We have assessed the bone phenotype of the osteocyte-specific SOCS3 null mouse, and have found that they have significant sex-specific changes in bone mass.|Normal|C57BL/6|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|20-Nov-2018|Cryopreserved sperm|40.0|0.0|Unknown|||Yes| 5694.0|CMV/Sox 9||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 159.0|Murdoch|STOCK H2 Zap70/AnuApb|STOCK H2 Zap70/AnuApb|Recessive|Zap70, zeta-chain (TCR) associated protein kinase|Zap70|Nil|Zap-70, Srk, TZK|MGI:99613|Murdoch|Zap70|MGI:3614796|1|ENSMUSG00000026117|ENSMUST00000027291|Zap70-201|1099|1190|A to T|ENSMUSE00000448670|9|366|Isoleucine to Phenylalanine|||||GCATGCGCAAGAAGCAGATTGACGTGGCCATCAAGGTGCTGAAGCAGGGCACAGAGAAGGC|No||||histocompatibility-2, MHC|H2||H-2, MHC-II|MGI:95894|histocompatibility-2, MHC; k2 variant|H2|MGI:4936842|17|Reduced naïve CD4⁺ and CD8⁺ T cells which are hyperactivated, reduced CD4⁺ cells, defect in TCR signal transduction, impaired but not severe response to anti-TCR stimulation, T cell intrinsic defect, Elevated serum levels of IgG2b||B10.BR x C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||10|hom x hom|No|07-Mar-2006|Cryopreserved sperm|165.0|0.0|Unknown||T cell, zap70, B cell, TCR, signalling, ENU|Yes| 7667.0|ENU23:032:Lrig1:B6:G2|C57BL/6NCrlAnu-Lrig1/AnuApb|C57BL/6NCrlAnu-Lrig1/AnuApb|Recessive|leucine-rich repeats and immunoglobulin-like domains 1|Lrig1|Unknown|Img, LIG-1|MGI:107935|leucine-rich repeats and immunoglobulin-like domains 1; mutation 1, The Australian National University|Lrig1|MGI:5563390|6|ENSMUSG00000030029|ENSMUST00000101126|Lrig1-002|1763|2215|G to T|ENSMUSE00000194515|13|588|Threonine to Lysine|||||GTGTATCATCACAAACCACTTTGGCTCCACATACTCCCACAAAGCCAGGCTCACTGTGAAT||||||||||||||Normal blood lymphocyte populations as measured by expression of following proteins: B220, CD3, CD4, CD44, KLRG1, NK1.1, IgM, IgD by flow cytometry.|Normal|C57BL/6NCrlAnu|Yes|Unknown|Yes|Yes|Unknown|Yes|No|Unknown||||No|29-Apr-2014|Cryopreserved sperm|10.0|0.0|Unknown||ENU, immunoglobulin, lymphocyte|Yes| 8609.0|ENU43:030:Jak3|C57BL/6NCrlAnu-Jak3/AnuApb||Recessive|Janus kinase 3|Jak3|Unknown||MGI:99928||||8|||||||||||||||||||||||||||||||C57BL/6NCrlAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|21-Nov-2018||0.0|0.0|Unknown|||Yes| 7364.0|BCL6-flox x CD19-cre|B6.129-Bcl6 Tg(Cd19-cre)||Recessive|B cell leukemia/lymphoma 6|Bcl6|Normal|Bcl5|MGI:107187|B cell leukemia/lymphoma 6; targeted mutation 1.1, Alexander Dent|Bcl6|MGI:5518542|16|||||||||||||||||cre recombinase|CD19|||||||||||||C57BL/6NCrlAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|01-Jul-2013||0.0|0.0|Unknown||T cell, transcription, follicular|Yes| 1541.0|Kapil Dev|C57BL/6-Gzma Prf1 Tg(TcraTcrb)1100Mjb/AnuApb||Recessive|granzyme A|Gzma|Nil|BLT esterase, Ctla-3, Ctla3, H factor, Hanukah factor, Hf, SE1, serine esterase 1, TSP-1, TSP1|MGI:109266|targeted mutation 1, Markus M Simon|Gzma|MGI:2449926|13||||||||||||||||Yes|transgene insertion 1100, Michael J Bevan||High - 49 Copies||||||||||||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|06-Jul-2007|Cryopreserved sperm|30.0|0.0|Unknown||T cell receptor, CD8, ovalbumin, Natural Killer cell|No| 1541.0|Kapil Dev|C57BL/6-Gzma Prf1 Tg(TcraTcrb)1100Mjb/AnuApb||Recessive|perforin 1 (pore forming protein)|Prf1|Nil|perforin, Pfp, Prf-1|MGI:97551|targeted mutation 1, Sandoz Pharmaceutical|Prf1|MGI:1857235|10|||||||||||||||||||||||||||||||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|06-Jul-2007|Cryopreserved sperm|||Unknown||T cell receptor, CD8, ovalbumin, Natural Killer cell|No| 7338.0|SerpinB5 cKO x FLPe|C57BL/6J-SerpinB5/MarpApb||Dominant|serine (or cysteine) peptidase inhibitor, clade B, member 5|Serpinb5|Nil|1110036M19Rik, Maspin, ovalbumin, Spi7|MGI:109579|targeted mutation 1.2, Phil Bird|Serpinb5|MGI:5484765|1||||||||||Unknown to Unknown|||||||||||||||||||Unknown|Unknown|C57BL/6J|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|22-May-2013|Cryopreserved sperm|45.0|0.0|Unknown||serpin|No| 10354.0|RnaseH2 cKO (3)|C57BL/6NCrl-RnaseH2em1/Anu||Dominant|ribonuclease H2|RnaseH2|||MGI:1914403 ||||14|||||||||||||||||||||||||||||unkown|normal|C57Bl/6N|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|21-Aug-2023|Cryopreserved sperm|66.0|146.0|Unknown|||Possibly| 6224.0|B6del535/bakM|B6del535/C57BL/6/Bak knockout |||| bok bak ||||||||||||||||||||||||||||||||||||Bak - Homozygous females may have occluded vaginal opening. ||C57BL/6|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 7662.0|ENU23 32 (PPM1E) Asb3|C57BL/6NCrlAnu-Asb3/AnuApb|C57BL/6NCrlAnu-Asb3/AnuApb|Recessive|ankyrin repeat and SOCS box-containing 3|Asb3|Unknown|2400011J03Rik|MGI:1929749|ankyrin repeat and SOCS box-containing 3; mutation 1, The Australian National University|Asb3|MGI:5563516|11|ENSMUSG00000020305|ENSMUST00000020551|Asb3-001|632|820|G to A|ENSMUSE00001205336|6|211|Aspartic acid to Asparagine|||||TGGTGCAAATGTCAATTGCCAAGCCTTGGATAAAGCTACTCCTTTGTTTATTGCTGCACAA||||||||||||||Reduced CD44 protein expression on B cells.|Normal|C57BL/6NCrlAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|11-Apr-2014|Cryopreserved sperm|39.0|0.0|Unknown||ENU, B cell, lymphocyte|Possibly| 5549.0|Tg5C2 ; Eales|C.CBA-Tg(CD2-IL5)5C2Ldt/AnuApb|C.CBA-Tg(CD2-IL5)5C2Ldt/AnuApb|Dominant||||||||||||||||||||||||||transgene insertion 5C2, Lindsay A Dent|the dominant control region (DCR) of the gene encoding human CD2|High - 49 Copies||||||||||Constitutive expression of the IL5 gene is sufficient to induce lifelong high-level eosinophilia. Northern blotanalysis identified 11,5 mRNA in the thymus, Peyer's patches, and subcutaneous (pooled inguinal and axillary) lymph nodes. No IL5 mRNA was detected in liver, heart, brain, or skeletal muscle tissues from transgenics, nor in any tissues from normal littermates. Do not maintain as homozygotes. While this is apparently possible, survival of homozygotes likely to be lower.|Appear normal with peripheral blood eosinophilia and increased numbers of eosinophils in the spleen (with splenomegaly), bone marrow. Heterozygous BALB/c and C57BL/6 IL-5 Tg2 mice are resistant to methylcholanthrene-induced carcinogenesis - see Simson, L, et al., 2007, Regulation of carcinogenesis by IL-5 and CCL11: a potential role for eosinophils in tumor immune surveillance. J. Immunol., 178:4222-4229.|BALB/c|No|No|Yes|No|No|Yes|No|Excellent|20||Transgenic male with wild type female|No|08-Aug-2011|Cryopreserved sperm|50.0|0.0|Yes||eosinophil, immune surveillance, resistance to helminthic parasites, asthma, allergy|Yes| 8610.0|ENU43:054:Lck|C57BL/6NCrlAnu-Lck/Anu||Recessive|ymphocyte protein tyrosine kinase|Lck|Unknown|Hck-3, p56|MGI:96756||||4|||||||||||||||||||||||||||||||C57BL/6NCrlAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|21-Nov-2018||0.0|0.0|Unknown|||Yes| 7239.0|TCRF5|C57BL/10-Tg(Cd2-TcraF5,CD2-TcrbF5)1Kio/CbnApb|C57BL/10-Tg(Cd2-TcraF5,CD2-TcrbF5)1Kio/CbnApb|Dominant||||||||||||||||||||||||||transgene insertion 1, Dimitris Kioussis|CD2 minigene|||||||||||This clone is CD8+ and recognises amino acids 366-374 of the nucleoprotein (NP 366-374) of influenza virus (A/NT/60/68), in the context of Class I MHC Db (Townsend et al., 1986). The usage of V beta 11 makes this TcR reactive to Class II IE molecules and an endogenous ligand recently identified as a product of the endogenous mammary tumour viruses (Mtv) 8, 9, and 11 (Dyson et al., 1991). The development of F5 transgenic T cells and their function in mice of the appropriate MHC (C57BL/10 H-2b, IE-) or in mice expressing Class II MHC IE (e.g., CBA/Ca H-2k and BALB/c H-2d) and the endogenous Mtv ligands. Positive selection of CD8+ T cells expressing the V beta 11 is seen in C57BL/10 transgenic mice (H-2b). Peripheral T cells from these mice are capable of killing target cells in an antigen-dependent manner after a period of in vitro culture with IL-2. In the presence of Class II MHC IE molecules and the endogenous Mtv ligand, most of the single-positive cells carrying the transgenic T-cell receptor are absent in the thymus. Unexpectedly, CD8+ peripheral T-cells in these (H-2k or H-2d) F5 mice are predominantly V beta 11 positive and also have the capacity to kill targets in an antigen-dependent manner. This is true even following backcrossing of the F5 TcR transgene to H-2d scid/scid mice, in which functional rearrangement of endogenous TcR alpha- and beta-chain genes is impaired.||C57BL/10|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|30-Nov-2012|Cryopreserved sperm|20.0|0.0|No||T cell receptor, T cell, influenza, cytotoxic, CD8|Yes| 5483.0||C57BL/6-Tg(UBC-GFP)30Scha/JAdelApb||Recessive||||||||||||||||||||||||||transgene insertion 30, Brian Schaefer|Human ubiquitin C|Higher than normal||||||||||Normal|Normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Excellent|||Homozygous x homozygous|No|15-Apr-2011|Cryopreserved sperm|50.0|0.0|No||GFP|Possibly| 5465.0|MLR37|FVB/N-Tg(Cryaa-cre)37Mlr/MelbApb||Dominant||||||||||||||||||||||||||transgene insertion 39, Mike Robinson|alpha A crystallin promoter|||||||||||Unknown|MLR37 transgenic line made from the CPV2/Cre construct, showed little or no LacZ activity in the lens epithelium.The staining patterns of these transgenic lines were characterized by positive staining in the embryonic lens. Although all transgenic embryos stained with x-gal in the eye, extraocular staining patterns were unique to each transgenic line and varied widely, probably due to different transgene integration sites.|FVB/N|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|17-Mar-2011|Cryopreserved sperm|50.0|0.0|Unknown||lens, epithelium, Pax6, alphaA-crystallin, Cre recombinase|Yes| 7586.0|ADAR3+/-|C57BL/6-Adarb2/StvApb||Dominant|adenosine deaminase, RNA-specific, B2|Adarb2 |Nil|Adar3, RED2 |MGI:2151118|Adar3|Adar3+/-||13|||||||||||||||||||||||||||||Normal as far as investigator / depositor of strain can tell.|Normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|4||+/- to +/- (can breed -/- to -/- happily also)|No|14-Feb-2014|Cryopreserved sperm|30.0|0.0|No||ADAR3, Adarb2|Yes| 8611.0|ENU43:139:Pax5|C57BL/6NCrlAnu-Pax5/AnuApb|C57BL/6NCrlAnu-Pax5/AnuApb|Recessive|paired box gene 5|Pax5|Unknown|EBB-1, Pax-5|MGI:97489|paired box gene 5; mutation 4, The Australian National University|Pax5||4||||||||||Unknown to Unknown||||||Yes|||||||||||||||C57BL/6NCrlAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|21-Nov-2018|Cryopreserved sperm|22.0|0.0|Unknown||B cell, lymphocyte, ENU|Possibly| 4859.0|Kaos ; ENU9CAT:053|STOCK Lrguk/AnuApb||Recessive|leucine-rich repeats and guanylate kinase domain containing|Lrguk|Unknown||MGI:1921604||||6|ENSMUSG00000056215|ENSMUST00000070189|Lrguk-001|1582|1591|C to T|ENSMUSE00000459708|14|528|Arginine to STOP|||||GAAGTTTGAAATATTCTTATTTTGAGCCTCGATATATCTTGGTGGTGCCTATGGACAAGGA|Yes|transgene insertion 3, Christopher C Goodnow|Rat insulin promoter|Expression of the inserted sequence specifically to pancreatic islet beta cells||||||||||Male infertility. Mutant found in HEL:TCR ENU library.HEL:TCR transgenes not required for mutant phenotype||C57BL/6 x CBA x C57BL/10BR|Yes|Yes|Yes|Yes|No|Yes|No|Poor||||No|24-Sep-2009|Cryopreserved sperm|120.0|0.0|Yes|Male Infertility|ENU, fertility, sperm|Yes| 4859.0|Kaos ; ENU9CAT:053|STOCK Lrguk/AnuApb||Recessive||||||||||||||||||||||||||transgene insertion 1, Mark M Davis||||||||||||Male infertility. Mutant found in HEL:TCR ENU library.HEL:TCR transgenes not required for mutant phenotype||C57BL/6 x CBA x C57BL/10BR|Yes|Yes|Yes|Yes|No|Yes|No|Poor||||No|24-Sep-2009|Cryopreserved sperm|||Yes|Male Infertility|ENU, fertility, sperm|Yes| 2360.0|TCRF5|C57BL/10-Tg(Cd2-TcraF5,CD2-TcrbF5)1Kio/AnuApb|C57BL/10-Tg(Cd2-TcraF5,CD2-TcrbF5)1Kio/AnuApb|Dominant||||||||||||||||||||||||||transgene insertion 1, Dimitris Kioussis|CD2 minigene|||||||||||This clone is CD8+ and recognises amino acids 366-374 of the nucleoprotein (NP 366-374) of influenza virus (A/NT/60/68), in the context of Class I MHC Db (Townsend et al., 1986). The usage of V beta 11 makes this TcR reactive to Class II IE molecules and an endogenous ligand recently identified as a product of the endogenous mammary tumour viruses (Mtv) 8, 9, and 11 (Dyson et al., 1991). The development of F5 transgenic T cells and their function in mice of the appropriate MHC (C57BL/10 H-2b, IE-) or in mice expressing Class II MHC IE (e.g., CBA/Ca H-2k and BALB/c H-2d) and the endogenous Mtv ligands. Positive selection of CD8+ T cells expressing the V beta 11 is seen in C57BL/10 transgenic mice (H-2b). Peripheral T cells from these mice are capable of killing target cells in an antigen-dependent manner after a period of in vitro culture with IL-2. In the presence of Class II MHC IE molecules and the endogenous Mtv ligand, most of the single-positive cells carrying the transgenic T-cell receptor are absent in the thymus. Unexpectedly, CD8+ peripheral T-cells in these (H-2k or H-2d) F5 mice are predominantly V beta 11 positive and also have the capacity to kill targets in an antigen-dependent manner. This is true even following backcrossing of the F5 TcR transgene to H-2d scid/scid mice, in which functional rearrangement of endogenous TcR alpha- and beta-chain genes is impaired.||C57BL/10|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|13-Dec-2007|Cryopreserved sperm|20.0|0.0|No||T cell receptor, T cell, influenza, cytotoxic, CD8|Yes| 9291.0|Col1a2-cre_ERFGFR1OP2floxed|C57Bl/6J-Tg-FGFR1OP2/AnuApb||Recessive|FGFR1 oncogene partner 2|Fgfr1op2 ||1500031J01Rik |MGI:1914779 |FGFR1 oncogene partner 2|Fgfr1op2 ||6|||||||||||||||||Col1a2-cre|Procollagen|||||||||||Normal|Normal|C57Bl/6J|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|26-Oct-2021|Cryopreserved sperm|50.0|0.0|Unknown|||Possibly| 7587.0|Adar3 LacZ|C57BL/6N-Adarb2/MarpStvApb||Dominant|adenosine deaminase, RNA-specific, B2|Adarb2|Reduced|Adar3, RED2|MGI:2151118|adenosine deaminase, RNA-specific, B2; targeted mutation 1a, Mouse Biology Program, UCDavis|Adarb2|MGI:4944293|13|||||||||||||||||||||||||||||none apparent|none apparent|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|generated on a C57bl6 background||ki/+ to KI/+ or WT female|No|14-Feb-2014|Cryopreserved sperm|50.0|0.0|No||Adar3 LacZ|Yes| 1525.0|Chilcott|C57BL/6-Myd88/AnuApb||Recessive|myeloid differentiation primary response gene 88|Myd88|Nil||MGI:108005|targeted mutation 1, Shizuo Akira|Myd88|MGI:2385681|9||||||||||||||||Yes|||||||||||||Increased apoptosis:* 5 days after lung injury, mutants show significantly increased numbers of apoptotic lung epithelial and inflammatory cells.Increased physiological sensitivity to xenobiotics:* knockout mice are more susceptible to bleomycin-induced lung injury.Abnormal dendritic cell differentiation:* dendritic cell maturation fails to occur in vivo upon exposure to TLR9 agonists.Increased dendritic cell number:* increased numbers of dendritic cells in brains of mice infected with Plasmodium.Abnormal immune system physiology:* response to LPS and CpG is completely abrogatedAbnormal dendritic cell physiology:* cytokine secretion elicited by zymosan or LPS is impaired.* following infection with attenuated yellow fever vaccine 17D (YF-17D), dendritic cells produce less IL-12p40, IL-6 and interferon-gamma relative to wild-type mice.Abnormal macrophage physiology:* TNF production is impaired in thioglycollate-elicited macrophages treated with intact zymosan.* cytokine production by macrophages cultured with P. carinii cysts is reduced compared to wild-type.Abnormal NK cell physiology:* NK cells fail to make IFN-gamma in response to injections of TLR9 agonists.Abnormal T cell physiology:* induction of the antigen-specific CD8+ T-cell response by immunizing with soluble ovalbumin and TLR9 agonists, but not TLR2 and TLR6 agonists, was severely impaired.Abnormal cytokine secretion:* LPS-induced cytokine production by BMDCs is almost abolished compared to controls and Myd88-sufficient mutantsAbnormal chemokine secretion:* hyaluronan fragment-induced expression of chemokines by peritoneal macrophages is completely abolished in double knockout mice.Decreased interferon-alpha secretion:* CpG-A or RNA polyuridylic acid induced production of interferon-alpha was abolished in plasmacytoid dendritic cells.Decreased interferon-gamma secretion:* less up regulation of INF-gamma in Plasmodium infection.* following infection with attenuated yellow fever vaccine 17D (YF-17D), dendritic cells produce less interferon-gamma.Decreased interleukin-12 secretion:* after stimulation with zymosan, TNF production is significantly reduced in Myd88-deficient animals.Decreased interleukin-12b secretion:* less upregulation of IL-12b in Plasmodium infection>* following infection with attenuated yellow fever vaccine 17D (YF-17D), dendritic cells produce less IL-12p40 relative to wild-type mice.Decreased interleukin-6 secretion:* following treatment with PbA(Plasmodium bergbei ANKA)-parasitized erythrocytes or LPS-stimulation, IL-6 secretion is reduced.* following infection with attenuated yellow fever vaccine 17D (YF-17D), dendritic cells produce less IL-6 relative to wild-type mice.Decreased tumor necrosis factor secretion:* less upregulation of TNF-alpha in Plasmodium infection.* following treatment with PbA(Plasmodium bergbei ANKA)-parasitized erythrocytes or LPS-stimulation, TNF secretion is reduced.* after stimulation with zymosan, TNF production is significantly reduced in Myd88-deficient animals.Decreased inflammatory response:* in a model of induced pneumococcal meningitis-associated labyrinthitis, homozygotes exhibit a significantly lower granulocytic infiltration of the labyrinth and increased bacterial density in the cochlea at 24 hrs post-infection relative to wild-type control mice.Abnormal response to infection:* following treatment with PbA (Plasmodium bergbei ANKA)-parasitized erythrocytes, mice have a decreased immune response in terms of TNF and IL-6 secretion and response to CpG.Decreased susceptibility to parasitic infection:* resistant to cerebral malaria but eventually die of extremely high parasitemia.Increased susceptibility to viral infection:* increased susceptibility to encephalomyocarditis virus (EMCV) infection compared to wildtype.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|05-Jul-2007|Cryopreserved sperm|81.0|0.0|Unknown||T cell, Natural Killer, IL-18, IL-1 receptor, interferon, eosinophil, dendritic cell, cytokine, infection|Yes| 5126.0|B6-ANU.A2G-Mx1 (Mx1+/+)|B6.A2G-Mx1/AnuApb||Dominant|myxovirus (influenza virus) resistance 1|Mx1|Normal|Mx, Mx-1, myxovirus (influenza) resistance 1 polypeptide|MGI:97243|myxovirus (influenza virus) resistance 1; myxovirus resistance|Mx1|MGI:3715151|16|||||||||||||||||||||||||||||Normal, i.e. highly influenza resistant.|Normal.|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|19-May-2010|Cryopreserved sperm|99.0|0.0|Unknown||Infection, resistance, Interferon|Possibly| 7659.0|ENU26:041:(Bach2)|C57BL/6NCrlAnu-Bach2/AnuApb|C57BL/6NCrlAnu-Bach2/AnuApb|Recessive|BTB and CNC homology 2|Bach2||E030004N02Rik|MGI:894679|BTB and CNC homology 2; mutation 2, Christopher C Goodnow|Bach2|MGI:5563501|4|ENSMUSG00000040270|ENSMUST00000108180|Bach2-001|239|793|A to G|ENSMUSE00000361532|4|81|Glutamic acid to Glycine|||||GAAAGATGACTTGGTGGTCAGCTTGCCTGAGGAGGTCACGGCCAGGGGCTTTGGGCCACTG||||||||||||||Increased numbers of immature B cells, decreased numbers of mature B cells and increased expression of IgM on B cells. Increased CD44 protein expression on B, CD4<+> and CD8<+> T cells.|Normal|C57BL/6NCrlAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|11-Apr-2014|Cryopreserved sperm|50.0|0.0|Unknown||B cell, lymphocyte|No| 7660.0|ENU27:039:PRC1|C57BL/6NCrlAnu-Prc1/AnuApb|C57BL/6NCrlAnu-Prc1/AnuApb|Recessive|protein regulator of cytokinesis 1|Prc1||D7Ertd348e, MGC:6745|MGI:1858961|protein regulator of cytokinesis 1; mutation 1, The Australian National University|Prc1|MGI:5563437|7|ENSMUSG00000038943|ENSMUST00000163812|Prc1-002||||||||80307696|8|||GAGAGCTGGAAACTTTTCCTAGAGTTTGAGGTAATATCCCTGTTTTAGCTGTGTTGCTCT||||||||||||||Embryonic lethal|normal|C57BL/6NCrlAnu|No|No|Yes|No|No|Yes|No|Unknown||||No|11-Apr-2014|Cryopreserved sperm|29.0|0.0|Unknown||embryonic lethal, ENU|No| 5125.0|BALB-ANU"X".A2G-Mx1 (Mx1+/+)|BALB/c.A2G-Mx1/AnuApb||Dominant|myxovirus (influenza virus) resistance 1|Mx1|Normal|Mx, Mx-1, myxovirus (influenza) resistance 1 polypeptide|MGI:97243|myxovirus (influenza virus) resistance 1; myxovirus resistance|Mx1|MGI:3715151|16|||||||||||||||||||||||||||||Normal, i.e. highly influenza resistant.|Normal.|BALB/c x C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|19-May-2010||0.0|0.0|Unknown||influenza, infection, resistance, Interferon|Possibly| 5695.0|Col1a2 ||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5124.0|B6-ANU.A2G-Mx1/IFNAR-/-Mx1+/+|B6.A2G-Mx1 Ifnar1/AnuApb||Dominant|interferon (alpha and beta) receptor 1|Ifnar1|Nil|Ifar, IFN-alpha/betaR, Ifrc|MGI:107658|interferon (alpha and beta) receptor 1; targeted mutation 1, Michel Aguet|Ifnar1|MGI:1930950|16||||||||||||||||No|||||||||||||Due to the lack of a functional type I interferon receptor (IFNAR), mice don't respond to interferon (IFN) alpha/beta. Consequently they are highly susesptible to virus infections.|Normal in respect to IFN signalling, but highly resistant to influenza virus infections due to Mx1 (note that most inbred strains such as B6 and Balb don't have functional Mx genes). |C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|More than 10|||No|19-May-2010|Cryopreserved sperm|60.0|0.0|Unknown||influenza, infection, resistance, Interferon|Possibly| 5124.0|B6-ANU.A2G-Mx1/IFNAR-/-Mx1+/+|B6.A2G-Mx1 Ifnar1/AnuApb||Dominant|myxovirus (influenza virus) resistance 1|Mx1|Normal|Mx, Mx-1, myxovirus (influenza) resistance 1 polypeptide|MGI:97243|myxovirus (influenza virus) resistance 1; myxovirus resistance|Mx1|MGI:3715151|16|||||||||||||||||||||||||||||Due to the lack of a functional type I interferon receptor (IFNAR), mice don't respond to interferon (IFN) alpha/beta. Consequently they are highly susesptible to virus infections.|Normal in respect to IFN signalling, but highly resistant to influenza virus infections due to Mx1 (note that most inbred strains such as B6 and Balb don't have functional Mx genes). |C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|More than 10|||No|19-May-2010|Cryopreserved sperm|||Unknown||influenza, infection, resistance, Interferon|Possibly| 7588.0|Recql4 LacZ|C57BL/6N-Recql4/MarpStvApb||Dominant|RecQ protein-like 4|Recql4||RECQ4|MGI:1931028|RecQ protein-like 4; targeted mutation 3, Wellcome Trust Sanger Institute|Recql4|MGI:5050948|15|||||||||||||||||||||||||||||Embryonic lethal|Normal|C57BL/6|No|No|Yes|No|No|Yes|No|Good|generated on a C57bl6 background||ki/+ to ki/+|No|14-Feb-2014|Cryopreserved sperm|20.0|0.0|Yes|Rothmund-Thomson syndrome|Recql4, Recql4-LacZ|Yes| 5115.0|ENU14Yaa:016a|B6.Cg-Btk Yaa/AnuApb|B6.Cg-Btk Yaa/AnuApb|Recessive|Bruton agammaglobulinemia tyrosine kinase|Btk|Unknown|Bruton's tyrosine kinase, X-linked immune deficiency, xid|MGI:88216|Bruton agammaglobulinemia tyrosine kinase; mutation 1, The Australian National University|Btk|MGI:5563504|X|ENSMUSG00000031264|ENSMUST00000033617|Btk-001||||||||131089223|11|||GTGTCTGTGTTTGCTAAATCTACTGGGTACGTGTTATGGTTCCAGTGATATGGGGTTAAA|Yes|||||||||||||Low B cell numbers in peripheral blood.While mice carry Yaa allele the phenotype does not appear to be dependent upon Yaa.||C57BL/6JAnu x B6.SB-Yaa|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|11-May-2010|Cryopreserved sperm|50.0|0.0|Unknown||Monocytes, T cell, lymphoma, autoantibody, ENU, B cell|Yes| 5115.0|ENU14Yaa:016a|B6.Cg-Btk Yaa/AnuApb|B6.Cg-Btk Yaa/AnuApb|Recessive|accelerated autoimmunity and lymphoproliferation transposition|Yaa||Tp(X;Y)1Ekw|MGI:99140|accelerated autoimmunity and lymphoproliferation transposition; accelerated autoimmunity and lymphoproliferation|Yaa|MGI:1856277|Y|||||||||||||||||||||||||||||Low B cell numbers in peripheral blood.While mice carry Yaa allele the phenotype does not appear to be dependent upon Yaa.||C57BL/6JAnu x B6.SB-Yaa|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|11-May-2010|Cryopreserved sperm|||Unknown||Monocytes, T cell, lymphoma, autoantibody, ENU, B cell|Yes| 7318.0|Nessy|B6(Cg)-Ncaph2/AnuApb|B6(Cg)-Ncaph2/AnuApb|Recessive|non-SMC condensin II complex, subunit H2|Ncaph2|Unknown|Kleisin beta|MGI:1289164|nessy|Ncaph2|MGI:3710093|15|ENSMUSG00000008690|ENSMUST00000074552|Ncaph2-001|44|144|T to A|ENSMUSE00000504356|1|15|Isoleucine to Asparagine|||||GGTGCGCTTTGCTCACCTCTTGCAGCCCATCCGGGATCTCACTAAGAACTGGGAGGTGGAC|Yes|||||||||||||The nessy mouse has a defect in T lymphocyte development that decreases circulating T cell numbers, increases their expression of the activation/memory marker CD44, and dramatically decreases the numbers of CD4(+)CD8(+) thymocytes and their immediate DN4 precursors. Thymic T cell differentiation defect at DN-DP transition, low peripheral T cell numbers, remaining cells all CD44high, Two fold more gd T cells, Defect resembles mice with exaggerated TCR signalling due to defects in c-cbl and slap proteins and defects in cbl plus cbl-b. No defect in B cells. Homozygotes grow at normal rate, size and are fertile. Intrinsic to T cells.Despite the ubiquitous expression and role of condensins, kleisin beta(nes/nes) mice were viable, fertile, and showed no defects even in the parallel pathway of B cell lymphocyte differentiation. ||C57BL/6JAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|6|||No|17-Apr-2013|Cryopreserved sperm|77.0|0.0|Unknown||T cell, lymphocyte, condensin, differentiation, ENU|Yes| 7591.0|R26-CreER Recql4fl/fl pRbfl/fl|C57BL/6-Gt(ROSA)26Sor Recql4 Trp53/StvApb||Dominant|transformation related protein 53|Trp53|Nil|p53|MGI:98834|transformation related protein 53; targeted mutation 1, Anton Berns|Trp53|MGI:1931011|11|||||||||||||||||||||||||||||Normal in absence of tamoxifen treatment.|Normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|generated on a C57bl6 background||R26-CreERki/+ homozygous Recql4 and p53 intercrosses|No|14-Feb-2014|Cryopreserved sperm|20.0|0.0|Yes|Rothmund-Thomson syndrome|R26-CreER, p53fl/fl, Recql4fl/fl|Possibly| 7591.0|R26-CreER Recql4fl/fl pRbfl/fl|C57BL/6-Gt(ROSA)26Sor Recql4 Trp53/StvApb||Dominant|gene trap ROSA 26, Philippe Soriano|Gt(ROSA)26Sor |Normal|beta geo, Gtrgeo26, Gtrosa26, R26, ROSA26|MGI:104735|gene trap ROSA 26, Philippe Soriano; targeted mutation 1, Tyler Jacks|Gt(ROSA)26Sor|MGI:3699244|6|||||||||||||||||||||||||||||Normal in absence of tamoxifen treatment.|Normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|generated on a C57bl6 background||R26-CreERki/+ homozygous Recql4 and p53 intercrosses|No|14-Feb-2014|Cryopreserved sperm|||Yes|Rothmund-Thomson syndrome|R26-CreER, p53fl/fl, Recql4fl/fl|Possibly| 7591.0|R26-CreER Recql4fl/fl pRbfl/fl|C57BL/6-Gt(ROSA)26Sor Recql4 Trp53/StvApb||Dominant|RecQ protein-like 4|Recql4|Reduced|RECQ4 |MGI:1931028 |Recql4|Recql4fl/fl||15|||||||||||||||||||||||||||||Normal in absence of tamoxifen treatment.|Normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|generated on a C57bl6 background||R26-CreERki/+ homozygous Recql4 and p53 intercrosses|No|14-Feb-2014|Cryopreserved sperm|||Yes|Rothmund-Thomson syndrome|R26-CreER, p53fl/fl, Recql4fl/fl|Possibly| 6902.0|Cornell|B6.129-Rel/AnuApb||Recessive|reticuloendotheliosis oncogene|Rel|Unknown|c-Rel|MGI:97897|targeted mutation 1, Steve Gerondakis|Rel|MGI:2179622|11||||||||||||||||No|||||||||||||In mice with an inactivated c-rel gene, whereas development of cells from all hemopoietic lineages appeared normal, humoral immunity was impaired and mature B and T cells were found to be unresponsive to most mitogenic stimuli. Phorbol ester and calcium ionophore costimulation, in contrast to certain membrane receptor-mediated signals, overcame the T cell-proliferative defect, demonstrating that T cell proliferation occurs by Rel-dependent and -independent mechanisms.This colony gets dermatitis.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|28-May-2012|Cryopreserved sperm|77.0|0.0|Unknown||Lymphocyte, IL-2, humoral immunity|Yes| 10366.0|RnaseH2 cKO (6)|C57BL/6NCrl-RnaseH2/Anu||Dominant|ribonuclease H2|RnaseH2|||MGI:1914403 ||||14|||||||||||||||||||||||||||||unkown|normal|C57Bl/6N|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|06-Oct-2023|Cryopreserved sperm|66.0|0.0|Unknown|||Possibly| 5234.0|APN 42 ; RNF31|C57BL/6-Rnf31||Recessive|ring finger protein 31|Rnf31|Unknown|HOIP, Paul, BC031509, AL033293|MGI:1934704||||14||||||||||||||||No|||||||||||||Unknown|Normal|C57BL/6N|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Good|||Chimeras mated with wildtype C57BL/6N|No|08-Oct-2010|Cryopreserved sperm|50.0|0.0|Unknown||ES cell|Yes| 7590.0|R26-CreER p53fl/fl pRbfl/fl|C57BL/6-Gt(ROSA)26Sor Rb1 Trp53/StvApb||Dominant|transformation related protein 53|Trp53|Nil|p53|MGI:98834|transformation related protein 53; targeted mutation 1, Anton Berns|Trp53|MGI:1931011|11|||||||||||||||||||||||||||||Normal in absence of tamoxifnen treatment.|no phenotype|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|generated on a C57bl6 background||R26-CreERki/+ homozygous pRb and p53 intercrosses|No|14-Feb-2014|Cryopreserved sperm|50.0|0.0|Yes|Osteosarcoma|R26-CreER, p53fl/fl, pRbfl/fl|Yes| 7590.0|R26-CreER p53fl/fl pRbfl/fl|C57BL/6-Gt(ROSA)26Sor Rb1 Trp53/StvApb||Dominant|retinoblastoma 1|Rb1|Nil|pRb, Rb, Rb-1|MGI:97874|retinoblastoma 1; targeted mutation 3, Tyler Jacks|Rb1|MGI:2450162|14|||||||||||||||||||||||||||||Normal in absence of tamoxifnen treatment.|no phenotype|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|generated on a C57bl6 background||R26-CreERki/+ homozygous pRb and p53 intercrosses|No|14-Feb-2014|Cryopreserved sperm|||Yes|Osteosarcoma|R26-CreER, p53fl/fl, pRbfl/fl|Yes| 7590.0|R26-CreER p53fl/fl pRbfl/fl|C57BL/6-Gt(ROSA)26Sor Rb1 Trp53/StvApb||Dominant|gene trap ROSA 26, Philippe Soriano|Gt(ROSA)26Sor |Normal|beta geo, Gtrgeo26, Gtrosa26, R26, ROSA26|MGI:104735|gene trap ROSA 26, Philippe Soriano; targeted mutation 1, Tyler Jacks|Gt(ROSA)26Sor|MGI:3699244|6|||||||||||||||||||||||||||||Normal in absence of tamoxifnen treatment.|no phenotype|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|generated on a C57bl6 background||R26-CreERki/+ homozygous pRb and p53 intercrosses|No|14-Feb-2014|Cryopreserved sperm|||Yes|Osteosarcoma|R26-CreER, p53fl/fl, pRbfl/fl|Yes| 6194.0|E�Myc/565foxo|B6. E�-myc 292-1/565foxo|||| Myc 565 ||||||||||||||||||||||||||||||||||||Animals develop high incidence pre-B and B lymphoma - Adult mortality: 80% Display excess pre-B cells in bone marrow, and develop lymphoma around 3 months of age. All Emu-myc mice will be visually checked twice a week from 4 weeks of age with particular attention paid to evidence of lymph node enlargement or general signs of ill health. Additionally, commencing at four weeks of age, transgenic animals will be examined once a week for swollen lymph nodes by gentle palpation of lymph node sites (axillary and inguinal regions). Mice with moderately enlarged lymph nodes indicating early lymphoma are usually otherwise healthy and normal. This is the appropriate point in disease progression for therapeutic/experimental intervention (e.g. doxycycline treatment), as lymphoma responses can be readily monitored by changes in lymph node size. Disease progression resulting in visually obvious lymph nodes, presence of ruffled fur, restricted movement, loss of weight, difficulty in breathing or obvious signs of distress will prompt euthanasia. Lymphoma tissue and other organs will be harvested post-euthanasia. ||C57BL/6|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6867.0|SM02-Pro|SuprMam02-(B6.Balb/C-SM1)-Pro/AnuApb||Recessive|||||||||||||||||||||||||||||SuprMam|SuprMam|||||||7|Mice are more susceptible to mammary tumours.|Unknown|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|11|||No|03-Apr-2012|Cryopreserved sperm|69.0|0.0|Unknown||mammary, tumour, DMBT1, p53, modifier|Possibly| 6190.0|APOE|B6.129P2-Apoe/JWehi||Recessive|apolipoprotein E|Apoe|Nil||MGI:88057|apolipoprotein E; targeted mutation 1, University of North Carolina|Apoe|MGI:1857129|7|||||||||||||||||||||||||||||premature death (J:73202)35% dead by 18 monthscardiovascular systemabnormal aorta wall morphology (J:101576, J:142083)endothelial nitric oxide synthase (eNOS) in mutant aortic wall is distinctly reduced (J:101576)Cx43 distribution at cell-cell junction shows significant disruption (J:142083)abnormal spiral modiolar artery morphology (J:101576)homozygotes fed an atherosclerotic diet develop atherosclerotic alterations in the spiral modiolar artery (SMA)in contrast, no such changes are detected in the SMA of homozygotes fed a normal dietarteriosclerosis (J:108154)homozygotes exhibit a 13% increase in aortic pulse-wave velocity (PWV) relative to wild-type mice (428 ? 14.5 cm/s vs 379 ? 10.1 cm/s), indicating increased arterial stiffness and reduced vascular elasticityatherosclerotic lesions (J:133606, J:73202, J:108154, J:97385, J:101576, J:60364, J:105736, J:142083)advanced atherosclerotic lesions; massive atheromas with abundant cholesterol crystals, neutral lipids, and diminished extracellular matrix in arotic roots and coronary arteries (J:73202)at 13 months, homozygotes display atherosclerotic lesions extending from the carotid arteries, heart, and aorta down to the renal arteries and the iliac bifurcation (J:108154)lesions are most severe in the proximal aorta and at the bifurcation of carotid arteries; the proximal carotid arteries are relatively free of lesions (J:108154)regular exercise does not reduce atherosclerotic lesion formation in homozygotes, as shown by a comparable % oil red-O staining of whole aortas from sedentary and exercised mutant mice (J:97385)at 24 weeks of age, homozygotes fed a normal diet (but not similarly-fed C57BL/6J control mice) show obvious atherosclerotic lesions in the aortic sinus and ascending aorta (J:101576)the number of atherosclerotic lesions in aortic sinus and ascending aorta is significantly increased in homozygotes fed an atherosclerotic diet vs a normal diet (J:101576)plaques in the luminal surface of the aorta are significantly larger in atherosclerotic diet homozygotes than in normal diet homozygotes (J:101576)23% of luminal surface in the aortic arch and thoracic aorta is covered by plaques at 4 months of age (J:60364)61% covered by plaques at 13 months of age (J:60364)thickened intima, foam cell accumulation and thin collagen cap (J:60364)focal fragmentation of elastic laminae (J:60364)intimal lesions are observed in atherosclerotic aortas in mutants (J:105736)major lesions are observed on lesser curvature of aortic arch in males and females with minor lesions found at branches of aortic arch (J:142083)lesions comprise around 14-16% of total aortic arch area in male and female mutants (J:142083)aortic lesions are observed in aortic sinus at level of aortic valve leaflets; lesions are about 27% of total aortal area (J:142083)increased susceptibility to atherosclerosis (J:101576, J:43846)severity of atherosclerosis is 2-fold and 99-fold higher in atherosclerotic diet homozygotes than in normal diet homozygotes and C57BL/6J control mice, respectively (J:101576)on a high fat, high cholesterol diet, mutants exhibit moderate to severe aortic and carotid atherosclerosis (J:43846)vascular stenosis (J:101576)vascular stenosis is significantly increased in homozygotes fed an atherosclerotic diet vs a normal dietspiral modiolar artery stenosis (J:101576)lumen stenosis of the spiral modiolar artery in the cochlea is exacerbated by an atherosclerotic diet relative to a normal dietincreased heart weight (J:108154)at 13 months, homozygotes show a 23% increase in heart weight relative to wild-type mice (186 ? 7.1 vs. 151 ? 2.5 mg)cardiac hypertrophy (J:108154)at 13 months, homozygotes show a 59% increase in heart weight-to-body weight ratio relative to wild-type miceabnormal blood flow velocity (J:108154)anesthetized homozygotes show significantly increased transaortic blood velocities relative to wild-type mice with peak aortic velocity at 133.4 ? 7.8 cm/s vs 89.2 ? 5.8 cm/s, and mean aortic velocity at 35.9 ? 2.7 vs 22.0 ? 1.6 cm/s, respectivelyin addition, anesthetized homozygotes show significantly increased transmitral blood velocities relative to wild-type mice with peak mitral velocities at 92 ? 7.2 cm/s vs 47.2 ? 5.3 cm/s, and mean mitral velocities at 20.6 ? 1.7 vs 11.4 ? 1.3 cm/s, respectivelyno significant differences in heart rate, peak aortic acceleration or ejection time are observed in the conscious or anesthetized state, when normalized to body weighthowever, homozygotes show alterations in aortic arch acceleration suggestive of increased peripheral wave reflectionsincreased cardiac output (J:108154)under anesthesia, homozygotes exhibit elevated flow velocities suggesting elevated cardiac outputabnormal cardiac stroke volume (J:108154)under anesthesia, homozygotes appear to exhibit significantly increased stroke volumedecreased systemic vascular resistance (J:108154)under anesthesia, homozygotes appear to exhibit significantly reduced peripheral vascular resistance and compliance in the presence of normal blood pressuresabnormal blood vessel physiology (J:60364)pulse wave velocity is insignificantly elevated at 4 monthspulse wave velocity significantly elevated at 13 monthsabnormal blood-brain barrier function (J:69455)impaired blood-brain barrier and blood-nerve barrier as indicated by extensive extravasation of serum proteins into sciatic nerve, spinal cord and cerebellum and occasional extravasation into cortex and subcortexdecreased vasodilation (J:101576)homozygotes fed a normal or atherosclerotic diet show severely impaired endothelium-dependent relaxation to acetylcholine in aortic rings relative to age-matched C57BL/6J control micemuscledecreased vasodilation (J:101576)homozygotes fed a normal or atherosclerotic diet show severely impaired endothelium-dependent relaxation to acetylcholine in aortic rings relative to age-matched C57BL/6J control miceimpaired muscle relaxation (J:60364)relaxation response to acetylcholine in blood vessels is significantly attenuated at 13 months of agemaximal response to acetylcholine is considerably reducedhomeostasis/metabolismabnormal circulating homocysteine level (J:73202)decrease in plasma total homocysteine levelsdecreased circulating glucose level (J:73202)abnormal circulating cholesterol level (J:73202)decreased HDL/total cholesterol ratiodecreased HDL/LDL ratioincreased circulating cholesterol level (J:73202, J:97385, J:101576, J:125978, J:104609, J:133606)increasing with age; 4-fold increase in plasma total cholesterol levels in 10-12 week old mutants and 13-fold increase at 29 weeks (J:73202)exercise (15 or 60 min/day swim) causes no significant changes in total cholesterol levels among homozygotes or wild-type mice relative to sedentary, genotype-matched controls (J:97385)on a normal diet, homozygotes display significantly increased plasma total cholesterol (TC) levels relative to C57BL/6J control mice (J:101576)on an atherosclerotic diet, homozygotes show a further significant increase in plasma TC levels relative to homozygotes on a normal diet (J:101576)5 fold increase in total cholesterol at 24 and 36 weeks (J:125978)total serum cholesterol 70 fold higher than controls on a normal diet (J:104609)total serum cholesterol 20 fold higher than controls on high fat diet where controls show 4 fold increase over normal diet (J:104609)significantly increased relative to wild-type controls at 24 weeks of age; levels in mutants after induction of chronic graft versus host disease (cGVH) to induce systemic lupus erythematosus (SLE) are equivalent to the Apoe-null mice (J:133606)increased circulating LDL cholesterol level (J:93987, J:101576)on a normal diet, homozygotes display significantly increased plasma LDL cholesterol levels relative to C57BL/6J control mice (J:101576)on an atherosclerotic diet, homozygotes show a further significant increase in plasma LDL levels relative to homozygotes on a normal diet (J:101576)increased circulating VLDL cholesterol level (J:93987, J:101576)on a normal diet, homozygotes display significantly increased plasma VLDL cholesterol levels relative to C57BL/6J control mice (J:101576)on an atherosclerotic diet, homozygotes show a further significant increase in plasma VLDL cholesterol levels relative to homozygotes on a normal diet (J:101576)decreased circulating triglyceride level (J:93987)hyperlipidemia (J:101576)homozygotes develop hyperlipidemia; however, HDL cholesterol levels, body weight and blood glucose remain unchanged relative to C57BL/6J control mice on a normal diet, with no further differences noted on an atheroscletoric dietincreased circulating triglyceride level (J:73202, J:101576)2-fold increase in plasma triglyceride levels in 10-12 week old mutants (J:73202)on a normal diet, homozygotes display significantly increased plasma triglyceride levels relative to C57BL/6J control mice (J:101576)on an atherosclerotic diet, homozygotes show a further significant increase in plasma triglyceride levels relative to homozygotes on a normal diet (J:101576)xanthoma (J:43846, J:73202)1 of 11 aged mice on a normal diet develops cerebral xanthoma (J:43846)eruptive xanthomas on shoulder and back areas with lipids and extracellular matix as the predominant components (J:73202)abnormal enzyme/coenzyme activity (J:73202)activity of cholesterol synthesis enzyme HMG-CoA reductase is reduced up to 60% in aging mice compared to 30% in wild-type aging micegrowth/sizedecreased body length (J:136630)nose to rump length less than controls at both 1 and 3 monthsincreased susceptibility to weight gain (J:136630)body weight was less than controls at 3 months but identical at 8 monthsdecreased body weight (J:60364, J:108154)at 13 months, homozygotes show a 22% reduction in body weight relative to wild-type mice (34.5 ? 0.9 vs. 44.5 ? 1.1 g) (J:108154)hematopoietic systemdecreased hematocrit (J:108154)at 13 months, awake, unanesthetized homozygotes display slightly but significantly reduced hematocrits ( 11%) relative to wild-type mice at 41.7 ? 1.1% vs 46.6 ? 0.4%; in contrast, systolic blood pressures remain unaffected (140 ? 7.6 mmHg vs 136 ? 7.4 mmHg)decreased follicular B cell number (J:133606)decreased relative to controlsdecreased marginal zone B cell number (J:133606)with induction of SLE by cGVH, levels are slightly decreased compared to wild-typeincreased B cell number (J:133606)newly formed B cells are significantly increased compared to wild-typeincreased marginal zone B cell number (J:133606)increased 2-fold compared to wild-typeabnormal T cell number (J:47027)increased numbers of cytokine producing T cellsabnormal CD4-positive T cell number (J:108154, J:47027)clusters of CD4+ cells found in fatty streak lesions (J:47027)ratio of Th2 to Th1 cells is increased from 4.4 to 11.4 on a normal diet and up to 20.9 on a high cholesterol diet (J:47027)increased T-helper 2 cell number (J:47027)abnormal B cell activation (J:133606)spleen cells display polyclonal B cell activation, with increased expression of MHC II, Fas, and CD86 and lower expression of CD21, CD22, and CD23increased spleen weight (J:61564)increased spleen weight while the thymus weight remains normalcellularoxidative stress (J:97385)regular exercise fails to reduce endogenous oxidant load and mitochondrial damage in hypercholesterolemic mutant micein contrast, regular exercise results in reduced mitochondrial damage and oxidant load and increased SOD2 and adenine nucleotide translocator activities in normocholesterolemic control micehearing/vestibular/earabnormal cochlea morphology (J:101576)endothelial nitric oxide synthase (eNOS) in mutant cochlea is distinctly reducedabnormal basilar membrane (J:101576)on an atherosclerotic diet, homozygotes display a sclerosed and atrophic basilar membranecochlear inner hair cell degeneration (J:101576)at 24 weeks, homozygotes fed a normal diet show almost complete loss of IHCs in the basal turn and some IHC loss in the middle turnIHC loss at the base turn is exacerbated by an atherosclerotic dietcochlear outer hair cell degeneration (J:101576)at 24 weeks, homozygotes fed a normal diet show almost complete loss of OHCs in the basal turn and some OHC loss in the middle turnOHC loss at the base turn is exacerbated by an atherosclerotic dietorgan of Corti degeneration (J:101576)at 24 weeks, homozygotes fed a normal diet show significant degeneration of the organ of Corti in the basal turn while the middle turn is relatively normaldegeneration of the organ of Corti is excerbated by an atherosclerotic diet, with complete loss noted in the basal turn in some animalsabnormal stria vascularis morphology (J:101576)on an atherosclerotic diet, homozygotes display a sclerosed and atrophic stria vascularisabnormal tectorial membrane morphology (J:101576)on an atherosclerotic diet, homozygotes display a sclerosed and atrophic tectorial membranedecreased brainstem auditory evoked potential (J:101576)at 10 weeks, homozygotes fed a normal diet display higher ABR thresholds than C57BL/6J control mice at all test frequencies, with more hearing loss noted at 32 kHz; by 24 weeks, further hearing loss is detected at all test stimuli levelshomozygotes fed an atherosclerotic diet show higher ABR thresholds than homozygotes fed a normal dietdeafness (J:101576)homozygotes fed a normal diet display hearing loss esp. at high frequencies as compared with C57BL/6J control micea high positive correlation between ABR thresholds at 16 and 8 kHz, or click and atherosclerotic lesions, and atherosclerotic plaque area of the aorta, and plasma total choelsterol levels is observed in both normal diet and high-fat diet homozygotesnervous systemabnormal blood-brain barrier function (J:69455)impaired blood-brain barrier and blood-nerve barrier as indicated by extensive extravasation of serum proteins into sciatic nerve, spinal cord and cerebellum and occasional extravasation into cortex and subcortexcochlear inner hair cell degeneration (J:101576)at 24 weeks, homozygotes fed a normal diet show almost complete loss of IHCs in the basal turn and some IHC loss in the middle turnIHC loss at the base turn is exacerbated by an atherosclerotic dietcochlear outer hair cell degeneration (J:101576)at 24 weeks, homozygotes fed a normal diet show almost complete loss of OHCs in the basal turn and some OHC loss in the middle turnOHC loss at the base turn is exacerbated by an atherosclerotic dietcochlear ganglion degeneration (J:101576)at 24 weeks, homozygotes fed a normal diet show a reduced number of spiral ganglion cells in the basal turn of the cochlealoss of ganglion cells is excerbated by an atherosclerotic dietimmune systemabnormal immune system morphology (J:47027)decreased follicular B cell number (J:133606)decreased relative to controlsdecreased marginal zone B cell number (J:133606)with induction of SLE by cGVH, levels are slightly decreased compared to wild-typeincreased B cell number (J:133606)newly formed B cells are significantly increased compared to wild-typeincreased marginal zone B cell number (J:133606)increased 2-fold compared to wild-typeabnormal T cell number (J:47027)increased numbers of cytokine producing T cellsabnormal CD4-positive T cell number (J:108154, J:47027)clusters of CD4+ cells found in fatty streak lesions (J:47027)ratio of Th2 to Th1 cells is increased from 4.4 to 11.4 on a normal diet and up to 20.9 on a high cholesterol diet (J:47027)increased T-helper 2 cell number (J:47027)abnormal B cell activation (J:133606)spleen cells display polyclonal B cell activation, with increased expression of MHC II, Fas, and CD86 and lower expression of CD21, CD22, and CD23increased spleen weight (J:61564)increased spleen weight while the thymus weight remains normalabnormal immune system physiology (J:61564)decreased susceptibility to type IV hypersensitivity reaction (J:61564)decreased antigen specific delayed hypersensitivity responseabnormal immune serum protein physiology (J:61564)increased immunoglobulin level (J:133606)mutants with cGVH-induced SLE show greatly increased levels compared to wild-type controls or untreated mutantsincreased IgM level (J:61564)IgM response to tetanus toxoid is significantly increased as compared to controlsdecreased interferon-gamma secretion (J:47027)production is reduced when fed a high cholesterol dietincreased susceptibility to systemic lupus erythematosus (J:133606)increased autoantibody level (J:133606)after induction of cGVH-SLE, IgG and IgM anti-oxidized LDL and anti-cardiolipin antibodies are increased compared to wild-type or Apoe-null controlsincreased anti-nuclear antigen antibody level (J:133606)after induction of cGVH-SLE, mice display greatly increased levels of anti-chromatin antibodies compared to wild-type controls or non-cGVH mutantsincreased anti-double stranded DNA antibody level (J:133606)after induction of cGVH-SLE, mice display greatly increased levels compared to wild-type controls or non-cGVH-SLE mutantsbehavior/neurologicalincreased thigmotaxis (J:120203)elevated thigmotaxis in Morris maze testsabnormal spatial learning (J:120203)longer latency to find the platform in Morris maze testsslow to acquire a preference for the target quadrant and the magnitude of the preference is always less than controlsrenal/urinary systemabnormal renal glomerulus morphology (J:125978)glomerular foam cells in the mesangium, capillary lumina and within the glomerular stalk close to the vascular polelipid deposits in arteriolar walls in the vascular poleslipid droplets filling glomerular capillary lumina at 36 weeks in about 50% of miceloss of mesangial matrix sometimes at 36 weeks but never at 24 weeks or in controlsincreased glomerular tuft areaglomerular cell numbers are increasedliver/biliary systemabnormal liver physiology (J:104609)no significant change in serum alanine transaminase with high fat diet as is seen in controls (marker for liver damage)hepatic uptake of LDL is increased two foldvision/eyeabnormal retinal inner nuclear layer morphology (J:70245)perinuclear vacuolation on a high cholesterol dietthin retinal inner nuclear layer (J:70245)cell numbers reducedthin retinal outer nuclear layer (J:70245)cell numbers reducedabnormal eye electrophysiology (J:84688, J:70245)implicit times increased for a and b waves of dark adapted electroretinogram (J:70245)wave amplitudes attenuated for a and b waves of dark adapted electroretinogram (J:70245)taste/olfactionimpaired olfaction (J:89344)preference for plain water over 0.1% iso-amyl alcohol moderate compared to the strong preference shown by controlsslower than control to find buried food pellet although found pellets visually more rapidlylatency to taste vanillin-cued quinine significantly increased only at day 5skeletonabnormal bone structure (J:111209)increased bone mineral density (J:111209)higher bone mineralization density in vertebral bodiesincreased bone volume to tissue volume ratioincreased compact bone thickness (J:111209)in vertebral bodies and tibiaincreased bone trabecula number (J:111209)increased number of trabeculaeabnormal skeleton physiology (J:111209)abnormal osteoblast physiology (J:111209)increased rate of bone formationrespiratory systemabnormal pulmonary alveolus morphology (J:136630)fewer but larger alveoli at 3 months of ageless surface area to volumeabnormal lung hysteresivity (J:136630)percent increase in hysteresivity with age greater than in controlsabnormal lung volume (J:136630)lung volume similar to controls at 3 months but 2.5 fold greater at 8 months of ageincreased airway resistance (J:136630)resistance to airflow greater than controls at 3 months but not at 8 months of ageincreased lung compliance (J:136630)dynamic and static compliance greater than controls at 8 months of ageintegumentskin lesions (J:73202)progressive skin lesions, mainly seen as eruptive xanthomas on shoulder and back areas with lipids and extracellular matix as the predominant components||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown||lipoprotein, cholesterol, atherosclerosis|Possibly| 6827.0|Dockland ; ENU16NIH19a|C57BL/6JAnu-Dock2/AnuApb|C57BL/6JAnu-Dock2/AnuApb|Recessive|dedicator of cyto-kinesis 2|Dock2|Unknown|CED-5, Hch, MBC|MGI:2149010|dedicator of cyto-kinesis 2; mutation 1, The Australian National University|Dock2|MGI:5563487|11|ENSMUSG00000020143|ENSMUST00000093193|Dock2-001|2323|2392|G to T|ENSMUSE00000249670|23|775|Glutamic acid to STOP|||||AGTTTGAAGAATCCATGAGACGGCTCTTCGAATCCATCAACAACCTGATGAAAAGTCAGTA||||||||||||||Low numbers of T cells, low numbers of activated B cells and T cells|Unknown|C57BL/6JAnu|Yes|Unknown|Yes|Yes|Yes|Yes|No|Good||G7||No|29-Feb-2012|Cryopreserved sperm|46.0|0.0|Unknown||T cell, B cell, lymphocyte, ENU|Possibly| 6196.0|EμMyc/Fox03|B6.Cg-Foxo3 Tg(IghMyc)22Bri/Wehi||Recessive|forkhead box O3|Foxo3||1110048B16Rik, 2010203A17Rik, Fkhr2, FKHRL1, Foxo3a|MGI:1890081|forkhead box O3; targeted mutation 1, Noboru Motoyama|Foxo3|MGI:3719789|10|||||||||||||||||transgene insertion 22, Ralph L Brinster|Igh (E mu) enhancer and Myc promoter|B cell lineage||||||||||Excess pre-B cells in bone marrow. Animals develop high incidence pre-B and B lymphoma - Adult mortality: 80% EμMyc/Fox03 T/+ -/- may have acceleration of tumour onset.||C57BL/6|Yes|Unknown|Yes|Yes|Unknown|Yes|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown||bim, B cell, lymphoma , Endoplasmic reticulum (ER), transcription factor|Possibly| 6853.0|BRINP1 Flpe ; DBC Flpe|C57BL/6-Fam5a/Marp||Recessive|bone morphogenic protein/retinoic acid inducible neural specific 1|Brinp1|Unknown|Dbc1, Dbccr1, Fam5a|MGI:1928478||||4|||||||||||||||||||||||||||||Unknown. |Unknown|C57BL/6J|Yes|Yes|Yes|Yes|Yes|Yes|No|Poor||||No|14-Mar-2012|Cryopreserved sperm|50.0|0.0|Unknown|||Possibly| 6188.0|472/Del|B6.129S1-Bcl2l11||Recessive|BCL2-like 11 (apoptosis facilitator) |Bcl2l11|Nil|1500006F24Rik, Bim, Bod |MGI:1197519 |BCL2-like 11 (apoptosis facilitator); targeted mutation 1, Andreas Strasser |Bcl2l11|MGI:2156494|2|||||||||||||||||||||||||||||Abnormal hippocampus morphology:*2 days after neonatal hypoxia-ischemia (HI) injury, ispsilateral hippocampal area loss (7.8%) is half of that seen in wild-type mice (16.8%) after HI.Gliosis:*Reactive gliosis is significantly decreased in hippocampi of mutants 2 days after neonatal HI compared to wild-type.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown||Bcl-2|Yes| 6195.0|EμMyc/CHOP|B6.Cg-Ddit3 Tg(IghMyc)22Bri/Wehi||Recessive|DNA-damage inducible transcript 3|Ddit3||C/EBP homoologous protein 10, chop, CHOP-10, CHOP10, gadd153|MGI:109247|DNA-damage inducible transcript 3; targeted mutation 1, Masakata Mori|Ddit3|MGI:2179046|10|||||||||||||||||transgene insertion 22, Ralph L Brinster|MGI:2447604|B cell lineage||||||||||Excess pre-B cells in bone marrow. Animals develop high incidence pre-B and B lymphoma - Adult mortality: 80% ||C57BL/6|Yes|Unknown|Yes|Yes|Unknown|Yes|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown||lymphadenopathy, B cell, lymphoma, immunoglobulin|Possibly| 6198.0|DEC-205|B6.129P-Ly75/Wehi||Recessive|lymphocyte antigen 75|Ly75|Nil|CD205, DEC-205|MGI:106662|lymphocyte antigen 75; targeted mutation 1, Michel C Nussenzweig|Ly75|MGI:3575119|2|||||||||||||||||||||||||||||Abnormal CD8-positive T cell morphology:*Splenic CD8a+ dendritic cells occur at slightly higher levels while CD8- dendritic cells occur at slightly lower levels.Abnormal cytotoxic T cell physiology:*Cytotoxic lymphocyte response to immunization with foreign splenocytes is absent.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown||DEC-205, Dendritic cells, Macrophage mannose receptor|Yes| 6197.0|EμMyc/Fox03/CHOP|B6.Cg-Ddit Foxo3 Tg(IghMyc)22Bri/Wehi||Recessive|DNA-damage inducible transcript 3|Ddit3||C/EBP homoologous protein 10, chop, CHOP-10, CHOP10, gadd153|MGI:109247|DNA-damage inducible transcript 3; targeted mutation 1, Masakata Mori|Ddit3|MGI:2179046|10|||||||||||||||||transgene insertion 22, Ralph L Brinster|Igh (E mu) enhancer and Myc promoter|B cell lineage||||||||||Excess pre-B cells in bone marrow. Animals develop high incidence pre-B and B lymphoma - Adult mortality: 80% ||C57BL/6|Yes|Unknown|Yes|Yes|Unknown|Yes|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown||B cell, transcription, bim|Possibly| 6197.0|EμMyc/Fox03/CHOP|B6.Cg-Ddit Foxo3 Tg(IghMyc)22Bri/Wehi||Recessive|forkhead box O3|Foxo3|Unknown|1110048B16Rik, 2010203A17Rik, Fkhr2, FKHRL1, Foxo3a|MGI:1890081|forkhead box O3; targeted mutation 1, Noboru Motoyama|Foxo3|MGI:3719789|10|||||||||||||||||||||||||||||Excess pre-B cells in bone marrow. Animals develop high incidence pre-B and B lymphoma - Adult mortality: 80% ||C57BL/6|Yes|Unknown|Yes|Yes|Unknown|Yes|No|Unknown||||No|13-Sep-2011||||Unknown||B cell, transcription, bim|Possibly| 6199.0|MLL-Af9|B6.129P2(Cg)-Mll1/KsyJ||Dominant|myeloid/lymphoid or mixed-lineage leukemia 1|Mll1||ALL-1, All1, Cxxc7, HTRX1, KMT2A, Mll, trithorax Drosophila |MGI:96995|myeloid/lymphoid or mixed-lineage leukemia 1; targeted mutation 2, Terrence H Rabbitts|Mll1|MGI:2671905|9|||||||||||||||||||||||||||||Prenatal lethality|Leukemia:*Predominantly acute myeloid leukemia (AML) involving immature myeloblasts and extramedullary leukemia.*A minority of the observed leukemia is acute lymphoblastic leukemia (ALL).*50% of heterozygotes succumb to AML at 5 months of age.*Almost all mice develop malignancy within 1 1/2 years.Abnormal hematopoiesis:*Abnormal hematopoietic differentiation resulting in an accumulation of Mac-1/Gr-1 double-positive mature myeloid cells in the bone marrow preceded the onset of AML, as early as 6 days of age.Enlarged spleenEnlarged liverPale kidney|C57BL/6 x 129|No|No|Yes|No|No|Yes|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown||chromosomal translocations, Mll-AF9, t(9;11) , transcription, leukaemia|Yes| 6735.0|KIf3-bYAC-BL6|KIf3-bYAC-BL6/Ausb||Recessive||Klf3,bYAC||||||||||||||||||||||||||||||||||||||C57BL6|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|02-Dec-2011||0.0|0.0|Unknown|||Possibly| 8615.0|H2-T15|C57BL/6-H2-T15/MarpApb||Recessive|histocompatibility 2, T region locus 15|H2-T15||H-2T15|MGI:95947||||17|||||||||||||||||||||||||||||Unknown|Normal|C57BL/6|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|27-Nov-2018|Cryopreserved sperm|20.0|0.0|Unknown|||Yes| 6868.0|SM02-Dist|SuprMam02-(B6.BALB/c-SM1)-Dist/AnuApb||Recessive|||||||||||||||||||||||||||||SuprMam|SuprMam||||SuprMam-BALB/c|SuprMam-BALB||7|Mice are more susceptible to mammary tumours.|Unknown|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|11|||No|03-Apr-2012|Cryopreserved sperm|82.0|0.0|Unknown||mammary, tumour, DMBT1, p53, modifier|Possibly| 6207.0|B6/Moz3/Bmi|B6;129-Bmi1 Myst3||Recessive|Bmi1 polycomb ring finger oncogene|Bmi1|Normal|Bmi-1, Bmi1, Pcgf4|MGI:88174|Bmi1 polycomb ring finger oncogene; targeted mutation 1, Anton Berns|Bmi1|MGI:1857632|2|||||||||||||||||||||||||||||||C57BL/6|Yes|Unknown|Yes|Yes|Unknown|Yes|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown||bmi-1 proto-oncogene, Monocytic leukemia zinc finger protein (MOZ)|Yes| 6207.0|B6/Moz3/Bmi|B6;129-Bmi1 Myst3||Recessive|MYST histone acetyltransferase (monocytic leukemia) 3|Myst3|Nil|9930021N24Rik, KAT6A, MOZ, Zfp220|MGI:2442415|MYST histone acetyltransferase (monocytic leukemia) 3; targeted mutation 1, Anne K Voss|Myst3|MGI:3626344|8|||||||||||||||||||||||||||||||C57BL/6|Yes|Unknown|Yes|Yes|Unknown|Yes|No|Unknown||||No|13-Sep-2011||||Unknown||bmi-1 proto-oncogene, Monocytic leukemia zinc finger protein (MOZ)|Yes| 6228.0|Bad|B6.129X1-Bad||Recessive|BCL2-associated agonist of cell death|Bad|Nil|Bbc2|MGI:1096330|BCL2-associated agonist of cell death; targeted mutation 1, Stanley J Korsmeyer|Bad|MGI:2675966|19|||||||||||||||||||||||||||||Abnormal hippocampus morphology:*2 days after neonatal hypoxia-ischemia (HI) injury, ispsilateral hippocampal area loss (10.3%) is half of that seen in wild-type mice (21%) after HI.Gliosis:*Reactive gliosis is significantly decreased in hippocampi of mutants 2 days after neonatal HI compared to wild-type.||129/Sv|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown||BAD, Tumorigenesis|Yes| 6205.0|Rag1/J|B6.129S7-Rag1||Recessive|recombination activating gene 1|Rag1|Nil|Rag-1|MGI:97848|recombination activating gene 1; targeted mutation 1, Peter Mombaerts|Rag1|MGI:1857241|2|||||||||||||||||||||||||||||Decreased vascular permeability:*After reperfusion mice do not have detectable IgM whereas wild-type have levels of 437 ug/ml.Ear inflammationIncreased eosinophil cell numberDecreased immunoglobulin level Decreased IgM level: *Upeon reperfusion of ischemic intestine, permeability index (PI) of injured Rag1-deficient mice is reduced compared to control treated wild-type (PI of 1.34 vs 3.26 in controls. *Rag1-deficient mice reconstituted with IgM show PI reduction similar to controls (PI of 2.86).Dermatitis:*After 16 days of MC903 treatment.Mixed cellular infiltration to dermis:*MC903-treated ears showed a dermal infiltrate.Epidermal hyperplasia:*MC903-treated ears display epidermal hyperplasia.Scaly skin:*After 16 days of MC903 treatment.Thick skin:*After 16 days of MC903 treatment.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown||RAG-1, Fibroblast|Yes| 6214.0|�LCRgamma|B6/�LCRg|||| �LCRg mpl ||||||||||||||||||||||||||||||||||||Phenotype does not differ from a wildtype of the same genetic background. Produce human haemoglobin gamma A||C57BL/6|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6216.0|B6CIS|C57BL/6-Socs2||Recessive|suppressor of cytokine signaling 2|Socs2|Nil|CIS2, Cish2, cytokine-inducible SH2 protein 2, D130043N08Rik, JAB, SOCS-2, SSI-2, STAT-induced STAT inhibitor 2|MGI:1201787|suppressor of cytokine signaling 2; targeted mutation 1, Walter and Eliza Hall Institute of Medical Research|Socs2|MGI:1934557|10|||||||||||||||||||||||||||||Increased body length:*Male homozygotes display significantly a increased body length relative to wild-type males, although tail length is normal.*A similar but less pronounced trend is noted in the body length of female homozygotes.Increased body weight:*At 6 weeks of age, male homozygotes weigh significantly more than wild-type males; as adults, mutant males are, on average, 40% heavier than wild-type males.*Increased growth is also significant but less pronounced in females, though adult female homozygotes typically attain the weight of wild-type males.*Increased body weight results from the proportionate enlargement of most visceral organs and is not attributed to accumulated fatty tissue.*Sexually dimorphic or male-specific organs are not disproportionately enlarged.*Carcass weight is also increased, indicating that muscle and bone may contribute to increased size.Increased growth rate:*Homozygotes display accelerated growth after weaning i.e. beginning at around 3-4 weeks of age.Long radius:*The mutant tibia is significantly longer than in wild-type controls.Increased length of long bones:*Male homozygotes display significantly increased long bone lengths relative to wild-type males.*A similar but less pronounced trend is noted in the long bone lengths of female homozygotes.*However, bone architecture, including the epiphiseal growth plates of the femur and tibia, is histologically normal. Long humerus Long femur Long tibiaAbnormal lung morphology:*At 2 months of age, 6 of 9 male, but only 3 of 10 female homozygotes show increased collagen deposition around the bronchi and vessels of the lungs; some alveolar sacs are occasionally involved.Abnormal hepatobiliary system morphology:*At 2 months of age, a minority of both male and female homozygotes display excess collagen accumulation around occasional hepatic vessels and bile ducts.Abnormal pancreatic duct morphology:*At 2 months of age, a minority of both male and female homozygotes display excess collagen accumulation in duct tissue of the pancreas.Abnormal salivary gland duct morphology:*At 2 months of age, a minority of both male and female homozygotes display excess collagen accumulation in duct tissue of the salivary glands.Abnormal insulin-like growth factor I level:*RNase protection assays indicate increased IGF-I production in several organs (heart, lungs and spleen), but not in liver, bone, fat or muscle.*However, no increase in serum IGF-I concentration is observed, consistent with normal production in the liver (major source of circulating IGF-I).Abnormal urine homeostasis:*At 6-7 weeks of age, all male and female homozygotes studied show decreased levels of major urinary protein (MUP) in their urine.Adipose tissue phenotype:*Neither male nor female mutants accumulate significantly more abdominal fatty tissue than wild-type mice.Thick dermal layer:*Adult homozygotes display a significantly thickened dermis, although most organs (including kidney, heart, spleen, thymus, lymph nodes, femur, sternum, gonads and bladder) appear histologically normal*Dermal thickening is associated with excessive collagen accumulation in all of male (7/7), and less prominently in female (6/8) homozygotes.|Increased body weight:*At 12 weeks of age, adult male heterozygotes show an intermediate body weight relative to wild-type and homozygous mutant littermates.*In contrast, female heterozygotes are not significantly heavier than wild-type females.|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown||SOCS-2, Janus kinase (JAK), Transducers and activators of transcription (STAT), IGF|Yes| 6217.0|339/OT-1|B6.129S1-Bcl2l11 Tg(TcraTcrb)1100Mjb||Semi-dominant|BCL2-like 11 (apoptosis facilitator)|Bcl2l11|Nil|1500006F24Rik, Bim, Bod|MGI:1197519|BCL2-like 11 (apoptosis facilitator); targeted mutation 1, Andreas Strasser |Bcl2l11|MGI:2156494|2|||||||||||||||||transgene insertion 1100, Michael J Bevan||||||||||||Unknown|Unknown|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown||Bim, Hematopoietic homeostasis, TCR|Yes| 6213.0|B6/G-CSF3R|B6.129X1-Csf3r/Wehi||Recessive|colony stimulating factor 3 receptor (granulocyte)|Csf3r||Cd114, Csfgr, G-CSFR|MGI:1339755|colony stimulating factor 3 receptor (granulocyte); targeted mutation 1, Daniel C Link|Csf3r|MGI:2156982|4|||||||||||||||||||||||||||||Normal development. Neutropenic. Mild immuno-compromised Keep hooded.Impaired neutrophil chemotaxis: no mobilization in response to granulocyte-colony stimulating factor (G-CSF)||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown||stem cell, progenitor, neutrophil, granulopoiesis|Possibly| 6215.0|bclx/bim|B6.129-Bcl2l1 Bcl2l11||Recessive|BCL2-like 1|Bcl2l1|Reduced|Bcl(X)L, bcl-x, Bcl-XL, Bcl-Xs, BclX|MGI:88139|BCL2-like 1; targeted mutation 1, Lothar Hennighausen|Bcl2l1|MGI:2176699|2|||||||||||||||||||||||||||||||C57BL/6|No|No|Yes|No|No|Yes|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown||Bcl-x, Bax, Bcl-2|Yes| 6215.0|bclx/bim|B6.129-Bcl2l1 Bcl2l11||Recessive|BCL2-like 11 (apoptosis facilitator)|Bcl2l11|Nil|1500006F24Rik, Bim, Bod|MGI:1197519|BCL2-like 11 (apoptosis facilitator); targeted mutation 1, Andreas Strasser|Bcl2l11|MGI:2156494|2|||||||||||||||||||||||||||||||C57BL/6|No|No|Yes|No|No|Yes|No|Unknown||||No|13-Sep-2011||||Unknown||Bcl-x, Bax, Bcl-2|Yes| 6229.0|Bak/Bmf|B6.129-Bak1 Bmf||Recessive|BCL2-antagonist/killer 1|Bak1|Nil|Bak, N-Bak|MGI:1097161|BCL2-antagonist/killer 1; targeted mutation 1, Craig B Thompson |Bak1|MGI:2159364|17|||||||||||||||||||||||||||||||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown||bak, Bcl2-modifying factor (Bmf)|Yes| 6229.0|Bak/Bmf|B6.129-Bak1 Bmf||Recessive|BCL2 modifying factor |Bmf|Nil||MGI:2176433|BCL2 modifying factor; targeted mutation 1, Roger J Davis|Bmf|MGI:4421178|2|||||||||||||||||||||||||||||||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|13-Sep-2011||||Unknown||bak, Bcl2-modifying factor (Bmf)|Yes| 10365.0|Irf5|C57BL/6NCrl-Irf5/Anu||Recessive|interferon regulatory factor 5|Irf5|Unknown|mirf5 |MGI:1350924 |Irf5; endonuclease-mediated mutation 1, Australian National University|Irf5||6|ENSMUSG00000029771 |ENSMUST00000163511.7||||G to T||||Unknown to Unknown|||||||||||||||||||unknown|unknown|C57Bl/6N|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|28-Sep-2023|Cryopreserved sperm|11.0|0.0|Unknown|||Possibly| 10367.0|129X1/SvJ:B6/Ncrl::APB|129X1/SvJ:B6/Ncrl::APB||Dominant|caspase 4, apoptosis-related cysteine peptidase|Casp4||Casp11, Caspase-11|MGI:107700||||9|ENSMUSG00000033538|ENSMUST00000027012|||||||||||||||||||||||||||high incidence of spontaneous testicular teratomas| |129S1/Sv|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|10-Oct-2023|Cryopreserved sperm|55.0|0.0|Unknown|||No| 6209.0|B6.Rel-10|B6.129S1-Rel/Wehi||Semi-dominant|reticuloendotheliosis oncogene|Rel|Normal|c-Rel|MGI:97897|reticuloendotheliosis oncogene; targeted mutation 1, Steve Gerondakis|Rel|MGI:2179622|11|||||||||||||||||||||||||||||Decreased B cell proliferation: * in culture, splenic B cells respond less efficiently to mitogenic stimulation; proliferative response is 0.5-2.5% of normal * B cell colonies are 100-fold less numerous compared with wild-type cells when splenocytes are seed onto agar cultures containing LPS * treatment of stimulated B cells with Il2 does not reverse proliferative defect in B cells.Decreased T cell proliferation: * in response to PMA stimulation, cultured T cells show only ~20% of normal response at 72 hours but in response to ionomycin, response is ~70% of normal * concanavalin A- or anti-CD3/anti-DC28-stimulated T cells cultured with exogenous Il2 show similar proliferative response to stimulated wild-type cells.Abnormal macrophage physiology: * resident peritoneal macrophages activated with LPS + interferon gamma show impaired cytotoxic killing ability towards tumor cells in vitro compared to wild-type macrophages * elicited macrophages from both genotypes show equal cytotoxic abilities * resident macrophages produce only ~20% of normal nitric oxide levelsAbnormal humoral immune response: * in response to a T cell-independent antigen (NP-LPS), IgG3 production is marginally reduced at 7 days after immunization, continuing to decrease over the next 14 days * NP-specific IgG1 production production is 50- to 100-fold lower than in wild-type in response to a T cell-dependent antigen (NP-KHL)Decreased IgG1 level: * levels are 100-fold less than in wild-type naive mice * IgG1 production production is 50- to 100-fold lower than in wild-type in response to a T cell-dependent antigen (NP-KHL)Decreased IgG2a level: levels are almost undetectable in naive mutants.Decreased IgG2b level: levels are 6-fold less than in wild-type naive mice.Decreased IgG3 level: levels are 4-fold less than in wild-type naive mice.Decreased IgM level: levels are 3-fold less than in wild-type naive mice.Abnormal cytokine secretion: * concanavalin A-stimulated T cells produce Il2 at levels that are 50-fold lower than wild-type; levels are several fold lower than normal in wild-type cultures stimulated with PMA or ionomycin. * with LPS treatment, GM-CSF and G-CSF production by resident macrophages is ~10- and 5-fold greater in wild-type macrophages. * levels of Il6 produced by unstimulated resident and peritoneal macrophages are elevated ~3-fold compared to wild-type; levels of Il6 after LPS stimulation are 3-5-fold higher than stimulated wild-type macrophages.Decreased susceptibility to parasitic infection.|Decreased B cell proliferation: * in culture, splenic B cells respond less efficiently to mitogenic stimulation; proliferative response is 14-20% of normal * B cell colonies are 10-fold less numerous compared with wild-type cells when splenocytes are seed onto agar cultures containing LPSAbnormal humoral immune response: NP-specific IgG1 production in response to a T cell-dependent antigen (NP-KHL) is intermediate between wild-type and homozygous mice; IgG3 response to NP-LPS is normal.|C57BL/6|Yes|Unknown|Yes|Yes|Unknown|Yes|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown||c-rel proto-oncogene, NF-kappaB, lymphocyte|Yes| 6212.0|B6/bcl-xflox/Eumyc|B6.Cg-Bcl2l1 Tg(IghMyc)22Bri/Wehi||Semi-dominant|BCL2-like 1|Bcl2l1|Reduced|Bcl(X)L, bcl-x, Bcl-XL, Bcl-Xs, BclX|MGI:88139|BCL2-like 1; targeted mutation 1.1, Lothar Hennighausen|Bcl2l1|MGI:2176700|2|||||||||||||||||transgene insertion 22, Ralph L Brinster|Igh (E mu) enhancer and Myc promoter|B cell lineage||||||||||Mice will develop lymphoma (mice with the Eumyc transgene) at 90-120 days. These mice are essentially wild-type.. The bcl-x gene is flanked (boarded) by loxP sites (ie Flanked by lox = flox). These mice have the EμMyc transgene and therefore behave the same as EμMyc mice. Bcl-x flox mice are agouti. ||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown||Bcl-x, Bax, myc|Yes| 5460.0|ENU16NIH:003b|C57BL/6JAnu-Klrg1/AnuApb|C57BL/6JAnu-Klrg1/AnuApb|Recessive|killer cell lectin-like receptor subfamily G, member 1|Klrg1|Unknown|2F1-Ag|MGI:1355294|killer cell lectin-like receptor subfamily G, member 1; mutation 1, The Australian National University|Klrg1|MGI:5563460|6|ENSMUSG00000030114|ENSMUST00000032207|Klrg-1||||||||122232913||||GGGATTTGGTAGAGATGGCTGACAGCTCTATCTATTCAACACTAGAGCTGCCGGAGGCAC|Yes|||||||||||||No KLRG1 expression on NK cells||C57BL/6JAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|07-Mar-2011|Cryopreserved sperm|46.0|0.0|Unknown||Natural Killer cell, ENU|Yes| 6226.0|B6NFKB2/lpr|B6NFKB2/B6.MRL-Fas/J COPY||Recessive|| NFKB2 Faslpr |||||||Unknown|||||||||||||||||||||||||||||Mice homozygous for the lymphoproliferation spontaneous mutation (Faslpr) show systemic autoimmunity, massive lymphadenopathy associated with proliferation of aberrant T cells, arthritis, and immune complex glomerulonephrosis. Onset and severity of symptoms is dependent on genetic background, with the original MRL/MpJ background being most severely affected beginning about 8 weeks of age. Females die at an average age of 17 weeks of age and males at 22 weeks. This mouse is a model for systemic lupus erythematosus-like autoimmune syndromes. ||C57Bl/6|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6219.0|B6del478/B6P50|B6del478/B6P50|||| FasL P50 ||||||||||||||||||||||||||||||||||||B6del478 - KI/KI develop enlarged lymphnodes and spleen. Not tumour at this stage. Mice at 10-12 months of age may develop lukaemia. T cell large granulocytic lukaemia. May have autoimmune disease. B6del478/P50 - Enhanced infection rate, some runting but not that much wrong until older, when splenomegaly can develop, survival drops off. Skin looks translucent. ||C57Bl/6|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6220.0|B6del478/NFKB2|B6del478/NFKB2|||| FasL NFKB2 ||||||||||||||||||||||||||||||||||||B6del478 - KI/KI develop enlarged lymphnodes and spleen. Not tumour at this stage. Mice at 10-12 months of age may develop lukaemia. T cell large granulocytic lukaemia. May have autoimmune disease. B6del478/NFKB2 - unknown.||C57Bl/6|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6221.0|B6del494|B6del494|||| FasL ||||||||||||||||||||||||||||||||||||Check with Researcher||C57Bl/6|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6222.0|bok/bax/bak|B6del535/Bax/Bak |||| bok bax bak ||||||||||||||||||||||||||||||||||||Bak +/- and Bax -/- are largely non-viable. A few survive. Generally runted and grey. Triple -/- unlikely to be born. Perhaps 5% may be born but will be very runted. Mainly grey colored.||C57BL/6|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6223.0|B6del535/baxC|B6del535/bax/bax|||| Bok bax ||||||||||||||||||||||||||||||||||||Bax - Male sterility in -/-. Otherwise, grossly normal. Most -/- mice have grey fur compared to +/- and +/+ which are black.||C57BL/6|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6236.0|vavbcl69/bax|B6.129-Bax Tg(Vav-BCL2)1Jad||Semi-dominant|BCL2-associated X protein|Bax|Nil||MGI:99702|BCL2-associated X protein; targeted mutation 1, Stanley J Korsmeyer|Bax|MGI:1857429|7|||||||||||||||||transgene insertion 1, Jerry M Adams|mouse Vav promoter|Overexpression||||||||||||C57BL/6|Yes|Unknown|Yes|Yes|No|Yes|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown||Bax, Bcl-2, Hematopoietic system|Yes| 6237.0|Bcl-2ko/myc|B6.129-Bcl2 Tg(IghMyc)22Bri||Semi-dominant|B-cell leukemia/lymphoma 2|Bcl2|Nil|Bcl-2, C430015F12Rik, D830018M01Rik|MGI:88138|B-cell leukemia/lymphoma 2; targeted mutation 1, Stanley J Korsmeyer|Bcl2|MGI:1857134|1|||||||||||||||||transgene insertion 22, Ralph L Brinster|Myc promoter|||||||||||||C57BL/6 129/SV|Yes|No|Yes|Yes|No|Yes|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown||Bcl-2, Thymocyte, c-myc|Yes| 6235.0|Bax/Bmf/472 |B6.129-Bax Bcl2l11 Bmf||Recessive|BCL2 modifying factor|Bmf|Nil||MGI:2176433|BCL2 modifying factor; targeted mutation 1, Roger J Davis|Bmf|MGI:4421178|2|||||||||||||||||||||||||||||||C57BL/6|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown||Bax, Bmf, Bim, Leukocyte homeostasis, Autoimmunity|Yes| 6235.0|Bax/Bmf/472 |B6.129-Bax Bcl2l11 Bmf||Recessive|BCL2-associated X protein|Bax|Nil||MGI:99702|BCL2-associated X protein; targeted mutation 1, Stanley J Korsmeyer|Bax|MGI:1857429|7|||||||||||||||||||||||||||||||C57BL/6|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|13-Sep-2011||||Unknown||Bax, Bmf, Bim, Leukocyte homeostasis, Autoimmunity|Yes| 6235.0|Bax/Bmf/472 |B6.129-Bax Bcl2l11 Bmf||Recessive|BCL2-like 11 (apoptosis facilitator)|Bcl2l11|Nil|1500006F24Rik, Bim, Bod|MGI:1197519|BCL2-like 11 (apoptosis facilitator); targeted mutation 1, Andreas Strasser |Bcl2l11|MGI:2156494|2|||||||||||||||||||||||||||||||C57BL/6|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|13-Sep-2011||||Unknown||Bax, Bmf, Bim, Leukocyte homeostasis, Autoimmunity|Yes| 6240.0|Blimp424/CD3|C57BL/6-Cd3e Prdm1||Semi-dominant|CD3 antigen, epsilon polypeptide|Cd3e|Reduced|CD3, CD3epsilon, T3e|MGI:88332|CD3 antigen, epsilon polypeptide; targeted mutation 1, Bernard Malissen |Cd3e|MGI:2155092|9|||||||||||||||||||||||||||||||C57BL/6|No|No|Yes|No|No|Yes|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown||CD3, T cell development, B cell, blimp-1|Yes| 6240.0|Blimp424/CD3|C57BL/6-Cd3e Prdm1||Semi-dominant|PR domain containing 1, with ZNF domain|Prdm1|Normal|Blimp-1, Blimp1, PRDI-BF1 |MGI:99655|PR domain containing 1, with ZNF domain; targeted mutation 1, Stephen L Nutt|Prdm1|MGI:3510704|10|||||||||||||||||||||||||||||||C57BL/6|No|No|Yes|No|No|Yes|No|Unknown||||No|13-Sep-2011||||Unknown||CD3, T cell development, B cell, blimp-1|Yes| 6241.0|Bmf/472|B6.129-Bcl2l11 Bmf||Recessive|BCL2-like 11 (apoptosis facilitator)|Bcl2l11 |Normal|1500006F24Rik, Bim, Bod|MGI:1197519|BCL2-like 11 (apoptosis facilitator); targeted mutation 1.1, Philippe Bouillet|Bcl2l11|MGI:4366749|2|||||||||||||||||||||||||||||Unknown|Unknown|C57BL/6|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown||Bim, Bad, Bmf|Yes| 6241.0|Bmf/472|B6.129-Bcl2l11 Bmf||Recessive|BCL2 modifying factor|Bmf|Nil||MGI:2176433|BCL2 modifying factor; targeted mutation 1, Roger J Davis|Bmf|MGI:4421178|2|||||||||||||||||||||||||||||Unknown|Unknown|C57BL/6|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|13-Sep-2011||||Unknown||Bim, Bad, Bmf|Yes| 6238.0|Bcl-x/flox/Mcl-1flox/E�Myc|B6-Bcl2l1 Mcl1 Tg(IghMyc)22Bri||Semi-dominant|BCL2-like 1|Bcl2l1|Reduced|Bcl(X)L, bcl-x, Bcl-XL, Bcl-Xs, BclX|MGI:88139|BCL2-like 1; platelet 16|Bcl2l1|MGI:3847886|2|||||||||||||||||transgene insertion 22, Ralph L Brinster|Myc promoter|||||||||||||C57BL/6|Yes|Yes|Yes|Yes|No|Yes|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown||Platelets, Bcl-x, Mcl1, c-myc|Yes| 6238.0|Bcl-x/flox/Mcl-1flox/E�Myc|B6-Bcl2l1 Mcl1 Tg(IghMyc)22Bri||Semi-dominant|myeloid cell leukemia sequence 1|Mcl1|Normal|Mcl-1|MGI:101769|myeloid cell leukemia sequence 1; targeted mutation 3, Stanley J Korsmeyer|Mcl1|MGI:2684151|3|||||||||||||||||||||||||||||||C57BL/6|Yes|Yes|Yes|Yes|No|Yes|No|Unknown||||No|13-Sep-2011||||Unknown||Platelets, Bcl-x, Mcl1, c-myc|Yes| 6246.0|SCID/Arc|CB17-Prkdc||Recessive|protein kinase, DNA activated, catalytic polypeptide|Prkdc|Nil|DNA-PK, DNA-PKcs, DNAPDcs, DOXNPH, dxnph, slip, XRCC7|MGI:104779|protein kinase, DNA activated, catalytic polypeptide; severe combined immunodeficiency|Prkdc|MGI:1857113|16|||||||||||||||||||||||||||||Premature death:*Lifespan is shortened in conventional housing, however, in an SPF environment homozygotes can live to more than one year.Immune system phenotype:*In contrast to homozygotes on the NOD background, spleen cell suspensions from homozygous CB17 mice exhibit NK cell activity. Salivary gland inflammation: *In mice injected i.p. with cells from submandibular gland tissue of diseased Fas mice, inflammatory lesions are observed in salivary and lacrimal glands. *Infiltrating cells are CD4<+> and Vbeta8<+> with a minority being CD4<+> and Vbeta6<+>. *Mice injected with cells pretreated with anti-CD4 or anti-Vbeta8 do not develop inflammatory lesions or only minor lesions are seen in parotid, submandibular, sublingual and lacrimal glands in majority of transplanted mice. Decreased leukocyte cell number: *Homozygotes are leukopenic. Absent B cells: *B cells cannot be detected in the spleen with Ig or Lyb-8 (Cd22) markers. Absent pre-B cells: *Pre-B cells cannot be detected in the bone marrow. Decreased B cell proliferation: *Spleen cells do not proliferate in response to LPS. Decreased T cell proliferation: *Splenic T cells do not proliferate in response to concanavalin A or to a one-way mixed lymphocyte reaction. Abnormal spleen white pulp morphology: *Splenic follicles are devoid of lymphocytic cells. Abnormal thymus morphology: *The remaining thymocytes that express the Thy1 marker are larger than normal thymocytes. Abnormal thymus cortex morphology: *Lymphocytic cortex is not evident in thymus. *Mucinous cysts are occasionally found. Small thymus: *1/10th to 1/100th normal size. Absent Peyer's patches: *Peyer?s patches are rarely visible. Lymph node hypoplasia: *Lymph nodes have only a few lymphoid cells, however, sinuses are well-formed and contain macrophages. Small lymphoid organs Lymphoid hypoplasia: *Lymphid organs are 1/10th or less of normal size. *Lymph organs consist mostly of supportive tissue with varying numbers of fibroblasts, macrophages and histiocytes. Abnormal humoral immune response: *Mice are unable to produce specific antibody to two T-independent antigens. Decreased immunoglobulin level: *31/206 mice tested have low levels of serum immunoglobulin, all 31 have an IgG isotype and of these, 17 also have an IgM isotype. *The remaining 175/206 mice do not have detectable serum immunoglobulin. *Only 1/11 homozygotescan produce greater than 1 ug/ml serum Ig at up to 100 days of age, however, 21/29 homozygotes produce greater than 1 ug/ml between 100-200 days of age. Decreased IgG level: *Hypogammaglobulinemic. Abnormal response to transplant: *Following injection of human T lymphoblastoid cells, 40% of nucleated spleen cells are of human origin by 4 weeks post injection. Increased length of allograft survival: *Homozygotes do not reject full thickness skin allografts. *1/5 homozygotes (5-6 weeks of age) reject orthotopic tail skin allografts throughout a 3 month observation period.Hematopoietic system phenotype:*In contrast to homozygotes on the NOD background, homozygous CB17 mice exhibit normal erythrocyte mean cell volumes.T cell derived lymphoma:*Spontaneous T cell lymphomas are found in greater than 10% of homozygotes at 5-9 months of age.*Tumors arise in the thymus and are highly invasive and are transplantable.Thymic lymphoma||CB17|Yes|No|Yes|Yes|No|Yes|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown||SCID|Yes| 6244.0|Bmf/473/Bax|B6.129-Bax Bcl2l11 Bmf||Recessive|BCL2-associated X protein|Bax|Nil||MGI:99702|BCL2-associated X protein; targeted mutation 1, Stanley J Korsmeyer|Bax|MGI:1857134|7|||||||||||||||||||||||||||||Unknown|Unknown|C57BL/6|Yes|No|Yes|Yes|No|Yes|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown||Bax, Bim, Noxa, Bmf|Yes| 6244.0|Bmf/473/Bax|B6.129-Bax Bcl2l11 Bmf||Recessive|BCL2 modifying factor|Bmf|Nil||MGI:2176433|BCL2 modifying factor; targeted mutation 1, Roger J Davis|Bmf|MGI:4421178|2|||||||||||||||||||||||||||||Unknown|Unknown|C57BL/6|Yes|No|Yes|Yes|No|Yes|No|Unknown||||No|13-Sep-2011||||Unknown||Bax, Bim, Noxa, Bmf|Yes| 6244.0|Bmf/473/Bax|B6.129-Bax Bcl2l11 Bmf||Recessive|BCL2-like 11 (apoptosis facilitator)|Bcl2l11|Normal|1500006F24Rik, Bim, Bod|MGI:1197519|BCL2-like 11 (apoptosis facilitator); targeted mutation 2.1, Philippe Bouillet|Bcl2l11|MGI:4366751|2|||||||||||||||||||||||||||||Unknown|Unknown|C57BL/6|Yes|No|Yes|Yes|No|Yes|No|Unknown||||No|13-Sep-2011||||Unknown||Bax, Bim, Noxa, Bmf|Yes| 6243.0|Bmf/473/Bak |B6.129-Bak1 Bcl2l11 Bmf||Recessive|BCL2-antagonist/killer 1|Bak1|Nil|Bak, N-Bak|MGI:1097161|BCL2-antagonist/killer 1; targeted mutation 1, Craig B Thompson|Bak1|MGI:2159364|17|||||||||||||||||||||||||||||Unknown|Unknown|C57BL/6|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown||Bak, Bim, Noxa, Bmf|Yes| 6243.0|Bmf/473/Bak |B6.129-Bak1 Bcl2l11 Bmf||Recessive|BCL2 modifying factor|Bmf|Nil||MGI:2176433|BCL2 modifying factor; targeted mutation 1, Roger J Davis|Bmf|MGI:4421178|2|||||||||||||||||||||||||||||Unknown|Unknown|C57BL/6|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|13-Sep-2011||||Unknown||Bak, Bim, Noxa, Bmf|Yes| 6243.0|Bmf/473/Bak |B6.129-Bak1 Bcl2l11 Bmf||Recessive|BCL2-like 11 (apoptosis facilitator)|Bcl2l11|Normal|1500006F24Rik, Bim, Bod|MGI:1197519|BCL2-like 11 (apoptosis facilitator); targeted mutation 2.1, Philippe Bouillet|Bcl2l11|MGI:4366751|2|||||||||||||||||||||||||||||Unknown|Unknown|C57BL/6|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|13-Sep-2011||||Unknown||Bak, Bim, Noxa, Bmf|Yes| 6247.0|MHCII|C57BL/6-H2-Aa||Recessive|histocompatibility 2, class II antigen A, alpha|H2-Aa|Nil|A alpha, Aalpha, H-2Aa, I-Aalpha, Ia-1, Ia1|MGI:95895|histocompatibility 2, class II antigen A, alpha; targeted mutation 1, Horst Bluethmann|H2-Aa|MGI:2157977|17|||||||||||||||||||||||||||||Abnormal T cell morphology: Decreased CD4-positive T cell number: *Very few or no CD4+ T-cells in thymus. *About 4% CD4+ peripheral T-cells as opposed to 60% normally. Increased CD8-positive T cell number: *About 90% of lymph node T-cells are CD8+.Enlarged thymus:*Slightly enlarged. Thymus hyperplasia: *Slightly increased cell number.Aabnormal splenocyte physiology:*No splenocyte response to staphylococcal enterotoxin B.*Response to T-cell independent antigens is normal.Enlarged lymph nodes:*Slightly enlarged.Abnormal MHC II cell surface expression on macrophages:*Class II expression is absent on bone-marrow derived macrophages.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown||MHC class II gene Aa, CD4, CD8|Yes| 6248.0|B6/IRF4-enu/Blimp|C57BL/6-Irf4 Prdm1||Recessive|interferon regulatory factor 4|Irf4|Normal|IRF-4, Spip|MGI:1096873|interferon regulatory factor 4; mutation 1, Bruce Beutler|Irf4|MGI:4456226|13|||||||||||||||||||||||||||||||B6 x BALB mixed|No|No|Yes|No|No|Yes|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown||Blimp-1, GFP|Yes| 6248.0|B6/IRF4-enu/Blimp|C57BL/6-Irf4 Prdm1||Recessive|PR domain containing 1, with ZNF domain|Prdm1|Reduced|Blimp-1, Blimp1, PRDI-BF1|MGI:99655|PR domain containing 1, with ZNF domain; targeted mutation 1, Stephen L Nutt|Prdm1|MGI:3510704|10|||||||||||||||||||||||||||||||B6 x BALB mixed|No|No|Yes|No|No|Yes|No|Unknown||||No|13-Sep-2011||||Unknown||Blimp-1, GFP|Yes| 6249.0|RAG1-GFP|C57BL/6-RAG1||Recessive|recombination activating gene 1|Rag1|Nil|Rag-1|MGI:97848|recombination activating gene 1; targeted mutation 1, Nobuo Sakaguchi|Rag1|MGI:2388344|2|||||||||||||||||||||||||||||Abnormal immunoglobulin V(D)J recombination:*Bone marrow B cells lack recombination of the immunoglobulin gene segments.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown||RAG1, GFP|Yes| 6253.0|B6/TLR4 x DEC-205 |B6.129P-Ly75 Tlr4/J ||Recessive|lymphocyte antigen 75|Ly75|Nil|CD205, DEC-205|MGI:106662|lymphocyte antigen 75; targeted mutation 1, Michel C Nussenzweig|Ly75|MGI:3575119|2|||||||||||||||||||||||||||||||C3H/He & C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown||Dendritic cell, DEC-205, LPS, Tlr4|Yes| 6253.0|B6/TLR4 x DEC-205 |B6.129P-Ly75 Tlr4/J ||Recessive|toll-like receptor 4|Tlr4|Normal|lipopolysaccharide response, Lps, Rasl2-8 |MGI:96824|toll-like receptor 4; defective lipopolysaccharide response|Tlr4|MGI:1857718|4|||||||||||||||||||||||||||||||C3H/He & C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|13-Sep-2011||||Unknown||Dendritic cell, DEC-205, LPS, Tlr4|Yes| 6254.0|tcasp-8|B6.129P2-Casp8 Tg548Jxm||Semi-dominant|caspase 8|Casp8|Normal|Caspase-8, FLICE, MACH, Mch5|MGI:1261423|caspase 8; targeted mutation 1, Razqallah Hakem|Casp8|MGI:2655730|1|||||||||||||||||transgene insertion 548, Jamey Marth|mouse lck promoter|||||||||||Premature death:*Die at an average age of 51.7 weeks, however lethality is sometimes seen as early as 14 weeks of age.Decreased body size Decreased body weightDecreased leukocyte cell number:*Peripheral T cell lymphopenia is seen early in life but is no longer apparent in older mutants. Decreased T cell number: *Relative proportion of splenic and lymph node T cells is significantly lower in young mutants. Decreased CD4-positive T cell number: *Lower numbers of CD4+ T cells in young mutants. Decreased CD8-positive T cell number: *Lower numbers of CD8+ T cells in young mutants.Abnormal lymphocyte morphology:*Peripheral lymphocyte populations from spleens and lymph nodes of old mutants show a decreased B-to-T cell ratio. Increased lymphocyte cell number: *Lymphoproliferation in older mutants is confirmed by increased total lymphocyte counts. Increased B cell number: *Older mutants exhibit a balanced expansion of both B and T lymphocyte numbers in the periphery. Increased T cell number: *Older mutants exhibit a balanced expansion of both B and T lymphocyte numbers in the periphery. Abnormal T cell morphology Abnormal T cell subpopulation ratio: *The CD4+ to CD8+ T-cell ratio is increased in spleen, lymph node, and peripheral blood. *Peripheral lymphocyte populations from spleens and lymph nodes of old mutants show a decreased proportion of CD8+ T cells relative to CD4+ T cells Abnormal T cell activation: *Isolated T cells from old mutants are in a perpetual state of activation. Abnormal T cell proliferation: *T cells derived from older mutants exhibit defective in vitro proliferative responses to various stimuli and activated T cells are resistant to CD95L-induced apoptosis. Decreased T cell proliferation: *Exhibit defective activation-induced expansion of peripheral T cells.Enlarged spleenAbnormal lymph node morphology:*Lymphoid hyperplasia is apparent in older mutants. Enlarged lymph nodes: *In older mutants. Abnormal CD8-positive T cell physiology: *Do not exhibit an expansion of CD8+ T cells in the peripheral blood 6 days after lymphocytic choriomeningitis virus (LCMV) infection and show decreased representation of CD62LCD44 (memory) T cells. *LCMV-infected mutants are unable to generate CD8+ cytotoxic T cells specific for LCMV. Decreased T cell apoptosis: *Thymocytes and activated T cells are resistant to CD95L-induced apoptosis, however mitochondria-mediated apoptosis is normal.Abnormal liver morphology:*Livers from 30-week old mutants display T cell accumulation as focal perivascular infiltrates.Abnormal kidney morphology:*Kidneys from 30-week old mutants show focal interstitial and periglomerular T cell infiltration.Abnormal lung morphology:*Lungs from 30-week old mutants contain obvious interstitial peribronchiovascular T cell infiltration.*At about 1 year of age, disrupted lung tissue organization is associated with much more widespread and abundant T cell infiltration.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown||Caspase 8, T cell|Yes| 6258.0|CD40/B-GFP|B6.129P2-Cd40 Prdm1||Recessive|CD40 antigen|Cd40|Nil|Bp50, Cd40, p50, Tnfrsf5|MGI:88336|CD40 antigen; targeted mutation 1, Hitoshi Kikutani|Cd40|MGI:1857457|2|||||||||||||||||||||||||||||||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown||CD40, CD23, Germinal center formation, Blimp-1|Yes| 6258.0|CD40/B-GFP|B6.129P2-Cd40 Prdm1||Recessive|PR domain containing 1, with ZNF domain|Prdm1|Nil|Blimp-1, Blimp1, PRDI-BF1|MGI:99655|PR domain containing 1, with ZNF domain; targeted mutation 1, Stephen L Nutt|Prdm1|MGI:3510704|10|||||||||||||||||||||||||||||||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|13-Sep-2011||||Unknown||CD40, CD23, Germinal center formation, Blimp-1|Yes| 6252.0|PLT4/GFP|C57BL/6-Mpl Myb Tg(UBC-GFP)30Scha/JWehi||Semi-dominant|myeloproliferative leukemia virus oncogene|Mpl|Nil|c-mpl, c-mpl-I, c-mpl-II, CD110, hlb219, thrombopoietin receptor, TPO-R|MGI:97076|myeloproliferative leukemia virus oncogene; targeted mutation 1, Warren S Alexander|Mpl|MGI:2660811|4|||||||||||||||||transgene insertion 30, Brian Schaefer|human ubiquitin C promoter|||||||||||||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown||CD8, GFP, c-Mpl, c-Myb|Yes| 6252.0|PLT4/GFP|C57BL/6-Mpl Myb Tg(UBC-GFP)30Scha/JWehi||Semi-dominant|myeloblastosis oncogene|Myb|Normal|c-myb|MGI:97249|myeloblastosis oncogene; Plt4 |Myb|MGI:3045843|10|||||||||||||||||||||||||||||||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|13-Sep-2011||||Unknown||CD8, GFP, c-Mpl, c-Myb|Yes| 6251.0|B6113/GFP|C57BL/6-Mpl Tg(UBC-GFP)30Scha/JWehi||Semi-dominant|myeloproliferative leukemia virus oncogene|Mpl|Nil|c-mpl, c-mpl-I, c-mpl-II, CD110, hlb219, thrombopoietin receptor, TPO-R |MGI:97076|myeloproliferative leukemia virus oncogene; targeted mutation 1, Warren S Alexander|Mpl|MGI:2660811|4|||||||||||||||||transgene insertion 30, Brian Schaefer|human ubiquitin C promoter|||||||||||||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown||c-Mpl, GFP, CD8|Yes| 6259.0|cKit/TOM|cKit-rttA3-GFP/Tet-O c-myc|||| cKitrtA c-myc ||||||||||||||||||||||||||||||||||||This strain carries the human c-myc gene and the rttA3-IRES-GFP cassette which are controlled by the Tet/O and the cKit promoter respectively. The expression of myc is induced in cKit expressing cells only in the presence of doxycycline. Normal monitoring - This stain should not have any obvious phenotype without treatment of doxycycline. DOX - The phenotypes of this strain with treatment of doxycycline remain unknown. But this strain may potentially develop tumors in certain tissues upon treatment with doxycycline. ||FVB|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6260.0|CLVav69|CLVav69|||| Clec9A Cre Bcl-2 ||||||||||||||||||||||||||||||||||||Vav-bcl 69 -Excess B cells throughout life. Develop glomerulonephritis, lymphoma and plasmacytoma Enlarged spleens lymphadenopathy (more white blood cells), larger (2-3fold) spleen and lymph nodes Clec9A1088 - Phenotype does not differ from a wildtype of the same genetic background. ||C57BL/6|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6261.0|B6 Deleter|CMV cre |||| del-cre ||||||||||||||||||||||||||||||||||||This line has a sex-linked gene (carried on the X chromosome). This CRE mouse cuts out the neo/hygro cassette at the lox P site. In transgenic mice, in conjunction with a transgene carrying a loxP-flanked gene, deletion of the loxP-flanked gene occurs in all tissues including germ cells. Molecular Note: This transgene expresses Cre recombinase under the control of a human cytomegalovirus (CMV) promoter, active in most cells and tissues.||C57BL/6|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6262.0|539/del|DEF2 4A8 |||| Bim ||||||||||||||||||||||||||||||||||||Phenotype does not differ from a wildtype of the same genetic background.||C57BL/6|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6263.0|541/del|DEF2 5A1 /B6deleter|||| Bim flpE ||||||||||||||||||||||||||||||||||||Contact Researcher||C57BL/6|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6265.0|del376/266|B6.129S-Bcl2l11 Bmf||Recessive|BCL2-like 11 (apoptosis facilitator)|Bcl2l11|Nil|1500006F24Rik, Bim, Bod |MGI:1197519|BCL2-like 11 (apoptosis facilitator); targeted mutation 1, Andreas Strasser|Bcl2l11|MGI:2156494|2|||||||||||||||||||||||||||||||C57BL/6|Yes|No|Yes|Yes|No|Yes|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown||Bim, Bmf|Yes| 6265.0|del376/266|B6.129S-Bcl2l11 Bmf||Recessive|BCL2 modifying factor|Bmf|Nil||MGI:2176433|BCL2 modifying factor; targeted mutation 1, Roger J Davis|Bmf|MGI:4421178|2|||||||||||||||||||||||||||||||C57BL/6|Yes|No|Yes|Yes|No|Yes|No|Unknown||||No|13-Sep-2011||||Unknown||Bim, Bmf|Yes| 6266.0|Puma/p21|B6.129S-Bbc3 Cdkn1a||Recessive|BCL2 binding component 3|Bbc3|Nil|PUMA|MGI:2181667|BCL2 binding component 3; targeted mutation 1, Andreas Strasser|Bbc3|MGI:2681654|7|||||||||||||||||||||||||||||||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown||p53, Puma, p21|Yes| 6266.0|Puma/p21|B6.129S-Bbc3 Cdkn1a||Recessive|cyclin-dependent kinase inhibitor 1A (P21)|Cdkn1a|Nil|CAP20, CDKI, Cdkn1, CIP1, mda6, P21, p21, p21Cip1, p21WAF, SDI1, Waf1 |MGI:104556|cyclin-dependent kinase inhibitor 1A (P21); targeted mutation 1, Tyler Jacks|Cdkn1a|MGI:1933751|17|||||||||||||||||||||||||||||||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|13-Sep-2011||||Unknown||p53, Puma, p21|Yes| 6267.0|Puma/p21/Noxa|B6.129S-Bbc3 Cdkn1a Pmaip1||Recessive|BCL2 binding component 3|Bbc3|Nil|PUMA|MGI:2181667|BCL2 binding component 3; targeted mutation 1, Andreas Strasser|Bbc3|MGI:2681654|7|||||||||||||||||||||||||||||||C57BL/6|Yes|No|Yes|Yes|No|Yes|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown||p21, p53, Puma, Noxa|Yes| 6267.0|Puma/p21/Noxa|B6.129S-Bbc3 Cdkn1a Pmaip1||Recessive|cyclin-dependent kinase inhibitor 1A (P21)|Cdkn1a|Nil|CAP20, CDKI, Cdkn1, CIP1, mda6, P21, p21, p21Cip1, p21WAF, SDI1, Waf1|MGI:104556|cyclin-dependent kinase inhibitor 1A (P21); targeted mutation 1, Tyler Jacks|Cdkn1a|MGI:1933751|17|||||||||||||||||||||||||||||||C57BL/6|Yes|No|Yes|Yes|No|Yes|No|Unknown||||No|13-Sep-2011||||Unknown||p21, p53, Puma, Noxa|Yes| 6267.0|Puma/p21/Noxa|B6.129S-Bbc3 Cdkn1a Pmaip1||Recessive|phorbol-12-myristate-13-acetate-induced protein 1|Pmaip1|Nil|Noxa|MGI:1930146|phorbol-12-myristate-13-acetate-induced protein 1; targeted mutation 1, Andreas Strasser |Pmaip1|MGI:2681649|18|||||||||||||||||||||||||||||||C57BL/6|Yes|No|Yes|Yes|No|Yes|No|Unknown||||No|13-Sep-2011||||Unknown||p21, p53, Puma, Noxa|Yes| 6271.0|ERTF5/NEU|ERTF5-rttA3-GFP/Tet-O NEU|||| ERTF5tA NEU ||||||||||||||||||||||||||||||||||||Phenotype does not differ from a wildtype of the same genetic background.||FVB|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6272.0|ERTF5-rttA-GFP|ERTF5-rttA3-IRES-GFP|||| ERTF5tA ||||||||||||||||||||||||||||||||||||Phenotype does not differ from a wildtype of the same genetic background.||FVB|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6273.0|B6bcl 22|C57BL/6-Tg(BCL2)22Wehi||Semi-dominant||||||||||||||||||||||||||transgene insertion 22, Walter and Eliza Hall Institute of Medical Research|SV40 promoter|||||||||||Increased B cell number||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown||BCL2, immunoglobulin heavy chain enhancer (Emu)|Yes| 6276.0|E�Myc/delmnt/KO50|B6.129-Mnt Trp53 Tg(IghMyc)22Bri||Semi-dominant|max binding protein|Mnt|Nil|bHLHd3, Rox|MGI:109150|max binding protein; targeted mutation 1.1, Anthony Wynshaw-Boris|Mnt|MGI:3044352|11|||||||||||||||||transgene insertion 22, Ralph L Brinster|Myc promoter|||||||||||||C57BL/6|Yes|Unknown|Yes|Yes|Unknown|Yes|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown||Mnt, Miller-Dieker syndrome (MDS), p53, c-myc, Lymphoid malignancy|Possibly| 6276.0|E�Myc/delmnt/KO50|B6.129-Mnt Trp53 Tg(IghMyc)22Bri||Semi-dominant|transformation related protein 53 |Trp53|Nil|p44, p53|MGI:98834|transformation related protein 53; targeted mutation 1, Tyler Jacks|Trp53|MGI:1857263|11|||||||||||||||||||||||||||||||C57BL/6|Yes|Unknown|Yes|Yes|Unknown|Yes|No|Unknown||||No|13-Sep-2011||||Unknown||Mnt, Miller-Dieker syndrome (MDS), p53, c-myc, Lymphoid malignancy|Possibly| 6274.0|E�Myc/Bax|B6.SJL-Bax Tg(IghMyc)22Bri||Semi-dominant|BCL2-associated X protein|Bax|Nil||MGI:99702|BCL2-associated X protein; targeted mutation 1, Stanley J Korsmeyer|Bax|MGI:1857429|7|||||||||||||||||transgene insertion 22, Ralph L Brinster|Myc promoter|||||||||||||C57BL/6|Yes|Unknown|Yes|Yes|Unknown|Yes|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown||c-myc, Lymphoma, Leukemia, Bax|Yes| 8619.0|NODScid|NOD-Prkdc/AnuApb||Recessive|protein kinase, DNA activated, catalytic polypeptide|Prkdc|Nil|DNA-PK, DNA-PKcs, DNAPDcs, slip, XRCC7|MGI:104779|severe combined immunodeficiency|Prkdc|MGI:1857113|16||||||||||||||||Yes|||||||||||||SCID mutation prevents TCR and BCR rearrangements. This prevents maturation of B and T cells at very early stages of development. These mice, therefore lack, T and B cells in periphery. Please refer to MGI allele page for further information using the link above.||NOD|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||19||No|14-Dec-2018|Cryopreserved sperm|44.0|0.0|Yes||SCID, severe combined immunodeficiency, transplant, T cell, B cell|Yes| 6275.0|Myc/Puma/Noxa|B6.SJL-Bbc3 Pmaip1 Tg(IghMyc)22Bri||Semi-dominant|BCL2 binding component 3|Bbc3|Nil|PUMA|MGI:2181667|BCL2 binding component 3; targeted mutation 1, Andreas Strasser|Bbc3|MGI:2681654|7|||||||||||||||||transgene insertion 22, Ralph L Brinster|Myc promoter|||||||||||||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown||c-myc, Lymphoid malignancy, p53, puma, noxa|Yes| 6275.0|Myc/Puma/Noxa|B6.SJL-Bbc3 Pmaip1 Tg(IghMyc)22Bri||Semi-dominant|phorbol-12-myristate-13-acetate-induced protein 1|Pmaip1|Nil|Noxa|MGI:1930146|phorbol-12-myristate-13-acetate-induced protein 1; targeted mutation 1, Andreas Strasser|Pmaip1|MGI:2681649|18|||||||||||||||||||||||||||||||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|13-Sep-2011||||Unknown||c-myc, Lymphoid malignancy, p53, puma, noxa|Yes| 6277.0|Myc/Puma/Bim|C57BL/6-Bbc3 Bcl2l11 Tg(IghMyc)22Bri||Semi-dominant|BCL2 binding component 3|Bbc3|Nil|PUMA|MGI:2181667|BCL2 binding component 3; targeted mutation 1, Andreas Strasser|Bbc3|MGI:2681654|7|||||||||||||||||transgene insertion 22, Ralph L Brinster|Myc promoter|||||||||||||C57BL/6|Yes|Unknown|Yes|Yes|Unknown|Yes|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown||p53, Bbc3, Bcl-2, c-myc|Yes| 6277.0|Myc/Puma/Bim|C57BL/6-Bbc3 Bcl2l11 Tg(IghMyc)22Bri||Semi-dominant|BCL2-like 11 (apoptosis facilitator)|Bcl2l11|Nil|1500006F24Rik, Bim, Bod|MGI:1197519|BCL2-like 11 (apoptosis facilitator); targeted mutation 1, Andreas Strasser|Bcl2l11|MGI:2156494|2|||||||||||||||||||||||||||||||C57BL/6|Yes|Unknown|Yes|Yes|Unknown|Yes|No|Unknown||||No|13-Sep-2011||||Unknown||p53, Bbc3, Bcl-2, c-myc|Yes| 10369.0|CRISP4 KO/BL6/J|C57BL/6J-Crisp4/MarpApb||Dominant|cysteine-rich secretory protein 4|CRISP4|||MGI:1925331 ||Crisp4||1|ENSMUSG00000025774|||||||||Unknown to Unknown|||||||||||||||||||Sub-fertile: issues binding sperm to zona pellucida and regulation of acrosome reaction. No in vitro fertilisation possible|Normal|C57Bl/6J|Yes|Yes|Yes|Unknown|Unknown|Unknown|Yes|Unknown||||No|12-Oct-2023|Cryopreserved sperm|40.0|0.0|Unknown|||No| 5088.0|Kandy ; ENU11B6:021|Kandara||Recessive|integrin alpha 4|Itga4|Unknown|VLA-4 receptor, alpha 4 subunit|MGI:96603||||2|ENSMUSG00000027009|ENSMUST00000099972|Itga4-001|1540|1700|G to A|ENSMUSE00000165394|14|513|Valine to Isoleucine|||||ATAAAGGCAAAGAGGTCCCAGGCTACATCGTTTTGTTTTACAATGTGAGCTTGGATGTGCA|Yes|||||||||||||Embryonic death around e12.5.Embryos appear completely pale with no blood formation. Other physical features relatively normal. Total failure of hematopoesis.|Normal|C57BL/6 x C57BL/10|No|No|Yes|No|No|Yes|No|Good||||No|12-Apr-2010|Cryopreserved sperm|20.0|0.0|Unknown||blood, ENU, embryonic lethal|Possibly| 6278.0|E�Myc/Mcl1-1(33)/bim|E�Myc/vavMcl-1(33)/bim|||| Myc Mcl-1 bim ||||||||||||||||||||||||||||||||||||E�-Myc transgenics succumb to lymphoma from 3-12 months of age. We expect double heterozugous mice to succumb to lymphoma earlier, perhaps around 6 weeks of age. They may have large spleens and lymph nodes.||C57BL/6|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6280.0|Fox03/myc10|Fox03/vav-myc10 x vav-myc10|||| Fox03 myc10 ||||||||||||||||||||||||||||||||||||Late onset (~10 months) thymoma or histiocytic sarcoma (subcutaneous tumour or enlarged liver or spleen). Might see acceleration with Fox03 -/- (not sure how many, if any).||C57BL/6|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6282.0|FVB/Bim|FVB-Bcl2l11||Recessive|BCL2-like 11 (apoptosis facilitator)|Bcl2l11|Nil|1500006F24Rik, Bim, Bod|MGI:1197519|BCL2-like 11 (apoptosis facilitator); targeted mutation 1, Andreas Strasser|Bcl2l11|MGI:2156494|2|||||||||||||||||||||||||||||||FVB|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown||Bcl-2, Bim|Yes| 6281.0|FVB/F2ROSA-26|B6.FVB-Gt(ROSA)26Sor||Dominant||||||||||||||||||||||||||gene trap ROSA 26, Philippe Soriano||||||||||||||FVB|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown||Embryonic stem cells, ROSA26|Yes| 6285.0|Mtkneo2|ICR-M-tkneo2|||| Neo2 ||||||||||||||||||||||||||||||||||||No phenotype, Neomycin Resistance ||Balb/c|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6286.0|ID4/Tet GFP|ID4-rttA3-GFP/TRE GFP shLuc|||| ID4rtta TetGFP ||||||||||||||||||||||||||||||||||||No special monitoring required This stain should not have any obvious phenotype without or with treatment of doxycycline||FVB|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6284.0|B6Flpe|C57BL/6-Tg(ACTFLPe)9205Dym||Dominant||||||||||||||||||||||||||transgene insertion 9205, Susan Dymecki|human ACTB promoter|||||||||||||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown||Cre, Flp|Yes| 6287.0|IL-7 -/-|C57BL/6-Il7||Recessive|interleukin 7|Il7|Nil|A630026I06Rik, hlb368, Il-7|MGI:96561|interleukin 7; targeted mutation 1, DNAX Research Institute of Cellular and Molecular Biology|Il7|MGI:1857652|3|||||||||||||||||||||||||||||Decreased thymocyte number:*At E14, thymocytes are about 100-fold lower than in heterozygous littermates.*However, differentiation of thymic progenitors into pro-T cells appears to be normal.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown||IL-7, Cytokine|Yes| 6288.0|HA-BBCD3|C57BL/6-Cd3e Ighm Prdm1||Semi-dominant|CD3 antigen, epsilon polypeptide|Cd3e|Nil|CD3, CD3epsilon, T3e|MGI:88332|CD3 antigen, epsilon polypeptide; targeted mutation 1, Bernard Malissen|Cd3e|MGI:2155092|9|||||||||||||||||||||||||||||||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown||CD3, T cell development, Bcl6, Blimp-1|Yes| 6288.0|HA-BBCD3|C57BL/6-Cd3e Ighm Prdm1||Semi-dominant|immunoglobulin heavy constant mu|Ighm|Increased|BCR, Ig mu, Igh-M, Igh6, IgM, muH, muMT|MGI:96448|immunoglobulin heavy constant mu; targeted mutation 1, Riccardo Dalla-Favera|Ighm|MGI:3581517|12|||||||||||||||||||||||||||||||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|13-Sep-2011||||Unknown||CD3, T cell development, Bcl6, Blimp-1|Yes| 6288.0|HA-BBCD3|C57BL/6-Cd3e Ighm Prdm1||Semi-dominant|PR domain containing 1, with ZNF domain|Prdm1|Normal|Blimp-1, Blimp1, PRDI-BF1|MGI:99655|PR domain containing 1, with ZNF domain; targeted mutation 1, Stephen L Nutt|Prdm1|MGI:3510704|10|||||||||||||||||||||||||||||||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|13-Sep-2011||||Unknown||CD3, T cell development, Bcl6, Blimp-1|Yes| 6289.0|K/BxN|B6.NOD-Tg(TcraR28,TcrbR28)KRNDim||Semi-dominant||||||||||||||||||||||||||transgene insertion KRN, Diane Mathis|natural TCR alpha and -beta promoter/enhancer elements|||||||||||Abnormal lymphocyte cell number Increased B cell number: *Spleen and lymph node B cell numbers are increased 1.75-fold in mice suffering from arthritis. Decreased CD4-positive T cell number: *CD4+ T cells are virtually absent in the spleens of mice under 2 weeks of age. *CD4+ T cell numbers are reduced by 3.1-fold in the spleens of adult mice. Decreased CD8-positive T cell number: *CD8+ T cells numbers are reduced in mice under 3 weeks of age.Abnormal T cell activation:*A greater proportion of T cells express late activation markers (CD44 CD62L, CD45RB) than in transgene negative controls. Abnormal T cell proliferation: *T cells expressing the transgenic TCR proliferate in response to antigen presenting cells expressing Class II MHC from a H2 locus in the absence of any antigen.Abnormal T cell clonal deletion:*Clonal deletion is evident in the thymus of neonatal mice with reduced numbers of total cells and aberrant percentages of single-positive populations.*Single-positive populations normalize by 4 weeks of age though total cell numbers are still reduced.*Clonal deletion affects T cell populations in the periphery with a paucity of single-positive T cells in young mice and chronically reduced CD4<+> population in adults.Enlarged spleen:*Splenomegaly is often observed.Increased IgG1 level:*Serum IgG1 levels are dramatically increased.Abnormal macrophage recruitment:*Macrophage cells make up a large number of cells found in inflamed joints.Impaired neutrophil recruitment:*Neutrophils make up a large number of cells found in inflamed joints.Abnormal T cell anergy:*Background Sensitivity: transgenic T cells from mice on a NOD background have lower levels of T cell receptor expressed.*Background Sensitivity: transgenic T cells from mice on a NOD background have a severe reduction in response to its cognate antigen (RNAse peptide) presented by A than do transgenic T cells from a C57BL/6 background.*Hybridomas created from these T cells respond normally to antigen suggesting a cell intrinsic anergy.Rheumatoid arthritis:*Background Sensitivity: transgenic mice crossed to a NOD background develop rheumatoid arthritis.*Distal paws become red and swollen.*All transgenic mice have significantly swollen ankles by 30 days of age with the degree of swelling symmetrical on either limb.*As mice age hyperextension of the ankle, valgus deviation of the knee and hyperpronation of the toes occur.*Arthritis occurs in almost all joints with the exception of hip joints.*Arthritis starts as fibrinoid material and a few cells are found in the articular cavity; edema sets in under the synovial lining, accompanied by neovascularithezation and some infiltration of inflammatory cells.*After a few weeks, disease is marked by extensive synovitis, affecting all areas of the joint with massive infiltration of inflammatory cells and beginnings of fibrosis.*After several months, the inflammation recedes leaving massive fibrosis, very little cartilage, and irregular shaped bone.Abnormal phalanx morphology:*Bones are eroded from arthritis with anarchic reconstruction occurring afterwards.Clinodactyly:*Rheumatoid arthritis leads to hyperpronation of the toes.Abnormal metatarsal bone morphology:*Bones are eroded from arthritis with anarchic reconstruction occurring afterwards.Abnormal intervertebral disk morphology:*Intervertebral inflammation occurs sporadically in these mice.||C57BL/6 x NOD|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown||Rheumatoid arthritis (RA), TCR, Systemic autoimmunity|Yes| 6290.0|Lg-GFP|C57BL/6-Cd207||Dominant|CD207 antigen|Cd207|Normal|Langerin|MGI:2180021|CD207 antigen; targeted mutation 1, Bernard Malissen|Cd207|MGI:3581825|6|||||||||||||||||||||||||||||||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown||Langerhans cells (LCs), Dendritic cells (DCs), CD207, EGFP|Yes| 6291.0|lck-GM-CSF-19/94B6|lck-GM-CSF-19 x 94B6|||| Lck-19 94B6 ||||||||||||||||||||||||||||||||||||Contact Researcher 94B6: These mice are immuno-compromised. Alveolar proteinosis, normal lifespan Mild lung pathology develops 6-14 weeks of age - ususally does not cause major problems. LckGM: These mice have enlarged spleen and LN and can suffer from anaemia and thrombocytopenia. LckGM/94B6 cross: we expect the same phenotype as 94B6.||C57BL/6|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6292.0|l-fadd 64|Lckpr-FADDdn-64|||| FADD ||||||||||||||||||||||||||||||||||||Low incidences of plasmacytoma. Look out for dragging hind legs, enlarged spleen, enlarged menteric lymph nodes - tumours. Visually check. 1-2% will die at 20 weeks of age, 19-20% will die at 1 year. Mice die as a result of plasmcytoma. Mice will bear one of the following tumours: lymphoma, splenomegaly, messentary associated, abdominal, caecal, Peyer's Patches. They may also suffer from small bowel obstruction, intestinal haemorrhage, hind leg paralysis, intussusception,||C57BL/6|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6293.0|Lgr5/Tet GFP|Lgr5-rttA3-GFP/TRE GFP shLuc|||| Lgr5rta Tet GFP ||||||||||||||||||||||||||||||||||||No speical monitoring required This strain should not have any obvious phenotype without or with treatment of doxycycline. ||FVB|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6294.0|B6/mb1cre|C57BL/6-Cd79a||Dominant|CD79A antigen (immunoglobulin-associated alpha)|Cd79a|Nil|Cd79a, Ig alpha, Ig-alpha, Iga, Igalpha, Ly-54, Ly54, mb-1 |MGI:101774|CD79A antigen (immunoglobulin-associated alpha); targeted mutation 1, Michael Reth|Cd79a|MGI:3687451|7|||||||||||||||||||||||||||||Normal|Normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown||mb1, B cell|Yes| 6295.0|Mcl-1 flox/CD19cre/E�-myc|Mcl-1 flox/CD19cre x Mcl-1 flox/E�-myc|||| Mcl-1 CD19cre E�-myc ||||||||||||||||||||||||||||||||||||Lymphoma Development at around 80 days for T/+ myc mice.||C57BL/6|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6296.0|Mcl-1flox/Eu-myc|C57BL/6-Mcl1 Tg(IghMyc)22Bri||Semi-dominant|myeloid cell leukemia sequence 1|Mcl1|Normal|Mcl-1|MGI:101769|myeloid cell leukemia sequence 1; targeted mutation 3, Stanley J Korsmeyer|Mcl1|MGI:2684151|3|||||||||||||||||transgene insertion 22, Ralph L Brinster|Myc promoter|||||||||||||C57BL/6|Yes|Yes|Yes|Yes|No|Yes|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown||Mcl-1, B cells, c-myc, Immunoglobulin|Yes| 6297.0|Mcl-1flox|C57BL/6-Mcl1||Recessive|myeloid cell leukemia sequence 1|Mcl1|Normal|Mcl-1|MGI:101769|myeloid cell leukemia sequence 1; targeted mutation 3, Stanley J Korsmeyer|Mcl1|MGI:2684151|3|||||||||||||||||||||||||||||||C57BL/6|Yes|Yes|Yes|Yes|No|Yes|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown||Mcl-1, Apoptosis|Yes| 6299.0|Mcl-1flox/Bcl-2|C57BL/6-Bcl2 Mcl1||Recessive|B-cell leukemia/lymphoma 2|Bcl2|Nil|Bcl-2, C430015F12Rik, D830018M01Rik|MGI:88138|B-cell leukemia/lymphoma 2; targeted mutation 1, Stanley J Korsmeyer|Bcl2|MGI:1857134|1|||||||||||||||||||||||||||||||C57BL/6|Yes|Yes|Yes|Yes|No|Yes|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown||Bcl-2, Mcl-1, Apoptosis|Yes| 6299.0|Mcl-1flox/Bcl-2|C57BL/6-Bcl2 Mcl1||Recessive|myeloid cell leukemia sequence 1|Mcl1|Normal|Mcl-1|MGI:101769|myeloid cell leukemia sequence 1; targeted mutation 3, Stanley J Korsmeyer|Mcl1|MGI:2684151|3|||||||||||||||||||||||||||||||C57BL/6|Yes|Yes|Yes|Yes|No|Yes|No|Unknown||||No|13-Sep-2011||||Unknown||Bcl-2, Mcl-1, Apoptosis|Yes| 6300.0|Mcl-1flox/Bcl-xflox|C57BL/6-Bcl2l1 Mcl1||Recessive|BCL2-like 1|Bcl2l1|Reduced|Bcl(X)L, bcl-x, Bcl-XL, Bcl-Xs, BclX|MGI:88139|BCL2-like 1; targeted mutation 1, Lothar Hennighausen|Bcl2l1|MGI:2176699|2|||||||||||||||||||||||||||||||C57BL/6|Yes|Yes|Yes|Yes|No|Yes|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown||Bcl-x, Germ cells, Mcl-1, Apoptosis|Yes| 6300.0|Mcl-1flox/Bcl-xflox|C57BL/6-Bcl2l1 Mcl1||Recessive|myeloid cell leukemia sequence 1|Mcl1|Normal|Mcl-1|MGI:101769|myeloid cell leukemia sequence 1; targeted mutation 3, Stanley J Korsmeyer|Mcl1|MGI:2684151|3|||||||||||||||||||||||||||||||C57BL/6|Yes|Yes|Yes|Yes|No|Yes|No|Unknown||||No|13-Sep-2011||||Unknown||Bcl-x, Germ cells, Mcl-1, Apoptosis|Yes| 6302.0|239/B6|C57BL/6-Xiap||X-linked|X-linked inhibitor of apoptosis|Xiap|Nil|1110015C02Rik, Aipa, Api3, Birc4, IAP3, ILP-1|MGI:107572|X-linked inhibitor of apoptosis; targeted mutation 1, Craig B Thompson|Xiap|MGI:2158344|X|||||||||||||||||||||||||||||Normal|Normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown||Inhibitor of apoptosis protein (IAP), X-linked IAP (XIAP)|Yes| 6303.0|GFP/MTB|MMTV-rttA/TRE GFP shLuc|||| Tet GFP MTB |||||||||||||||||||||||||||||||||||| Unknown||FVB/Black6|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6304.0|MTKN/H|MTKN/H|||| Neo hygro ||||||||||||||||||||||||||||||||||||Neomycin & Hygromycin resistant ||Balb/c|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6305.0|Mx-cre|C57BL/6-Tg(Mx1-cre)1Cgn||Semi-dominant||||||||||||||||||||||||||transgene insertion 1, University of Cologne|inducible Mx1 promoter|||||||||||Normal|Normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown||Cre|Yes| 6306.0|myc/bcl-x|C57BL/6-Bcl2l1 Tg(IghMyc)22Bri||Semi-dominant|BCL2-like 1|Bcl2l1|Reduced|Bcl(X)L, bcl-x, Bcl-XL, Bcl-Xs, BclX |MGI:88139|BCL2-like 1; targeted mutation 1, Lothar Hennighausen|Bcl2l1|MGI:2176699|2|||||||||||||||||transgene insertion 22, Ralph L Brinster|Myc promoter|||||||||||||C57BL/6|Yes|No|Yes|Yes|Yes|Yes|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown||Bcl-x, c-myc|Yes| 6307.0|Myd88|C57BL/6-Myd88||Recessive|myeloid differentiation primary response gene 88|Myd88|Nil||MGI:108005|myeloid differentiation primary response gene 88; targeted mutation 1, Shizuo Akira|Myd88|MGI:2385681|9|||||||||||||||||||||||||||||Increased apoptosis:*5 days after lung injury, mutants show significantly increased numbers of apoptotic lung epithelial and inflammatory .Increased physiological sensitivity to xenobiotic:*Knockout mice are more susceptible to bleomycin-induced lung injury.Increased dendritic cell number:*Increased numbers of dendritic cells in brains of mice infected with Plasmodium.Abnormal dendritic cell differentiation:*Dendritic cell maturation fails to occur in vivo upon exposure to TLR9 agonists.Abnormal immune system physiology:*Response to LPS and CpG is completely abrogated. Abnormal dendritic cell physiology: *Cytokine secretion elicited by zymosan or LPS is impaired. *Following infection with attenuated yellow fever vaccine 17D (YF-17D), dendritic cells produce less IL-12p40, IL-6 and interferon-gamma relative to wild-type mice. Abnormal macrophage physiology: *TNF production is impaired in thioglycollate-elicited macrophages treated with intact zymosan. *Cytokine production by macrophages cultured with P. carinii cysts is reduced compared to wild-type. Abnormal NK cell physiology: *NK cells fail to make IFN-gamma in response to injections of TLR9 agonists. Abnormal T cell physiology: Induction of the antigen-specific CD8+ T-cell response by immunizing with soluble ovalbumin and TLR9 agonists, but not TLR2 and TLR6 agonists, was severely impaired. Abnormal cytokine secretion: *LPS-induced cytokine production by BMDCs is almost abolished compared to controls and Myd88-sufficient mutants. Abnormal chemokine secretion: *Hyaluronan fragment-induced expression of chemokines by peritoneal macrophages is completely abolished in double knockout mice. Decreased interferon-alpha secretion: *CpG-A or RNA polyuridylic acid induced production of interferon-alpha was abolished in plasmacytoid dendritic cells. Decreased interferon-gamma secretion: *Less up regulation of INF-gamma in Plasmodium infection. *Following infection with attenuated yellow fever vaccine 17D (YF-17D), dendritic cells produce less interferon-gamma. Decreased interleukin-12 secretion: *After stimulation with zymosan, TNF production is significantly reduced in Myd88-deficient animals. Decreased interleukin-12b secretion: *Less upregulation of IL-12b in Plasmodium infection. *Following infection with attenuated yellow fever vaccine 17D (YF-17D), dendritic cells produce less IL-12p40 relative to wild-type mice. Decreased interleukin-6 secretion: *Following treatment with PbA(Plasmodium bergbei ANKA)-parasitized erythrocytes or LPS-stimulation, IL-6 secretion is reduced. *Following infection with attenuated yellow fever vaccine 17D (YF-17D), dendritic cells produce less IL-6 relative to wild-type mice. Decreased tumor necrosis factor secretion: *Less upregulation of TNF-alpha in Plasmodium infection. *Following treatment with PbA(Plasmodium bergbei ANKA)-parasitized erythrocytes or LPS-stimulation, TNF secretion is reduced. *After stimulation with zymosan, TNF production is significantly reduced in Myd88-deficient animals. Decreased inflammatory response: *In a model of induced pneumococcal meningitis-associated labyrinthitis, homozygotes exhibit a significantly lower granulocytic infiltration of the labyrinth and increased bacterial density in the cochlea at 24 hrs post-infection relative to wild-type control mice. Abnormal response to infection: *Following treatment with PbA (Plasmodium bergbei ANKA)-parasitized erythrocytes, mice have a decreased immune response in terms of TNF and IL-6 secretion and response to CpG. Decreased susceptibility to parasitic infection: *Resistant to cerebral malaria but eventually die of extremely high parasitemia. Increased susceptibility to viral infection. *Increased susceptibility to encephalomyocarditis virus (EMCV) infection compared to wildtype.Abnormal susceptibility to hearing loss:*In a model of induced pneumococcal meningitis-associated labyrinthitis, homozygotes exhibit significantly less hearing impairment at 24 hrs post-infection in response to click, 1- or 10-kHz stimuli relative to wild-type control mice.Abnormal neuron differentiation:*Improved differentiation of progenitor cells into neurons.*Survival of newly formed neurons is reduced.Abnormal nervous system physiology:*After cold induced cortical injury, recruitment of neutrophiles to lesion site is reduced by 85% in comparison to controls.*Cold induced cortical lesion volume is reduced by 25% compared to controls.*Fewer cortical cells have damaged DNA compared to controls after cold induced cortical injury.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown||Myd88, IL-1, IL-18, NF-kappaB|Yes| 8621.0|K5-creERt R26-YAP5SA|STOCK Gt(ROSA)26Sor<(CAGGS-Yap5SA,LacZ)Mao> Tg(KRT5-cre/ERT2)2Ipc||Recessive||||||||||||||||||||||||||||||||||||||Overexpression of activated YAP (NLS-YAP-5SA) with Keratin-5 (K5-CreERt) is sufficient to induce rapid formation of both SCC and spSCC in mice. spSCC tumours arise at sites of epithelial scratch wounding, where tumour-initiating epithelial cells undergo EMT to generate spSCC. Expression of the EMT transcription factor ZEB1 arises upon wounding and is a defining characteristic of spSCC in mice and humans. Thus, the wound healing response synergises with YAP to drive metaplastic transformation of SCC to spSCC.||C57BL/6J|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|18-Dec-2018|Cryopreserved sperm|58.0|52.0|Unknown||Hippo, epithelium, Squamous cell carcinoma (SCC) |Yes| 6314.0|OT-II|C57BL/6-Tg(TcraTcrb)425Cbn/Wehi||Dominant||||||||||||||||||||||||||transgene insertion 425, Frank Carbone||||||||||||Abnormal cytokine level:*CD4 T cells cultured with OVA peptide-loaded spleen cells from B7 (CD80/86) deficient mice then restimulated with anti-CD3 produce lower amounts of IL-4, Il-17a, and interferon gamma (Ifng) than wild-type T cells.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|13-Sep-2011|Cryopreserved sperm|21.0|0.0|Unknown||MHC II, TCR|Yes| 6301.0|MclYAN|C57BL/6-Mcl1 Tg(Tek-cre)1Ywa||Semi-dominant|myeloid cell leukemia sequence 1|Mcl1|Normal|Mcl-1|MGI:101769|myeloid cell leukemia sequence 1; targeted mutation 3, Stanley J Korsmeyer|Mcl1|MGI:2684151|3|||||||||||||||||transgene insertion 1, Masashi Yanagisawa|mouse Tek promoter and enhancer|||||||||||||C57BL/6|Yes|Yes|Yes|Yes|No|Yes|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown||Mcl-1, Apoptosis, Tie2-Cre, Endothelial cell-lineage|Yes| 6308.0|N1C1 |N1C1 |||| Nlrp1a Casp-1 ||||||||||||||||||||||||||||||||||||Phenotype does not differ from a wildtype of the same genetic background.||Balb/c and C57bl/6|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6309.0|NALP1/NALP3|C57BL/6-Nlrp3||Semi-dominant|NLR family, pyrin domain containing 3|Nlrp3|Nil|Cias1, cryopyrin, Mmig1, NALP3, Pypaf1|MGI:2653833|NLR family, pyrin domain containing 3; targeted mutation 1, Hal M Hoffman|Nlrp3|MGI:3850011|11|||||||||||||||||||||||||||||Normal|Normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown||NLRP3, cryopyrin-associated periodic syndromes (CAPS)|Yes| 6311.0|Noxa/339|C57BL/6-Bcl2l11 Pmaip1||Recessive|BCL2-like 11 (apoptosis facilitator)|Bcl2l11|Nil|1500006F24Rik, Bim, Bod |MGI:1197519|BCL2-like 11 (apoptosis facilitator); targeted mutation 1, Andreas Strasser|Bcl2l11|MGI:2156494|2|||||||||||||||||||||||||||||||C57BL/6|Yes|No|Yes|Yes|Yes|Yes|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown||Bcl-2, Bim, p53|Yes| 6311.0|Noxa/339|C57BL/6-Bcl2l11 Pmaip1||Recessive|phorbol-12-myristate-13-acetate-induced protein 1|Pmaip1|Nil|Noxa|MGI:1930146|phorbol-12-myristate-13-acetate-induced protein 1; targeted mutation 1, Andreas Strasser|Pmaip1|MGI:2681649|18|||||||||||||||||||||||||||||||C57BL/6|Yes|No|Yes|Yes|Yes|Yes|No|Unknown||||No|13-Sep-2011||||Unknown||Bcl-2, Bim, p53|Yes| 6313.0|del 377|C57BL/6-Pmaip1||Recessive|phorbol-12-myristate-13-acetate-induced protein 1|Pmaip1|Nil|Noxa|MGI:1930146|phorbol-12-myristate-13-acetate-induced protein 1; targeted mutation 1, Andreas Strasser|Pmaip1|MGI:2681649|18|||||||||||||||||||||||||||||Decreased sensitivity to induced cell death:*Modest but significant resistance to etoposide induced apoptosis in mouse embryo fibroblasts but not in thymocytes and other lymphocytes.Abnormal NK cell morphology:*Following expansion in culture, NK cells survive IL-15 withdrawal better than wild-type cells.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown||p53, Noxa|Yes| 6324.0|QkfTg-15|QkfBACRP23-360F23 Transgenic|||| Qkf ||||||||||||||||||||||||||||||||||||Contact Researcher||CBA x C57Bl/6|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6740.0|LauraKlf3KO|LauraKlf3KO/Ausb||||Klf3||||||||||||||||||||||||||||||||||||Mild.||FVBn|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|02-Dec-2011||0.0|0.0|Unknown|||Possibly| 6872.0|A1f|C57BL/6-Acaca/AusbApb|C57BL/6-Acaca/Ausb|Dominant|acetyl-Coenzyme A carboxylase alpha|Acaca|Normal|A530025K05Rik, Acac, Acc1, acetyl-CoA carboxylase, LOC327983|MGI:108451|acetyl-Coenzyme A carboxylase alpha; targeted mutation 1, David E James|Acaca|MGI:5618483|11||||||||||Unknown to Unknown|||||||||||||||||||Normal|Normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|17-Apr-2012|Cryopreserved sperm|50.0|0.0|No||ACC1|Yes| 5651.0|C57Bl/6 (Pink)||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6317.0|RaR|B6;129-Gt(ROSA)26Sor Pdgfra||Dominant|gene trap ROSA 26, Philippe Soriano|Gt(ROSA)26Sor|Normal|beta geo, Gtrgeo26, Gtrosa26, R26, ROSA26|MGI:104735|gene trap ROSA 26, Philippe Soriano; targeted mutation 1, Philippe Soriano|Gt(ROSA)26Sor|MGI:1861932|6|||||||||||||||||||||||||||||||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown||Receptor tyrosine kinases (RTKs), mitogen-activated protein (MAP) kinase|Yes| 6317.0|RaR|B6;129-Gt(ROSA)26Sor Pdgfra||Dominant|platelet derived growth factor receptor, alpha polypeptide|Pdgfra|Normal|CD140a, Pdgfr-2|MGI:97530|platelet derived growth factor receptor, alpha polypeptide; targeted mutation 11, Philippe Soriano|Pdgfra|MGI:2663656|5|||||||||||||||||||||||||||||||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|13-Sep-2011||||Unknown||Receptor tyrosine kinases (RTKs), mitogen-activated protein (MAP) kinase|Yes| 6316.0|Raf/R26R|B6;129-Gt(ROSA)26Sor Pdgfra/JWehi||Semi-dominant|gene trap ROSA 26, Philippe Soriano|Gt(ROSA)26Sor|Normal|beta geo, Gtrgeo26, Gtrosa26, R26, ROSA26|MGI:104735|gene trap ROSA 26, Philippe Soriano; targeted mutation 1, Philippe Soriano|Gt(ROSA)26Sor|MGI:1861932|6|||||||||||||||||||||||||||||||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown||Cardiac and cephalic neural crest cells (NCCs), Cre, ROSA26|Yes| 6318.0|RaW|B6;129-Pdgfra Wt1||Semi-dominant|Wilms tumor 1 homolog|Wt1|Nil|D630046I19Rik, Wt-1|MGI:98968|Wilms tumor 1 homolog; targeted mutation 1, William T Pu|Wt1|MGI:3801681|2|||||||||||||||||||||||||||||Normal||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown||Receptor tyrosine kinases (RTKs), mitogen-activated protein (MAP) kinase, Nkx2-5, Isl1|Yes| 6318.0|RaW|B6;129-Pdgfra Wt1||Semi-dominant|platelet derived growth factor receptor, alpha polypeptide|Pdgfra|Normal|CD140a, Pdgfr-2|MGI:97530|platelet derived growth factor receptor, alpha polypeptide; targeted mutation 11, Philippe Soriano|Pdgfra|MGI:2663656|5|||||||||||||||||||||||||||||Normal||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|13-Sep-2011||||Unknown||Receptor tyrosine kinases (RTKs), mitogen-activated protein (MAP) kinase, Nkx2-5, Isl1|Yes| 6319.0|PdxGFP|129S1/Sv-Pdx1||Dominant|pancreatic and duodenal homeobox 1|Pdx1|Normal|IDX-1, IPF-1, Ipf1, Mody4, pdx-1, STF-1|MGI:102851|pancreatic and duodenal homeobox 1; targeted mutation 1, Edouard G Stanley|Pdx1|MGI:3688420|5|||||||||||||||||||||||||||||||129/Sv|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown||ES cell, GFP, Pdx1|Yes| 6320.0|Plt4 Rag|C57BL/6-Myb Rag1||Semi-dominant|myeloblastosis oncogene|Myb|Normal|c-myb|MGI:97249|myeloblastosis oncogene; Plt4|Myb|MGI:3045843|10|||||||||||||||||||||||||||||||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown||c-Myc, Platelet, RAG1, GFP|Yes| 6320.0|Plt4 Rag|C57BL/6-Myb Rag1||Semi-dominant|recombination activating gene 1|Rag1|Nil|Rag-1|MGI:97848|recombination activating gene 1; targeted mutation 1, Nobuo Sakaguchi|Rag1|MGI:2388344|2|||||||||||||||||||||||||||||||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|13-Sep-2011||||Unknown||c-Myc, Platelet, RAG1, GFP|Yes| 6321.0|del403|C57BL/6-Bbc3||Recessive|BCL2 binding component 3|Bbc3|Nil|PUMA|MGI:2181667|BCL2 binding component 3; targeted mutation 1, Andreas Strasser|Bbc3|MGI:2681654|7|||||||||||||||||||||||||||||Decreased sensitivity to induced cell death:*Thymocytes and MEFs show enhanced resistance to genotoxic damage induced by etoposide or gamma irradiation. Decreased cellular sensitivity to gamma-irradiation: *In thymocytes and MEFs.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown||p53, Puma, Bbc3|Yes| 6323.0|QkfTg|CBA.B6-Myst4||Dominant|MYST histone acetyltransferase monocytic leukemia 4|Myst4|Normal|B130044K16Rik, KAT6B, monocytic leukemia, Morf, qkf, querkopf|MGI:1858746|MYST histone acetyltransferase monocytic leukemia 4; gene trap 1, Peter Gruss|Myst4|MGI:2679726|14|||||||||||||||||||||||||||||||CBA x C57BL/6|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown||Cerebral cortex, MYST|Yes| 6325.0|QkfTg-21|QkfBACRP23-360F23 Transgenic|||| Qkf ||||||||||||||||||||||||||||||||||||Contact Researcher||CBA x C57Bl/6|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6326.0|QkfTg-24|QkfBACRP23-360F23 Transgenic|||| Qkf ||||||||||||||||||||||||||||||||||||Contact Researcher||CBA x C57Bl/6|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6327.0|QkfTg-26|QkfBACRP23-360F23 Transgenic|||| Qkf ||||||||||||||||||||||||||||||||||||Contact Researcher||CBA x C57Bl/6|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6328.0|377SCID|RIP-B7.NOD.SCID|||| Rip |||||||||||||||||||||||||||||||||||| Phenotype does not differ from a wildtype of the same genetic background.||NOD SCID backcross|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6329.0|RorYtTbx21|RorYt.573Id2Tbx21|||| RorYGPF Tbet Id2-GFP ||||||||||||||||||||||||||||||||||||Mice have a restricted T cell receptor which can make them more susceptible to infection under some conditions. This does not appear to occur under routine housing. Mice are Immuno-compromised.||C57BL/6|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6330.0|50-1/SCID/IL2R|NOD.Cg-IL2rg Prkdc||Recessive|interleukin 2 receptor, gamma chain|Il2rg|Nil|[g]c, CD132, common cytokine receptor gamma chain, common gamma chain, gamma C receptor, gamma(c), gc|MGI:96551|interleukin 2 receptor, gamma chain; targeted mutation 1, Warren J Leonard|Il2rg|MGI:1857455|X|||||||||||||||||||||||||||||Premature death:*Median survival time is lengthened to between 59-95 weeks (median 89 weeks) in contrast to the shorter lifespan observed homozygous Prkdc controls.*The majority of autopsies indicate no evidence of lymphomas.Decreased leukocyte cell number:*Decrease in peripheral leukocytes at 10 weeks as compared to to Prkdc controls. Decreased immature B cell number: *Flow cytometric analysis indicates that spleen cells exhibit a reduction in B220+ IgK- immature B cells in comparison to Prkdc controls. Decreased mature B cell number: *Spleens are deficient in B220+ IgK+ B cells. Decreased NK cell number: *Mice are deficient in cells expressing NK cell markers in comparison to Prkdc controls. *Spleen cells from poly(I:C) stimulated 6-8 week old mice exhibit very low levels of NK cell cytotoxic activity. Decreased CD4-positive T cell number: *Spleens are deficient in mature T cells. Decreased CD8-positive T cell number: *Spleens are deficient in mature T cells.Abnormal immune system organ morphology: Lymph tissues are severely depleted of lymphoid cells. Abnormal spleen B cell follicle morphology: *Spleens do not have detectable follicles. Abnormal splenic cell ratio: *Two fold reduction in nucleated spleen cell numbers in comparison to Prkdc controls. Abnormal thymus morphology: *Thymus consists mostly of stromal cells with sporadic cyst structures. Small lymph nodes: *Lymph nodes in the double mutant are markedly smaller than those of homozygous Prkdc mice. Lymph node hypoplasia: *Lymph nodes are hypocellular.Decreased immunoglobulin level:*No detectable immunoglobulin in mice at 394-426 days of age.Abnormal response to transplant:*Mice support CD34+ human stem cell engraftment at much higher levels than Prkdc controls.*Human CD45+ cells comprise almost 50% of cells in the spleen, approximately 35% in bone marrow and thymus, and 6% in blood at 10 weeks post-engraftment.Decreased mean corpuscular volume:*Slight decrease in packed cell volume at 10 weeks as compared to to Prkdc controls.Increased cellular sensitivity to X-ray irradiation:*Mice do not survive doses above or equal to 400cGy.Decreased incidence of ionizing radiation-induced tumors:*Mice irradiated with doses below 400cGy do not exhibit thymic lymphomas in contrast to homozygous Prkdc controls.Abnormal glucose homeostasis:*Streptozotocin-diabetic mice are not restored to euglycemia after receiving transplants of 1000 to 3000 IEQ, while 4000 IEQ transplant was successful in two long-term survivors. Hyperglycemia: *Streptozotocin effectively induced hyperglycemia essentially equally in male and female mice at doses of 120to 160 mg/kg; some mice do not become hyperglycemic at all doses of streptozotocin administered.||CBAxB10.BR F2-NODSCID|Yes|No|Yes|Yes|No|Yes|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown||Human hemopoietic stem cells (HSC), IL-2R gamma, TCR, Lymphoid development, SCID|Yes| 6330.0|50-1/SCID/IL2R|NOD.Cg-IL2rg Prkdc||Recessive|protein kinase, DNA activated, catalytic polypeptide|Prkdc|Nil|DNA-PK, DNA-PKcs, DNAPDcs, DOXNPH, dxnph, slip, XRCC7|MGI:104779|protein kinase, DNA activated, catalytic polypeptide; severe combined immunodeficiency|Prkdc|MGI:1857113|16|||||||||||||||||||||||||||||Premature death:*Median survival time is lengthened to between 59-95 weeks (median 89 weeks) in contrast to the shorter lifespan observed homozygous Prkdc controls.*The majority of autopsies indicate no evidence of lymphomas.Decreased leukocyte cell number:*Decrease in peripheral leukocytes at 10 weeks as compared to to Prkdc controls. Decreased immature B cell number: *Flow cytometric analysis indicates that spleen cells exhibit a reduction in B220+ IgK- immature B cells in comparison to Prkdc controls. Decreased mature B cell number: *Spleens are deficient in B220+ IgK+ B cells. Decreased NK cell number: *Mice are deficient in cells expressing NK cell markers in comparison to Prkdc controls. *Spleen cells from poly(I:C) stimulated 6-8 week old mice exhibit very low levels of NK cell cytotoxic activity. Decreased CD4-positive T cell number: *Spleens are deficient in mature T cells. Decreased CD8-positive T cell number: *Spleens are deficient in mature T cells.Abnormal immune system organ morphology: Lymph tissues are severely depleted of lymphoid cells. Abnormal spleen B cell follicle morphology: *Spleens do not have detectable follicles. Abnormal splenic cell ratio: *Two fold reduction in nucleated spleen cell numbers in comparison to Prkdc controls. Abnormal thymus morphology: *Thymus consists mostly of stromal cells with sporadic cyst structures. Small lymph nodes: *Lymph nodes in the double mutant are markedly smaller than those of homozygous Prkdc mice. Lymph node hypoplasia: *Lymph nodes are hypocellular.Decreased immunoglobulin level:*No detectable immunoglobulin in mice at 394-426 days of age.Abnormal response to transplant:*Mice support CD34+ human stem cell engraftment at much higher levels than Prkdc controls.*Human CD45+ cells comprise almost 50% of cells in the spleen, approximately 35% in bone marrow and thymus, and 6% in blood at 10 weeks post-engraftment.Decreased mean corpuscular volume:*Slight decrease in packed cell volume at 10 weeks as compared to to Prkdc controls.Increased cellular sensitivity to X-ray irradiation:*Mice do not survive doses above or equal to 400cGy.Decreased incidence of ionizing radiation-induced tumors:*Mice irradiated with doses below 400cGy do not exhibit thymic lymphomas in contrast to homozygous Prkdc controls.Abnormal glucose homeostasis:*Streptozotocin-diabetic mice are not restored to euglycemia after receiving transplants of 1000 to 3000 IEQ, while 4000 IEQ transplant was successful in two long-term survivors. Hyperglycemia: *Streptozotocin effectively induced hyperglycemia essentially equally in male and female mice at doses of 120to 160 mg/kg; some mice do not become hyperglycemic at all doses of streptozotocin administered.||CBAxB10.BR F2-NODSCID|Yes|No|Yes|Yes|No|Yes|No|Unknown||||No|13-Sep-2011||||Unknown||Human hemopoietic stem cells (HSC), IL-2R gamma, TCR, Lymphoid development, SCID|Yes| 6332.0|Spin|C57BL/6-Ptpn6||Recessive|protein tyrosine phosphatase, non-receptor type 6|Ptpn6|Nil|hcp, Hcph, Ptp1C, SHP-1, Spin|MGI:96055|protein tyrosine phosphatase, non-receptor type 6; targeted mutation 1, Klaus Rajewsky|Ptpn6|MGI:3719625|6|||||||||||||||||||||||||||||||C57BL/6|Yes|No|Yes|Yes|Yes|Yes|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown||Shp1, Systemic autoimmunity, B cell|Yes| 6341.0|1010|vav-Myc 10 x vav-Myc 10|||| vav-myc ||||||||||||||||||||||||||||||||||||Tumour development T/+ mice develop thymoma or sub-cutaneous tumours (hystiocytic sarcoma) with a median onset of 41 weeks. T/T mice develop thymoma with a median onset of 13 weeks.||C57BL/6|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6339.0|VAV-bcl-472|C57BL/6-Bcl2l11 Tg(Vav-BCL2)1Jad||Semi-dominant|BCL2-like 11 (apoptosis facilitator)|Bcl2l11|Nil|1500006F24Rik, Bim, Bod|MGI:1197519|BCL2-like 11 (apoptosis facilitator); targeted mutation 1, Andreas Strasser|Bcl2l11|MGI:2156494|2|||||||||||||||||transgene insertion 1, Jerry M Adams|mouse Vav promoter|Overexpression||||||||||||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown||Bim, Bcl-2|Yes| 6335.0|Tbn5|C57BL/6-Taf8||Dominant|TAF8 RNA polymerase II, TATA box binding protein (TBP)-associated factorq|Taf8|Normal|Taf8, Tbn|MGI:1926879|TAF8 RNA polymerase II, TATA box binding protein (TBP)-associated factorq; gene trap 9, Peter Gruss|Taf8|MGI:3033758|17|||||||||||||||||||||||||||||||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown||Pluripotent cell, Taube nuss (Tbn)|Yes| 6345.0|1010/delmnt|Vavmyc 10 x Vavmyc10/delmnt|||| 1010 delmnt ||||||||||||||||||||||||||||||||||||delmnt are embryonic lethal in C57 background. T/+ +/+ succumb to thymoma or hystiocytic sarcoma with a median onset of 41 weeks. We have predicted that T/+ +/- mice should succumb to thymoma earlier than T/+ +/+. T/T +/+ median 13 weeks||C57BL/6|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6343.0|17/delmnt|vav-myc17/delmnt|||| myc17 delmnt ||||||||||||||||||||||||||||||||||||Transgenic mice succumb to Lymphoma from 7 weeks of age.||C57BL/6|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6347.0|Vavbcl/506|VavP-BCL2-69/BPH3 19B2|||| Bcl-2 Bim/Pum ||||||||||||||||||||||||||||||||||||Excess B cells throughout life. Develop glomerulonephritis, lymphoma and plasmacytoma Enlarged spleens lymphadenopathy (more white blood cells), larger (2-3fold) spleen and lymph nodes ||C57BL/6|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 7290.0|GzmB KO x OT-1|B6.129-Gzmb Tg(TcraTcrb)1100Mjb/PibMarpApb|B6.129-Gzmb Tg(TcraTcrb)1100Mjb/Pib|Recessive|granzyme B|Gzmb||CCP1, CCP-1/C11, Ctla1, Ctla-1, GZB|MGI:109267|granzyme B; targeted mutation 1, Timothy J Ley|Gzmb|MGI:1857156|14|||||||||||||||||transgene insertion 1100, Michael J Bevan|H-2Kb promoter|||||||||||Immunocompromised|Normal|C57BL/6J|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|18-Mar-2013|Cryopreserved sperm|50.0|0.0|Unknown||T cell, natural killer, apoptosis, cytotoxic|Possibly| 5653.0|C57xCD11||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5654.0|C5aR Het||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5656.0|C5L2 KO||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6360.0|PDX1cre|B6.FVB-Tg(Ipf1-cre)1Tuv/Ausb||Dominant||||||||||||||||||||||||||transgene insertion 1, David A Tuveson|Ipf1 promoter|||||||||||Unknown||B6/FVB|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown||Oncogenic RAS mutations, Pancreatic tumorigenesis|Yes| 6358.0|NOGIL2|NOD.Cg-Il2rg Prkdc/SzJAusb||Recessive|interleukin 2 receptor, gamma chain|Il2rg|Nil|[g]c, CD132, common cytokine receptor gamma chain, common gamma chain, gamma C receptor, gamma(c), gc |MGI:96551 |interleukin 2 receptor, gamma chain; targeted mutation 1, Warren J Leonard |Il2rgtm1|MGI:1857455|X|||||||||||||||||||||||||||||Premature death:*Median survival time is lengthened to between 59-95 weeks (median 89 weeks) in contrast to the shorter lifespan observed homozygous Prkdc controls.*The majority of autopsies indicate no evidence of lymphomas.Decreased leukocyte cell number:*Decrease in peripheral leukocytes at 10 weeks as compared to to Prkdc controls Decreased immature B cell number: *Flow cytometric analysis indicates that spleen cells exhibit a reduction in B220+ IgK- immature B cells in comparison to Prkdc controls Decreased mature B cell number: *Spleens are deficient in B220+ IgK+ B cells Decreased NK cell number: *Mice are deficient in cells expressing NK cell markers in comparison to Prkdc controls *Spleen cells from poly(I:C) stimulated 6-8 week old mice exhibit very low levels of NK cell cytotoxic activity Decreased CD4-positive T cell number: *Spleens are deficient in mature T cells Decreased CD8-positive T cell number: *Spleens are deficient in mature T cellsAbnormal immune system organ morphology:*Lymph tissues are severely depleted of lymphoid cells Abnormal spleen B cell follicle morphology: *Spleens do not have detectable follicles Abnormal splenic cell ratio: *Two fold reduction in nucleated spleen cell numbers in comparison to Prkdc controls Abnormal thymus morphology: *Thymus consists mostly of stromal cells with sporadic cyst structures Small lymph nodes: *Lymph nodes in the double mutant are markedly smaller than those of homozygous Prkdc mice Lymph node hypoplasia: *Lymph nodes are hypocellularDecreased immunoglobulin level:*No detectable immunoglobulin in mice at 394-426 days of ageAbnormal response to transplant:*Mice support CD34+ human stem cell engraftment at much higher levels than Prkdc controls*Human CD45+ cells comprise almost 50% of cells in the spleen, approximately 35% in bone marrow and thymus, and 6% in blood at 10 weeks post-engraftmentDecreased mean corpuscular volume:*Slight decrease in packed cell volume at 10 weeks as compared to to Prkdc controlsDecreased leukocyte cell number:*Decrease in peripheral leukocytes at 10 weeks as compared to to Prkdc controls Decreased immature B cell number: *Flow cytometric analysis indicates that spleen cells exhibit a reduction in B220+ IgK- immature B cells in comparison to Prkdc controls Decreased mature B cell number: *Spleens are deficient in B220+ IgK+ B cells Decreased NK cell number: *Mice are deficient in cells expressing NK cell markers in comparison to Prkdc controls *Spleen cells from poly(I:C) stimulated 6-8 week old mice exhibit very low levels of NK cell cytotoxic activity Decreased CD4-positive T cell number: *Spleens are deficient in mature T cells Decreased CD8-positive T cell number: *Spleens are deficient in mature T cellsAbnormal spleen B cell follicle morphology:*Spleens do not have detectable folliclesAbnormal splenic cell ratio:*Two fold reduction in nucleated spleen cell numbers in comparison to Prkdc controlsAbnormal thymus morphology:*Thymus consists mostly of stromal cells with sporadic cyst structuresIncreased cellular sensitivity to X-ray irradiation:*Mice do not survive doses above or equal to 400cGyDecreased incidence of ionizing radiation-induced tumors:*Mice irradiated with doses below 400cGy do not exhibit thymic lymphomas in contrast to homozygous Prkdc controlsAbnormal glucose homeostasis:*Streptozotocin-diabetic mice are not restored to euglycemia after receiving transplants of 1000 to 3000 IEQ, while 4000 IEQ transplant was successful in two long-term survivors Hyperglycemia: *Treptozotocin effectively induced hyperglycemia essentially equally in male and female mice at doses of 120to 160 mg/kg; some mice do not become hyperglycemic at all doses of streptozotocin administered||CB17/129S4SvJae|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Yes| 6358.0|NOGIL2|NOD.Cg-Il2rg Prkdc/SzJAusb||Recessive|protein kinase, DNA activated, catalytic polypeptide|Prkdc|Nil|DNA-PK, DNA-PKcs, DNAPDcs, DOXNPH, dxnph, slip, XRCC7|MGI:104779 |protein kinase, DNA activated, catalytic polypeptide; severe combined immunodeficiency |Prkdc|MGI:1857113|16|||||||||||||||||||||||||||||Premature death:*Median survival time is lengthened to between 59-95 weeks (median 89 weeks) in contrast to the shorter lifespan observed homozygous Prkdc controls.*The majority of autopsies indicate no evidence of lymphomas.Decreased leukocyte cell number:*Decrease in peripheral leukocytes at 10 weeks as compared to to Prkdc controls Decreased immature B cell number: *Flow cytometric analysis indicates that spleen cells exhibit a reduction in B220+ IgK- immature B cells in comparison to Prkdc controls Decreased mature B cell number: *Spleens are deficient in B220+ IgK+ B cells Decreased NK cell number: *Mice are deficient in cells expressing NK cell markers in comparison to Prkdc controls *Spleen cells from poly(I:C) stimulated 6-8 week old mice exhibit very low levels of NK cell cytotoxic activity Decreased CD4-positive T cell number: *Spleens are deficient in mature T cells Decreased CD8-positive T cell number: *Spleens are deficient in mature T cellsAbnormal immune system organ morphology:*Lymph tissues are severely depleted of lymphoid cells Abnormal spleen B cell follicle morphology: *Spleens do not have detectable follicles Abnormal splenic cell ratio: *Two fold reduction in nucleated spleen cell numbers in comparison to Prkdc controls Abnormal thymus morphology: *Thymus consists mostly of stromal cells with sporadic cyst structures Small lymph nodes: *Lymph nodes in the double mutant are markedly smaller than those of homozygous Prkdc mice Lymph node hypoplasia: *Lymph nodes are hypocellularDecreased immunoglobulin level:*No detectable immunoglobulin in mice at 394-426 days of ageAbnormal response to transplant:*Mice support CD34+ human stem cell engraftment at much higher levels than Prkdc controls*Human CD45+ cells comprise almost 50% of cells in the spleen, approximately 35% in bone marrow and thymus, and 6% in blood at 10 weeks post-engraftmentDecreased mean corpuscular volume:*Slight decrease in packed cell volume at 10 weeks as compared to to Prkdc controlsDecreased leukocyte cell number:*Decrease in peripheral leukocytes at 10 weeks as compared to to Prkdc controls Decreased immature B cell number: *Flow cytometric analysis indicates that spleen cells exhibit a reduction in B220+ IgK- immature B cells in comparison to Prkdc controls Decreased mature B cell number: *Spleens are deficient in B220+ IgK+ B cells Decreased NK cell number: *Mice are deficient in cells expressing NK cell markers in comparison to Prkdc controls *Spleen cells from poly(I:C) stimulated 6-8 week old mice exhibit very low levels of NK cell cytotoxic activity Decreased CD4-positive T cell number: *Spleens are deficient in mature T cells Decreased CD8-positive T cell number: *Spleens are deficient in mature T cellsAbnormal spleen B cell follicle morphology:*Spleens do not have detectable folliclesAbnormal splenic cell ratio:*Two fold reduction in nucleated spleen cell numbers in comparison to Prkdc controlsAbnormal thymus morphology:*Thymus consists mostly of stromal cells with sporadic cyst structuresIncreased cellular sensitivity to X-ray irradiation:*Mice do not survive doses above or equal to 400cGyDecreased incidence of ionizing radiation-induced tumors:*Mice irradiated with doses below 400cGy do not exhibit thymic lymphomas in contrast to homozygous Prkdc controlsAbnormal glucose homeostasis:*Streptozotocin-diabetic mice are not restored to euglycemia after receiving transplants of 1000 to 3000 IEQ, while 4000 IEQ transplant was successful in two long-term survivors Hyperglycemia: *Treptozotocin effectively induced hyperglycemia essentially equally in male and female mice at doses of 120to 160 mg/kg; some mice do not become hyperglycemic at all doses of streptozotocin administered||CB17/129S4SvJae|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|13-Sep-2011||||Unknown|||Yes| 6367.0|M0DTRtg|C57Bl/6-tg(DTR)||||DTR||||||||||||||||||||||||||||||||||||Nil in absence of diptheria toxin||C57BL6|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6373.0|BERT|B6.Cg-Cd79a/Max||Dominant|CD79A antigen (immunoglobulin-associated alpha)|Cd79a|Normal|Cd79a, Ig alpha, Ig-alpha, Iga, Igalpha, Ly-54, Ly54, mb-1 |MGI:101774 |CD79A antigen (immunoglobulin-associated alpha); targeted mutation 1, Michael Reth|Cd79a|MGI:3687451|7|||||||||||||||||||||||||||||Unknown|Normal|C57BL/6|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown||B cell antigen receptor, B cell development and function|Yes| 6361.0|RAREtg|CD1-Tg(RARE-Hspa1b/lacZ)12Jrt/Ausb|CD1-Tg(RARE-Hspa1b/lacZ)12Jrt/Ausb|Dominant||||||||||||||||||||||||||transgene insertion 12, Janet Rossant||||||||||||No phenotypic analysis:*Mice were used for expression analysis only||CD1|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|13-Sep-2011|Embryo|0.0|0.0|Unknown||Retinoic acid, RA response element|Yes| 6363.0|TRp53f|129S4-Trp53/Ausb|129S4-Trp53/Ausb|Recessive|Transformation related protein 53|Trp53 |Nil|p44, p53 |MGI:98834 |transformation related protein 53; targeted mutation 2, Tyler Jacks|Trp53|MGI:3039263|11|||||||||||||||||||||||||||||||129S4/SvJae|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|13-Sep-2011|Embryo|0.0|0.0|Unknown||p53|Yes| 6380.0|CreER|C57BL/6-Gt(ROSA)26Sor/TACAusb||Dominant|gene trap ROSA 26, Philippe Soriano|Gt(ROSA)26Sor|Normal|beta geo, Gtrgeo26, Gtrosa26, R26, ROSA26|MGI:104735|gene trap ROSA 26, Philippe Soriano; targeted mutation 9, Artemis Pharmaceuticals|Gt(ROSA)26Sor|MGI:3763211|6|||||||||||||||||||||||||||||Unknown|Unknown|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown||Cre recombinase-steroid receptor fusion, loxP-flanked lacZ reporter gene|Yes| 6390.0|OT2tgTHY1cn40LKO|B6.Cg-Cd40lg Thy1 Tg(TcraTcrb)425Cbn/Ausb||Recessive|CD40 ligand|Cd40lg|Nil|CD154, Cd40L, gp39, HIGM1, IMD3, Ly-62, T-BAM, Tnfsf5|MGI:88337|CD40 ligand; targeted mutation 1, Immunex|Cd40lg|MGI:1857145|X|||||||||||||||||transgene insertion 425, Frank Carbone||||||||||||Unknown|Unkown|C57BL/6|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown||CD40 ligand, Thymus-independent antigens, AKR thymic antigen, T cell receptor|Yes| 6390.0|OT2tgTHY1cn40LKO|B6.Cg-Cd40lg Thy1 Tg(TcraTcrb)425Cbn/Ausb||Recessive|thymus cell antigen 1, theta|Thy1|Normal|CD90, T25, theta, Thy 1.2, Thy-1, Thy-1.2, Thy1.1, Thy1.2 |MGI:98747|thymus cell antigen 1, theta; a variant|Thy1|MGI:3579311|9|||||||||||||||||||||||||||||Unknown|Unkown|C57BL/6|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|13-Sep-2011||||Unknown||CD40 ligand, Thymus-independent antigens, AKR thymic antigen, T cell receptor|Yes| 6383.0|H3Xf|B6.Cg-HEL3XRbr/Ausb ?||Recessive||H3X|||||||Unknown|||||||||||||||||||||||||||||none||C57BL/6|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6393.0|PODcre|129S6.Cg-Tg(NPHS2-cre)295Lbh/BroAusb|129S6.Cg-Tg(NPHS2-cre)295Lbh/BroAusb|Dominant||||||||||||||||||||||||||transgene insertion 295, Lawrence B Holzman|The human NPHS2 promoter|||||||||||Unknown|Unknown|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown||Podocyte, Human NPHS2 promoter|Yes| 6410.0|Kaede|C57BL/6-tg(Kaede)Rik/Ausb?||||Kaede||||||||||||||||||||||||||||||||||||||C57BL6|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6401.0|Stat3fOT2ThyLcre|B6.Cg-Stat3 Thy1 Tg(Lck-cre)548Jxm Tg(TcraTcrb)425Cbn/Ausb||Dominant|signal transducer and activator of transcription 3|Stat3|Nil|1110034C02Rik, Aprf|MGI:103038|signal transducer and activator of transcription 3; targeted mutation 1, Stephen Desiderio|Stat3|MGI:2673309|11|||||||||||||||||transgene insertion 548, Jamey Marth|mouse lck promoter|||||||||||Unknown|Unknown|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown||IL-6, T cell receptor, AKR lymphocyte, UDP-N-acetylgalactosamine (GalNAc)|Yes| 6401.0|Stat3fOT2ThyLcre|B6.Cg-Stat3 Thy1 Tg(Lck-cre)548Jxm Tg(TcraTcrb)425Cbn/Ausb||Dominant|thymus cell antigen 1, theta|Thy1|Normal|CD90, T25, theta, Thy 1.2, Thy-1, Thy-1.2, Thy1.1, Thy1.2|MGI:98747|thymus cell antigen 1, theta; a variant|Thy1|MGI:3579311|9|||||||||||||||||transgene insertion 425, Frank Carbone||||||||||||Unknown|Unknown|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|13-Sep-2011||||Unknown||IL-6, T cell receptor, AKR lymphocyte, UDP-N-acetylgalactosamine (GalNAc)|Yes| 6403.0|TOMGREtg|B6.129(Cg)-Gt(ROSA)26Sor/JAusb||Dominant|gene trap ROSA 26, Philippe Soriano|Gt(ROSA)26Sor|Normal|beta geo, Gtrgeo26, Gtrosa26, R26, ROSA26|MGI:104735|gene trap ROSA 26, Philippe Soriano; targeted mutation 4, Liqun Luo|Gt(ROSA)26Sor|gene trap ROSA 26, Philippe Soriano|6|||||||||||||||||||||||||||||Normal|Unknown|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown||Cre/loxP, Mutagenesis|Yes| 6405.0|TR3B?|B6.Cg-Cd19 Traf3/JAusb||Dominant|CD19 antigen|Cd19|Normal||MGI:88319|CD19 antigen; targeted mutation 1, University of Cologne|Cd19|MGI:1931143|7|||||||||||||||||||||||||||||Unknown|Unknown|C57BL/6|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown||CD19, B cell development, TRAF3, Nuclear factor-kappaB2 (NF-kappaB2)|Yes| 6405.0|TR3B?|B6.Cg-Cd19 Traf3/JAusb||Dominant|TNF receptor-associated factor 3|Traf3|Normal||MGI:108041|TNF receptor-associated factor 3; targeted mutation 1, Robert Brink|Traf3|MGI:3777324|12|||||||||||||||||||||||||||||Unknown|Unknown|C57BL/6|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|13-Sep-2011||||Unknown||CD19, B cell development, TRAF3, Nuclear factor-kappaB2 (NF-kappaB2)|Yes| 5213.0|mIMPα4FL (high level expression)|C57BL/6-Tg(EGFP-Kpna4 full length)high||Dominant|karyopherin (importin) alpha 4|Kpna4|Unknown|IPOA3|MGI:1100848||||Unknown||||||||||||||||Yes|EGFP fused to full length Kpna4|Protamine 1|high level expression||||||||||Fertility maybe reduced||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|30-Aug-2010|Cryopreserved sperm|50.0|0.0|Unknown||importin, testis, nuclear transport, fertility, protamine 1|No| 6411.0|Kaede lox|B6;B6D2-Tg(Oct4deltaPE-KikumeGR)1Rbrc/RbrcAusb||Dominant|||||||||||||||||||||||||||POU domain, class 5, transcription factor 1, Pou5f1||||||||||||Cells are fluorescent.|C57BL/6|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown||green, red|Possibly| 6412.0|LYScre|B6.129P2-Lyz2/JAusb||Dominant|lysozyme 2|Lyz2|Normal|Lys, Lysm, Lyzs, Lzm, Lzm-s1, Lzp|MGI:96897|lysozyme 2; targeted mutation 1, Irmgard Forster|Lyz2|MGI:1934631|10|||||||||||||||||||||||||||||Unknown|Enlarged spleen:*Rare|C57BL/6|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown||Macrophage, Granulocyte, Conditional mutagenesis|Yes| 6880.0|Krüppel-like Factor 3 (KLF3) Cherry Knock-in|Klf3-mCherry-loxP-neo-loxP||Recessive|Kruppel-like factor 3 (basic)|Klf3|Nil|BKLF, Bklf, Tef-2|MGI:1342773||||5||||||||||||||||Yes|||||||||||||No visible phenotype. Cells express "Cherry" fluorescence.|Same as homozygous|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Excellent||||No|01-May-2012|Cryopreserved sperm|50.0|0.0|Unknown||Kruppel-like Factor 3, Basic Kruppel-like Factor, KLF, Obesity, adipose|Possibly| 10349.0||ANU:ENU60:G2||Recessive|Unknown||||||||Unknown||||||||||||||||||||||||||||| | |C57Bl/6N|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|11-Jul-2023||0.0|0.0|Unknown|||Possibly| 6450.0|CART|cart flox, cart cre and cart m cherry?||||cart,rGFP,car.t,cart?||||||||||||||||||||||||||||||||||||||B6/129SvJ|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6428.0|BR1?|B6.Cg-Tnfrsf13b/Ausb||Recessive|tumor necrosis factor receptor superfamily, member 13b|Tnfrsf13b|Nil|1200009E08Rik, Taci|MGI:1889411|tumor necrosis factor receptor superfamily, member 13b; targeted mutation 1, Charles R Mackay|Tnfrsf13b|MGI:3052983|11|||||||||||||||||||||||||||||Immune system phenotype:*Allograft survival is unaffectedIncreased B cell number:*Mice have B cell hyperplasiaEnlarged spleen||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown||BAFF, BAFF-R, BCMA, TACI, Systemic autoimmune disease|Yes| 1487.0|B6.CCR-5-/-|B6.129P2-Ccr5/AnuApb|B6.129P2-Ccr5/AnuApb|Recessive|chemokine (C-C motif) receptor 5|Ccr5|Nil|CD195, Cmkbr5|MGI:107182|targeted mutation 1, William A Kuziel|Ccr5|MGI:1861911|9||||||||||||||||Yes|||||||||||||Decreased susceptibility to induced colitis:* null mice show clinically less severe DSS-mediated colitis than wild-type or Ccr2-nulls.Increased NK T cell number:* null mice show a significant increase in NK 1.1+ T cells by day 3 and 7 of DSS-treatment; wild-type and Ccr2-null mice do not show as large of an increase.Abnormal CD4-positive T cell morphology:* intestinal mucosa shows enhanced infiltration of CD4+ lymphocytes by day 7 compared to wild-type or Ccr2-deficient mice.* mice have an increased number of CD4+ T cells before and during DSS-induced colitis.Abnormal CD8-positive T cell morphology.Abnormal cytokine level:* mice expression one fifth the wild-type level of Ifng after day 3 and 7, while Il-4 is increased 75-fold and a 2-fold increase in Il-5 and -10 over wild-type.Impaired macrophage recruitment:* 80% fewer macrophages compared to control in Ag-loaded gelatin sponge DTH assay.* delay in induced peritoneal macrophage accumulation, however, accumulation of neutrophils/eosinophils is unchanged.Increased susceptibility to fungal infection:* reduced survival following inoculation with Cryptococcus neoformans, 40% die by week 8 due to CNS infection (hydrocephalus).* infected mice exhibit increased mononuclear cell recruitment to lungs, but not brain.* by week 5 infected mice exhibit cryptococcal meningitis ? cranial swelling, ruffled fur, staggered gait, lethargy and unresponsiveness, and decreased limb function.* brains of infected mice develop loss of neural tissue integrity , and large amounts of extracellelular cryptococcal polysaccharide capsule.Abnormal locomotor activity:* mice show little reduction in activity with DSS treatment, unlike wild-type which become very lethargic with time.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|10|||No|02-Jul-2007|Cryopreserved sperm|144.0|0.0|Unknown||innate immunity, leukocyte, trafficking, chemotaxis|Yes| 6444.0|Endo-cre|B6.Cg-Tg(PDGFB-cre)/Ausb?||||||||||||||||||||||||||||||||||||||||?||C57BL6|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6434.0|RN2|B6.Cg-Traf2 Tg(Lck-cre)448Jxm/Ausb||Semi-dominant|TNF receptor-associated factor 2|Traf2|Normal||MGI:101835|TNF receptor-associated factor 2; targeted mutation 1, Robert Brink|Traf2|MGI:3511494|2|||||||||||||||||transgene insertion 548, Jamey Marth|mouse lck promoter|||||||||||Unknown|Unknown|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown||TRAF2, NF-kappaB, GalNAc|Yes| 6446.0|GEMf|B6.Cg-Gem/?Ausb||Recessive||GEM|||||||Unknown|||||||||||||||||||||||||||||||C57BL6|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6461.0|AdqCre|B6.Cg-Tg(Adipoq-cre)#Pesch/Ausb||Dominant||||||||||||||||||||||||||Transgene insertion, Philipp E Scherer; transgene insertion, Philipp E Scherer|adiponectin promoter|||||||||||Unknown|Unknown|C57BL/6|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown||Adiponectin|Yes| 6438.0|TRAF2-RIP|B6.Cg-Traf2 Tg(Ins2-cre)25Mgn/Ausb||Dominant|TNF receptor-associated factor 2|Traf2|Normal||MGI:101835|TNF receptor-associated factor 2; targeted mutation 1, Robert Brink|Traf2|MGI:3511494|2|||||||||||||||||transgene insertion 25, Mark A Magnuson|rat insulin promoter (Ins2)|||||||||||Unknown|Unknown|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown||TRAF2, Nuclear factor kappaB (NF-kappaB), Glucokinase, MODY-2|Yes| 6441.0|BI?|B6.Cg-Hif1a Tg(Ins2-cre)25Mgn/Ausb||Semi-dominant|hypoxia inducible factor 1, alpha subunit|Hif1a|Nil|bHLHe78, HIF-1alpha, HIF1alpha, MOP1|MGI:106918|hypoxia inducible factor 1, alpha subunit; targeted mutation 1, Shuhei Tomita|Hif1a|MGI:2677892|12|||||||||||||||||transgene insertion 25, Mark A Magnuson|rat insulin promoter (Ins2)|||||||||||Unknown|Unknown|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown||Glucokinase, HIF-1alpha, Human T2D islets|Yes| 6442.0|bVDR|B6.Cg-Vdr/Ausb||Dominant|vitamin D receptor|Vdr|Normal|Nr1i1|MGI:103076|vitamin D receptor; targeted mutation 1, Geert Carmeliet|Vdr|MGI:2183407|15|||||||||||||||||||||||||||||Unknown|Unknown|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown||Vitamin D receptor, CaT1|Yes| 6454.0|Y6?|B6;129P2-Npy6r/Ausb||Recessive||Y6|||MGI:3528882|||||||||||||||||||||||||||||||||||Mixed - mice|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6462.0|D2B|B6.129P2-Doc2b/Ausb?||Recessive|double C2, beta|Doc2b|Nil||MGI:1100497|double C2, beta; targeted mutation 1, Alexander J Groffen|Doc2b|MGI:4440451|11|||||||||||||||||||||||||||||Abnormal CNS synaptic transmission:*Purkinje cells exhibit continuous spiking without interruption unlike wild-type cells. Abnormal inhibitory postsynaptic currents: *Spontaneous inhibitory postsynaptic currents are decreased to one-fourth of wild-type.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown||Doc2, SNARE|Yes| 6458.0|1D15Δ|C57BL/6-Tbc1d15/Ausb||Recessive|TBC1 domain family, member 15|Tbc1d15||4432405K22Rik, Ly6dl|MGI:1913937|TBC1 domain family, member 15; gene trap RRR232, BayGenomics|Tbc1d15|MGI:4397430|10|||||||||||||||||||||||||||||Unknown||C57BL/6|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6455.0|Y7Δ|B6.129-Npy7r?||Recessive||Y7|||||||Unknown|||||||||||||||||||||||||||||||B6/129SVJ|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6456.0|Y7f|B6.129-Npy7r?||Recessive||Y7|||||||Unknown|||||||||||||||||||||||||||||||B6/129SVJ|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6464.0|HSAcre|B6.Cg-Tg(ACTA1-cre)/Ausb ?||Dominant||||||||||||||||||||||||||Cre recombinase|Human Skeletal Actin Promoter|skeletal muscle||||||||||||C57BL/6|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown||muscle, Cre recombinase, skeletal|Possibly| 6490.0|OB|B6.V-Lep/JAusb ||Recessive|Leptin|Lep|Nil||MGI:104663|leptin; obese|Lep|MGI:1856424|6|||||||||||||||||||||||||||||Abnormal body weight:*Treatment with triiodothyronine significantly reduces body weight relative to the reduction seen in controls.*Body weight reduced by treatment with Leptin.Obese:*12-week old males are obese.*Develop progressive obesity.Increased growth rate:*Mice reach 60-70 g by 10 months of age.Decreased insulin secretion:*Leptin-treated islet cells exhibit decreased insulin secretion compared to similarly treated wild-type islets.Increased insulin secretion:*Insulin content in the pancreata is increased compared to in wild-type mice.Abnormal circulating glucose level: Decreased circulating glucose level: *After feeding, serum glucose levels are more than 30% lower than in wild-type mice. Hypoglycemia: *Older mice are usually hypoglycemic. Hyperglycemia: *Serum glucose is 320 mg/dl compared to 134 mg/dl in wild-type controls. *Transient hyperglycemia. *Blood sugar peaks at 2-3 months. *Returns to normal by 4-5 months of age.Increased circulating insulin level:*Seen in 12-week old males.*Serum insulin is 41.5 ng/ml compared to 0.8 ng/ml in wild-type.*At 2 weeks, insulin levels are increased 2.5-fold compared to in wild-type mice.*Insulin levels increase rapidly to over 50X normal controls.*However, mice treated with isoproterenol exhibit lowered serum levels of insulin.Abnormal circulating cholesterol level Increased circulating cholesterol level *Fasting plasma total cholesterol concentration is increased 2-3 fold over controls. Increased circulating HDL cholesterol level Increased circulating LDL cholesterol level Increased circulating VLDL cholesterol levelIncreased circulating triglyceride level:*Seen in 12-week old males.*Triglyceride levels are elevated 1.5- to 2-fold.Decreased body temperature:*Body temperature is maintained a basal level when the ambient temperature is gradually reduced to 4C. Abnormal oxygen consumption:*Insulin stimulated oxygen consumption by the soleus muscle is little affected by triiodothyronine.*Oxygen consumption about 2/3 that observed in controls.*Increased by treatment with triiodothyronine. Decreased oxygen consumption: *In the epididymal and brown fat pads. Increased oxygen consumption: *In the liver.Impaired glucose tolerance:*Glucose intolerance which improved when treated with rosiglitazone.*Following an acute intraperitoneal glucose injection, the post-challenge glucose level remained elevated up to 120 min compared to controls, indicating glucose intolerance.Insulin resistanceAbnormal protein level:*Total body protein lower than in controls.*Total body protein increased by treatment with triiodothyronine. Abnormal urine homeostasis:*Less epinephrine in the urine of ad libitum fed mice.*Males show elevated levels of dopamine, serotonin, 5'hydroxyindolineacetic acid in urine.*Urine levels of norepinephrine only slightly elevated.Abnormal myocardial fiber morphology:*Exhibit extensive focal damage in myocardial tissue, showing an abundance of lipid droplets in myocytes and damaged mitochondria that are swelled, have disorganized cristae and show loss of integrity.*Exhibit myocyte hypertrophy, with increased myocyte diameter and distorted nuclear architecture.*Cardiomyocytes exhibit a significantly enlarged cross-sectional area. Enlarged myocardial fiber: *Cardiomyocytes display larger resting cell length and cross-sectional area.Heart left ventricle hypertrophy:*Increase in left ventricle wall thickness and mass is seen by 6 months of age but not at 2 months of age.*Induced weight loss via leptin infusion, but not via caloric restriction, partially resolves the hypertrophy.Decreased cardiac muscle contractility.*Exhibit cardiac contractile dysfunction that is due to leptin deficiency and not obesity as high fat diet-induced obese controls show normal cardiomyocyte morphology and contractile function.*Cardiomyocytes exhibit a reduced contractile capacity.*Decreased peak shortening.*Prolonged relengthening.*Elevated resting peak calcium ion concentration.*Slowed intracellular calcium ion decay.Abnormal myocardial fiber physiology:*Cardiomyocytes exhibit decreased peak shortening and maximal velocity of shortening/relengthening, prolonged time-to-90% relengthening, reduced intracellular calcium release upon electrical stimulus associated with a slowed intracellular calcium decay rate, and significantly higher oxygen levels.Decreased cardiac muscle contractility:*Exhibit cardiac contractile dysfunction that is due to leptin deficiency and not obesity as high fat diet-induced obese controls show normal cardiomyocyte morphology and contractile function.*Cardiomyocytes exhibit a reduced contractile capacity.*Decreased peak shortening.*Prolonged relengthening.*Elevated resting peak calcium ion concentration.*Slowed intracellular calcium ion decay.Abnormal muscle morphology:*Muscle protein content is reduced.Abnormal myocardial fiber morphology:*Exhibit extensive focal damage in myocardial tissue, showing an abundance of lipid droplets in myocytes and damaged mitochondria that are swelled, have disorganized cristae and show loss of integrity.*Exhibit myocyte hypertrophy, with increased myocyte diameter and distorted nuclear architecture.*Cardiomyocytes exhibit a significantly enlarged cross-sectional area.Enlarged myocardial fiber:*Cardiomyocytes display larger resting cell length and cross-sectional area.Decreased skeletal muscle fiber size:*Cross-sectional area of muscle fibers is generally smaller.Abnormal skeletal muscle fiber type ratio:*Lower proportion of faster myosin heavy chain isoforms.Decreased skeletal muscle mass:*Mean muscle mass consistently less than controls but magnitude of difference is muscle specific.Abnormal adipose tissue amount:*Treatment with triiodothyronine significantly reduces adipocyte numbers relative to the degree of reduction seen in controls.*Treatment with triiodothyronine reduces adipocyte numbers.Increased percent body fat:*Mice have fat mass of ~42 g compared to ~3 g in wild-type at 16 weeks.Abnormal epididymal fat pad morphology:*Treatment with triiodothyronine significantly reduces epididymal fat pad weight relative to the degree of reduction seen in controls.*Adipocyte size remains larger after treatment with triiodothyronine relative to controls.Increased interscapular fat pad weight:*Greater weight than for controls.*Affected less by treatment with triiodothyronine than controls.*Brown adipocyte numbers are normal.Abnormal food intake:*Food intake is reduced by Leptin treatment.Increased eating behavior:*Increased food intake when ambient temperature drops from 28 to 21C.Polyphagia:*Mice eat 70% more than wild-type controls.Hypoactivity:*Significantly reduced activity relative to wild-type controls.*Less wheel running activity.*More wheel running activity in light phase and less in dark phase.Abnormal pain threshold:Allodynia:*Resistant to tactile allodynia caused by partial sciatic nerve ligation.*Epineural application of leptin treated peritoneal macrophage induces tactile allodynia.Hyperalgesia:*Display thermal hyperalgesia after partial sciatic nerve ligation.Abnormal sleep pattern:*Increased total sleep time in a 24 hour period.*Additional sleep primarily in the dark phase.*Increased non-REM sleep time.*Recovery from sleep deprivation involves increased duration of non-REM bouts rather than increased number of bouts as seen in controls.Abnormal frequency of paradoxical sleep:*Reduced REM in light phase.*Increased REM in dark phase.Fragmentation of sleep/wake states:*Sleep more fragmented.*More arousals.*Shorter wake periods.Female infertility:*Females do not produce litters.Lung inflammation:*Ozone induces significantly elevated levels of TNFR1.*Ozone induces a nonsignificant elevation of TNFR2 levels.Enlarged pancreatic isletsAbnormal pancreatic beta cell physiology:*Background Sensitivity: less beta cell degranulation than seen on the "BKS" background.Decreased insulin secretion:*Leptin-treated islet cells exhibit decreased insulin secretion compared to similarly treated wild-type islets.Increased insulin secretion:*Insulin content in the pancreata is increased compared to in wild-type mice.Decreased NK cell number:*Reduced numbers can be restored by treatment with leptin.Increased metastatic potential:*Increased metastasis to the lung of both melanoma cell lines and lung cancer cell lines initially injected in the tail vein.*Leptin reduces the level of metastasis.Abnormal sympathetic nervous system physiologyAbnormal liver weight:*Treatment with triiodothyronine significantly reduces relative and absolute liver weight.||C57BL/6|Yes|No|Yes|Yes|Unknown|Yes|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown||Leptin, Obesity|Yes| 6491.0|Shaker2|Myo15/JAusb||Recessive|myosin XV|Myo15|Nil||MGI:1261811|myosin XV; shaker 2|Myo15|MGI:1857036|11|||||||||||||||||||||||||||||Abnormal cochlear outer hair cell morphology:*Most outer hair cells exhibit a non-convex region on their apical circumference unlike wild-type cells.*Outer hair cells exhibit a slight flattening of their neural side compared to in wild-type mice Short outer hair cell stereocilia: *Hair cell stereocilia are shorter than in wild-type mice.||Mixed mice|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Yes| 6881.0|ENU15Ch:020a:mTOR|C57BL/6JAnu-Mtor/AnuApb|C57BL/6JAnu-Mtor/AnuApb|Recessive|mechanistic target of rapamycin (serine/threonine kinase)|Mtor|Unknown|2610315D21Rik, FKBP-rapamycin-associated protein FRAP, flat, Frap1, RAFT1, RAPT1 |MGI:1928394|mechanistic target of rapamycin (serine/threonine kinase); mutation 1, The Australian National University|Mtor|MGI:5484589|4|ENSMUSG00000028991|ENSMUST00000103221|mtor-001|614|705|T to G|ENSMUSE00000524008|5|205|Isoleucine to Serine|||||TGTGGCTGTGTGGGACCCCAAGCAGGCCATCCGGGAAGGCGCTGTAGCGGCCCTTCGTGCC||||||||||||||Low numbers of NK cells, few KLRG1 expressing NK cells, low CD44 protein expression on CD4<+> T cells in the blood|Normal|C57BL/6JAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||G5N1||No|02-May-2012|Cryopreserved sperm|45.0|0.0|Unknown||lymphocyte, T cell, NK cell, ENU|No| 6494.0|PRLACZKI|B6.Cg-Pgr/Ausb||Dominant|progesterone receptor|Pgr|Normal|9930019P03Rik, ENSMUSG00000074510, NR3C3, PR, PR-A, PR-B|MGI:97567|progesterone receptor; targeted mutation 1, John P Lydon|Pgr|MGI:3032652|9|||||||||||||||||||||||||||||Unknown|Unknown|129/B6|Yes|No|Yes|Yes|Unknown|Yes|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown||Progesterone|Yes| 7596.0||SJL/ASAM||Dominant|unknown|unknown|Reduced||||||Unknown|||||||||||||||||||||||||||||Unknown|The mice displays a growth retardation phenotype without other gross abrnomalities. The mice are viable and fertile.|SJL/J|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Good|8|||No|18-Feb-2014|Cryopreserved sperm|72.0|0.0|Unknown||growth retardation, ENU|Yes| 6499.0|PKCef|B6.129Sv-Prkce/Ausb||Recessive|protein kinase C, epsilon|Prkce|Nil|5830406C15Rik, PKC[e], Pkce, PKCepsilon|MGI:97599||||17|||||||||||||||||||||||||||||Normal|Normal|129SV/B6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown||Protein kinase Cepsilon, Diabetes|Yes| 6529.0|HY|B6.Cg-Tg(TcraH-Y,TcrbH-Y)71Vbo/WehiAusb||Dominant||||||||||||||||||||||||||transgene insertion 71, Harald von Boehmer||||||||||||Abnormal T cell differentiation:*Female mice have substantial numbers of HY-specific CD8<+> T cells but not HY-specific CD4<+> T cells.Abnormal cytotoxic T cell physiology:*Virtually all CD8<+> T cells from female mice recognize HY antigen in the context of H-2D.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown||Class I H-2Db MHC antigens, CD4<+>, CD8<+>|Yes| 6531.0|IL15?|B6.Cg-Il15/ScrAusb||Recessive|interleukin 15|Il15|Nil||MGI:103014|nterleukin 15; targeted mutation 1, Immunex Research and Development Corporation|Il15|MGI:2136897|8|||||||||||||||||||||||||||||Abnormal dendritic cell physiology:*In culture, dendritic cells are resistant to cytokine withdrawal-induced apoptosis.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown||IL-15, NK T cells, Memory phenotype CD8<+> T cells, intestinal intraepithelial lymphocytes (IELs)|Yes| 6532.0|IL2B6?|?||||IL2||||||||||||||||||||||||||||||||||||||C57BL6|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6883.0|MKB ; Met-Kb|STOCK-Tg(sMt1-H2-K)||Dominant||||||||||||||||||||||||||mouse H2-K (MHC class I)|Sheep metallothionein promoter|variable and slightly lower than wild type H2-K. Expression can be induced with Zinc||||||||||Normal|Normal|B10.BR|Yes|Yes|Yes|Yes|Yes|Yes|No|Excellent|more than 10|||No|02-May-2012||0.0|0.0|No||tolerance, liver, CD8 T cells, MHC class I, autoimmunity|Possibly| 6521.0|2CTHY1.1tg|STOCK Thy1 Tg(Tcra2C,Tcrb2C)1Dlo/Ausb||Recessive|thymus cell antigen 1, theta|Thy1|Normal|CD90, T25, theta, Thy 1.2, Thy-1, Thy-1.2, Thy1.1, Thy1.2|MGI:98747|thymus cell antigen 1, theta; a variant|Thy1|MGI:3579311|9|||||||||||||||||transgene insertion 1, Dennis Y Loh||||||||||||||Unknown|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown||T cell receptor, MHC|Possibly| 6524.0|CAB?|?||||CAB||||||||||||||||||||||||||||||||||||||C57BL6|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6527.0|FoxDT|B6.Cg-Foxp3/TacAusb?||Dominant|forkhead box P3|Foxp3|Normal|JM2, scurfin|MGI:1891436|forkhead box P3; targeted mutation 3, Alexander Y Rudensky|Foxp3|MGI:3698131|X|||||||||||||||||||||||||||||Unknown|Unknown|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown||Foxp3, Self-activated T cells|Yes| 6537.0|JA18?|B6.Cg-Tcra-J/Ausb?||Recessive|T-cell receptor alpha, joining region|Tcra-J|Nil|Jalpha281|MGI:98555|T-cell receptor alpha, joining region; targeted mutation 1, Masaru Taniguchi|Tcra-J|MGI:2180736|Unknown|||||||||||||||||||||||||||||Unknown|Unknown|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown||Valpha 14 NKT cells, IL-12|Yes| 6534.0|IL7tg|B6.Cg-Tg(H2-Ea-Il7)10Rhdr/ScrAusb||Semi-dominant||||||||||||||||||||||||||transgene insertion 10, Rhodri Ceredig|H2-Ea promoter|||||||||||Abnormal B cell morphology:*Proportion of pro/pre-B cells in the thymus is significantly increased.Abnormal double-negative T cell morphology:*5.3% of double negative cells in 6 week old thymus are CD19+, a significant increase compared to controls.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown||IL-7, E alpha (MHC class II) promoter, Lymphoproliferative disorders|Yes| 6555.0|G2f|GR2FloxISO||Recessive||G2,CRE|||||||Unknown|||||||||||||||||||||||||||||||C57BL6|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6539.0|MHC1?|B6.Cg-B2m/ScrAusb?||Recessive|beta-2 microglobulin|B2m|Nil|beta 2 microglobulin, beta2-m, Ly-m11|MGI:88127|beta-2 microglobulin; targeted mutation 1, University of North Carolina|B2m|MGI:1857133|2|||||||||||||||||||||||||||||Unknown|Unknown|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown||beta 2-microglobulin|Yes| 6541.0|PKCT?|B6.129P2-Prkcq/ScrAusb?||Recessive|protein kinase C, theta|Prkcq|Nil|A130035A12Rik, PKC theta, PKC-0, PKC-theta, Pkcq, PKCtheta|MGI:97601|protein kinase C, theta; targeted mutation 1, Dan Littman|Prkcq|MGI:2664379|2|||||||||||||||||||||||||||||Immune system phenotype:*Mice exhibit normal lung inflammation driven by Th1 cytokines. Abnormal T-helper 1 cell differentiation: *Th1 stimulated T cells exhibit delayed differentiation and accumulation compared with similarly treated wild-type cells. *However, Th1 cytokine production is normal in antigen airway challenge. Decreased T cell proliferation: *In mice immunized with ovalbumin in alum. *However, proliferation of T cells in mice stimulated with ovalbumin and complete Freund's adjuvant is normal. Decreased splenocyte proliferation: *On day 14, but not day 21, following induction of experimental autoimmune encephalomyelitis (EAE). Abnormal CD4-positive T cell physiology: *Accumulation of antigen-induced CD4 cells in lung draining lymph nodes during Th2 lung inflammation is decreased compared to in similarly treated wild-type mice. Abnormal T-helper 2 physiology: *Following ovalbumin challenge, production of Th2 cytokines (Il4, Il5, and Il13) compared to in similarly treated wild-type mice. *Stimulated CD4 T cells exhibit impaired early Th2 and Th1 differentiation compared with similarly treated wild-type cells. Decreased interferon-gamma secretion: *From CD4 T cells stimulated by anti-CD3, anti-CD28 antibodies but not when IL2 was present. *From CD4 T cells from mice stimulated subcutaneously with ovalbumin and complete Freund's adjuvant. *Following induction of experimental autoimmune encephalomyelitis (EAE). Decreased interleukin-13 secretion: *In the bronchoalveolar lavage fluid of ovalbumin challenged mice. Decreased interleukin-17 secretion: *Following induction of experimental autoimmune encephalomyelitis (EAE), splenocytes produce less IL17 compared to in similarly treated wild-type mice. *IL23-stimulated spleen cultures produce less IL17 compared with similarly treated wild-type cultures. *However, ovalbumin-stimulated splenocytes exhibit normal IL17 production. Decreased interleukin-2 secretion: *From CD4 T cells from mice stimulated subcutaneously with ovalbumin and complete Freund's adjuvant. *From splenocytes on day 14, but not day 21, following induction of experimental autoimmune encephalomyelitis (EAE). Decreased interleukin-4 secretion: *In the bronchoalveolar lavage fluid of ovalbumin challenged mice. *From CD4 T cells stimulated by anti-CD3, anti-CD28 antibodies with or without IL2. *From CD4 T cells from mice stimulated with ovalbumin in alum. *From splenocytes on day 14, but not day 21, following induction of experimental autoimmune encephalomyelitis (EAE). Decreased interleukin-5 secretion: *In the bronchoalveolar lavage fluid of ovalbumin challenged mice. *From CD4 T cells from mice stimulated with ovalbumin in alum. Decreased susceptibility to experimental autoimmune encephalomyelitis: *Mice treated with MOG35-55 are completely resistance to experimental autoimmune encephalomyelitis (EAE) induction (reduced inflammation, no demyelinating lesions, decreased production of Th1 cytokines IFN-gamma, IL2, and IL4, and IL17 production) compared with similarly treated wild-type mice.Decreased airway responsiveness:*Mice exhibit attenuated methacholine sensitivity compared with similarly treated wild-type mice.Abnormal nervous system development:*Developmental dennervation of polyinnervated neuromuscular junctions is delayed compared to in wild-type mice.Abnormal neuromuscular synapse morphology:*In a twitch assay, PMA-treated muscles even with normal nerves and glia in the preparation fail to exhibit synapse loss unlike similarly treated wild-type muscles.*In a twitch assay, PMA-treated neurons with normal muscles and glia in the preparation fail to exhibit synapse loss unlike similarly treated wild-type muscles.Abnormal endplate potential:*Following stimulation, myotubes fail to exhibit a decrement in endplate potential (EPP) amplitude unlike in similarly treated wild-type cells.*Following PMA treatment, muscles with wild-type nerves and glia or ventral spinal cord nerves with wild-type muscles and glia fail to exhibit a decrease in endplate amplitude compared with similarly treated wild-type muscles.*However, ventral spinal cord neurons treated with PMA and TTX exhibit a normal decrease in EPP amplitude.Decreased physiological sensitivity to xenobiotic:*Mice exhibit attenuated methacholine sensitivity compared with similarly treated wild-type mice.*Ovalbumin-treated mice exhibit a reduction in accumulation of leukocytes, including eosinophils and lymphocytes, in bronchoalveolar lavage fluid and lung tissue, relatively normal bronchial epithelium, reduced mucus, and reduced Th2 cytokines compared with similarly treated wild-type mice.|Abnormal neuromuscular synapse morphology:*PMA-treated neurons with normal muscles and glia in the preparation fail to exhibit synapse loss unlike similarly treated wild-type muscles that is not as severe as in samples from homozygotes.|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown||PKC-theta, NF-kappaB, TCR|Yes| 6545.0|C3Ttg|FVB/N-Tg(C3-1-TAg)cJeg/NAusb||Dominant||||||||||||||||||||||||||transgene insertion c, Jeffrey E Green|rat prostatic binding protein C3 promoter (Pbpc3)|||||||||||Increased prostate gland tumor incidence Prostate intraepithelial neoplasia: *Mice develop prostate intraepithelial neoplasia (PIN) unlike wild-type mice. *PIN is higher in the ventral lobe compared to in the dorsal lobe.||FVB/N|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown||rat prostatic steroid binding protein [C3(1)] gene, Adenoma, Adenocarcinoma, Prostate cancer|Yes| 6551.0|CONB6KI|CONEDKIxto B6||Recessive||CONED||||||||||||||||||||||||||||||||||||||C57BL6|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6560.0|GR5?B6|GluR5KO x B6||Recessive||GR5||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6558.0|Gcre|GLIcreER||Recessive||G|||||||Unknown|||||||||||||||||||||||||||||||C57BL6|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6557.0|GAPB6f|ROSA26GAP x B6||Recessive||GAPB6||||||||||||||||||||||||||||||||||||||C57BL6|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011|Embryo|0.0|0.0|Unknown|||Possibly| 6569.0|NR1f|NR1flox+/-CA1||Recessive||NR1|||||||Unknown|||||||||||||||||||||||||||||||SVEV|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011|Embryo|0.0|0.0|Unknown|||Possibly| 6567.0|LES6?|LEDS6? x CAMcretg||Recessive||CAM,LES6|||||||Unknown|||||||||||||||||||||||||||||||SVEV|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6568.0|MyD88|B6.129P2-Myd88/Ausb ?||Recessive|myeloid differentiation primary response gene 88|Myd88|Nil||MGI:108005|myeloid differentiation primary response gene 88; targeted mutation 1, Shizuo Akira|Myd88|MGI:2385681|9|||||||||||||||||||||||||||||Increased apoptosis:*5 days after lung injury, mutants show significantly increased numbers of apoptotic lung epithelial and inflammatory cells.Increased physiological sensitivity to xenobiotic:*Knockout mice are more susceptible to bleomycin-induced lung injury.Increased dendritic cell number:*Increased numbers of dendritic cells in brains of mice infected with Plasmodium.Abnormal dendritic cell differentiation:*Dendritic cell maturation fails to occur in vivo upon exposure to TLR9 agonists.Abnormal immune system physiology:*Response to LPS and CpG is completely abrogated. Abnormal dendritic cell physiology: *Cytokine secretion elicited by zymosan or LPS is impaired. *Following infection with attenuated yellow fever vaccine 17D (YF-17D), dendritic cells produce less IL-12p40, IL-6 and interferon-gamma relative to wild-type mice. Abnormal macrophage physiology: *TNF production is impaired in thioglycollate-elicited macrophages treated with intact zymosan. *Cytokine production by macrophages cultured with P. carinii cysts is reduced compared to wild-type. Abnormal NK cell physiology: *NK cells fail to make IFN-gamma in response to injections of TLR9 agonists. Abnormal T cell physiology: *Induction of the antigen-specific CD8+ T-cell response by immunizing with soluble ovalbumin and TLR9 agonists, but not TLR2 and TLR6 agonists, was severely impaired. Abnormal cytokine secretion: *LPS-induced cytokine production by BMDCs is almost abolished compared to controls and Myd88-sufficient mutants. Abnormal chemokine secretion: *Hyaluronan fragment-induced expression of chemokines by peritoneal macrophages is completely abolished in double knockout mice. Decreased interferon-alpha secretion: *CpG-A or RNA polyuridylic acid induced production of interferon-alpha was abolished in plasmacytoid dendritic cells. Decreased interferon-gamma secretion: *Less up regulation of INF-gamma in Plasmodium infection. *Following infection with attenuated yellow fever vaccine 17D (YF-17D), dendritic cells produce less interferon-gamma. Decreased interleukin-12 secretion: *After stimulation with zymosan, TNF production is significantly reduced in Myd88-deficient animals. Decreased interleukin-12b secretion: *Less upregulation of IL-12b in Plasmodium infection. *Following infection with attenuated yellow fever vaccine 17D (YF-17D), dendritic cells produce less IL-12p40 relative to wild-type mice. Decreased interleukin-6 secretion: *Following treatment with PbA(Plasmodium bergbei ANKA)-parasitized erythrocytes or LPS-stimulation, IL-6 secretion is reduced. *Following infection with attenuated yellow fever vaccine 17D (YF-17D), dendritic cells produce less IL-6 relative to wild-type mice. Decreased tumor necrosis factor secretion: *Less upregulation of TNF-alpha in Plasmodium infection. *Following treatment with PbA(Plasmodium bergbei ANKA)-parasitized erythrocytes or LPS-stimulation, TNF secretion is reduced. *After stimulation with zymosan, TNF production is significantly reduced in Myd88-deficient animals. Decreased inflammatory response: *In a model of induced pneumococcal meningitis-associated labyrinthitis, homozygotes exhibit a significantly lower granulocytic infiltration of the labyrinth and increased bacterial density in the cochlea at 24 hrs post-infection relative to wild-type control mice. Abnormal response to infection: *Following treatment with PbA (Plasmodium bergbei ANKA)-parasitized erythrocytes, mice have a decreased immune response in terms of TNF and IL-6 secretion and response to CpG. Decreased susceptibility to parasitic infection: *Resistant to cerebral malaria but eventually die of extremely high parasitemia. Increased susceptibility to viral infection: *Increased susceptibility to encephalomyocarditis virus (EMCV) infection compared to wildtype.Abnormal susceptibility to hearing loss:*In a model of induced pneumococcal meningitis-associated labyrinthitis, homozygotes exhibit significantly less hearing impairment at 24 hrs post-infection in response to click, 1- or 10-kHz stimuli relative to wild-type control mice.Abnormal neuron differentiation:*Improved differentiation of progenitor cells into neurons.*Survival of newly formed neurons is reduced.Abnormal nervous system physiology:*After cold induced cortical injury, recruitment of neutrophiles to lesion site is reduced by 85% in comparison to controls.*Cold induced cortical lesion volume is reduced by 25% compared to controls.*Fewer cortical cells have damaged DNA compared to controls after cold induced cortical injury.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown||MyD88, IL-1, IL-18, NF-kappaB, c-Jun N-terminal kinase (JNK)|Yes| 6571.0|R5RKI|GluR5(Q636R)-N6-bx129S6||Recessive||R5R|||||||Unknown|||||||||||||||||||||||||||||||SVEV|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011|Embryo|0.0|0.0|Unknown|||Possibly| 6572.0|R6EΔ|GR6ΔECS||Recessive||R6E|||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011|Embryo|0.0|0.0|Unknown|||Possibly| 6552.0|CONEDKI|CONEDKI||Recessive||CONED||||||||||||||||||||||||||||||||||||||SVEV|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011|Embryo|0.0|0.0|Unknown|||Possibly| 6562.0|GR7?|GLUR7?||Recessive||GR7||||||||||||||||||||||||||||||||||||||C57BL6|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011|Embryo|0.0|0.0|Unknown|||Possibly| 6561.0|GR6S6?|GLUR6? x SVEV||Recessive||GR6S6||||||||||||||||||||||||||||||||||||||SVEV|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011|Embryo|0.0|0.0|Unknown|||Possibly| 7302.0||SJL/Mrit||Dominant|Unknown||||||||Unknown|||||||||||||||||||||||||||||Severe macrocytosis|Macrocytosis|SJL/J|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|03-Apr-2013|Cryopreserved sperm|47.0|0.0|No||haematology, macrocytosis, ENU|Yes| 6574.0|THGtg|hTHGFPTg||Dominant||THG|||||||Unknown|||||||||||||||||||||||||||||||C57BL6|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6563.0|GR7S6?|GR7S6?||Recessive||GR7S6||||||||||||||||||||||||||||||||||||||SVEV|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 9171.0|Rpl41:F0:19|C57BL/6NCrlAnu-Rpl41/AnuApb||Semi-dominant|ribosomal protein L41|Rpl41||1810055P16Rik, 2210411K19Rik |MGI:1915195|Rpl41|Rpl41:F0:19||10|||||||||||||||||||||||||||||unknown |unknown|C57Bl/6N|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|07-Apr-2021|Cryopreserved sperm|12.0|0.0|Unknown|||Possibly| 3310.0|APP23|C57BL/6-Tg(Thy1-APP)3Somm||Recessive||||||||||||||||||||||||||The human amyloid precursor protein (APP) cDNA carrying the Swedish double mutation at positions 670/671 (KM->NL).|murine Thy1.2|High, in brain|||||||||||These mice are an animal model for Alzheimer’s disease; Mice develop Aβ-plaques from 6 months onwards and show memory impairment|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|Yes|Good|10||T6 x B6|No|09-Jun-2008||0.0|0.0|Yes||Alzheimer, Aβ, plaque, memory, neurodegeneration|Possibly| 6878.0|EL20 ; Embryonic Lethal 20|B6.129-Inpp5d/MarpApb|B6.129-Inpp5d/Marp|Recessive|inositol polyphosphate-5-phosphatase D|Inpp5d|Reduced|SHIP, SHIP1, SHIP-1, Src homology 2 domain-containing inositol-5-phosphatase, s-SHIP|MGI:107357|inositol polyphosphate-5-phosphatase D; early lethal|Inpp5d|MGI:5050823|1|||||||||||||||||||||||||||||From birth homozygous mutants exhibit runting and by 5-6 weeks of age, will develop myeloid leukemia characterised by anemia, leukopenia, thrombocytopenia and splenomegaly. Mice will die by 7 weeks of age due to myeloid infiltration of the lungs.|Normal|C57BL/6|Yes|No|Yes|Yes|No|Yes|No|Excellent|10|10+|Heterozygous x Heterozygous|No|26-Apr-2012|Cryopreserved sperm|50.0|0.0|Yes|Leukemia|Ship1, sShip, myeloid, leukemia, ENU mutation|Yes| 3484.0|uMT|C57BL/6-Igh-6/Wehi||Recessive|immunoglobulin heavy chain 6 (heavy chain of IgM)|Igh-6|Nil|BCR, Ig mu, Igh-M, Igh6, IgM, muH, muMT|MGI:96448|targeted mutation 1, University of Cologne|Igh-6|MGI:1857187|12||||||||||||||||Yes|||||||||||||B cell deficient and therefore immuno-compromised (no immunoglobulin but CTL intact).||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|23-Jul-2008||0.0|0.0|Unknown||immunoglobulin, B cell, Ig, differentiation, infection|Yes| 6583.0|RalGDS|BALB/c-Ralgds/Apb|3574574|Semi-dominant|ral guanine nucleotide dissociation stimulator|Ralgds|Nil|Gnds, mKIAA1308, RalGDS, Rgds|MGI:107485||||2|||||||||||||||||||||||||||||Normal|Normal|BALB/c|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|||homozygous cross to heterozygous mouse|No|19-Sep-2011|Cryopreserved sperm|50.0|0.0|No|||No| 235.0|Twist|B6.129-Twist1||Semi-dominant|twist gene homolog 1 (Drosophila)|Twist1|Nil|charlie chaplin, M-Twist, pdt, Pluridigite, Skam10Jus, Ska10|MGI:98872|targeted mutation 1, Richard R Behringer|Twist1|MGI:1857265|12||||||||||||||||Yes|||||||||||||Homozygous mutant embyros have neural tube defects and die around E11.|Heterozygous mutants are viable and exhibit features of human Saethre-Chotzen syndrome, including hindlimb polydactyly, craniofacial defects, long bone abnormalities, an abnormal gait and a small size.||No|No|Yes|No|No|Yes|No|Unknown||||No|25-Apr-2006||0.0|0.0|Yes||polydactyly, neural tube, mesenchyme, cranial, morphogenesis|Yes| 5303.0|B6.Myd88 Rag KO|C57BL/6-Myd88 Rag1||Recessive|myeloid differentiation primary response gene 88|Myd88|Nil||MGI:108005|targeted mutation 1, Shizuo Akira|Myd88|MGI:2385681|9||||||||||||||||Yes|||||||||||||Deficient in mature B cells||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|05-Nov-2010||0.0|0.0|Unknown||T cell, Natural Killer, IL-18, IL-1 receptor, interferon, B cell|Yes| 5303.0|B6.Myd88 Rag KO|C57BL/6-Myd88 Rag1||Recessive|recombination activating gene 1|Rag1|Nil|Rag-1|MGI:97848|recombination activating gene 1; targeted mutation 1, Peter Mombaerts|Rag1|MGI:1857241|2||||||||||||||||No|||||||||||||Deficient in mature B cells||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|05-Nov-2010||||Unknown||T cell, Natural Killer, IL-18, IL-1 receptor, interferon, B cell|Yes| 5306.0||C57BL/6-Mrc1||Recessive|mannose receptor, C type 1|Mrc1|Nil|CD206, MR|MGI:97142|mannose receptor, C type 1; targeted mutation 1, Michel C Nussenzweig|Mrc1|MGI:2448258|2||||||||||||||||No|||||||||||||Defective macrophage function.MR-/- mice were defective in clearing proteins bearing accessible mannose and N-acetylglucosamine residues and had elevated levels of eight different lysosomal hydrolases.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|05-Nov-2010||0.0|0.0|Unknown||glycoprotein, mannose|Possibly| 7021.0|SphK1 Tg|C57BL/6-Tg(CAG-Sphk1)/MarpApb||Dominant||||||||||||||||||||||||||Sphingosine kinase 1a|chicken beta-actin promoter, CAG|Moderate - High||||||||||Normal|Normal|C57BL/6|No|Yes|Yes|No|Yes|Yes|No|Excellent|more than 9 times||WT (-/-) x Het (+/-)|No|19-Jul-2012|Cryopreserved sperm|40.0|0.0|No||Ceramide, Insulin resistance|Possibly| 7597.0||SJL/ASAM||Dominant|unknown|unknown|Reduced||||||Unknown|||||||||||||||||||||||||||||Unknown|The mice displays a growth retardation phenotype without other gross abrnomalities. The mice are viable and fertile.|SJL/J|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Good|8|||No|18-Feb-2014|Cryopreserved sperm|103.0|0.0|Unknown||growth retardation, ENU|Yes| 4869.0|B6.HTF1.Tg|C57BL/6-Tg(H2-K-huFUT1)1/Apb||Dominant||||||||||||||||||||||||||human fucosyltransferase 1|H2-K|All blood/tissue samples express human fucosyltransferase 1||||||||||Attempts to breed homozygous animals failed. Unknown if homozygous transgene expression is embryonic lethal.|All blood/tissue samples express human fucosyltransferase.Develop colitis from 6 weeks of age, skin disease from around 12 weeks of age, highly susceptible to infections such as MHV.|C57BL/6|No|No|Yes|No|No|Yes|No|Unknown||||No|28-Sep-2009|Cryopreserved sperm|90.0|0.0|Unknown||glycosylation, xenotransplantation, transplantation, transferase, lectins, H transferase, antibody|Yes| 5526.0|Klf8-LoxP|B6;129-Klf8||X-linked|Kruppel-like factor 8|Klf8||BKLF3, ZNF74|MGI:2442430||||X||||||||||||||||Yes|||||||||||||Normal|Normal|C57BL/6-129SV/J|Yes|Unknown|Yes|Yes|Yes|Yes|No|Unknown||||No|21-Jun-2011|Cryopreserved sperm|50.0|0.0|No|||Possibly| 5713.0|CYP 26 KO ||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5715.0|CYPC2||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6884.0|AKB ; Alb-Kb|STOCK-Tg(Alb-H2-K)||Dominant||||||||||||||||||||||||||mouse H2-K (MHC class I)|Mouse albumin promoter|similar to wild type H2-K expression||||||||||Normal|Normal|B10.BR|Yes|Yes|Yes|Yes|Yes|Yes|No|Excellent|more than 10|||No|02-May-2012||0.0|0.0|No||tolerance, liver, CD8 T cells, MHC class I, autoimmunity|Possibly| 7023.0|Ndfip1-Tg|B6;CBA-Tg(CAG-Ndfip1/tdTomato)/Apb||Dominant||||||||||||||||||||||||||Nedd4 family interacting protein 1|chicken beta actin (CAG)|Low||||||||||Unknown|Unknown|B6/CBA F1|No|Unknown|Unknown|No|Unknown|Unknown|No|Unknown|none|||No|19-Jul-2012||0.0|0.0|Unknown|||No| 3581.0||NOD.Cg-Prkdc IL2rg||Recessive|interleukin 2 receptor, gamma chain|Il2rg|Nil|[g]c, CD132, common cytokine receptor gamma chain, common gamma chain, gamma C receptor, gamma(c)|MGI:96551||||X||||||||||||||||Yes|||||||||||||Mutant mice are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Histological examination of lymphoid tissues reveals absence of lymphoid cells and some cystic structures in the thymus, an absence of follicles in the spleen and markedly diminished celluarity of lymph nodes. Double mutants are deficient in mature lymphocytes, serum Ig is not detectable and natural killer (NK) cell cytotoxic activity is extremely low. These mice are resistant to lymphoma development even after sublethal irradiation treatment. These mice have been shown to readily support engraftment of human CD34+ hematopoietic stem cells and represent a superior, long-lived model suitable for studies employing xenotransplantation strategies. Hemizygous males display: • immune system, other dysmorphology: • thymus: small, hypoplastic, cortex reduced in size, ndistinct corticomedullary junction • peripheral lymph nodes absent • mesenteric lymph node: small, contained few lymphoid follicles, contained few lymphocytes, contained no germinal centers, gut-associated lymph tissue absent in small and large intestine • spleens at 3 weeks: modestly decreased size, severe lymphocyte hypoplasia evident in white pulp, B cell and marginal zones absent • spleens at 4 to 9 weeks: increase in splenic lymphocytes, splenomegaly, dendritic epidermal T cells absent, gamma-delta-positive intestinal intraepithelial lymphocytes absent, immune system, lymphoid development/T lymphocyte defects: • thymic T cells showed: reduction in absolute numbers, increase in ratio of CD4+ to CD8+ single-positive cells, increased percentage of CD4+ single-positivecells • splenic T cells at 3 weeks showed: increase in ratio of CD4+ to CD8+ single-positive cells, decreased percentage of CD8+ single-positive cells, marked increase in CD4 to CD8 ratio at 4 to 9 weeks, NK cells absent • immune system, lymphoid development/B lymphoid defects: overall decrease in B cell numbers, nearly absent in bone marrow, markedly reduced in spleen, decreased concentrations of immunoglobulins in mice greater than 5 weeks of age • digestive system, dysmorphology: inflammation of the cecum and colitis|Heterozygous females display: • no obvious phenotype, no defect detected|NOD|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|04-Aug-2008||0.0|0.0|Unknown||IL-2, T cell, lymph node, germinal centre, Natural Killer cell (NK)|Yes| 6882.0|CKB|STOCK-Tg(Crp-H2-K)/Apb||Dominant||||||||||||||||||||||||||mouse H2-K (MHC class I)|C-reactive protein promoter|low in the absence of inflammation, induced upon inflammation||||||||||Normal|Normal|B10.BR|Yes|Yes|Yes|Yes|Yes|Yes|No|Excellent|more than 10|||No|02-May-2012|Cryopreserved sperm|50.0|0.0|No||tolerance, liver, CD8 T cells, MHC class I, autoimmunity|Yes| 5541.0|ENU18Ch:065a|C57BL/6JAnu-Fcer2a/AnuApb|C57BL/6JAnu-Fcer2a/AnuApb|Dominant|Fc receptor, IgE, low affinity II, alpha polypeptide|Fcer2a |Reduced|CD23, FC epsilon RII, Fce2, low-affinity IgE receptor, Ly-42 |MGI:95497|Fc receptor, IgE, low affinity II, alpha polypeptide; mutation 1, The Australian National University|Fcer2a|MGI:5563468|8|ENSMUSG00000005540|ENSMUST00000005678|fcer2a-201|54|226|C to A|ENSMUSE00000484893|3|18|Cysteine to STOP|||||TACTGGGAACCTCCTAGAAAGCGTTGCTGCTGTGCAAGACGTGGGACACAGCTCATGTTGG||||||||||||||Reduced CD23 protein expression on B cells in peripheral blood. |Reduced CD23 protein expression on B cells in peripheral blood. |C57BL/6JAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|6|4|Sib x sib|No|18-Jul-2011|Cryopreserved sperm|62.0|0.0|Unknown||B cell, lymphocyte, ENU|Yes| 6741.0|Cassie Klf3|Cassie Klf3/Ausb||||Klf3||||||||||||||||||||||||||||||||||||Homozygous females are less fertile; some die between 4 and 6 month of age.||FVBn|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|02-Dec-2011||0.0|0.0|Unknown|||Possibly| 5580.0|APN 170|C57BL/6N-Tnfsf12/Marp||Dominant|tumor necrosis factor (ligand) superfamily, member 12|Tnfsf12|Unknown|APO3L, DR3L, Tweak |MGI:1196259|tumor necrosis factor (ligand) superfamily, member 12; targeted mutation 1, Velocigene|Tnfsf12|MGI:4415424|11|||||||||||||||||||||||||||||Unknown|Normal|C57BL/6N|Unknown|Unknown|Unknown|Unknown|Unknown|Yes|No|Unknown||||No|08-Sep-2011|Cryopreserved sperm|50.0|0.0|Unknown|||Possibly| 6744.0|LN-KIf3KIf8FV|Laura KIf3KIf8-GT-FVB/N/Ausb||||Klf3,Klf8||||||||||||||||||||||||||||||||||||Homozygous lethal||FVBn|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|02-Dec-2011||0.0|0.0|Unknown|||Possibly| 9315.0|Muscle mouse|C57BL/6.hcm||Recessive|Unknown||Unknown||||||Unknown|||||||||||||||||||||||||||||Spontaneous mutation arising in a C57BL/6 mouse colony that results in hypertrophic centronuclear myopathy and increased gross muscularity|unknown|C57Bl/6J|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||4|brother-sister mating or first cousin mating|No|07-Dec-2021|Cryopreserved sperm|40.0|0.0|Yes|Muscle development disorders|hypertrophic centronuclear myopathy, muscle development, muscular dystrophy|Possibly| 7301.0|CPEB|SJL-CPEB1/Apb||Dominant|cytoplasmic polyadenylation element binding protein 1|Cpeb1|Unknown||MGI:108442||||7|ENSMUSG00000025586|ENSMUST00000098331|Cpeb1-001||||||||||||||||||||||||||The homozygous females displays an infertility phenotype associated with a dysmorphology of the internal reproductive organs (uterus and ovaries)|The phenotype is normal|SJL/J|Yes|No|Yes|Yes|Yes|Yes|No|Poor||||No|03-Apr-2013|Cryopreserved sperm|50.0|0.0|No||Fertility, ovaries, ENU|Yes| 5716.0|D SOX||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5717.0|D-Cre||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 231.0|Zp3-Cre|C57BL/6-Tg(Zp3-cre)93Knw||Recessive||||||||||||||||||||||||||transgene insertion 93, Barbara B Knowles|mouse zona pellucida 3 (Zp3) promoter|female germ line||||||||||Normal||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|25-Apr-2006||0.0|0.0|Unknown||zona pellucida, oocyte, expression|Yes| 232.0|CMV-Cre|STOCK Tg(CMV-cre)1Cgn||Dominant||||||||||||||||||||||||||transgene insertion 1, University of Cologne|human cytomegalovirus (CMV) promoter|||||||||||Normal|||Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|25-Apr-2006||0.0|0.0|Unknown||Cre, cytomegalovirus, CMV, deleter|Yes| 6745.0|KIf3-Cherry|KIf3m-Cherry/Ausb||||Klf3||||||||||||||||||||||||||||||||||||KO generally mild but appear less healthy than WT littermates.KO are smaller than WT littermates.KO lifespan suspected to be reduced.||C57BL6/129SV/J|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|02-Dec-2011||0.0|0.0|Unknown|||Possibly| 6746.0|KIf8-129GT|KIf8-129GT/Ausb||||Klf8||||||||||||||||||||||||||||||||||||Mild.||129|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|02-Dec-2011||0.0|0.0|Unknown|||Possibly| 230.0|Meox2-Cre|B6.129-Meox2||Recessive|mesenchyme homeobox 2|Meox2|Unknown|Gax, Mox-2, Mox2|MGI:103219|targeted mutation 1, Philippe Soriano|Meox2|MGI:2176174|12||||||||||||||||Yes|||||||||||||Normal|Normal||Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|25-Apr-2006||0.0|0.0|Unknown||epiblast, Cre, embryonic|Yes| 6192.0|CDKN1A (p21ko)|B6;129S2-Cdkn1a||Recessive|cyclin-dependent kinase inhibitor 1A (P21)|Cdkn1a|Nil|CAP20, CDKI, Cdkn1, CIP1, mda6, P21, p21, p21Cip1, p21WAF, SDI1, Waf1 |MGI:104556|cyclin-dependent kinase inhibitor 1A (P21); targeted mutation 1, Tyler Jacks |Cdkn1a|MGI:1933751|17|||||||||||||||||||||||||||||Decreased monocyte cell number:*Circulating inflammatory monocytes are reduced compared to in wild-type mice.Impaired macrophage recruitment:*In a serum transfer model of inflammatory arthritis, fewer macrophages are recruited to the site of inflammation compared to in similarly treated wild-type mice.*Following intraperitoneal thioglycollate injection, fewer macrophages are recruited into the peritoneum compared to in similarly treated wild-type mice.*However, in vitro migration of bone marrow derived macrophages is normal in response to several chemoattractants.Decreased susceptibility to induced arthritis:*In a serum transfer model of inflammatory arthritis, mice exhibit no inflammation, lower histological scores, and reduced macrophage infiltration compared with similarly treated wild-type mice.*However, adoptive transfer of wild-type bone marrow restores susceptibility to induced arthritis.Hearing/vestibular/ear phenotype:*Contrary to expectation, homozygotes display a normal inner ear morphology relative to wild-type mice.*At E16.5, E18.5, P2 and 2 months of age, no significant differences in the cytoarchitecture of vestibular and auditory sensory epithelia or aberrant mitoses in developing hair cells are observed.Abnormal bone marrow cell morphology/development:*Fewer monocyte precursors are found within the bone marrow compared to in wild-type mice.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown||p21, proliferating-cell nuclear antigen (PCNA), p53|Yes| 6586.0|MMP13KO BALB/c|C.FVB(Cg)-Mmp13/Apb||Recessive|matrix metallopeptidase 13|MMP13|Nil|Clg, collagenase-1, Collagenase-3, interstitial collagenase, MMP-13, Mmp1|MGI:1340026|matrix metallopeptidase 13; targeted mutation 1.1, Zena Werb|Mmp13|MGI:3521938|9|||||||||||||||||||||||||||||Increased width of hypertrophic chondrocyte zone: * the hypertrophic zone is expanded in the tibia and metatarsals, at E17 and 1 week after birth, respectively, however by 12 weeks of age the size of the hypertrophic zone is similar to wild-type. * chondrocytes proliferate and differentiate normally but accumulate in the most terminally differentiated hypertrophic state. * establishment of the primary ossification centers is normal.Abnormal cancellous bone morphology: * the amount of trabecular bone is increased in the tibia and metatarsals by 3 weeks or 1 week of age, respectively, however by 1 year of age the amount of trabecular bone was similar to wild-type. * the organization of the trabecular bone is also irregular.OA was surgically induced in the knees of MMP-13-knockout mice. No difference between wildtype and KO mice for aggrecan loss or cartilage erosion at 4 weeks. here was less tibial cartilage erosion in knockout mice than in wild-type mice at 8 weeks. Cartilaginous osteophytes were larger in knockout mice at 4 weeks, but by 8 weeks osteophyte maturity and size were no different from those in wild-type mice. Articular chondrocyte hypertrophy with positive type X collagen and DIPEN staining occurred in both wild-type and knockout mouse joints. Authors conclude Chondrocyte hypertrophy is not regulated by MMP-13 activity in this model and does not in itself lead to cartilage erosion. MMP-13 deficiency can inhibit cartilage erosion in the presence of aggrecan depletion, supporting the potential for therapeutic intervention in established OA with MMP-13 inhibitors.||BALB/c|Yes|Yes|Yes|Yes|Yes|Yes|No|Poor|10||Het x Het|No|22-Sep-2011|Cryopreserved sperm|80.0|0.0|Yes|spondyloepimetaphyseal dysplasia|extracellular matrix, collagenase, chondrocyte, osteoblast, growth plate|Possibly| 5659.0|Caggsbow (Rainbow)||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 3935.0|RRF|BALB/c-Gt(ROSA)26Sor/AnuApb||Dominant|gene trap ROSA 26, Philippe Soriano|Gt(ROSA)26Sor||beta geo, Gtrgeo26, Gtrosa26, R26, ROSA26|MGI:104735|gene trap ROSA 26, Philippe Soriano; targeted mutation 1, Hugh D Campbell|Gt(ROSA)26Sor|MGI:4939369|6|||||||||||||||||||||||||||||Normal|Normal.No analysis performed|BALB/c|Yes|Yes|Yes|Yes|Yes|Yes|No|Excellent|4||Hom x Hom|No|16-Oct-2008|Cryopreserved sperm|80.0|0.0|Unknown||ROSA, flightless, wound healing|Yes| 8631.0|TLR9 ApoE double knock out mice|C57BL/6-Apoe Tlr9||Recessive|apolipoprotein E|Apoe|Nil||MGI:88057|apolipoprotein E; targeted mutation 1, University of North Carolina|Apoe|MGI:1857129|7|||||||||||||||||||||||||||||Genetic deletion of the innate immune receptor TLR9 exacerbated atherosclerosis in ApoE−/− mice fed a high-fat diet. CD4+ T cells were identified as potential mediators of this effect.|Normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|19-Dec-2018|Cryopreserved sperm|40.0|0.0|Unknown||Atherosclerosis, Plaque, low-density-lipoprotein cholesterol|Yes| 8631.0|TLR9 ApoE double knock out mice|C57BL/6-Apoe Tlr9||Recessive|toll-like receptor 9|Tlr9|Nil||MGI:1932389|toll-like receptor 9; targeted mutation 1, Shizuo Akira|Tlr9|MGI:2660562|9|||||||||||||||||||||||||||||Genetic deletion of the innate immune receptor TLR9 exacerbated atherosclerosis in ApoE−/− mice fed a high-fat diet. CD4+ T cells were identified as potential mediators of this effect.|Normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|19-Dec-2018|Cryopreserved sperm|||Unknown||Atherosclerosis, Plaque, low-density-lipoprotein cholesterol|Yes| 8634.0||Fut 7 KO Line 1||Semi-dominant|Fut 7 |Fut 7|||||||Unknown|||||||||||||||||||||||||||||Normal|Normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|15-Jan-2019||0.0|0.0|Unknown|||Yes| 6591.0|TRPC1|B6;129S-Trpc1/Dfat||Recessive|transient receptor potential cation channel, subfamily C, member 1|Trpc1|Nil|Mtrp1, Trp1, Trrp1|MGI:109528|transient receptor potential cation channel, subfamily C, member 1; targeted mutation 1, Lutz Birnbaumer|Trpc1|MGI:3764882|9|||||||||||||||||||||||||||||Normal||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|29-Sep-2011||0.0|0.0|Unknown||Ca channel, motor, salivary|Yes| 1228.0|T-Bird|C57BL/6JAnu-Dsg4/AnuApb|C57BL/6JAnu-Dsg4/AnuApb|Recessive|desmoglein 4|Dsg4|Unknown|CDHF13, lah|MGI:2661061|T-Bird|Dsg4|MGI:5007752|18|ENSMUSG00000001804|ENSMUST00000019426|Dsg4-001|643|777|A to C|ENSMUSE00000445469|6|215|Threonine to Proline|||||GTGCACCCATGTTCATGGTGAACAGGTACACTGGAGAAGTCCGCACGATGTCCAATTTCCT|No|||||||||||||Greasy Coat. Affected mice develop a dull, sparse and greasy coat at about ~40 days of age. ||C57BL/6 x C57BL10|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|5|||No|15-Jun-2007|Cryopreserved sperm|27.0|0.0|Unknown||Coat, greasy, hair, ENU|Yes| 1549.0||BALB/c-Tg(iFABPp-IL9)/AnuApb||Recessive||||||||||||||||||||||||||interleukin 9|rat intestinal fatty acid binding protein (nucleotides -1178 - +28) - iFABP , i-FABP linked to nucleotides 3–2,150 of the human growth hormone (hGH) gene (except for its 5' regulatory sequences). |High||||||||||Restricted expression of IL9 transgene to intestine - duodenum and proximal jejunum.||BALB/c|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|06-Jul-2007|Cryopreserved sperm|103.0|0.0|Unknown||intestine, interleukin, mast cell, anaphylaxis, mastocytosis, allergy|Yes| 5183.0|Ggn knockout clone 16|B6.129-Ggn/16MarpApb||Recessive|gametogenetin|Ggn|Unknown|GGN1, GGN2, GGN3|MGI:2181461|gametogenetin; targeted mutation 1, Duangporn Jamsai|Ggn|MGI:5503309|7||||||||||||||||Yes|||||||||||||Embryonic Lethal|Appear normal.Abnormal double-strand DNA break repair:• increased unrepaired double-strand breaks in pachytene spermatocytes|C57BL/6J x129Sv|No|No|Yes|No|No|Unknown|No|Unknown||||No|23-Jul-2010|Cryopreserved sperm|50.0|0.0|Unknown||Sperm, testis, embryonic lethal, DNA repair|Possibly| 8632.0|Dmp1Cre.Efnb2|B6.Cg-Efnb2 Tg(Dmp1-cre)1Jqfe||Recessive|ephrin B2|Efnb2||ELF-2, Epl5, Eplg5, Htk-L, Lerk5, LERK-5, NLERK-1|MGI:105097|ephrin B2; targeted mutation 2, David J Anderson|Efnb2|MGI:2176538|8|||||||||||||||||transgene insertion 1, Jian Q Feng|Dmp1|odontoblast-specific||||||||||Normal bone shape and cortical width with a low bone material strength due to hypermineralization|Unknown|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|20-Dec-2018|Cryopreserved sperm|48.0|0.0|Unknown||homeostasis, osteoblasts, EphB4|Yes| 6838.0|APN 228|C57Bl/6N-mir-196a-2/MarpApb||Recessive|microRNA 196a-2 |Mir196a-2 |Unknown|mir 196a-2, Mirn196a-2, mmu-mir-196a-2|MGI:3618739||||15|||||||||||||||||||||||||||||Unknown|Normal|C57Bl/6N|Unknown|Unknown|Unknown|Unknown|Unknown|Yes|No|Unknown||||No|07-Mar-2012|Cryopreserved sperm|50.0|0.0|Unknown|||Possibly| 6886.0|APN174|C57Bl/6N-Map3k5/MarpApb||Recessive|mitogen-activated protein kinase kinase kinase 5|Map3k5|Unknown|7420452D20Rik, ASK, ASK1, Mekk5|MGI:1346876|mitogen-activated protein kinase kinase kinase 5; targeted mutation 1a, Helmholtz Zentrum Muenchen GmbH |Map3k5|MGI:4434801|10|||||||||||||||||||||||||||||Unknown|Normal|C57Bl/6N|Unknown|Unknown|Unknown|Unknown|Unknown|Yes|No|Good||||No|03-May-2012|Cryopreserved sperm|50.0|0.0|Unknown|||Possibly| 10375.0||ENU43:055::B6||Semi-dominant|01-87620512-IGL3903 (Inpp5d)|||||Inpp5d:m1Anu|||Unknown|||||||||||||||||||||||||||||Unknown|Unknown|C57Bl/6N|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|14-Nov-2023|Cryopreserved sperm|57.0|0.0|Unknown|||No| 4989.0|IL-4 -/-|B6.129-Il4||Recessive|interleukin 4|Il4|Unknown|Il-4|MGI:96556|interleukin 4; targeted mutation 1, Manfred Kopf|Il4|MGI:2176268|11|||||||||||||||||||||||||||||Decreased IgE level: unlike in wild-type mice, IgE levels are undetectable prior to and following immunization.Decreased IgG1 level:* IgG1 levels are reduced 20-fold compared to in wild-type mice and following immunization IgG1 levels are 12-fold lower than in immunized wild-type mice.* following immunization with DNP-ovalbumin, IgG1 antibodies are 10-fold lower than in wild-type mice.Increased IgG level:* following infection with N. brasiliensis, IgG2 and IgG3 levels are slightly higher than in wild-type mice.* following immunization with DNP-ovalbumin, IgG2 and IgG3 levels are 100- to 500-fold higher than in wild-type mice.Decreased interleukin-10 secretion: stimulated CD4+ T cells in vitro fail to produce IL-10.Decreased interleukin-3 secretion: in stimulated CD4+ T cells, the production of IL-3 is reduced more than 70% of wild-type value.Decreased interleukin-4 secretion: stimulated CD4+ T cells in vitro fail to produce IL-4.Decreased interleukin-5 secretion: stimulated CD4+ T cells in vitro fail to produce IL-5.Abnormal response to infection: * following infection with N. brasiliensis, CD4+ T cells produce reduced levels of Th2 cytokines, increased levels of interferon-gamma, and reduced blood eosinophilia levels compared to infected wild-type mice.* however, CD8+ T cells do produce IL-5 following infection with N. brasiliensis.||C57BL/6 x 129|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|28-Jan-2010|Cryopreserved sperm|39.0|0.0|Unknown||T cell, infection, asthma, hyperresponsiveness, eosinophil, IFN, IL2|Yes| 6413.0|ACC2Δ|C57BL/6-Acacb/Ausb||Recessive|acetyl-Coenzyme A carboxylase beta|Acacb|Nil|Acc2, Accb|MGI:2140940|acetyl-Coenzyme A carboxylase beta; targeted mutation 1, David James|Acacb|MGI:4430244|5|||||||||||||||||||||||||||||Mice are leaner and smaller than wildtype siblings.Abnormal fatty acid oxidation:*Increase in fatty acid oxidation in isolated soleus muscle.*Increase in whole-body fatty-acid oxidation in the dark cycle.Abnormal aerobic energy metabolism:*Decrease in malonyl-CoA levels in skeletal and cardiac muscle.Growth/size phenotype:*Despite changes in fatty acid oxidation, no changes in body weight or responses to a high fat diet are detected.Homeostasis/metabolism phenotype:*Despite changes in fatty acid oxidation, no change in energy expenditure is detected. Abnormal glucose homeostasis: *Utilization of glucose for lipid synthesis is increased. Increased skeletal muscle glycogen level: *Muscle glycogen stores are elevated.Abnormal lipid homeostasis:*Utilization of glucose for lipid synthesis is increased.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown||AMPK, ACC2, Adiposity|Yes| 6608.0|BXD-75|BXD75/RwwJArc||Recessive||||||||||||||||||||||||||||||||||||||Normal|Normal|C57BL/6J x DBA/2|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|||brother x sister|No|04-Oct-2011|Embryo|0.0|0.0|Unknown|||Possibly| 4964.0|Ptch1|B6.129-Ptch1/Apb||Recessive|patched homolog 1|Ptch1|Normal|Patched 1, Ptc, Ptc1|MGI:105373|patched homolog 1; targeted mutation 1, Brandon J Wainwright|Ptch1|MGI:2675356|13|||||||||||||||||||||||||||||Normal|Normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Excellent|12|||No|15-Jan-2010|Cryopreserved sperm|93.0|0.0|Unknown||BCC, neuroblastoma, hedgehog signalling, stem cell|Possibly| 5660.0|CamK||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6605.0|BXD-51|BXD51/RwwJArc||Recessive||||||||||||||||||||||||||||||||||||||Normal|Normal|C57BL/6J x DBA/2|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|||brother x sister|No|04-Oct-2011|Embryo|0.0|0.0|Unknown|||Possibly| 6609.0|BXD-96|BXD96/RwwJArc||Recessive||||||||||||||||||||||||||||||||||||||Normal|Normal|C57BL/6J x DBA/2|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|||brother x sister|No|04-Oct-2011|Embryo|0.0|0.0|Unknown|||Possibly| 7592.0||SJL/ASAM||Dominant|unknown|unknown|Reduced||||||Unknown|||||||||||||||||||||||||||||Unknown|The mice displays an harmonious growth retardation phenotype without other gross abrnomalities. The mice are viable and fertile.|SJL/J|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Good|5|||No|18-Feb-2014|Cryopreserved sperm|50.0|0.0|Unknown||growth retardation, ENU|Yes| 6604.0|BXD-48|BXD48/RwwJArc||Recessive||||||||||||||||||||||||||||||||||||||Normal|Normal|C57BL/6J x DBA/2|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|||brother x sister|No|04-Oct-2011|Embryo|0.0|0.0|Unknown|||Possibly| 6756.0|TRPC3KO|129S/SvEv-Trpc3/Ausb||Recessive|transient receptor potential cation channel, subfamily C, member 3 |Trpc3|Nil|Trcp3, Trp3, Trrp3 |MGI:109526|transient receptor potential cation channel, subfamily C, member 3; targeted mutation 1.1, Arthur Konnerth|Trpc3|MGI:3810122|3|||||||||||||||||||||||||||||Abnormal eye physiology:*Intrinsically photosensitive retinal ganglion cells exhibit decreased firing frequency at most light intensities compared with wild-type cells.*However, sensitivity is normal.||SVEV|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|02-Dec-2011||0.0|0.0|Unknown||Trpc3, metabotropic glutamate receptors (mGluRs), Purkinje cells, Synaptic transmission, Motor coordination|Yes| 10376.0|CTNSCGins|C57BL/6NCrl/Anu-CTNSem1/Apb||Dominant|cystinosis, nephropathic|CTNS|Unknown||MGI:1932872||||11|ENSMUSG00000005949||||751|ACCA to gt||8||Unknown to Unknown|||||||||||||||||||unknown|normal|C57Bl/6N|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Good||||No|15-Nov-2023|Cryopreserved sperm|22.0|0.0|Unknown|||Possibly| 7593.0||SJL/ASAM||Dominant|unknown|unknown|Reduced||||||Unknown|||||||||||||||||||||||||||||Unknown|The mice displays a growth retardation phenotype without other gross abrnomalities. The mice are viable and fertile.|SJL/J|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Good|8|||No|18-Feb-2014|Cryopreserved sperm|83.0|0.0|Unknown||growth retardation, ENU|Yes| 7391.0|B6.pIgR-/-|C57BL/6-Pigr/Apb||Recessive|polymeric immunoglobulin receptor|Pigr|Nil||MGI:103080|polymeric immunoglobulin receptor; targeted mutation 1, Richard A Strugnell|Pigr|MGI:2651659|1|||||||||||||||||||||||||||||These mice are unable to secrete IgA and IgM into the secretions. This results in 50-100 fold increased levels of IgA in blood, and very low to undetectable levels of IgA in faecal samples.|normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Excellent||||Yes|06-Aug-2013|Cryopreserved sperm|50.0|0.0|No||polymeric immunoglobulin receptor, IgA, SIgA, mucosal immunology|No| 6755.0|P2X2KO|B6.129-P2rx2/J/Ausb||Recessive|purinergic receptor P2X, ligand-gated ion channel, 2 |P2rx2|Nil|P2x2, P2X2a |MGI:2665170|purinergic receptor P2X, ligand-gated ion channel, 2; targeted mutation 1, Debra A Cockayne |P2rx2|MGI:2687349|5|||||||||||||||||||||||||||||Decreased pulmonary ventilation:*In response to hypoxia (10% O2), adult homozygotes (4-6 months of age) display a significantly reduced ventilatory response showing an increase of only 261 +/- 202 ml/min/kg in minute ventilation (VE) relative to 1008 +/- 154 ml/min/kg in wild-type controls.*In response to further hypoxia (7.5% O2), homozygotes display a severe ventilatory depression with the VE reduced below prehypoxic levels by 606 +/- 209 ml/min/kg, unlike wild-type controls where no additional increase in ventilation is observed but the VE remains above normoxic levels.*However, adult homozygotes display normal resting ventilation during normoxia and show normal ventilatory responses to a mild (15% O2) hypoxia relative to wild-type controls.Abnormal carotid body physiology:*Homozygotes show a dramatic reduction in afferent nerve responses of the carotid sinus nerve to a decrease in oxygen tension (PO2).*Unlike in in vitro carotid body-sinus nerve preparations from wild-type mice where sinus nerve discharge increases from baseline to a peak of 130.82 +/- 10.79 spikes/sec during hypoxia, the afferent discharge in preparations from mutant mice only reaches a peak of 58.13 +/- 9.40 spikes/sec, indicating that carotid body function is impaired.*The average peak firing rate of single units induced by hypoxia is significantly lower in carotid body-sinus nerve preparations from mutant mice (1.64 +/- 0.11 spikes/sec) relative to that observed in wild-type preparations (7.96 +/- 0.88 spikes/sec).Homeostasis/metabolism phenotype:*In response to hypoxia (7.5% O2), adult homozygotes display normal decreases in body temperature relative to wild-type controls (0.9 +/- 0.2 vs 0.8 +/- 0.1 degress Celsius, respectively).||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|02-Dec-2011||0.0|0.0|Unknown||Interneuron, ATP modulation|Yes| 6885.0|ARNEZ 2 MTf Tg #2|B6.129-Tg(UBC-Mfi2)43Drrn/Apb||Dominant||||||||||||||||||||||||||murin melanotransferrin|human unbiquitin c|ubiquitous||||||||||Normal.Mild but significant decrease of erythrocyte number in both male and female MTf Tg mice compared to the wildtype counterparts|Normal.Mild but significant decrease of erythrocyte number in both male and female MTf Tg mice compared to the wildtype counterparts|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|03-May-2012|Cryopreserved sperm|50.0|0.0|Unknown||melanoma, melanotransferrin, iron, erythrocyte, p97, ARNEZ , ARNEZ 2, MTf Tg|Yes| 6888.0|APN157|C57Bl/6N-Tgm5/MarpApb||Recessive|transglutaminase 5|Tgm5|Unknown|2310007C07Rik, TGx |MGI:1921426 |transglutaminase 5; targeted mutation 2a, Wellcome Trust Sanger Institute|Tgm5 |MGI:4451573|2|||||||||||||||||||||||||||||Unknown|Normal|C57Bl/6N|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Good||||No|03-May-2012|Cryopreserved sperm|50.0|0.0|Unknown|||Possibly| 8636.0|Swiss:Green|Swiss Webster Outbred:Green||Dominant||||||||||||||||||||||||||||||||||||||Normal.High fecundity, excellent mothers, ideal for recipients.||Swiss Webster|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|15-Jan-2019||0.0|35.0|Unknown||Swiss|Yes| 6757.0|PeripherinΔ|B6.129-Prph/Ausb||Recessive|peripherin|Prph|Nil|Prph1 |MGI:97774|peripherin; targeted mutation 1, Jean-Pierre Julien |Prph|MGI:2180052|15|||||||||||||||||||||||||||||Nervous system phenotype:*Overall axonal structure was normal.*Overall, number and caliber of large myelinated axons from spinal motor neurons was normal.*Retinal ganglion cells morphologically similar to control mice. Abnormal axon morphology: *Reduced numbers of unmyelinated sensory axons. Abnormal sensory neuron morphology: *Reduced numbers of unmyelinated sensory axons.||129/C57BL6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|02-Dec-2011|Embryo|0.0|0.0|Unknown||Peripherin, Intermediate filament, Unmyelinated sensory axons|Yes| 6750.0|CD11cDTR|B6.Cg-Tg(Itgax-DTR/EGFP)57Lan/Ausb||Semi-dominant||||||||||||||||||||||||||transgene insertion 57, Richard A Lang|mouse Itgax promoter (CD11c)|||||||||||||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|02-Dec-2011||0.0|0.0|Unknown||Cytotoxic T lymphocytes (CTL) , Dentritic cells|Yes| 6892.0|Gp130/IL10) (ME-263)|B6-Il6st Il10/LudApb||Dominant|interleukin 6 signal transducer|Il6st|Unknown|5133400A03Rik, CD130, D13Ertd699e, gp130|MGI:96560|interleukin 6 signal transducer; targeted mutation 1, Matthias Ernst |Il6st|MGI:2388478|13|||||||||||||||||||||||||||||Homozygous mice do not breed when mated together.gp130 mice develop gastric polyps.|Unknown|C57BL/6|Yes|No|Unknown|Yes|No|Unknown|No|Unknown||||No|10-May-2012|Cryopreserved sperm|49.0|0.0|Unknown||il10, il6st, signal transduction, infection|Possibly| 6892.0|Gp130/IL10) (ME-263)|B6-Il6st Il10/LudApb||Dominant|interleukin 10|Il10||cytokine synthesis inhibitory factor, IL-10|MGI:96537|interleukin 10; targeted mutation 1, University of Cologne|Il10|MGI:1857199|1|||||||||||||||||||||||||||||Homozygous mice do not breed when mated together.gp130 mice develop gastric polyps.|Unknown|C57BL/6|Yes|No|Unknown|Yes|No|Unknown|No|Unknown||||No|10-May-2012|Cryopreserved sperm|||Unknown||il10, il6st, signal transduction, infection|Possibly| 6889.0|APN218|C57Bl/6N-mir-196b/MarpApb||Recessive|microRNA 196b|Mir196b |Unknown|mir 196b, Mirn196b, mmu-mir-196b |MGI:3618741 ||Mir196b ||6|||||||||||||||||||||||||||||Unknown|Normal|C57Bl/6N|Unknown|Unknown|Unknown|Unknown|Unknown|Yes|No|Good||||No|03-May-2012|Cryopreserved sperm|50.0|0.0|Unknown|||Possibly| 7111.0|APN278 (ARL SPF)|C57BL/6N-Dsg2Mu||Recessive|desmoglein 2|Dsg2 ||D18Ertd293e |MGI:1196466 |desmoglein 2; targeted mutation 1a, Wellcome Trust Sanger Institute |Dsg2tm1a(EUCOMM)Wtsi|MGI:4432319|18|||||||||||||||||||||||||||||Unknown|Normal|C57Bl/6N|Unknown|Unknown|Yes|Unknown|Unknown|Unknown|No|Unknown||||No|24-Oct-2012|Cryopreserved sperm|50.0|0.0|Unknown|||Possibly| 8639.0|Swiss:Blue|Swiss Webster Outbred:Blue||Dominant||||||||||||||||||||||||||||||||||||||Normal.High fecundity, excellent mothers, ideal for recipients.||Swiss Webster|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|15-Jan-2019||0.0|180.0|Unknown||Swiss|Yes| 8638.0|Swiss:Red|Swiss Webster Outbred:Red||Dominant||||||||||||||||||||||||||||||||||||||Normal.High fecundity, excellent mothers, ideal for recipients.||Swiss Webster|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|15-Jan-2019||0.0|0.0|Unknown||Swiss|Yes| 8637.0|Swiss:Yellow|Swiss Webster Outbred:Yellow||Dominant||||||||||||||||||||||||||||||||||||||Normal.High fecundity, excellent mothers, ideal for recipients.||Swiss Webster|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|15-Jan-2019||0.0|174.0|Unknown||Swiss|Yes| 255.0||B6,129-Csf3||Recessive|colony stimulating factor 3 (granulocyte)|Csf3|Nil|Csfg, G-CSF, MGI-IG|MGI:1339751|targeted mutation 1, Ashley R Dunn|Csf3|MGI:1857155|11||||||||||||||||Yes|||||||||||||Mutant mice were viable and fertile, with no overt signs of disease. They suffered, however, a severe neutropenia, with blood neutrophil levels in homozygotes 20 to 30% of those in normal mice, and intermediate levels in heterozygotes. Granulocyte precursor cell levels were reduced 50% in homozygotes, and the ability of these mice to resist Listeria monocytogenes infections was reduced (J:20400).|Decreased neutrophil cell number (chronic neutropenia).|C57BL/6 x 129|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|28-Apr-2006||0.0|0.0|Unknown||neutropenia, monocyte, progenitor stem cell, granulocyte|Yes| 642.0||Un.129-Atm||Recessive|ataxia telangiectasia mutated homolog (human)|Atm|Unknown|C030026E19Rik|MGI:107202|targeted mutation 1, Philip Leder|Atm|MGI:1926875|9||||||||||||||||No|||||||||||||Atm-deficient mice are retarded in growth, do not produce mature sperm, and exhibit severe defects in T cell maturation while going on to develop thymomas.Atm-deficient fibroblasts grow poorly in culture and display a high level of double-stranded chromosome breaks. Atm-deficient thymocytes undergo spontaneous apoptosis in vitro significantly more than controls.Homozygotes for null mutations may exhibit locomotor abnormalities, motor learning deficits, growth retardation, sterility due to meiotic arrest, and susceptibility to thymic lymphomas.||Unknown|Yes|Yes|Yes|Yes|No|Yes|Yes|Poor||||No|25-Apr-2007||0.0|0.0|Yes|ataxia-telangiectasia|ATM, locomotor, thymoma, sperm, T cell, ataxia-telangiectasia|Yes| 331.0||B6,129-Tgfa||Semi-dominant|transforming growth factor alpha|Tgfa|Unknown||MGI:98724|targeted mutation 1, Ashley R Dunn|Tgfa|MGI:1856577|6||||||||||||||||Yes|||||||||||||Homozygous mutants have curly vibrissae, wavy hair with misaligned hair follicles, reduced body weight, and eye defects including open eyelids at birth, corneal scarring and microphthalmia.||C57BL/6 x 129|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|05-May-2006||0.0|0.0|Unknown||Coat, hair, cornea, curly, wavy|Yes| 247.0||C57BL/10-T||Recessive|brachyury|T|Unknown|Bra, cou, Low, low ratio, Lr, me75, T1, Tl2, Tl3|MGI:98472|brachyury|T|MGI:1856184|17||||||||||||||||Yes|||||||||||||Homozygotes exhibit defects in notochord differentiation and mesoderm formation, lack a trunk and tail, and die around embryonic day 10.|Shortened tail and abnormal sacral vertebrae|C57BL/10|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|26-Apr-2006||0.0|0.0|Unknown||heart, ventricular loops, situs, embryonic|Yes| 223.0|Paf|Patchy Fur||Semi-dominant|patchy fur|Paf|Unknown||MGI:97472|patchy fur|Paf|MGI:1856622|X||||||||||||||||Yes|||||||||||||Semi-dominant causing a random loss of fur resulting in a striped or patchy coat. Hemizygous male and homozygous female show more severe hair loss than heterozygous female.||C3H|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|25-Apr-2006||0.0|0.0|Unknown||Coat, fur, Y chromosome, meiosis|Yes| 191.0|FAP -/-|C57BL/6-Fap||Recessive|fibroblast activation protein|Fap|Nil||MGI:109608|targeted mutation 1, Andreas Schnapp|Fap|MGI:2386791|2||||||||||||||||No|||||||||||||None detected. No change in cancer susceptibility||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|17-Apr-2006||0.0|0.0|Unknown||Knockout, fibroblast|Yes| 8640.0|Swiss:Orange|Swiss Webster Outbred:Orange||Dominant||||||||||||||||||||||||||||||||||||||Normal.High fecundity, excellent mothers, ideal for recipients.||Swiss Webster|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|15-Jan-2019||0.0|196.0|Unknown||Swiss|Yes| 10361.0|ENU:Ninj1|C57BL/6JAnu-Ninji/Anu||Dominant|ninjurin 1|Ninj1|||MGI:1196617 |Ninji: mutation 1, Australian National University|Ninji||13|ENSMUSG00000037966||||||||||||||||||||||||||||Normal|Normal|C57Bl/6N|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|20-Sep-2023|Cryopreserved sperm|56.0|0.0|Unknown|||Possibly| 229.0||ECFP||Dominant||||||||||||||||||||||||||Cyan Fluorescent Protein||||||||||||Mice that are homozygous for the transgenic insert are viable, fertile, normal in size and do not display any gross physical or behavioural abnormalities. All tissues from hemizygous animals display fluorescence in all cell types under appropriate lighting conditions. Homozygotes fluoresce with twice the intensity of the hemizygotes. Notable exceptions to this phenotype are erythrocytes and adipocytes in with fluorescence is negligible or absent. Coat colour expected from breeding: albino, agouti|||Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|25-Apr-2006||0.0|0.0|Unknown||CFP|Yes| 256.0||B6,129-Csf2||Recessive|colony stimulating factor 2 (granulocyte-macrophage)|Csf2|Nil|Csfgm, Gm-CSf, MGI-IGM|MGI:1339752|targeted mutation 1, Ashley R Dunn|Csf2|MGI:1930997|11||||||||||||||||No|||||||||||||Homozygotes for targeted null mutations exhibit lung abnormalities with lymphocytic infiltration and accumulation of surfactant lipids. Litter sizes from homozygous breeding pairs are smaller at weaning due to perinatal mortality. Appearance of lungs resembles alveolar proteinosis. Lung pathology renders these mice susceptible to opportunistic bacterial and fungal lung infection. If mice are kept in hooded boxes they should be OK for at least 10 months.||C57BL/6 x 129|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|28-Apr-2006||0.0|0.0|Unknown||growth factor, receptor, signal transduction, lung infiltrate, macrophage|Yes| 8641.0|Chloe|C57BL/6-Acan/AfosSyd||Recessive|aggrecan|Acan||Agc1, b2b183Clo, Cspg1|MGI:99602|aggrecan; targeted mutation 1, Amanda J Fosang|Acan|MGI:3577026|7|||||||||||||||||||||||||||||Normal|Normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|17-Jan-2019||0.0|0.0|Unknown||Skeletal, metalloproteinases|Yes| 7308.0|mRI61689|B6.BKS-Lepr Ank1/Apb|B6.BKS-Lepr Ank1|Dominant|ankyrin 1, erythroid|Ank1|Unknown|Ank-1, pale|MGI:88024||||8|ENSMUSG00000031543|ENSMUST00000121802|Ank1-004||||||||23106021|17|||CTTCCCTGGCTTAAAGTTGGTGCACATCTGTTTCTTTTTAGAGTGGACTCACTCCCCTCC||||||||||||||Pre and Perinatal mortality with Jaundice, enlarge spleen and fragmented red blood cells|Heterozygous mice display a microcytic anaemia with increase osmotic fragility, splenomegaly and survival advantage to Plasmodium chabaudi|B6.BKS-Lepr|No|No|Yes|No|No|Yes|No|Good||||No|09-Apr-2013|Cryopreserved sperm|45.0|0.0|Yes|Hereditary spherocytosis|Hereditary spherocytosis, microcytosis, ENU|Yes| 7308.0|mRI61689|B6.BKS-Lepr Ank1/Apb|B6.BKS-Lepr Ank1|Dominant|leptin receptor|Lepr|||MGI:104993|leptin receptor; diabetes|Lepr|MGI:1856009|4|||||||||||||||||||||||||||||Pre and Perinatal mortality with Jaundice, enlarge spleen and fragmented red blood cells|Heterozygous mice display a microcytic anaemia with increase osmotic fragility, splenomegaly and survival advantage to Plasmodium chabaudi|B6.BKS-Lepr|No|No|Yes|No|No|Yes|No|Good||||No|09-Apr-2013|Cryopreserved sperm|||Yes|Hereditary spherocytosis|Hereditary spherocytosis, microcytosis, ENU|Yes| 7598.0|Stk35KO or Clik1KO|B6.129-Stk35/MarpApb||Semi-dominant|serine/threonine kinase 35 |Stk35|Nil|1700054C12Rik, CLIK1, CLP-36 interacting kinase|MGI:1914583||||2|||||||||||||||||||||||||||||Male and female subfertility/infertility and abnormal eye development|Variable from subfertility to normal.|SV129/C57Bl6|Yes|Yes|Yes|Yes|Yes|Yes|Yes|Poor||||No|19-Feb-2014|Cryopreserved sperm|50.0|0.0|Unknown|||Possibly| 5535.0|Crash|STOCK Celsr1/MarpApb||Recessive|cadherin, EGF LAG seven-pass G-type receptor 1 (flamingo homolog, Drosophila)|Celsr1|Reduced|crash, Crsh, Scy|MGI:1100883|cadherin, EGF LAG seven-pass G-type receptor 1 (flamingo homolog, Drosophila); crash|Celsr1|MGI:2668337|15|ENSMUSG00000016028|ENSMUST00000016172|Celsr1-201|3119|3126|A to G|ENSMUSE00001038472|1|1040|Aspartic acid to Glycine|||||TTCAGTGGTAGCAAGAATAAGGGCCAACGACCCGGACGAAGGTCCGAATGCTCAGATCATG||||||||||||||Homozygous mice aren't viable. They have neural tube defects and planar cell polarity defects.|Heterozygous mice display a curly tail.|C57BL/6|No|No|Yes|No|No|Yes|No|Good|||+/- x +/+|No|07-Jul-2011|Cryopreserved sperm|40.0|0.0|No||planar cell polarity, neural tube, ENU|No| 6788.0|APN 253|C57BL/6N-Kat5 /Marp||Recessive|K(lysine) acetyltransferase 5 |Kat5 |Unknown|Htatip, mHTATIP/CPLA2, PLIP, Tip60 |MGI:1932051 | gene trap IST12384G7, Texas A&M Institute for Genomic Medicine |Gt(IST12384G7)Tigm|MGI:4076960|19||||||||||||||||Yes|||||||||||||Unknown - Not bred to homozygocity |Normal |C57BL/6N|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|18-Jan-2012|Cryopreserved sperm|50.0|0.0|Unknown||ES cell, Gene Trap|Yes| 225.0|H253|Tg(Hmgcr-lacZ)H253Sest||X-linked||||||||||||||||||||||||||transgene insertion H253, Seong-Seng Tan|mouse 3-hydroxy-3-methylglutaryl coenzyme A reductase (HMG CoA)|||||||||||Mice that are homozygous for the transgenic insert are viable, fertile, normal in size and do not display any gross physical or behavioural abnormalities. ||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|25-Apr-2006||0.0|0.0|No||X-linked, inactivation, implantation, embryo|Yes| 10368.0|Sting KO_SPT ; goldenticket|B6(Cg)-Tmem173/JAnu||Dominant|stimulator of interferon response cGAMP interactor 1|Sting1 |Nil|Tmem173 |MGI:1919762||||18|ENSMUSG00000024349.11||||||||||||||||||||||||||||Homozygotes do not produce IFN-β in response to cyclic dinucleotides or Listeria monocytogenes infection.|normal|C57Bl/6N|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|||homxhom|No|10-Oct-2023|Cryopreserved sperm|55.0|0.0|Unknown|||Possibly| 6798.0|TRAMPtg|C57BL/6-Tg(TRAMP)8247Ng/JAusb||Dominant||||||||||||||||||||||||||transgene insertion 8247, Norman M Greenberg |probasin|Expression of the SV40 early region tumor antigen was driven in mouse prostrate epithelium ||||||||||Unknown|Progressive forms of prostate cancer with distant site metastasis as early as ten weeks of age. (8.2 pre-weaning loss).|C57BL/6|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown|20+ generations||hemizygous females with C57BL/6 males|No|19-Jan-2012||0.0|0.0|Yes|Prostate Cancer|intraepithelial hyperplasia , malignant neoplasia, androgen receptor , prostate|Yes| 7687.0|ENU26:017:Mef2c|C57BL/6NCrlAnu-Mef2c/AnuApb||Recessive|myocyte enhancer factor 2C|Mef2c|Unknown|5430401D19Rik, 9930028G15Rik|MGI:99458|myocyte enhancer factor 2C; mutation 1, The Australian National University|Mef2c|MGI:5571303|13|ENSMUSG00000005583|ENSMUST00000163888|Mef2c-202|374|952|A to T|ENSMUSE00000680752|5|125|Aspartic acid to Valine|||||CAAGTACAGGAAAATTAACGAAGATATTGATCTAATGATCAGCAGGCAAAGATTGTGTGCT||||||||||||||Embryonic Lethal|Appear normal|C57BL/6NCrlAnu|No|No|Yes|No|No|Yes|No|Unknown||G5|Het x Het|No|22-May-2014|Cryopreserved sperm|45.0|0.0|Unknown||ENU, embryonic lethal|Yes| 5037.0|ENU11B6:221d ; ambrosius|C57BL/6JAnu-Atp11c/AnuApb|C57BL/6JAnu-Atp11c/AnuApb|X-linked|ATPase, class VI, type 11C|Atp11c||Ig|MGI:1859661|ambrosius|Atp11c|MGI:4456247|X|ENSMUSG00000062949|ENSMUST00000154051|Atp11c-001||||||||57491646|27|||TTTCTCATTCTTCTGGGGAGGAATTATTTGGTAAGCAGCTGTACCTGTGTGAGCAATATT|Yes|||||||||||||No B cells.Defective ATP11C resulted in a lower rate of phosphatidylserine translocation in pro-B cells and much lower pre-B cell and B cell numbers despite expression of pre-rearranged immunoglobulin transgenes or enforced expression of the prosurvival protein Bcl-2 to prevent apoptosis and abolished pre-B cell population expansion in response to a transgene encoding interleukin 7. ||C57BL/6JAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|22-Feb-2010|Cryopreserved sperm|93.0|0.0|Unknown||ENU, B cell, NIH, Wellcome Trust|Yes| 6890.0|ENU23:G2|ANU:ENU23:G2||Recessive||||||||||||||||||||||||||||||||||||||Unknown|Unknown|C57BL/6NCrlAnu|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|04-May-2012|Cryopreserved sperm|1312.0|0.0|Unknown||ENU, mutagenesis, random, screen|Yes| 2379.0|Dorian, ENU6AT:HELxTCR:035|B6JSfdAnu;CBA-Bcl2/AnuApb|B6JSfdAnu;CBA-Bcl2/AnuApb|Recessive|B-cell leukemia/lymphoma 2|Bcl2|Unknown|Bcl-2|MGI:88138|B-cell leukemia/lymphoma 2; dorian|Bcl2|MGI:3844731|1|ENSMUSG00000057329|ENSMUST00000080103|Bcl2-201|70|1244|T to C|ENSMUSE00000466735|2|24|Serine to Proline|||||TCGTGATGAAGTACATACATTATAAGCTGTCACAGAGGGGCTACGAGTGGGATGCTGGAGA|No|||||||||||||Coat colour change.Diluted coat colour.Irregular coat pigmentation.Affected mice undergo dramatic greying/whitening of their coat from about 4 - 5 weeks of age. Both black and agouti mice are affected. "Salt 'n' Pepper". Mice do not appear to "age" at a greater rate.||C57BL/6JStdAnu x CBA/CaJ|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|14-Dec-2007|Cryopreserved sperm|100.0|0.0|Unknown||Coat, grey, salt and pepper, ageing, ENU, hair, Bcl2|Yes| 8643.0|Dap10/Dap12 double knock out (Dap10/12 DKO)|B6.129-Hcst/Tyrobp/Ttk||Recessive|hematopoietic cell signal transducer|Hcst|Nil|DAP10, KAP10|MGI:1344360|hematopoietic cell signal transducer; targeted mutation 1, Toshiyuki Takai|Hcst/Tyrobp|MGI:3840566|7|||||||||||||||||||||||||||||Normal; Mice lack Ly49H on cell surface |Normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|23-Jan-2019|Cryopreserved sperm|50.0|0.0|Unknown||NK cell|Yes| 8643.0|Dap10/Dap12 double knock out (Dap10/12 DKO)|B6.129-Hcst/Tyrobp/Ttk||Recessive|TYRO protein tyrosine kinase binding protein|Tyrobp|Nil|DAP12, KARAP, killer cell activating receptor associated protein|MGI:1277211|TYRO protein tyrosine kinase binding protein; targeted mutation 1, Toshiyuki Takai|Hcst/Tyrobp|MGI:3840567|7|||||||||||||||||||||||||||||Normal; Mice lack Ly49H on cell surface |Normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|23-Jan-2019|Cryopreserved sperm|||Unknown||NK cell|Yes| 7079.0|Momme D26|FVB/NJ-Rlf Tg(Hba1-Gfp)1Ew/QimrApb||Semi-dominant|rearranged L-myc fusion sequence|Rlf|Unknown|9230110M18Rik, MommeD8|MGI:1924705|modifier of murine metastable epialleles, D26|||4|||||||||||||||||transgene insertion 1, Emma Whitelaw|human alpha-globin promoter and enhancer region|11 copies||||||||||Normal|Normal|FVB/NJ|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|||MommeD26<+/->;Tg(Hba1-Gfp)1Ew x Tg(Hba1-Gfp)1Ew|No|13-Sep-2012|Cryopreserved sperm|50.0|0.0|Unknown||ENU, epigenetics, suppressor of variegation|Possibly| 5668.0|CBB6F1||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5664.0|Caspase11xC57||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5665.0|Cav-1 KO||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5667.0|Caveolin Balb/c||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5669.0|CCSP-rt/TA/Tet0-NFIen ||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5670.0|CD1/Z Red||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6773.0|DBC3 KO Cre deleted ; BRINP3 KO|C57BL/6-Fam5c||Recessive|family with sequence similarity 5, member C|Fam5c|Nil|B830045N13Rik; Brinp3|MGI:2443035||||1|||||||||||||||||||||||||||||Normal|Normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Excellent||||No|11-Jan-2012||0.0|0.0|Unknown|||No| 7602.0||SJL/ASAM||Dominant|unknown|unknown|Reduced||||||Unknown|||||||||||||||||||||||||||||Unknown|Normal|SJL/J|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Good|2|||No|24-Feb-2014|Cryopreserved sperm|50.0|0.0|Unknown||ENU|Yes| 6770.0|Hck/Stat6|STOCK Hck Stat6/LudApb||Recessive|hemopoietic cell kinase|Hck|Reduced|Bmk, Hck-1|MGI:96052|hemopoietic cell kinase; targeted mutation 1, Matthias Ernst|Hck|MGI:3663799|2|||||||||||||||||||||||||||||When maintained on a C57BL/6 background Hck mutant mice develop an age dependant inflammation that is restricted to the lung|Normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|20-Dec-2011|Cryopreserved sperm|60.0|0.0|Unknown||signal transduction|Yes| 6770.0|Hck/Stat6|STOCK Hck Stat6/LudApb||Recessive|signal transducer and activator of transcription 6|Stat6|Nil||MGI:103034|signal transducer and activator of transcription 6; targeted mutation 1, Shizuo Akira|Stat6|MGI:2386746|10|||||||||||||||||||||||||||||When maintained on a C57BL/6 background Hck mutant mice develop an age dependant inflammation that is restricted to the lung|Normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|20-Dec-2011|Cryopreserved sperm|||Unknown||signal transduction|Yes| 5380.0|TSW ; TS1(SW)|BALB/c-Tg(Tcra/Tcrb) Rag2/Apb||Dominant|recombination activating gene 2|Rag2|Nil|Rag-2|MGI:97849||||2|||||||||||||||||T cell receptor alpha, T cell receptor beta||||||||||||Mice lack mature T and B cells|Normal|BALB/c|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|||Hom x Hom|Yes|06-Jan-2011|Cryopreserved sperm|50.0|0.0|No||TCR transgenic, CD4, influenza|Possibly| 5478.0|Latte ; ADAMTS 5 flox/flox Col2A1Cre|C57BL/6-Adamts5 Tg(Col2a1-cre)1Asz/Mrch||Dominant|a disintegrin-like and metallopeptidase (reprolysin type) with thrombospondin type 1 motif, 5 (aggrecanase-2)|Adamts5|Unknown|ADAM-TS5|MGI:1346321||||16||||||||||||||||No|transgene insertion 1, Attila Aszodi|mouse type II collagen gene|7 copies||||||||||Normal|Normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||Yes|07-Apr-2011|Cryopreserved sperm|45.0|0.0|No||Arthritis , collagen, chondrocyte|Possibly| 7042.0|Loco|ENU20 Bcl2:016:a:B6||Recessive|caspase recruitment domain family, member 11|Card11|Unknown||MGI:1916978|loco|||5|||||||||||||||||transgene insertion 1, Jerry M Adams|mouse Vav promoter|||||||||||No Treg cells|Decreased circulating Treg cells.|C57BL/6NCrlAnu|Yes|Yes|Yes|Yes|Yes|Yes|Yes|Poor|G6|3|best to maintain clony with Het breeders, hom's produced small litters size|No|06-Aug-2012|Cryopreserved sperm|65.0|0.0|Unknown||T cell|Possibly| 10374.0|C57BL/6NCrlAnu-Kat6a/Anu|ENU53:456:Kat6a:B6||Dominant|K(lysine) acetyltransferase 6A|Kat6a||MOZ, Myst3, Zfp220 |MGI:2442415||Kat6a||8|ENSMUSG00000031540 |ENSMUST00000238975|||||||||||||||||||||||||||Unknown|Normal|C57Bl/6N|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|14-Nov-2023|Cryopreserved sperm|51.0|0.0|Unknown|||Possibly| 6893.0|tet(o)kras (ME-78)|FVB/N-Tg(tetO-Kras2)12Hev/LudApb||Dominant||||||||||||||||||||||||||transgene insertion 12, Harold E Varmus|tetracycline-responsive promoter element (tTA)|||||||||||This strain allows for the inducible and tissue-specific activation of Kras when crossed into a rtTA or rTA expressing line.||FVB/N|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|10-May-2012|Cryopreserved sperm|40.0|0.0|Unknown||inducible|Possibly| 6804.0|Nox2 / ApoE KO|B6.129-Apoe Cybb/MarpApb||Recessive|apolipoprotein E|Apoe|Nil||MGI:88057|apolipoprotein E; targeted mutation 1, University of North Carolina|Apoe|MGI:1857129|7|||||||||||||||||||||||||||||The absence of Nox2 in Nox2−/y/ApoE−/− double-knockout mice had minimal effects on plasma lipids or lesion development in the aortic sinus in animals up to 19 wk of age. However, an en face examination of the aorta from the arch to the iliac bifurcation revealed a 50% reduction in lesion area in Nox2−/y/ApoE−/− versus ApoE−/− mice, and this was associated with a marked decrease in aortic ROS production and an increased NO bioavailability.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|27-Jan-2012|Cryopreserved sperm|58.0|0.0|Unknown||nitric oxide, atherosclerotic plaque, macrophage|Possibly| 6804.0|Nox2 / ApoE KO|B6.129-Apoe Cybb/MarpApb||Recessive|cytochrome b-245, beta polypeptide|Cybb|Nil|Cgd, gp91, gp91phox, Nox2|MGI:88574|cytochrome b-245, beta polypeptide; targeted mutation 1, Mary C Dinauer|Cybb|MGI:1857284|X|||||||||||||||||||||||||||||The absence of Nox2 in Nox2−/y/ApoE−/− double-knockout mice had minimal effects on plasma lipids or lesion development in the aortic sinus in animals up to 19 wk of age. However, an en face examination of the aorta from the arch to the iliac bifurcation revealed a 50% reduction in lesion area in Nox2−/y/ApoE−/− versus ApoE−/− mice, and this was associated with a marked decrease in aortic ROS production and an increased NO bioavailability.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|27-Jan-2012|Cryopreserved sperm|||Unknown||nitric oxide, atherosclerotic plaque, macrophage|Possibly| 6894.0|GSTA3-/-|BALB/c-Gsta3/AnuApb||Recessive|glutathione S-transferase, alpha 3|GstA3|Nil|Gst2-3|MGI:95856||||1|||||||||||||||||||||||||||||Altered metabolism of aflatoxinB1|Unknown|BALB/c|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|N4||homozygote matings|No|11-May-2012|Cryopreserved sperm|46.0|0.0|Yes|This mouse is a model of normal human sensitivity to aflatoxinB1 carcinogenesis.||Yes| 7307.0|RIP-OVAlo|C57BL/6-Tg(Ins2-OVA)307Wehi/WehiApb|C57BL/6-Tg(Ins2-OVA)307Wehi/WehiApb|Dominant||||||||||||||||||||||||||transgene insertion 307, Walter and Eliza Hall Institute of Medical Research|rat insulin 2|low (relative to RIP-OVAhi mice)||||||||||Normal. Mice express OVA in the pancreas beta cells. |Normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Excellent||>30|brother-sister or Tg x C57BL/6|No|09-Apr-2013|Cryopreserved sperm|50.0|0.0|No||pancreas, autoimmunity, ovalbumin|Yes| 7081.0|Momme D20|FVB/NJ-D14Abb1e Tg(Hba1-Gfp)1Ew/QimrApb||Semi-dominant|transcription activation suppressor, DNA segment, Chr 14, Abbott 1 expressed|D14Abb1e|Unknown|4933409E02Rik, Tasor|MGI:1921694|DNA segment, Chr 14, Abbott 1 expressed; modifier of murine metastable epialleles, D20|D14Abb1e|MGI:5659903|14||||||||||Unknown to Unknown|||||||transgene insertion 1, Emma Whitelaw|human alpha-globin promoter and enhancer region|11 copies||||||||||Death at E6-E8|Normal|FVB/NJ|No|No|Yes|No|No|Yes|No|Good|||MommeD20<+/->;Tg(Hba1-Gfp)1Ew x Tg(Hba1-Gfp)1Ew|No|13-Sep-2012|Cryopreserved sperm|20.0|0.0|Unknown||ENU, epigenetics, modifier|Possibly| 4885.0|NODH/Kb|NOD.Cg-Tg(IE-Atp4b)1Ird||Dominant||||||||||||||||||||||||||ATPase, H+/K+ exchanging, beta polypeptide|major histocompatibility complex class II I-Ek alpha promoter|||||||||||Unknown|Transgene prevents the onset of autoimmune gastritis after neonatal thymectomy on the Balb/c genetic background. Incidence of type I diabetes in NOD/Lt mice is the same as wild type NOD/Lt mice.|NOD/Lt|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown|10|||No|28-Sep-2009||0.0|0.0|Unknown||Diabetes, autoimmunity, gastritis, proton pump, H+/K+ transporter|Yes| 8646.0|EGFL6 global KO|B6.129X1-Egfl6||Recessive|EGF-like-domain, multiple 6|Egfl6||Maeg|MGI:1858599|EGF-like-domain, multiple 6; gene trap 485H8, Centre for Modeling Human Disease|Egfl6|MGI:4954036|X|||||||||||||||||||||||||||||Unknown|Normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|24-Jan-2019|Cryopreserved sperm|50.0|0.0|Unknown|||Yes| 5325.0|Acc2 floxed|C57BL/6-Acacb/Apb||Dominant|acetyl-Coenzyme A carboxylase beta|Acacb|Normal|Acc2, Accb|MGI:2140940||||5||||||||||||||||No|||||||||||||Normal|Normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|||Homozygous pairs|No|18-Nov-2010|Cryopreserved sperm|50.0|0.0|No||fatty acid, adipose, liver, glycogen|Yes| 5221.0|GRQ|B6.129-Fxn Tg(FXN-EGFP)CSars/Apb|SARS|Recessive|frataxin|Fxn||Frda|MGI:1096879|frataxin; targeted mutation 1, Michel Koenig|Fxn|MGI:2177162|19||||||||||||||||No|Human FRATAXIN gene|FXN endogenous promoter|||||||||||Homozygous FXN-EGFP transgene: Normal.Homozygous Fxn knockout: embryonic lethal, but completely complemented by presence of FXN-EGFP transgene.|Hemizygous FXN-EGFP transgene: Normal.Heterozygous Fxn knockout: Normal.|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||16|Hemizygous FXN-EGFP transgene X Homozygous FXN knockout|Yes|23-Sep-2010|Cryopreserved sperm|45.0|0.0|Yes|Friedreich ataxia|Friedreich ataxia, neurodegenerative disease, GAA repeat expansion, iron-sulfur clusters|Yes| 10372.0|C57BL/6NCrlAnu-Dpp3/Anu|ENU54:044:Dpp3:B6 ||Dominant|dipeptidylpeptidase 3|Dpp3|||MGI:1922471||Dpp3||19|ENSMUSG00000063904 |NM_133803|||||||||||||||||||||||||||Unknown|Normal|C57Bl/6N|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|13-Nov-2023|Cryopreserved sperm|60.0|0.0|Unknown|||Possibly| 7311.0|K5rTA-Rae1-33|C57BL/6-Tg(K5-rTA)04Cbn Tg(TetO-RaeT1e)33Cbn/Apb|C57BL/6-Tg(K5-rTA)04Cbn Tg(TetO-RaeT1e)33Cbn|Dominant||||||||||||||||||||||||||tetracycline-regulated transcriptional transactivator|bovine keratin-5|||||||||||In these mice following oral doxycyline treatment, rTA expresssion induced in the skin activates the TetO promoter driving RaeT1e expression in the skin.Following doxycycline treatment, RaeT1e expression is patchy in these mice.|As for homozygous mice.|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||4|Tg Tg x Tg Tg|No|09-Apr-2013|Cryopreserved sperm|45.0|0.0|Yes||etinoic acid early transcript 1E, doxycyline inducible|Yes| 7311.0|K5rTA-Rae1-33|C57BL/6-Tg(K5-rTA)04Cbn Tg(TetO-RaeT1e)33Cbn/Apb|C57BL/6-Tg(K5-rTA)04Cbn Tg(TetO-RaeT1e)33Cbn|Dominant||||||||||||||||||||||||||retinoic acid early transcript 1E|CMV minimal promoter and 7 TetO sequences|||||||||||In these mice following oral doxycyline treatment, rTA expresssion induced in the skin activates the TetO promoter driving RaeT1e expression in the skin.Following doxycycline treatment, RaeT1e expression is patchy in these mice.|As for homozygous mice.|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||4|Tg Tg x Tg Tg|No|09-Apr-2013|Cryopreserved sperm|||Yes||etinoic acid early transcript 1E, doxycyline inducible|Yes| 5321.0|NfiA Ko|C57BL/6-Nfia||Dominant|Nuclear Factor i A|Nfia |Unknown|NF1-A, NF1A|MGI:108056|nuclear factor I/A; targeted mutation 1, Richard M Gronostajski|Nfia|MGI:2449024|4||||||||||||||||Yes||||||||||||4|Absence of corpus callosum. >= 95% Die on day of birth or within two weeks of birth. Adults have hydrocepahly. Males infertile. Females decreased fecundity. Tremors if survive to adulthood. Postnatal lethality: more than 90% die postnatally.Abnormal corpus callosum morphology: sling cells, which contribute to the development of the corpus callosum, are generated but migrate abnormally into the septum and do not form a sling.Absent corpus callosum: in E18 mice and adults.Abnormal hippocampal commissure morphology: hippocampal commissure is absent or reduced.Abnormal hippocampus morphology: glia within the hippocampus, particularly the dentate gyrus and the fimbria are reduced.Abnormal glial cell morphology: * glia within the indusium griseum and the glial wedge are greatly reduced or absent. * glia within the hippocampus, particularly the dentate gyrus and the fimbria are reduced. * formation of the midline zipper glial population is disrupted, with glia either absent or shifted position. * glial tunnel is greatly reduced surrounding a smaller anterior commissure.Abnormal axon outgrowth: * although callosal axons approach the midline, they fail to cross and extend aberrantly into the septum. * overlap of the axons in the corpus callosum and fornix and the corpus callosum and the hippocampal commissure.Decreased body size: the rare survivors are runted for the first two weeks of life.Hydroencephaly: survivors display hydrocephalus, however this phenotype diminishes with time in most mutants except for a few rare adults that exhibit severe hydrocephalus.Dilated lateral ventricles: rare adults show dilation of the lateral ventricles.Dilated third ventricle: rare adults show dilation of the third ventricles.Absent corpus callosum: in E18 mice and adults.Tremors: rare surviving mice possess a tremor.Reduced female fertility: surviving females have low fecundity but are able to give birth and suckle young.Male infertility: adult males appear sterile, however histological examination of testes reveals no gross abnormalities.Abnormal head morphology: the rare survivors have a domed head, however this phenotype diminishes with time and adults appear relatively normal.Abnormal spinal cord central canal morphology: 66% of newborns exhibit syringomyelia that is manifested as an enlarged central canal and confined to the lumbear region.Abnormal kidney morphology: 68% of newborns display agenesis, dysplastic, cystic, or duplex kidneys.Hydronephrosis: two mice that survive to P16 develop severe hydronephrosis.Dilated renal tubules.Absent kidney: some newborns exhibit bilateral renal agenesis.Duplex kidney: in some newborns.Kidney cysts: in some newborns.Abnormal ureter morphology: newborns exhibit duplication and dilatation of the ureter at the ureteropelvic junction.|Het males to wild type females. Haploinsufficiency - wt males to NFia- females results in <50% NFia- +/-.Maternal effect: loss of heterozygous progeny is seen only when the mutant allele is transmitted from the female parent, suggesting a maternal effect.Hydronephrosis: 22% of newborns exhibit hydronephrosis.Abnormal ureter morphology: * newborns exhibit duplication and dilatation of the ureter at the ureteropelvic junction. * some newborns exhibit dilation of the ureterovesical junction.|C57BL/6|No|No|Yes|No|No|Yes|Yes|Good|||Het x wt|No|16-Nov-2010||0.0|0.0|Yes|Hydrocephaly. Agenesis of the corpus callosum.|embryonic lethality, corpus callosum, glia, kidney, ferility, hydrocephaly|Possibly| 4896.0|Lym1|BALB/c-Nfkb2/Apb||Recessive|nuclear factor of kappa light polypeptide gene enhancer in B-cells 2, p49/p100|Nfkb2|Unknown|NF kappaB2, p52|MGI:1099800|nuclear factor of kappa light polypeptide gene enhancer in B cells 2, p49/p100; Lym1|Nfkb2|MGI:4412046|19|||||||||||||||||||||||||||||Increased circulating lymphocytes.A comprehensive histopathological analysis of these mice, however, revealed an absence of peripheral LN (inguinal, brachial, axillary, cervical) and Peyer’s patches. Mesenteric LN were present, but were reduced in size and cellularity.presence of inflammatory cell infiltrates in the lung and liver.The number of mature recirculating B cells was significantly reduced.Nfkb2 bone marrow was almost completely unresponsive to RANKL with osteoclast formation <0.5% of that seen with wt.Mild osteopetrosis, with significantly increased trabecular bone volume|The ability of Nfkb2 cells to form osteoclasts in response to RANKL stimulation was significantly reduced|BALB/c|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|09-Oct-2009|Cryopreserved sperm|93.0|0.0|Unknown||noncanonical, p52, signal transduction, lymph node, osteopetrosis, B cell|Yes| 10377.0|Rbm20R636H(6)|C57BL6/NCrl-Rbm20em2||Dominant|RNA binding motif protein 20|Rbm20|||MGI:1920963|Rbm20 |||Unknown| ENSMUSG00000043639| ENSMUST00000164202|||||||||||||||||||||||||||Potential arrythmia |Unknown|C57Bl/6N|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|16-Nov-2023|Cryopreserved sperm|54.0|0.0|Unknown|||Possibly| 4941.0|Linie 5706|Swiss-Tg(tPA-LacZ)5706/MarpApb||Dominant||||||||||||||||||||||||||Beta-galactosidase|9.5kb of human t-PA gene promoter|||||||||||Normal.Expression of LacZ in brain. Very high expression in hippocampus, dentate gyrus and cortex.||Swiss white|Yes|Yes|Yes|Yes|Yes|Yes|No|Excellent|||Tg Het x WT Swiss white|No|04-Dec-2009|Cryopreserved sperm|60.0|0.0|No||tissue type plasminogen activator, brain, hippocampus, medial habenula, dentate gyrus|Yes| 4871.0|B6.HTF2.Tg|C57BL/6-Tg(H2-K-huFUT1)2/Apb||Dominant||||||||||||||||||||||||||human fucosyltransferase 1|H2-K|All blood/tissue samples express human fucosyltransferase 1||||||||||Attempts to breed homozygous animals failed. Unknown if homozygous transgene expression is embryonic lethal.|All blood/tissue samples express human fucosyltransferase.Mice develop colitis.HFUT1 mice were profoundly lymphopenic, with aberrant T-cell markers and thymic medullary hypoplasia. Reconstitution with wild type bone marrow restored thymic morphology and prevented colitis in hFUT1 mice.|C57BL/6|No|No|Yes|No|No|Yes|No|Unknown||||No|28-Sep-2009|Cryopreserved sperm|88.0|0.0|Unknown||glycosylation, xenotransplantation, transplantation, transferase, lectins, H transferase, antibody, T cell|Yes| 5554.0|N1A-dko|Nox1-ApoE double knockout mouse||Recessive|NADPH oxidase 1|Nox1|Unknown|GP91 phox homolog, Nox-1|MGI:2450016||||X|||||||||||||||||||||||||||||Normal|Normal|C57BL/6J|Yes|Yes|Unknown|Yes|Yes|Unknown|No|Unknown||||No|11-Aug-2011|Cryopreserved sperm|50.0|0.0|Unknown|||Possibly| 5554.0|N1A-dko|Nox1-ApoE double knockout mouse||Recessive|apolipoprotein E|Apoe|||MGI:88057||||7|||||||||||||||||||||||||||||Normal|Normal|C57BL/6J|Yes|Yes|Unknown|Yes|Yes|Unknown|No|Unknown||||No|11-Aug-2011|Cryopreserved sperm|||Unknown|||Possibly| 5326.0|Robo1 DuLox|C57BL/6-Robo1||Dominant|roundabout homolog 1 (Drosophila)|Robo1|Nil|DUTT1|MGI:1274781|roundabout homolog 1 (Drosophila); targeted mutation 1, William Andrews|Robo1tm1Wian|MGI:3772898|16||||||||||||||||No|||||||||||||Homozygous mice viable as adults.Increased number of cortical interneurons.Abnormal embryonic/fetal subventricular zone morphology: cell cultures of ganglionic eminence exhibit increased cell proliferation compared to wild-type cells.Abnormal neurite morphology: in the subventricular zone/intermediate zone and subplate, mic exhibit an increased in neurite process length is, the number of neurites, and the degree of branching.|Heterozygous mice viable as adults.|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|||Hom x hom, Hom x Het, Het x Het, Hom x Wildtype|No|18-Nov-2010||0.0|0.0|Unknown||corticogenesis, migration, interneuron, proliferation|Possibly| 8648.0|ENU45:G2|ANU:ENU45:G2||Recessive|Unknown||||||||Unknown||||||||||||||||Unknown|||||||||||||Unknown|Unknown|C57BL/6NCrlAnu|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||1||No|31-Jan-2019|Cryopreserved sperm|1957.0|0.0|Unknown||ENU, random, mutagenesis, screen|Yes| 4758.0|NOD H-2Kb|NOD-Tg(H2K)1Rms/MarpApb||Dominant||||||||||||||||||||||||||transgene insertion 1, Robyn M Slattery|MHC Class II|||||||||||Normal NOD phenotype.|Normal NOD phenotype.|NOD|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|30-Apr-2009|Cryopreserved sperm|150.0|0.0|Unknown||Major Histocompability, autoimmunity, diabetes, T cell|Yes| 4943.0|osteocalcin-cre|C57BL/6-Tg(BGLAP-cre)1Clem/Apb||Dominant||||||||||||||||||||||||||transgene insertion 1, Thomas L Clemens|human osteocalcin (BGLAP) promoter|Osteoblasts|||||||||||Normal.Cre recombinase expression restricted to osteoblasts.|C57BL/6|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|04-Dec-2009|Cryopreserved sperm|68.0|0.0|Unknown||osteoblast, osteocalcin, Cre recombinase, IGF, mineralization|Yes| 4944.0|Mck-cre|C57BL/6-Tg(Ckmm-cre)5Khn/Apb||Dominant||||||||||||||||||||||||||transgene insertion 5, C Ronald Kahn|muscle creatine kinase promoter|heart and skeletal muscle|||||||||||Expression of Cre recombinase in heart and skeletal muscle.|C57BL/6|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown|10|||No|04-Dec-2009|Cryopreserved sperm|95.0|0.0|Unknown||skeletal muscle, muscle, Cre recombinase|Yes| 4947.0|amylin KO|B6.129-Iapp/Apb||Recessive|islet amyloid polypeptide|Iapp|Nil|amylin|MGI:96382|islet amyloid polypeptide; targeted mutation 1, Samuel Gebre-Medhin|Iapp|MGI:2656235|6||||||||||||||||Yes|||||||||||||Homeostasis/metabolism phenotype: normal basal circulating insulin and glucose levels.Increased circulating insulin level: males, but not females, show an increased plasma insulin response to a glucose tolerance test.Improved glucose tolerance:* following glucose administration, males exhibit rapid glucose clearance associated with an increased insulin response.* following glucose administration, females exhibit rapid glucose clearance but show no increase in insulin response relative to wild-type.Increased body weight: from 18 weeks of age, males show a 20% increase in body mass.On 129 background animals show increased osteoclast number and greater bone resorption and corresponding decrease in trabecular thickness.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|04-Dec-2009|Cryopreserved sperm|66.0|0.0|Unknown||osteoclast, resorption, insulin, amylin|Yes| 5201.0|GOSSIP|C57BL/6J-Zfp397||Recessive|zinc finger protein 397|Zfp397|Nil||MGI:1916506||||18||||||||||||||||Yes|||||||||||||Normal|Normal|C57BL/6J|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|05-Aug-2010|Cryopreserved sperm|50.0|0.0|No||centromere, kinetochore, zinc finger, SCAN domain|No| 5671.0|CD11c-DTR x K14E7.C57 ||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6625.0|TG2KI.129T2|129T2;B6-Tgm2||Semi-dominant|transglutaminase 2, C polypeptide|Tgm2||G[a]h, protein-glutamine gamma-glutamyltransferase, TG C, TG2, TGase2, tissue transglutaminase, tTG, tTGas|MGI:98731||||2|||||||||||||||||||||||||||||||129T2|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|19-Oct-2011||0.0|0.0|Unknown||Transgluatminase, Gh, G-protein, cross-linking|Yes| 5406.0|GM.G CSF.C57 (L-01) ;GM(-/-) G(-/-). C57|C57BL/6-Csf2 Csf3/LudApb||Recessive|colony stimulating factor 2 (granulocyte-macrophage)|Csf2|Nil|Csfgm, Gm-CSf, MGI-IGM|MGI:1339752|colony stimulating factor 2 (granulocyte-macrophage); targeted mutation 1, Ashley R Dunn|Csf2|MGI:1930997|11||||||||||||||||No|||||||||||||The phenotype of mice lacking both G-CSF and GM-CSF was additive to the features of the constituent genotypes, with three novel additional features: a greater degree of neutropenia among newborn mice than in those lacking G-CSF alone, an increased neonatal mortality rate, and a dominant influence of the lack of G-CSF on splenic hematopoiesis resulting in significantly reduced numbers of splenic progenitors. In contrast to newborn animals, adult mice lacking both G-CSF and GM-CSF exhibited similar neutrophil levels as G-CSF-deficient animals.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|02-Feb-2011|Cryopreserved sperm|50.0|0.0|Unknown||granulocyte, lung, progenitor, neutropenia|Yes| 5406.0|GM.G CSF.C57 (L-01) ;GM(-/-) G(-/-). C57|C57BL/6-Csf2 Csf3/LudApb||Recessive|colony stimulating factor 3 (granulocyte)|Csf3|Nil|Csfg, G-CSF, MGI-IG|MGI:1339751|colony stimulating factor 3 (granulocyte); targeted mutation 1, Ashley R Dunn|Csf3|MGI:1857155|11||||||||||||||||No|||||||||||||The phenotype of mice lacking both G-CSF and GM-CSF was additive to the features of the constituent genotypes, with three novel additional features: a greater degree of neutropenia among newborn mice than in those lacking G-CSF alone, an increased neonatal mortality rate, and a dominant influence of the lack of G-CSF on splenic hematopoiesis resulting in significantly reduced numbers of splenic progenitors. In contrast to newborn animals, adult mice lacking both G-CSF and GM-CSF exhibited similar neutrophil levels as G-CSF-deficient animals.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|02-Feb-2011|Cryopreserved sperm|||Unknown||granulocyte, lung, progenitor, neutropenia|Yes| 4879.0|Bc.Rag1.KO|C.B6-Rag1/ArcStvApb||Recessive|recombination activating gene 1|Rag1|Nil|Rag-1|MGI:97848|targeted mutation 1, Peter Mombaerts|Rag1|MGI:1857241|2||||||||||||||||No|||||||||||||Homozygotes for targeted null mutations exhibit arrested development of T and B cell maturation at the CD4-8- thymocyte or B220+/CD43+pro-B cell stage due to inability to undergo V(D)J recombination.||BALB/c x C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|6|||No|28-Sep-2009|Cryopreserved sperm|90.0|0.0|Unknown||T cell, B cell, eosinophil, inflammation, interferon|Yes| 4946.0|CMV-cre|C57BL/6-Tg(CMV-cre)1Cgn/Apb||Dominant||||||||||||||||||||||||||transgene insertion 1, University of Cologne|human cytomegalovirus (CMV) promoter||||||||||||Cre recombinase under the control of a human cytomegalovirus (CMV) promoter, active in most cells and tissues.|C57BL/6|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|04-Dec-2009|Cryopreserved sperm|89.0|0.0|Unknown||CMV, Cre recombinase, ubiquitous, deleter|Yes| 4948.0|a-actin-cre|C57BL/6-Tg(ACTA1-cre)1Jdz/Apb||Dominant||||||||||||||||||||||||||transgene insertion 1, Jeffrey D Zajac|human actin, alpha 1, skeletal muscle promoter||||||||||||Cre expression in heart and skeletal muscle.|C57BL/6|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|04-Dec-2009|Cryopreserved sperm|99.0|0.0|Unknown||Cre recombinase, skeletal muscle, muscle, heart|Yes| 7312.0|R26-Confetti|B6J.129P2-Gt(ROSA)26Sor/JApb||Dominant|gene trap ROSA 26, Philippe Soriano|Gt(ROSA)26Sor|Unknown|beta geo, Gtrgeo26, Gtrosa26, R26, ROSA26|MGI:104735|gene trap ROSA 26, Philippe Soriano; targeted mutation 1, Hans Clevers|Gt(ROSA)26Sor|MGI:4835542|6|||||||||||||||||||||||||||||none - reporter mouse|none - reporter mouse|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Excellent|obtained from Jackson Lab as a C57Bl/6 backcrossed line (stock number 017492)|||No|10-Apr-2013|Cryopreserved sperm|40.0|0.0|No||R26-confetti, reporter mouse|Yes| 8649.0|ENU45:G3|ANU:ENU45:G3||Recessive|Unknown||||||||Unknown||||||||||||||||Unknown|||||||||||||Unknown|Unknown|C57BL/6NCrlAnu|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||1||No|31-Jan-2019|Cryopreserved sperm|110.0|0.0|Unknown||ENU, random, mutagenesis, screen|Yes| 5331.0|Pdx1-GFP|C57BL/6-Pdx1/MarpApb||Recessive|Pancreatic and duodedenal homeobox gene 1|Pdx1|Reduced|IDX-1, IPF-1, Ipf1, Mody4, pdx-1, STF-1|MGI:102851|pancreatic and duodenal homeobox 1; targeted mutation 1, Edouard G Stanley|Pdx1|MGI:3688420|5||||||||||||||||Yes|||||||||||||Pdx1 null mice lack a pancreas|Reduce glucose responsiveness|C57BL/6|No|No|Yes|No|No|Yes|No|Excellent|more than 15 back-crossed to B6||Pdx1-GFP males mated with C57BL/6 hets |No|24-Nov-2010|Cryopreserved sperm|50.0|0.0|Unknown||Pancreas, endoderm, embryo|Yes| 5477.0|Espresso ; Ts5 flox/flox|C57BL/6-Adamts5/Mrch||Dominant|a disintegrin-like and metallopeptidase (reprolysin type) with thrombospondin type 1 motif, 5 (aggrecanase-2)|Adamts5|Normal|ADAM-TS5|MGI:1346321||||16||||||||||||||||No|||||||||||||Normal|Normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|6|no||Yes|07-Apr-2011|Cryopreserved sperm|57.0|0.0|Unknown||Surgical model for Arthritis, cartilage, inflammation, aggrecan|No| 5278.0|Lyn -/-|B6.129P2-Lyn/LudApb|B6.129P2-Lyn/LudApb|Recessive|Yamaguchi sarcoma viral (v-yes-1) oncogene homolog|Lyn|Nil|Hck-2|MGI:96892|Yamaguchi sarcoma viral (v-yes-1) oncogene homolog; targeted mutation 1, Ashley R Dunn|Lyn|MGI:2157129|4||||||||||||||||No|||||||||||||Peritoneal inflammation: there is about a doubling in the number of T cells found in the peritoneum.Increased T cell number: there is about a doubling in the number of T cells found in the peritoneum.Abnormal B cell morphology: B cells express lower levels of CD21 and higher levels of CD23 on the cell surface compared to controls.Decreased transitional stage B cell number: profound reduction in transitional stage-2 B cells.Decreased follicular B cell number: about a five-fold reduction in follicular B cells.Decreased marginal zone B cell number: profound reduction in marginal zone B cells.Abnormal B cell activation: * significant expression of MHCII complexes by circulating B cells suggest these B cells are in an activated state. * B cells have enhanced calcium flux upon activation.Abnormal myelopoiesis: * myelopoiesis is greatly enhanced in these mice. * there is a significant increase in the number of colonies generated by bone marrow cells or splenocytes in response to in vitro culturing with GM-CSF, M-CSF, or IL-3.Spleen hypoplasia: spleen cellularity is reduced by more than half due to B cell lymphopenia.Increased anti-nuclear antigen antibody level: auto-antibodies of the IgA, IgG IgM classes develop as the mice age.Increased anti-double stranded DNA antibody level: mice develop anti-DS DNA IgG antibodies as they age with high levels detectable in all mice by 20 weeks of age.Glomerulonephritis: * all mice have immunoglobulin complex deposition in the kidney by 8 weeks of age. * 83% of mice also have C3 complement deposition in the kidney. * severe glomerulonephritis occurs in these mice by one year of age.Increased basophil cell number: in cervical and inguinal lymph nodes and spleen.Increased mast cell number: in the peritoneum.Increased neutrophil cell number: mice exhibit decreased platelet numbers that becomes more pronounced with age (at 6 to 8 weeks in peripheral blood, 1089+/-242 per ul compared to 609+/-207 per ul in wild-type mice; at 52 to 58 weeks in peripheral blood, 2540+/-1050 per ul compared to 1264+/-434 per ul in wild-type mice).Decreased platelet cell number.Extramedullary hematopoiesis: * red and white pulp are often replaced with of red and white pulp with myelomonocytic cells that are often centers of extramedullary hematopoiesis. * myelomonocytic cells often accumulate in other organs and on the surface of the ears, tails and legs.Decreased spleen red pulp amount: red and white pulp are often replaced with myelomonocytic cells that are often centers of extramedullary hematopoiesis.Enlarged spleen: * mice develop age-dependent splenomegaly * 20% of mice greater than 1 year of age exhibit severe splenomegaly with partial to complete replacement of red and white pulp with myelomonocytic cells that are often centers of extramedullary hematopoiesis.Decreased spleen white pulp amount: red and white pulp are often replaced with myelomonocytic cells that are often centers of extramedullary hematopoiesis.Abnormal circulating complement protein level: increased circulating immune complexes reactive to complement component 1 q.Abnormal level of surface class II molecules: basophils show high MHC II expression.Increased IgA level.Increased IgE level.Increased IgG2b level.Increased IgM level.Increased anti-nuclear antigen antibody level: of IgE isotype.Increased anti-double stranded DNA antibody level: of IgE isotype.Young mice are apparently healthy, but they start to show signs of autoimmune disease at >12 wks of age. The disease resembles the human condition systemic lupus erythematosus (SLE). The mice develop serum anti-nuclear antibodies and acquire crescentic glomerulonephritis due to immune complex deposition in kidney, leading to renal dysfunction. They show hematologic disorders such as lymphopenia and thrombocytopenia, and they develop lymphadenopathy and splenomegaly. They develop inflammatory lesions in multiple organs including skin, lung and kidney, and occasionally we observe neurologic disorders such as seizures and hind limb paralysis. Similar to SLE patients, the mice also have hyperactive B lymphocytes.|Normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|20||Hom x Hom|No|28-Oct-2010|Cryopreserved sperm|38.0|0.0|Yes|Systemic Lupus Erythematosus; SLE|B cell, immunoglobulin, spleen, kinase, signal transduction, src family, autoimmunity, lymphocyte|Yes| 5147.0|Cx40.354 ; Tie2Cx40.354|B6;CBA-Tg(Tie2-Gja5)/AnuApb||Dominant|gap junction protein, alpha 5|Gja5|Increased|connexin 40, Cx40, Gja-5|MGI:95716||||Unknown|||||||||||||||||overexpression of Cx40|Tie2 endothelial specific|||||||||||Unknown|unknown|N2 B6|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Good|2|||No|03-Jun-2010|Cryopreserved sperm|60.0|0.0|Yes|hypertension|connexins, hypertension, gap junctions|Possibly| 7355.0|MommeR1|FVB-Foxo3/QimrAnuApb||Recessive|forkhead box O3|Foxo3|Unknown|Fkhr2, FKHRL1, Foxo3a|MGI:1890081|modifier of murine metastable epialleles, R1|Foxo3|MGI:4949204|10||||||||||Unknown to Unknown||||||Yes|Green Fluorescent Protein|human alpha-globin promoter and enhancer region|||||||||||Percentage of cells expressing the Line3 GFP transgene is decreased (enhancer of variegation).||FVB/NJ|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Poor|||MommeD5<+/->;Tg(α-Globin-GFP)3EWh x Tg(α-Globin-GFP)3EWh|No|19-Jun-2013|Cryopreserved sperm|20.0|0.0|No||epigenetics, histone modification|Yes| 5149.0||Crisp3 Flox Allele||Semi-dominant|cysteine-rich secretory protein 3|Crisp3|Normal|Aeg2, CRISP-3, CRS3, SGP28|MGI:102552||||17||||||||||||||||Yes|||||||||||||Unknown|Unknown|C57BL/6J|Yes|Unknown|Yes|Yes|Unknown|Yes|No|Unknown||||No|08-Jun-2010|Cryopreserved sperm|50.0|0.0|Unknown|||No| 5532.0|PbT-I-27 ; C57BL/6-Tg(TCRaB4-46TcrbB4-46)27Cbn|C57BL/6-Tg(H2-K-Tcra,-Tcrb)27Cbn/Apb||Dominant||||||||||||||||||||||||||transgene insertion 27, Francis Carbone|H-2Kb|||||||||||Majority of CD8 T cells express the transgenic T cell recepter Va8Vb10 specific for Plasmodium berghei (Pb) parasites.|As for homozygous|C57BL/6|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Excellent||4|brother-sister or Tg positive to C57BL/6|No|07-Jul-2011|Cryopreserved sperm|50.0|0.0|Yes|Used to model cerebral/severe malaria|malaria, Plasmodium berghei, CD8 TCR transgenic|Yes| 5312.0|Ship.C57BL/6|B6.129-Inpp5d/JAcbdLudApb||Recessive|inositol polyphosphate-5-phosphatase D|Inpp5d|Nil|s-SHIP, SHIP, SHIP-1, SHIP1, Src homology 2 domain-containing inositol-5-phosphatase|MGI:107357|inositol polyphosphate-5-phosphatase D; targeted mutation 1, Dan Dumont|Inpp5d|MGI:1861956|1||||||||||||||||No|||||||||||||Young mice are apparently healthy, but they start to show signs of inflammatory lung disease at >12 wks of age.|Normal to 12 months of age.|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|7|||No|09-Nov-2010|Cryopreserved sperm|50.0|0.0|Unknown||phosphorylation, phosphatase, signal transduction, myeloid hyperplasia, apoptosis, PI3'K, inflammatory lung disease|Yes| 7356.0|CD28 :Ly5a|B6.129S2-Cd28 Ptprc/AnuApb|B6.129S2-Cd28 Ptprc/Anu|Recessive|CD28 antigen|CD28|Nil||MGI:88327|targeted mutation 1, Tak Mak|Cd28|MGI:1857150|1||||||||||||||||Yes|||||||||||||Homozygous mutation of this gene results in impairment of some T cell responses and decreased basal immunoglobulin levels. Mutant animals have reduced T helper cell activity and impaired T cell response to lectins, but cytotoxic T cells can still be induced||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|19-Jun-2013|Cryopreserved sperm|50.0|0.0|No||T cell, immunoglobulin, costimulation, lymphocyte, lectin|Yes| 7356.0|CD28 :Ly5a|B6.129S2-Cd28 Ptprc/AnuApb|B6.129S2-Cd28 Ptprc/Anu|Recessive|protein tyrosine phosphatase, receptor type, C|Ptprc||B220, CD45, Ly-5, Lyt-4, T200|MGI:97810|protein tyrosine phosphatase, receptor type, C; a variant|Ptprc|MGI:4819849|1|||||||||||||||||||||||||||||Homozygous mutation of this gene results in impairment of some T cell responses and decreased basal immunoglobulin levels. Mutant animals have reduced T helper cell activity and impaired T cell response to lectins, but cytotoxic T cells can still be induced||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|19-Jun-2013|Cryopreserved sperm|||No||T cell, immunoglobulin, costimulation, lymphocyte, lectin|Yes| 5311.0|Robo 2 KO|C57BL/6-Robo2||Dominant|roundabout homolog 2 (Drosophila)|Robo2|||MGI:1890110|roundabout homolog 2 (Drosophila); targeted mutation 1.1, Richard Maas|Robo2|MGI:3759448|16||||||||||||||||No|||||||||||||Fail to survive after birth. Multiple ureter buds resulting in multiple ureters. May have midline defects in the brain.|Unknown. Heterozygous mice used to maintain colony.|C57BL/6|No|No|Yes|No|No|Yes|No|Unknown|||Heterozygous x Wild Type|No|08-Nov-2010||0.0|0.0|Unknown||kidney, ureter, urinary tract, cortex, interneuron|Possibly| 5148.0||Crisp3 Knockout||Recessive|cysteine-rich secretory protein 3|Crisp3||Aeg2, CRISP-3, CRS3, SGP28|MGI:102552||||17||||||||||||||||Yes|||||||||||||Unknown|Unknown|C57BL/6J|Yes|Unknown|Yes|Yes|Unknown|Yes|No|Unknown||||No|08-Jun-2010|Cryopreserved sperm|50.0|0.0|Unknown|||No| 5155.0|APN 22 ;RRR502, TBC1D1|B6;129-tbc1d1/Marp||Recessive|TBC1 domain family, member 1|TBC1D1|Unknown||1889508|TBC1 domain family, member 1; gene trap RRR502, BayGenomics|Tbc1d1|MGI:4330552|5|||||||||||||||||||||||||||||Unknown|Normal|C57BL/6J|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Good||||No|17-Jun-2010|Cryopreserved sperm|50.0|0.0|Unknown||Muscle, myotubes, skeletal, contraction, ES cell|Yes| 5439.0| Men1fl/fl ; Miles|B6;129T2-Men1/Apb|B6;129T2-Men1|Recessive|multiple endocrine neoplasia type 1|Men1|Nil|menin|MGI:1316736|multiple endocrine neoplasia 1; targeted mutation 1, Graham F Kay|Men1|MGI:2384620|19||||||||||||||||No|||||||||||||Normal.However tissue specific deletion of Men1 using RIP-Cre transgenic mice (C57BL/6-Tg(Ins2-cre)25Mgn/J) results in tumour formation in pancreatic islets and pituitary.|Normal|mixed C57BL/6 and 129T2/SvEms|Yes|Yes|Yes|Yes|Yes|Yes|No|Excellent|N/A|8|homozygous cross|No|17-Feb-2011|Cryopreserved sperm|50.0|0.0|Yes|With tissue specific deletion can be used to model human MEN1|menin, men1, pancreas, islet, transcription factor, Multiple Endocrine Neoplasia, Type I; MEN1, Jun|Yes| 5440.0|Men1 del/wt (Marcel S)|129T2-Men1/Apb|129T2-Men1|Recessive|multiple endocrine neoplasia 1|Men1|Nil|menin|MGI:1316736|multiple endocrine neoplasia 1; targeted mutation 1.1, Graham F Kay|Men1|MGI:2384622|19||||||||||||||||No|||||||||||||Embryonic lethal.|Tumours with age predominantly in pancreas, pituitary and parathyroids.|129T2/SvEms|No|No|Yes|No|No|Yes|No|Good|N/A|6|heterozygote cross wildtype|No|17-Feb-2011|Cryopreserved sperm|50.0|0.0|Yes|Used to model human MEN1|menin, men1, transcription factor, pancreas, Jun, Multiple Endocrine Neoplasia, Type I; MEN1|Yes| 5536.0|C57 Rln-/-|B6.B10-Rln1||Dominant|relaxin 1|Rln1|Nil|Rlx, Rln1|MGI:97931|relaxin 1; targeted mutation 1, Marelyn Wintour|Rln1|MGI:2668458|19|||||||||||||||||||||||||||||The phenotypes are well established. The mice have no known behavioural defects and their life span is not adversely affected (they live to over 18 months of age). There are no premature signs of ageing or tumour development. The main phenotype is that the mothers are unable to suckle their young because the nipples do not develop. Therefore, young born to Rln-/- mice die within 24 hours. The pregnant Rln-/- females may also have difficulty giving birth (dystocia) because the cervix does not dilate and the pubic symphysis does not elongate. Therefore Rln-/- mice must be generated from a heterozygous mother.|Normal|C57BL/6J|Yes|Yes|Unknown|Yes|Yes|Unknown|No|Good|14|||No|08-Jul-2011||0.0|0.0|Unknown||lactation, milk|Possibly| 5534.0|Chuzhoi|B6;C-Ptk7/Apb||Recessive|protein tyrosine kinase 7|Ptk7|Reduced|hz, mPTK7/CCK4|MGI:1918711|PTK7 protein tyrosine kinase 7; chuzhoi|Ptk7|MGI:3640803|17|||||||||||||||||||||||||||||Homozygouse mice do not survive past birth. They suffer from impaired neural tube, heart and lung development, rib defects, polydactyly, failed eyelid closure and altered cell polarity.|normal|C57BL/6|No|No|Yes|No|No|Yes|Yes|Good|||+/- x +/+|No|07-Jul-2011|Cryopreserved sperm|40.0|0.0|Unknown||planar cell polarity, neural tube, ENU|No| 7057.0|Rbm5 KO|B6;129P2-Rbm5/Marp||Recessive|RNA binding motif protein 5|Rbm5|Unknown||MGI:1933204|RNA binding motif protein 5; gene trap PST20293, Mammalian Functional Genomics Centre|Rbm5|MGI:3902497|9||||||||||||||||No|||||||||||||Unknown|Unknown|C57BL/6 x 129P2/OlaHsd|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Good||||No|22-Aug-2012|Cryopreserved sperm|50.0|0.0|Unknown||ES cell|Yes| 4757.0|NOD floxed IEα|NOD-Tg(H2-Ea)/MarpApb||Dominant||||||||||||||||||||||||||MHC class II H2-Ea|MHC Class II|||||||||||Mice maintained in hemizygous state|Normal NOD phenotype|NOD|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|30-Apr-2009|Cryopreserved sperm|94.0|0.0|Unknown||Major Histocompability, I-E alpha-chain (E alpha)|Yes| 4973.0|DSCR1 P77 Tg|B6.CBA-Tg(RCAN1)77Mapr/MarpApb||Dominant||||||||||||||||||||||||||human regulator of cacineurin 1|RCAN1|low||||||||||Transgenics are indistinguishable from wild type animals|Normal|C57BL/6 x CBA|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|||Homozygous Tg x Homozygous Tg|No|22-Jan-2010|Cryopreserved sperm|100.0|0.0|Yes|Down syndrome|Down Syndrome, vesicle trafficking|Yes| 5476.0|Gin ; Col2a1Cre|C57BL/6-Tg(Col2a1-cre)1Asz/MrchApb||Dominant|||||||||X|||||||||||||||||transgene insertion 1, Attila Aszodi|mouse type II collagen gene|7 copies||||||||||Normal|Normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|16 generation|1||Yes|07-Apr-2011|Cryopreserved sperm|45.0|0.0|Unknown||Surgical model for Arthritis, chondrocyte, cartilage|Possibly| 5508.0|Fh2|FVB/N-Tg(ACTA1-Fhl1)12Hrd/Apb||Dominant||||||||||||||||||||||||||human four and a half LIM domains 1|Human Skeletal Actin Promoter|||||||||||Unknown|Increased whole-body strength and fatigue resistance|FVB/N|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Good|N.A.|N.A.|heterozygote males crossed with FVB/N females|No|20-May-2011|Cryopreserved sperm|100.0|0.0|No||FHL1, Transgenic Mouse, Muscle hypertrophy, Mouse skeletal muscle|Yes| 4571.0||STOCK Asic2/Apb||Recessive|acid-sensing (proton-gated) ion channel 2|Asic2|Nil|ASIC2, BNaC1a, BNC1, Mdeg|MGI:1100867|acid-sensing (proton-gated) ion channel 2; targeted mutation 1, Michael J Welsh|Asic2|MGI:2180111|11||||||||||||||||Yes|||||||||||||Normal appearance, growth, size, temperature, fertility and life span, and show no obvious behavioural abnormalities.Abnormal nervous system electrophysiology:• low threshold, rapid adapting mechanoreceptors exhibit reduced sensitivity compared with wild-type mechanoreceptors• low threshold, rapid adapting mechanoreceptor stimulus response function exhibits reduced discharge frequency and flattens unlike in wild-type mechanoreceptors• low threshold, rapid adapting mechanoreceptors exhibit reduced sensitivity between 5 and 20 um displacement unlike wild-type mechanoreceptor• the stimulus-response of slowly adapting mechanoreceptor exhibits decreased sensitivity compared to wild-type mechanoreceptors• however, sensory neurons exhibit normal response to current injectionAbnormal hearing electrophysiology:• pH changes fail to generate firing of action potentials in spiral ganglion unlike similarly treated wild-type cells• proton-induced current flows in spiral ganglion compared with wild-type cells• following exposure to 110 dB white-band noise, mice exhibit a decrease in their susceptibilities to noise-induced temporary threshold shifts compared with wild-type mice• however, auditory brainstem response is normalDecreased vasoconstriction-• mice exhibit decreased pressure-induced constriction of the middle cerebral artery in the presence of calcium unlike similarly treated wild-type mice• mice develop myogenic tone with increases in intraluminal pressure but generate less tone at every pressure step compared with similarly treated wild-type mice|||Yes|Yes|Yes|Yes|Yes|Yes|No|Good|||Sibling Het x Het|No|07-Mar-2009|Cryopreserved sperm|135.0|0.0|Unknown||touch sensation, sodium channel, visceral afferents, mechanosensation, vasoconstriction|Yes| 8654.0|Prx1-Cre Dynll1|B6-Dynll1 Tg(Prx1-cre)/Jhh||Recessive|dynein light chain LC8-type 1|Dynll1||8kDa LC, DLC8, Dnclc1, Pin|MGI:1861457|dynein light chain LC8-type 1; targeted mutation 1.1, Jorg Heierhorst|Dynll1|MGI:5463937|5|||||||||||||||||Cre|Prx1|||||||||||Homozygous deleters (Prx1-Cre +/T Dynll1 fl/fl) have very short legs and lack of hair in areas where the Cre is active|Normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|15-Feb-2019|Cryopreserved sperm|50.0|0.0|Unknown|||Yes| 5511.0|CTR1 Tg|C57BL/6-Tg(CMV/CAG-SLC31A1)Jmer/Apb||Dominant||||||||||||||||||||||||||human Solute carrier family 31, member 1|Composite CMV chicken beta actin promoter (CAG)|Higher than endogenous||||||||||The hCTR1 transgenic mice display no overt phenotype resulting from the over-expression of the human CTR1 protein, however, in many tissues, copper levels are elevated compared to the non-transgenic mice consistent with enhanced copper uptake capacity of the cells expressing high levels of CTR1. |Same as homozygous. |C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|10|10|brother x sister mating|No|24-May-2011|Cryopreserved sperm|50.0|0.0|No||copper transport|Yes| 5513.0|prkfl/fl|C57BL/6-Prkar1a/Apb||Dominant|protein kinase, cAMP dependent regulatory, type I, alpha|Prkar1a|Normal|RIalpha, Tse-1, Tse1|MGI:104878||||11||||||||||||||||No|||||||||||||Normal|Normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Excellent|More than 10|||No|25-May-2011|Cryopreserved sperm|50.0|0.0|Unknown|||No| 5488.0|B6NRG|C57BL/6-Tg(Vav1-Nup98/Rap1gds1)1Apla/Apb||Dominant||||||||||||||||||||||||||Nup98-Rap1GDS1|Vav1|||||||||||Normal|Normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|||T/+ male X +/+ female, maintain on c56Bl/6 background|No|20-Apr-2011|Cryopreserved sperm|50.0|0.0|Yes|Leukemia||Yes| 7605.0|Rbm5 KO|B6.129P2-Rbm5/Marp||Recessive|RNA binding motif protein 5|Rbm5|Unknown||MGI:1933204|RNA binding motif protein 5; gene trap PST20293, Mammalian Functional Genomics Centre|Rbm5|MGI:3902497|9||||||||||||||||No|||||||||||||Unknown|Unknown|C57BL/6 x 129P2/OlaHsd|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Good|13|||No|27-Feb-2014||0.0|0.0|Unknown||ES cell|Yes| 8655.0|129.8|129X1/Sv-Rec8/Cjo||Recessive|REC8 meiotic recombination protein|Rec8|Nil|mrec, Rec8L1|MGI:1929645|REC8 meiotic recombination protein; targeted mutation 1, Michael J McKay|Rec8|MGI:3583574|14|||||||||||||||||||||||||||||Prenatal lethality, incomplete penetrance:• only 12% of pups from heterozygous matings are homozygous and at E13.5 only 16% of embryos are homozygousAbnormal seminiferous tubule morphology: • more apoptotic cells are seen in the tubules compared to wild-type miceAbnormal female reproductive system morphology: • the genital tract is involutedAbnormal ovary morphology:• dense fibrovascular stoma is seenAbsent ovarian follicles. Abnormal gametogenesis.Absent oocytes:• complete absence of oocytesAzoospermia:• no mature sperm or spermatids are seen and testes are almost depleted of primary spemtocytes by 19 days of ageAbnormal female meiosis:• homozygous meiocytes fail to complete meiotic prophase I and abnormal synaptonemal complexes form between sister chromatids rather than between homologous chromososmes• leptotene chromosomes are seen at E16.5-E18.5 but normal pachytene nuclei are never seenArrest of male meiosis:• homozygous meiocytes fail to complete meiotic prophase I and abnormal synaptonemal complexes form between sister chromatids rather than between homologous chromososmes• zygotene but not pachytene nuclei are seenFemale infertility.Male infertility.Postnatal growth retardation. Decreased fetal size: • reduced size at E15.5||129S1/Sv|Yes|No|Yes|Yes|No|Yes|No|Unknown||||No|15-Feb-2019|Cryopreserved sperm|50.0|0.0|Unknown||Meiotic cohesin, chromatid|Yes| 5344.0|NfiB KO|C57BL/6-Nfib/Apb||Dominant|nuclear factor I/B|NFib|Normal||MGI:103188|nuclear factor I/B; targeted mutation 1, Richard M Gronostajski|Nfib|MGI:3530139|4||||||||||||||||No|||||||||||||Lung maturation and cortical development defects. Do not survive past birth due to lung defect. Abnormal cerebellar, corpus callosum, glia and hippocampal development.Abnormal lung morphology: * E17.5 lungs lacked saccules * observed minor surface indentations in E15.5 lungs and deep clefts or ruffles at E18.5 * higher levels of proliferation in E18.5 lung as detected by a fourfold increase in PCNA transcripts and a substantial increase in the total DNA in the lung but no differences in lung size.Abnormal lung development: E17.5 lungs were severely defective in maturation and resembled the less-mature E15.5 wildtype lungs however morphology at E15.5 was normal indicating that lung development is arrested between E15.5 and E16.5.Abnormal hippocampus development: a reduction in the entire hippocampal primordium at E15.5 and displayed more severe disruptions in the formation of the hippocampus, with the entire CA3 region absent or severely reduced, than on a mixed Black Swiss/129P2 background.Absent cerebellar foliation: cerebellum appears unfoliated at E18.5.Abnormal brain ventricle morphology: enlarged ventricles.Abnormal corpus callosum morphology: * exhibit agenesis of the corpus callosum * complete absence of GFAP labeling in the indusium griseum and the glial wedge and a reduction in the midline zipper glia, indicating a loss or reduction of glial populations in these areas.Absent dentate gyrus: at E17.5 the dentate gyrus was absentAbnormal hippocampal fimbria: greatly reduced fimbria in E17.5 hippocampus.Abnormal cerebellar granule cell morphology: at E18, axon formation by cerebrellar granule neurons (GCNs) is altered.Abnormal pons morphology: the basilar pons was virtually absent in the hindbrain, with only a small cap of cells remaining at E16.5 to E18.5 and the rest of the hindbrain appeared normal.Abnormal glial cell morphology: complete absence of GFAP labeling in the indusium griseum and the glial wedge and a reduction in the midline zipper glia, indicating a loss or reduction of glial populations in the midline.|Abnormal corpus callosum development and abnormal glial morphology.Postnatal lethality: only about 55% survive to 14 days after birth.Abnormal lung morphology: E17.5 lungs had smaller saccules.Abnormal lung development: E17.5 lungs had a developmental delay in maturation.Abnormal corpus callosum morphology: * displayed a less severe callosal phenotype with the formation of Probst bundles at the midline than heterozygotes on the mixed Black Swiss background * reduction in all three midline glial populations of the corpus callosum.Abnormal glial cell morphology: reduction in all three midline glial populations of the corpus callosum.|C57BL/6|No|No|Yes|No|No|Yes|No|Unknown||||No|14-Dec-2010|Cryopreserved sperm|50.0|0.0|Yes|Agenesis of the corpus callosum|respiratory system, lung, cerebellar, corpus callosum, transcription|Possibly| 5539.0|Looptail|A.C3H-Vangl2/MarpApb||Semi-dominant|vang-like 2 (van gogh, Drosophila)|Vangl2|Reduced| loop-tail, Lpp1, Ltap, mKIAA1215, ska, ska17, strabismus|MGI:2135272|vang-like 2 (van gogh, Drosophila); loop tail|Vangl2|MGI:1857642|1|||||||||||||||||||||||||||||Embryonic lethal - craniorachischisis|Heterozygous mice have a curly tail, abnormal head movement - rocking or wobbling, impaired balance, spina bifida in 5% of mice.|C3H|No|No|Yes|No|No|Yes|Yes|Good|||wildtype x heterzygote|No|18-Jul-2011|Cryopreserved sperm|50.0|0.0|No||planar cell polarity, neural tube, hearing, shake, ENU|No| 5182.0|Ggn Knockout clone 42|B6.129-Ggn/42MarpApb||Recessive|gametogenetin|Ggn||GGN1, GGN2, GGN3|MGI:2181461|gametogenetin; targeted mutation 1, Duangporn Jamsai|Ggn|MGI:5503309|7||||||||||||||||Yes|||||||||||||Embryonic lethal|Appear normal.Abnormal double-strand DNA break repair:• increased unrepaired double-strand breaks in pachytene spermatocytes|C57BL/6J x 129Sv|No|No|Yes|No|No|Unknown|No|Unknown||||No|22-Jul-2010|Cryopreserved sperm|50.0|0.0|Unknown||sperm, testis, embryonic lethal|Possibly| 5240.0|MIP-GFP|C57BL/6-Tg(Ins2-EGFP)1Hara/Arc||Dominant||||||||||||||||||||||||||transgene insertion 1, Manami Hara|mouse insulin 1 gene|high||||||||||Normal C57BL/6 phenotype. GFP expression in pancreatic islet beta cells. |Normal C57BL/6 phenotype. GFP expression in pancreatic islet beta cells. |C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|10|||No|13-Oct-2010|Cryopreserved sperm|57.0|0.0|No||diabetes, pancreas, beta-cell, GFP, insulin|No| 8666.0|NOD.NfKb|NOD-Tg(TK-Nfkb*-EGFP/Luc)/Het||Dominant||||||||||||||||||||||||||eGFP-Luciferase|NfKappab enhancer- HSV-Thymidine Kinase promoter|||||||||||Normal|Normal|NOD/Lt|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|27-Feb-2019|Cryopreserved sperm|50.0|0.0|Unknown|||Yes| 7315.0|RNAi-9|C57BL/6J-HDAC1 219F||Dominant|histone deacetylase 1|Hdac1|Unknown|HD1, MommeD5, RPD3|MGI:108086||||4|||||||||||||||||||||||||||||Unknown|Normal|C57BL/6J|Unknown|Unknown|Unknown|Unknown|Unknown|Yes|No|Good||||No|11-Apr-2013|Cryopreserved sperm|50.0|0.0|Unknown||RNAi|Possibly| 5098.0|VR1 knock out|B6.129X1-Trpv1/JApb||Recessive|transient receptor potential cation channel, subfamily V, member 1|Trpv1|Nil|capsaicin receptor, OTRPC1, VR-1, Vr1|MGI:1341787|transient receptor potential cation channel, subfamily V, member 1; targeted mutation 1, David Julius|Trpv1|MGI:1934023|11||||||||||||||||Yes|||||||||||||Homozygous mutant mice demonstrate abnormal nociception, abnormal anxiety- and conditioning-related behaviors, increased sensitivity to DOCA-salt-induced renal damage, resistance to diet-induced obesity, altered taste sensitivity, and impaired febrile response.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|27-Apr-2010|Cryopreserved sperm|49.0|32.0|Unknown||capsaicin receptor, nociception, neuron, taste|Possibly| 5453.0|HH8-Ly5.1|C57BL/6-H2 Ptpcr Tg(Cd4-CD4)2362Litt Tg(HLA DR3-DQ2)303 Tg(TcraHH8,TcrbHH8)/Apb||Dominant|histocompatibility-2, MHC|H2|Nil|H-2, MHC-II|MGI:95894|histocompatibility-2, MHC; targeted deletion, H2 complex|H2|MGI:2658725|17||||||||||||||||No|human leukocyte antigen class II|||protein tyrosine phosphatase, receptor type, C|Ptprc||B220, CD45, Ly-5, Lyt-4, T200|MGI:97810|protein tyrosine phosphatase, receptor type, C; a variant|Ptprc|MGI:4819849|1|Expression of HLA DR and DQ evident on B cells, dendritic cells and a proportion of macrophages.These mice Tg for hCD4.DR3-DQ2.MHCII<Δ/Δ> express functional HLA-DR3 and DQ2 molecules that mediate thymic selection generating Ag-specific CD4<+> T cell immunity. Although about one in five Europeans homozygous for HLA-DQ2 develops celiac disease, homozygous and heterozygous hCD4.DR3-DQ2.MHCII<Δ/Δ> Tg mice do not spontaneously develop hypersensitivity to gluten. However, standard immunization protocols do produce HLA-DQ2-restricted CD4+ T cells in hCD4.DR3-DQ2.MHCII<Δ/Δ> Tg mice that preferentially recognize the deamidated α-gliadin 17-mer immunodominant in human celiac disease. Nevertheless, we have found that preexisting DQ2-restricted CD4<+> T cell immunity to deamidated α-gliadin 17-mer in hCD4.DR3-DQ2.MHCII<Δ/Δ> Tg mice is not sufficient for gluten ingestion to cause measurable intestinal pathology.TCR Tg T cells proliferated following systemic administration of Α-gliadin{57–73} Q65E or chymotrypsin-digested gliadin in vivo and secreted Th1-type cytokines implicated in Celiac disease in vitro. But ingestion of gluten or Α-gliadin{57–73} Q65E did not trigger intestinal pathology in TCR Tg mice, either spontaneously or induced by immunization strategies that have produced autoimmune disease in other TCR Tg models.Findings indicate that gluten ingestion in humanized mice expressing functional HLA-DQ2 and possessing a substantial population of CD4+ T cells specific for gluten is not sufficient to cause celiac-like enteropathy.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|20||intercross|No|03-Mar-2011|Cryopreserved sperm|50.0|0.0|Unknown||MHC, B cell, selection, autoimmunity, celiac disease|No| 5453.0|HH8-Ly5.1|C57BL/6-H2 Ptpcr Tg(Cd4-CD4)2362Litt Tg(HLA DR3-DQ2)303 Tg(TcraHH8,TcrbHH8)/Apb||Dominant||||||||||||||||||||||||||transgene insertion 2362, Dan R Littman|murine Cd4 and human CD4|equivalent to human CD4+ cells||||||||||Expression of HLA DR and DQ evident on B cells, dendritic cells and a proportion of macrophages.These mice Tg for hCD4.DR3-DQ2.MHCII<Δ/Δ> express functional HLA-DR3 and DQ2 molecules that mediate thymic selection generating Ag-specific CD4<+> T cell immunity. Although about one in five Europeans homozygous for HLA-DQ2 develops celiac disease, homozygous and heterozygous hCD4.DR3-DQ2.MHCII<Δ/Δ> Tg mice do not spontaneously develop hypersensitivity to gluten. However, standard immunization protocols do produce HLA-DQ2-restricted CD4+ T cells in hCD4.DR3-DQ2.MHCII<Δ/Δ> Tg mice that preferentially recognize the deamidated α-gliadin 17-mer immunodominant in human celiac disease. Nevertheless, we have found that preexisting DQ2-restricted CD4<+> T cell immunity to deamidated α-gliadin 17-mer in hCD4.DR3-DQ2.MHCII<Δ/Δ> Tg mice is not sufficient for gluten ingestion to cause measurable intestinal pathology.TCR Tg T cells proliferated following systemic administration of Α-gliadin{57–73} Q65E or chymotrypsin-digested gliadin in vivo and secreted Th1-type cytokines implicated in Celiac disease in vitro. But ingestion of gluten or Α-gliadin{57–73} Q65E did not trigger intestinal pathology in TCR Tg mice, either spontaneously or induced by immunization strategies that have produced autoimmune disease in other TCR Tg models.Findings indicate that gluten ingestion in humanized mice expressing functional HLA-DQ2 and possessing a substantial population of CD4+ T cells specific for gluten is not sufficient to cause celiac-like enteropathy.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|20||intercross|No|03-Mar-2011|Cryopreserved sperm|||Unknown||MHC, B cell, selection, autoimmunity, celiac disease|No| 5453.0|HH8-Ly5.1|C57BL/6-H2 Ptpcr Tg(Cd4-CD4)2362Litt Tg(HLA DR3-DQ2)303 Tg(TcraHH8,TcrbHH8)/Apb||Dominant||||||||||||||||||||||||||T cell receptor alpha, T cell receptor beta||||||||||||Expression of HLA DR and DQ evident on B cells, dendritic cells and a proportion of macrophages.These mice Tg for hCD4.DR3-DQ2.MHCII<Δ/Δ> express functional HLA-DR3 and DQ2 molecules that mediate thymic selection generating Ag-specific CD4<+> T cell immunity. Although about one in five Europeans homozygous for HLA-DQ2 develops celiac disease, homozygous and heterozygous hCD4.DR3-DQ2.MHCII<Δ/Δ> Tg mice do not spontaneously develop hypersensitivity to gluten. However, standard immunization protocols do produce HLA-DQ2-restricted CD4+ T cells in hCD4.DR3-DQ2.MHCII<Δ/Δ> Tg mice that preferentially recognize the deamidated α-gliadin 17-mer immunodominant in human celiac disease. Nevertheless, we have found that preexisting DQ2-restricted CD4<+> T cell immunity to deamidated α-gliadin 17-mer in hCD4.DR3-DQ2.MHCII<Δ/Δ> Tg mice is not sufficient for gluten ingestion to cause measurable intestinal pathology.TCR Tg T cells proliferated following systemic administration of Α-gliadin{57–73} Q65E or chymotrypsin-digested gliadin in vivo and secreted Th1-type cytokines implicated in Celiac disease in vitro. But ingestion of gluten or Α-gliadin{57–73} Q65E did not trigger intestinal pathology in TCR Tg mice, either spontaneously or induced by immunization strategies that have produced autoimmune disease in other TCR Tg models.Findings indicate that gluten ingestion in humanized mice expressing functional HLA-DQ2 and possessing a substantial population of CD4+ T cells specific for gluten is not sufficient to cause celiac-like enteropathy.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|20||intercross|No|03-Mar-2011|Cryopreserved sperm|||Unknown||MHC, B cell, selection, autoimmunity, celiac disease|No| 5479.0|Stat 3/MMTV neu|B6.Cg-Stat3 Tg(MMTVneu)202Mul/LudApb||Recessive|Signal transducer and activator of transcription 3|Stat3||Aprf|MGI:103038|signal transducer and activator of transcription 3; targeted mutation 1, Shizuo Akira|Stat3|MGI:1926814|11|||||||||||||||||transgene insertion 202, William Muller|MMTV|||||||||||Unknown|Unknown|C57BL/6|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|11-Apr-2011|Cryopreserved sperm|100.0|0.0|Unknown||signal transduction, kinase|Yes| 342.0|ATM 7271 T⇒G|B6.129-ATM ||Recessive|ataxia telangiectasia mutated homolog (human)|Atm|Normal|C030026E19Rik|MGI:107202|targeted mutation 1, Georgia Chenevix-Trench|ATM||9||||||||||Unknown to Unknown||||||No|||||||||||||Infertile. Increased sensitivity to ionizing radiation. Immune deficiencies. Increased susceptability to lymphoid tumours|Normal|C57BL/6|Yes|No|Yes|Yes|No|Yes|Yes|Good|14|4|sib x sib|No|22-Sep-2006|Cryopreserved sperm|90.0|0.0|Yes||ATM, cancer, Radiation, Breast|No| 5226.0|APN 55|C57BL/6N-Hsd11b1||1||||||||||||||||No|||||||||||||Unknown|Normal|C57BL/6N|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Excellent|||Chimeras mated with wildtype C57BL/6N|No|01-Oct-2010|Cryopreserved sperm|50.0|0.0|Unknown||glucose, adipose, cholesterol, fat pad, ES cell|Yes| 5351.0|Stat 3 loxP|B6;129P2-Stat3/LudApb||Recessive|signal transducer and activator of transcription 3|Stat3|Normal||MGI:103038|signal transducer and activator of transcription 3; targeted mutation 2, Shizuo Akira|Stat3|MGI:1926816|11||||||||||||||||No|||||||||||||No overt phenotype|No overt phenotype|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|16-Dec-2010|Cryopreserved sperm|45.0|0.0|Unknown||signal transduction, IL-6|Yes| 5322.0|shRNA-Stat3, RNAi1|TRE-Stat3.1348||Dominant|Col1A1|||||TRE-Stat.1348|||11|||||||||||||||||||||||||||||Unknown|Stat3 gene expression is inhibited (knocked-down) when TRE-Stat3.1348 mice are bi-transgenic for the TRE-Stat3.1348 allele and an rtTA allele (Tet-ON) and are treated with doxycycline. Mice with the single TRE-Stat3.1348 allele exhibit no phenotype and bi-transgenics have no phenotype in the absence of doxycycline treatment.|Mixed|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|17-Nov-2010|Cryopreserved sperm|50.0|0.0|Unknown||shRNA, Stat3, Stat3 knock-down, RNAi|Possibly| 5464.0|Kuche ; ENU18embryo:001|B6JAnu;B10SnJ-Casp8/AnuApb|B6JAnu;B10SnJ-Casp8/AnuApb|Recessive|caspase 8|Casp8|Unknown|Caspase-8, FLICE, MACH, Mch5|MGI:1261423|caspase 8; mutation 1, The Australian National University|Casp8|MGI:5563498|1|ENSMUSG00000026029|ENSMUST00000027189|Casp8-201|950|1343|T to A|ENSMUSE00000155085|8|317|Leucine to Glutamine|||||GAACAAAGACTGCTTCATCTGCTGTATCCTATCCCACGGTGACAAGGGTGTCGTCTATGGA|Yes|||||||||||||Reduced fetal liver size and haematopoetic failure at E14.5|not known|C57BL/6JAnu x C57BL/10Anu|No|No|Yes|No|No|Yes|No|Good||||No|11-Mar-2011|Cryopreserved sperm|10.0|0.0|Unknown||embryonic lethal|No| 5319.0|F/F x Mal ; gp130Y757F x Mal|B6;129-Il6st Tirap/MarpApb||Dominant|interleukin 6 signal transducer|Il6st|Unknown|CD130, D13Ertd699e, gp130|MGI:96560|interleukin 6 signal transducer; targeted mutation 1, Matthias Ernst|Il6st|MGI:2388478|13||||||||||||||||Yes|||||||||||||Mice develop gastric and inflammation and tumours, as well as splenomegaly and lymphadenopathy.|If the mice are heterozygous for the gp130 knock-in mutation (F+) then the mice appear normal. |C57BL/6 x 129Sv|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|||homozogous x homozygous|No|12-Nov-2010|Cryopreserved sperm|50.0|0.0|Yes|Gastric cancer|gastric, cancer, gp130, TLR4|No| 5319.0|F/F x Mal ; gp130Y757F x Mal|B6;129-Il6st Tirap/MarpApb||Dominant|toll-interleukin 1 receptor (TIR) domain-containing adaptor protein|Tirap|Unknown|Mal, Mal, MyD88-adapter-like, wyatt|MGI:2152213|toll-interleukin 1 receptor (TIR) domain-containing adaptor protein; targeted mutation 1.1, Paul J Hertzog|Tirap|MGI:4939795|9||||||||||||||||Unknown|||||||||||||Mice develop gastric and inflammation and tumours, as well as splenomegaly and lymphadenopathy.|If the mice are heterozygous for the gp130 knock-in mutation (F+) then the mice appear normal. |C57BL/6 x 129Sv|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|||homozogous x homozygous|No|12-Nov-2010|Cryopreserved sperm|||Yes|Gastric cancer|gastric, cancer, gp130, TLR4|No| 4863.0||FVB/N-CD151/Apb||Recessive|CD151 antigen|Cd151|Normal|PETA-3, SFA-1, Tspan24|MGI:1096360||||7||||||||||||||||Yes|||||||||||||Normal|Normal|FVB/N|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|24-Sep-2009|Cryopreserved sperm|135.0|0.0|Unknown||tetraspanin, integrin, wound repair, cell migration, angiogenesis|Yes| 4861.0||C57BL/6-Tg(ICAM2-huCD55,huCD59)/Apb||Dominant||||||||||||||||||||||||||human CD55/CD59 dual construct|ICAM2|endothelial cells and neutrophils||||||||||Expression of membrane bound human CD55 and CD59 on endothelial cells and neutrophils.|Expression of membrane bound human CD55 and CD59 on endothelial cells and neutrophils.|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|24-Sep-2009|Cryopreserved sperm|86.0|0.0|Unknown||complement, heart, endothelial, ischemia, reperfusion, xenotransplantation|Yes| 4872.0|Bc.HTF2.Tg|BALB/c-Tg(H2-K-huFUT1)2/Apb||Dominant||||||||||||||||||||||||||human fucosyltransferase 1|H2-K|All blood/tissue samples express human fucosyltransferase 1||||||||||Attempts to breed homozygous animals failed. Unknown if homozygous transgene expression is embryonic lethal.|Normal.All blood/tissue samples express human fucosyltransferase.|BALB/c|No|No|Yes|No|No|Yes|No|Unknown|15|||No|28-Sep-2009|Cryopreserved sperm|82.0|0.0|Unknown||glycosylation, xenotransplantation, transplantation, transferase, lectins, H transferase, antibody|Yes| 4873.0|B6.TFPI.Tg|C57BL/6-Tg(H2-K-huTFPI)/Apb||Dominant||||||||||||||||||||||||||human Tissue Factor Pathway Inhibitor|H2-K|All blood/tissue samples express human human Tissue Factor Pathway Inhibitor||||||||||Not attempted|Normal.All blood/tissue samples express human Tissue Factor Pathway Inhibitor.|C57BL/6|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|28-Sep-2009|Cryopreserved sperm|63.0|0.0|Unknown||glycosylation, xenotransplantation, transplantation, transferase, lectins, antibody|Yes| 6895.0|Germaine|STOCK Gstp1/Gstp2/Anu||Recessive|glutathione S-transferase, pi 1|Gstp1|Nil|Gst p-1, GstpiB|MGI:95865|glutathione S-transferase, pi 1; targeted mutation 1, C Roland Wolf|Gstp1/Gstp2|MGI:3046099|19|||||||||||||||||||||||||||||Altered drug metabolism |unknown|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|N3||homozygote matings|No|11-May-2012|Cryopreserved sperm|50.0|0.0|Yes|This mouse is a model of normal human sensitivity to carcinogens||Possibly| 6895.0|Germaine|STOCK Gstp1/Gstp2/Anu||Recessive|glutathione S-transferase, pi 2|Gstp2|Nil|Gst3, Gst-3, Gst p-2, GSTpiA|MGI:95864|glutathione S-transferase, pi 2; targeted mutation 1, C Roland Wolf|Gstp1/Gstp2|MGI:3046101|19|||||||||||||||||||||||||||||Altered drug metabolism |unknown|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|N3||homozygote matings|No|11-May-2012|Cryopreserved sperm|||Yes|This mouse is a model of normal human sensitivity to carcinogens||Possibly| 5232.0|Ben|C57BL/6-Tigd2||Recessive|tigger transposable element derived 2|Tigd2|Nil||MGI:1915390||||6||||||||||||||||Yes|||||||||||||Normal|Normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|08-Oct-2010|Cryopreserved sperm|50.0|0.0|Unknown||chromosomal, Epigenetics|Possibly| 5231.0|K14gBlo|C57BL/6-Tg(K14-HSVgB)35Cbn/WehiApb||Dominant||||||||||||||||||||||||||Herpes Simplex Virus-1 glycoprotein B - transgene insertion 35, Frank Carbone|human keratin-14 (K14)|low||||||||||Unknown|Normal|C57BL/6|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Excellent||at least 12|transgenic x C57BL/6|No|06-Oct-2010|Cryopreserved sperm|50.0|0.0|No||Herpes Simplex Virus (HSV-1), tolerance, T cell, CTL, cytotoxic, autoimmunity|Yes| 8660.0|SHMR|B6.Cg-Msh2 Rag1 Samhd1/Cjo||Recessive|mutS homolog 2|Msh2|||MGI:101816||||17|||||||||||||||||||||||||||||Unknown||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|15-Feb-2019|Cryopreserved sperm|50.0|0.0|Unknown|||Yes| 8660.0|SHMR|B6.Cg-Msh2 Rag1 Samhd1/Cjo||Recessive|recombination activating gene 1|Rag1||Rag-1|MGI:97848|recombination activating gene 1; targeted mutation 1, David Baltimore|Rag1|MGI:2448994|2|||||||||||||||||||||||||||||Unknown||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|15-Feb-2019|Cryopreserved sperm|||Unknown|||Yes| 8660.0|SHMR|B6.Cg-Msh2 Rag1 Samhd1/Cjo||Recessive|SAM domain and HD domain, 1|Samhd1||E330031J07Rik|MGI:1927468||||2|||||||||||||||||||||||||||||Unknown||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|15-Feb-2019|Cryopreserved sperm|||Unknown|||Yes| 7603.0||SJL/ASAM||Dominant|unknown|unknown|Reduced||||||Unknown|||||||||||||||||||||||||||||Unknown|Normal|SJL/J|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Good|2|||No|24-Feb-2014|Cryopreserved sperm|50.0|0.0|Unknown||ENU|Yes| 4883.0|Fas10|NOD-Tg(RIP7-dnhFAS)10Het/Apb||Dominant||||||||||||||||||||||||||human Fas (Fas5)|rat insulin promoter (RIP7)|High, restricted to pancreatic beta cells||||||||||Unknown|Mice do not develop diabetes and have a delayed onset of insulitis.|NOD/Lt|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Good|15||NOD/Lt x Fas-10 transgenic positive|No|28-Sep-2009|Cryopreserved sperm|80.0|0.0|Unknown||Cytotoxic, T cell, Pancreatic beta cell, non obese diabetic, diabetes|Yes| 4900.0||B6.129-CdKn2a/Apb||Recessive|cyclin-dependent kinase inhibitor 2A|Cdkn2a|Nil|Arf, ARF-INK4a, INK4a-ARF, Ink4a/Arf, MTS1, p16, p16INK4a, p19, p19ARF, Pctr1|MGI:104738|targeted mutation 1, Charles J Sherr|Cdkn2a|MGI:1926877|4|||||||||||||||||||||||||||||fibrohistocytomalymphomacarcinomafibrosarcomaincreased incidence of ionizing radiation-induced tumorsincreased incidence of chemically-induced tumorsMEFs (embryonic fibroblasts showed increased proliferative capacity and less responsive to contact inhibition.Abnormal lens morphology: at around P14, the lens undergoes degenerative changes characterized by vacuolization and lens material degradation; an attempt at lens repair beyond P14 is manifested by the accumulation of lens epithelial cells lining a regenerated posterior capsuleattachment of the retrolental tissue to the posterior lens and extrusion of lens material into the retrolental tissue.primary vitreous hyperplasia.MicrophthalmiaRetinal detachment||C57BL/6 x 129|Yes|No|Yes|Yes|No|Yes|No|Good||||No|09-Oct-2009|Cryopreserved sperm|90.0|0.0|Unknown||tumour, lymphoma, tumour supressor, kinase, cyclin, oncogene, p53, Rb|Yes| 7601.0||SJL/ASAM||Dominant|unknown|unknown|Reduced||||||Unknown|||||||||||||||||||||||||||||Unknown|Normal|SJL/J|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Good|2|||No|24-Feb-2014|Cryopreserved sperm|82.0|0.0|Unknown||ENU|Yes| 4770.0|B6.Asciz|C57BL/6-Atmin/JhhApb||Dominant|ATM interactor|Atmin|Normal|Asciz, MGC:79206, mKIAA0431|MGI:2682328|ATM interactor; targeted mutation 1.2, Jorg Heierhorst|Atmin|MGI:5463937|8||||||||||||||||Yes|||||||||||||Normal|Normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Excellent||||No|06-May-2009|Cryopreserved sperm|90.0|0.0|Unknown||Base excision repair, embryonic lethal, zinc finger, ATM kinase|Yes| 5238.0|IL-6 knockout ; C57.IL-6 -/-|C57BL/6-IL6/LudApb||Recessive|interleukin 6|Il6|Nil|Il-6|MGI:96559|interleukin 6; targeted mutation 1, Manfred Kopf|Il6|MGI:1857197|5||||||||||||||||No|||||||||||||Decreased pro-B cell number: the percentage of CD19+ B cell progenitors in the bone marrow is decreased from 58% to 35%.Decreased interferon-gamma secretion: after restimulation of spleen cells with keyhole limpet hemocyanin one week following immunization of mutant mice, reduced interferon gamma production is observed.Increased interleukin-4 secretion: after restimulation of spleen cells with keyhole limpet hemocyanin one week following immunization of mutant mice, enhanced Il-4 secretion is observed.Abnormal interleukin-6 secretion: intraperitoneal administration of LPS does not induce production of Il6 in the livers of mutants compared to wild-type where expression is increase.Increased body temperature: injection of Il1beta results in body temperature elevation by about 0.5C.Abnormal glucose homeostasis: inhibition of hepatic glucose production by ICV infusion of insulin is attenuatedinhibition of hepatic glucose production assessed by a euglycemic hyperinsulinemic clamp is also attenuated.Impaired glucose tolerance: impaired glucose tolerance on a high fat diet.Abnormal emotion/affect behavior.Behavioral despair: increased latency to "give up" in a forced swim test.Increased anxiety-related response: * less time spent in the illuminated areas of a light-dark box. * significantly decreased time spent in the open arms of an elevated maze. * significantly decreased number of entries into the open arms of an elevated maze.Increased fear-related response: * lower latency to escape adverse stimuli. * fewer failures to escape adverse stimuliHyperactivity: * increased locomotor activity in open field testsabnormal sleep pattern. * injection of Il1beta results in reduced dark phase wakefulness. * injection of Il1beta results in increased non REM sleep. * increased time in non-REM sleep after sleep deprivation persists longer than for controls but increase in time is equivalent.Decreased body weight: lower body weight at 4 months of age is due largely to lower fat mass.Obese: obesity develops by 8 months of age.Increased susceptibility to induced colitis: severe erosion of the intestinal epithelium from exposure to 3.5% dextran sodium sulfate.Decreased T cell number: T cells are reduced in the periphery by 20-40%.Abnormal T cell differentiation: thymocytes are consistently reduced by 20-40%.Abnormal microglial cell morphology: modest increase in microglial density after haloperidol treatment relative to the increase seen in controls.Abnormal acute phase protein level: 100-fold reduction in SAA production by the liver in response to turpentine injection or listeria infection.Defective cytotoxic T cell cytolysis: cytolytic activity of CD8 T cells to vaccinia virus infected cells is reduced 3-10 fold.Increased susceptibility to bacterial infection: 10 to 100 fold increase in bacterial titers in the liver and spleen of mice infected with Listeria.Increased susceptibility to viral infection: viral titers are 10-1000 fold higher in the ovaries and lungs of vaccinia virus infected mice.Abnormal capillary morphology: fewer capillaries in the heartabnormal heart morphology.Abnormal heart development: * loss of cell-cell interaction between myocytes and fibroblasts. * increased number of fibroblasts and decreased numbers of myocytes.Decreased heart weight: heart weight/body weight and heart weight/tibia length ratios both significantly reduced.Abnormal heart ventricle morphology.Abnormal interventricular septum morphology: modestly increased interstitial collagen.Dilated heart left ventricle.Thin ventricular wall: * both anterior and posterior walls of the left ventricle are thin. * increased interstitial collagen in the free walls of both left and right ventricles.Abnormal cardiovascular system physiology: * increased cell proliferation and apoptosis in 5 day old hearts. * proliferation at 5 days primarily by non myocytes. * apoptosis at 5 days primarily of myocytes.Decreased cardiac muscle contractility: * both fractional shortening and ejection fraction are decreased in adults and at 5 and 15 days of age. * cardiac dysfunction beginning at 15 days of age. * cardiac dilation is more or less normal at 5 days of age.Abnormal learning/memory/conditioning.Abnormal object recognition memory: * increased exploration in novel object recognition tests. * reduced exploration in initial phase of novel object recognition tests.Abnormal long term object recognition memory: reduced object recognition when retested.Greater object recognition memory.Abnormal spatial learning: * longer escape latencies in a Morris water maze. * shorter time spent in the target quadrant of a Morris water maze. * slower to relocate platform after it is moved.Abnormal brain interneuron morphology: parvalbumin positive interneurons in the hippocampus suffer less loss in numbers with age.Abnormal CNS glial cell morphology:Abnormal microglial cell morphology: modest increase in microglial density after haloperidol treatment relative to the increase seen in controls.Abnormal astrocyte morphology: density fails to increase in response to neurotoxin (6-OHDA) lesioning.Aabnormal neuron morphology:Abnormal axon morphology: * axon terminal tree is 25% larger in the substantia nigra pars compacta than for controls. * resistant to the effects of haloperidol treatment on terminal trees. * neurotoxin lesion results in reduced terminal tree density.Abnormal nervous system physiology:Abnormal neuron physiology: age induced increase in oxygen consumption in synaptosomes is attenuated.Decreased cardiac muscle contractility: * both fractional shortening and ejection fraction are decreased in adults and at 5 and 15 days of age. * cardiac dysfunction beginning at 15 days of age. * cardiac dilation is more or less normal at 5 days of age.Abnormal muscle progenitor cell migration: migration of primary myoblasts is reduced relative to controls.Abnormal skeletal muscle fiber morphology: * cross-sectional area of myofibers does not increase after overload of the plantaris muscle by incapacitation of the gastrocnemius, measured 14 and 42 days after overload. * no change in myonuclear numbers.Abnormal skeletal muscle satellite cell proliferation: proliferation is defective.Retinal outer nuclear layer degeneration: * higher level of apoptosis after retinal separation from the retinal pigment epithelium. * higher rate of photoreceptor cell death after 1 month.Abnormal bone healing: * callus formed after bone fracture is denser after 2 weeks than is true in controls. * tissue mineral density is less at 4 and 6 weeks after injury than for controls. * greater collagen content at 2 weeks after fracture but not at 4 or 6 weeks.Decreased bone mineral density: * mineral density of cortical bone reduced * reduced crystallinity relative to controls * reduced mineral/matrix ratio in cortical bone at both 2 and 4 weeks.Decreased incidence of chemically-induced tumors: reduced incidence of hepatocellular cancer in males treated with diethyl nitrosamine relative to incidence in control males.Hepatic necrosis: less necrosis resulting from diethyl nitrosamine treatment.Liver degeneration: * less hepatic injury in males from treatment with diethyl nitrosamine. * less apoptosis due to diethyl nitrosamine treatmentless compensatory proliferation as a result of diethyl nitrosamine treatment.Abnormal pulmonary gas exchange: elevated respiratory exchange rate in young mice.Abnormal homeostasis.Increased circulating glucose level: * elevated basal glucose levels at 8 months but not in younger mice. * glucose levels do not differ from controls in young mice after 1 hour of exercise.Abnormal oxygen consumption: oxygen consumption is not maintained at as high a level after 12 minutes of running as in controls.Abnormal acute phase protein level: 100-fold reduction in SAA production by the liver in response to turpentine injection or listeria infection.Abnormal exercise endurance: reduced treadmill endurance.Abnormal bone healing: * callus formed after bone fracture is denser after 2 weeks than is true in controls. * tissue mineral density is less at 4 and 6 weeks after injury than for controls. * greater collagen content at 2 weeks after fracture but not at 4 or 6 weeks.Abnormal involution of the mammary gland: develops more slowly.Increased susceptibility to induced colitis: severe erosion of the intestinal epithelium from exposure to 3.5% dextran sodium sulfate.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|12-Oct-2010|Cryopreserved sperm|50.0|0.0|Unknown||IL11, stat, signal transduction, receptor, phosphorylation, B cell, germinal centre|Possibly| 5235.0|PbT-I-25 ; C57BL/6-Tg(TCRaB4-46TcrbB4-46)25Cbn|C57BL/6-Tg(H2-K-Tcra,-Tcrb)25Cbn/Apb||Dominant||||||||||||||||||||||||||transgene insertion 25, Francis Carbone|H-2Kb|||||||||||Majority of CD8 T cells express the transgenic T cell recepter Va8Vb10 specific for Plasmodium berghei (Pb) parasites.|As for homozygous|C57BL/6|Yes|Yes|Yes|Unknown|Unknown|Unknown|No|Excellent||4|brother-sister|No|11-Oct-2010|Cryopreserved sperm|50.0|0.0|Yes|Used to model cerebral/severe malaria|malaria, Plasmodium berghei, CD8 TCR transgenic|Yes| 5505.0|Sleeping Beauty|B6.Cg-Gt(ROSA)26Sor TgTn(sb-T2/Onc2)6070Njen/Apb||Recessive|gene trap ROSA 26, Philippe Soriano|Gt(ROSA)26Sor||beta geo, Gtrgeo26, Gtrosa26, R26, ROSA26|MGI:104735|gene trap ROSA 26, Philippe Soriano; targeted mutation 2, Nancy A Jenkins|Gt(ROSA)26Sor|MGI:3839796|6||||||||||||||||Yes|transgenic transposon concatemer 6070, Nancy A Jenkins|CMV enhancer/chicken beta-actin promoter|||||||||||normal|normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|12-May-2011|Cryopreserved sperm|50.0|0.0|Unknown||tumour|Possibly| 5320.0|Robo 1 KO|B6,129-Robo1/Apb||Dominant|roundabout homolog 1 (Drosophila)|Robo1|Nil|DUTT1|MGI:1274781|roundabout homolog 1 (Drosophila); targeted mutation 1.1, Linda J Richards|Robo1|MGI:3641236|16||||||||||||||||No|||||||||||||Malformation in the corpus callosum (axons tracing a dorso-ventral path instead of medio-lateral). Disruption of the hippocampal commissure. Fornix malformation. Some disruption of midline zipper glia.|Normal callosal projections.|C57BL/6|No|No|Yes|No|No|Yes|No|Good|||Het x Wt|No|16-Nov-2010|Cryopreserved sperm|50.0|0.0|Yes|Agenesis of the corpus callosum.|axon, interneuron migration, corticothalamic, thalamocortical, Slit|Possibly| 5569.0|HYf|B6;129-Hif1a/AusbApb||Recessive|hypoxia inducible factor 1, alpha subunit|Hif1a|Normal|bHLHe78, HIF-1alpha, HIF1alpha, MOP1|MGI:106918|hypoxia inducible factor 1, alpha subunit; targeted mutation 3, Randall S Johnson|Hif1a|MGI:2386679|12|||||||||||||||||||||||||||||Normal|Normal|C57BL/6 x 129|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|29-Aug-2011|Cryopreserved sperm|50.0|0.0|Unknown|||Possibly| 5353.0|Crbp1|B6;129-Rbp1/Apb||Recessive|retinol binding protein 1, cellular|Rbp1|Nil|Crbp, CRBPI, Rbp-1|MGI:97876|retinol binding protein 1, cellular; targeted mutation 1, Pierre Chambon|Rbp1|MGI:2181412|9||||||||||||||||Yes|||||||||||||Mutantmice fed a vitA-enriched diet are healthy and fertile.They do not present any of the congenital abnormalitiesrelated to retinoic acid (RA) deficiency, indicating thatCRBPI is not indispensable for RA synthesis. However,CRBPI deficiency results in an ~50% reduction ofretinyl ester (RE) accumulation in hepatic stellate cells.This reduction is due to a decreased synthesis and a6-fold faster turnover, which are not related to changesin the levels of RE metabolizing enzymes, but probablyreflect an impaired delivery of ROL to lecithin:retinolacyltransferase. CRBPI-null mice fed a vitA-deficientdiet for 5 months fully exhaust their RE stores. Thus,CRBPI is indispensable for efficient RE synthesis andstorage, and its absence results in a waste of ROL thatis asymptomatic in vitA-sufficient animals, but leadsto a severe syndrome of vitA deficiency in animals feda vitA-deficient diet.|Unknown but probably same as normal.|Mixed 129/Sv-C57BL/6 genetic background|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|Unknown|0|Cross to C57BL/6|Yes|20-Dec-2010|Cryopreserved sperm|50.0|0.0|Unknown||retinol, vitamin A, knockout, retinol binding protein|Possibly| 4949.0|GreenSox|B6;CBA-Tg(Sox3-IRES-GFP)/Apb||Dominant||||||||||||||||||||||||||SRY-box containing gene 3 - green fluorescent protein fusion||||||||||||Normal|Normal|C57BL/6 x CBA|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Good|||Tg/+ male to wt female|No|04-Dec-2009|Cryopreserved sperm|90.0|0.0|Unknown||Sox3, SRY-box, growth retardation, hormone|Possibly| 5000.0|TRAP-cre|B6.CBA-Tg(Acp5-cre)3Rda/Apb||Dominant||||||||||||||||||||||||||transgene insertion 3, Rachel A Davey|promoters 1B and 1C from exon 1 of Acp5|||||||||||Transgenic mice express Cre recombinase in osteoclasts.||C57BL/6|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|01-Feb-2010|Cryopreserved sperm|64.0|0.0|Unknown||osteoclast, Cre recombinase, tartrate-resistant acid phosphatase, chondrocytes|Yes| 5130.0|CBf|B6.129-Cbl/AusbApb||Recessive|Casitas B-lineage lymphoma|Cbl||c-Cbl, Cbl-2|MGI:88279|Casitas B-lineage lymphoma; targeted mutation 2.1, David E James|Cbl|MGI:6822331|9||||||||||Unknown to Unknown|||||||||||||||||||Mice appear normal||C57BL/6 x 129|Yes|Yes|Yes|Yes|Yes|Yes|Yes|Good||||No|21-May-2010|Cryopreserved sperm|53.0|0.0|Unknown||Cre recombinase, transcription factor, signal transduction, phosphorylation, insulin|Yes| 5444.0|NODGrzB|NOD.B6-Gzmb/LtJApb||Dominant|granzyme B|Gzmb|Nil|CCP-1/C11, CCP1, Ctla-1, Ctla1, GZB|MGI:109267|granzyme B; targeted mutation 1, Timothy J Ley|Gzmb|MGI:1857156|14||||||||||||||||No|||||||||||||Gzm B−/− mice develop normally and have normal hematopoiesis and lymphopoiesis.Mice develop diabetes at the same rate as wild type NOD mice|Mice develop diabetes similar to NOD mice|NOD/Lt|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|11|8|Sister X Brother|Yes|23-Feb-2011|Cryopreserved sperm|50.0|0.0|Unknown||Cytotoxic T lymphocytes, Granzymes, Type 1 Diabetes, Apoptosis, Pancreatic beta cell|Possibly| 4876.0|Bc.Gal KO|BALB/c-Ggta1/Apb||Recessive|glycoprotein galactosyltransferase alpha 1, 3|Ggta1||alpha Gal, alpha3GalT, Gal, GALT, Ggta, Ggta-1, glycoprotein alpha galactosyl transferase 1|MGI:95704||||2|||||||||||||||||||||||||||||Matings between mice heterozygous for the inactivated GalT gene produced genotype ratios that deviated significantly from the predicted Mendelian 1:2:1 (wild type:heterozygote:homozygote) ratio. Cortical cataracts developed in all GalT-/- mice at 4-6 weeks of age.||BALB/c|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|11|||No|28-Sep-2009|Cryopreserved sperm|85.0|0.0|Unknown||Xenotransplantation, Transplantation, antibody, transferase, galactose|Yes| 5672.0|CD11c-DTR/GFP||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5675.0|CD11xC57xBALB/c||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5720.0|DBA/2J||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5504.0|Ctsk-cre|B6.CBA-Tg(Ctsk-cre)8Rda/Apb|B6.CBA-Tg(Ctsk-cre)8Rda|Dominant||||||||||||||||||||||||||transgene insertion 8, Rachel A Davey|5kb of Ctsk promoter (nucleotides -3359 - +1660)|||||||||||Transgenic mice express Cre recombinase in osteoclasts.|Transgenic mice express Cre recombinase in osteoclasts.|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Excellent|15||maintained in heterozygous state by backcrossing to C57BL/6|No|11-May-2011|Cryopreserved sperm|50.0|0.0|No||osteoclast, Cre recombinase, cathepsin K, Cre/loxP|No| 5404.0|G-/-|C57BL/6-Csf3/LudApb||Recessive|colony stimulating factor 3 (granulocyte)|Csf3|Nil|Csfg, G-CSF, MGI-IG|MGI:1339751|colony stimulating factor 3 (granulocyte); targeted mutation 1, Ashley R Dunn|Csf3|MGI:1857155|11||||||||||||||||Yes|||||||||||||Decreased leukocyte cell number: * homozygotes are viable, fertile, and developmentally normal with no overt signs of disease or significant changes in hemoglobin or platelet levels. * however, homozygotes exhibit leukopenia as a result of significant selective neutropenia. * some homozygotes exhibit reduced circulating lymphocyte levels; however, these changes are inconsistent.Decreased neutrophil cell number: * homozygotes exhibit a severe chronic neutropenia, with blood neutrophil levels reduced to ~30% of wild-type levels * however, no significant changes in circulating eosinophil numbers are observed.Decreased monocyte cell number: homozygotes display significantly reduced monocyte levels relative to wild-type miceImpaired myelopoiesis: * homozygotes show a 50% decrease in granulopoietic precursor cells in the bone marrow, with reduced levels of granulocyte, macrophage, and blast progenitor cells. * G-CSF administration reverses the granulopoietic defect: one day of G-CSF administration increases circulating neutrophil levels to normal, and after 4 days of G-CSF administration, mutant bone marrows are morphologically indistinguishable from wild-type marrows.Abnormal neutrophil physiology: homozygotes exhibit impaired neutrophil mobilization in response to a single dose of G-CSF, with only 21% of wild-type circulating neutrophil levels at 3 hrs post-treatment.Increased susceptibility to bacterial infection: homozygotes display a significantly impaired ability to control infection with Listeria monocytogenes, as shown by a 50% mortality rate at day 5 post-inoculation as well as diminished neutrophil and delayed monocyte increases in blood and reduced infection-driven granulopoiesis.|Decreased neutrophil cell number: heterozygotes exhibit a chronic neutropenia, with blood neutrophil levels reduced to ~67% of wild-type levels, suggesting a gene-dosage effect.|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|02-Feb-2011|Cryopreserved sperm|50.0|0.0|Unknown||granulocyte, haemopoiesis, neutrophil, stem cell, progenitor|Yes| 5081.0|Slc2a6 (Glut6) conditional KO|C57BL/6-Slc2a6||Recessive|solute carrier family 2 (facilitated glucose transporter), member 6|Slc2a6|Normal|Glut6, Glut9|MGI:2443286||||2||||||||||||||||Yes|||||||||||||Normal|Normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|25-Mar-2010|Cryopreserved sperm|60.0|0.0|Unknown||transporter, glucose, channel|Possibly| 5417.0|A33:Lgp130YFKO ; line 6 backcross (ME-248)|CB;129-Tg(Gpa33-Il6st*)6Ern/Lud||Dominant|||||||||||||||||||||||||||glycoprotein A33 (transmembrane)|||||||||||Unknown|Unknown|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|04-Feb-2011|Cryopreserved sperm|50.0|0.0|Unknown||stat, epithelium, colon|Yes| 5313.0|Bombay ; Rosa26/col2a1Cre|C57BL/6-Tg(Col2a1-cre)1Asz Gt(ROSA)26Sor/Apb||Dominant||||||||||||||||||||||||||transgene insertion 1, Attila Aszodi|Col2a1|7 copies||||||||||Normal|Normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Excellent||||No|09-Nov-2010|Cryopreserved sperm|70.0|0.0|No||Arthritis |Yes| 5313.0|Bombay ; Rosa26/col2a1Cre|C57BL/6-Tg(Col2a1-cre)1Asz Gt(ROSA)26Sor/Apb||Dominant||||||||||||||||||||||||||gene trap ROSA 26, Philippe Soriano; targeted mutation 1, Philippe Soriano||||||||||||Normal|Normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Excellent||||No|09-Nov-2010|Cryopreserved sperm|||No||Arthritis |Yes| 5500.0|H2az|C.129P2-H2afz/Apb||Recessive|H2A histone family, member Z|H2afz|Nil|H2A.Z|MGI:1888388|H2A histone family, member Z; targeted mutation 1, Ian Lyons|H2afz|MGI:2387764|3||||||||||||||||Yes|||||||||||||Embryonic Lethality: Homozygous lethal with embryos dying from 3.5-6.5 d.p.c.Abnormal inner cell mass: cells derived from the inner cell mass of cultured blastocysts fail to persist whereas trophectoderm does persist|Heterozygotes appear normal and are fertile.|BALB/c|No|No|Yes|No|No|Yes|No|Good|Unknown but over 10|Unknown|Heterozygous intercross or Heterozygote x WT|No|09-May-2011|Cryopreserved sperm|50.0|0.0|Unknown||Histone variant, epigenetics, embryo, transcription, chromatin|Yes| 5053.0|NOD.B6 R7 N12|NOD.B6(D1Mit48-D1Mit495)N12||Recessive||||||||||||||||||||||||||||||||||||||The incidence of diabetes in female mice is 80% after 43-weeks, which is significantly higher than the incidence of diabetes in female NOD/Lt mice in host facility (50-60% at 43-weeks of age). The incidence of diabetes in male mice is 58% after 43 weeks of age, which is significantly higher than the incidence of diabetes in male NOD/Lt mice in host facility (5-10% at 43-weeks of age).|The incidence of diabetes has not been tested in heterozygotes of this mouse strain.|NOD/Lt|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|12|8|Hom x Hom|No|26-Feb-2010|Cryopreserved sperm|45.0|0.0|Yes|Type 1 Diabetes|IgA, IgM, Idd5.4, B cell|Yes| 10382.0|ASD688:Tigger; Ddit3|C57BL/6NCrlAnu-Ddit3/Anu||Semi-dominant|DNA-damage inducible transcript 3|Ddit3||CHOP-10, gadd153|MGI:109247|Ddit3:endonuclease-mediated mutation 1, Australian National University|Ddit3||10|ENSMUSG00000025408||||||||||||||||||||||||||||Normal|Normal||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|26-Nov-2023|Cryopreserved sperm|21.0|0.0|Unknown|||Possibly| 5242.0|FF:IFNAR2KO ; gp130Y757F x IFNAR2|B6;129/Sv-Il6st Ifnar2/Apb||Dominant|interleukin 6 signal transducer|Il6st|Normal|CD130, D13Ertd699e, gp130|MGI:96560|interleukin 6 signal transducer; targeted mutation 1, Matthias Ernst|Il6st|MGI:2388478|13||||||||||||||||Yes|||||||||||||Gastric tumoursSplenomegalyLymphadenopathy|unknown|C57BL/6 x 129/Sv |Yes|Yes|Yes|Yes|Yes|Yes|No|Poor||||No|14-Oct-2010|Cryopreserved sperm|40.0|0.0|Yes|gastric cancer|signal transduction, phosphorylation, Src, STAT, SHP|Possibly| 5242.0|FF:IFNAR2KO ; gp130Y757F x IFNAR2|B6;129/Sv-Il6st Ifnar2/Apb||Dominant|interferon (alpha and beta) receptor 2|Ifnar2|Nil|Ifnar-2|MGI:1098243|interferon (alpha and beta) receptor 2; targeted mutation 1, Paul J Hertzog|Ifnar2|MGI:2680693|16||||||||||||||||Yes|||||||||||||Gastric tumoursSplenomegalyLymphadenopathy|unknown|C57BL/6 x 129/Sv |Yes|Yes|Yes|Yes|Yes|Yes|No|Poor||||No|14-Oct-2010|Cryopreserved sperm|||Yes|gastric cancer|signal transduction, phosphorylation, Src, STAT, SHP|Possibly| 5087.0|APN25|B6.129Ola-Tcfcp2l1/MIMR||Recessive|transcription factor CP2-like 1|Tcfcp2l1|Unknown|Cp2l1, Crtr-1, D930018N21Rik, LBP-9|MGI:2444691|transcription factor CP2-like 1; gene trap AS0519, Wellcome Trust Sanger Institute|Tcfcp2l1|MGI:4346711|1|||||||||||||||||||||||||||||Unknown for this mutant.Targeted mutation is postnatal lethal.||C57BL/6 x 129|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|09-Apr-2010|Cryopreserved sperm|56.0|0.0|Unknown||transcription factor, Genetrap, APN, ES cell|No| 5095.0|Lzt-I.1|C57BL/6-Tg(TcraP3A4TcrbP3A4)37Cbn/JWehiApb||Dominant||||||||||||||||||||||||||transgene insertion P3A4 Tcrb, Francis R Carbone|Tcrb|||||||||||Preferential CD8 T cell development resulting in a decreased CD4/CD8 ratio. 80% of peripheral CD8 T cells express the transgenic TCR.|As for homozygous mice|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Excellent||9|brother x sister mating|Yes|19-Apr-2010|Cryopreserved sperm|100.0|0.0|No||TCR tansgenic, beta-galactosidase|Possibly| 5095.0|Lzt-I.1|C57BL/6-Tg(TcraP3A4TcrbP3A4)37Cbn/JWehiApb||Dominant||||||||||||||||||||||||||transgene insertion P3A4 Tcra, Francis R Carbone|H-2Kb|||||||||||Preferential CD8 T cell development resulting in a decreased CD4/CD8 ratio. 80% of peripheral CD8 T cells express the transgenic TCR.|As for homozygous mice|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Excellent||9|brother x sister mating|Yes|19-Apr-2010|Cryopreserved sperm|||No||TCR tansgenic, beta-galactosidase|Possibly| 6637.0|BALB/c-Her2|C.(Cg)-Tg(Wap-ERBB2)229Wzw||Dominant||||||||||||||||||||||||||transgene insertion 229 Wei-Zen Wei|Whey acidic protein (Wap)|High in brain and lactating breast||||||||||Human Her-2 protein expressed in brain and lactating breast.|Human Her-2 protein expressed in brain and lactating breast.|BALB/c|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Good|10|||No|27-Oct-2011||0.0|0.0|No||Her-2, mammary epithelia, Bergman glia cells, tumour, vaccine|Possibly| 5245.0|Orana; ENU15:B10:025 ; ENU15b10_25 ; ENU15embryo:015|C57BL/6JAnu-Dhfr/AnuApb|C57BL/6JAnu-Dhfr/AnuApb|Recessive|dihydrofolate reductase|Dhfr|Unknown||MGI:94890|dihydrofolate reductase; orana|Dhfr|MGI:5563476|13|ENSMUSG00000021707|ENSMUST00000022218|Dhfr-201|409|885|A to G|ENSMUSE00000120178|5|137|Threonine to Alanine|||||ATCAACCAGGCCACCTCAGACTCTTTGTGACAAGGATCATGCAGGAATTTGAAAGTGACAC|Yes|||||||||||||Blood development defect in mouse embryos at e14.5. Reduced number of RBCs, Pale embryos, prominent fetal liver with changed progenitor cell subsets.|Normal, at time of information submission.|C57BL/6JAnu|No|No|Yes|No|No|Yes|No|Good||||No|15-Oct-2010|Cryopreserved sperm|10.0|0.0|Unknown||embryonic lethal, blood, progenitor, RBC, ENU|No| 7279.0|B6 RIIa Tg y-/-|B6;SJL-Tg(FCGR2A)11Mkz Fcer1g/J|HOGA|Semi-dominant|Fc receptor, IgE, high affinity I, gamma polypeptide|Fcer1g|Nil|FcR-gamma, FcRgamma, Ly-50|MGI:95496|Fc receptor, IgE, high affinity I, gamma polypeptide; targeted mutation 1, Jeffrey V Ravetch|Fcer1g|MGI:1857165|1|||||||||||||||||transgene insertion 11, Steven E McKenzie||||||||||||normal|normal|C57BL/6J|Yes|Yes|Yes|Yes|Yes|Yes|Yes|Good|12|||Yes|15-Feb-2013|Cryopreserved sperm|50.0|0.0|Yes|immune complex disease and allergy|Fc receptor, antibody, immune complex, inflammation, arthritis, thrombocytopenia, osteopetrosis, allergy|Possibly| 3312.0|DOM5|B6.DBA1-Tg(Thy1-PP2ACα*L309A)||Recessive||||||||||||||||||||||||||protein phosphatase 2 (formerly 2A), catalytic subunit, alpha isoform (L309A mutant)|murine Thy1||||||||||||Transgene expressed in Brain and Harderian (lacrimal) gland. Slit eye : 100 % penetrance. Tau phosphorylation in brain vimentin.Authors found a delayed postnatal development and hypoplasia of the gland, causing enophthalmos. To determine why expression of the L309A mutant caused this phenotype, we determined the PP2A subunit composition. We found an altered subunit composition in the transgenic gland that was accompanied by pronounced changes of proteins regulating cell adhesion. Specifically, cadherin and β-catenin were dramatically reduced and shifted to the cytosol. Furthermore, we found an inactivating phosphorylation of the cadherin-directed glycogen synthase kinase-3β.|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|6||T6 x C57BL/6|No|09-Jun-2008||0.0|0.0|Yes||protein phosphatase 2A, lacrimal gland, brain, tau phosphorylation, cadherin|Yes| 5096.0|Lzt-I.2|B6-Tg(TcrLzT-I)39Cbn/WehiApb||Dominant||||||||||||||||||||||||||Tcrb|Cbeta2|yes||||||||||Normal|Normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Excellent|||brother x sister mating|Yes|19-Apr-2010|Cryopreserved sperm|50.0|0.0|No||TCR tansgenic, beta-galactosidase|Possibly| 5096.0|Lzt-I.2|B6-Tg(TcrLzT-I)39Cbn/WehiApb||Dominant||||||||||||||||||||||||||Tcra|H-2|yes||||||||||Normal|Normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Excellent|||brother x sister mating|Yes|19-Apr-2010|Cryopreserved sperm|||No||TCR tansgenic, beta-galactosidase|Possibly| 5092.0|Strummer|SPIF-1 FRT KO||Recessive|SPIF-1|SPIF-1|||||||15|||||||||||||||||||||||||||||Unknown|Unknown|C57BL/6|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|16-Apr-2010|Cryopreserved sperm|50.0|0.0|Unknown|||No| 5093.0|Iggy|SPIF-1 NEO KO||Recessive|SPIF-1|SPIF-1|||||||15|||||||||||||||||||||||||||||Unknown|Unknown|C57BL/6|Unknown|Unknown|Yes|Unknown|Unknown|Unknown|No|Unknown||||No|16-Apr-2010|Cryopreserved sperm|30.0|0.0|Unknown|||No| 5249.0|FGFPC|C57BL/6-Tg(FXN/EGFP)CSars/Apb|C57BL/6-Tg(FXN/EGFP)CSars/Apb|Recessive||||||||||||||||||||||||||Human FRATAXIN gene|FXN endogenous promoter|Normal||||||||||Normal|Normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|10|21|Hemizygous FXN-EGFP transgene X Hemizygous FXN-EGFP transgene|No|20-Oct-2010|Cryopreserved sperm|50.0|0.0|Yes|Friedreich ataxia|Friedreich ataxia, neurodegenerative disease, GAA repeat expansion, iron-sulfur clusters|Yes| 3313.0|K369I tau ; K3|C57BL/6-Tg(Thy1-MAPT*K369I)K3Gotz/Apb||Recessive||||||||||||||||||||||||||transgene insertion K3, Jurgen Gotz|murine Thy1|High|||||||||||Transgene expression high in brain including Substantia nigra. Parkinsonism and amyotrophy (incl hind limbs clasping); memory impairment; Pick’s pathology; age of onset 4 weeks|C57BL/6|No|No|Yes|No|No|Yes|No|Good|10||T6 x C57BL/6|No|09-Jun-2008|Cryopreserved sperm|10.0|0.0|Yes||Parkinsonism, Pick’s disease, axonal transport, memory impairment, amyotrophy, tau, microtubule-associated protein tau|No| 5252.0|BMP4/LacZneo|STOCK BMP4/MarpApb||Semi-dominant|bone morphogenetic protein 4|Bmp4|Nil|Bmp-4, Bmp2b, Bmp2b-1, Bmp2b1|MGI:88180|bone morphogenetic protein 4; targeted mutation 2, Brigid L Hogan|Bmp4|MGI:2158495|14||||||||||||||||No|beta-galactosidase|endogenous Bmp4|||||||||||Prenatal lethality.Embryonic lethality during organogenesis: die at E8.5|Kidney anomalies|129/SvEv x Black Swiss|No|No|Yes|No|No|Yes|No|Good|||heterozygotes x wild-types within the colony|No|20-Oct-2010|Cryopreserved sperm|60.0|0.0|Yes|CAKUT- congenital anomalies of the kidney and urinary tract|CAKUT, kidney, ureter, hydronephrosis, duplicated ureter|Possibly| 3311.0|Δtau ; delta Tau74|C57BL/6-Tg(Thy1.2-hTau)||Recessive||||||||||||||||||||||||||truncated human tau 40 (projection domain) aa 1-255|murine Thy1.2||||||||||||No obvious altered phenotype|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|5||T6 x C57BL/6|No|09-Jun-2008|Cryopreserved sperm|20.0|0.0|Unknown||phosphorylation, tau, mitochondria, transport, membrane localization|Possibly| 5362.0|HH8-Ly5.1|C57BL/6-Ptprc H2 Tg(Cd4-CD4)2362Litt Tg(HLA DR3-DQ2)303 Tg(TcraHH8,TcrbHH8)||Dominant|histocompatibility-2, MHC|H2|Nil|H-2, MHC-II|MGI:95894|histocompatibility-2, MHC; targeted deletion, H2 complex|H2|MGI:2658725|17||||||||||||||||No|human leukocyte antigen class II|||protein tyrosine phosphatase, receptor type, C|Ptprc||B220, CD45, Ly-5, Lyt-4, T200|MGI:97810|protein tyrosine phosphatase, receptor type, C; a variant|Ptprc|MGI:4819849|1|Expression of HLA DR and DQ evident on B cells, dendritic cells and a proportion of macrophages.These mice Tg for hCD4.DR3-DQ2.MHCII<Δ/Δ> express functional HLA-DR3 and DQ2 molecules that mediate thymic selection generating Ag-specific CD4<+> T cell immunity. Although about one in five Europeans homozygous for HLA-DQ2 develops celiac disease, homozygous and heterozygous hCD4.DR3-DQ2.MHCII<Δ/Δ> Tg mice do not spontaneously develop hypersensitivity to gluten. However, standard immunization protocols do produce HLA-DQ2-restricted CD4+ T cells in hCD4.DR3-DQ2.MHCII<Δ/Δ> Tg mice that preferentially recognize the deamidated α-gliadin 17-mer immunodominant in human celiac disease. Nevertheless, we have found that preexisting DQ2-restricted CD4<+> T cell immunity to deamidated α-gliadin 17-mer in hCD4.DR3-DQ2.MHCII<Δ/Δ> Tg mice is not sufficient for gluten ingestion to cause measurable intestinal pathology.TCR Tg T cells proliferated following systemic administration of Α-gliadin{57–73} Q65E or chymotrypsin-digested gliadin in vivo and secreted Th1-type cytokines implicated in Celiac disease in vitro. But ingestion of gluten or Α-gliadin{57–73} Q65E did not trigger intestinal pathology in TCR Tg mice, either spontaneously or induced by immunization strategies that have produced autoimmune disease in other TCR Tg models.Findings indicate that gluten ingestion in humanized mice expressing functional HLA-DQ2 and possessing a substantial population of CD4+ T cells specific for gluten is not sufficient to cause celiac-like enteropathy.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|21-Dec-2010||0.0|0.0|Unknown||MHC, B cell, selection, autoimmunity, celiac disease|Yes| 5362.0|HH8-Ly5.1|C57BL/6-Ptprc H2 Tg(Cd4-CD4)2362Litt Tg(HLA DR3-DQ2)303 Tg(TcraHH8,TcrbHH8)||Dominant||||||||||||||||||||||||||transgene insertion 2362, Dan R Littman|murine Cd4 and human CD4|equivalent to human CD4+ cells||||||||||Expression of HLA DR and DQ evident on B cells, dendritic cells and a proportion of macrophages.These mice Tg for hCD4.DR3-DQ2.MHCII<Δ/Δ> express functional HLA-DR3 and DQ2 molecules that mediate thymic selection generating Ag-specific CD4<+> T cell immunity. Although about one in five Europeans homozygous for HLA-DQ2 develops celiac disease, homozygous and heterozygous hCD4.DR3-DQ2.MHCII<Δ/Δ> Tg mice do not spontaneously develop hypersensitivity to gluten. However, standard immunization protocols do produce HLA-DQ2-restricted CD4+ T cells in hCD4.DR3-DQ2.MHCII<Δ/Δ> Tg mice that preferentially recognize the deamidated α-gliadin 17-mer immunodominant in human celiac disease. Nevertheless, we have found that preexisting DQ2-restricted CD4<+> T cell immunity to deamidated α-gliadin 17-mer in hCD4.DR3-DQ2.MHCII<Δ/Δ> Tg mice is not sufficient for gluten ingestion to cause measurable intestinal pathology.TCR Tg T cells proliferated following systemic administration of Α-gliadin{57–73} Q65E or chymotrypsin-digested gliadin in vivo and secreted Th1-type cytokines implicated in Celiac disease in vitro. But ingestion of gluten or Α-gliadin{57–73} Q65E did not trigger intestinal pathology in TCR Tg mice, either spontaneously or induced by immunization strategies that have produced autoimmune disease in other TCR Tg models.Findings indicate that gluten ingestion in humanized mice expressing functional HLA-DQ2 and possessing a substantial population of CD4+ T cells specific for gluten is not sufficient to cause celiac-like enteropathy.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|21-Dec-2010||||Unknown||MHC, B cell, selection, autoimmunity, celiac disease|Yes| 5362.0|HH8-Ly5.1|C57BL/6-Ptprc H2 Tg(Cd4-CD4)2362Litt Tg(HLA DR3-DQ2)303 Tg(TcraHH8,TcrbHH8)||Dominant||||||||||||||||||||||||||T cell receptor alpha, T cell receptor beta||||||||||||Expression of HLA DR and DQ evident on B cells, dendritic cells and a proportion of macrophages.These mice Tg for hCD4.DR3-DQ2.MHCII<Δ/Δ> express functional HLA-DR3 and DQ2 molecules that mediate thymic selection generating Ag-specific CD4<+> T cell immunity. Although about one in five Europeans homozygous for HLA-DQ2 develops celiac disease, homozygous and heterozygous hCD4.DR3-DQ2.MHCII<Δ/Δ> Tg mice do not spontaneously develop hypersensitivity to gluten. However, standard immunization protocols do produce HLA-DQ2-restricted CD4+ T cells in hCD4.DR3-DQ2.MHCII<Δ/Δ> Tg mice that preferentially recognize the deamidated α-gliadin 17-mer immunodominant in human celiac disease. Nevertheless, we have found that preexisting DQ2-restricted CD4<+> T cell immunity to deamidated α-gliadin 17-mer in hCD4.DR3-DQ2.MHCII<Δ/Δ> Tg mice is not sufficient for gluten ingestion to cause measurable intestinal pathology.TCR Tg T cells proliferated following systemic administration of Α-gliadin{57–73} Q65E or chymotrypsin-digested gliadin in vivo and secreted Th1-type cytokines implicated in Celiac disease in vitro. But ingestion of gluten or Α-gliadin{57–73} Q65E did not trigger intestinal pathology in TCR Tg mice, either spontaneously or induced by immunization strategies that have produced autoimmune disease in other TCR Tg models.Findings indicate that gluten ingestion in humanized mice expressing functional HLA-DQ2 and possessing a substantial population of CD4+ T cells specific for gluten is not sufficient to cause celiac-like enteropathy.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|21-Dec-2010||||Unknown||MHC, B cell, selection, autoimmunity, celiac disease|Yes| 5361.0|HH8-1|C57BL/6-H2 Tg(Cd4-CD4)2362Litt Tg(HLA DR3-DQ2)303 Tg(TcraHH8,TcrbHH8)/Apb||Dominant|histocompatibility-2, MHC|H2|Nil|H-2, MHC-II|MGI:95894|histocompatibility-2, MHC; targeted deletion, H2 complex|H2|MGI:2658725|17||||||||||||||||No|human leukocyte antigen class II||||||||||||Expression of HLA DR and DQ evident on B cells, dendritic cells and a proportion of macrophages.These mice Tg for hCD4.DR3-DQ2.MHCII<Δ/Δ> express functional HLA-DR3 and DQ2 molecules that mediate thymic selection generating Ag-specific CD4<+> T cell immunity. Although about one in five Europeans homozygous for HLA-DQ2 develops celiac disease, homozygous and heterozygous hCD4.DR3-DQ2.MHCII<Δ/Δ> Tg mice do not spontaneously develop hypersensitivity to gluten. However, standard immunization protocols do produce HLA-DQ2-restricted CD4+ T cells in hCD4.DR3-DQ2.MHCII<Δ/Δ> Tg mice that preferentially recognize the deamidated α-gliadin 17-mer immunodominant in human celiac disease. Nevertheless, we have found that preexisting DQ2-restricted CD4<+> T cell immunity to deamidated α-gliadin 17-mer in hCD4.DR3-DQ2.MHCII<Δ/Δ> Tg mice is not sufficient for gluten ingestion to cause measurable intestinal pathology.TCR Tg T cells proliferated following systemic administration of Α-gliadin{57–73} Q65E or chymotrypsin-digested gliadin in vivo and secreted Th1-type cytokines implicated in Celiac disease in vitro. But ingestion of gluten or Α-gliadin{57–73} Q65E did not trigger intestinal pathology in TCR Tg mice, either spontaneously or induced by immunization strategies that have produced autoimmune disease in other TCR Tg models.Findings indicate that gluten ingestion in humanized mice expressing functional HLA-DQ2 and possessing a substantial population of CD4+ T cells specific for gluten is not sufficient to cause celiac-like enteropathy.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|21-Dec-2010|Cryopreserved sperm|40.0|0.0|Unknown||MHC, B cell, selection, autoimmunity, celiac disease|Yes| 5361.0|HH8-1|C57BL/6-H2 Tg(Cd4-CD4)2362Litt Tg(HLA DR3-DQ2)303 Tg(TcraHH8,TcrbHH8)/Apb||Dominant||||||||||||||||||||||||||transgene insertion 2362, Dan R Littman|murine Cd4 and human CD4|equivalent to human CD4+ cells||||||||||Expression of HLA DR and DQ evident on B cells, dendritic cells and a proportion of macrophages.These mice Tg for hCD4.DR3-DQ2.MHCII<Δ/Δ> express functional HLA-DR3 and DQ2 molecules that mediate thymic selection generating Ag-specific CD4<+> T cell immunity. Although about one in five Europeans homozygous for HLA-DQ2 develops celiac disease, homozygous and heterozygous hCD4.DR3-DQ2.MHCII<Δ/Δ> Tg mice do not spontaneously develop hypersensitivity to gluten. However, standard immunization protocols do produce HLA-DQ2-restricted CD4+ T cells in hCD4.DR3-DQ2.MHCII<Δ/Δ> Tg mice that preferentially recognize the deamidated α-gliadin 17-mer immunodominant in human celiac disease. Nevertheless, we have found that preexisting DQ2-restricted CD4<+> T cell immunity to deamidated α-gliadin 17-mer in hCD4.DR3-DQ2.MHCII<Δ/Δ> Tg mice is not sufficient for gluten ingestion to cause measurable intestinal pathology.TCR Tg T cells proliferated following systemic administration of Α-gliadin{57–73} Q65E or chymotrypsin-digested gliadin in vivo and secreted Th1-type cytokines implicated in Celiac disease in vitro. But ingestion of gluten or Α-gliadin{57–73} Q65E did not trigger intestinal pathology in TCR Tg mice, either spontaneously or induced by immunization strategies that have produced autoimmune disease in other TCR Tg models.Findings indicate that gluten ingestion in humanized mice expressing functional HLA-DQ2 and possessing a substantial population of CD4+ T cells specific for gluten is not sufficient to cause celiac-like enteropathy.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|21-Dec-2010|Cryopreserved sperm|||Unknown||MHC, B cell, selection, autoimmunity, celiac disease|Yes| 5361.0|HH8-1|C57BL/6-H2 Tg(Cd4-CD4)2362Litt Tg(HLA DR3-DQ2)303 Tg(TcraHH8,TcrbHH8)/Apb||Dominant||||||||||||||||||||||||||T cell receptor alpha, T cell receptor beta||||||||||||Expression of HLA DR and DQ evident on B cells, dendritic cells and a proportion of macrophages.These mice Tg for hCD4.DR3-DQ2.MHCII<Δ/Δ> express functional HLA-DR3 and DQ2 molecules that mediate thymic selection generating Ag-specific CD4<+> T cell immunity. Although about one in five Europeans homozygous for HLA-DQ2 develops celiac disease, homozygous and heterozygous hCD4.DR3-DQ2.MHCII<Δ/Δ> Tg mice do not spontaneously develop hypersensitivity to gluten. However, standard immunization protocols do produce HLA-DQ2-restricted CD4+ T cells in hCD4.DR3-DQ2.MHCII<Δ/Δ> Tg mice that preferentially recognize the deamidated α-gliadin 17-mer immunodominant in human celiac disease. Nevertheless, we have found that preexisting DQ2-restricted CD4<+> T cell immunity to deamidated α-gliadin 17-mer in hCD4.DR3-DQ2.MHCII<Δ/Δ> Tg mice is not sufficient for gluten ingestion to cause measurable intestinal pathology.TCR Tg T cells proliferated following systemic administration of Α-gliadin{57–73} Q65E or chymotrypsin-digested gliadin in vivo and secreted Th1-type cytokines implicated in Celiac disease in vitro. But ingestion of gluten or Α-gliadin{57–73} Q65E did not trigger intestinal pathology in TCR Tg mice, either spontaneously or induced by immunization strategies that have produced autoimmune disease in other TCR Tg models.Findings indicate that gluten ingestion in humanized mice expressing functional HLA-DQ2 and possessing a substantial population of CD4+ T cells specific for gluten is not sufficient to cause celiac-like enteropathy.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|21-Dec-2010|Cryopreserved sperm|||Unknown||MHC, B cell, selection, autoimmunity, celiac disease|Yes| 7316.0|ENU19 WT 23b|ANU:ENU19WT:023b||Recessive|Unknown|Unknown|||||||Unknown|||||||||||||||||||||||||||||Mice have increased population of CD8+CD44 T cells|Het mice have not been assessed|C57BL/6JAnu|Yes|Unknown|Unknown|Yes|Unknown|Unknown|No|Good|0|4|affected by affacted or unaffected by affected|No|12-Apr-2013|Cryopreserved sperm|37.0|0.0|No||ENU, T cell|Possibly| 5364.0|B6.hCD4.IAE.427-3 ; triple 427|C57BL/6-H2 Tg(Cd4-CD4)2362Litt Tg(HLA DR4-DQ8)427/Apb||Dominant|histocompatibility-2, MHC|H2|Nil|H-2, MHC-II|MGI:95894|histocompatibility-2, MHC; targeted deletion, H2 complex|H2|MGI:2658725|17||||||||||||||||No|human leukocyte antigen class II||||||||||||HLA DR4 and DQ3 expression was evident on B cell but not T cells, dendritic cells and a proportion of macrophages.DR4-DQ3 mice develop protective immunity following infectious challenge with S. typhimurium.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|21-Dec-2010|Cryopreserved sperm|50.0|0.0|Unknown||MHC, B cell, selection, autoimmunity, celiac disease|Yes| 5364.0|B6.hCD4.IAE.427-3 ; triple 427|C57BL/6-H2 Tg(Cd4-CD4)2362Litt Tg(HLA DR4-DQ8)427/Apb||Dominant||||||||||||||||||||||||||transgene insertion 2362, Dan R Littman|murine Cd4 and human CD4|equivalent to human CD4+ cells||||||||||HLA DR4 and DQ3 expression was evident on B cell but not T cells, dendritic cells and a proportion of macrophages.DR4-DQ3 mice develop protective immunity following infectious challenge with S. typhimurium.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|21-Dec-2010|Cryopreserved sperm|||Unknown||MHC, B cell, selection, autoimmunity, celiac disease|Yes| 8668.0|CRISP2 flox|B6(Cg)-Crisp2/Marp||Recessive|cysteine-rich secretory protein 2|Crisp2||CRISP-2, GAPDL5, Tpx1, Tpx-1|MGI:98815|cysteine-rich secretory protein 2; targeted mutation 1c, Mouse Biology Program, UC Davis|Crisp2|MGI:6369005|17||||||||||Unknown to Unknown|||||||||||||||||||Normal|Normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|01-Mar-2019|Cryopreserved sperm|50.0|0.0|Unknown|||Yes| 7276.0|B6.RIIa Tg|B6.Fcgr 2a Tg|HOGA|Semi-dominant|Fcgamma r2a|FcgR2a|Normal||||||Unknown|||||||||||||||||human FcyR2a|human FcyR2a|normal||||||||||normal|not known|C57BL/6J|Yes|Yes|Yes|Yes|Yes|Yes|Yes|Good|12|||Yes|15-Feb-2013|Cryopreserved sperm|50.0|0.0|Yes|immune complex disease|Fc receptor, antibody, immune complex, inflammation, arthritis, thrombocytopenia|Possibly| 5133.0|Delta 359 ; Tie2DeltaCx40.359|B6;CBA-Tg(Tie2-Gja5)/AnuApb||Dominant|gap junction protein, alpha 5|Gja5|Increased|connexin 40, Cx40, Gja-5|MGI:95716||||Unknown|||||||||||||||||dominant negative of Cx40|Tie2 endothelial specific|||||||||||Unknown|Mild Hypertension|N3 B6|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Good|3|||No|25-May-2010|Cryopreserved sperm|50.0|0.0|Yes|hypertension|connexins, hypertension, gap junctions|Possibly| 5271.0|Vegfb knockout|B6.129T2-Vegfb/QimrApb|Gfk|Recessive|vascular endothelial growth factor B|Vegfb|Nil|VEGF-B, Vrf|MGI:106199 |vascular endothelial growth factor B; targeted mutation 1, Graham F Kay|Vegfb|MGI:2178819|19||||||||||||||||No|||||||||||||Corneal vascularization: corneal injection of a plasmid encoding short hairpin RNA targeting secreted Flt1 (pshRNA-sflt1) induces corneal vascularization within 3 days of injection in wild-type and mutant mice.Small heart.Decreased heart weight: heart weight is reduced in juveniles but not in early postnatal mice, indicating impaired growth of hearts in the first few weeks after birth.Abnormal cardiovascular system physiology: abnormal reactive hyperemic response to coronary occlusion, with a lower overall flow-debt repayment during the initial 60 sec of reperfusion, although peak hyperemic flow was normal.Increased time of peak ischemic contracture: peak contracture during ischemia is greater, diastolic pressure is elevated during reperfusion and recovered only minimally, and the recovery of contractile function is slightly depressed throughout reperfusion, with the rate-pressure product lower at 30 min compared with controls.|Normal|C57BL/6J|Yes|Yes|Yes|Yes|Yes|Yes|No|Excellent|20||sib-mated homozygous mice|No|25-Oct-2010|Cryopreserved sperm|45.0|0.0|No||blood vessel, heart, angiogenesis, ischmia, myocardia|Yes| 5405.0| GM CSF (L.02) ; GM(-/-).C57|C57BL/6-Csf2/LudApb||Recessive|colony stimulating factor 2 (granulocyte-macrophage)|Csf2|Nil|Csfgm, Gm-CSf, MGI-IGM|MGI:1339752|colony stimulating factor 2 (granulocyte-macrophage); targeted mutation 1, Ashley R Dunn|Csf2|MGI:1930997|11||||||||||||||||No|||||||||||||Perinatal lethality: despite normal numbers of implantation sites in early pregnancy, homozygotes exhibit fetal loss during the second half of gestation and in the perinatal period.Postnatal lethality: during the first 3 weeks of life, the survival rate of pups is affected by parental genotype, with 91.1% survival of pups born to homozygous females vs 98.0% survival of pups born to heterozygous females.Prenatal lethality: * despite normal numbers of implantation sites in early pregnancy, homozygotes exhibit fetal loss during the second half of gestation and in the perinatal period. * on day 17 of pregnancy, the mean number of resorbing and malformed embryos is twice as high in pregnant female homozygotes (21%) vs female heterozygotes (11%).Abnormal placenta development: * mutant placentas show a ~28% reduction in the ratio of labyrinthine to spongiotrophoblast areas. * structural changes in placental architecture are associated with diminished nutrient transfer and appear to contribute to embryonic growth retardation.Abnormal glycogen cell morphology: the proportion of vacuolated trophoblast glycogen cells in the mutant spongiotrophoblast zone is reduced by 20%.Abnormal spongiotrophoblast layer morphology: on day 15 of pregnancy, mutant placentas exhibit a 22% increase in the area occupied by the spongiotrophoblast relative to wild-type placentas.Placental labyrinth hypoplasia: on day 15 of pregnancy, mutant placentas exhibit a 13% reduction in the area occupied by the labyrinth relative to wild-type placentas.Abnormal alveolar macrophage morphology: by 24 weeks, mutant intraalveolar macrophages exhibit phagosomes with "onion-like" structures resembling type-C lamellar bodies.Abnormal spleen size: on day 7 postinfection, P. chabaudi AS-infected homozygotes exhibit impaired development of malarial splenomegaly relative to wild-type mice.Lymphoid hyperplasia: by 11 weeks, mutant lungs display moderate to extensive lymphoid hyperplasia around central and peripheral vessels.Abnormal leukocyte physiology: * during the periovulatory period, homozygotes exhibit a normal size and composition of ovarian leukocyte populations in the stroma and follicle theca. * however, the number of macrophages/dendritic cells expressing MHC class II (Ia) is significantly reduced in mutant ovaries at ovulation. * after parturition, the number of ovarian macrophages and neutrophils is significantly decreased, with significantly reduced CD11b+ (Mac-1) staining in the stromal region.Abnormal MHC II cell surface expression on macrophages: at ovulation, mutant ovarian macrophages and/or dendritic cells exhibit reduced MHC class II (Ia) expression, suggesting impaired macrophage activation within the ovarian stroma and theca.Impaired macrophage recruitment: during the postpartum period, mutant ovaries exhibit reduced recruitment of macrophages and neutrophils in the stromal region.Lung inflammation: * starting at ~3 weeks, all homozygotes exhibit a nonfatal lung pathology, with local accumulation of surfactant protein within alveoli and a high incidence of bacterial and fungal infection resembling human alveolar proteinosis. * by 12-16 weeks, mutant lungs display extensive peribronchovascular infiltration with lymphocytes, primarily B cells and ~20% T cells (mostly CD4+).Increased susceptibility to bacterial infection: * one 4-week-old homozygote has been shown to die of purulent acute Pasteurella pneumotropica lobar pneumonia. * Gram-positive coccobacilli are detected in 7-week-old pneumonic consolidated areas. * virgin homozygotes exhibit an increased incidence of subclinical bacterial colonization of the uterus, with Pasteurella pneumotropica recovered from 50% of mutant uteri; clearance of bacterial organisms from the reproductive tract occurs normally after mating.Increased susceptibility to fungal infection: at 16 weeks, 3 of 15 mutant lungs contain foci of infection with Grocott-positive fungal particles.Increased susceptibility to parasitic infection: homozygotes are more susceptible to infection with P. chabaudi AS, as shown by higher peak parasitemia, recurrent recrudescent parasitemia, and significantly increased mortality relative to wild-type mice.Abnormal lung morphology.Abnormal respiratory alveoli morphology: * at 6-12 weeks, mutant alveoli contain large foamy macrophages, neutrophils, and eosinophilic alveolar debris. * surfactant-producing type-II alveolar cells are readily identifiable by their cytoplasmic type-C lamellar bodies.Abnormal alveolar macrophage morphology: by 24 weeks, mutant intraalveolar macrophages exhibit phagosomes with "onion-like" structures resembling type-C lamellar bodies.Emphysema: a number of older homozygotes display lungs with enlarged alveolar spaces, suggestive of emphysematous processes with peristent peribronchovascular lymphoid hyperplasia.Absent mature ovarian follicles: homozygotes exhibit impaired ovarian follicle maturation.Decreased ovary weight: * on day 4 of natural pregnancy, homozygotes show a significant reduction in ovarian weight relative to wild-type mice * in contrast, the number of corpora lutea remains normal.Abnormal uterus morphology: * homozygotes exhibit normal uterine development with no discernible differences in the process of decidualization and normal size and distribution of uterine granulocyte and macrophage populations during the estrous cycle, early pregnancy, and midgestation. * however, recently mated or parous mice are occasionally found to have chronic uterine abscesses, as a result of Pasteurella pneumotropica infection.Abnormal ovulation: * immature homozygotes primed with gonadotropins and naturally cycling adult homozygotes exhibit normal ovulation rates relative to wild-type counterparts. * however, in vitro, 70% of wild-type ovaries perfused with LH ovulate one or more oocytes vs 93% of homozygous mutant ovaries; the mean number of oocytes ovulated per mutant ovary is 2.8-fold higher but addition of rmGM-CSF has no effect on the ovulation rate in mutant ovaries. * in vitro, LH-perfused mutant ovaries show a 57% increase in nitrate/nitrite secretion relative to media-perfused and LH-perfused wild-type ovaries; however, addition of rmGM-CSF to mutant ovaries does not increase NO liberation.Prolonged diestrus: a significantly longer diestrus stage is observed.Prolonged metestrus: a significantly longer metestrus-2 stage is observed.Prolonged estrous cycle: in homozygotes, the mean duration of estrous cycle is extended by 1.5 days, with a significantly longer metestrus-2 and/or diestrus stage relative to wild-type mice.Impaired luteinization: * homozygotes display impaired luteinization and steroidogenic function of the corpus luteum during early pregnancy, as a result of altered recruitment and activation of ovarian myeloid leukocytes. * notably, homozygotes exhibit no differences in the time frame of corpus luteum demise, as the length of pseudopregnancy is comparable to that observed in wild-type mice.Abnormal fertility/fecundity.Decreased litter size: * the mean litter sizes of homozygous mutant breeding pairs are 25% smaller at weaning compared with heterozygous pairs, due to fetal death late in gestation and early in postnatal life. * reduced litter size appears to reflect a selective loss of male pups, with approximately one male less per litter weaned from homozygous mutant females than from heterozygous females.Reduced fertility: homozygotes display a moderate decrease in fertility, manifested as a 25% reduction in litter size at weaning.Decreased body size: * at weaning, surviving homozygous mutant pups are significantly smaller than wild-type pups. * in males, reduced body size persists into adulthood.Postnatal growth retardation: homozygotes exhibit slow growth kinetics after birth.Decreased fetal size: * on day 17 of pregnancy, the number of very small fetuses (< 500 mg) is 9-times as high in pregnant female homozygotes (23%) vs female heterozygotes (2.5%). * the mean fetal weight and the mean fetal:placental ratio in surviving conceptuses are reduced by 7% and 6%, respectively.Fetal growth retardation: homozygotes exhibit slow growth kinetics in utero.Decreased circulating progesterone level: * on day 4 of natural pregnancy, adult homozygotes exhibit significantly reduced plasma progesterone levels (116.5 ± 6 nM) relative to wild-type mice (141.6 ± 10.3 nM) * however, no major alterations in steroid secretion are noted at ovulation.Maternal effect: * litter sizes in homozygous deficient mothers are less severely affected in pregnancies sired by wild-type males, with resorption rates, fetal weights, and fetal:placental ratios being more comparable to normal values. * conversely, fetal weights and fetal:placental ratios are not reduced in homozygous deficient embryos gestating in replete mothers.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|02-Feb-2011|Cryopreserved sperm|50.0|0.0|Yes|Surfactant Metabolism Dysfunction, Pulmonary, 1; SMDP1|macrophage, lung, B cell, surfactant, progenitor|Yes| 5262.0|gp130fl/fl|C57BL/6-Il6st||Recessive|interleukin 6 signal transducer|Il6st|Normal|CD130, gp130|MGI:96560|interleukin 6 signal transducer; targeted mutation 1, Werner Mueller|Il6st|MGI:1931239|13||||||||||||||||Yes|||||||||||||Abnormal heart development.Abnormal erythropoiesis: resynthesis of erythrocytes is impaired after mice are treated with 5-fluoro-5'-deoxyuridine.Increased leukocyte cell number: there is an increased number of circulating leukocytes.Abnormal T cell differentiation.Decreased thymocyte number: the T-cell population is reduced by 30%.Abnormal thrombopoiesis: * there is a reduced thrombocyte count in the peripheral blood. * resynthesis of thrombocytes is impaired after mice are treated with 5-fluoro-5'-deoxyuridine.Increased leukocyte cell number.Abnormal immunoglobulin level: * there is an increase in the circulating level of IgG1 * there is an increase in the circulating level of IgE.Abnormal Schwann cell morphology: in myocardium and gut incomplete Schwann cell covering of small and thick bundles noted.Abnormal myelination: range of defects are noted from loss of laminar structure to loss of myelin sheath and axon lysis.|Unknown|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|21-Oct-2010||0.0|0.0|Unknown||osteocytes, signal transduction, gp130|Possibly| 7610.0|DBM/J|BKS.Cg-Dock7 +/+ Lepr/JAusb||Dominant|dedicator of cytokinesis 7|Dock7||3110056M06Rik, LOC242555, m, mKIAA1771|MGI:1914549|dedicator of cytokinesis 7; misty|Dock7|MGI:1856946|4|||||||||||||||||||||||||||||Displays a mellitus diabetes at 3-4 weeks of age||C57BL/6|Yes|No|Yes|Yes|No|Yes|No|Unknown||||No|28-Feb-2014||0.0|0.0|Unknown||melanocyte|Yes| 7610.0|DBM/J|BKS.Cg-Dock7 +/+ Lepr/JAusb||Dominant|leptin receptor|Lepr||Leprb, LEPROT, leptin receptor gene-related protein, Modb1, obese-like, obl, Obr, OB-RGRP|MGI:104993|leptin receptor; diabetes|Lepr|MGI:1856009|4|||||||||||||||||||||||||||||Displays a mellitus diabetes at 3-4 weeks of age||C57BL/6|Yes|No|Yes|Yes|No|Yes|No|Unknown||||No|28-Feb-2014||||Unknown||melanocyte|Yes| 5482.0|TGF (-/-) L-05|STOCK Tgfa/LudApb||Recessive|transforming growth factor alpha|Tgfa|||MGI:98724|transforming growth factor alpha; targeted mutation 1, Ashley R Dunn|Tgfa|MGI:1856577|6||||||||||||||||No|||||||||||||Increased incidence of corneal inflammation.Eyelids open at birth.Increased incidence of corneal inflammation.Waved hair: attenuated slightly with age.Increased curvature of hairs.Abnormal hair follicle orientation.Curly vibrissae: attenuated slightly with age.|Normal|Un|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|14-Apr-2011|Cryopreserved sperm|50.0|0.0|Unknown||cornea, coat, fur|Yes| 5573.0|Par2 KO|129X1/Sv-PAR2/Apb||Recessive|coagulation factor II (thrombin) receptor-like 1|F2rl1|Nil|Gpcr11, PAR-2, Par2, Protease-activated receptor-2, proteinase-activated receptor-2|MGI:101910|coagulation factor II (thrombin) receptor-like 1; targeted mutation 1, Mary Stevens|F2rl1|MGI:2389587|13|||||||||||||||||||||||||||||Normal|Normal|129Sv|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|01-Sep-2011|Cryopreserved sperm|50.0|0.0|Unknown||protease, infection, eosinophil, inflammation|Yes| 7611.0|Cr6-GFP|B6.129S6-Ccr6/JAusb||Dominant|chemokine (C-C motif) receptor 6|Ccr6|Normal|Cmkbr6|MGI:1333797|chemokine (C-C motif) receptor 6; targeted mutation 1, Ifor R Williams|Ccr6|MGI:2179543|17|||||||||||||||||||||||||||||The B cell lineage expression pattern from this allele visualized using EGFP matches that of wild-type gene expression previously described using a mouse-specific monoclonal antibody. |The B cell lineage expression pattern from this allele visualized using EGFP matches that of wild-type gene expression previously described using a mouse-specific monoclonal antibody. |C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|28-Feb-2014||0.0|0.0|Unknown||B cell, CD4, CD8, T cell, CD11b|Yes| 4455.0||B6.129-Rel/WehiAnuApb||Recessive|reticuloendotheliosis oncogene|Rel|Unknown|c-Rel|MGI:97897|targeted mutation 1, Steve Gerondakis|Rel|MGI:2179622|11||||||||||||||||No|||||||||||||In mice with an inactivated c-rel gene, whereas development of cells from all hemopoietic lineages appeared normal, humoral immunity was impaired and mature B and T cells were found to be unresponsive to most mitogenic stimuli. Phorbol ester and calcium ionophore costimulation, in contrast to certain membrane receptor-mediated signals, overcame the T cell-proliferative defect, demonstrating that T cell proliferation occurs by Rel-dependent and -independent mechanisms.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|20-Feb-2009|Cryopreserved sperm|120.0|0.0|Unknown||Lymphocyte, IL-2, humoral immunity|Yes| 5218.0|ATM null 129/SvJ|129/SvJ-Atm/AnuApb||Recessive|ataxia telangiectasia mutated homolog (human)|Atm|Nil||MGI:107202|ataxia telangiectasia mutated homolog (human); targeted mutation 1, Frederick W Alt|Atm|MGI:1933748|9|||||||||||||||||||||||||||||Smaller than littermate controls (about 20% reduction in size). ATM null male and females are infertile; 1% develop B or T cell lymphomas by >9 mths.|Normal|129/SvJ|Yes|No|Yes|Yes|No|Yes|Yes|Poor|||ATM het to ATM het crossings required|No|14-Sep-2010|Cryopreserved sperm|90.0|0.0|Yes|ataxia-telangiectasia (A-T)|human hepatocellular carcinoma (HCC), p53, kinase, Ataxia Telangiectasia Mutated (ATM), DNA repair, Purkinje cells, T cell (CD4+CD8+)|Possibly| 8678.0|Slc17a9 mutant|C57BL/6-Slc17a9/Marp||Recessive|solute carrier family 17, member 9|Slc17a9||1700019H03Rik, MGC:28538, Vnut|MGI:1919107||||2|||||||||||||||||||||||||||||No visual phenotype.Otherwise unknown.|Unknown|C57BL/6JArc|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|19-Mar-2019|Cryopreserved sperm|50.0|0.0|Unknown|||Yes| 10378.0|C57Bl/6-TFF2(CreERT2)-ROSA26tdTomato |B6(Cg)-Tg(Tff2-cre/ERT2)#Tcw (Cg)-Gt(ROSA)26Sor/J||Semi-dominant|gene trap ROSA 26, Philippe Soriano|Gt(ROSA)26Sor ||Gtrosa26, R26|MGI:104735|gene trap ROSA 26, Philippe Soriano; targeted mutation 4, Liqun Luo|Gt(ROSA)26Sor|MGI:3716464|6|ENSMUSG00000086429||||||||||||||||||||||||||||Normal|Normal|C57Bl/6J|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|21-Nov-2023|Cryopreserved sperm|11.0|0.0|Unknown|||Possibly| 8670.0|Bmi1|B6J;129-Bmi1/JAnu||Dominant|Bmi1 polycomb ring finger oncogen|Bmi1||Bmi1, Bmi-1, Pcgf4|MGI:88174|Bmi1 polycomb ring finger oncogene; targeted mutation 1, Mario R Capecchi|Bmi1|MGI:3805814|2||||||||||||||||||||||||||||||These targeted mutant mice carry tamoxifen-inducible Cre under the transcriptional control of the mouse Bmi1 (Bmi1 polycomb ring finger oncogene) promoter. When crossed with a strain containing a loxP-flanked sequence of interest, the offspring are useful for generating tamoxifen-induced, Cre-mediated targeted deletions, and when crossed with a floxed reporter strain, lineage tracing of Bmi1-expressing cells is possible. |C57BL/6J|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|04-Mar-2019|Cryopreserved sperm|11.0|0.0|Unknown||Cre, Crypt|Yes| 5094.0|gBT-I.1xA/J|A.B6-Tg(TcraHsv2.3,TcrbHsv2.3)L118-1Cbn/Apb||Dominant||||||||||||||||||||||||||transgene insertion L118-1, Francis R Carbone|2 kb fragment of the H-2Kb and a 700 bp fragment including the Igh enhancer|||||||||||Normal|Normal|A/J|Yes|Yes|Yes|Yes|Yes|Yes|No|Poor|10|7|brother x sister mating|Yes|19-Apr-2010|Cryopreserved sperm|50.0|0.0|No||TCR tansgenic, Herpes Simplex Virus (HSV-1), glycoprotein B, cytotoxic T lymphocyte|Possibly| 5132.0|gBT-I.3beta|C57BL/6-Tg(TcrbHsv2.3)L118-3Cbn/CbnApb||Dominant||||||||||||||||||||||||||transgene insertion L118-3, Frank Carbone|Tcrb|||||||||||The majority of CD8 T cells express the transgenic Vb8.1 T cell receptor. The development of CD8 T cells is enhanced and CD4 T cells is diminished.In other respects the mouse has a similar phenotype to C57BL/6 mice.|As for homozygous|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||24|brother x sister mating|Yes|24-May-2010|Cryopreserved sperm|50.0|0.0|No||TCR tansgenic, Herpes Simplex Virus (HSV-1), glycoprotein B, cytotoxic T lymphocyte|Yes| 5138.0|Vb4-10|C57BL/6-Tg(Tcrb4BH-98)10Cbn/JWehiApb||Dominant||||||||||||||||||||||||||transgene insertion 4BH-98 TCRbeta, Francis R Carbone|Tcrb|||||||||||Greater than 95% of CD8+ T cells and 75% of CD4 T cell in the lymph node express the transgenic TCRbeta.|As for homozygous|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|||brother-sister|No|27-May-2010|Cryopreserved sperm|50.0|0.0|No||TCR beta transgenic, murine gamma herpesvirus|Possibly| 5384.0|Stx16|C57BL/6-Stx16||Dominant|Syntaxin 16|Stx16|Unknown|SYN16|MGI:1923396||||2||||||||||||||||No|||||||||||||Unknown|Normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|||Homozygous pairs|No|11-Jan-2011|Cryopreserved sperm|50.0|0.0|No||SNAREs, GLUT4 recycling, Trafficking, Trans Golgi Network|Possibly| 5421.0|Pax-6|C57BL/6-Pax6/Apb||Dominant|paired box gene 6|Pax6|Unknown|AEY11, Dey, Dickie's small eye, Gsfaey11, Pax-6|MGI:97490|paired box gene 6; small eye, Neuherberg|Pax6|MGI:1856158|2||||||||||||||||No|||||||||||||No remnants of eye formation, and a much shorter snout. Abnormal craniofacial morphology.|Smaller eye than wild type mice. Abnormal craniofacial morphology.|C57BL/6|No|No|Yes|No|No|Yes|No|Unknown||||No|07-Feb-2011|Cryopreserved sperm|50.0|0.0|Unknown||Lens, eye, retina|Possibly| 5185.0|MMP13KO RAG1KO FVBn|FVB/N(Cg)-Mmp13 Rag1/Apb||Recessive|matrix metallopeptidase 13|MMP13|Nil|Clg, collagenase-1, Collagenase-3, interstitial collagenase, MMP-13, Mmp1|MGI:1340026|matrix metallopeptidase 13; targeted mutation 1.1, Zena Werb|Mmp13||9||||||||||Unknown to Unknown|||||||||||||||||||Increased width of hypertrophic chondrocyte zone: * the hypertrophic zone is expanded in the tibia and metatarsals, at E17 and 1 week after birth, respectively, however by 12 weeks of age the size of the hypertrophic zone is similar to wild-type. * chondrocytes proliferate and differentiate normally but accumulate in the most terminally differentiated hypertrophic state. * establishment of the primary ossification centers is normal.Abnormal cancellous bone morphology: * the amount of trabecular bone is increased in the tibia and metatarsals by 3 weeks or 1 week of age, respectively, however by 1 year of age the amount of trabecular bone was similar to wild-type. * the organization of the trabecular bone is also irregular.OA was surgically induced in the knees of MMP-13-knockout mice. No difference between wildtype and KO mice for aggrecan loss or cartilage erosion at 4 weeks. here was less tibial cartilage erosion in knockout mice than in wild-type mice at 8 weeks. Cartilaginous osteophytes were larger in knockout mice at 4 weeks, but by 8 weeks osteophyte maturity and size were no different from those in wild-type mice. Articular chondrocyte hypertrophy with positive type X collagen and DIPEN staining occurred in both wild-type and knockout mouse joints. Authors conclude Chondrocyte hypertrophy is not regulated by MMP-13 activity in this model and does not in itself lead to cartilage erosion. MMP-13 deficiency can inhibit cartilage erosion in the presence of aggrecan depletion, supporting the potential for therapeutic intervention in established OA with MMP-13 inhibitors.||FVB/N|Yes|Yes|Yes|Yes|Yes|Yes|No|Poor|10|||No|28-Jul-2010|Cryopreserved sperm|50.0|0.0|Yes|spondyloepimetaphyseal dysplasia|extracellular matrix, collagenase, chondrocyte, osteoblast, growth plate|Possibly| 5185.0|MMP13KO RAG1KO FVBn|FVB/N(Cg)-Mmp13 Rag1/Apb||Recessive|recombination activating gene 1|Rag1||Rag-1|MGI:97848||Rag1||2||||||||||Unknown to Unknown||||||No|||||||||||||Increased width of hypertrophic chondrocyte zone: * the hypertrophic zone is expanded in the tibia and metatarsals, at E17 and 1 week after birth, respectively, however by 12 weeks of age the size of the hypertrophic zone is similar to wild-type. * chondrocytes proliferate and differentiate normally but accumulate in the most terminally differentiated hypertrophic state. * establishment of the primary ossification centers is normal.Abnormal cancellous bone morphology: * the amount of trabecular bone is increased in the tibia and metatarsals by 3 weeks or 1 week of age, respectively, however by 1 year of age the amount of trabecular bone was similar to wild-type. * the organization of the trabecular bone is also irregular.OA was surgically induced in the knees of MMP-13-knockout mice. No difference between wildtype and KO mice for aggrecan loss or cartilage erosion at 4 weeks. here was less tibial cartilage erosion in knockout mice than in wild-type mice at 8 weeks. Cartilaginous osteophytes were larger in knockout mice at 4 weeks, but by 8 weeks osteophyte maturity and size were no different from those in wild-type mice. Articular chondrocyte hypertrophy with positive type X collagen and DIPEN staining occurred in both wild-type and knockout mouse joints. Authors conclude Chondrocyte hypertrophy is not regulated by MMP-13 activity in this model and does not in itself lead to cartilage erosion. MMP-13 deficiency can inhibit cartilage erosion in the presence of aggrecan depletion, supporting the potential for therapeutic intervention in established OA with MMP-13 inhibitors.||FVB/N|Yes|Yes|Yes|Yes|Yes|Yes|No|Poor|10|||No|28-Jul-2010|Cryopreserved sperm|||Yes|spondyloepimetaphyseal dysplasia|extracellular matrix, collagenase, chondrocyte, osteoblast, growth plate|Possibly| 7317.0|ENU22:49rik|C57BL/6NCrlAnu-Atp6v0a4/AnuApb|C57BL/6NCrlAnu-Atp6v0a4/AnuApb|Recessive|ATPase, H+ transporting, lysosomal V0 subunit A4|Atp6v0a4||Atp6n1b, V-ATPase alpha 4|MGI:2153480|ATPase, H+ transporting, lysosomal V0 subunit A4; mutation 1, The Australian National University|Atp6v0a4|MGI:5563513|6|ENSMUSG00000038600|ENSMUST00000114908|Atp6v0a4-002|166|464|G to A|ENSMUSE00001242165|4|56|Arginine to STOP|||||GCTTCCAGAGGAAGTTTGTGAATGAAGTCCGAAGGTGTGAGTCACTGGAGAGAATCCTGCG||||||||||||||Premature death|Unknown|C57BL/6NCrlAnu|Yes|No|Yes|Yes|No|Yes|No|Unknown||G4||No|12-Apr-2013|Cryopreserved sperm|26.0|0.0|Unknown||ENU, premature death|Yes| 5383.0|Thy1.1|CBy.PL(B6)-Thy1a/ScrJ||Dominant|||||||||||||||||||||||||||||thymus cell antigen 1, theta|Thy1||CD90, T25, theta, Thy 1.2, Thy-1, Thy-1.2, Thy1.1, Thy1.2|MGI:98747|thymus cell antigen 1, theta; a variant|Thy1|MGI:3579311|9|Normal|Normal|BALB/c|Yes|Yes|Unknown|Yes|Yes|Unknown|No|Excellent|||Homozygous|Yes|07-Jan-2011|Cryopreserved sperm|20.0|0.0|Unknown||Thy1.1, congenic, Balb/c|Yes| 5424.0|PRrtTAKI|129.Cg-Pgr/Apb||Dominant|progesterone receptor|Pgr||NR3C3, PR, PR-A, PR-B|MGI:97567|progesterone receptor; targeted mutation 3, John P Lydon|Pgr|MGI:3768562|9||||||||||||||||Yes|||||||||||||Abnormal female reproductive system morphology: authors state that the phenotype is identical to that of Pgr homozygotes.Female infertility: authors state that the phenotype is identical to that of Pgr homozygotes.|Unknown|crossed within line|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||4 @ Host institution|All genotypes are viable and fertile, any combination can be used. We often cross Male Het with Female Hom|No|09-Feb-2011|Cryopreserved sperm|50.0|0.0|Unknown||Progesterone Receptor, mammary gland, corpus luteum, ovarian follicle, uterus|Possibly| 5507.0|Blimp-Gfp|C57BL/6JWehi-Prdm1/AnuApb||Dominant|PR domain containing 1, with ZNF domain|Prdm1|Normal|Blimp-1, Blimp1, PRDI-BF1|MGI:99655|PR domain containing 1, with ZNF domain; targeted mutation 1, Stephen L Nutt|Prdm1|MGI:3510704|10||||||||||||||||Yes|||||||||||||Prenatal lethality: homozygotes die in late gestation||C57BL/6|No|No|Yes|No|No|Yes|No|Unknown||||No|16-May-2011|Cryopreserved sperm|38.0|0.0|No||B cell, plasma cell|Yes| 7612.0|MIP-Cre|B6.CD1-Tg(Ins1-Cre/ERT)/Ausb||Dominant||||||||||||||||||||||||||transgene insertion 1, Louis Philipson|Ins1|||||||||||Normal||C57BL/6|Yes|Unknown|Yes|Yes|Unknown|Yes|No|Unknown||||No|28-Feb-2014||0.0|0.0|Unknown||Cre recombinase, pancreas|Yes| 7685.0|Notch4null|B6(Cg)-Notch4/Apb||Recessive|notch 4|Notch4|Nil|Int3, Int-3, N4|MGI:107471|notch 4; targeted mutation 1, Velocigene|Notch4|MGI:4842905|17|||||||||||||||||||||||||||||Mild delay in retinal angiogenesis|Normal|C57BL/6J|Yes|Yes|Unknown|Yes|Yes|Unknown|No|Good|7 generations|||No|22-May-2014|Cryopreserved sperm|48.0|0.0|Unknown|||Yes| 5473.0|Gpc3 knockout|B6;Cg-Gpc3/Apb||Dominant|glypican 3|Gpc3|Nil|OCI-5|MGI:104903|glypican 3; targeted mutation 1, Jorge Filmus|Gpc3|MGI:2159356|X||||||||||||||||No|||||||||||||Phenotype is highly strain dependent. For example, as the proportion of C57BL/6 background increases, phenotypic effects typical of Simpson-Golabi-Behmel syndrome begin to manifest and become more severe with increasing proportion of C57BL/6 background. For females, affected tissues include, craniofacial, skeletal, renal, urinary, respiratory and reproductive systems. Animals are also larger. Postnatal lethality: phenotype is stated to be similar to that of Gpc3tm1Fil male hemizygotes; however, no data are presented in.Mandible hypoplasia.Abnormal perineum morphology: mutant females with an imperforate vagina display swelling of the perineum.Abnormal perineum morphology: mutant females with an imperforate vagina display swelling of the perineum.Dilated uterus: mutant females with an imperforate vagina have a dilated, fluid-filled uterus.Vagina atresia: mutant females exhibit an imperforate vagina at a higher frequency (30%) than wild-type females (4%).Lung inflammation.Increased susceptibility to bacterial infection.Abnormal kidney development.Abnormal ureteric bud morphology.Abnormal ureteric bud branching morphogenesis.Kidney cysts.Increased body weight.|Because Gpc3 is on the X chromosome, affected males are hemizygous and show many of the phenotypic characteristics of homozygous females.Females:Abnormal kidney development: * from N4 on, some heterozygous females display dysplastic kidneys (also noted in a large proportion of mice from earlier backcrosses) * the degree of renal dysplasia varies from mouse to mouse.Abnormal ureteric bud morphology.Abnormal ureteric bud branching morphogenesis.Kidney cysts: from N4 on, some heterozygous females display cystic kidneys (also noted in a large proportion of mice from earlier backcrosses).Increased body weight: heterozygotes display an intermediate size between hemizygous mutant males and wild-type controls at all time points.|C57BL/6 x CD-1|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|unknown||Complex. Maintain on 50:50 C57BL/6 x CD-1 (or Swiss) until required to study phenotypic effects. Then, cross to C57BL/6 to "develop" phenotype.|No|01-Apr-2011|Cryopreserved sperm|45.0|0.0|Yes|Simpson-Golabi-Behmel syndrome|glypican, heparan sulfate proteoglycans, Simpson-Golabi-Behmel syndrome, Gpc 3|Possibly| 8672.0|Il1r1 KO|B6-129S-Il1r1/JAnu||Recessive|interleukin 1 receptor, type I|Il1r1|Nil|CD121a, Il1r-1, IL-1R1, IL-1 receptor alpha chain, IL-iR|MGI:96545|interleukin 1 receptor, type I; targeted mutation 1, Immunex Research and Development Corporation|Il1r1|MGI:1861112|1|||||||||||||||||||||||||||||Increased circulating interleukin-1 beta level:• 96 hours following S. aureus infection.Decreased circulating interleukin-18 level: • 24 hours following S. aureus infection.Increased circulating interleukin-18 level:• 96 hours following S. aureus infection.Decreased circulating interleukin-6 level: • 4 and 24 hours following S. aureus infection.Decreased interleukin-6 secretion: • in spleen cells stimulated with formalin-killed S. aureus infection for 48 hours• within wound fluids on days 1, 3, 5, 10, and 14 of wound healing.Decreased tumor necrosis factor secretion:• in spleen cells stimulated with formalin-killed S. aureus infection.Increased susceptibility to induced arthritis:• following S. aureus infection.Increased susceptibility to bacterial infection:• following S. aureus infection, mice exhibit severe septicemia, increased weight loss, increased frequency and severity of arthritis, increased bacterial load, and decreased survival compared with wild-type mice.Increased susceptibility to bacterial infection induced morbidity/mortality:• following S. aureus infection.Sepsis:• following S. aureus infectionAbnormal vascular wound healing:• following carotid ligation, mice exhibit a 19-fold reduction in neointima/media area, 3.4-fold increase in lumen area, and decrease in total vessel area compared with wild-type mice• neointima formation following carotid ligation is disrupted to a greater extent when null mice transplanted with null bone marrow compared when null mice are receive wild-type bone marrow or wild-type mice receive null bone marrow.Increased circulating insulin level:• 2-fold in 9 and 11 month old mice.Increased circulating insulin-like growth factor I level:• in older mice.Increased circulating leptin level:• 2-fold in 9 and 11 month old mice.Increased respiratory quotient:• during the first half of the dark cycle.Impaired glucose tolerance:• following glucose challenge, older mice exhibit impaired plasma glucose elimination compared with wild-type mice.Insulin resistance:• in older mice.Decreased transforming growth factor level:• within wound fluids on day 1 of wound healing.Enhanced wound healing:• after wound healing, mice exhibit decreased scar width and depth compared with wild-type mice• deep tissue wounds exhibit 3-fold less fibrosis compared to in wild-type mice• however, mice exhibit normal cellular infiltration and tensile strength of skin woundsIncreased body mass index:• in older mice.Abnormal lean body mass:• older mice exhibit a decrease in percentage lean body mass but an increase in absolute lean body mass compared with wild-type mice.Weight loss:• following S. aureus infection.Increased body weight:• after 5 to 6 months.Increased body length:• in older mice.Increased susceptibility to age related obesity.Increased growth rate:• in older miceIncreased total body fat amount:• 2-fold at 9 months of age• however, mice exhibit normal body fat at 4 months of age.Increased gonadal fat pad weight:• in older mice.Increased inguinal fat pad weight:• in older mice.Increased mesenteric fat pad weight:• in older mice.Increased retroperitoneal fat pad weight:• in older mice.Increased abdominal fat pad weight:• at 19 months, intra-abdominal fat mass is increased 1.5- to 1.7-fold compared with wild-type mice.Increased percent body fat/body weight:• in older miceEnhanced contextual conditioning behavior. Abnormal food intake:• preobese mice exhibit mild leptin resistance compared with wild-type mice.Decreased anxiety-related response:• mice exhibit reduced latency to drink in a novelty-induced hypophagia test compared with wild-type mice• mice spend more time in the open arms of an elevated plus maze compared with wild-type mice• mice exhibit increased latency to enter into the dark chamber in a light/dark test compared with wild-type mice.Hypoactivity :• during the dark phase at 4 months.Increased liver weight:• in older mice.Abnormal nervous system electrophysiolog:• following administration of kainate, Purkinje cells fail to exhibit an increase in firing rate unlike wild-type cells||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|04-Mar-2019||0.0|0.0|Unknown||LPS, IL-1|Yes| 10380.0|C57BL/6NCrlAnu-Tex2/Anu|ENU54:272:Tex2:B6||Semi-dominant|testis expressed gene 2|Tex2||Def-5, mKIAA1738, Taz4|MGI:102465|Tex2 |||11|ENSMUSG00000040548|ENSMUST00000042780|||||||||||||||||||||||||||unknown|unknown|C57Bl/6N|Yes|Unknown|Yes|Yes|Yes|Yes|No|Good||||No|24-Nov-2023|Cryopreserved sperm|20.0|0.0|Unknown|||No| 5425.0|Tpcn1∆|129S5/SvEvBrd-Tpcn1/Apb||Dominant|two pore channel 1|Tpcn1|Unknown||MGI:2182472|two pore channel 1; gene trap OST359423, Lexicon Genetics|Tpcn1|MGI:3529820|5||||||||||||||||No|||||||||||||Unknown|Unknown|129S5/SvEvBrd|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||4 @ Garvan|We keep Homozygous|No|09-Feb-2011|Cryopreserved sperm|35.0|0.0|Unknown||channel, Pore|Possibly| 5426.0|ELFBtgxMTBtg|FVB/N-Tg(MMTV-rtTA)1Lach Tg(tetO-Elf5-EGFP)1Cor||Dominant||||||||||||||||||||||||||transgene insertion 1, Lewis A Chodosh|MMTV LTR|||||||||||Unknown|Unknown|FVB/N|Unknown|Unknown|Yes|Unknown|Unknown|Unknown|Yes|Poor||17|Researchers cross Male WT, WT with female ELFBtg/+, MTBtg/+ or male WT, MTBtg/+ with female ELFBtg/+, WT|No|09-Feb-2011||0.0|0.0|Unknown|||No| 5426.0|ELFBtgxMTBtg|FVB/N-Tg(MMTV-rtTA)1Lach Tg(tetO-Elf5-EGFP)1Cor||Dominant||||||||||||||||||||||||||Transgene insertion 1 Chris Ormandy|tetracycline operon|||||||||||Unknown|Unknown|FVB/N|Unknown|Unknown|Yes|Unknown|Unknown|Unknown|Yes|Poor||17|Researchers cross Male WT, WT with female ELFBtg/+, MTBtg/+ or male WT, MTBtg/+ with female ELFBtg/+, WT|No|09-Feb-2011||||Unknown|||No| 5428.0|TnI.1; cTnIwt.1|C57BL/6-Tg(Myh6-TNNI3*wt)1Chs/Apb||Dominant||||||||||||||||||||||||||transgene insertion wild type 1, Christopher Semsarian|cardiac specific mouse αMHC promoter (alpha myosin heavy chain)|50% of endogenous (hemizygous)||||||||||Unknown|Indistinguishable from non-transgenic wild type C57BL/6 mice |C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Excellent||17, of which 13 have been maintaned as homozygous|Homozygous transgenic x homozygous transgenic sibs|No|10-Feb-2011|Cryopreserved sperm|45.0|0.0|Yes|Hypertrophic cardiomyopathy (HCM) is a primary disorder of the myocardium characterized by cardiac hypertrophy. The clinical course of HCM is variable, with inter- and intra-familial variations ranging from benign asymptomatic disease to a malignant phenotype with a high risk of cardiac failure or sudden cardiac death.|Hypertrophy, Cardiomyopathy, Calcium, Troponin I gene|Yes| 7613.0|FcgR2Δ|C57BL/6-Fcgr2b/Ausb||Recessive|Fc receptor, IgG, low affinity IIb|Fcgr2b|Nil|CD32, F630109E10Rik, FcgammaRIIB, Fc gamma RIIB, Fcgr2, Fcgr2a, FcgRII, Fc[g]RII, Fcr-2, Fcr-3, Ly-17, LyM-1, Ly-m20|MGI:95499|Fc receptor, IgG, low affinity IIb; targeted mutation 1.2, J Sjef Verbeek|Fcgr2b|MGI:5427927|1||||||||||||||||||||||||||||||Modifier of autoimmune susceptibility.|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|28-Feb-2014||0.0|0.0|Unknown||autoimmunity|Yes| 3325.0|TGM2 KO|B6.129-Tgm2/Apb||Recessive|transglutaminase 2, C polypeptide|Tgm2|Nil|G[a]h, protein-glutamine gamma-glutamyltransferase, TG C, TG2, tissue transglutaminase, tTG, tTGas|MGI:98731|targeted mutation 1.1, Robert M Graham|Tgm2|MGI:3527996|2||||||||||||||||No|||||||||||||Abnormal cell adhesion: fewer homozygous fibroblasts (20% versus 79% of wild-type) adhered to poly-L-coated or fibronectin coated slidesAbnormal T cell physiology: 24 hours after induction of apoptosis by dexamethasone treatment, homozygotes had smaller thymuses due to decreased viability of thymocytes and increased clearance of dead cells compared to controls, however mutants are viable, normal in size and weight, have normal separation of digits and open eyelids and no difference in thymocyte numbers, indicating that developmental apoptosis was not impaired.||129S1/SvImJ * C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|15-Jun-2008|Cryopreserved sperm|50.0|0.0|Unknown||transgluatminase, Gh, G-protein, cross linking, T cell|Yes| 7319.0|Raptorfl/fl|B6.129-Rptor/Adel||Dominant|regulatory associated protein of MTOR, complex 1|Rptor||4932417H02Rik, mKIAA1303, Rap, raptor|MGI:1921620|regulatory associated protein of MTOR, complex 1; targeted mutation 1, Markus A Ruegg|Rptor|MGI:3829770|11|||||||||||||||||||||||||||||Normal|Unknown|C57BL/6|Yes|Yes|Unknown|Yes|Yes|Unknown|No|Good|||homozygote x homozygote|No|18-Apr-2013|Cryopreserved sperm|75.0|0.0|Unknown||Muscle, mTor|Possibly| 7320.0|Rictorfl/fl|B6.129-Rictor/Adel||Dominant|RPTOR independent companion of MTOR, complex 2|Rictor||921505C17Rik, 6030405M08Rik, D530039E11Rik|MGI:1926007|RPTOR independent companion of MTOR, complex 2; targeted mutation 1, Markus Ruegg|Rictor|MGI:3829768|15|||||||||||||||||||||||||||||Normal|Unknown|C57BL/6|Yes|Yes|Unknown|Yes|Yes|Unknown|No|Good|||homozygote x homozygote|No|18-Apr-2013|Cryopreserved sperm|75.0|0.0|Unknown||mTOR, muscle|Possibly| 5294.0|CZ-SOD ; B6.huSOD1.Tg (TD)|C57BL/6-Tg(H2-K-SOD1)Apb||Dominant||||||||||||||||||||||||||human superoxide dismutase 1, soluble|H2-K|||||||||||These mice contain human CuZn superoxide dismutase (SOD1) with a hemagglutinin epitope tag expressed from the mouse H-2Kb (MHC Class I) promoter. The antioxidant enzyme is expressed in most nucleated cells, which should therefore be protected from (superoxide anion) oxidative injury. This has been demonstrated using pancreatic islets isolated from the transgenic mice.The mice show no overt phenotype. Phenotype does not differ from a wildtype of the same genetic background.||C57BL/6|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Good|10|||No|29-Oct-2010|Cryopreserved sperm|50.0|0.0|Unknown||transplantation, rejection, oxidative stress, islet, reactive oxygen species (ROS) , hypoxia/reoxygenation|Possibly| 5295.0|EC-SOD ; B6.huSOD3.Tg (TE)|C57BL/6-Tg(H2-K-SOD3)/StvApb||Dominant||||||||||||||||||||||||||human superoxide dismutase 1, extracellular|H2-K|||||||||||These mice contain human extracellular superoxide dismutase (SOD3) modified to include a glycosyl phosphatidylinositol (GPI) membrane linkage signal & tagged with a FLAG epitope tag. SOD3 is expressed from the mouse H-2Kb (MHC Class I) promoter. The antioxidant enzyme is expressed in most nucleated cells, which should therefore be protected from (extracellular superoxide anion) oxidative injury. This has been demonstrated using pancreatic islets isolated from the transgenic mice.The mice show no overt phenotype. Phenotype does not differ from a wildtype of the same genetic background.||C57BL/6|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Good|10|||No|29-Oct-2010|Cryopreserved sperm|70.0|0.0|Unknown||transplantation, rejection, oxidative stress, islet, reactive oxygen species (ROS) , hypoxia/reoxygenation|Possibly| 5509.0|New York MPS IIIA|Stock Sgsh/Apb||Recessive|N-sulfoglucosamine sulfohydrolase (sulfamidase)|Sgsh|Reduced|sulphamidase|MGI:1350341|N-sulfoglucosamine sulfohydrolase (sulfamidase); mucopolysaccharidosis IIIA|Sgsh|MGI:2151181|11||||||||||||||||Yes|||||||||||||Newborn MPS IIIA pups do not appear different to their unaffected coutnerparts. Significant changes in open-field activity are observed from 3 weeks in MPS IIIA mice. Abnormalities in tests of gait, grip strength and in the assessment of the negative geotaxis response are observable from ∼15 weeks of age (Hemsley & Hopwood, 2005). Memory and learning deficits in the Morris Water Maze are observed from 20 weeks of age (Gliddon & Hopwood, 2004). Behavioural changes were often detected in male MPS-IIIA mice before they appeared in females.Premature death: most died between 7 and 10 months of age with a small number living to 14 months.Circling:observed in some mice over 1 year of age.Abnormal heart morphology: endomysium and perivascular space is often expanded by abnormal fibroblasts and macrophages.Abnormal myocardium layer morphology: myocardiocytes ultimately undergo degenerative changes and are replaced by fibroblasts with foamy cytoplasm.Abnormal heart valve morphology: valvular cusps and arterial perivascular spaces are also invaded by fibroblasts.Abnormal cell content/ morphology: Vacuolated or vesiculated cells with enlarged cytoplasm in: * fibroblasts * cerebral and cerebellar neurons as well as other cells in and around the brain, dense inclusions * dorsal root ganglion * cells of the eye * kidney * cardiac tissuesAbnormal lysosome morphology: * "zebra body" type storage material identifiable by EM in the brain and skeletal muscle * lysosomal storage is particularly prominent in the liver and spleenAbnormal neurocranium morphology: thickened calvariumEnlarged spleen.Enlarged liver.Abnormal kidney morphology.Hydronephrosis: unilateral or bilateral hydronephrosis frequently seenAbnormal renal tubule morphology: microvesiculated cytoplasm in the distal convoluted tubules, podocytes, and epithelial cells lining the collecting tubules.Distended urinary bladder: * at death the bladder is grossly distended and contains 1-2 ml of turbid urine * heparan sulfate accumulation in the urineAbnormal neurocranium morphology: thickened calvariumAbnormal vertebrae morphology: vertebrae become deformed.Corneal opacity: corneal opacity develops around 7 months of age.Abnormal hair texture.Disheveled coat: appeared normal at birth but developed a scruffy, ill appearance around 6-7 months of age.|Normal|Mixed genetic background including predominantly 129SvJ and CD1, with some C57BL/6 and SJL strain contributions|Yes|Yes|Yes|Yes|Yes|Yes|No|Excellent||||No|20-May-2011|Cryopreserved sperm|50.0|0.0|Yes|Progressive neurodegenerative lysosomal storage disorder||Possibly| 5250.0|CAM|C57BL/6-Tg(PRPH1-EGFP)CSars/Apb||Recessive||||||||||||||||||||||||||Human Peripherin gene|PRPH1 endogenous promoter|Normal||||||||||Normal|Normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|10|16|Hemizygous PRPH1-EGFP transgene X Hemizygous PRPH1-EGFP transgene|No|20-Oct-2010|Cryopreserved sperm|44.0|0.0|Unknown|Friedreich ataxia|Peripherin, Neurodegenerative disease, Neuroregeneration|Yes| 8676.0|ASD1030:Bmi1:fl|STOCK Bmi1/JAnu||Recessive|Bmi1 polycomb ring finger oncogene|Bmi1|Unknown|Bmi1, Bmi-1, Pcgf4 |MGI:88174 |Bmi1 polycomb ring finger oncogene; targeted mutation 1.1, Sean J Morrison|Bmi1|MGI:5638198|2|||||||||||||||||||||||||||||Normal|Normal|C57BL/6J|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|14-Mar-2019|Cryopreserved sperm|10.0|0.0|Unknown||Bmi-1, fate-mapping, forebrain, prospective identification, stem cell|Yes| 5253.0|Hoxb7/GFP|B6;CBA-Tg(Hoxb7-EGFP)33Cos/MarpApb||Dominant||||||||||||||||||||||||||transgene insertion 33, Franklin Costantini|Hoxb7|High level expression||||||||||GFP is too strong in homozygote state and embryos don't survive|Normal.GFP expression controlled by the activity of the HoxB7 promoter.GFP expressed in ureteric epithelium of the kidney, snout of pup and in regions of the brain.|(C57BL/6 x CBA)F2|No|Unknown|Yes|No|Unknown|Yes|No|Good||||No|20-Oct-2010|Cryopreserved sperm|90.0|0.0|No||GFP, expression pattern, kidney, ureteric bud, nephron|Yes| 7328.0|ENU25:009:BTK|C57BL/6NCrlAnu-Btk/AnuApb|C57BL/6NCrlAnu-Btk/AnuApb|Recessive|Bruton agammaglobulinemia tyrosine kinase|Btk|Unknown|Bruton's tyrosine kinase, X-linked immune deficiency, xid|MGI:88216|Bruton agammaglobulinemia tyrosine kinase; mutation 2, The Australian National University|Btk|MGI:5563503|X|ENSMUSG00000031264|ENSMUST00000033617|Btk-001|454|614|A to G|ENSMUSE00001191399|6|152|Tyrosine to Histidine|||||ACCATCCTTGCTTCTGGATTGATGGACAGTATCTCTGCTGCTCTCAGACAGCCAAGAATGC|Unknown|||||||||||||Mild BTK phenotype. Normal % peripheral B cells, increased numbers of immature B cells. Increased IgM expression on mature B cells.|Hemizygous phenotype same as homozygous females|C57BL/6NCrlAnu|Yes|Yes|Yes|Yes|Unknown|Yes|No|Excellent||G3||No|01-May-2013|Cryopreserved sperm|37.0|0.0|Unknown||B cell, immunoglobulin, IgM, IgD, ENU|Yes| 7346.0|EphA1 conditional full knockout (EA1C KO)|B6.129-Epha1/QimrApb||Recessive|Eph receptor A1|Epha1|Normal|5730453L17Rik, Eph, Esk|MGI:107381|targeted mutation 2, Shannon L Duffy|Epha1||6||||||||||||||||Yes|||||||||||||Normal|Normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|10|3|Hom x Hom|No|04-Jun-2013|Cryopreserved sperm|45.0|0.0|Unknown||Receptor Tyrosine Kinase, ephrin, epithelium, uterus, tail, embryonic|Yes| 2370.0|ENU6WTNIH:033|C57BL/6JSfdAnu-Stat1/AnuApb|C57BL/6JSfdAnu-Stat1/AnuApb|Recessive|signal transducer and activator of transcription 1|Stat1|||MGI:103063|signal transducer and activator of transcription 1; mutation 1, The Australian National University|Stat1|MGI:5563415|1|ENSMUSG00000026104|ENSMUST00000070968|Stat1-201|1633|1983|T to A|ENSMUSE00000630006|19|545|Tryptophan to Arginine|||||CTAATGCTGGCCCTGATGGTCTTATTCCATGGACAAGGTTTTGTAAGGAAAATATTAATGA|Yes|||||||||||||Defective antibody response to immunization: failure to mount a normal Th1 polarized IgG2c antibody response to heat killed B pertussis bacteria. Spontaneous formation of B cell lymphomas has also been observed in this pedigree, but it is not yet known if the two traits are linked.||C57BL/6JSfdAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||8||No|14-Dec-2007|Cryopreserved sperm|79.0|0.0|Unknown||B cell, immunization, Th1, ENU, Wellcome Trust, NH|Yes| 5941.0|NfiB/Gad67||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 8677.0|Chloe - Acan tm1Afos|C57BL/6-Acan/AfosSyd||Recessive|aggrecan|Acan||Agc1, b2b183Clo, Cspg1|MGI:99602|aggrecan; targeted mutation 1, Amanda J Fosang|Acan|MGI:3577026|7|||||||||||||||||||||||||||||No abnormal phenotype detected:• mutants develop normally with no skeletal abnormalities but do not accumulate aggregan in cartilage even though Agc1 is not cleaved by matrix metalloproteases|knock In|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|14-Mar-2019|Cryopreserved sperm|40.0|0.0|Unknown|||Yes| 5332.0|ENU16NIH:024a|C57BL/6JAnu-Lepr/AnuApb|C57BL/6JAnu-Lepr/AnuApb|Recessive|leptin receptor|Lepr||Leprb, LEPROT, leptin receptor gene-related protein, Modb1, obese-like, obl, Obr, OB-RGRP|MGI:104993|leptin receptor; mutation 1, The Australian National University|Lepr|MGI:5563456|4|ENSMUSG00000057722|ENSMUST00000036552|Lepr-001|2148|2703|T to A|ENSMUSE00000278589|14|716|Asparagine to Lysine|||||GCGCACACTGTTACAGTTCTGGCTGTCAATTCCCTCGGCGCTTCCCTTGTGAATTTTAACC||||||||||||||Noted as obese from 6 weeks of age. Continue to gain weight throughout their life. Heaviest mouse so far is a female at 49.4g|Normal|C57BL/6JAnu|Yes|No|Yes|Yes|No|Yes|Yes|Poor||4|Het x Het|No|25-Nov-2010|Cryopreserved sperm|19.0|0.0|Yes|Obesity|Obesity, ENU|Possibly| 7322.0|Pdx1-cre|B6(Cg)-Tg(Ipf1-cre)1Tuv/AusbAnuApb||Dominant||||||||||||||||||||||||||transgene insertion 6, David A Tuveson|Ipf1|Islet cells of pancreas||||||||||Normal.Islet cells express Cre recombinase|Normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|20-Apr-2013|Cryopreserved sperm|66.0|0.0|Unknown||Cre recombinase, islet, pancreas|Possibly| 7321.0|R26eYFP|B6.129-Gt(ROSA)26Sor/Adel||Dominant|gene trap ROSA 26, Philippe Soriano|Gt(ROSA)26Sor||beta geo, Gtrgeo26, Gtrosa26, R26, ROSA26|MGI:104735|gene trap ROSA 26, Philippe Soriano; targeted mutation 1, Frank Costantini|Gt(ROSA)26Sor|MGI:2449038|Unknown|||||||||||||||||||||||||||||Normal|Normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Excellent||||No|19-Apr-2013|Cryopreserved sperm|74.0|0.0|Unknown||eYFP, Cre recombinase|Possibly| 7365.0|BCL6-flox x CD4-cre|B6.129-Bcl6 Tg(Cd4-cre)||Recessive|B cell leukemia/lymphoma 6|Bcl6|Normal|Bcl5|MGI:107187|B cell leukemia/lymphoma 6; targeted mutation 1.1, Alexander Dent|Bcl6|MGI:5518542|16|||||||||||||||||cre recombinase|CD14|||||||||||||C57BL/6NCrlAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|01-Jul-2013|Cryopreserved sperm|10.0|0.0|Unknown||T cell, transcription, follicular|Yes| 5461.0|ENU18NIH:030b|C57BL/6JAnu-Atp11c/AnuApb|C57BL/6JAnu-Atp11c/AnuApb|X-linked|ATPase, class VI, type 11C|Atp11c|Reduced|Ig|MGI:1859661|ATPase, class VI, type 11C; mutation 2, The Australian National University|Atp11c|MGI:5006936|X|ENSMUSG00000062949|ENSMUST00000101527|Atp11c-202||||||||57493948|26|||CAGTCTTAGTATTCACCGTAACTCTGAAGGTTAGATTTTTATTCATTCAAATATATTTTG|Yes|||||||||||||Near complete block at pro-B cell stage; normal marginal zone B cell development from fetal liver but not from bone marrow.Defective ATP11C resulted in a lower rate of phosphatidylserine translocation in pro-B cells and much lower pre-B cell and B cell numbers despite expression of pre-rearranged immunoglobulin transgenes or enforced expression of the prosurvival protein Bcl-2 to prevent apoptosis and abolished pre-B cell population expansion in response to a transgene encoding interleukin 7. The only other abnormalities we noted were anemia, hyperbilirubinemia and hepatocellular carcinoma.||C57BL/6JAnu|Yes|No|Unknown|Yes|Unknown|Yes|Yes|Poor||||No|07-Mar-2011|Cryopreserved sperm|45.0|0.0|Unknown||ENU, B cell, lymphocyte|Possibly| 7347.0|CSTCR|BALB/c-Tg(TcraTcrb)1Zav||Dominant||||||||||||||||||||||||||T cell receptor alpha, T cell receptor beta|||||||||||||The mice express a monoclonal TCR specific for SYVPSAEQI in context of H2-K|BALB/c|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|04-Jun-2013||0.0|0.0|Unknown||T cell receptor, Plasmodium yoelii, CD8|Possibly| 7348.0|Bmp2|Bone morphogenic protein 2 5'Bac Transgenic line 85011||Dominant|Bone morphogenic protein 2|Bmp2|||||||Unknown|||||||||||||||||||||||||||||Normal|Normal|C57BL/5|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Good||||No|06-Jun-2013||0.0|0.0|Unknown|||Possibly| 4881.0|Bc.Rag1/Gal KO|C.B6-Rag1 Ggta1/Apb||Recessive|recombination activating gene 1|Rag1|Nil|Rag-1|MGI:97848|targeted mutation 1, Peter Mombaerts|Rag1|MGI:1857241|2||||||||||||||||No|||||||||||||Homozygotes for targeted null mutations exhibit arrested development of T and B cell maturation at the CD4-8- thymocyte or B220+/CD43+pro-B cell stage due to inability to undergo V(D)J recombination.All blood/tissue samples lack Gal expression.Cortical cataracts developed in all GalT-/- mice at 4-6 weeks of age.Mice are deficient in mature B and T cells.||BALB/c|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|28-Sep-2009|Cryopreserved sperm|83.0|0.0|Unknown||T cell, B cell, eosinophil, inflammation, interferon, Xenotransplantation, antibody, transferase, galactose|Yes| 4881.0|Bc.Rag1/Gal KO|C.B6-Rag1 Ggta1/Apb||Recessive|glycoprotein galactosyltransferase alpha 1, 3|Ggta1|Nil|alpha Gal, alpha3GalT, Gal, GALT, Ggta, Ggta-1, glycoprotein alpha galactosyl transferase 1|MGI:95704||||2|||||||||||||||||||||||||||||Homozygotes for targeted null mutations exhibit arrested development of T and B cell maturation at the CD4-8- thymocyte or B220+/CD43+pro-B cell stage due to inability to undergo V(D)J recombination.All blood/tissue samples lack Gal expression.Cortical cataracts developed in all GalT-/- mice at 4-6 weeks of age.Mice are deficient in mature B and T cells.||BALB/c|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|28-Sep-2009|Cryopreserved sperm|||Unknown||T cell, B cell, eosinophil, inflammation, interferon, Xenotransplantation, antibody, transferase, galactose|Yes| 5572.0|Zic5N|B6.CBA-Zic5/AnuApb|B6.CBA-Zic5/Anu|Semi-dominant|zinc finger protein of the cerebellum 5|Zic5|Nil|odd-paired related, Opr|MGI:1929518|zinc finger protein of the cerebellum 5; targeted mutation 1, Shinichi Aizawa|Zic5|MGI:3574814|14|||||||||||||||||||||||||||||Complete neonatal lethality: most mutants were live-born but died within 24 hours.Absent mandible: 2 out of 68 embryos exhibited agnathiaMicrognathia: one fifth of embryos exhibited mild micrognathiaMicrocephaly:most mutants were microcephalic.Abnormal optic vesicle formation:preoptic area was somewhat reduced medially in E12.5 and E18.5 embryos.Microphthalmia: found in some mutants.Anophthalmia:found in some mutants.Abnormal forebrain development: subtle defects in the ventromedial region of the forebrain at E12.5.Abnormal hippocampus development: development of hippocampus was somewhat poor at E18.5.Abnormal telencephalon development: * subtle defects in the dorsomedial region of the telencephalon at E12.5 * rostrally, development of the septum was poor at E12.5 and E18.5 and the fornix that normally becomes remarkable in septum at E15 was hardly visibleAbnormal folding of telencephalic vesicles: invagination of the telencephalic roof was less pronounced at E12.5.Exencephaly: observed in 9% of mutant embryos.Dilated lateral ventricles: the septum, striatum, and pallidum were underdeveloped, causing expansion of lateral ventricles at E18.5.Dilated third ventricle: at E18.5, the thalamus, hypothalamus, and preoptic area were reduced in the medial region, resulting in the expansion of the third ventricle.Abnormal choroid plexus morphology: choroid plexus was distorted at E12.5.Abnormal globus pallidus morphology: swelling of the pallidum was poor mediocaudally at E12.5 and was underdeveloped at E18.5.Abnormal striatum morphology: swelling of the striatum was poor mediocaudally at E12.5 and was underdeveloped at E18.5.Abnormal hypothalamus morphology: hypothalamus was reduced medially in E12.5 and E18.5 embryos.Abnormal thalamus morphology: swelling of the thalamus was poor ventrally at E15 and at E18.5 the thalamus was reduced in the medial region.Abnormal cerebral cortex morphology: * reduced medial pallium at E12.5. * the cortex was thinner at E18.5Abnormal axon morphology: the fornix that normally becomes remarkable in septum at E15 was hardly visible.Abnormal cranial ganglia morphology: mild reduction in facial ganglia.Abnormal glossopharyngeal ganglion morphology: mild reduction in glossopharyngeal ganglia.Abnormal trigeminal ganglion morphology: mild reduction in trigeminal ganglia.|Low prevalence of ventral spots and hydrocephaly on some genetic backgrounds.|C57BL/6|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Good|10|0|Heterozygous carrier aniamals are paired with C57BL/6 animals|No|31-Aug-2011|Cryopreserved sperm|70.0|0.0|Unknown||Cerebellum, Forebrain, Zic|Possibly| 5942.0|NfibCond/Emx1Cre||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 7323.0|ENU19:B6:Trim7|C57BL/6-Trim7/AnuApb|C57BL/6-Trim7/AnuApb|Recessive|tripartite motif-containing 7|Trim7|||MGI:2137353|mutation 1, The Australian National University|Trim7||11|ENSMUSG00000040350|ENSMUST00000109213|Trim7-001|124|370|A to G|ENSMUSE00000679460|2|44|Asparagine to Aspartic acid|||||TGCTGTCCCGGGAAGTGACACAGAAACAGAATGAGAACCTGGCCCAGCTGGAGGGTGAGAT||||||||||||||Unknown||C57BL/6JAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|22-Apr-2013|Cryopreserved sperm|20.0|0.0|Unknown||ENU|Yes| 5581.0|LMN|B6;129S1(Cg)-Lmna/Dfat||Dominant|lamin A|Lmna|Nil|Dhe, lamin A/C|MGI:96794|lamin A; targeted mutation 1, Colin L Stewart|Lmna|MGI:2177930|3|||||||||||||||||||||||||||||Lethal by 6-8weeks.Postnatal growth retardation.Muscle weakness.Small seminiferous tubules.Small testis.Azoospermia: spermatids and spermatozoa are largely absentArrest of male meiosis: * increased frequency of leptotene and zygotene spermatocytes and decreased frequency of pachytene and diplotene spermatocytes resulting from arrest and apoptosis of spermatocytes during the pachytene stage * unpaired chromosomes and/or improperly paired sex chromosomes and failure to progress through prophase I are seen * however, oogenesis in females is normal.|Viable, fertile.Abnormal nucleus morphology: in many MEFs, nuclei appear elongated but distribution of nuclear envelope proteins is normal except for increased levels of cytoplasmic emerin.|Mixed background, B6;129S1|No|Unknown|Yes|No|Unknown|Yes|No|Unknown||||No|09-Sep-2011|Cryopreserved sperm|50.0|0.0|Unknown||muscular dystrophy, membrane, interphase, spermatogenesis|Yes| 7324.0|PW1-LacZ|C57BL/6-Tg(Peg3-LacZ)/MarpApb||Semi-dominant||||||||||||||||||||||||||LacZ|paternally expressed gene 3 (PW1/Peg3) |||||||||||Unknown|Normal.|C57BL/6|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Good||||No|23-Apr-2013|Cryopreserved sperm|60.0|0.0|Unknown||LacZ|Possibly| 6592.0|GQI|B6.(Cg)-Tg(Myh6-Gnaq*)Wjk/Vccr||Dominant|||||||||||||||||||||||||||murine adult myosin, heavy polypeptide 6, cardiac muscle, alpha (Myh6) promoter|heart muscle||||||||||Viable, fertile||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|29-Sep-2011||0.0|0.0|Unknown||guanine, Gq, cardiomyocyte, hypertrophy|Yes| 6593.0|GSK3b|B6;CBA-Tg((Myh6-Gsk3b*S9A)1Eno/Vccr||Dominant||||||||||||||||||||||||||transgene insertion 1, Eric N Olson|alpha-myosin heavy chain (MHC) promoter and human GH (hGH) poly(A) signal|||||||||||Viable and fertile||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|29-Sep-2011||0.0|0.0|Unknown||heart, myocardium, Calcineurin, Glycogen synthase kinase-3 (GSK-3), signal transduction|Yes| 7550.0|ENU25:009:TNIK:B6|C57BL/6NCrlAnu-Tnik/AnuApb|C57BL/6NCrlAnu-Tnik/AnuApb|Recessive|TRAF2 and NCK interacting kinase|Tnik||1500031A17Rik, 4831440I19Rik, C530008O15Rik, C630040K21Rik|MGI:1916264|TRAF2 and NCK interacting kinase; mutation 1, The Australian National University|Tnik|MGI:5571275|3|ENSMUSG00000027692|ENSMUST00000160307|Tnik-007|317|397|A to G|ENSMUSE00000593159|5|106|Glutamic acid to Glycine|||||CATGGATGACCAACTCTGGTTGGTTATGGAGTTCTGTGGTGCTGGCTCTGTCACTGACCTG||||||||||||||Normal blood lymphocyte populations as measured by expression of following proteins: B220, CD3, CD4, CD44, KLRG1, NK1.1, IgM, IgD by flow cytometry.|Normal blood lymphocyte populations as measured by expression of following proteins: B220, CD3, CD4, CD44, KLRG1, NK1.1, IgM, IgD by flow cytometry.|C57BL/6NCrlAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|19-Dec-2013|Cryopreserved sperm|36.0|0.0|Unknown||ENU|Yes| 7349.0|Bmp2 - BAC clone RP23-85011 ; 5' Bac|B6.DBA-Tg(Bmp2)/VccriApb||Dominant||||||||||||||||||||||||||Bac Bmp2||||||||||||||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|06-Jun-2013|Cryopreserved sperm|54.0|0.0|Unknown||Lac Z|Possibly| 7411.0|ENU26:040:Dock8:B6|C57BL/6NCrlAnu-Dock8/AnuApb|C57BL/6NCrlAnu-Dock8/AnuApb|Recessive|dedicator of cytokinesis 8|Dock8|Unknown|1200017A24Rik, 5830472H07Rik, A130095G14Rik|MGI:1921396|dedicator of cytokinesis 8; mutation 2, The Australian National University|Dock8|MGI:5563483|19|ENSMUSG00000052085|ENSMUST00000025831|Dock8-201|4888|5010|A to T|ENSMUSE00000145935|38|1630|Arginine to STOP|||||ACCCTGAGATGCTTATGGACCTCATGTACAGAATTGCCAAGAGCTACCAGGCATCGCCTGA||||||||||||||Peripheral blood shows reduced T cells, activated CD8<+> T cells (high CD44) and low IgM expression on mature B cells. No Margnal Zone B cells in spleen.Parameters measured by flow cytometry using antibodies against following antigens: B220, CD3, CD4, CD44, KLRG1, NK1.1, IgM, IgD|Normal blood lymphocyte populations as measured by expression of following proteins: B220, CD3, CD4, CD44, KLRG1, NK1.1, IgM, IgD by flow cytometry.|C57BL/6NCrlAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||2||No|23-Aug-2013|Cryopreserved sperm|41.0|0.0|Unknown||T cell, B cell, antibody, ENU|Yes| 7367.0|ENU25:027:Mll3:B6:G2|C57BL/6NCrlAnu-Kmt2c/Anu||Recessive|lysine (K)-specific methyltransferase 2C|Kmt2c|Unknown|E330008K23Rik, HALR, mKIAA1506, Mll3|MGI:2444959|mutation 1, The Australian National University|Kmt2c||5|ENSMUSG00000038056|ENSMUST00000045291|Mll3-001|11740|11935|A to T|ENSMUSE00000655235|45|3914|Phenylalanine to Isoleucine|||||CTATGGCTTGCCAGAAGATGGCAAATGGTTTTGCAACGACTGAAGAACTTGCTGGAAAAGC||||||||||||||Unknown||C57BL/6NCrlAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|05-Jul-2013||0.0|0.0|Unknown||ENU|Yes| 5943.0|NfixCond||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 10350.0|Nr4a1|B6;129S2-Nr4a1tm1Jmi/J||Dominant|nuclear receptor subfamily 4, group A, member 1|Nr4a1|Nil|GFRP1, Hbr1, Hmr, N10, NGFI-B, NP10, Nur77, TIS1, TR3 |MGI:1352454 |nuclear receptor subfamily 4, group A, member 1; targeted mutation 1, Jeffrey Milbrandt|Nr4a1tm1Jmi|MGI:2182325|15|ENSMUSG00000023034 |ENSMUST00000023779|||||||||||||||||||||||||||NormalEight-month-old homozygotes develop systemic inflammation (PMID 26113803), demonstrating splenomegaly, and severe infiltration of inflammatory cells in several organs including liver, lung, spleen and kidney, in addition to increased hyperplasia of fibrous tissue in the lung, and enlargement of kidney glomeruli. Homozygotes also show increased production of pro-inflammatory cytokines and immunoglobulin, and elicit pro-inflammatory M1-like polarization in macrophages as revealed by increased expression of CXCL11 and INDO, and decreased expression of MRC1. |Normal|C57Bl/6J|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|bred to C57BL/6 for more than 10 generations and then intercrossed to homozygosity |||No|19-Jul-2023||0.0|0.0|Unknown|||Yes| 6897.0|APN188|C57Bl/6NTac-Notch4/Marp||Recessive|Notch gene homolog 4 (Drosophila|Notch4|Unknown|Int3, Int-3, N4|MGI:107471 |Notch gene homolog 4 (Drosophila); targeted mutation 1, Velocigene |Notch4 |MGI:4842905 |17|||||||||||||||||||||||||||||Unknown|Normal|C57Bl/6N|Unknown|Unknown|Unknown|Unknown|Unknown|Yes|No|Good||||No|17-May-2012|Cryopreserved sperm|50.0|0.0|Unknown|||Possibly| 8682.0|Nlrp9b KO ; Rice|C57BL/6NCrlAnu-Nlrp9b/AnuApb||Recessive|NLR family, pyrin domain containing 9B|Nlrp9b|Unknown|Nalp9b, Nalp-delta|MGI:2675377|Nlrp9b, endonuclease-mediated mutation 1, Australian National University|Nlrp9b||7||||||||||Unknown to Unknown|||||||||||||||||||Unknown|Normal|C57BL/6NCrlAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|02-Apr-2019|Cryopreserved sperm|21.0|20.0|Unknown|||Yes| 5758.0|eNos+/- Cav+/-||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5052.0|NOD.B6 R3 N12|NOD.B6(D1Mit48-D1Mit92)N12||Recessive||||||||||||||||||||||||||||||||||||||The incidence of diabetes in female mice is 78% after 43-weeks, which is higher than the incidence of diabetes in female NOD/Lt mice in our facility (50-60% at 43-weeks of age). The incidence of diabetes in male mice is 27% after 43 weeks of age, which is significantly higher than the incidence of diabetes in male NOD/Lt mice in host facility (5-10% at 43-weeks of age).|The incidence of diabetes has not been tested in heterozygotes of this mouse strain.|NOD/Lt|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|13|8|Hom x Hom|No|26-Feb-2010|Cryopreserved sperm|45.0|0.0|Yes|Type 1 Diabetes|IgA, IgM, Idd5.4, B cell|Yes| 6898.0|APN212|C57Bl/6N-Crisp2/MarpApb||Recessive|cysteine-rich secretory protein 2|Crisp2|Unknown|CRISP-2, GAPDL5, Tpx1, Tpx-1 |MGI:98815 |cysteine-rich secretory protein 2; targeted mutation 1a, Mouse Biology Program, UCDavis|Crisp2 |MGI:4888856|17|||||||||||||||||||||||||||||Unknown|Normal|C57Bl/6N|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Good||||No|17-May-2012|Cryopreserved sperm|50.0|0.0|Unknown|||Possibly| 10384.0|Itk T503S |C57BL6/NCrl-ItkAnu/Apb||Semi-dominant|IL2 inducible T cell kinase|Itk|||MGI:96621|Itk |||11|ENSMUSG00000020395||||||||||||||||||||||||||||Unknown|Unknown|C57Bl/6N|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|30-Nov-2023|Cryopreserved sperm|31.0|0.0|Unknown|||No| 7325.0||SJL-Tfrc/Apb||Dominant|transferrin receptor|Tfrc||2610028K12Rik, CD71, E430033M20Rik, Mtvr1, Mtvr-1, p90, TfR1, Trfr|MGI:98822||Tfrc||16|ENSMUSG00000022797|ENSMUST00000023486|Tfrc-001|218|358|T to G|ENSMUSE00000130494|3|73|Leucine to Arginine|||||TGGAAGACTCTGCTTTGCAGCTATTGCACTAGTCATTTTCTTCTTGATTGGATTCATGAGT||||||||||||||Severe microcytosis associated with erythrocytosis and normochromia. The homozygous are not viable.|Microcytosis associated with erythrocytosis and normochromia|SJL/J|No|No|Yes|No|No|Yes|No|Good||||No|23-Apr-2013|Cryopreserved sperm|50.0|0.0|Unknown||microcytosis, ENU, transferrin|Yes| 7115.0||ENU11B6053b||Recessive|Unknown|Unknown|||||||Unknown|||||||||||||||||||||||||||||Increased susceptibility to infection with ECTV|Unknown|C57BL/6J|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|29-Oct-2012|Cryopreserved sperm|50.0|0.0|Unknown||ENU, viral infection|Possibly| 7116.0||ENU11B6070b||Recessive|Unknown|Unknown|||||||Unknown|||||||||||||||||||||||||||||Increased susceptibility to infection with Ectromelia virus||C57BL/6J|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|29-Oct-2012|Cryopreserved sperm|46.0|0.0|Unknown||ENU, viral infection|Possibly| 7117.0||ENU11B6074c||Recessive|Unknown|Unknown|||||||Unknown|||||||||||||||||||||||||||||Increased susceptibility to infection with Ectromelia virus|Unknown|C57BL/6J|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Good||||No|29-Oct-2012|Cryopreserved sperm|30.0|0.0|Unknown||ENU, viral infection|Possibly| 7107.0|Nude|B6-Foxn1/AnuApb||Recessive|forkhead box N1|Foxn1|Unknown|D11Bhm185e, Hfh11, whn|MGI:102949|nude|Foxn1|MGI:1856108|11||||||||||||||||Yes|||||||||||||Postnatal lethality:some mice die within 1 week of birth55% mortality within 2 weeksPremature death:100% mortality by 25 weeksDecreased body size and weight.Postnatal growth retardation.Abnormal T cell differentiation.Athymia.Abnormal cell-mediated immunity.Abnormal liver morphology:liver lobes were atrophied and covered with red scarsvariable degrees of severity, typically increasing with age at time of death.Small ovaryCoiled sperm flagellum: many sperm had coiled tailsAbnormal estrous cycle: many females exhibited continuous dioestrus and metaoestrus phasesFemale infertility: severely reduced fertilityReduced male fertility.Asthenozoospermia.Nude: sparse hair growth around 5 weeks of agein some mice, cephalo-caudal migration of an irregular band of short sparse hairThin skin:reduction in skin thickness at 3 weeks of age, corresponding to the catagen stage of normal skinAbsent vibrissae: absent at birthShort and wavy vibrissae: older mice show repeated growth and loss of short and wavy vibrissae.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|17-Oct-2012|Cryopreserved sperm|18.0|0.0|Unknown||hair loss, T cell, thymus, body size / mass, growth retardation, alopecia, keratin|Yes| 7327.0|B6.SJL|B6.SJL-Ptprc Pep3/BoyJAnuApb||Recessive|||||||||||||||||||||||||||||protein tyrosine phosphatase, receptor type, C|Ptprc||B220, CD45, Ly-5, Lyt-4, T200|MGI:97810|protein tyrosine phosphatase, receptor type, C; a variant|Ptprc|MGI:4819849|Unknown|Normal||C57BL/6JAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|24-Apr-2013|Cryopreserved sperm|10.0|0.0|Unknown|||No| 7327.0|B6.SJL|B6.SJL-Ptprc Pep3/BoyJAnuApb||Recessive|||||||||||||||||||||||||||||peptidase C|Pepc||Dip-1, Pep3, Pep-3|MGI:97541|peptidase C; b variant|Pepc|MGI:4819861|1|Normal||C57BL/6JAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|24-Apr-2013|Cryopreserved sperm|||Unknown|||No| 7533.0|ENU24:014:Trps1|C57BL/6NCrlAnu-Trps1/AnuApb|C57BL/6NCrlAnu-Trps1/AnuApb|Recessive|trichorhinophalangeal syndrome I (human)|Trps1||D15Ertd586e|MGI:1927616|trichorhinophalangeal syndrome I (human); mutation 1, The Australian National University|Trps1|MGI:5563401|15|ENSMUSG00000038679|ENSMUST00000165201|Trps1-001|3436|3526|A to T|ENSMUSE00000478584|6|1146|Threonine to Serine|||||ATCCTTGCCAAAACTATGTGCCTTATCCCACCTTCAATCTGCCTCCTCATTTCTCAGCTGT||||||||||||||Normal blood lymphocyte populations as measured by expression of following proteins: B220, CD3, CD4, CD44, KLRG1, NK1.1, IgM, IgD by flow cytometry.|Normal blood lymphocyte populations as measured by expression of following proteins: B220, CD3, CD4, CD44, KLRG1, NK1.1, IgM, IgD by flow cytometry.|C57BL/6NCrlAnu|Yes|Unknown|Yes|Yes|Unknown|Yes|No|Unknown||G2N1||No|06-Dec-2013|Cryopreserved sperm|17.0|0.0|Unknown||ENU|Yes| 10351.0||C57Bl/6-TFF2(CreERT2)-Rosa26-delta(D3muc)/Apb||Semi-dominant|trefoil factor 2 (spasmolytic protein 1)|Tff2 |||MGI:1306805 |TFF2|||17|ENSMUSG00000024028 ||||||||||||||||||||||||||||Normal|Normal|C57Bl/6J|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|20-Jul-2023|Cryopreserved sperm|33.0|0.0|Unknown|||Possibly| 7551.0|ENU25:010:RAP1GAP2:B6|C57BL/6NCrlAnu-Rap1gap2/AnuApb|C57BL/6NCrlAnu-Rap1gap2/AnuApb|Recessive|RAP1 GTPase activating protein 2|Rap1gap2|Unknown|Garnl4, LOC380710, mKIAA1039|MGI:3028623|RAP1 GTPase activating protein 2; mutation 1, The Australian National University|Rap1gap2|MGI:5563432|11|ENSMUSG00000038807|ENSMUST00000102521|Rap1gap2-001|830|1071|T to A|ENSMUSE00000578461|12|277|Aspartic acid to Valine|||||TTTCAAGGAGTTTTTGGATCTCCTGGGAGACACCATCACACTGCAGGATTTCAAAGGTTTC||||||||||||||Normal blood lymphocyte populations as measured by expression of following proteins: B220, CD3, CD4, CD44, KLRG1, NK1.1, IgM, IgD by flow cytometry.|Normal blood lymphocyte populations as measured by expression of following proteins: B220, CD3, CD4, CD44, KLRG1, NK1.1, IgM, IgD by flow cytometry.|C57BL/6NCrlAnu|Yes|Unknown|Yes|Yes|Unknown|Yes|No|Good||G4||No|19-Dec-2013|Cryopreserved sperm|46.0|0.0|Unknown||ENU|Yes| 7114.0||ENU10B6043a||Recessive|Unknown|Unknown|||||||Unknown|||||||||||||||||||||||||||||Increased susceptibility to infection with Ectromelia.|Unknown|C57BL/6J|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|29-Oct-2012|Cryopreserved sperm|47.0|0.0|Unknown||ENU, viral infection|Possibly| 7110.0|ROS-iePLA|ROS-iePLA||Dominant||||||||||||||||||||||||||ROS-iePLA||||||||||||Mouse express GFP|Mouse express GFP|C57BL/6N|Yes|Yes|Yes|Yes|Yes|Yes|No|Excellent||||No|19-Oct-2012|Cryopreserved sperm|50.0|0.0|Unknown||green fluorescent protein|Yes| 7118.0|CD11c-Cre|B6.Cg-Tg(Itgax-cre)1-1Reiz/JMarpApb||Dominant||||||||||||||||||||||||||transgene insertion 1-1, Boris Reizis|Itgax, integrin alpha X, CD11c|||||||||||Unknown|Normal|C57BL/6J|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|29-Oct-2012|Cryopreserved sperm|60.0|0.0|Unknown||Dendritic cell, Cre recombinase|Yes| 7120.0|ANU:ENU22:Nr4a1:B6|C57BL/6NCrlAnu-Nr4a1/AnuApb||Recessive|nuclear receptor subfamily 4, group A, member 1|Nr4a1||Gfrp, GFRP1, Hbr1, Hbr-1, Hmr, N10, NGFI-B, NP10, Nur77, TIS1, TR3|MGI:1352454|nuclear receptor subfamily 4, group A, member 1; mutation 1, The Australian National University|Nr4a1|MGI:5570322|15|ENSMUSG00000023034 |ENSMUST00000023779|Nr4a1-201|815|943|T to C|ENSMUSE00000132956|2|272|Valine to Alanine|||||TTCAGGTGGCAGCGAGGGCCGCTGTGCAGTCTGTGGTGACAATGCTTCGTGTCAGCACTAT||||||||||||||Unknown|Unknown|C57BL/6NCrlAnu|Yes|Unknown|Yes|Yes|Unknown|Yes|No|Unknown||G3||No|30-Oct-2012|Cryopreserved sperm|26.0|0.0|Unknown||ENU|Yes| 5515.0|ENU15NIH36a|ENU15NIH:036a||Recessive|Unknown|Unknown|||||||Unknown|||||||||||||||||||||||||||||High % of NKT cells.|Higher % of NKT cells then WT mice.|C57BL/6JAnu|Yes|Yes|Yes|Yes|Yes|Yes|Yes|Poor||5|Sib x sib|No|26-May-2011|Cryopreserved sperm|70.0|0.0|Unknown||ENU|No| 5747.0|Eddie||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5750.0|EKLF/P53||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 10373.0||ENU43:040::B6||Semi-dominant|Unknown||||||||Unknown|||||||||||||||||||||||||||||Unknown|Unknown|C57Bl/6N|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Nov-2023|Cryopreserved sperm|153.0|0.0|Unknown|||No| 7113.0|TLR9 KO|B6.129P2-Tlr9/Marp||Dominant|toll-like receptor 9|Tlr9|Unknown||MGI:1932389|toll-like receptor 9; targeted mutation 1, Shizuo Akira|Tlr9|MGI:2660562|9|||||||||||||||||||||||||||||Abnormal immune system physiology: response to LPS and CpG is completely abrogated.Impaired natural killer cell mediated cytotoxicity: no NK cell activation is observed following infection with L. infantum.Decreased interferon-alpha secretion: * following infection with Leishmania baziliensis * however, secretion could be restored by treatment with GU-rich ssRNA, a TLR7 ligandDecreased interferon-beta secretion: * following infection with Leishmania baziliensis * however, secretion could be restored by treatment with GU-rich ssRNA, a TLR7 ligand.Decreased interleukin-12b secretion: * following infection with attenuated yellow fever vaccine 17D (YF-17D), dendritic cells produce less IL-12p40 relative to wild-type mice * unlike in wild-type mice, IL-12p40 production from dendritic cells following infection with Leishmania infantum is indetectable .Decreased tumor necrosis factor secretion: following treatment with PbA(Plasmodium bergbei ANKA)-parasitized erythrocytes or LPS-stimulation, TNF secretion is reduced.Decreased susceptibility to experimental autoimmune encephalomyelitis: * myelin oligodendrocyte glycoprotein injection results in delayed onset of disease, 17.9 days after injection rather than 15.9 days as in controls * fewer infiltrating foci in the spinal cordAbnormal response to infection: following treatment with PbA (Plasmodium bergbei ANKA)-parasitized erythrocytes, mice have a partially decreased immune response in terms of TNF secretion and response to CpG.Decreased susceptibility to parasitic infection: * resistant to cerebral malaria * reduced accumulation of hemozoin * less upregulation of TNF-alpha in Plasmodium infection|Normal|C57BL/6J|Yes|Yes|Unknown|Yes|Yes|Unknown|No|Unknown||||No|25-Oct-2012||0.0|0.0|Unknown||toll like receptor, DNA, bacteria, CpG|Yes| 5751.0|Emx1||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5752.0|Emx1-EGFP||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5753.0|Emx1/gad67||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5754.0|Emx1/Parvalbumin||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5755.0|Emx1Cre||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 10381.0|ENU56:403:IKAROS:B6|C57BL/6NCrlAnu-Ikzf1/Anu||Semi-dominant|IKAROS family zinc finger 1|Ikzf1||LyF-1, Zfpn1a1|MGI:1342540|Ikzf1|||11|ENSMUSG00000018654 |ENSMUST00000065433|||||||||||||||||||||||||||Homozygous mice develop tumours @12 weeks|Unknown|C57Bl/6N|Unknown|No|Yes|Unknown|Unknown|Yes|No|Good||||No|24-Nov-2023|Cryopreserved sperm|32.0|0.0|Unknown|||No| 7351.0|uGFP|C57BL/6-Tg(UBC-GFP)30Scha/JWehiAnuApb||Dominant||||||||||||||||||||||||||transgene insertion 30, Brian Schaefer|uman ubiquitin C promoter|||||||||||Homozygous transgenic mice are viable, fertile, normal in size, and do not display any gross physical or behavioral abnormalities. These mice express GFP in all tissues examined. Expression levels vary between certain hematapoetic cell types. GFP expression is uniform within a cell type lineage and remains constant throughout development. T cells have a 2-fold higher GFP expression than CD19+B220+ B cells or peripheral blood cells. Leukocytes and red blood cells from homozygous transgenic mice fluoresce at approximately twice the level of cells from hemizygous mice.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|07-Jun-2013|Cryopreserved sperm|60.0|0.0|Unknown||GFP, T cell, B cell, Dendritic|Possibly| 7125.0|AC2|B6;129R-Acta1 tm1(H40Y;neo)1Hrd/Ausb||||AC2||||||||||||||||||||||||||||||||||||MyopathyMale die by 12 weeks of age.Also male mice may be sterile||C57Bl6/JArc/R1-129|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|02-Nov-2012||0.0|0.0|Unknown|||Possibly| 7123.0|ENU26:G2|ANU:ENU26:G2||Recessive||||||||||||||||||||||||||||||||||||||Unknown|Unknown|C57BL/6Crl|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown|1|||No|01-Nov-2012|Cryopreserved sperm|1539.0|78.0|Unknown||ENU, mutagenesis, screen, random|Yes| 7330.0|ENU12NIH2b|ENU12NIH2b||Recessive|unknown|unknown|||||||Unknown|||||||||||||||||||||||||||||Increased IgE in plamsa|unknown|C57BL/6JAnu|Yes|Yes|Unknown|Yes|Yes|Unknown|No|Good||G13||No|03-May-2013|Cryopreserved sperm|30.0|0.0|Unknown||IgE, Allergy, B cell, T cell, ENU|Possibly| 7329.0|ENU19 WT:029:a:B6:F3|C57BL/6JAnu-Gucd1/Anu||Recessive|guanylyl cyclase domain containing 1|Gucd1|Unknown|1110038D17Rik|MGI:1916028|mutation 1, The Australian National University|Gucd1||10|ENSMUSG00000033416|||536|721|G to C|ENSMUSE00000226356|5|179|Arginine to Proline|||||TACTCCCAGTGGCCACCGCTGCTTCTGCCGCACCCCCGACTACCAAGGCCACTTCATCGTC|Unknown|||||||||||||Unknown|Unknown|C57BL/6JAnu|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|01-May-2013|Cryopreserved sperm|50.0|0.0|Unknown||ENU|Yes| 7105.0|ADAR1 fl/fl|B6.129-Adar/StvApb||Dominant|adenosine deaminase, RNA-specific|Adar|Nil|ADAR1, mZaADAR|MGI:1889575|adenosine deaminase, RNA-specific; targeted mutation 1.1, Peter H Seeburg|Adar|MGI:3828307|3|||||||||||||||||||||||||||||Homozygous animals normal and healthy, breed normally in the absence of Cre|Heterozygous animals normal and healthy, breed normally in the absence of Cre|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Excellent|more than 6|unknown/not collected|fl/fl to fl/fl|No|12-Oct-2012|Cryopreserved sperm|44.0|0.0|Yes|Mutations in ADAR1 cause Aicardi-Goutières syndrome associated with a type I interferon signature. Nat Genet. 2012 Sep 23. doi: 10.1038/ng.2414|ADAR1, RNA editing|Yes| 7129.0|SIRT5a|Sirtuin5 #36/Ausb||||Sirt5||||||||||||||||||||||||||||||||||||None||C57BL6|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|02-Nov-2012||0.0|0.0|Unknown|||Possibly| 7122.0|ENU26:G1|ANU:ENU26:G1||Recessive|Unknown||||||||Unknown||||||||||||||||Unknown|||||||||||||Unknown|Unknown|C57BL/6NCrl|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||1||No|01-Nov-2012|Cryopreserved sperm|467.0|0.0|Unknown||ENU, random, mutagenesis, screen|Yes| 7128.0|SIGMA-J20|B6.Cg-Tg(PDGFB-APPSwInd)20Lms/JAusb/Ausb||||APP|||MGI:3057148|||||||||||||||||||||||||||||||||||C57BL6|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|02-Nov-2012||0.0|0.0|Unknown|||Possibly| 7139.0|mFasL|B6.Cg-Fasl/WEHIAusb/Ausb||||mFasL|||MGI:4366050|||||||||||||||||||||||||||||||||Lymphoproliferative disease on old (>6 months) mice.||C57BL/6|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|02-Nov-2012||0.0|0.0|Unknown|||Possibly| 7131.0|SIRT5^|129-Sirt5/JAusb||Recessive||Sirt5|||MGI:3769236||||Unknown|||||||||||||||||||||||||||||Not Known||129|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|02-Nov-2012||0.0|0.0|Unknown|||Possibly| 7135.0|Moe|B6129S5-Cma1/TAC/Ausb||||mMCP5|||MGI:96941|||||||||||||||||||||||||||||||||||C57BL6|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|02-Nov-2012||0.0|0.0|Unknown|||Possibly| 7132.0|Monty|B6129S5-Ndst2/TAC/Ausb||Recessive||NDST2|||MGI:3529198||||Unknown|||||||||||||||||||||||||||||||C57BL6|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|02-Nov-2012||0.0|0.0|Unknown|||Possibly| 8688.0|Cish wt/wt|BALB/c-Cish/||Dominant|cytokine inducible SH2-containing protein|Cish|Normal|Cis, CIS1, cytokine-inducible SH2 protein, F23|MGI:103159|Wildtype|||9|||||||||||||||||||||||||||||Normal|Normal|BALB/c|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|11-Apr-2019||0.0|0.0|Unknown|||Yes| 8687.0|Rag2 del 15B|C57BL/6-Rag2/15BCsl||Recessive|recombination activating gene 2|Rag2||Rag-2|MGI:97849||||2|||||||||||||||||||||||||||||Fail to generate mature T or B lymphocytes.|||Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|04-Apr-2019|Cryopreserved sperm|50.0|0.0|Unknown|||Yes| 10386.0|hRhDTg|C57BL/6J-Rhdem1(hRhd_p2a_hRhag)MAGEC||Recessive|Rh blood group, D antigen|Rhd||Rh, Rhced, Rhl1|MGI:1202882|Rhesus D|||4|ENSMUSG00000028825 ||||||||||||||||||||||||||||Normal|Normal|C57Bl/6J|Yes|Yes|Yes|Yes|Yes|Unknown|No|Good||||No|01-Dec-2023|Cryopreserved sperm|40.0|0.0|Unknown|||Possibly| 7140.0|Manni|B6.129S1-Ill2b/Ausb||||IL12p40|||MGI:1857201|||||||||||||||||||||||||||||||||||C57BL/6|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|02-Nov-2012||0.0|0.0|Unknown|||Possibly| 7130.0|SIRT5b|Sirtuin5 #38/Ausb||Recessive||Sirt5||||||||||||||||||||||||||||||||||||None||C57BL6|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|02-Nov-2012||0.0|0.0|Unknown|||Possibly| 7141.0|PAR1|Protease receptor 1 deficient mice/Ausb||||PAR1|||MGI:101802|||||||||||||||||||||||||||||||||Slow breeders; they may have a reduced innate immune response.||C57BL/6|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|02-Nov-2012||0.0|0.0|Unknown|||Possibly| 7144.0|DAVID|C57BL/6-Prss22Gt(ROSA)26SorGt(Rosa)26 Sor/TAC/Ausb||||Prss22||||||||||||||||||||||||||||||||||||||C57BL6|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|02-Nov-2012||0.0|0.0|Unknown|||Possibly| 7145.0|BOWIE|C57BL/6-Tpsg1/6tm2072_239.1Arte>Gt(Rosa)26SorGt(Rosa)26Sor/TAC/Ausb||||Prss31||||||||||||||||||||||||||||||||||||||C57BL6|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|02-Nov-2012||0.0|0.0|Unknown|||Possibly| 7153.0|IKK2FL|C57BL/6-Ikbkb/Ausb/Ausb||||IKK2|||MGI:2652651|||||||||||||||||||||||||||||||||||C57BL/6|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|02-Nov-2012||0.0|0.0|Unknown|||Possibly| 7151.0|KrasG12D|B6.129-Kras/Ausb||Recessive||Kras|||MGI:2429948|||||||||||||||||||||||||||||||||||B6/129|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|02-Nov-2012||0.0|0.0|Unknown|||Possibly| 7155.0|NMNAT3|B6.J.B6D2-Tg(CAG-Nmnat3)1Ara/Ausb||||NMNAT3|||MGI:1921330|||||||||||||||||||||||||||||||||||C57BL/6|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|02-Nov-2012||0.0|0.0|Unknown|||Possibly| 7146.0|Shemp|RasGRP4KO/Ausb||||RasGRP4||||||||||||||||||||||||||||||||||||||C57BL/6|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|02-Nov-2012||0.0|0.0|Unknown|||Possibly| 7147.0|p65flox|C57BL/6-Rela/Ausb /Ausb||||p65|||MGI:3803795|||||||||||||||||||||||||||||||||||C57BL/6|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|02-Nov-2012||0.0|0.0|Unknown|||Possibly| 7148.0|Nemo flox|C57BL/6-Ikbkg/Ausb||||Ikkg|||MGI:2679024|||||||||||||||||||||||||||||||||||C57BL/6|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|02-Nov-2012||0.0|0.0|Unknown|||Possibly| 7156.0|T1germTg|Germline SIRT1 transgenics/Ausb||||Sirt1||||||||||||||||||||||||||||||||||||Improved glucose tolerance,resistance to ageing, expected prolonged lifespan.||C57BL/6|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|02-Nov-2012||0.0|0.0|Unknown|||Possibly| 7164.0|PUMA|C57BL/6-Bbc3/WEHIAusb/Ausb||||Bbc3|||MGI:2181667|||||||||||||||||||||||||||||||||decreased sensitivity to induced cell death||C57BL/6|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|02-Nov-2012||0.0|0.0|Unknown|||Possibly| 7159.0|T2Tg|Germline SIRT2 transgenic./Ausb||||SIRT2||||||||||||||||||||||||||||||||||||Resistance to ageing, improved cardiac function in old mice, expected prolonged lifespan.||C57BL/6|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|02-Nov-2012||0.0|0.0|Unknown|||Possibly| 7167.0|GFP-LC3|B6.B6D2-Tg(CAG-RGFP/LC3)53Nmz/NmzRbrc/Ausb||||LC3gFP|||MGI:3759813|||||||||||||||||||||||||||||||||||C57BL/6JJcl|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|02-Nov-2012||0.0|0.0|Unknown|||Possibly| 7161.0|nat81-KO|C57BL/6-Nat81/Ausb||||nat81|||MGI:3808552|||||||||||||||||||||||||||||||||Neurological abnormalitiesHomozygous mutants have never been generated but are expected to show neurological impairments( gait abnormalities and reduced body weight).||C57BL/6|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|02-Nov-2012||0.0|0.0|Unknown|||Possibly| 7157.0|iT1KO|Tamoxifen inducible SIRT1 KO/Ausb||Recessive||Sirt1, ERT||||||||||||||||||||||||||||||||||||Only upon treatment with Tamoxifen does phenotype become apparent,with decreased glucose tolerance and mitochondrial dysfuction, resulting in accelerated ageing.||C57BL/6|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|02-Nov-2012||0.0|0.0|Unknown|||Possibly| 7171.0|iAkt-F3|iAkt-Founder3/Ausb||||iAKT||||||||||||||||||||||||||||||||||||||C57BL/6|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|02-Nov-2012||0.0|0.0|Unknown|||Possibly| 7165.0|NOXA|C57BL/6-Pmaip1/WEHIAusb/Ausb||||Pmaip1|||MGI:1930146 |||||||||||||||||||||||||||||||||homozygous null mice develop normally and show no evidence of tumorigenesis.||C57BL/6|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|02-Nov-2012||0.0|0.0|Unknown|||Possibly| 7168.0|ATG7|B6.Cg-ATg7/Rbrc/Ausb||||ATG7|||MGI:3587769|||||||||||||||||||||||||||||||||||C57BL/6|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|02-Nov-2012||0.0|0.0|Unknown|||Possibly| 7178.0|C57BLKaLwRij|C57BL/KaLwRij/AnuApb||Recessive||||||||||||||||||||||||||||||||||||||May have reduced litter size.||C57BL/6|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|02-Nov-2012|Cryopreserved sperm|66.0|273.0|Yes|Multiple Myeloma|Multiple Myeloma, Samsn1, Tnfrsf22, Tnfrsf23|Yes| 7172.0|MaFIA|C57BL/6-Tg(Csf1r-EGFP-NGFR/FKBP1A/TNFRSF6)2Bck/JAusb||Dominant||MaFIA|||MGI:3051865||||Unknown|||||||||||||||||||||||||||||GFP positive macrophages||C57BL/6|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|02-Nov-2012||0.0|0.0|Unknown|||Possibly| 7169.0|UBR5Frt_Fi|C57BL/6N-Ubr5/Ausb/Ausb||||Ubr5|||MGI:4455996|||||||||||||||||||||||||||||||||||C57BL/6N|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|02-Nov-2012||0.0|0.0|Unknown|||Possibly| 7177.0|129S1|129S1/SvImJAusb||Dominant||||||||||||||||||||||||||||||||||||||||129S1/SvImJ|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|02-Nov-2012||0.0|0.0|Unknown|||Possibly| 7174.0|ApoDnullAPP|ApoDnull x B6.Cg-Tg(APPswePSEN1dE9)85Dbo/JAusb||Dominant||ApoD,APP,PSEN1|||||||Unknown|||||||||||||||||||||||||||||Early onset of Alzheimer's disease.||C57BL/6|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|02-Nov-2012||0.0|0.0|Unknown|||Possibly| 7170.0|iAkt-F2|iAkt-Founder2/Ausb||||iAKT||||||||||||||||||||||||||||||||||||||C57BL/6|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|02-Nov-2012||0.0|0.0|Unknown|||Possibly| 7175.0|IL21rSNP|IL21rSNP/Ausb||||IL21r||||||||||||||||||||||||||||||||||||||C57BL/6|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|02-Nov-2012||0.0|0.0|Unknown|||Possibly| 7176.0|MavsSNP|MavsSNP/Ausb||||Mavs||||||||||||||||||||||||||||||||||||||C57BL/6|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|02-Nov-2012||0.0|0.0|Unknown|||Possibly| 7183.0|p16luc/SKH1|p16-luciferase, SKH1 hairless/Ausb||||P16luc,SKH1||||||||||||||||||||||||||||||||||||Mice homozygous for SK1 point mutation (SKH1+/+) will lose all body hair prior to 8 weeks of age. No special care requirements are needed for this phenotype.||C57BL/6|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|02-Nov-2012||0.0|0.0|Unknown|||Possibly| 6381.0|CYANtg|B6.129(ICR)-Tg(CAG-ECFP)CK6Nagy/JAusb||Dominant||||||||||||||||||||||||||transgene insertion CK6, Andras Nagy|chicken beta actin promoter|||||||||||Unknown|Unknown|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown||EGFP|Yes| 7189.0|Beta-cateninLoxP|B6.129-Ctnnb1/KnwJAusb||Recessive|||||MGI:88276||||Unknown|||||||||||||||||||||||||||||none||C57BL/6|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|02-Nov-2012||0.0|0.0|Unknown|||Possibly| 7182.0|Sf1-SIRT1tg|Sf1Cre SIRT1 Transgenic/Ausb||||SIRT1tg, SF1||||||||||||||||||||||||||||||||||||When Sf1 cre and SIRT1 floxed alleles are crossed, SIRT1 is over-expressed in the hypothalamus. This leads to improved protection against diet induced diabetes.||C57BL/6|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|02-Nov-2012||0.0|0.0|Unknown|||Possibly| 7186.0|Spns2|C57BL/6DnkSpns2 (?)/Ausb||||Spns2|||MGI:2384936 |||||||||||||||||||||||||||||||||Absent pinna reflex,abnormal corneal vascularisation,abnormal braistem auditory evoked potencial,decrease leukocyte cell number,altered peripheral blood lymphocytes LSRII,decreased circulating glucose level,abnormal eye pigmenttation,increase bone mineral||BL/6NTac/Den,BL/6J-TTyrcBrd;BL/6N|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|02-Nov-2012||0.0|0.0|Unknown|||Possibly| 7187.0|R-FLPo|unknown/Ausb||Dominant||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|02-Nov-2012||0.0|0.0|Unknown|||Possibly| 5696.0|Col1a2 x B6 ROSA26A-EGFP ||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 7693.0|Tpbpa-Cre|C57BL/6-Tg(Tpbpa-cre-EGFP)5Jcc||Dominant||||||||||||||||||||||||||transgene insertion 5, James C Cross|trophoblast specific protein alpha|||||||||||Normal|Normal|C57BL/6|Yes|Yes|Unknown|Yes|Yes|Unknown|No|Unknown||||No|26-May-2014|Cryopreserved sperm|50.0|0.0|Unknown||Cre recombinase, trophoblast|Possibly| 7188.0|CD3e?|C57BL/6-Cd3etm1Mal/Orl/Ausb||||||||||||||||||||||||||||||||||||||||Mildly immunodeficient.||C57BL/6|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|02-Nov-2012||0.0|0.0|Unknown|||Possibly| 7594.0||SJL/ASAM||Dominant|unknown|unknown|Reduced||||||Unknown|||||||||||||||||||||||||||||Unknown|The mice displays a growth retardation phenotype without other gross abrnomalities. The mice are viable and fertile.|SJL/J|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Good|8|||No|18-Feb-2014|Cryopreserved sperm|50.0|0.0|Unknown||growth retardation, ENU|Yes| 7195.0|Thy1-aSyn-B6|B6.DBA/2-Tg(Thy1-SNCA)61Ema/Ausb||Dominant||||||||||||||||||||||||||transgene insertion 61, Eliezer Masliah|mouse Thy1|brain, including the basal ganglia, thalamus, substantia nigra, and brainstem|||||||||||Alpha-synuclein inclusion body: alpha-synuclein protein accumulates in synapses and neurons throughout the brain, including the neuropil of presynaptic terminals, thalamus, substantia nigra, neocortex, limbic system, hippocampus; in both pyramidal and nonpyramidal cells.Slight movement disorder at 6-9 months in males|C57BL/6|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|05-Nov-2012||0.0|0.0|Yes|Parkinson Disease 1, Autosomal Dominant; PARK1|Parkinson Disease, alpha-synuclein, Lewy body disease , atrophy|Yes| 5944.0|NfixCond/Emx1Cre||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5946.0|Nfixcond/Tomato||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 7201.0|Cx3cr1-GFP|B6.129-Cx3cr1/JAusb||Dominant|chemokine (C-X3-C) receptor 1|Cx3cr1|Nil||MGI:1333815|chemokine (C-X3-C) receptor 1; targeted mutation 1, Dan R Littman|Cx3cr1|MGI:2670351|9|||||||||||||||||||||||||||||Normal||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|05-Nov-2012||0.0|0.0|Unknown||neurotactin, FKN, endothelium, neuron, monocyte, NK cell, dendritic cell|Yes| 7199.0|GFAP-GFP|B6.Cg-Tg(Gfap-EGFP)3739Sart/JAusb||Dominant||||||||||||||||||||||||||transgene insertion 3739, Vijay P Sarthy|glial fibrillary acidic protein|Muller cells||||||||||Normal|Transgene expression is observed during retinal development, specifically in Muller cells and astrocytes.|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|05-Nov-2012||0.0|0.0|Unknown||Muller cell, eye, GFP, astrocytes|Yes| 7200.0|Thy1-YFP|B6.Cg-Tg(Thy1-YFP)HJrs/JAusb||Dominant||||||||||||||||||||||||||transgene insertion H, Joshua R Sanes|mouse Thy1||||||||||||Hemizygotes will express YFP in motor and sensory neurons and cortical layer V pyramidal cells.|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|05-Nov-2012||0.0|0.0|Unknown|||Yes| 7694.0|ENU30:G3|ANU:ENU30:G3||Recessive|Unknown|Unknown|||||||Unknown|||||||||||||||||||||||||||||Unknown|Unknown|C57BL/6NCrlAnu|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown|1|||No|27-May-2014|Cryopreserved sperm|242.0|0.0|Unknown||ENU, mutagenesis, screen, random|Yes| 7332.0|bm1|B6.C-H2-K/ByApb||Dominant|histocompatibility 2, K region|H2-K|||MGI:3040519|histocompatibility 2, K region; b haplotype mutation 1|H2-K|MGI:3618114|17||||||||||||||||||||||||||||17|Normal|Normal|C57BL/6J|Yes|Yes|Yes|Yes|Unknown|Unknown|No|Excellent|||bm1 x bm1|Yes|09-May-2013|Cryopreserved sperm|50.0|0.0|Unknown||H-2Kbm1, cross-presentation, antigen presentation|Possibly| 5583.0|129X1/SUJ x Epha4KO||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5584.0|202 F1(B57)||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5585.0|202 KO B57||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 1545.0|C57BL/6.gZB-/- OT-1|C57BL/6-Gzmb Tg(TcraTcrb)1100Mjb/AnuApb||Recessive|granzyme B|Gzmb|Unknown|CCP-1/C11, CCP1, Ctla-1, Ctla1, GZB|MGI:109267|targeted mutation 1, Timothy J Ley|Gzmb|MGI:1857156|14||||||||||||||||Yes|transgene insertion 1100, Michael J Bevan||||||||||||||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|06-Jul-2007|Cryopreserved sperm|20.0|0.0|Unknown||Fas, Natural Killer Cell, cytotoxic T cell|Yes| 2328.0|C57BL6.gZAB-/-OT-1 ; Shastri|B6.129S2-Gzmb Gzma Tg(TcraTcrb)1100Mjb/AnuApb||Recessive|granzyme A|Gzma|Nil|BLT esterase, Ctla-3, Ctla3, H factor, Hanukah factor, Hf, SE1, serine esterase 1, TSP-1, TSP1|MGI:109266|targeted mutation 1, Markus M Simon|Gzma|MGI:2449926|13||||||||||||||||Yes|transgene insertion 1100, Michael J Bevan||||||||||||||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|04-Dec-2007|Cryopreserved sperm|50.0|0.0|No||T cell, Natural Killer Cell, cytotoxicity, receptor, ovalbumin|No| 2328.0|C57BL6.gZAB-/-OT-1 ; Shastri|B6.129S2-Gzmb Gzma Tg(TcraTcrb)1100Mjb/AnuApb||Recessive|granzyme B|Gzmb|Nil|CCP-1/C11, CCP1, Ctla-1, Ctla1, GZB|MGI:109267|targeted mutation 1, Timothy J Ley|Gzmb|MGI:1857156|14|||||||||||||||||||||||||||||||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|04-Dec-2007|Cryopreserved sperm|||No||T cell, Natural Killer Cell, cytotoxicity, receptor, ovalbumin|No| 5697.0|Col1a2 x C57BL/6 ||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 7204.0|AR2.3-tg|B6(Cg)-Tg(Col1a1*2.3-Ar)/Apb||Dominant||||||||||||||||||||||||||AR2.3-tg|2.3kb fragment of the rat type 1 alpha 1 collagen gene|||||||||||Low bone turnover phenotype with compromised bone quality and strength.|Unknown|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|>10|||No|07-Nov-2012|Cryopreserved sperm|50.0|0.0|No||receptor, osteogenesis, osteoblast, androgen|Possibly| 7205.0|AR3.6-tg|B6(Cg)-Tg(Col1a1*3.6-Ar)/Apb||Dominant||||||||||||||||||||||||||AR3.6-tg|3.6kb fragment of the type 1 alpha 1 collagen gene|||||||||||Low bone turnover phenotype with compromised bone quality and strength.|Unknown|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|>10|||No|07-Nov-2012|Cryopreserved sperm|50.0|0.0|No||receptor, androgen, osteoblast|Possibly| 5318.0|LDLr knockouts|B6.129S7-Ldlr/J||Dominant|Low density lipoprotein receptor|Ldlr|||MGI:96765|low density lipoprotein receptor; targeted mutation 1, Joachim Herz|Ldlr|MGI:1857212|9||||||||||||||||No|||||||||||||Mice will exhibit high circulating cholesterol levels and develop atherosclerotic lesions after being fed a western style diet|Intermediate to homozygote|C57BL/6J|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|10|||No|12-Nov-2010|Cryopreserved sperm|50.0|0.0|Yes|Familial hypercholesterolemia|cholesterol, atherosclerosis, low density lipoprotein|Possibly| 7571.0|37L1ConR|C57BL/6N-A Gpr37L1/Apb||Dominant|G protein-coupled receptor 37-like 1|Gpr37l1|Unknown|CAG-18, D0Kist8|MGI:1928503|G protein-coupled receptor 37-like 1; targeted mutation 1a, Wellcome Trust Sanger Institute|Gpr37l1|MGI:4441736|1|||||||||||||||||||||||||||||Unknown. Predicted loss of expression mutant.|Unknown. Predicted loss of expression mutant.|C57BL/6N|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Excellent|Pure background||het x het|No|20-Jan-2014|Cryopreserved sperm|47.0|0.0|No|||Possibly| 7571.0|37L1ConR|C57BL/6N-A Gpr37L1/Apb||Dominant|nonagouti|a|||MGI:87853|nonagouti; targeted mutation 1, Allan Bradley|A|MGI:3842513|2|||||||||||||||||||||||||||||Unknown. Predicted loss of expression mutant.|Unknown. Predicted loss of expression mutant.|C57BL/6N|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Excellent|Pure background||het x het|No|20-Jan-2014|Cryopreserved sperm|||No|||Possibly| 7072.0|ABCA1ABCG1 Betacell KO|Ins2Cre ABCA1fl/flABCG1fl/fl||Recessive|ABCA1|ABCA1|||||||9|||||||||||||||||Ins2Cre|Rat insulin promoter|||||||||||Pancreatic beta islet cells do not express ABCA1 and ABCG1. Impaired glucose tolerance|Normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Excellent||||No|03-Sep-2012|Cryopreserved sperm|50.0|0.0|Unknown||ABCA1, ABCG1, B cell, diabetes, cholesterol|Possibly| 7072.0|ABCA1ABCG1 Betacell KO|Ins2Cre ABCA1fl/flABCG1fl/fl||Recessive|ABCG1|ABCG1|||||||17|||||||||||||||||||||||||||||Pancreatic beta islet cells do not express ABCA1 and ABCG1. Impaired glucose tolerance|Normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Excellent||||No|03-Sep-2012|Cryopreserved sperm|||Unknown||ABCA1, ABCG1, B cell, diabetes, cholesterol|Possibly| 7203.0|Vdr flox|B6-Vdr/Apb||Dominant|vitamin D (1,25-dihydroxyvitamin D3) receptor|Vdr|Normal|Nr1i1|MGI:103076|vitamin D (1,25-dihydroxyvitamin D3) receptor; targeted mutation 1, Pierre Chambon|Vdr|MGI:3663379|15|||||||||||||||||||||||||||||Normal|Normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|>10|||No|07-Nov-2012|Cryopreserved sperm|46.0|0.0|No||rickets, hyperparathyroidism, calcium, 1,25(OH)(2) vitamin D|Possibly| 7211.0||SJL-Ank1/MriApb|SJL-Ank1|Dominant|ankyrin 1, erythroid|Ank1|Reduced|Ank-1, pale|MGI:88024|ankyrin 1, erythroid; MRI23420|Ank1|MGI:5438699|8|ENSMUSG00000031543|ENSMUST00000121802|Ank1-004||||||||||||||||||||||||||Pre and Perinatal mortality with Jaundice, enlarge spleen and fragmented red blood cells|Heterozygous mice display a microcytic anaemia with increase osmotic fragility, splenomegaly and survival advantage to Plasmodium chabaudi |SJL|No|No|Yes|No|No|Yes|No|Good||||No|14-Nov-2012|Cryopreserved sperm|50.0|0.0|Yes|Hereditary spherocytosis|Hereditary spherocytosis, Malaria resistance, microcytosis, ENU|Yes| 8695.0|VWF/FVIII dKO|B6.129-F8 Vwf/||Recessive|coagulation factor VIII|F8||Cf8, Cf-8, Factor VIII, FVIII|MGI:88383||||X|||||||||||||||||||||||||||||Increased susceptibility to bleeding|Normal|C57BL/6|Yes|Unknown|Yes|Yes|Unknown|Yes|No|Unknown||||No|12-Apr-2019|Cryopreserved sperm|50.0|0.0|Unknown|||Yes| 8695.0|VWF/FVIII dKO|B6.129-F8 Vwf/||Recessive|Von Willebrand factor|Vwf|||MGI:98941||||6|||||||||||||||||||||||||||||Increased susceptibility to bleeding|Normal|C57BL/6|Yes|Unknown|Yes|Yes|Unknown|Yes|No|Unknown||||No|12-Apr-2019|Cryopreserved sperm|||Unknown|||Yes| 7027.0|CAG-H2B-GFP|C57BL/6N-Tg(CAG-H2/GFP)/MarpApb||Recessive||||||||||||||||||||||||||histocompatibility-2|chicken beta actin (CAG)|||||||||||Expresses H2B-GFP from CAG promoter|Expresses H2B-GFP from CAG promoter|C57BL/6N|Yes|Yes|Yes|Yes|Yes|Yes|No|Excellent||||No|24-Jul-2012|Cryopreserved sperm|50.0|0.0|Unknown|||No| 5698.0|CreHetFloxHet||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 7212.0|APN329|C57Bl/6NSrsf3/Marp||Recessive|serine/arginine-rich splicing factor 3|Srsf3|Unknown|Sfrs3, X16|MGI:98285|serine/arginine-rich splicing factor 3; targeted mutation 1a, Mouse Biology Program, UCDavis|Srsf3tm1a(KOMP)Mbp|MGI:4462527|17|||||||||||||||||||||||||||||Unknown|Normal|C57Bl/6N|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|15-Nov-2012|Cryopreserved sperm|50.0|0.0|Unknown|||Possibly| 7041.0|alpha-gus-, alpha-gustducin null, Gust KO|B6.129S1-Gnat3||Dominant|guanine nucleotide binding protein, alpha transducing 3|Gnat3|Nil|alpha-gustducin, Ggust, Gtn|MGI:3588268|uanine nucleotide binding protein, alpha transducing 3; targeted mutation 1, Robert F Margolskee|Gnat3|MGI:2152966|5|||||||||||||||||||||||||||||Homozygotes exhibit normal taste epithelia, with no significant differences in the three types of taste papillae, number of taste buds in each papilla or complement of taste receptor cells per bud relative to wild-type mice.Homozygotes display normal responses to a range of salty (NaCl) and sour (HCl) solutionsnotably, although the electrophyiological (chorda tympani) response is greater for sweet than for bitter compounds, the aversive behavioral effect is greater with bitter compounds.Homozygotes exhibit reduced aversive behavioral and electrophysiological responses to bitter compounds (denatorium and quinine) relative to wild-type mice.Homozygotes also exhibit reduced behavioral and electrophysiological responses to sweet compounds (sucrose and sweetener SC45647) relative to wild-type mice.Homozygotes show reduced preference for MSG at concentrations normally preferred by control mice.|Normal|C57BL/6J|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|06-Aug-2012||0.0|0.0|Unknown||G protein, taste, receptor|No| 7043.0|Trpm5-, Trpm5 KO|C57BL/6-Trpm5||Dominant|transient receptor potential cation channel, subfamily M, member 5|Trpm5|Nil|9430099A16Rik, Ltrpc5, Mtr1|MGI:1861718|transient receptor potential cation channel, subfamily M, member 5; targeted mutation 1, Sami Damak|Trpm5|MGI:3612408|7|||||||||||||||||||||||||||||Abnormal bitter taste sensitivity (J:103852)chorda tympani nerve responses to bitter compounds similar to response to sweet compounds.Abnormal salty taste sensitivity (J:103852)chorda tympani nerve responses to salt similar to response to sweet compounds.Abnormal sour taste sensitivity (J:103852)chorda tympani nerve responses to acid compounds similar to response to sweet compounds.Abnormal sweet taste sensitivity (J:103852)chorda tympani nerve response to sweet compounds applied to the anterior taste field of the tongue is greatly reduced but not eliminatedno enhancement of response to sweet compounds by increased temperature.Abnormal umami taste sensitivity (J:103852, J:104626)chorda tympani nerve responses to monosodium glutamate similar to response to sweet compounds (J:103852).residual responses to 100 and 300 mM monosodium glutamate in a two bottle preference test (J:104626).|Normal|C57BL/6J|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|06-Aug-2012||0.0|0.0|Unknown||taste, receptor|No| 7101.0|Cd8b KO|B6.129S-Cd8b/NIHAnuApb||Recessive|CD8 antigen, beta chain 1|Cd8b1|Nil|Ly-3, Ly-C, Lyt-3|MGI:88347|CD8 antigen, beta chain 1; targeted mutation 1, Dan R Littman|Cd8b1|MGI:3654103|6|||||||||||||||||||||||||||||Abnormal enzyme/coenzyme activity: thymocytes display 6-fold less CD8-associated Lck activity vs wild-type.Decreased thymocyte number: mice have 5-fold fewer CD8-lineage thymocytes compared to wild-type; there is a lack of mature CD8-lineage T cells.Decreased CD8-positive T cell number: * there is a lack of mature CD8-lineage T cells * number of mature single positive CD8+ thymocytes is reduced 5-fold vs wild-type * numbers in peripheral lymph nodes are reduced 5-fold also.Abnormal T cell subpopulation ratio: CD8 to CD4 ratio is 6.6 fold lower than in wild-type.Abnormal cytotoxic T cell physiology: splenocytes from mutants show a normal cytotoxic T lymphocyte response comparable to heterozygous mice to allogeneic stimuli even though mutants have only 20% of normal numbers of CD8+ T cells.||C57BL/6NCrlAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|05-Oct-2012|Cryopreserved sperm|52.0|0.0|Unknown||T cell, MHC, TCR, CD8, selection|Possibly| 5587.0|49.1A||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 7094.0|RNAi-14|C57Bl/6J-HDAC3/MarpApb||X-linked|histone deacetylase 3|Hdac3|Unknown||MGI:1343091||||X|||||||||||||||||||||||||||||Unknown|Normal|C57Bl/6N|Unknown|Unknown|Unknown|Unknown|Unknown|Yes|No|Good||||No|27-Sep-2012|Cryopreserved sperm|50.0|0.0|Unknown|||Possibly| 6931.0|APN 256|C57BL/6N-Sema3d/Marp||Recessive| sema domain, immunoglobulin domain (Ig), short basic domain, secreted, (semaphorin) 3D|Sema3d ||4631426B19Rik |MGI:1860118 |sema domain, immunoglobulin domain (Ig), short basic domain, secreted, (semaphorin) 3D; targeted mutation 1a, Wellcome Trust Sanger Institute |Sema3dtm1a(KOMP)Wtsi|MGI:4820051|5|||||||||||||||||||||||||||||Unknown|Normal|C57Bl/6N|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|03-Jul-2012|Cryopreserved sperm|50.0|0.0|Unknown|||Possibly| 7025.0|APN239|C57BL/6N-A Adarb2/Marp||Recessive|adenosine deaminase, RNA-specific, B2|Adarb2 |Unknown|Adar3, RED2 |MGI:2151118 |adenosine deaminase, RNA-specific, B2; targeted mutation 1a, Mouse Biology Program, UCDavis |Adarb2 |MGI:4944293|13|||||||||||||||||||||||||||||Unknown|Normal|C57BL/6N|Unknown|Unknown|Unknown|Unknown|Unknown|Yes|No|Unknown||||No|20-Jul-2012|Cryopreserved sperm|50.0|0.0|Unknown||ES cell clone|Possibly| 7037.0|zeta-SV129 390|129Sv-Ywhaz/Apb||Recessive|tyrosine 3-monooxygenase/tryptophan 5-monooxygenase activation protein, zeta polypeptide|Ywhaz|Nil|1110013I11Rik, 14-3-3 zeta|MGI:109484|tyrosine 3-monooxygenase/tryptophan 5-monooxygenase activation protein, zeta polypeptide; gene trap OST405390, Lexicon Genetics|Ywhaz||15|||||||||||||||||||||||||||||Infertile, reduced survival of KO pups at 21 days|None|129Sv/B6|Yes|No|Yes|Yes|No|Yes|Yes|Good|N/A||het x het|No|06-Aug-2012|Cryopreserved sperm|50.0|0.0|Unknown||14-3-3, signal transduction|Possibly| 7695.0|Dynll-loxP|C57BL/6-Dynll1/Stv||Dominant|dynein light chain LC8-type 1|Dynll1|Normal|8kDa LC, DLC8, Dnclc1, Pin|MGI:1861457|dynein light chain LC8-type 1; targeted mutation 1.1, Jorg Heierhorst|Dynll1|MGI:5463937|5||||||||||||||||Yes|||||||||||||Normal|Normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Excellent||||No|03-Jun-2014|Cryopreserved sperm|99.0|0.0|Unknown||Dynll-1, ASCIZ|Possibly| 4722.0|Joey-RSA|C57BL/6-Rbm5/MarpApb|C57BL/6-Rbm5/MarpApb|Recessive|RNA binding motif protein 5|Rbm5|Unknown||MGI:1933204|RNA binding motif protein 5; sda|Rbm5|MGI:5563424|9|ENSMUSG00000032580|ENSMUST00000035199|Rbm5-201|788|940|G to C|ENSMUSE00000251397|10|263|Arginine to Proline|||||CTATGCTTCCTTAGCTGTCAATAACATTCGCCTCATAAAAGACAAACAGACACAACAGAAC|Yes|||||||||||||Round spermatid arrest.Spermatid differentiation arrest, germ cell sloughing and apoptosis, which ultimately led to azoospermia (no sperm in the ejaculate) and male sterility.||C57BL/6|Yes|Yes|Yes|Yes|No|Yes|No|Unknown||||No|09-Apr-2009|Cryopreserved sperm|70.0|0.0|Unknown||infertility, sperm, arrest, ENU|Yes| 5588.0|49.1B||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5589.0|a-actin-cre||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 4808.0|River|ENU8BAT:038||Recessive|||||||||Unknown|||||||||||||||||transgene insertion 3, Christopher C Goodnow|Rat insulin promoter|Expression of the inserted sequence specifically to pancreatic islet beta cells||||||||||Male infertility. Mutant found in HEL:TCR ENU library.HEL:TCR transgenes not required for mutant phenotype||C57BL/6 x CBA x C57BL/10BR|Yes|Yes|Yes|Yes|No|Yes|No|Poor||||No|24-Sep-2009|Cryopreserved sperm|30.0|0.0|Yes|Male Infertility|ENU, fertility, sperm|Possibly| 4808.0|River|ENU8BAT:038||Recessive||||||||||||||||||||||||||transgene insertion 1, Mark M Davis||||||||||||Male infertility. Mutant found in HEL:TCR ENU library.HEL:TCR transgenes not required for mutant phenotype||C57BL/6 x CBA x C57BL/10BR|Yes|Yes|Yes|Yes|No|Yes|No|Poor||||No|24-Sep-2009|Cryopreserved sperm|||Yes|Male Infertility|ENU, fertility, sperm|Possibly| 7024.0|APN97|C57BL/6N-A Ubr5/Marp||Recessive|ubiquitin protein ligase E3 component n-recognin 5|Ubr5 |Unknown|4432411E13Rik, Edd, Edd1, mKIAA0896 |MGI:1918040 |ubiquitin protein ligase E3 component n-recognin 5; targeted mutation 1a, Wellcome Trust Sanger Institute |Ubr5 |MGI:4455996|15|||||||||||||||||||||||||||||Unknown|Normal|C57BL/6N|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|20-Jul-2012|Cryopreserved sperm|50.0|0.0|Unknown||ES cell clone|Possibly| 7029.0|APN257|C57BL/6N-Ift140/Marp||Recessive|intraflagellar transport 140 homolog (Chlamydomonas)|Ift140 |Unknown|mKIAA0590, Tce5, Wdtc2 |MGI:2146906 |intraflagellar transport 140 homolog (Chlamydomonas); targeted mutation 1a, Wellcome Trust Sanger Institute |Ift140tm1a(KOMP)Wtsi|MGI:4363217|17||||||||||||||||Yes|||||||||||||Unknown - Not bred to homozygocity |Normal |C57BL/6N |Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|26-Jul-2012|Cryopreserved sperm|50.0|0.0|Unknown||ES cell|Possibly| 7059.0|B6.BlGpA|C57BL/6-Tg(ICAM2-FUT1, NAGAT)/StV||Dominant||||||||||||||||||||||||||human H transferase and human A transferase|human ICAM2||||||||||||Expression of human blood group A on endothelial cells and red blood cells|C57BL/6|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Good||||No|24-Aug-2012|Cryopreserved sperm|100.0|0.0|Unknown||blood group|Possibly| 5175.0||ENU15China:001b||Recessive|Unknown|Unknown|Unknown||||||Unknown|||||||||||||||||||||||||||||Increased Germinal Centre B cells in unimmunised mice|Unknown|C57BL/6JAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|12-Jul-2010|Cryopreserved sperm|10.0|0.0|Unknown||B cell, germinal centre, ENU|Possibly| 4851.0|Inara|ENU6AT:23||Recessive|Unknown||||||||Unknown|||||||||||||||||transgene insertion 3, Christopher C Goodnow|Rat insulin promoter|Expression of the inserted sequence specifically to pancreatic islet beta cells||||||||||Male infertility. Mutant found in HEL:TCR ENU library.HEL:TCR transgenes not required for mutant phenotype||C57BL/6 x CBA x C57BL/10BR|Yes|Yes|Yes|Yes|No|Yes|No|Poor||||No|24-Sep-2009|Cryopreserved sperm|70.0|0.0|Yes|Male Infertility|ENU, fertility, sperm|No| 4851.0|Inara|ENU6AT:23||Recessive||||||||||||||||||||||||||transgene insertion 1, Mark M Davis||||||||||||Male infertility. Mutant found in HEL:TCR ENU library.HEL:TCR transgenes not required for mutant phenotype||C57BL/6 x CBA x C57BL/10BR|Yes|Yes|Yes|Yes|No|Yes|No|Poor||||No|24-Sep-2009|Cryopreserved sperm|||Yes|Male Infertility|ENU, fertility, sperm|No| 4852.0|Kaylee|ENU6AT:52||Recessive|Unknown||||||||Unknown|||||||||||||||||transgene insertion 3, Christopher C Goodnow|Rat insulin promoter|Expression of the inserted sequence specifically to pancreatic islet beta cells||||||||||Male infertility. Mutant found in HEL:TCR ENU library.HEL:TCR transgenes not required for mutant phenotype||C57BL/6 x CBA x C57BL/10BR|Yes|Yes|Yes|Yes|No|Yes|No|Poor||||No|24-Sep-2009|Cryopreserved sperm|80.0|0.0|Yes|Male Infertility|ENU, fertility, sperm|Yes| 4852.0|Kaylee|ENU6AT:52||Recessive||||||||||||||||||||||||||transgene insertion 1, Mark M Davis||||||||||||Male infertility. Mutant found in HEL:TCR ENU library.HEL:TCR transgenes not required for mutant phenotype||C57BL/6 x CBA x C57BL/10BR|Yes|Yes|Yes|Yes|No|Yes|No|Poor||||No|24-Sep-2009|Cryopreserved sperm|||Yes|Male Infertility|ENU, fertility, sperm|Yes| 7334.0|ENU3_4|Infertility screen||Recessive|Unknown||||||||Unknown|||||||||||||||||||||||||||||Male infertility screen||C57BL/6JSfdAnu|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-May-2013|Cryopreserved sperm|140.0|0.0|Unknown||ENU|No| 5590.0|A107CYPOE||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 4457.0|Singh|C57BL/6-Gzmb Tg(TcraTcrb)1100Mjb/AnuApb||Recessive|granzyme B|Gzmb|Unknown|CCP-1/C11, CCP1, Ctla-1, Ctla1, GZB|MGI:109267|targeted mutation 1, Timothy J Ley|Gzmb|MGI:1857156|14||||||||||||||||Yes|transgene insertion 1100, Michael J Bevan||||||||||||||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|20-Feb-2009|Cryopreserved sperm|20.0|0.0|Unknown||T cell, Natural Killer, cytotoxicity, receptor, ovalbumin|Yes| 7078.0|APN245|C57Bl/6NTac-Gpbar1/Marp||Recessive|G protein-coupled bile acid receptor 1|Gpbar1|Unknown|BG37, GPR131, M-BAR, TGR5 |MGI:2653863|G protein-coupled bile acid receptor 1; targeted mutation 1, Velocigene|Gpbar1|MGI:4399435|1||||||||||Unknown to Unknown|||||||||||||||||||Unknown|Normal|C57Bl/6N|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2012|Cryopreserved sperm|50.0|0.0|Unknown|||Possibly| 7108.0|APN197|C57BL/6N(Ag)-Scmh1Mu||Recessive|sex comb on midleg homolog 1|Scmh1 ||Scml3 |MGI:1352762 |sex comb on midleg homolog 1; targeted mutation 1a, Helmholtz Zentrum Muenchen GmbH|Scmh1tm1a(EUCOMM)Hmgu|MGI:4456695|4|||||||||||||||||||||||||||||Unknown|Normal|C57Bl/6N|Unknown|Unknown|Yes|Unknown|Unknown|Unknown|No|Unknown||||No|17-Oct-2012|Cryopreserved sperm|50.0|0.0|Unknown|||Possibly| 4854.0|Shepherd|ENU6AT:045||Recessive|Unknown||||||||Unknown|||||||||||||||||transgene insertion 3, Christopher C Goodnow|Rat insulin promoter|Expression of the inserted sequence specifically to pancreatic islet beta cells||||||||||Male infertility. Mutant found in HEL:TCR ENU library.HEL:TCR transgenes not required for mutant phenotype||C57BL/6 x CBA x C57BL/10BR|Yes|Yes|Yes|Yes|No|Yes|No|Poor||||No|24-Sep-2009|Cryopreserved sperm|50.0|0.0|Yes|Male Infertility|ENU, fertility, sperm|Yes| 4854.0|Shepherd|ENU6AT:045||Recessive||||||||||||||||||||||||||transgene insertion 1, Mark M Davis||||||||||||Male infertility. Mutant found in HEL:TCR ENU library.HEL:TCR transgenes not required for mutant phenotype||C57BL/6 x CBA x C57BL/10BR|Yes|Yes|Yes|Yes|No|Yes|No|Poor||||No|24-Sep-2009|Cryopreserved sperm|||Yes|Male Infertility|ENU, fertility, sperm|Yes| 5239.0|Lyn knockout Viable Motheaten mice ; C57.Lyn-/- Me v/+|C57BL/6-Lyn Ptpn6/Apb||Recessive|Yamaguchi sarcoma viral (v-yes-1) oncogene homolog|Lyn|Nil|Hck-2|MGI:96892|Yamaguchi sarcoma viral (v-yes-1) oncogene homolog; targeted mutation 1, Ashley R Dunn|Lyn|MGI:2157129|4||||||||||||||||No|||||||||||||B6-Lyn<-/-> Ptpn6 mice develop exaggerated autoimmune disease compared with Lyn<-/-> miceAbnormal mature B cell morphology: mature B cells have about 4-fold lower surface IgM levels.|Double heterozygotes develop autoimmunity with earlier onset than single heterozygote mice|C57BL/6|No|No|Yes|No|No|Yes|No|Unknown|20 for Lyn<-/->||B6-Lyn<-/-> Ptpn6 x B6-Lyn<-/-> Ptpn6|No|12-Oct-2010|Cryopreserved sperm|50.0|0.0|Unknown||B cell, signal transduction, src kinase, phosphorylation, phosphatase, autoimmunity, inflammation|Yes| 5239.0|Lyn knockout Viable Motheaten mice ; C57.Lyn-/- Me v/+|C57BL/6-Lyn Ptpn6/Apb||Recessive|protein tyrosine phosphatase, non-receptor type 6|Ptpn6||hcp, Hcph, Ptp1C, SHP-1, Spin|MGI:96055|protein tyrosine phosphatase, non-receptor type 6; viable motheaten|Ptpn6|MGI:1856074|6||||||||||||||||No|||||||||||||B6-Lyn<-/-> Ptpn6 mice develop exaggerated autoimmune disease compared with Lyn<-/-> miceAbnormal mature B cell morphology: mature B cells have about 4-fold lower surface IgM levels.|Double heterozygotes develop autoimmunity with earlier onset than single heterozygote mice|C57BL/6|No|No|Yes|No|No|Yes|No|Unknown|20 for Lyn<-/->||B6-Lyn<-/-> Ptpn6 x B6-Lyn<-/-> Ptpn6|No|12-Oct-2010|Cryopreserved sperm|||Unknown||B cell, signal transduction, src kinase, phosphorylation, phosphatase, autoimmunity, inflammation|Yes| 4853.0|Taily ; ENU8CAT:006|CBA;B6JSfdAnu-Katnb1/AnuApb||Recessive|katanin p80 (WD40-containing) subunit B 1|Katnb1|Unknown|KAT|MGI:1921437|katanin p80 (WD40-containing) subunit B 1; taily|Katnb1|MGI:5428740|8|ENSMUSG00000031787|ENSMUST00000034239|Katnb1-201|700|972|G to T|ENSMUSE00000212968|9|234|Valine to Phenylalanine|||||TGAGCTGCATTGAAGGGGAGCCCGGGCCCGTCAGGAGTGTCCTCTTCAACCCCGACGGCTG|Yes|||||||||||||Male infertility. Reproductive system phenotype: • number of Sertoli cells, spermatogonia and spermatocytes are similar to controls.Small testis: • testes from 8-12 week old homozygous mice are 18.7% smaller than controls.Oligozoospermia: • epididymes from mutant males contain significantly lower sperm counts.Abnormal sperm flagellum morphology: • flimsy or absent outer dense fibers.Abnormal sperm axoneme morphology:• missing central microtubules and hemi-axenomes are present.Globozoospermia: • abnormally shaped spermatid heads.• all sperm in the cauda epididymis have abnormally shaped heads.Abnormal spermatid morphology:• ~30% fewer spermatids (round and elongating) compared to controls.Abnormal manchette morphology:• mutant spermatids exhibit constricted perinuclear rings, nuclear distortion and abnormally long microtubules extending in to the distal cytoplasm.• although the manchettes eventually resolved, the removal of manchettes was delayed at step 13.Abnormal male meiosis: • abnormal male meiotic cells appear at metaphase-anaphase; many cells are stalled in late anaphase in mutant males.• reduction in spermatid number is due to a decrease in the number of cells exiting meiosis.• apoptotic cells are present in the stage XII and stage I tubules where final events of meiosis occur.• telophase cells with prominent midbody microtubules are seen in testes from mutant male mice• binucleated haploid spermatids frequently appear.Abnormal meiotic spindle morphology:• metaphase spindles are more densely populated with microtubules and project from the poles at a wider angle than controls pole to pole measurements in metaphase spindles are longer than controls.Increased Sertoli cell phagocytosis: • 36-fold increase in the number of spermatozoa being phagocytosed by Sertoli cells in stages IX-X1 tubules.Asthenozoospermia:• all sperm in the cauda epididymis display compromised motility, with very few capable of forward (progressive) motility.||C57BL/6 x CBA x C57BL/10BR|Yes|Yes|Yes|Yes|No|Yes|No|Poor||||No|24-Sep-2009|Cryopreserved sperm|175.0|0.0|Yes|Male Infertility|ENU, fertility, sperm|Yes| 4912.0|Wombi ; ENU9CAT:006|B6;CBA(Cg)-Pou1f1/Apb||Recessive|POU domain, class 1, transcription factor 1|Pou1f1|Unknown|GHF-1, Hmp1, Pit-1, Pit1, Pit1-rs1, Snell dwarf|MGI:97588|wombi|Pou1f1||16|ENSMUSG00000004842|ENSMUST00000116588|Pou1f1-202|470|585|T to A|ENSMUSE00000131906|4|156|Leucine to Glutamine|||||ATACACCCAGACAAACGTGGGCGAAGCGCTGGCTGCTGTCCACGGCTCAGAATTCAGTCAA|No|||||||||||||Male infertility. Dwarf, affected mice are smaller than littermates.Mutant found in HEL:TCR ENU library. HEL:TCR transgenes not required for mutant phenotype||C57BL/6 x CBA|Yes|Yes|Yes|Yes|No|Yes|No|Poor|||Het x Het|No|16-Oct-2009|Cryopreserved sperm|210.0|0.0|Yes|Male Infertility|ENU, fertility, sperm, Dwarf|Yes| 5243.0|MMP13KO FVBn|FVB/N-Mmp13/Apb||Recessive|matrix metallopeptidase 13|MMP13|Nil|Clg, collagenase-1, Collagenase-3, interstitial collagenase, MMP-13, Mmp1|MGI:1340026|matrix metallopeptidase 13; targeted mutation 1.1, Zena Werb|Mmp13|MGI:3521938|9||||||||||Unknown to Unknown|||||||||||||||||||Increased width of hypertrophic chondrocyte zone: * the hypertrophic zone is expanded in the tibia and metatarsals, at E17 and 1 week after birth, respectively, however by 12 weeks of age the size of the hypertrophic zone is similar to wild-type. * chondrocytes proliferate and differentiate normally but accumulate in the most terminally differentiated hypertrophic state. * establishment of the primary ossification centers is normal.Abnormal cancellous bone morphology: * the amount of trabecular bone is increased in the tibia and metatarsals by 3 weeks or 1 week of age, respectively, however by 1 year of age the amount of trabecular bone was similar to wild-type. * the organization of the trabecular bone is also irregular.OA was surgically induced in the knees of MMP-13-knockout mice. No difference between wildtype and KO mice for aggrecan loss or cartilage erosion at 4 weeks. here was less tibial cartilage erosion in knockout mice than in wild-type mice at 8 weeks. Cartilaginous osteophytes were larger in knockout mice at 4 weeks, but by 8 weeks osteophyte maturity and size were no different from those in wild-type mice. Articular chondrocyte hypertrophy with positive type X collagen and DIPEN staining occurred in both wild-type and knockout mouse joints. Authors conclude Chondrocyte hypertrophy is not regulated by MMP-13 activity in this model and does not in itself lead to cartilage erosion. MMP-13 deficiency can inhibit cartilage erosion in the presence of aggrecan depletion, supporting the potential for therapeutic intervention in established OA with MMP-13 inhibitors.||FVB/N|Yes|Yes|Yes|Yes|Yes|Yes|No|Poor|10|||No|14-Oct-2010|Cryopreserved sperm|90.0|0.0|Yes|spondyloepimetaphyseal dysplasia|extracellular matrix, collagenase, chondrocyte, osteoblast, growth plate|Possibly| 7071.0|APN209|C57Bl/6N(Ag)-Rabl2/Marp||Recessive|RAB, member of RAS oncogene family-like 2|Rabl2|Unknown|1110031N17Rik, Rabl2a|MGI:1915958 |RAB, member of RAS oncogene family-like 2; targeted mutation 1, Wellcome Trust Sanger Institute |Rabl2/Marp |MGI:4431454|15|||||||||||||||||||||||||||||Unknown|Normal|C57Bl/6N|Unknown|Unknown|Unknown|Unknown|Unknown|Yes|No|Good||||No|30-Aug-2012|Cryopreserved sperm|50.0|0.0|Unknown|||Possibly| 5254.0|CNTFKO|C57BL/6-Cntf/StvApb||Recessive|ciliary neurotrophic factor|Cntf|Nil||MGI:88439|ciliary neurotrophic factor; targeted mutation 1, Max Planck Institute for Neurobiology|Cntf|MGI:1857773|19||||||||||||||||No|||||||||||||Abnormal microglial cell morphology: atrophic and degenerative changes in spinal motor neurons are accompanied by an increase in the numbers of activated microglial cells.Abnormal motor neuron morphology: at 8 weeks of age, lumbar motor neuron cell bodies are smaller and the nuclei are swollen, resulting in an increase in the ratio between nuclear and cytoplasmic areas of about 40%, however by 14 weeks of age, both cell area and nuclear area are smaller.Decreased motor neuron number: 22% reduction in facial motor neurons at 28 weeks of age but not at 4 weeks of age.Motor neuron degeneration: * with increasing age, spinal motor neurons exhibit progressive atrophy and finally degeneration. * trophy becomes apparent by 8 weeks of age and the first signs of degeneration are seen at 22 weeks of age.Muscle weakness: small but significant reduction in muscle strength at 28 weeks of age, as indicated by forelimb grip strength.Decreased grip strength: small but significant reduction in forelimb grip strength at 28 weeks of age.Abnormal microglial cell morphology: atrophic and degenerative changes in spinal motor neurons are accompanied by an increase in the numbers of activated microglial cells.This knockout results in progressive atrophy and loss of motor neurons in adult mice, functionally this means a small reduction in muscle strength.||C57BL/6|Yes|Unknown|Yes|Yes|Unknown|Yes|No|Unknown||||No|21-Oct-2010|Cryopreserved sperm|50.0|0.0|Unknown||Schwann cell, motor neuron, muscle, atrophy, growth factor|No| 5169.0|Idd5D|NOD.B6-Idd5CD/ArcApb||Dominant||||||||||||||||||||||||||||||||||||||As per the parental strain (NOD/Lt).Delayed onset of Type 1 diabetes.||NOD/Lt|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|||Hom x Hom|No|29-Jun-2010|Embryo|0.0|0.0|Yes|All of these 4 strains are derived from the Non Obese Diabetes (NOD) model where we have bred a small section of the protective mouse (C57BL/6) into the Idd locus. This generated 4 congenic mouse strains that have enabled us to evaluate the effectiveness of a protective allele in a known Type 1 Diabetic region in the NOD/Lt mouse.||Yes| 4911.0|Per-gAB|C57BL/6-Gzma Gzmb Prf1/AnuApb||Recessive|granzyme A|Gzma|Nil|BLT esterase, Ctla-3, Ctla3, H factor, Hanukah factor, Hf, SE1, serine esterase 1, TSP-1, TSP1|MGI:109266|targeted mutation 1, Markus M Simon|Gzma|MGI:2449926|13||||||||||||||||Yes|||||||||||||Increased sensitivity to induced morbidity/mortality: West Nile Virus-infected triple homozygotes display prolonged mean survival time (MST) but significantly increased mortality (50%) relative to either wild-type (29%) or Prf1 (18%) mice.Immune system phenotype: triple homozygotes develop a normal contact hypersensitivity (CHS) response (based on increase in ear thickness) to trinitrophenyl (TNP) relative to wild-type mice.Increased susceptibility to parasitic infection: decreased clearance and survival after infection with Trypanosoma cruziIncreased susceptibility to viral infection: triple homozygotes display increased susceptibility to West Nile flavivirus (WNV) infection relative to wild-type. Triple mutants show a higher level of infectious virus in brain relative to wild-type or Prf1 mice at the same time point||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|12-Oct-2009|Cryopreserved sperm|50.0|0.0|No||T cell, Natural Killer Cell, cytotoxicity, receptor, ovalbumin|Yes| 4911.0|Per-gAB|C57BL/6-Gzma Gzmb Prf1/AnuApb||Recessive|granzyme B|Gzmb|Unknown|CCP-1/C11, CCP1, Ctla-1, Ctla1|MGI:109267|targeted mutation 1, Timothy J Ley|Gzmb|MGI:1857156|14|||||||||||||||||||||||||||||Increased sensitivity to induced morbidity/mortality: West Nile Virus-infected triple homozygotes display prolonged mean survival time (MST) but significantly increased mortality (50%) relative to either wild-type (29%) or Prf1 (18%) mice.Immune system phenotype: triple homozygotes develop a normal contact hypersensitivity (CHS) response (based on increase in ear thickness) to trinitrophenyl (TNP) relative to wild-type mice.Increased susceptibility to parasitic infection: decreased clearance and survival after infection with Trypanosoma cruziIncreased susceptibility to viral infection: triple homozygotes display increased susceptibility to West Nile flavivirus (WNV) infection relative to wild-type. Triple mutants show a higher level of infectious virus in brain relative to wild-type or Prf1 mice at the same time point||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|12-Oct-2009|Cryopreserved sperm|||No||T cell, Natural Killer Cell, cytotoxicity, receptor, ovalbumin|Yes| 4911.0|Per-gAB|C57BL/6-Gzma Gzmb Prf1/AnuApb||Recessive|perforin 1 (pore forming protein)|Prf1|Nil|perforin, Pfp, Prf-1|MGI:97551|targeted mutation 1, Sandoz Pharmaceutical|Prf1|MGI:1857235|10|||||||||||||||||||||||||||||Increased sensitivity to induced morbidity/mortality: West Nile Virus-infected triple homozygotes display prolonged mean survival time (MST) but significantly increased mortality (50%) relative to either wild-type (29%) or Prf1 (18%) mice.Immune system phenotype: triple homozygotes develop a normal contact hypersensitivity (CHS) response (based on increase in ear thickness) to trinitrophenyl (TNP) relative to wild-type mice.Increased susceptibility to parasitic infection: decreased clearance and survival after infection with Trypanosoma cruziIncreased susceptibility to viral infection: triple homozygotes display increased susceptibility to West Nile flavivirus (WNV) infection relative to wild-type. Triple mutants show a higher level of infectious virus in brain relative to wild-type or Prf1 mice at the same time point||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|12-Oct-2009|Cryopreserved sperm|||No||T cell, Natural Killer Cell, cytotoxicity, receptor, ovalbumin|Yes| 7333.0|ENU17China14|ENU17China14||Recessive|Unknown|Unknown|||||||Unknown|||||||||||||||||||||||||||||Reduced % MZB cells in spleen. |unknown|C57BL6/JAnu|Yes|Unknown|Unknown|Yes|Unknown|Unknown|No|Good||7|unknown x unknown (lethal screen, breed unknown siblings of affected individuals)|No|10-May-2013|Cryopreserved sperm|10.0|0.0|Unknown||B cell, Marginal zone, MZB, B cell development, spleen, ENU|No| 8703.0|ASD752:Ssbp4|C57BL/6NCrlAnu-Ssbp4/Anu||Recessive|single stranded DNA binding protein 4|Ssbp4||1210002E11Rik|MGI:1924150||||8|||||||||||||||||||||||||||||Unknown|unknown|C57BL/6NCrlAnu|Yes|Unknown|Yes|Yes|Unknown|Yes|No|Unknown||||No|16-Apr-2019|Cryopreserved sperm|92.0|0.0|Unknown|||Yes| 8702.0|PDCD2LKO|C57BL/6-Pdcd2l/MkobMarp||Recessive|programmed cell death 2-like|Pdcd2l||6030457N17Rik|MGI:1915329||||7|||||||||||||||||||||||||||||Embryonic lethal|Normal|C57BL/6J|No|No|Yes|No|No|Yes|No|Unknown||||No|15-Apr-2019|Cryopreserved sperm|50.0|0.0|Unknown|||Yes| 7335.0||SJL/Mrit||Dominant|Unknown|Unknown|||||||Unknown|||||||||||||||||||||||||||||Pre and Perinatal mortality with Jaundice, enlarge spleen and fragmented red blood cells|Heterozygous mice display a microcytic anaemia with increase osmotic fragility and splenomegaly|SJL/J|No|No|Yes|No|No|Yes|No|Good||||No|14-May-2013|Cryopreserved sperm|70.0|0.0|Yes|hereditary spherocytosis|haematology, red blood cells, hereditary spherocytosis, ENU|Yes| 5269.0|Lyn IL-6 double knockout ; C57.Lyn-/- IL-6-/-|C57BL/6-Lyn IL6/Apb||Recessive|Yamaguchi sarcoma viral (v-yes-1) oncogene homolog|Lyn|Nil|Hck-2|MGI:96892|Yamaguchi sarcoma viral (v-yes-1) oncogene homolog; targeted mutation 1, Ashley R Dunn|Lyn|MGI:2157129|4||||||||||||||||No|||||||||||||As compared to Lyn mice genetic deletion of IL-6 on a Lyn-deficient background does not alter B cell development, plasma cell accumulation, or dendritic cell hypermaturation, suggesting that these characteristics are intrinsic to the loss of Lyn. However, hyperactivation of B and T cell compartments, extramedullary hematopoiesis, expansion of the myeloid lineage and autoimmune disease are all ameliorated in Lyn<-/-> IL-6<-/-> mice. Importantly, our studies show that although Lyn<-/-> B cells may be autoreactive, it is the IL-6-dependent inflammatory environment they engender that dictates their disease-causing potential.|Unknown|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|20|||No|25-Oct-2010|Cryopreserved sperm|50.0|0.0|Unknown||B cell, autoimmune disease, dendritic cell, signal transduction|Yes| 5269.0|Lyn IL-6 double knockout ; C57.Lyn-/- IL-6-/-|C57BL/6-Lyn IL6/Apb||Recessive|interleukin 6|Il6|Nil|Il-6|MGI:96559|interleukin 6; targeted mutation 1, Manfred Kopf|Il6|MGI:1857197|5||||||||||||||||No|||||||||||||As compared to Lyn mice genetic deletion of IL-6 on a Lyn-deficient background does not alter B cell development, plasma cell accumulation, or dendritic cell hypermaturation, suggesting that these characteristics are intrinsic to the loss of Lyn. However, hyperactivation of B and T cell compartments, extramedullary hematopoiesis, expansion of the myeloid lineage and autoimmune disease are all ameliorated in Lyn<-/-> IL-6<-/-> mice. Importantly, our studies show that although Lyn<-/-> B cells may be autoreactive, it is the IL-6-dependent inflammatory environment they engender that dictates their disease-causing potential.|Unknown|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|20|||No|25-Oct-2010|Cryopreserved sperm|||Unknown||B cell, autoimmune disease, dendritic cell, signal transduction|Yes| 5236.0|Viable Motheaten mice ; C57.Me v/+|C57BL/6J-Ptpn6/LudApb||Recessive|protein tyrosine phosphatase, non-receptor type 6|Ptpn6|Unknown|hcp, Hcph, Ptp1C, SHP-1, Spin|MGI:96055|protein tyrosine phosphatase, non-receptor type 6; viable motheaten|Ptpn6|MGI:1856074|6||||||||||||||||Yes|||||||||||||Decreased B cell number: lambda1 and lambda2, 3 B cells are reduced 14- and 4-fold, respectively, in the spleen and 5.9- and 2.2-fold, respectively, in the bone marrow compared to B cell numbers in wild-type mice.Decreased mature B cell number: a result of a rapid expansion of the plasma cell population.Increased plasma cell number: due to a factor in serum of mutant mice that increases cell maturation by three orders of magnitude.Abnormal immunoglobulin level: uncontrolled levelsAbnormal inflammatory response: * resembles rheumatoid arthritis. * immunosuppressant drugs inhibit arthritic symptoms, but non-steroid anti-inflammatory drugs do notRheumatoid arthritis.Chronic inflammation: * reactions in the paws consist mainly of polymorphonuclear and mononuclear cell infiltration in the subcutaneous tissue extending to the periosteum and joint * paws become deformed causing progressive problems walkingInterstitial pneumonia: pneumonitis progression is slower than in Ptpn6 homozygotes but still causes death.Premature death: * mice die at about 9 weeks instead of at 3 weeks as in Ptpn6 homozygotes * death is due to a progressive and fatal autoimmune syndromeAbsent skin pigmentation: at 3-4 days of age mice have focal depigmentation of the skin.Focal hair loss: patchy absence of hair follows focal skin depigmentation giving the coat an uneven or motheaten appearance.Spontaneous skin ulceration: necrotic lesions can develop on paws, tail and ears.Abnormal skin condition.Interstitial pneumonia: pneumonitis progression is slower than in Ptpn6 homozygotes but still causes death.Decreased body size.Homozygous Motheaten viable mice develop early onset systemic autoimmune and inflammatory disease. The lungs of the mice become consolidated with neutrophils and activated chitinase-laden macrophages. The mice do not thrive, are runted and their skin, paws and ears shows signs of inflammatory disease, which is observable at weaning. The mice are usually euthanized before 8 wks of age.|Heterozygous mice develop low level antinuclear antibodies at about 12 months of age.|C57BL/6J|Yes|No|Yes|Yes|No|Yes|No|Unknown|||Het x Het|No|11-Oct-2010|Cryopreserved sperm|50.0|0.0|Unknown||src kinase, B cell, autoimmunity, neutrophil, inflammation, pigmentation|Possibly| 5292.0|SHIP(Flox47).C57|B6.Cg-Inpp5d/LudApb||Semi-dominant|inositol polyphosphate-5-phosphatase D|Inpp5d|Normal|s-SHIP, SHIP, SHIP-1, SHIP1, Src homology 2 domain-containing inositol-5-phosphatase|MGI:107357|inositol polyphosphate-5-phosphatase D; targeted mutation 1, Jeffrey V Ravetch|Inpp5d|MGI:3715982|1||||||||||||||||No|||||||||||||Normal|Normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|7|||No|29-Oct-2010|Cryopreserved sperm|50.0|0.0|Unknown||phosphatase, phosphorylation, signal transduction, PI3'K, myeloid cells, apoptosis, recceptor, inflammatory lung disease, hyperplasia|Yes| 5381.0|MF-04 ; EGFP|C57BL/6-Tg(CAG-EGFP)131Osb/LudApb||Dominant||||||||||||||||||||||||||transgene insertion 131, Research Institute for Microbial Diseases, Osaka University|ytomegalovirus immediate early + chicken beta-actin gene + rabbit hemoglobin beta gene|Ubiquitous||||||||||Ubiquitous expression of EGFP.|Ubiquitous expression of EGFP but weaker signal than homozygote.|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|06-Jan-2011|Cryopreserved sperm|50.0|0.0|Unknown||GFP|Yes| 5337.0|C57.p110d KD/KD ; C57.p110d D910A|C57BL/6-Pik3cd/Apb||Recessive|phosphatidylinositol 3-kinase catalytic delta polypeptide|Pik3cd|Unknown|p110delta|MGI:1098211|phosphatidylinositol 3-kinase catalytic delta polypeptide; targeted mutation 1, Bart Vanhaesebroeck|Pik3cd|MGI:2385595|4||||||||||||||||Yes|||||||||||||Mice have a number of immune system disorders including impaired T and B cell function||C57BL/6|Yes|No|Yes|Yes|Yes|Yes|No|Unknown|||Female Het x Male Hom|No|09-Dec-2010|Cryopreserved sperm|47.0|0.0|Unknown||T cell, B cell, signal transduction, PI3'K, receptor|Yes| 5501.0|A33crePR2 |C57BL/6-Gpa33/LudApb||Dominant|glycoprotein A33 (transmembrane)|Gpa33||A33 antigen|MGI:1891703|glycoprotein A33 (transmembrane) targeted mutation 1, Matthias Ernst|Gpa33||1||||||||||||||||Yes|||||||||||||Unknown|Cre recombinase expressed in the intestinal epithelium.|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|09-May-2011|Cryopreserved sperm|50.0|0.0|Unknown||Cre recombinase, epihelium, A33, RU486|Yes| 5510.0|gp130/stat3/MMTVneu|STOCK Il6st Stat3 Tg(MMTVneu)202Mul/LudApb||Dominant|interleukin 6 signal transducer|Il6st|Unknown|CD130, D13Ertd699e, gp130|MGI:96560|interleukin 6 signal transducer; targeted mutation 1, Matthias Ernst|Il6st|MGI:2388478|13||||||||||||||||Yes|transgene insertion 202, William Muller|MMTV|||||||||||Unknown|Unknown|C57BL/6, 129, FVB/N mix|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|23-May-2011|Cryopreserved sperm|50.0|0.0|Unknown||signal transduction, kinase, proliferation|Yes| 5510.0|gp130/stat3/MMTVneu|STOCK Il6st Stat3 Tg(MMTVneu)202Mul/LudApb||Dominant|signal transducer and activator of transcription 3|Stat3|Unknown|Aprf|MGI:103038|signal transducer and activator of transcription 3; targeted mutation 1, Shizuo Akira|Stat3|MGI:1926814|11||||||||||||||||Unknown|||||||||||||Unknown|Unknown|C57BL/6, 129, FVB/N mix|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|23-May-2011|Cryopreserved sperm|||Unknown||signal transduction, kinase, proliferation|Yes| 5407.0|Stat 3 B6|B6.129P2-Stat3/LudApb||Recessive|Signal transducer and activator of transcription 3|Stat3|Nil|Aprf|MGI:103038|targeted mutation 1, Shizuo Akira|Stat3|MGI:1926814|11||||||||||||||||Yes|||||||||||||Embryonic lethality before somite formation: * homozygotes develop into the egg cylinder stage until E6.0 but start undergoing rapid degeneration at E6.5 * all homozygotes are completely resorbed by E7.5.Failure to gastrulate: homozygotes die at ~E7.0, the day at which gastrulation initiates.Absent mesoderm: homozygotes show absence of mesoderm formation between E6.5 and E7.5.Decreased embryo size: at E6.0, homozygoys mutant embryos are smaller than wild-type embryos.Abnormal inner cell mass proliferation: in culture, E3.5 mutant blastocysts exhibit a reduced ICM outgrowth relative to wild-type blastocysts.||C57BL/6|No|No|Yes|No|No|Yes|No|Unknown||||No|02-Feb-2011|Cryopreserved sperm|50.0|0.0|Unknown||embryonic lethal, signal transduction, phosphorylation, cytokine, IL6|Yes| 6923.0|ERT2/Pten/Gp130F (Black); A33(CreERT2)/Pten loxP/Gp130y757F (ME-276)|STOCK Gpa33 Il6st Pten/Lud||Dominant|glycoprotein A33 (transmembrane)|Gpa33||A33 antigen|MGI:1891703|glycoprotein A33 (transmembrane) targeted mutation 1, Matthias Ernst|Gpa33||1|||||||||||||||||||||||||||||Unknown|Unknown|Mixed 129 and C57BL/6|No|No|Yes|No|No|Yes|No|Unknown||||No|27-Jun-2012||0.0|0.0|Unknown|||Possibly| 6923.0|ERT2/Pten/Gp130F (Black); A33(CreERT2)/Pten loxP/Gp130y757F (ME-276)|STOCK Gpa33 Il6st Pten/Lud||Dominant|interleukin 6 signal transducer|Il6st||5133400A03Rik, CD130, D13Ertd699e, gp130|MGI:96560|interleukin 6 signal transducer; targeted mutation 1, Matthias Ernst|Il6st|MGI:2388478|13|||||||||||||||||||||||||||||Unknown|Unknown|Mixed 129 and C57BL/6|No|No|Yes|No|No|Yes|No|Unknown||||No|27-Jun-2012||||Unknown|||Possibly| 6923.0|ERT2/Pten/Gp130F (Black); A33(CreERT2)/Pten loxP/Gp130y757F (ME-276)|STOCK Gpa33 Il6st Pten/Lud||Dominant|phosphatase and tensin homolog|Pten||2310035O07Rik, A130070J02Rik, B430203M17Rik, MMAC1, TEP1|MGI:109583|phosphatase and tensin homolog; targeted mutation 2, Tak W Mak|Pten|MGI:2182005|19|||||||||||||||||||||||||||||Unknown|Unknown|Mixed 129 and C57BL/6|No|No|Yes|No|No|Yes|No|Unknown||||No|27-Jun-2012||||Unknown|||Possibly| 5415.0|APC(580s).C57|C57BL/6-Apc/LudApb||Dominant|adenomatosis polyposis coli|Apc|Reduced|CC1, Min|MGI:88039|adenomatosis polyposis coli; targeted mutation 1, Tetsuo Noda|Apc|MGI:1857966|18||||||||||||||||Yes|||||||||||||Exposure to liver specific carcinogen diethynitrosamine results in higher tumour incidence than het mice including hepatocellular carcinoma.Colorectal adenomas observed when exon 14 was deleted by colorectal infection of an adenovirus exressing Cre recombinase.|Low incidence of hepatocellular carcinoma.|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|04-Feb-2011|Cryopreserved sperm|50.0|0.0|Unknown||Familial adenomatous polyposis coli (FAP), colorectal adenomas|Yes| 5592.0|A22Ca F25||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5595.0|ADLH1A1||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 8694.0|C57/Bl6 Gmcsf-/- Cish-lacZ/lacZ|C57BL/6-Csf2 Cish/||Recessive|colony stimulating factor 2 (granulocyte-macrophage)|Csf2|Nil|Csfgm, Gm-CSf, GMCSF, MGI-IGM|MGI:1339752|colony stimulating factor 2 (granulocyte-macrophage); targeted mutation 1, Ashley R Dunn|Csf2|MGI:1930997|11|||||||||||||||||||||||||||||Perturbed macrophage biology, disrupted haematopoiesis and metabolism|Normal|C57BL/6|Yes|Unknown|Yes|Yes|Unknown|Yes|No|Unknown||||No|11-Apr-2019||0.0|0.0|Unknown|||Yes| 8694.0|C57/Bl6 Gmcsf-/- Cish-lacZ/lacZ|C57BL/6-Csf2 Cish/||Recessive|cytokine inducible SH2-containing protein|Cish||Cis, CIS1, cytokine-inducible SH2 protein, F23|MGI:103159||||9|||||||||||||||||||||||||||||Perturbed macrophage biology, disrupted haematopoiesis and metabolism|Normal|C57BL/6|Yes|Unknown|Yes|Yes|Unknown|Yes|No|Unknown||||No|11-Apr-2019||||Unknown|||Yes| 6765.0|A33:Lgp130YFKQ|CBA;129-Tg(Gpa33-Il6*)6Ern/LudApb||Dominant||||||||||||||||||||||||||transgene insertion 6 Matthias Ernst|glycoprotein A33 (transmembrane)|||||||||||Unknown|Unknwon|CBA/129|Yes|Yes|Unknown|Yes|Yes|Unknown|No|Unknown||||No|16-Dec-2011|Cryopreserved sperm|50.0|0.0|Unknown||signal transduction, dimerization|Yes| 5480.0|TFF Cre/LacZ13|STOCK Tg(Tff1-CreERT2/Tff2-CreERT2/Tff3-LacZERT2)/LudApb||Dominant||||||||||||||||||||||||||trefoil1/2/3|Tff1/Tff2/Tff3|||||||||||No overt phenotype.|No overt phenotype.||Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|12-Apr-2011|Cryopreserved sperm|50.0|0.0|Unknown|||Yes| 5463.0|ENU16NIH:003b coat phenotype|C57BL/6JAnu-Rab27a/AnuApb|C57BL/6JAnu-Rab27a/AnuApb|Recessive|RAB27A, member RAS oncogene family|Rab27a|Unknown|2210402C08Rik, 2410003M20Rik, 4933437C11Rik |MGI:1861441 |RAB27A, member RAS oncogene family; mutation 1, The Australian National University|Rab27a|MGI:5563433|9|ENSMUSG00000032202|ENSMUST00000034722|Rab27a-201|217|386|T to A|ENSMUSE00000217627|3|72|Tryptophan to Arginine|||||GCCGAGGCCAGAGAATCCACCTGCAGTTATGGGACACGGCGGGGCAGGAGAGGTTTCGTAG|No|||||||||||||Silver coat color|Normal|C57BL/6JAnu|Yes|Unknown|Yes|Yes|Unknown|Yes|No|Good|n/a|5|sib x sib|No|09-Mar-2011|Cryopreserved sperm|17.0|0.0|Unknown||Coat, fur, melanocyte, melanin|Yes| 5436.0|Funky|C.Cg-Ndufs4/DrthApb|C.Cg-Ndufs4/Drth|Recessive|NADH dehydrogenase (ubiquinone) Fe-S protein 4|Ndufs4|Reduced|C1-18k|MGI:1343135|funky|Ndufs4|MGI:4942335|13||||||||||||||||Yes|||||||||||||Homozygous mice initially present with fur loss around postnatal day 14, which regrows in the next hair cycle. They show reduced growth and several behavioural abnormalities that appear from postnatal week five, such as tilting of the head, walking in circles and twisting of the body when suspended by the tail. Due to progressively wobbly gait and general deterioration in physical condition, all homozygous mice have to be euthanased around postnatal week eight in compliance with ethical guidelines.|Animals show reduced growth and several behavioural abnormalities that appear from postnatal week five to six, such as a ruffled appearance, tilting of the head, walking in circles and twisting of the body when suspended by the tail. Due to progressively wobbly gait and general deterioration in physical condition, all homozygous mice have to be euthanased around postnatal week nine in compliance with ethical guidelines.|BALB/c|Yes|Unknown|Yes|Yes|Unknown|Yes|No|Good|11||het X het|No|15-Feb-2011|Cryopreserved sperm|80.0|0.0|Yes|Mitochondrial Disease; Leigh Syndrome|Mitochondria, Oxidative Phosphorylation, Complex I|Possibly| 6794.0|S164|SJL/J-tg(TCR1640)/Ausb||Recessive||||||||||||||||||||||||||||||||||||||||SJL/J|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|19-Jan-2012||0.0|0.0|Unknown||Autoimmune, multiple sclerosis , Ataxia, Paralysis, Experimental autoimmune encephalomyelitis|Yes| 5591.0|A22ca (A22alpha) ||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6903.0|ERT2/Pten/Gp130F; A33(CreERT2)/Pten loxP/Gp130y757F (ME-276)|STOCK Gpa33 Il6st Pten/LudApb||Dominant|glycoprotein A33 (transmembrane)|Gpa33||A33 antigen|MGI:1891703|glycoprotein A33 (transmembrane) targeted mutation 1, Matthias Ernst|Gpa33||1|||||||||||||||||||||||||||||Unknown|Unknown|Mixed 129 and C57BL/6|No|No|Yes|No|No|Yes|No|Unknown||||No|28-May-2012|Cryopreserved sperm|50.0|0.0|Unknown|||Possibly| 6903.0|ERT2/Pten/Gp130F; A33(CreERT2)/Pten loxP/Gp130y757F (ME-276)|STOCK Gpa33 Il6st Pten/LudApb||Dominant|interleukin 6 signal transducer|Il6st||5133400A03Rik, CD130, D13Ertd699e, gp130|MGI:96560|interleukin 6 signal transducer; targeted mutation 1, Matthias Ernst|Il6st|MGI:2388478|13|||||||||||||||||||||||||||||Unknown|Unknown|Mixed 129 and C57BL/6|No|No|Yes|No|No|Yes|No|Unknown||||No|28-May-2012|Cryopreserved sperm|||Unknown|||Possibly| 6903.0|ERT2/Pten/Gp130F; A33(CreERT2)/Pten loxP/Gp130y757F (ME-276)|STOCK Gpa33 Il6st Pten/LudApb||Dominant|phosphatase and tensin homolog|Pten||2310035O07Rik, A130070J02Rik, B430203M17Rik, MMAC1, TEP1|MGI:109583|phosphatase and tensin homolog; targeted mutation 2, Tak W Mak|Pten|MGI:2182005|19|||||||||||||||||||||||||||||Unknown|Unknown|Mixed 129 and C57BL/6|No|No|Yes|No|No|Yes|No|Unknown||||No|28-May-2012|Cryopreserved sperm|||Unknown|||Possibly| 7054.0|Flp/E2acre|B6.Cg-Tg(ACTFLPe)9205Dym Tg((EIIa-cre)C5379Lmgd/LudApb||Dominant||||||||||||||||||||||||||transgene insertion 9205, Susan Dymecki|human ACTB promoter|spinal cord, heart, gonad, adrenal) as early as embryonic day 10.5||||||||||Normal|Normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|21-Aug-2012|Cryopreserved sperm|41.0|0.0|Unknown||Flp, Cre recombinase|Possibly| 7054.0|Flp/E2acre|B6.Cg-Tg(ACTFLPe)9205Dym Tg((EIIa-cre)C5379Lmgd/LudApb||Dominant||||||||||||||||||||||||||transgene insertion C5379, Laboratory of Mammalian Genes and Development, Heiner Westphal|adenovirus EIIa promoter|Expression in nearly all tissues||||||||||Normal|Normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|21-Aug-2012|Cryopreserved sperm|||Unknown||Flp, Cre recombinase|Possibly| 5481.0|APC (min) .C57 X C57 |C57BL/6-Apc/LudApb||Dominant|adenomatosis polyposis coli|Apc|Unknown|CC1, Min|MGI:88039|adenomatosis polyposis coli; multiple intestinal neoplasia|Apc|MGI:1856318|18||||||||||||||||Yes|||||||||||||Unknown|Increased colonic adenoma incidence: tubular adenomas in the colon.Increased intestinal adenoma incidence: tubular adenomas in the intestine.|Unknown|No|No|Yes|No|No|Yes|No|Unknown||||No|12-Apr-2011|Cryopreserved sperm|48.0|0.0|Yes|Adenomatous Polyposis of the Colon; APC; OMIM ID: 175100|adenoma, carcinoma, colon, mammary gland|Yes| 5576.0|∆SRI |B6.129T2-Atm/QimrApb||Recessive|ataxia telangiectasia mutated homolog (human)|Atm|Reduced|C030026E19RIK|MGI:107202|ataxia telangiectasia mutated homolog (human); targeted mutation 1, Martin F Lavin|Atm|MGI:2181756|9|||||||||||||||||||||||||||||Premature death: 50% mortality by 40 weeks of age Decreased body size: smaller size persists through adulthood Postnatal growth retardation: 20% growth reduction in males and 18% reduction in females from birth to 45 days of age. Increased tumor incidence: mice dying after 40 weeks of age usually have tumors that are not thymic lymphomas Thymic lymphoma: found in all mice dying before 40 weeks, diverse cell types involved, spongy tumors with a high proportion of cells undergoing apoptosis Abnormal immune system cell morphology: occasional increase in thymocyte size. Abnormal T lymphocyte development: lymph node T cells are primarily at early stages of development. Increased double-negative T cell count: occurs at random Abnormal effector T cell morphology/development: randomly observed increases in single positive T cells. Decreased thymocyte number: 10% reduction in thymocytes, 30-50% reduction in thymocytes expressing alpha and beta T cell receptors or CD3. Abnormal immune system organ morphology: enlarged spleen: usually found in mice dying after 40 weeks of age. small spleen: in mice under 40 weeks of age small thymus small lymph nodes Abnormal chromosome morphology: 3 fold increase in radiation induced chromosomal aberrations. Increased cellular sensitivity to ionizing radiation: increased sensitivity of thymocytes and splenocytes to ionizing radiation. Seminiferous tubule degeneration: tubules disrupted Abnormal testis development: poorly developed Abnormal gametogenesis: abnormal oogenesis: disrupted, lack of maturing follicles and oocytes. Abnormal spermatogenesis: disrupted spermatogenesis, degenerating spermatocytes, loss of spermatids Nervous system phenotype: no gross neuronal degeneration at time points between 2 and 16 months of age. Abnormal Purkinje cell morphology: survival of Purkinje cells in culture less than 60% of controls at 4 days and about 40% at 10 day, survival of cultured cells improves if cultured with cerebellar astroglial cells, develop simpler dendritic arboritization with reduced secondary branching, nitroxide free radicals improve survival and arborization Seminiferous tubule degeneration: tubules disrupted|Increased tumor incidence: average age at onset 18.6 months, varying tumor types including dermatoid cysts adenoma: 13% of total leukemia: 5% of total lymphoma:24% of total ovary tumor: 8% of total sarcoma: 32% of total, half of sarcomas are in Mammary glands|C57BL/6J x 129T2/Sv|Yes|No|Yes|Yes|Yes|Yes|Yes|Good|35|35|Hetrezygotes x Heterozygotes|Yes|05-Sep-2011|Cryopreserved sperm|50.0|0.0|Yes|A-T is characterized by immunodeficiency, neurological abnormalities and a |ataxia telangiectasia , T cell , spermatogenesis, thymocyte, lymphoma |Possibly| 6846.0|Slit1/2|CD-1.129S2-Slit1 Slit2/Uqbr||Dominant|slit homolog 1 (Drosophila)|Slit1|Nil|mKIAA0813, Slil1|MGI:1315203|slit homolog 1 (Drosophila); targeted mutation 1.1, Marc Tessier-Lavigne|Slit1|MGI:2179459|19|||||||||||||||||||||||||||||Complete perinatal lethality: mice die at birthNervous system phenotype: mice exhibit normal numbers of interneurons during development.Abnormal embryonic/fetal subventricular zone morphology: at E13.5 and E16.5, cell proliferation of ganglionic eminences in the subventricular zone is increased compared to in Slit1 homozygotes.Abnormal neurite morphology: in the subventricular zone/intermediate zone and subplate, mic exhibit an increased in neurite process length is, the number of neurites, and the degree of branching.||CD-1|No|No|Unknown|No|No|Unknown|No|Unknown||||No|13-Mar-2012||0.0|0.0|Unknown||Robo1, corpus callosum, midline, axon, glia, receptor|Possibly| 6846.0|Slit1/2|CD-1.129S2-Slit1 Slit2/Uqbr||Dominant|slit homolog 2 (Drosophila)|Slit2|Nil|Drad-1, E030015M03Rik, E130320P19Rik, Slil3|MGI:1315205|slit homolog 2 (Drosophila); targeted mutation 1, Marc Tessier-Lavigne|Slit2|MGI:2179460|5|||||||||||||||||||||||||||||Complete perinatal lethality: mice die at birthNervous system phenotype: mice exhibit normal numbers of interneurons during development.Abnormal embryonic/fetal subventricular zone morphology: at E13.5 and E16.5, cell proliferation of ganglionic eminences in the subventricular zone is increased compared to in Slit1 homozygotes.Abnormal neurite morphology: in the subventricular zone/intermediate zone and subplate, mic exhibit an increased in neurite process length is, the number of neurites, and the degree of branching.||CD-1|No|No|Unknown|No|No|Unknown|No|Unknown||||No|13-Mar-2012||||Unknown||Robo1, corpus callosum, midline, axon, glia, receptor|Possibly| 6847.0|Slit2|STOCK-Slit2/MmmhUqbr||Dominant|slit homolog 2 (Drosophila) |Slit2|Unknown|Drad-1, E030015M03Rik, E130320P19Rik, Slil3|MGI:1315205|slit homolog 2 (Drosophila); targeted mutation 1, Marc Tessier-Lavigne|Slit2|MGI:2179460|5|||||||||||||||||||||||||||||Partial perinatal lethality: almost all homozygotes die at birthAbnormal embryonic tissue morphology: * at E11.5 multiple ureteric buds (3 or more buds in 14/16 mutants, and 2 in 2/16) emerge from the nephric duct rather than a single bud as in wild-type mice * some of these buds project medially rather than dorsallyAbnormal kidney morphology: at E18.5 the region where new nephrons are being generated is not restricted to the periphery as in wild-type mice but extends into the interior of the kidney in homozygotes.Abnormal kidney development: * many of the multiple ureteric buds have developed to give rise to 2 or more adjacent kidneys * fusion of these adjacent kidneys may cause the interior nephrogenesis seen at E18.5.Abnormal ureter morphology: * multiple ureters arising from a single kidney are seen in all homozygous mutants * all of the ureters remain connected to the nephric duct rather than undergoing remodeling to connect to the bladder.Hydroureter: at E18.5 the collecting ducts and ureters are grossly dilated.||CD-1|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown|More than 10.|Unknown|Heterozygous x wild type|No|13-Mar-2012||0.0|0.0|Unknown||glia, axon guidance|No| 7337.0|Il7tg|B6.Cg-Tg(H2-Ea-Il7)10Rhdr/ScrAusbAnuApb||Recessive||||||||||||||||||||||||||transgene insertion 10, Rhodri Ceredig|H2-Ea promoter|||||||||||Normal||C57BL/6JAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|17-May-2013|Cryopreserved sperm|9.0|0.0|Unknown||il7, B cell|Yes| 6777.0|NODSCID|NOD.CB17-Prkdc/SzJAusb||Recessive|protein kinase, DNA activated, catalytic polypeptide |Prkdc||DNA-PK, DNA-PKcs, DNAPDcs, DOXNPH, dxnph, slip, XRCC7 |MGI:104779 |protein kinase, DNA activated, catalytic polypeptide; severe combined immunodeficiency |Prkdc |MGI:1857113|16|ENSMUSG00000022672|ENSMUST00000023352|Prkdc-201||||||||||||||||||||||||||Absence of functional T cells and B cells, lymphopenia, hypogammaglobulinemia, and a normal hematopoietic microenvironment|Normal|NOD/ShiLtSz |Yes|Yes|Yes|Yes|Yes|Yes|No|Good|10||Homozygote x Homozygote |No|12-Jan-2012||0.0|0.0|No||lymphocytes, immunodeficiency, xenografts, T cells, B cells|Yes| 5597.0|AGFP||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5598.0|Agr2-/-||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6782.0|MC4R^|C57BL/6-Mc4r/MmcdAusb||Semi-dominant|melanocortin 4 receptor |Mc4r||Fatboy|MGI:99457 |melanocortin 4 receptor; mutation 1, Bruce Beutler |Mc4rm1Btlr|MGI:3723065|18|ENSMUSG00000047259|ENSMUST00000057942|Mc4r-201 ||||||||||||||||||||||||||Homozygous mice are very obese at 6 weeks of age. Pre weaning mortality 13.9%, hyperphagia, fasting hyperinsulinemia. |Hets larger than wildtype mice|C57BL/6J |Yes|Yes|Yes|Yes|Unknown|Yes|No|Unknown|||het x het or het(F) x homo(M) breeding|No|13-Jan-2012||0.0|0.0|Unknown||Hyperphagia, hyperinsulinemia, Obesity|Yes| 8704.0|TcrP14|B6.SJL-Ptprc Tg(TcrLCMV)327Sdz/AnuApb||Dominant|protein tyrosine phosphatase, receptor type, C|Ptprc|Normal|B220, CD45, Ly-5, Lyt-4, T200|MGI:97810|protein tyrosine phosphatase, receptor type, C; a variant|Ptprc|MGI:4819849|1|||||||||||||||||transgene insertion 327, Birgit Ledermann||10 copies|||||||||||MIce express a T-cell receptor (Tcra-V2, Tcra-J TA31 / Tcrb-V8.1, Tcrb-D, Tcrb-J 2.4) specific for LCMV (lymphocytic choriomeningitis virus), H2-Db.|C57BL/6J|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|26-Apr-2019|Cryopreserved sperm|60.0|0.0|Unknown||T cell|Yes| 5246.0|BALB.Lyn knockout|BALB/c-Lyn/Apb||Semi-dominant|Yamaguchi sarcoma viral (v-yes-1) oncogene homolog|Lyn|Nil|Hck-2|MGI:96892|Yamaguchi sarcoma viral (v-yes-1) oncogene homolog; targeted mutation 1, Ashley R Dunn|Lyn|MGI:2157129|4||||||||||||||||No|||||||||||||Young mice are apparently healthy, but they start to show signs of autoimmune disease at >16 wks of age. The disease resembles the human condition systemic lupus erythematosus (SLE). The mice develop serum anti-nuclear antibodies and acquire crescentic glomerulonephritis due to immune complex deposition in kidney, leading to renal dysfunction. They show hematologic disorders such as lymphopenia and thrombocytopenia, and they develop lymphadenopathy and splenomegaly. They develop inflammatory lesions in multiple organs including skin, lung and kidney, and occasionally we observe neurologic disorders such as seizures and hind limb paralysis. Similar to SLE patients, the mice also have hyperactive B lymphocytes.|Heterozygous mice are autoimmune-prone, but the disease is of later onset and less severe.|BALB/c|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|5|||No|18-Oct-2010|Cryopreserved sperm|50.0|0.0|Yes|Systemic Lupus Erythematosus; SLE|B cell, src family, immunoglobulin, spleen, signal transduction, autoimmunity, lymphocyte|Yes| 7783.0|403sv, MHC-403sv|129(Cg)-Myh6/Apb |MGI:2182704|Dominant|myosin, heavy polypeptide 6, cardiac muscle, alpha;|Myh6|Unknown|A830009F23Rik, alpha cardiac MHC, alpha-MHC, alpha myosin, cardiomyopathy, hypertrophic 1, Myhca, Myhc-a|MGI:97255|myosin, heavy polypeptide 6, cardiac muscle, alpha; targeted mutation 1, Jonathan G Seidman|Myh6|MGI:2182704|14|||||||||||||||||||||||||||||Lethal|Hypertrophy of myocytes with large hyperchromatic nuclei by 30 weeks of age, myocardial fiber disarray becoming marked by 30 weeks of age, moderate diffuse interstitial fibrosis by 30 weeks of age, starting as early as 15 weeks|129/SvEv|No|No|Yes|No|No|Yes|No|Good||24|Myh6/MYH6+ x MYH6/MYH6 |No|12-Nov-2014|Cryopreserved sperm|40.0|0.0|Yes|Hypertrophic cardiomyopathy (HCM) is a primary disorder of the myocardium characterized by cardiac hypertrophy. The clinical course of HCM is variable, with inter- and intra-familial variations ranging from benign asymptomatic disease to a malignant phenotype with a high risk of cardiac failure or sudden cardiac death.|Hypertrophy, Cardiomyopathy, Calcium, Myosin heavy chain gene|Yes| 6772.0|DBC2 KO Cre deleted ; Brinp2 KO|C57BL/6-Fam5b/Marp||Recessive|family with sequence similarity 5, member B|Fam5b|Unknown|6430517E21Rik, mKIAA1747|MGI:2443333|6430517E21Rik|||1|||||||||||||||||||||||||||||Normal|Normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Excellent||||No|11-Jan-2012||0.0|0.0|Unknown|||No| 5123.0|IGF-1Ea ; sglt-2 IGF-1Ea|FVB-Tg(Slc5a2-rIGF1-Ea)UqbrApb||Dominant||||||||||||||||||||||||||rat Insulin-like growth factor-1 Ea isoform|mouse solute carrier family 5 (sodium/glucose cotransporter), member 2 (Slc5a2) ; Sglt2|high||||||||||No obvious developmental phenotype in kidneys. Adults show increase damage in kidneys after ischeamia reperfusion injury|Less severe than homozygous (damage model)|FVB|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|18-May-2010|Cryopreserved sperm|80.0|0.0|Unknown||kidney, nephron, renal|No| 5186.0||ENU18WT:005b||Recessive|Unknown||Unknown||||||Unknown|||||||||||||||||||||||||||||Unknown||C57BL/6JAnu|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|02-Aug-2010|Cryopreserved sperm|90.0|0.0|Unknown||ENU, Wellcome Trust|Possibly| 5190.0||ENU18WT:027b||Recessive|Unknown||Unknown||||||Unknown|||||||||||||||||||||||||||||Unknown||C57BL/6JAnu|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|02-Aug-2010|Cryopreserved sperm|47.0|0.0|Unknown||ENU, Wellcome Trust|Possibly| 7215.0|G11-23|Gast11-23||Recessive|ATPase, Na+/K+ transporting, alpha 1 polypeptide|Atp1a1||Atpa-1|MGI:88105||||3|||||||||||||||||||||||||||||A failure to thrive at gastrulation |Normal|C3H/HeH|No|No|Yes|No|No|Yes|No|Good|One generation backcrossed to C57BL/6, after 6 generation backcrossed C3H/HeH.|||No|16-Nov-2012|Cryopreserved sperm|50.0|0.0|Unknown||embryonic lethal, Na+/K+ transport, gastrulation , ENU|No| 7216.0||ENU17WT027b||Recessive|Unsure at the moment could be ATRN or TTC30A2|ATRN or TTC30A2|||||||2|||||||||||||||||||||||||||||Mice display increased susceptibility to infection with TB|NA|C57BL/6JAnu|Yes|Yes|Unknown|Yes|Yes|Unknown|No|Good|NA|7|Het x Het and Hom x Hom|No|19-Nov-2012|Cryopreserved sperm|30.0|0.0|Unknown||ENU, infection|Possibly| 6768.0||ENU12B6:C3H:020:G2||Recessive|Unknown||||||||Unknown|||||||||||||||||||||||||||||Ataxia||C57BL/6 x C3H|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|20-Dec-2011|Cryopreserved sperm|10.0|0.0|Unknown|||No| 7218.0|nZEGs|nZEG #2||Dominant||||||||||||||||||||||||||||||||||||||||C57BL/6|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|19-Nov-2012|Cryopreserved sperm|19.0|0.0|Unknown||EGFP|Possibly| 5363.0|MF-07 ; APC (580s)/ROSA26|B6;129/Sv-Apc Gt(ROSA)26Sor/Lud||Recessive|adenomatosis polyposis coli|Apc|Reduced|CC1, Min|MGI:88039|adenomatosis polyposis coli; targeted mutation 1, Tetsuo Noda|Apc|MGI:1857966|18||||||||||||||||Yes|gene trap ROSA 26, Philippe Soriano; targeted mutation 1, Philippe Soriano||||||||||||to come|to come|to come|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|21-Dec-2010|Cryopreserved sperm|50.0|0.0|Yes|Familial adenomatous polyposis coli (FAP)|Familial adenomatous polyposis coli (FAP), adenoma, epithelial|Yes| 7221.0|G11-68|Gas11-68||Recessive|Unknown|Unknown|||||||6|||||||||||||||||||||||||||||Patterning defects.The homozygous mutant embryos die before 8.5 dpc.|Normal|C3H/HeH|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Good|Three generation on C3H/HeH backround followed by two genertion on C47BL/6.|||No|20-Nov-2012|Cryopreserved sperm|79.0|0.0|Unknown||Gastrulation Screen, ENU|No| 7222.0|G16-7|Gast16-7||Recessive|Unknown|Unknown|||||||7|||||||||||||||||||||||||||||A failure to gastrulate|Normal|FVB|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Good|Four|||No|20-Nov-2012|Cryopreserved sperm|50.0|0.0|Unknown||Gastrulation Screen, ENU|No| 7224.0|G18-19|Gast18-19||Recessive|Unknown|Unknown|||||||Unknown|||||||||||||||||||||||||||||A failure to gastrulate.The homozygous mutant embryos die before 8.5 dpc.|Normal|BALB/c|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Good|Three|||No|20-Nov-2012|Cryopreserved sperm|50.0|0.0|Unknown||Gastrulation Screen, ENU|No| 6901.0|B6.3-PAPKO; C57BL/6-3-PAP knockout|C57BL/6-Mtmr12/Stv||Dominant|myotubularin related protein 12|Mtmr12|Nil|C730015A02Rik, mKIAA1682, Pip3ap|MGI:2443034||||15|||||||||||||||||||||||||||||Normal|Normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Excellent||15||No|24-May-2012|Cryopreserved sperm|50.0|0.0|No|||Possibly| 7217.0|Sppl2a KO1|C57BL/6N-A Sppl2a/1MarpAnu||Recessive|signal peptide peptidase like 2A|Sppl2a|Unknown|2010106G01Rik, C130089K23Rik|MGI:1913802|signal peptide peptidase like 2A; targeted mutation 1a, Helmholtz Zentrum Muenchen GmbH|Sppl2a|MGI:4887673|2|||||||||||||||||||||||||||||Unknown|Unknown|C57BL/6NCrlAnu|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|19-Nov-2012|Cryopreserved sperm|29.0|0.0|Unknown|||Possibly| 7225.0|G18-5|Gast18-5||Recessive|Unknown|Unknown|||||||Unknown|||||||||||||||||||||||||||||A failure to gastrulate.The homozygous mutant embryos die before 8.5 dpc.|Normal|BALB/c|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Good|Three|||No|20-Nov-2012|Cryopreserved sperm|106.0|0.0|Unknown||Gastrulation Screen, ENU|No| 7226.0|G16-5|Gast16-5||Recessive|Unknown|Unknown|||||||Unknown|||||||||||||||||||||||||||||A failure to thrive.The mutant homozygous embryos die before 8.5 dpc.|Normal|FVB|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Good|Three|||No|20-Nov-2012|Cryopreserved sperm|97.0|0.0|Unknown||Gastrulation Screen, ENU|No| 5377.0|hPI Triple 427|C57BL/6-H2 Tg(Cd4-CD4)2362Litt Tg(HLA DR4-DQ8)427 Tg(TcraINS1,TcrbINS1)/Apb||Dominant|histocompatibility-2, MHC|H2|Nil|H-2, MHC-II|MGI:95894|histocompatibility-2, MHC; targeted deletion, H2 complex|H2|MGI:2658725|17||||||||||||||||No|human leukocyte antigen class II||||||||||||||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|22-Dec-2010|Cryopreserved sperm|50.0|0.0|Unknown||MHC, B cell, selection, autoimmunity, celiac disease|Yes| 5377.0|hPI Triple 427|C57BL/6-H2 Tg(Cd4-CD4)2362Litt Tg(HLA DR4-DQ8)427 Tg(TcraINS1,TcrbINS1)/Apb||Dominant||||||||||||||||||||||||||transgene insertion 2362, Dan R Littman|murine Cd4 and human CD4|equivalent to human CD4+ cells||||||||||||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|22-Dec-2010|Cryopreserved sperm|||Unknown||MHC, B cell, selection, autoimmunity, celiac disease|Yes| 5377.0|hPI Triple 427|C57BL/6-H2 Tg(Cd4-CD4)2362Litt Tg(HLA DR4-DQ8)427 Tg(TcraINS1,TcrbINS1)/Apb||Dominant||||||||||||||||||||||||||T cell receptor alpha, T cell receptor beta||||||||||||||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|22-Dec-2010|Cryopreserved sperm|||Unknown||MHC, B cell, selection, autoimmunity, celiac disease|Yes| 7219.0|G18-22|Gas18-22||Recessive|Unknown|Unknown|||||||9|||||||||||||||||||||||||||||Patterning defects.The homozygous mutant embryos die before 8.5 dpc. |Normal|BALB/c|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Good|4|||No|20-Nov-2012|Cryopreserved sperm|86.0|0.0|Unknown||Gastrulation Screen, ENU|No| 7220.0|G18-10|Gas18-10||Recessive|Unknown|Unknown|||||||Unknown|||||||||||||||||||||||||||||Patterning defects.The homozygous mutant embryos die before 8.5 dpc.|Normal|BALB/c|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Good|3|||No|20-Nov-2012|Cryopreserved sperm|89.0|0.0|Unknown||Gastrulation Screen, ENU|No| 5390.0|Ndufs6gt/+|C.129P2-Ndufs6/MrchApb|C.129P2-Ndufs6/Mrch|Recessive|NADH dehydrogenase (ubiquinone) Fe-S protein 6|Ndufs6|Reduced|IP13|MGI:107932|NADH dehydrogenase (ubiquinone) Fe-S protein 6; gene trap AR0138, Wellcome Trust Sanger Institute|Ndufs6|MGI:4346527|13||||||||||||||||Yes|||||||||||||The homozygous mice seem unable to survive pass weaning. Further investigation is in progress.|Normal|BALB/c|No|No|Yes|No|No|Yes|No|Good|11|1|heterogygote X heterozygote|No|18-Jan-2011|Cryopreserved sperm|97.0|0.0|Yes|Mutations in human gene, NDUFS6, encoding one of the 45 subunits of Complex I, are one cause of Complex I deficiency. NDUFS6-/- patients suffer from seizures, hypotonia and abnormal eye movements and die in the first month of life. Currently, no effective treatment is available. |Mitochondria, Cardiac , Complex I, Oxidative phosphorylation, ES cell|Possibly| 7228.0|Mx-Cre pRb TNFa-/-|C57BL/6-Rb1 Tnf Tg(Mx1-cre)1Cgn/SviApb||Dominant|tumor necrosis factor|Tnf|Nil|DIF, Tnfa, TNFalpha, TNF alpha, TNF-alpha, Tnfsf1a, tumor necrosis factor-alpha|MGI:104798|tumor necrosis factor; targeted mutation 1, George Kollias|Tnf|MGI:2149024|17|||||||||||||||||transgene insertion 1, University of Cologne|Mx1|high after interferon stimulation||||||||||Normal if not treated with pIpC|Normal if not treated with pIpC|C57Bl/6|Yes|Yes|Yes|Unknown|Unknown|Unknown|No|Good|all were C57BL/6 when inbred, no further backcrossing done||Cre+ male to Cre-ve female (all Rbfl/fl TNFa-/-)|No|22-Nov-2012|Cryopreserved sperm|60.0|0.0|Unknown||Mx-Cre, Rb, TNFa|Yes| 7228.0|Mx-Cre pRb TNFa-/-|C57BL/6-Rb1 Tnf Tg(Mx1-cre)1Cgn/SviApb||Dominant|retinoblastoma 1|Rb1 |Nil|pRb, Rb, Rb-1 |MGI:97874|retinoblastoma 1; targeted mutation 3, Tyler Jacks |Rb1|MGI:2450162|14|||||||||||||||||||||||||||||Normal if not treated with pIpC|Normal if not treated with pIpC|C57Bl/6|Yes|Yes|Yes|Unknown|Unknown|Unknown|No|Good|all were C57BL/6 when inbred, no further backcrossing done||Cre+ male to Cre-ve female (all Rbfl/fl TNFa-/-)|No|22-Nov-2012|Cryopreserved sperm|||Unknown||Mx-Cre, Rb, TNFa|Yes| 5699.0|Crim1 C57 Tie2-Cre||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5600.0|Alb TVA ||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5599.0|Alb Cre ||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5601.0|Almasy||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5602.0|Alpha 4 ||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 7234.0|RIP-YMII|C57BL/6-Tg(Ins2-EYFP-MII)Wehi/WehiApb||Dominant||||||||||||||||||||||||||Ins2-EYFP-MII|Ins2|low||||||||||Normal. Mice express MHCI and MHCII resticted peptides from ovalbumin, influenza A virus and herpes simplex virus. The expression is directed to the pancreas under the rat insulin promoter. Expression of these peptides has no obvious effects on the life-span, well-being or breeding potential of the mice.|Normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Excellent|||brother-sister or Tg x C57BL/6|No|28-Nov-2012|Cryopreserved sperm|45.0|0.0|No||YFP|Yes| 7235.0|classI-mOVA|C57BL/6-Tg(H2-K1-TFRC/OVA)5Cbn/Apb||Dominant||||||||||||||||||||||||||ovalbumin residues 139-385 fused to transferrin receptor membrane domain|MHC class I|moderate||||||||||NormalClass I mOVA mice express a membrane-bound form of ovalbumin (transferrin receptor membrane domain and OVA residues 139-385) under the control of the MHC class I promoter. OVA expression is directed to the membranes of all cells except red blood cells.|Normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|28-Nov-2012|Cryopreserved sperm|50.0|0.0|No||MHC, ovalbumin, autoimmunity|Yes| 7282.0|Cathepsin-S Knockout|B6NCrl;129-Ctss/AnuApb||Recessive|cathepsin S|Ctss|Nil|Cat S|MGI:107341|cathepsin S; targeted mutation 1, Harold A Chapman|Ctss|MGI:2182133|3||||||||||||||||Yes|||||||||||||Defective CD4 T cell response and humoral responses, but no overt immunodeficiency. Homozygous null mice are resistant to the development of experimental autoimmune myasthenia gravis and showed reduced T and B cell responses to acetylcholine receptor.||C57BL/6NCrlAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|27-Feb-2013|Cryopreserved sperm|20.0|0.0|Unknown||T cell, MHC class II, cysteine proteinase, Humoral resposne, arthritis, germinal centre|Yes| 7227.0|APN281|C57Bl/6N-A Oas2/Marp||Recessive|2'-5' oligoadenylate synthetase 2|Oas2|Unknown|2'-5' oligoadenylate synthetase-like 11, Oasl11|MGI:2180852|2'-5' oligoadenylate synthetase 2; targeted mutation 1a, Helmholtz Zentrum Muenchen GmbH|Oas2/Marp|MGI:4434541|5|||||||||||||||||||||||||||||Unknown|Normal|C57Bl6N|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Good||||No|22-Nov-2012|Cryopreserved sperm|40.0|0.0|Unknown|||Possibly| 7231.0|Sftpc+/+ 129|129/Sv-Sftpc/MarpApb||Recessive|surfactant associated protein C|Sftpc|Nil|pro-SpC, Sftp2, Sftp-2, SP-C|MGI:109517||||14|||||||||||||||||||||||||||||Normal.Wildtype strain developed from Het x het mating of knockout mice.Used as control for experiments.|Normal|129/Sv|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|>20|||No|27-Nov-2012|Cryopreserved sperm|50.0|0.0|Yes|Interstitial Pneumonitis, Desquamative, Familial; DIP|lung, alveolar, surfactant, respiratory, WT control|Possibly| 7233.0|APN318|C57Bl/6N-A Sppl2a||Recessive|signal peptide peptidase like 2A|Sppl2a|Unknown|2010106G01Rik, C130089K23Rik|MGI:1913802|signal peptide peptidase like 2A; targeted mutation 1a, Helmholtz Zentrum Muenchen GmbH|Sppl2atm1a(EUCOMM)Hmgu|MGI:4887673|2|||||||||||||||||||||||||||||Unknown|Normal|C57Bl/6N|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Good||||No|28-Nov-2012|Cryopreserved sperm|50.0|0.0|Unknown|||Possibly| 7232.0|PbT-I-9 ; C57BL/6-Tg(TCRaB4-46TcrbB4-46)9Cbn|C57BL/6-Tg(H2-K-Tcra,-Tcrb)9Cbn/Apb||Dominant||||||||||||||||||||||||||transgene insertion 9, Francis Carbone|H-2Kb|||||||||||Majority of CD8 T cells express the transgenic T cell recepter Va8Vb10 specific for Plasmodium berghei (Pb) parasites.|As for homozygous|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Excellent||7|brother-sister or Tg positive to C57BL/6|No|28-Nov-2012|Cryopreserved sperm|50.0|0.0|Yes|Used to model cerebral/severe malaria|malaria, Plasmodium berghei, CD8 TCR transgenic|Yes| 7387.0|KRasG12D|B6.129-Kras/JAnuApb||Dominant|v-Ki-ras2 Kirsten rat sarcoma viral oncogene homolog|Kras|Normal|Ki-ras, K-ras, Kras2, Kras-2|MGI:96680|v-Ki-ras2 Kirsten rat sarcoma viral oncogene homolog; targeted mutation 4, Tyler Jacks|Kras|MGI:2429948|6|||||||||||||||||||||||||||||Normal until mice crossed with Cre expressing strain.Expression of adenovirus controlled Cre recombinase results in lung tun our development.Treatment with adenoviral Cre injection results in ovarian endometriosis like lesions.Abnormal peritoneum morphology: * 47% of mutants develop peritoneal endometriosis following ovarian intrabursal injection of an adenovirus expressing Cre * however, mice injected with adenovirus expressing Cre directly into the peritoneum do not develop peritoneal endometriosis.||C57BL/6|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|30-Jul-2013|Cryopreserved sperm|60.0|0.0|Unknown||lung, ovary, adenocarcinoma, Cre|Yes| 7238.0|K5rTA-TSLP 1714|C57BL/6-Tg(K5-rTA)17Cbn Tg(TetO-TSLP)14Cbn/Apb||Dominant||||||||||||||||||||||||||tetracycline-regulated transcriptional transactivator|bovine keratin-5|||||||||||In these mice following oral doxycyline treatment, rTA expresssion induced in the skin activates the TetO promoter driving TSLP expression in the skin.In the absence of doxycyline treatment the mice are normal for lifespan and breeding.|As for homozygous mice.|C57BL/6|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Good|||Tg/+ +/+ x +/+ Tg/+|No|28-Nov-2012|Cryopreserved sperm|70.0|0.0|Yes||thymic stromal lymphopoietin, dermatitis, doxycyline inducible|Possibly| 7238.0|K5rTA-TSLP 1714|C57BL/6-Tg(K5-rTA)17Cbn Tg(TetO-TSLP)14Cbn/Apb||Dominant||||||||||||||||||||||||||thymic stromal lymphopoietin|CMV minimal promoter and 7 TetO sequences|||||||||||In these mice following oral doxycyline treatment, rTA expresssion induced in the skin activates the TetO promoter driving TSLP expression in the skin.In the absence of doxycyline treatment the mice are normal for lifespan and breeding.|As for homozygous mice.|C57BL/6|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Good|||Tg/+ +/+ x +/+ Tg/+|No|28-Nov-2012|Cryopreserved sperm|||Yes||thymic stromal lymphopoietin, dermatitis, doxycyline inducible|Possibly| 5414.0||NOD.Mog7ag||Recessive|||||||||||||||||||||||||||||||||||||7|Unknown||NOD/Lt|Yes|Yes|Unknown|Yes|Yes|Unknown|No|Unknown|10||Hom x Hom|No|03-Feb-2011|Embryo|0.0|0.0|Unknown||QTL|Yes| 4842.0|Topsy-Turvy|ENU8C:063||Recessive|Unknown||Unknown||||||Unknown|||||||||||||||||||||||||||||Ataxia, tremors, jerky movements, falls over while walking, throws head back to look at ceiling.Affected mice shake constantly, roll onto their sides frequently while walking. These mice also seem to have difficulty righting themselves as they are often seen on their backs underneath the feeder. It seems likely that this is a spontaneous mutant as it was first seen in G10. Video available.|Normal|C57BL/6 x CBA|Yes|No|Yes|Yes|No|Yes|No|Unknown||||No|24-Sep-2009|Cryopreserved sperm|38.0|0.0|Unknown||ataxia, ENU, tremors, balance, jerky movement|Yes| 7194.0|Pw1|B6-Tg(Pw1)26sas/Ausb||Dominant||||||||||||||||||||||||||transgene insertion 26, David Sassoon|Pw1||||||||||||Reporter line driven by Pw1 that reveals cycling and quiescent progenitor/stem cells in all adult tissues thus far examined, including the intestine, blood, testis, central nervous system, bone, skeletal muscle, and skin. Neurospheres generated from the adult PW1-reporter mouse show near 100% reporter-gene expression following a single passage. Furthermore, epidermal stem cells can be purified solely on the basis of reporter-gene expression. These cells are clonogenic, repopulate the epidermal stem-cell niches, and give rise to new hair follicles. Finally, we demonstrate that only PW1 reporter-expressing epidermal cells give rise to follicles that are capable of self-renewal following injury. Heterozygous mutant females exhibit growth retardation, impaired maternal behavior and diminished milk ejection, and fewer oxytocin neurons.|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|05-Nov-2012||0.0|0.0|Unknown||stem cell, reporter, Peg3|Yes| 7384.0|B6.MHCII-GFP|B6.129S4-H2-Ab1/Apb||Dominant|histocompatibility 2, class II antigen A, beta 1|H2-Ab1||Abeta, A beta, H-2Ab, H2-Ab, Ia2, Ia-2, IAb, I-A, I-Abeta, Rmcs1|MGI:103070|histocompatibility 2, class II antigen A, beta 1; targeted mutation 1, Hidde Ploegh|H2-Ab1|MGI:2387946|17|||||||||||||||||||||||||||||Express MHCII GFP fusion protein.|Express MHCII GFP fusion protein.Mice are immunologically indistinguishable from wild-type controls|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Excellent||||No|28-Jul-2013|Cryopreserved sperm|41.0|48.0|Unknown||major histocompatibility complex, MHCII, antigen presentation, GFP|Yes| 7243.0|CTR flox|B6.129-Calcr/Apb||Dominant|calcitonin receptor|Calcr||Clr|MGI:101950|calcitonin receptor; targeted mutation 1, Rachel A Davey|Calcr|MGI:4352932|6|||||||||||||||||||||||||||||Normal.|Normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|>20|||No|06-Dec-2012|Cryopreserved sperm|60.0|0.0|Unknown||hypercalcemia|Possibly| 4972.0|DSCR1 P71 Tg|B6.CBA-Tg(RCAN1)71Mapr/MarpApb||Dominant||||||||||||||||||||||||||human regulator of cacineurin 1|RCAN1|low||||||||||Transgenics are indistinguishable from wild type animals|Normal|C57BL/6 x CBA|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|||Homozygous Tg x Homozygous Tg|No|22-Jan-2010|Cryopreserved sperm|155.0|0.0|Yes|Down syndrome|Down Syndrome, vesicle trafficking|Yes| 7445.0|ENU29:G1|ANU:ENU29:G1||Recessive|Unknown||||||||Unknown||||||||||||||||Unknown|||||||||||||Unknown|Unknown|C57BL/6NCrlAnu|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||1||No|24-Sep-2013|Cryopreserved sperm|1222.0|38.0|Unknown||ENU, random, mutagenesis, screen|Yes| 7554.0|ENU25:022:CASC5:B6|C57BL/6NCrlAnu-Casc5/AnuApb|C57BL/6NCrlAnu-Casc5/AnuApb|Recessive|cancer susceptibility candidate 5|Casc5|Unknown|2310043D08Rik, 5730505K17Rik|MGI:1923714|cancer susceptibility candidate 5; mutation 1, The Australian National University|Casc5|MGI:5563500|2|ENSMUSG00000027326|ENSMUST00000028802|Casc5-004|2645|2661|T to A|ENSMUSE00000642270|7|882|Isoleucine to Lysine|||||TCTACCAGCAAAAGGCAGCCAGCTAACAATATTAGAGGAAGGGTCTAATAGCGGGCTTGGA||||||||||||||Possible embryonic lethal.|Normal blood lymphocyte populations as measured by expression of following proteins: B220, CD3, CD4, CD44, KLRG1, NK1.1, IgM, IgD by flow cytometry.|C57BL/6NCrlAnu|Yes|Unknown|Yes|Yes|Unknown|Yes|No|Unknown||||No|19-Dec-2013|Cryopreserved sperm|50.0|0.0|Unknown||ENU|Yes| 8711.0|GLIPR1L1|C57BL/6J-Glipr1l1/MarpApb||Recessive|GLI pathogenesis-related 1 like 1|Glipr1l1|Nil|1700011E04Rik|MGI:1916536||||10|||||||||||||||||||||||||||||Subfertile|Normal|C57BL/6J|Yes|Unknown|Yes|Yes|Unknown|Yes|No|Unknown||||No|06-May-2019|Cryopreserved sperm|50.0|0.0|Unknown|||Yes| 7556.0|ENU26:042:SOAT1:B6|C57BL/6NCrlAnu-Soat1/AnuApb|C57BL/6NCrlAnu-Soat1/AnuApb|Recessive|sterol O-acyltransferase 1|Soat1|Unknown|8430426K15Rik, Acact, ACAT-1, hid|MGI:104665|sterol O-acyltransferase 1; mutation 1, The Australian National University|Soat1|MGI:5563410|1|ENSMUSG00000026600|ENSMUST00000051396|Soat1-201|1241|1452|A to C|ENSMUSE00000160863|13|414|Valine to Glycine|||||CAACTACTACAGGACCTGGAACGTGGTGGTGCACGACTGGCTCTACTACTATGTTTACAAA||||||||||||||Normal blood lymphocyte populations as measured by expression of following proteins: B220, CD3, CD4, CD44, KLRG1, NK1.1, IgM, IgD by flow cytometry.|Normal blood lymphocyte populations as measured by expression of following proteins: B220, CD3, CD4, CD44, KLRG1, NK1.1, IgM, IgD by flow cytometry.|C57BL/6NCrlAnu|Yes|Unknown|Yes|Yes|Unknown|Yes|No|Unknown||G4||No|19-Dec-2013|Cryopreserved sperm|59.0|0.0|Unknown||ENU|Yes| 7385.0|B6.bst2loxp|C57BL/6-Bst2/Apb||Dominant|bone marrow stromal cell antigen 2|Bst2||2310015I10Rik, Bst-2, C87040, GREG|MGI:1916800||||8|||||||||||||||||||||||||||||Express Bst2 flanked by loxp sites.|One allele will express Bst2 flanked by loxp sites.|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Excellent||||No|28-Jul-2013|Cryopreserved sperm|44.0|0.0|Unknown||Bst2, immunology, antigen presentation|Yes| 7464.0|ENU30:G1|ANU:ENU30:G1||Recessive|Unknown||||||||Unknown||||||||||||||||Unknown|||||||||||||Unknown|Unknown|C57BL/6NCrlAnu|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||1||No|29-Oct-2013|Cryopreserved sperm|1361.0|40.0|Unknown||ENU, random, mutagenesis, screen|Yes| 6599.0|BXD-24b|BXD24/TyJ-Cep290rd16/JArc||Recessive|centrosomal protein 290|Cep290|Normal|MGC:7859, Nphp6|MGI:2384917|centrosomal protein 290; retinal degeneration 16|Cep290|MGI:3624136|10|||||||||||||||||||||||||||||Normal.Mice exhibit complete degeneration of retinal photoreceptors (Seecharan et al. 2003) resulting in blindness.|Normal|C57BL/6J x DBA/2|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|||brother x sister|No|04-Oct-2011|Embryo|0.0|0.0|Unknown|||Possibly| 4134.0||C57BL/6-Gt(ROSA)26Sor/MarpApb||Dominant|gene trap ROSA 26, Philippe Soriano|Gt(ROSA)26Sor|Nil|R26R-EYFP, R26RYFP, ROSA26-stop-YFP reporter, Rosa26-YFPfl, ROSA26R-YFP|MGI:104735|targeted mutation 1, Frank Costantini|Gt(ROSA)26Sor|MGI:2449038|6||||||||||||||||Yes|||||||||||||Normal||129X1/SvJ x C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|11||C57Bl/6 female x C57Bl/6 eYFP male or vice versa|No|07-Dec-2008|Cryopreserved sperm|145.0|0.0|No||yellow fluorescence protein (YFP), GFP, ROSA|Yes| 8709.0|FANCM KO|FVB-Fancm/StVApb||Recessive|Fanconi anemia, complementation group M|Fancm|Nil|C730036B14Rik, D12Ertd364e|MGI:2442306||||11|||||||||||||||||||||||||||||Reduced fertility: smaller testis and epidydmis. Reduced sperm count and sperm motility.May have decreased lifespan.May have increased cancer susceptibility.|May have increased cancer susceptibility.|FVB/N|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|06-May-2019|Cryopreserved sperm|50.0|0.0|Unknown|||Yes| 7368.0|ENU25:018:Nup35:B6|C57BL/6NCrlAnu-Nup35/Anu||Recessive|nucleoporin 35|Nup35|Unknown|2310006I24Rik, 5330402E05Rik|MGI:1916732|nucleoporin; mutation 1, The Australian National University|Nup35|MGI:6154324|2|ENSMUSG00000026999|ENSMUST00000028382|Nup35-001|576|653|T to A|ENSMUSE00001214171|6|192|Phenylalanine to Leucine|||||GCATCTGCTTCTTATATATTATTACAGTTTGCACAATATGGGAATATCTTAAAGCATGTGA||||||||||||||Mega colon|Probably normal|C57BL/6NCrlAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|05-Jul-2013|Cryopreserved sperm|43.0|0.0|Unknown||ENU, Colon|Yes| 6611.0|BXD-62|BXD62/RwwJArc||Recessive||||||||||||||||||||||||||||||||||||||Normal|Normal|C57BL/6J x DBA/2|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|||brother x sister|No|04-Oct-2011|Embryo|0.0|0.0|Unknown|||Possibly| 7607.0|ENU19:Mcm5|C57BL/6JAnu-Mcm5/AnuApb|C57BL/6JAnu-Mcm5/AnuApb|Recessive|minichromosome maintenance deficient 5, cell division cycle 46 (S. cerevisiae)|Mcm5|Unknown|Cdc46, mCD46, Mcmd5|MGI:103197|minichromosome maintenance deficient 5, cell division cycle 46 (S. cerevisiae); mutation 1, The Australian National University|Mcm5|MGI:5563450|8|ENSMUSG00000005410|ENSMUST00000164309|Mcm5-202||||||||77648844|15|||GGATGCTGCTTTGTCTGGCAATCTGTCGGGTGAGTAAGCGCTGGACTGTGGTCTTGGACG||||||||||||||Embryonic Lethal.No pups carrying homozygous genotype are born||C57BL/6JAnu|No|No|Yes|No|No|Yes|No|Unknown||G3|Het x Het|No|27-Feb-2014|Cryopreserved sperm|40.0|0.0|Unknown||ENU, embryonic lethal|Yes| 7342.0|MommeD44|FVB/NJ-Nrf1 Tg(Hba1-Gfp)1Ew/QimrApb||Dominant|nuclear respiratory factor 1|Nrf1|Normal|D6Ertd415e|MGI:1332235|nuclear respiratory factor 1; modifiers of murine metastable epiallele D44|Nrf1||6|ENSMUSG00000058440|ENSMUST00000115212|Nrf1-001|||||||||||||Yes|transgene insertion 1, Emma Whitelaw|human alpha-globin promoter and enhancer region|||||||||||Homozygous lethality (~9.5dpc)|Percentage of cells expressing the GFP transgene is decreased (enhancer of variegation).|FVB/NJ|No|No|Yes|No|No|Yes|No|Good||||No|27-May-2013|Cryopreserved sperm|44.0|0.0|Unknown||epigenetics, modifier, ENU|Yes| 4525.0|ENU11B6:020b ; Servalan|C57BL/6JAnu-Ebf1/2AnuApb|C57BL/6JAnu-Ebf1/2AnuApb|Dominant|early B-cell factor 1|Ebf1|Unknown|O/E-1, Olf-1, Olf1|MGI:95275|early B-cell factor 1; Servalan|Ebf1|MGI:5007783|11|ENSMUSG00000057098|ENSMUST00000081265|Ebf1-001|||||||||||||No|||||||||||||Low B cell numbers in peripheral blood.|Low B cell numbers in peripheral blood.|C57BL/6JAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|27-Feb-2009|Cryopreserved sperm|27.0|0.0|Unknown||B cell, ENU, NIH|Yes| 7388.0|fur|ENU24:006 unknown||Recessive|Unknown||||||||Unknown|||||||||||||||||||||||||||||Wispy fur, looks to lack development of adult hair.||C57BL/6NCrlAnu|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|30-Jul-2013|Cryopreserved sperm|50.0|0.0|Unknown||Coat, hair, fur, ENU|Yes| 7784.0|403, MHC-403|B6.129-Myh6/Apb||Dominant|myosin, heavy polypeptide 6, cardiac muscle, alpha|Myh6|Unknown|A830009F23Rik, alpha cardiac MHC, alpha-MHC, alpha myosin, cardiomyopathy, hypertrophic 1, Myhca, Myhc-a|MGI:97255|myosin, heavy polypeptide 6, cardiac muscle, alpha; targeted mutation 1, Jonathan G Seidman|Myh6|MGI:2182704|14|||||||||||||||||||||||||||||Lethal|Hypertrophy of myocytes with large hyperchromatic nuclei by 30 weeks of age, myocardial fiber disarray becoming marked by 30 weeks of age, moderate diffuse interstitial fibrosis by 30 weeks of age, starting as early as 15 weeks|C57BL/6|No|No|Yes|No|No|Yes|No|Good|9|15|Myh6tm1Jse/MYH6+ x MYH6/MYH6 |No|12-Nov-2014|Cryopreserved sperm|68.0|0.0|Yes|Hypertrophic cardiomyopathy (HCM) is a primary disorder of the myocardium characterized by cardiac hypertrophy. The clinical course of HCM is variable, with inter- and intra-familial variations ranging from benign asymptomatic disease to a malignant phenotype with a high risk of cardiac failure or sudden cardiac death.|Hypertrophy, Cardiomyopathy, Calcium, Myosin heavy chain gene|Yes| 4977.0|ENU11B6:024b ; Servalan|C57BL/6JAnu-Ebf1/3AnuApb|C57BL/6JAnu-Ebf1/3AnuApb|Recessive|early B-cell factor 1|Ebf1|Unknown|O/E-1, Olf-1, Olf1|MGI:95275|early B-cell factor 1; Servalan|Ebf1|MGI:5007783|11|ENSMUSG00000057098|ENSMUST00000081265|Ebf1-001|||||||||||||No|||||||||||||Small decrease in peripheral blood B cell numbers.Slight decrease in spleen B cell numbers|Normal|C57BL/6JAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|22-Jan-2010|Cryopreserved sperm|18.0|0.0|Unknown||B cell, immunity, NIH|Yes| 7608.0|BALB/b|BALB/c-H2/AnuApb||Recessive|||||||||||||||||||||||||||||histocompatibility-2, MHC|H2||H-2, MHC-II|MGI:95894|histocompatibility-2, MHC; b variant|H2|MGI:3579319|17|Balb/c is usually H2. The H2 complex contains 3 major classes of highly polymorphic gene sets: class I (H2-K, H2-D, Q, H2-T18 genes), class II (H2-I genes), and class III (H2-S genes). These genes are involved in many processes, including graft rejection, immune response, antigen presentation and complement component.||BALB/c|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|28-Feb-2014|Cryopreserved sperm|50.0|0.0|Unknown||haplotype, presentation, antigen presentation, T cell|Yes| 5604.0|Ancient 3||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5606.0|Ap2-c-ski - Incomplete||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5607.0|APP/PS||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5608.0|ARC(S)||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5610.0|AT2||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5609.0|ASC-/-||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 7604.0|Crisp1 KO|B6.129-Crisp1/Marp||Recessive|Cysteine-rich secretory protien 1 C|Crisp1||Aeg1, CRISP-1|MGI:102553|cysteine-rich secretory protein 1; gene trap CMHD-GT_255A4-3, Centre for Modeling Human Disease|Crisp1|MGI:3879688|17||||||||||||||||Yes|||||||||||||Unknown|Normal|C57BL/6J|No|Unknown|Yes|No|Unknown|Unknown|No|Good|6|||No|27-Feb-2014|Cryopreserved sperm|50.0|0.0|Unknown||Genetrap, Sperm, fertilization, ES cell|Possibly| 5335.0|NOD.scid β2M-/- |NOD-B2m Prkdc/MarpApb||Recessive|beta-2 microglobulin|B2m|Unknown|beta 2 microglobulin, beta2-m, Ly-m11|MGI:88127|targeted mutation 1, Rudolf Jaenisch|B2m|MGI:1927183|2||||||||||||||||Yes|||||||||||||Severe combined immuno deficiency; no B or T cells.|Normal|NOD|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|01-Dec-2010|Cryopreserved sperm|50.0|0.0|Unknown||Autoimmunity, insulin, MHC I, beta cell|Possibly| 5335.0|NOD.scid β2M-/- |NOD-B2m Prkdc/MarpApb||Recessive|protein kinase, DNA activated, catalytic polypeptide|Prkdc|Unknown|DNA-PK, DNA-PKcs, DNAPDcs, slip, XRCC7|MGI:104779|protein kinase, DNA activated, catalytic polypeptide; severe combined immunodeficiency|Prkdc|MGI:1857113|16|||||||||||||||||||||||||||||Severe combined immuno deficiency; no B or T cells.|Normal|NOD|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|01-Dec-2010|Cryopreserved sperm|||Unknown||Autoimmunity, insulin, MHC I, beta cell|Possibly| 5336.0|Krüppel-like Factor 3 (KLF3/BKLF) Knockout |129/SvJ-Klf3/Apb||Recessive|Kruppel-like factor 3 (basic)|Klf3|Nil|BKLF, Bklf, Tef-2|MGI:1342773|targeted mutation 1, Merlin Crossley|Klf3|MGI:3799368|5||||||||||||||||Yes|||||||||||||Postnatal lethality, only 17% survive to weaning. Decreased adipose tissue, mice appear leaner, abnormal fat pads. Similar in size to wildtype at birth but significantly smaller than littermate controls from 3 to 12 weeks of age.||129/SvJ|Yes|No|Yes|Yes|No|Yes|Yes|Unknown|10|||No|02-Dec-2010|Cryopreserved sperm|50.0|0.0|Unknown||Kruppel-like Factor 3, Basic Kruppel-like Factor, KLF, Obesity, adipose|Yes| 5575.0|Setx; Setx on C57/BL6Jx129Sv background|B6;129-Setx/QimrApb|15|Recessive|senataxin|Setx|Nil|AOA2; Als4; Sen1; SCAR1; AW060766; mKIAA0625; A130090N03; A930037J23Rik.|MGI:2443480 ||||2|||||||||||||||||||||||||||||Black or bown coat, Normal size, normal body, weight, normal life span. Male sterility|Normal|C57BL/6J x 129Sv|Yes|No|Yes|Yes|No|Yes|Yes|Good||30|Hetrezygotes x Heterozygotes|No|01-Sep-2011|Cryopreserved sperm|50.0|0.0|Yes|ataxia oculomotor Apraxia type 2 (AOA2)|DNA damage, AOA2, Senataxin, Transcription regulation, sterility|No| 7285.0|ENU27:G2|ANU:ENU27:G2||Recessive||||||||||||||||||||||||||||||||||||||Unknown|Unknown|C57BL/6NCrlAnu|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown|1|||No|12-Mar-2013|Cryopreserved sperm|1600.0|21.0|Unknown||ENU, mutagenesis, screen, random|Yes| 7390.0|ENU24:G3|ANU:ENU24:G3||Recessive||||||||||||||||||||||||||||||||||||||Unknown|Unknown|C57BL/6NCrlAnu|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown|1|||No|02-Aug-2013|Cryopreserved sperm|30.0|0.0|Unknown||ENU, mutagenesis, screen, random|Yes| 5204.0|BCMA KO; BCMA 49.29 KO:G1|B6.129S2/Sv-Tnfrsf17/AusbApb||Recessive|tumor necrosis factor receptor superfamily, member 17|Tnfrsf17|Nil|BCM, Tnfrsf13, Tnfrsf13a|MGI:1343050|targeted mutation 1, Martin L Scott|Tnfrsf17|MGI:2387427|16||||||||||||||||No|||||||||||||Mice homozygous for targeted null mutations in this gene are viable and fertile with no apparent defects in immune system development or function.||C57BL/6 x 129|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|09-Aug-2010|Cryopreserved sperm|100.0|0.0|No||BAFF, B cell, receptor, lymphocyte|Yes| 5338.0|B6.tx|C57BL/6-Atp7b/Apb||Recessive|ATPase, Cu++ transporting, beta polypeptide|Atp7b|Normal|Atp7a, Wilson protein, WND|MGI:103297|ATPase, Cu++ transporting, beta polypeptide; toxic milk|Atp7b|MGI:1856220|8||||||||||||||||Yes|||||||||||||Postnatal lethality: * mice die at about 14 days of age. * severity of defects depends on genetic background (less severe on a mixes C57BL/6 background) and maternal age (decreasing severity with increasing maternal age). * however, fostering with wild-type dams reverses many defects depending on the age of onset of fostering.Reduced female fertility: older female mice exhibit decreased fertility compared to wild-type mice.Abnormal mineral level: mice exhibit an increase in zinc the brain, liver and muscle.Abnormal copper level: mice exhibit an increase copper accumulation in the kidney, spleen, brain, muscle, serum and red blood cells.Decreased circulating copper level.Decreased liver copper level: in postnatal mice.Increased liver copper level: in adult mice.Tremors: * mice exhibit tremors. * severity of defects depends on genetic background (less severe on a mixes C57BL/6 background) and maternal age (decreasing severity with increasing maternal age). * however, fostering with wild-type dams reverses many defects depending on the age of onset of fostering.Ataxia: * mice exhibit difficulty walking, listing from side to side, overbalancing, falling over and exerting great effort in righting themselves. * severity of defects depends on genetic background (less severe on a mixes C57BL/6 background) and maternal age (decreasing severity with increasing maternal age). * however, fostering with wild-type dams reverses many defects depending on the age of onset of fostering.Decreased body weight: * mice reach their maximal weight at day 9 (70% of wild-type) and exhibit weight loss until their death. * severity of defects depends on genetic background (less severe on a mixes C57BL/6 background) and maternal age (decreasing severity with increasing maternal age). * however, fostering with wild-type dams reverses many defects depending on the age of onset of fostering.Postnatal growth retardation: * apparent within a day or two after birth * severity of defects depends on genetic background (less severe on a mixes C57BL/6 background) and maternal age (decreasing severity with increasing maternal age). * however, fostering with wild-type dams reverses many defects depending on the age of onset of fostering.Abnormal muscle physiology: * mice exhibit hyperextension of hindlimbs and hyperflexion of wrists. * severity of defects depends on genetic background (less severe on a mixes C57BL/6 background) and maternal age (decreasing severity with increasing maternal age). * however, fostering with wild-type dams reverses many defects depending on the age of onset of fostering.Diluted coat colour: * mice exhibit pale coat color * severity of defects depends on genetic background (less severe on a mixes C57BL/6 background) and maternal age (decreasing severity with increasing maternal age).Hypopigmentation: * pigment contained within melanocytes is lighter than normalseverity of defects depends on genetic background (less severe on a mixes C57BL/6 background) and maternal age (decreasing severity with increasing maternal age). * however, fostering with wild-type dams reverses many defects depending on the age of onset of fostering.Curly vibrissae: * mice exhibit curly whiskers * severity of defects depends on genetic background (less severe on a mixes C57BL/6 background) and maternal age (decreasing severity with increasing maternal age). * however, fostering with wild-type dams reverses many defects depending on the age of onset of fostering.Maternal effect: pups suckled by homozygous mothers are deficient in copper concentration in their stomach contents and liver, and supplementing the drinking water of the homozygous mother with copper does not increase the copper content of the milk but rather increases the copper accumulation in the mammary gland.Endocrine/exocrine gland phenotype: * mammary glands are structurally normal by histology.Defects are less severe on C57BL/6 background compared to DL background.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|10|||No|11-Dec-2010|Cryopreserved sperm|89.0|168.0|Yes|Wilson's Disease||Yes| 5343.0|F/F:STAT1KO ; gp130Y757F x STAT1|B6;129-IL6st Stat1/MarpApb||Dominant|signal transducer and activator of transcription 1|Stat1|Nil||MGI:103063|signal transducer and activator of transcription 1; targeted mutation 1, Robert D Schreiber|Stat1|MGI:1861949|1||||||||||||||||No|||||||||||||Gastric tumors; splenomegaly; thrombocytosis; lymphadenopathy; multi-organ inflammation.|Gastric tumors; splenomegaly; thrombocytosis; lymphadenopathy; multi-organ inflammation.|C57BL/6 x 129S1/Sv|Yes|Yes|Yes|Yes|Yes|Yes|Yes|Good||||No|13-Dec-2010|Cryopreserved sperm|50.0|0.0|Unknown||signal transduction, JAK-STAT, cytokine, interferon, kinase, phosphorylation|Yes| 5343.0|F/F:STAT1KO ; gp130Y757F x STAT1|B6;129-IL6st Stat1/MarpApb||Dominant|interleukin 6 signal transducer|Il6st|Normal|CD130, D13Ertd699e, gp130|MGI:96560|interleukin 6 signal transducer; targeted mutation 1, Matthias Ernst|Il6st|MGI:2388478|13||||||||||||||||Yes|||||||||||||Gastric tumors; splenomegaly; thrombocytosis; lymphadenopathy; multi-organ inflammation.|Gastric tumors; splenomegaly; thrombocytosis; lymphadenopathy; multi-organ inflammation.|C57BL/6 x 129S1/Sv|Yes|Yes|Yes|Yes|Yes|Yes|Yes|Good||||No|13-Dec-2010|Cryopreserved sperm|||Unknown||signal transduction, JAK-STAT, cytokine, interferon, kinase, phosphorylation|Yes| 7382.0|ENU28:G1|ANU:ENU28:G1||Recessive|Unknown||||||||Unknown||||||||||||||||Unknown|||||||||||||Unknown|Unknown|C57BL/6NCrlAnu|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||1||No|26-Jul-2013|Cryopreserved sperm|522.0|0.0|Unknown||ENU, random, mutagenesis, screen|Yes| 6588.0|BALB/c x NOD/Lt|Nod/Lt.C-Idd5 Idd1/Arc||Recessive||||||||||||||||||||||||||||||||||||||As per background strain.||NOD/Lt|Yes|Yes|Yes|Yes|Yes|Yes|No|Excellent|10|||No|29-Sep-2011|Embryo|0.0|0.0|Yes|Multiple Sclerosis|Autoimmune Encephalitis, Idd, diabetes, MHC|Possibly| 8713.0|Kynu null|C57BL/6N-Kynu/DunwApb||Recessive|kynureninase|Kynu|Nil|4432411A05Rik, L-kynurenine hydrolase|MGI:1918039|kynureninase; endonuclease-mediated mutation 1, Sally L Dunwoodi|Kynu|MGI:6285803|2|||||||||||||||||||||||||||||Normal|Normal|C57BL/6N|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|13-May-2019|Cryopreserved sperm|50.0|0.0|Unknown||NAD, Haao, Niacin|Yes| 5410.0|NOD.HJ16-3|NOD/Lt-Tg(IL12B)HJ16-3Gem/Arc||Dominant||||||||||||||||||||||||||human interleukin 12b||||||||||||Mice express human interleukin 12B||NOD/Lt|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|10||Hom x Hom|No|03-Feb-2011|Embryo|0.0|0.0|Unknown||cytokine, interleukin, autoimmunity|Yes| 7386.0|B6.IAbloxp|C57BL/6-H2-Ab1/Apb||Dominant|histocompatibility 2, class II antigen A, beta 1|H2-Ab1|Normal|Abeta, A beta, H-2Ab, H2-Ab, Ia2, Ia-2, IAb, I-A, I-Abeta, Rmcs1|MGI:103070|histocompatibility 2, class II antigen A, beta 1; targeted mutation 1, Pandelakis A Koni|H2-Ab1|MGI:2384629|17|||||||||||||||||||||||||||||Express IAb flanked by loxp sites.|One allele will express IAb flanked by loxp sites.|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Excellent||||No|28-Jul-2013|Cryopreserved sperm|42.0|0.0|Unknown||MHCII, immunology, antigen presentation, major histocompatibility complex|Yes| 5170.0|NOD.NHE1|NOD.B6-idd11-NHE1/ArcApb||Dominant||||||||||||||||||||||||||||||||||||||Accelerated diabetes incidence (number and time)||NOD/Lt|Yes|Yes|Yes|Yes|Yes|Yes|No|Excellent|||Hom x Hom OR Het x Het|No|29-Jun-2010|Embryo|0.0|0.0|Yes|Type I Diabetes|NOD/Lt|Yes| 7248.0|IGF1 Exon5 total KO|B6.Cg-Igf1/MarpApb||Semi-dominant|insulin-like growth factor 1|Igf1|Nil|C730016P09Rik, Igf-1, Igf-I|MGI:96432||||10|||||||||||||||||||||||||||||Normal|Normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|12-Dec-2012|Cryopreserved sperm|60.0|0.0|Unknown|||Possibly| 5345.0|SS-11 ; Vegfd 2.2.36|C57BL/6-Figf/Apb||X-linked|c-fos induced growth factor|Figf|Nil|VEGF-D, Vegfd|MGI:108037|c-fos induced growth factor; targeted mutation 1, Marc G Achen|Figf|MGI:3576785|X|||||||||||||||||||||||||||||No abnormal phenotype detected: homozygous females are morphologically normal, can suckle, and have grossly normal lymphatic system morphology and function.Mice have reduced numbers of lymphatic vessels in lungs.|Normal|129S1/Sv x C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|0|||No|15-Dec-2010|Cryopreserved sperm|100.0|0.0|Unknown||growth factor, Vegf, lymphatics|Yes| 7284.0|ENU27:G1|ANU:ENU27:G1||Recessive|Unknown||||||||Unknown||||||||||||||||Unknown|||||||||||||Unknown|Unknown|C57BL/6NCrlAnu|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||1||No|12-Mar-2013|Cryopreserved sperm|473.0|34.0|Unknown||ENU, random, mutagenesis, screen|Yes| 7252.0|Nod il21R knock out|NOD(Cg)-Il21r/AusbApb||Dominant|interleukin 21 receptor|Il21r|Nil|NILR|MGI:1890475|interleukin 21 receptor; targeted mutation 1, Warren J Leonard|Il21r|MGI:2446509|7|||||||||||||||||||||||||||||Healthy and viable.Defect in IgG1 responses.NOD mice develop spontaneous diabetes type 1 but NOD mice carrying the IL21r mutation do not develop diabetes.|Healthy and viable|NOD|Yes|Yes|Unknown|Yes|Yes|Unknown|No|Unknown|10|||No|14-Dec-2012|Cryopreserved sperm|50.0|0.0|Unknown||Immunoglobulin, autoimmunity, B cell, T cell, CCR9|No| 7253.0|IL21ROT2tgThy|B6(Cg)-Thy1 Il21r Tg(Tg(TcraTcrb)425Cbn/AusbApb||Recessive|interleukin 21 receptor|Il21r|Nil|NILR|MGI:1890475|interleukin 21 receptor; targeted mutation 1, Warren J Leonard|Il21r|MGI:2446509|7|||||||||||||||||transgene insertion 425, Frank Carbone|||thymus cell antigen 1, theta|Thy1||CD90, T25, theta, Thy-1, Thy1.1, Thy 1.2, Thy-1.2, Thy1.2|MGI:98747|thymus cell antigen 1, theta; a variant|Thy1|MGI:3579311|9|Normal development and breeding|Normal development and breeding|C57BL6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|14-Dec-2012|Cryopreserved sperm|60.0|0.0|Unknown|||No| 7245.0||NOD.B6 Idd9/11||Recessive|||Unknown|||insulin dependent diabetes susceptibility 9; C57BL/6J|Idd9|MGI:3036801|4||||||||||||||||Yes|||||||||||||Non obese diabetic (NOD) mice exhibit a susceptibility to Spontaneous development of type 1 diabetes.||NOD|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|11-Dec-2012|Embryo|0.0|0.0|Unknown||Diabetic, insulin, T cell, autoimmunity|Yes| 7245.0||NOD.B6 Idd9/11||Recessive|||Unknown|||insulin dependent diabetes susceptibility 11|Idd11|MGI:3036811|4|||||||||||||||||||||||||||||Non obese diabetic (NOD) mice exhibit a susceptibility to Spontaneous development of type 1 diabetes.||NOD|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|11-Dec-2012|Embryo|||Unknown||Diabetic, insulin, T cell, autoimmunity|Yes| 7251.0|ENU22:4930473A06Rik|C57BL/6NCrlAnu-Ccdc171/AnuApb||Dominant|coiled-coil domain containing 171|Ccdc171|Unknown|4930418J05Rik, 4930473A06Rik, A330015D16Rik|MGI:1922152|coiled-coil domain containing 171; mutation 1, The Australian National University|Ccdc171|MGI:5570360|4|ENSMUSG00000052407|ENSMUST00000053414|Ccdc171-001|2586|2913|T to A|ENSMUSE00001208951|18|862|Cysteine to STOP|||||CCAAAACATCAGAGGGAACAGTTACGCTGTTTACAGGCACTCGCGTGGCTCACCAGTTCTG||||||||||||||Reduced peripheral B cells, high IgM and low IgD expression|Reduced peripheral B cells, increased population of IgM very high immature B cells|C57BL/6NCrlAnu|Yes|Unknown|Yes|Yes|Yes|Yes|No|Good||3||No|14-Dec-2012|Cryopreserved sperm|32.0|0.0|Unknown||B cell, B lymphocyte, IgM, B cell development, ENU|No| 5402.0|B6 x B6FVB; Dirc-2|B6;FVB/N-Dircq2/ArcApb||Dominant||||||||||||||||||||||||||||||||||||||As per parental strain.Once injected with Alloxan mice become diabetic (check via urine glucose or blood monitor), these mice show nephropathy and retinopathy disease consistent with the human conditions. Mice are identified by conventional genotyping but on induction of diabetes phenotypes relating to type 1 diabetic complication are observed i.e. Excessive urination, weight loss and proteinuria. |As per parental strain.|C57BL/6J|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|10|5|Hom x Hom|No|01-Feb-2011|Embryo|0.0|0.0|Yes|Once injected with Alloxan mice become diabetic (check via urine glucose or blood monitor), these mice show nephropathy and retinopathy disease consistent with the human conditions. |diabetic complications, retinopathy, nephropathy|Yes| 6891.0|ENU24:G2|ANU:ENU24:G2||Recessive||||||||||||||||||||||||||||||||||||||Unknown|Unknown|C57BL/6NCrlAnu|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown|1|||No|04-May-2012|Cryopreserved sperm|1647.0|0.0|Unknown||ENU, mutagenesis, screen, random|Yes| 5403.0|B6 x B6FVB; Dirc-3|B6;FVB/N-Dircq3/ArcApb||Dominant||||||||||||||||||||||||||||||||||diabetes induced renal changes 3|Dircq3||6|As per parental strain.Once injected with Alloxan mice become diabetic (check via urine glucose or blood monitor), these mice show nephropathy and retinopathy disease consistent with the human conditions. Mice are identified by conventional genotyping but on induction of diabetes phenotypes relating to type 1 diabetic complication are observed i.e. Excessive urination, weight loss and proteinuria. |As per parental strain.|C57BL/6J|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|10|5|Hom x Hom|No|01-Feb-2011|Embryo|0.0|0.0|Yes|Once injected with Alloxan mice become diabetic (check via urine glucose or blood monitor), these mice show nephropathy and retinopathy disease consistent with the human conditions. |diabetic complications, retinopathy, nephropathy|Yes| 5357.0|B6.427|C57BL/6-Tg(HLA DR4-DQ8)427/Apb||Dominant||||||||||||||||||||||||||human leukocyte antigen class II||||||||||||HLA DR4 and DQ3 expression was evident on B cell but not T cells, dendritic cells and a proportion of macrophages.DR4-DQ3 mice develop protective immunity following infectious challenge with S. typhimurium.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||31||No|20-Dec-2010|Cryopreserved sperm|45.0|0.0|Unknown||autoimmunity, B cell, HLA, MHC, selection|Yes| 5385.0|WOMBAT ; Ndufs6gt/+|B6;129P2-Ndufs6/MrchApb|B6;129P2-Ndufs6/MrchApb|Recessive|NADH dehydrogenase (ubiquinone) Fe-S protein 6|Ndufs6|Reduced|IP13|MGI:107932|NADH dehydrogenase (ubiquinone) Fe-S protein 6; gene trap AR0138, Wellcome Trust Sanger Institute|Ndufs6|MGI:4346527|13||||||||||||||||Yes|||||||||||||Ndufs6gt/gt mice are fertile. For the first 4 months of life, Ndufs6gt/gt mice have no overt phenotype, with normal weight gain and survival. After 4 months of age, Ndufs6gt/gt mice develop cardiac hypertrophy, which can lead to sudden weight loss, lethargy and death. Ndufs6gt/gt males are more severely affected than females. |Normal|129P2/OlaHsd x C57BL/6N|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||11|heterogygote X heterozygote|No|14-Jan-2011|Cryopreserved sperm|40.0|0.0|Yes|Mutations in human gene, NDUFS6, encoding one of the 45 subunits of Complex I, are one cause of Complex I deficiency. NDUFS6-/- patients suffer from seizures, hypotonia and abnormal eye movements and die in the first month of life. Currently, no effective treatment is available. |Mitochondria, Cardiac , Complex I, Oxidative phosphorylation, ES cell|Possibly| 7061.0|Momme D38|FVB/NJ-MommeD38 Tg(Hba1-Gfp)1Ew||Semi-dominant|eukaryotic translation initiation factor 3, subunit H|Eif3h|Unknown||MGI:1915385|eukaryotic translation initiation factor 3, subunit H; modifier of murine metastable epialleles, D38|Eif3h|MGI:5514384|15||||||||||Unknown to Unknown|||||||transgene insertion 1, Emma Whitelaw|human alpha-globin promoter and enhancer region|||||||||||Homozygous lethality (before E9.5 dpc)|Percentage of cells expressing the GFP transgene is decreased (enhancer of variegation).|FVB/NJ|No|No|Yes|No|No|Yes|No|Good|||MommeD38<+/->;Tg(Hba1-Gfp)1Ew x Tg(Hba1-Gfp)1Ew|No|24-Aug-2012|Cryopreserved sperm|47.0|0.0|Unknown||ENU, epigenetics, suppressor of variegation, modifier|Possibly| 7389.0|ENU19:G2|ANU:ENU19:G2||Recessive||||||||||||||||||||||||||||||||||||||Unknown|Unknown|C57BL/6JAnu|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||1||No|02-Aug-2013|Cryopreserved sperm|50.0|0.0|Unknown||ENU, random, mutagenesis, screen|Yes| 5700.0|Crim1 Flox BRE-LacZ C57||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5430.0|Idd14 R13|NOD.B6-Idd14/R13Apb||Recessive|||||||||||||||||||||||||||||insulin dependent diabetes susceptibility 14|Idd14|||MGI:99416||||13|Unknown|Unknown|NOD/Lt|Yes|Yes|Unknown|Yes|Yes|Unknown|No|Unknown||||Yes|14-Feb-2011|Cryopreserved sperm|80.0|0.0|Unknown|||No| 6639.0|ENU16Ch:069b|C57BL/6JAnu-Mpz/AnuApb||Recessive|myelin protein zero|Mpz|Unknown|Mpp, P0|MGI:103177|myelin protein zero; enu16|Mpz|MGI:5490251|1|ENSMUSG00000056569|ENSMUST00000070758|Mpz-001|362|530|A to G|ENSMUSE00000476648|5|121|Aspartic acid to Glycine|||||CATTGTCATACACAACCTAGACTACAGTGACAACGGCACTTTCACATGTGATGTCAAAAAC||||||||||||||Circling Behaviour.Tremors and hypermetric gait. Worsens with age||C57BL/6J|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|02-Nov-2011|Cryopreserved sperm|18.0|0.0|Yes|Charcot-Marie-Tooth disease type 1 (CMT1B)|circling, tremours, myelin, Alzheimer's disease|Yes| 7614.0|ENU24:029:Agtr2|C57BL/6NCrlAnu-Agtr2/AnuApb|C57BL/6NCrlAnu-Agtr2/AnuApb|Recessive|angiotensin II receptor, type 2|Agtr2|Unknown|AT2 receptor|MGI:87966|angiotensin II receptor, type 2; mutation 1, The Australian National University|Agtr2|MGI:5648447|X|ENSMUSG00000068122|ENSMUST00000089188|Agtr2-001|353|599|A to T|ENSMUSE00000556750|3|118|Lysine to STOP|||||TGATTGGCTTTTTGGACCTGTGATGTGCAAAGTGTTTGGTTCTTTTCTGACTCTGAACATG||||||||||||||Unknown|Unknown|C57BL/6NCrlAnu|Yes|Unknown|Yes|Yes|Yes|Yes|No|Excellent||G4||No|04-Mar-2014|Cryopreserved sperm|36.0|0.0|Unknown||ENU|Yes| 5413.0||NOD.Mog7w||Recessive|||||||||||||||||||||||||||||||||||||7|Unknown||NOD/Lt|Yes|Yes|Unknown|Yes|Yes|Unknown|No|Unknown|10||Hom x Hom|No|03-Feb-2011|Embryo|0.0|0.0|Unknown||QTL|Yes| 5358.0|NOD.427|NOD-Tg(HLA DR4-DQ8)427/Apb||Dominant||||||||||||||||||||||||||human leukocyte antigen class II||||||||||||HLA DR4 and DQ3 expression was evident on B cell but not T cells, dendritic cells and a proportion of macrophages.DR4-DQ3 mice develop protective immunity following infectious challenge with S. typhimurium.||NOD|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|19|7||No|20-Dec-2010|Cryopreserved sperm|45.0|0.0|Unknown||autoimmunity, B cell, HLA, MHC, selection|Yes| 4135.0||NOD.B6-Prkdc B2m Tg(B2m)1Rms/MarpApb||Semi-dominant|beta-2 microglobulin|B2m|Unknown|beta 2 microglobulin, beta2-m, Ly-m11|MGI:88127|targeted mutation 1, Rudolf Jaenisch|B2m|MGI:1927183|2||||||||||||||||Yes|||||||||||||NOD phenotype|NOD phenotype|NOD|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|11|||No|07-Dec-2008|Cryopreserved sperm|100.0|0.0|Yes||microglobulin, autoimmune disease|Yes| 4135.0||NOD.B6-Prkdc B2m Tg(B2m)1Rms/MarpApb||Semi-dominant|protein kinase, DNA activated, catalytic polypeptide|Prkdc|Unknown|DNA-PK, DNA-PKcs, DNAPDcs, slip, XRCC7|MGI:104779|protein kinase, DNA activated, catalytic polypeptide; severe combined immunodeficiency|Prkdc|MGI:1857113|16|||||||||||||||||||||||||||||NOD phenotype|NOD phenotype|NOD|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|11|||No|07-Dec-2008|Cryopreserved sperm|||Yes||microglobulin, autoimmune disease|Yes| 2393.0|BCMA KO; BCMA 49.29 KO:G1|B6.129-Tnfrsf17/AnuApb||Recessive|tumor necrosis factor receptor superfamily, member 17|Tnfrsf17|Nil|BCM, Tnfrsf13, Tnfrsf13a|MGI:1343050|targeted mutation 1, Martin L Scott|Tnfrsf17|MGI:2387427|16||||||||||||||||No|||||||||||||Mice homozygous for targeted null mutations in this gene are viable and fertile with no apparent defects in immune system development or function.||C57BL/6 x 129|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|20-Dec-2007|Cryopreserved sperm|80.0|0.0|No||BAFF, B cell, receptor, lymphocyte|Yes| 5422.0|203.1 ; cTnI-G203S.1|C57BL/6-Tg(Myh6-TNNI3*G203S)1Chs/Apb||Dominant||||||||||||||||||||||||||transgene insertion 1, Christopher Semsarian|cardiac specific mouse αMHC promoter (alpha myosin heavy chain)|48% of endogenous||||||||||Unknown|Mice develop cardiac phenotype - hypertrophic cardiomyopathy by age 50 weeks. No differences were observed in LV systolic function at any age.|C57BL/6|No|Unknown|Yes|No|Unknown|Yes|No|Excellent|||Transgenic x non-transgenic sibs|No|07-Feb-2011|Cryopreserved sperm|50.0|0.0|Yes|Hypertrophic cardiomyopathy (HCM) is a primary disorder of the myocardium characterized by cardiac hypertrophy. The clinical course of HCM is variable, with inter- and intra-familial variations ranging from benign asymptomatic disease to a malignant phenotype with a high risk of cardiac failure or sudden cardiac death.|Hypertrophy, Cardiomyopathy, Calcium, Troponin I gene|Yes| 5565.0|ENU22 MDX:::B6:F1|ENU22MDX.F1||X-linked|dystrophin, muscular dystrophy|Dmd|Unknown|Dp427, Duchenne muscular dystrophy, mdx, pke, X-linked muscular dystrophy|MGI:94909|X linked muscular dystrophy|Dmd|MGI:1856328|X||||||||||||||||No|||||||||||||Abnormal muscle morphology.dilated sarcoplasmic reticulum.Abnormal skeletal muscle fiber morphology: * development of electron-dense bodies in the mitochondria resulting in swelling and degenerating mitochondria, and disruption of the plasmalemma basal lamina. * the normal myofibrillar architecture of bands and lines disappears and myofilaments disintegrate and become misaligned.Increased variability of skeletal muscle fiber size: variable muscle fiber size; progressive starting at 3 weeks of age.Skeletal muscle fibrosis: exhibit mild muscle fibrosis, however there is no replacement of lost muscle by fat cells.Skeletal muscle necrosis: progressive starting at 9 weeks of age.Muscle degeneration: progressive starting at 3 weeks of age.Abnormal muscle physiology: increased intracellular sodium concentration in muscle; increased severity with age.Muscular atrophy: progressive starting at 3 weeks of age.Dystrophic muscle.Myopathy: progressive degenerative myopathy; increased severity with age.Abnormal circulating enzyme level: exhibit elevated blood levels of muscle creatine kinase and pyruvate kinase.Reduced female fertility: slight reduction in fertility.||C57BL/6 x C57BL/10|Unknown|Unknown|Yes|Unknown|Unknown|Yes|Yes|Unknown||||No|17-Aug-2011|Cryopreserved sperm|474.0|0.0|Yes||Muscular dystrophy, Duchenne Type, muscle, necrosis, degeneration|No| 5565.0|ENU22 MDX:::B6:F1|ENU22MDX.F1||X-linked|Unknown||||||||Unknown|||||||||||||||||||||||||||||Abnormal muscle morphology.dilated sarcoplasmic reticulum.Abnormal skeletal muscle fiber morphology: * development of electron-dense bodies in the mitochondria resulting in swelling and degenerating mitochondria, and disruption of the plasmalemma basal lamina. * the normal myofibrillar architecture of bands and lines disappears and myofilaments disintegrate and become misaligned.Increased variability of skeletal muscle fiber size: variable muscle fiber size; progressive starting at 3 weeks of age.Skeletal muscle fibrosis: exhibit mild muscle fibrosis, however there is no replacement of lost muscle by fat cells.Skeletal muscle necrosis: progressive starting at 9 weeks of age.Muscle degeneration: progressive starting at 3 weeks of age.Abnormal muscle physiology: increased intracellular sodium concentration in muscle; increased severity with age.Muscular atrophy: progressive starting at 3 weeks of age.Dystrophic muscle.Myopathy: progressive degenerative myopathy; increased severity with age.Abnormal circulating enzyme level: exhibit elevated blood levels of muscle creatine kinase and pyruvate kinase.Reduced female fertility: slight reduction in fertility.||C57BL/6 x C57BL/10|Unknown|Unknown|Yes|Unknown|Unknown|Yes|Yes|Unknown||||No|17-Aug-2011|Cryopreserved sperm|||Yes||Muscular dystrophy, Duchenne Type, muscle, necrosis, degeneration|No| 5359.0|B6.hCD4.IAE.303-4 ; triple 303|C57BL/6-H2 Tg(Cd4-CD4)2362Litt Tg(HLA DR3-DQ2)303/Apb||Dominant|histocompatibility-2, MHC|H2|Nil|H-2, MHC-II|MGI:95894|histocompatibility-2, MHC; targeted deletion, H2 complex|H2|MGI:2658725|17||||||||||||||||No|human leukocyte antigen class II||||||||||||Expression of HLA DR and DQ evident on B cells, dendritic cells and a proportion of macrophages.These mice Tg for hCD4.DR3-DQ2.MHCII<Δ/Δ> express functional HLA-DR3 and DQ2 molecules that mediate thymic selection generating Ag-specific CD4<+> T cell immunity. Although about one in five Europeans homozygous for HLA-DQ2 develops celiac disease, homozygous and heterozygous hCD4.DR3-DQ2.MHCII<Δ/Δ> Tg mice do not spontaneously develop hypersensitivity to gluten. However, standard immunization protocols do produce HLA-DQ2-restricted CD4+ T cells in hCD4.DR3-DQ2.MHCII<Δ/Δ> Tg mice that preferentially recognize the deamidated α-gliadin 17-mer immunodominant in human celiac disease. Nevertheless, we have found that preexisting DQ2-restricted CD4<+> T cell immunity to deamidated α-gliadin 17-mer in hCD4.DR3-DQ2.MHCII<Δ/Δ> Tg mice is not sufficient for gluten ingestion to cause measurable intestinal pathology.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|21-Dec-2010|Cryopreserved sperm|39.0|0.0|Unknown||MHC, B cell, selection, autoimmunity, celiac disease|Yes| 5359.0|B6.hCD4.IAE.303-4 ; triple 303|C57BL/6-H2 Tg(Cd4-CD4)2362Litt Tg(HLA DR3-DQ2)303/Apb||Dominant||||||||||||||||||||||||||transgene insertion 2362, Dan R Littman|murine Cd4 and human CD4|equivalent to human CD4+ cells||||||||||Expression of HLA DR and DQ evident on B cells, dendritic cells and a proportion of macrophages.These mice Tg for hCD4.DR3-DQ2.MHCII<Δ/Δ> express functional HLA-DR3 and DQ2 molecules that mediate thymic selection generating Ag-specific CD4<+> T cell immunity. Although about one in five Europeans homozygous for HLA-DQ2 develops celiac disease, homozygous and heterozygous hCD4.DR3-DQ2.MHCII<Δ/Δ> Tg mice do not spontaneously develop hypersensitivity to gluten. However, standard immunization protocols do produce HLA-DQ2-restricted CD4+ T cells in hCD4.DR3-DQ2.MHCII<Δ/Δ> Tg mice that preferentially recognize the deamidated α-gliadin 17-mer immunodominant in human celiac disease. Nevertheless, we have found that preexisting DQ2-restricted CD4<+> T cell immunity to deamidated α-gliadin 17-mer in hCD4.DR3-DQ2.MHCII<Δ/Δ> Tg mice is not sufficient for gluten ingestion to cause measurable intestinal pathology.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|21-Dec-2010|Cryopreserved sperm|||Unknown||MHC, B cell, selection, autoimmunity, celiac disease|Yes| 7916.0|Eu myc|B6.SJL-Tg(IghMyc)22Bri/WehiAnu||Dominant||||||||||||||||||||||||||transgene insertion 22, Ralph L Brinster|Igh (E mu) enhancer and Myc promoter||||||||||||Mice invariably develop lymphomas, 90% succumbing in the first 5 mo of life. to almost invariably develop lymphomas, 90% succumbing in the first 5 mo of life. The tumors typically presented as rapidly progressive lymphadenopathy with thymic involvement and were highly malignant by transplantation assay. Morphologically, they were lymphoblastic lymphomas, usually accompanied by lymphoid leukemia and granulocytosis, and were distinct from the tumors that arose much later in 37% of nontransgenic mice of the same (C57BL/6 x SJL)F2 genetic background.Premature death: mice die at 6 to 15 weeks of age with 94% of mice dying by 4 months of age.Increased tumor incidence: mice occasionally develop thyoma without involvement of peripheral lymphoid organsLeukemia: mice develop multicentric lymphosarcoma associated with leukemia.Lymphoma:* 13 of 15 mice develop lymphomas* mice develop multicentric lymphosarcoma associated with leukemia.B cell derived lymphoma: lymphomas develop from single B-lymphoid clones at different stages of differentiation.Sarcoma: mice develop multicentric lymphosarcoma associated with leukemia.Abnormal lymphopoiesis: mice exhibit an increased in the number of lymphoblasts in lymph tissues and the blood compared to wild-type mice.Enlarged spleen: two-fold.Enlarged thymus.Enlarged lymph nodes.|C57BL/6 x SJL|Yes|No|Yes|Yes|No|Yes|No|Unknown||||No|18-Jun-2015|Cryopreserved sperm|88.0|0.0|Unknown||B cell, lymphoma, c-myc, B cell|Yes| 7615.0|EphA3 Knockout|B6;129S1-Epha3/QimrApb||Recessive|Eph Receptor A3|EphA3|Nil|Cek4, End3, Hek, Hek4, Mek4, Tyro4|MGI:99612|Eph receptor A3; targeted mutation 1, Arthur Brown|Epha3|MGI:2681606|16|||||||||||||||||||||||||||||Partial perinatal lethality:• about 70-75% of homozygotes die within 48 hours of birth from pulmonary edema secondary to cardiac failure• mice surviving perinatal period develop normally with no cardiac or other abnormalities and normal grip strength, motor column organization and spinal nerve projections.Liver vascular congestion:• venous congestionPulmonary vascular congestion:• venous congestionVenoocclusion:• venous congestion is seen in the lungs, liver, and other organsabnormal cardiac epithelial to mesenchymal transition.• atrioventricular canal explants exhibit a reduced number of mesenchymal cells that invade a collagen gel compared to wild-type, indicating reduced epithelial-mesenchymal transition (EMT).Abnormal heart development.Abnormal atrioventricular cushion morphology:• mutants exhibit delayed fusion of endocardial cushions; 75% of atrioventricular endocardial cushions are not yet fused at E11.5• 78% of E12.5 embryos exhibit rounded atrioventricular endocardial cushion cells with few or no processes instead of the flatted cells with multiple processes seen in wild-type• atrioventricular endocardial cushions exhibit increased apoptosis, however show no difference in proliferation• stress fibers in endocardial cushions are reduced in size and disorganised.Decreased atrioventricular cushion size:• hypoplastic endocardial cushions; endocardial cushions are 28.8% smaller than wild-type at E12.5 due to a reduction in cells within the cushion.Ostium primum atrial septal defect:• P0 mutants that become cyanotic have an atrial septal defect; the infolding representing the septum secundum is occasionally seen and the septum primum is either totally absent or is only a thin remnant.Dilated heart atrium:• enlarged atria that are engorged with blood and dilatedAbnormal atrioventricular septum morphology.• atrioventricular septum is thinnerAbnormal cardiovascular system physiology.Pulmonary alveolar hemorrhage:• neonatal lungs exhibit alveoli filled with blood, indicating exceedingly high cardiac filling pressures leading to capillary disruption.Atrioventricular valve regurgitation:• atrioventricular orifices are enlarged and their valvular leaflets inadequate to close the right and left atrioventricular canals.Decreased heart rate:• significant bradycardia at P0; average heart rate is 297 bpm compared to 396 bpm for wild-type.Atrioventricular block.Prolonged PR interval:• first-degree atrioventricular block as evidenced by prolonged PR interval• however, mutants show no evidence of arrhythmia or of second- or third-degree AV conduction blockCongestive heart failure:• cardiac failure in 70-75% of mutantsCyanosis:• mutants quickly become cyanotic after birthPulmonary edema:• seen in 70% of mutantsPulmonary alveolar haemorrhage:• neonatal lungs exhibit alveoli filled with blood, indicating exceedingly high cardiac filling pressures leading to capillary disruption.Abnormal lung morphology:• neonatal lungs are poorly inflatedPulmonary vascular congestion:• venous congestionLethargy:• mutants quickly become lethargic after birthLiver vascular congestion:• venous congestion|Normal|Mixed|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|Unknown||Homozygous x Homozygous|No|06-Mar-2014|Cryopreserved sperm|50.0|0.0|Unknown||Tyrosine kinase, axon, atrial septa, atrioventricular endocardial cushions, hypoplastic, migration|No| 5676.0|Cd19.Cre (B6.129P2�-Cd19/J)||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5677.0|CD1d -/-||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5678.0|CD45.2 ||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5679.0|CD88 and C3aR||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5680.0|Cd88xCD1 (C5aR x CD1)||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5681.0|CDx2||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5682.0|Cep55-MMTV-cCe||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5683.0|CFP||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5686.0|ChAT-EGFP||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5688.0|CISH KO||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5689.0|CITED 2||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5690.0|Clone 5.9||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5691.0|Clone 741-304 B||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5692.0|CMV||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5702.0|Crim1 Flox CD1 ||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5703.0|Crim1 Flox:HoxB7GFP||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5704.0|Crim1 Flox/Pod-Cre||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5705.0|Crim1 FloxC57 TRANSGELIN-Cre||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5706.0|Crim1 KST264 C57||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5707.0|Crim1 KST264 CD1||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5708.0|Crystallin-MMTV-Cre||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5709.0|Ctsq-Cre||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5710.0|CX3 CR1||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5711.0|CX3 CR1 and C57||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5712.0|Cx3cr1; Cx3cr1-GFP||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5721.0|DBX1CreRosa26||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5722.0|DCC||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5726.0|DCX DTR (TOM)||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5727.0|DCX-EGFP/Gensat||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5728.0|Deb Black NesCreERT2||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5729.0|Dectin-1 KO Balb/C||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5730.0|Dectin-1 KO C57||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5733.0|DEREG||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5734.0|DHD||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5735.0|Dicer,Flox,Math1,CRE||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5736.0|DMRT||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5737.0|Donkey pZAP||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5738.0|DR4 DQ3||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5739.0|DS Zred||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5745.0|E2F8-/- (295/09)||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5746.0|E7TCR269||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5759.0|ENU6WTNIH (Eddie)- Strains grouped ||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5762.0|Epha4 KO||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5765.0|EphA4KO/129x1/SVj||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5766.0|EphA4Ko/129x1SVj||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5767.0|EPHA4Loxp||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5768.0|Epha4loxp/Emx1Cre||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5771.0|EYFP||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5772.0|EYFP Ptch1 c/c C57||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5769.0|Estella||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5770.0|ExtraToes||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5773.0|F1B-GFP||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5774.0|F2 MIR 202 GFPCre||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5775.0|FAB Cre ||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5779.0|Fgf8floxC57||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5781.0|Fgf8FloxC57/Rosa26/Emx1Cre||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5783.0|FGF8FloxC57/Rosa26EGFP/NesCreERT2||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5786.0|FgFr2 flox flox||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5787.0|Flox Flox||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5789.0|Fox 03 STAG||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5790.0|FOXP3-DTR||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5791.0|Francois C57||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5792.0|FVBN||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5793.0|G8C9||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5794.0|GAD 67||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5797.0|Gal4 Robin (C57)||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5798.0|GBx2||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5799.0|Gbx2 -mCherry||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5800.0|Genia||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5802.0|GFAP cre x C57||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5803.0|GFAP Cre, B6, Balb/c||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5804.0|GFAP Cre: Ptc1||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5805.0|Gfap-EGFP||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5810.0|GHR Box 1 ||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5811.0|GHR Null||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5812.0|GHRH-GFP||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5813.0|GHRH-GFPxC57BL/6||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5814.0|GKLF||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5816.0|GolliTau/NF1B||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5817.0|Gorgo (green)||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5818.0|Gregory C57||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5819.0|GsH2Cre-Rosa26||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5820.0|HAA Cre ||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5822.0|HBP 1 LacZ||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5825.0|Hes/Hey||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5826.0|Hes/Hey Cond||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5827.0|Hes/Hey Ptc1cond||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5828.0|Hes5 Aging||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5829.0|Hes5 Stock||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5830.0|Hes5-EGFP||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5833.0|HIT B6 A||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5831.0|HGT||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5832.0|HIT 391||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5834.0|Hopscotch||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5835.0|HoxB7 GFP||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5837.0|Hugo x CMV cre||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5838.0|Hugo x NestinCre||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5839.0|Hugo/ChatCre||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5841.0|ICE -/-||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5842.0|ICE -/-xC57BL/6||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5843.0|iDTR||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5844.0|iDTR/NesCreERT2||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5845.0|IfitmDel (MDAA) ||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5849.0|IFR7/3,IFR7-/-,IFR3/7-/-,IFR3-/-||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5850.0|IL-23R KO||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5851.0|IL-4 -/-||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5852.0|IL17-/-.C57||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5853.0|IRF3||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5854.0|IRF3-7||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5855.0|IRF7||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5856.0|Ja18-/-||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5857.0|K14Cre ||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5858.0|K14Cre; Sox9; Ptc1||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5859.0|K14Cre:Ptc1/Ptc2||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5860.0|K14Cre.FVB||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5861.0|K14E6.FVB||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5862.0|K14E7.C57||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5863.0|K14E7.C57 x IL17-/-.C57 F1||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5864.0|K14E7.C57 xCD11cDTR||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5867.0|K14hGH023.C57||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5868.0|K15 Cre PRG1||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5869.0|K5Cre||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5872.0|Kamu||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5873.0|KLF4 LOXP||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5874.0|KoAgc||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5875.0|KoagD||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5876.0|KoGeph||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5877.0|Kogeph x Komusk||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5878.0|KoMusk||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5879.0|KoRap||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5880.0|Kosla||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5881.0|KRT 14||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5882.0|KRT14 Cre x Caggsbow||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5883.0|Lavinia C57||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5884.0|Lawrence ||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5885.0|Lifeact-GFP||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5887.0|Lox-Stop-OVA - WEHI - F600||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5888.0|Lox-Stop-OVA WEHI F500 x CD19Cre||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5889.0|Lox.stop.OVA F500||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5892.0|Ly5.1 Tea x Balb/c ||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5893.0|Ly5.1 Tea x Ly5.1||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5894.0|Ly5.1 x TEa ||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5896.0|LysMCre||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5897.0|M72-GFP||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5898.0|Macblue ||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5899.0|Macgreen||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5901.0|Madu (Orange)||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5903.0|Mafia x C57 ||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5904.0|Math 1 GFP||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5905.0|MBP DTR 100A||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5907.0|McBride (Myd88-/-)||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5908.0|Mcx1Hb9-Cre||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5909.0|MDX||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5913.0|Mincle||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5914.0|MMTVCre||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5915.0|MNB||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5916.0|MNB.Clec4e||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5917.0|MNB.Clec4e x BALB/c ||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5918.0|Moody||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5919.0|Mortlock||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5920.0|Mulberry||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5921.0|MYBFLOX||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5923.0|N/C-Mcy||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5924.0|Nas1 ||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5925.0|Nas1 C57||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5926.0|Nas1 mixed||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5927.0|Neo -C57Bl/6||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5930.0|NesCreERT2||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5932.0|Nestin GFP (PN18)||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5953.0|NXAT x Emx1Cre||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5954.0|Ob/Ob ||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5955.0|OCT 4 Cre||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5956.0|OCT 4 GFP||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5957.0|Oct4 Cre||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5958.0|OIM||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5959.0|OIM Hom x Hom ||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5960.0|OMP-AIF Zsgreen||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5961.0|OMP-BIM3Zsgreen||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5963.0|OSMR-1-||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5965.0|Otx2 flox/flox||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5966.0|P19||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5967.0|P2-LacZ||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5968.0|P35||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5969.0|P40||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5970.0|P53HetBrca1WT (P53 Het)||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5971.0|Par2+/- Rag1-/-||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5972.0|Parvalbumin (Balb/C)||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5973.0|Parvalbumin (C57)||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5974.0|ParvCre||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5976.0|PCX: kik||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5977.0|pDC-DTR (Sonny Bill)||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5978.0|Peach ||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5979.0|Petra C57||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5980.0|Phr 1||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5981.0|Pik3cd||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5982.0|Pod Flox Flox||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5983.0|Pod Rosa||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5984.0|PRL||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5985.0|PRLR||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5986.0|Prox 1 GFP||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5987.0|PRX 1 Cre||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5988.0|Prx1Cre; Ptc||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5989.0|Prx1Cre/Ptch1||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5990.0|PTc Cond||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5991.0|PTC Cond, Balb/c||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5992.0|Ptc1 c/c C57||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5993.0|Ptc1 LacZ||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5994.0|Ptc1/Ptc2||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5995.0|Ptch 1 Balbc||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5996.0|Ptch 1 c/c C57||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5997.0|Ptch 1 Cond Neo||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5998.0|Ptch 1 Rosa||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5999.0|Ptch1 c/c stock||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6000.0|PTPRCA||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6001.0|PTRF||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6002.0|PTRF - null ||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6003.0|PTRF/Cavin/Trog-1-KO||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6004.0|PVALB||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6005.0|pZAP||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6006.0|QB GFP linked ||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6007.0|R26R Flox/Flox||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6008.0|R6/1 Huntingtons||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6009.0|R61(Huntington)/CBB6/F1 ||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6010.0|Rac2 ||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6011.0|Rag-1||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6012.0|RAG1 x BALB/c||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6013.0|Rag1KO; Rag1-/-||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6014.0|RaOpB6 & RaOpDBA ||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6015.0|RaOpxC57||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6016.0|RB flox/flox||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6017.0|RB x CMV||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6018.0|RBP-J Cond||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6020.0|RelBdel||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6021.0|RelbKO||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6022.0|RKO 129||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6023.0|RKO 44||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6024.0|RKO129Ludwig||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6025.0|Rob1Dulox/DccKanga||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6028.0|Robo1LoxPC57||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6032.0|Rolfe - Balb/c (493/09)||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6033.0|Rolfe - C5aR Het (493/09)||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6034.0|Rolfe - MacGreen (712/08)||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6035.0|Rolfe/Cheng - APOE (414/09)||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6036.0|Rolfe/Mooney - C57BL/6J (712/08)||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6037.0|RORg-loxP||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6038.0|Rosa||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6039.0|Rosa 26||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6040.0|Rosa/Pct1 c/c||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6041.0|ROSA26||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6042.0|ROSA26-eGFP-DTA||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6043.0|ROSA26A-EGFP||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6044.0|ROSA26A-EGFP x CD-1||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6045.0|RP105-/-||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6046.0|rtTA-Nagy||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6047.0|SAD ||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6048.0|Sat1||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6049.0|Sat1 C57||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6050.0|Satb2Cre x CD1||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6051.0|Schlafen Fuzzy||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6052.0|Sez 6||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6053.0|Sez6 C57||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6054.0|SF1-GFP||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6055.0|SFI-GFP (Homo x B6)||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6056.0|Sirt/NestinCreCROSS||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6057.0|Sirt1||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6058.0|Sirt1/NesCreERT2||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6059.0|Sirt1/NesCreERT2 x Sirt1/NesCreERT2||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6060.0|Sirt1/NesCreERT2Cross||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6061.0|Sirt1/NestinCre||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6062.0|Sirt1xSirt1/NestinCre||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6063.0|Six 2 EGFP||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6064.0|Six 2 x CD1||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6065.0|SIX TGC||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6066.0|Six2 Flox/Flox||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6067.0|Six2/ZRed||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6068.0|SJL||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6069.0|SKG ||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6070.0|SKG x FoxP3DTR ||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6071.0|Ski tm1 ||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6072.0|SLD ||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6074.0|Slit1/3||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6076.0|Slit2C57||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6077.0|Slit3||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6078.0|Slit3C57||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6079.0|Slp1 KO||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6080.0|SMO + Six TGE||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6081.0|SOD 1||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6082.0|SOD 1 x C5L2 KO||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6083.0|SOD 1 x Thyl-YFP||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6084.0|SOD1*G93A||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6085.0|SOD1/C3aR||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6086.0|SOD1/C5aR||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6087.0|SOD12Gur||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6088.0|SOD1G93A1Gur||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6089.0|Sortilin 25||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6090.0|Sortolin1/Sort1||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6091.0|SOST Tg||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6092.0|Sox 9 Flox||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6093.0|Sox 9 Ptch 1||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6094.0|SOX Cre||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6095.0|Sox18-/-&mix ||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6096.0|Sox9/Ptc1||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6097.0|Spring||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6098.0|SRY 5.7||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6099.0|SRY 741-302B||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6100.0|SRY Clone 18.1||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6101.0|SRY clone 18.2||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6102.0|SRY, Stu1 #3||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6103.0|SRY49,29||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6104.0|SrySal1 ||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6105.0|Staggerer (blue)||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6106.0|Stat 5||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6107.0|Stra 8 1.4 clone 205||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6108.0|Stra 8 2.5 clone C108||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6109.0|Stra 8 2.5 clone D103||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6110.0|Stra 8.1.4||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6111.0|Stra 8.1.5||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6112.0|Stu2||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6113.0|Super16TOPFLASH x C57||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6114.0|Super16Topflash x RaOp||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6115.0|T Crim||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6116.0|T-Wimp||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6117.0|T/Z Crim||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6118.0|Tagln - Cre||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6119.0|TARD||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6120.0|TARDBP||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6121.0|TdTomato/Emx1CreERT2||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6122.0|Tea||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6123.0|Teague||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6124.0|Teague KO x Genia KO||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6125.0|teaxptprca||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6126.0|Tet0-NFIB2||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6127.0|Teto- Nf1En/trta-nagy||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6128.0|Teto-Nf1B2/rtta-nagy||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6129.0|Tg Rare-LacZ||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6130.0|Tg(Appswe,PSEN1De9)85Dbo/J||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6131.0|Tg(Emx1-EGFP)||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6132.0|Tg(Gfap-EGFP)||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6133.0|Tg(Thy-1-CFP)||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6134.0|Tg(Thy-1-YFPG)||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6135.0|TgEpha4 GFP||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6136.0|Thy1 YFP||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6137.0|Thy1-CFP||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6138.0|Thy1CFP x Sod1||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6139.0|Thy1YFP x Sod 1||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6140.0|Tie-1 ||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6141.0|Tie2 One||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6142.0|TINDALL||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6143.0|Tindall N10||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6144.0|TLR2/RP105-/-||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6145.0|TLR4||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6146.0|TLR9||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6147.0|TNF?ARE||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6148.0|TNF?ARE X ERAP||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6149.0|Tom DCX-DTR||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6150.0|Tomato||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6151.0|Tomato/Satb2Cre||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6152.0|Topflash ||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6153.0|Topflash x C57 ||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6154.0|TP3||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6155.0|Trans Cre Flox||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6156.0|Transgelin Rosa||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6157.0|Tubbs-EGFP||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6158.0|Tubbs3 ||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6159.0|Tubbs3 EGFP||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6160.0|TVA||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6161.0|TVA x TYR CRE||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6162.0|TVM ||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6163.0|TVU||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6164.0|Twinkle toes||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6165.0|TWT||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6166.0|Twt (FVB)||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6167.0|Tyr Cre/ C57BL6||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6168.0|Tyr Cre/ Ptc1 C57||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6169.0|TYR-CRE||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6170.0|Vamp8 ||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6171.0|VEGFD||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6172.0|Vgat||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6173.0|Vgat x Komusk||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6174.0|Wdr19||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6175.0|We +/- ||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6176.0|Wnt1 Cre C57||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6177.0|Wnt1 Cre/Ptc1 Mix||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6178.0|Wnt1-Cre||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6179.0|Wnt1-Cre R26R||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6180.0|Wnt5a||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6181.0|Wnt5atm/Amc/J||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6182.0|WT1-MIR 202||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6183.0|Z Crim||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6184.0|Z/AP||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6185.0|Z/Red||||||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 5360.0|NOD.hCD4.IAE.303-4 ; NOD triple 303|NOD-H2 Tg(Cd4-CD4)2362Litt Tg(HLA DR3-DQ2)303/Apb||Dominant|histocompatibility-2, MHC|H2|Nil|H-2, MHC-II|MGI:95894|histocompatibility-2, MHC; targeted deletion, H2 complex|H2|MGI:2658725|17||||||||||||||||No|human leukocyte antigen class II||||||||||||Expression of HLA DR and DQ evident on B cells, dendritic cells and a proportion of macrophages.These mice Tg for hCD4.DR3-DQ2.MHCII<Δ/Δ> express functional HLA-DR3 and DQ2 molecules that mediate thymic selection generating Ag-specific CD4<+> T cell immunity. Although about one in five Europeans homozygous for HLA-DQ2 develops celiac disease, homozygous and heterozygous hCD4.DR3-DQ2.MHCII<Δ/Δ> Tg mice do not spontaneously develop hypersensitivity to gluten. However, standard immunization protocols do produce HLA-DQ2-restricted CD4+ T cells in hCD4.DR3-DQ2.MHCII<Δ/Δ> Tg mice that preferentially recognize the deamidated α-gliadin 17-mer immunodominant in human celiac disease. Nevertheless, we have found that preexisting DQ2-restricted CD4<+> T cell immunity to deamidated α-gliadin 17-mer in hCD4.DR3-DQ2.MHCII<Δ/Δ> Tg mice is not sufficient for gluten ingestion to cause measurable intestinal pathology.On the NOD background mice immunised with gliadin and co-injected with pertusis toxin remained healthy.||NOD|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|21-Dec-2010|Cryopreserved sperm|50.0|0.0|Unknown||MHC, B cell, selection, autoimmunity, celiac disease|Yes| 5360.0|NOD.hCD4.IAE.303-4 ; NOD triple 303|NOD-H2 Tg(Cd4-CD4)2362Litt Tg(HLA DR3-DQ2)303/Apb||Dominant||||||||||||||||||||||||||transgene insertion 2362, Dan R Littman|murine Cd4 and human CD4|equivalent to human CD4+ cells||||||||||Expression of HLA DR and DQ evident on B cells, dendritic cells and a proportion of macrophages.These mice Tg for hCD4.DR3-DQ2.MHCII<Δ/Δ> express functional HLA-DR3 and DQ2 molecules that mediate thymic selection generating Ag-specific CD4<+> T cell immunity. Although about one in five Europeans homozygous for HLA-DQ2 develops celiac disease, homozygous and heterozygous hCD4.DR3-DQ2.MHCII<Δ/Δ> Tg mice do not spontaneously develop hypersensitivity to gluten. However, standard immunization protocols do produce HLA-DQ2-restricted CD4+ T cells in hCD4.DR3-DQ2.MHCII<Δ/Δ> Tg mice that preferentially recognize the deamidated α-gliadin 17-mer immunodominant in human celiac disease. Nevertheless, we have found that preexisting DQ2-restricted CD4<+> T cell immunity to deamidated α-gliadin 17-mer in hCD4.DR3-DQ2.MHCII<Δ/Δ> Tg mice is not sufficient for gluten ingestion to cause measurable intestinal pathology.On the NOD background mice immunised with gliadin and co-injected with pertusis toxin remained healthy.||NOD|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|21-Dec-2010|Cryopreserved sperm|||Unknown||MHC, B cell, selection, autoimmunity, celiac disease|Yes| 7397.0|ENU23:037:DRD2:B6|C57BL/6NCrl-Drd2/AnuApb||Recessive|dopamine receptor D2|Drd2||D2R, D2 receptor, Drd-2|MGI:94924|dopamine receptor D2, mutation 1 Australian National University|||9|ENSMUSG00000032259|ENSMUST00000075764|Drd2-201|143|237|T to C|ENSMUSE00000462498|2|48|Isoleucine to Threonine|||||CATGCTGCTCACCCTCCTCATCTTTATCATCGTCTTTGGCAATGTGCTGGTGTGCATGGCT||||||||||||||Unknown||C57BL/6NCrlAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|16-Aug-2013|Cryopreserved sperm|37.0|0.0|Unknown||ENU, receptor|Yes| 7403.0|Cre-ERT2|B6.129-Gt(ROSA)26Sor/AusbAnu||Dominant|gene trap ROSA 26, Philippe Soriano|Gt(ROSA)26Sor |Unknown|Gt(ROSA)26Sor, R26, Rosa26|MGI:104735|gene trap ROSA 26, Philippe Soriano; targeted mutation 1, Tyler Jacks |Gt(ROSA)26Sor|MGI:3699244|6|||||||||||||||||||||||||||||Non tamoxifen treated animals are viable, fertile and are slightly smaller than wild-type controls|No apparent phenotype|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|20-Aug-2013|Cryopreserved sperm|74.0|0.0|Yes||Cre recombinase, R26-CreERT2|Yes| 63.0|Polly|B6JSfdAnu;NODAnu-Nphp3/AnuApb|B6JSfdAnu;NODAnu-Nphp3/AnuApb|Recessive|nephronophthisis 3 (adolescent)|Nphp3|Nil|nephrocystin 3, pcy|MGI:1921275|polly|Nphp3|MGI:3847130|9|ENSMUSG00000032558|ENSMUST00000116516|Nphp3-202|1319|1496|T to A|ENSMUSE00000220789|8|441|Valine to Glutamic acid|||||AGAGGGAGTGTGTAAGATTTACGTGGGTGTGGAAAAGATTATTAAACAGGACATCCTTGGC|No|||||||||||||Juvenile polycystic kidney disease, brain defects: exencephaly. Homozygous mutant mice display slowly progressing kidney cysts, enlarged kidneys, increased blood urea nitrogen, kidney inflammation and associated fibrosis, and premature death.||C57BL/6JSfdAnu x NOD|Yes|No|Yes|Yes|No|Yes|Yes|Good|6|||No|06-Feb-2006|Cryopreserved sperm|102.0|0.0|Unknown||kidney, exencephaly, polycystic, juvenile, ENU|Yes| 7400.0|Ins2-Cre|B6.Cg-Tg(Ins2-cre)25Mgn/JAusb||Dominant||||||||||||||||||||||||||transgene insertion 25, Mark A Magnuson |rat insulin promoter (Ins2)|9 copies||||||||||Expression of Cre recombinase in pancreatic beta cells and hypothalamus.|Expression of Cre recombinase in pancreatic beta cells and hypothalamus.|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|16-Aug-2013||0.0|0.0|Unknown||Cre recombinase, islet|Yes| 7402.0|Mb1-creERT2|B6.129-Cd79a/RethAnu||Dominant|CD79A antigen (immunoglobulin-associated alpha)|Cd79a|Unknown|Cd79a, Iga, Igalpha, Ig alpha, Ig-alpha, Ly54, Ly-54, mb-1|MGI:101774|CD79A antigen (immunoglobulin-associated alpha); targeted mutation 3, Michael Reth|Cd79a|MGI:5568505|7||||||||||Unknown to Unknown|||||||||||||||||||||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|20-Aug-2013|Cryopreserved sperm|44.0|0.0|Unknown||B cell, Cre recombinase, inducible|Yes| 7401.0|Senp2 Gt|B6;C3-Senp2/RbrcAnu||Recessive|SUMO/sentrin specific peptidase 2|Senp2|Unknown|2310007L05Rik, 4930538C18Rik, mKIAA1331|MGI:1923076||||16|||||||||||||||||||||||||||||Unknown||C57BL/6|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|20-Aug-2013||0.0|0.0|Unknown|||Yes| 7398.0|tagap|B6.Cg-TagapAusb||Recessive|T cell activation Rho GTPase activating protein|Tagap|Nil||MGI:3615484|T cell activation Rho GTPase activating protein; targeted mutation 1, Bernhard G Herrmann|Tagap|MGI:3603008|17|||||||||||||||||||||||||||||||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|16-Aug-2013||0.0|0.0|Unknown||t-complex, GTPase|Yes| 7399.0|Alk5loxp|B6.129P2-Tgfbr1/UscAusb||Recessive|transforming growth factor, beta receptor I|Tgfbr1|Normal|Alk-5, ALK5, TbetaRI, TbetaR-I|MGI:98728|transforming growth factor, beta receptor I; targeted mutation 1.1, Stefan Karlsson|Tgfbr1|MGI:2680164|4|||||||||||||||||||||||||||||Normal||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|16-Aug-2013||0.0|0.0|Unknown||angiogenesis, TGF|Yes| 7396.0|FoxP3-cre|B6.129X-Foxp3/StvAnuApb||Dominant|forkhead box P3|Foxp3||JM2, scurfin|MGI:1891436|forkhead box P3; targeted mutation 4, Alexander Y Rudensky|Foxp3|MGI:3790499|X|||||||||||||||||||||||||||||Normal||C57BL/6|Yes|Yes|Yes|Yes|Yes|Unknown|No|Unknown||||No|14-Aug-2013|Cryopreserved sperm|80.0|0.0|Unknown||T cell, Cre recombinase, Foxp3|Yes| 8719.0||TRAIL-R-flox||Recessive|Tnfrsf10b|||||TRAIL-R-flox||||||||||||||||||||||||||||||||Normal|Normal|C57BL/6|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|28-May-2019||0.0|0.0|Unknown|||Yes| 7407.0|P110-Tg|C57BL/6-Gt(ROSA)26Sor/JAnuapb||Dominant|gene trap ROSA 26, Philippe Soriano|Gt(ROSA)26Sor||beta geo, Gtrgeo26, Gtrosa26, R26, ROSA26|MGI:104735|gene trap ROSA 26, Philippe Soriano; targeted mutation 7, Klaus Rajewsky|Gt(ROSA)26Sor|MGI:4430527|6|||||||||||||||||||||||||||||Unknown||C57BL/6JAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|22-Aug-2013|Cryopreserved sperm|32.0|0.0|Unknown||B cell|Yes| 7406.0|ENU22 Bcl2:019:a|ANU:ENU22 Bcl2:019:a||Recessive|Unknown||||||||Unknown|||||||||||||||||||||||||||||Low CD4's, increased CD25's and CD44hi|Unknown|C57BL/6NCrlAnu|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|21-Aug-2013|Cryopreserved sperm|50.0|0.0|Unknown||ENU, mutagenised|No| 7690.0|Id3lox|B.129S6(Cg)-Id3/JAusb||Recessive|inhibitor of DNA binding 3|Id3|Normal|bHLHb25, HLH462, Idb3|MGI:96398|inhibitor of DNA binding 3; targeted mutation 2.1, Yuan Zhuang|Id3|MGI:5009711|4|||||||||||||||||||||||||||||Normal||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|22-May-2014||0.0|0.0|Yes|Sjögren's syndrome|T cell, B cell|Yes| 5216.0|Lyn -/-|B6;129P2-Lyn/LudApb|B6;129P2-Lyn|Recessive|Yamaguchi sarcoma viral (v-yes-1) oncogene homolog|Lyn|Nil|Hck-2|MGI:96892|Yamaguchi sarcoma viral (v-yes-1) oncogene homolog; targeted mutation 1, Ashley R Dunn|Lyn|MGI:2157129|4||||||||||||||||No|||||||||||||Peritoneal inflammation: there is about a doubling in the number of T cells found in the peritoneum.Increased T cell number: there is about a doubling in the number of T cells found in the peritoneum.Abnormal B cell morphology: B cells express lower levels of CD21 and higher levels of CD23 on the cell surface compared to controls.Decreased transitional stage B cell number: profound reduction in transitional stage-2 B cells.Decreased follicular B cell number: about a five-fold reduction in follicular B cells.Decreased marginal zone B cell number: profound reduction in marginal zone B cells.Abnormal B cell activation: * significant expression of MHCII complexes by circulating B cells suggest these B cells are in an activated state. * B cells have enhanced calcium flux upon activation.Abnormal myelopoiesis: * myelopoiesis is greatly enhanced in these mice. * there is a significant increase in the number of colonies generated by bone marrow cells or splenocytes in response to in vitro culturing with GM-CSF, M-CSF, or IL-3.Spleen hypoplasia: spleen cellularity is reduced by more than half due to B cell lymphopenia.Increased anti-nuclear antigen antibody level: auto-antibodies of the IgA, IgG IgM classes develop as the mice age.Increased anti-double stranded DNA antibody level: mice develop anti-DS DNA IgG antibodies as they age with high levels detectable in all mice by 20 weeks of age.Glomerulonephritis: * all mice have immunoglobulin complex deposition in the kidney by 8 weeks of age. * 83% of mice also have C3 complement deposition in the kidney. * severe glomerulonephritis occurs in these mice by one year of age.Increased basophil cell number: in cervical and inguinal lymph nodes and spleen.Increased mast cell number: in the peritoneum.Increased neutrophil cell number: mice exhibit decreased platelet numbers that becomes more pronounced with age (at 6 to 8 weeks in peripheral blood, 1089+/-242 per ul compared to 609+/-207 per ul in wild-type mice; at 52 to 58 weeks in peripheral blood, 2540+/-1050 per ul compared to 1264+/-434 per ul in wild-type mice).Decreased platelet cell number.Extramedullary hematopoiesis: * red and white pulp are often replaced with of red and white pulp with myelomonocytic cells that are often centers of extramedullary hematopoiesis. * myelomonocytic cells often accumulate in other organs and on the surface of the ears, tails and legs.Decreased spleen red pulp amount: red and white pulp are often replaced with myelomonocytic cells that are often centers of extramedullary hematopoiesis.Enlarged spleen: * mice develop age-dependent splenomegaly * 20% of mice greater than 1 year of age exhibit severe splenomegaly with partial to complete replacement of red and white pulp with myelomonocytic cells that are often centers of extramedullary hematopoiesis.Decreased spleen white pulp amount: red and white pulp are often replaced with myelomonocytic cells that are often centers of extramedullary hematopoiesis.Abnormal circulating complement protein level: increased circulating immune complexes reactive to complement component 1 q.Abnormal level of surface class II molecules: basophils show high MHC II expression.Increased IgA level.Increased IgE level.Increased IgG2b level.Increased IgM level.Increased anti-nuclear antigen antibody level: of IgE isotype.Increased anti-double stranded DNA antibody level: of IgE isotype.Young mice are apparently healthy, but they start to show signs of autoimmune disease at >12 wks of age. The disease resembles the human condition systemic lupus erythematosus (SLE). The mice develop serum anti-nuclear antibodies and acquire crescentic glomerulonephritis due to immune complex deposition in kidney, leading to renal dysfunction. They show hematologic disorders such as lymphopenia and thrombocytopenia, and they develop lymphadenopathy and splenomegaly. They develop inflammatory lesions in multiple organs including skin, lung and kidney, and occasionally we observe neurologic disorders such as seizures and hind limb paralysis. Similar to SLE patients, the mice also have hyperactive B lymphocytes.||C57BL/6 x 129|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|||Hom x Hom|No|13-Sep-2010|Cryopreserved sperm|50.0|0.0|Yes|Systemic Lupus Erythematosus; SLE|B cell, immunoglobulin, spleen, kinase, signal transduction, src family, autoimmunity, lymphocyte|Yes| 7408.0|Ikk2ca-Tg|C57BL/6-Gt(ROSA)26Sor/JAnuApb||Dominant|gene trap ROSA 26, Philippe Soriano|Gt(ROSA)26Sor||beta geo, Gtrgeo26, Gtrosa26, R26, ROSA26|MGI:104735|gene trap ROSA 26, Philippe Soriano; targeted mutation 4, Klaus Rajewsky|Gt(ROSA)26Sor|MGI:3687199|6|||||||||||||||||||||||||||||Unknown||C57BL/6JAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|22-Aug-2013|Cryopreserved sperm|30.0|0.0|Unknown||B cell|Yes| 7405.0|ENU23 Bcl2:036:a|ANU:ENU23 Bcl2:36:a||Recessive||||||||||||||||||||||||||||||||||||||Low lymphocytes, no tregs and increased granulocytes|Unknown|C57BL/6NCrlAnu|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|21-Aug-2013|Cryopreserved sperm|60.0|0.0|Unknown||ENU, mutagenesis|No| 7404.0|TOMGREtg ; mT/mG|B6.129(Cg)-Gt(ROSA)26Sor/JAusbAnu||Dominant|gene trap ROSA 26, Philippe Soriano|Gt(ROSA)26Sor|Normal|beta geo, Gtrgeo26, Gtrosa26, R26, ROSA26|MGI:104735|gene trap ROSA 26, Philippe Soriano; targeted mutation 4, Liqun Luo|Gt(ROSA)26Sor|MGI:3716464|6|||||||||||||||||||||||||||||Normal|Unknown|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|20-Aug-2013|Cryopreserved sperm|46.0|0.0|Unknown||Cre/loxP, Mutagenesis, tomato|Yes| 7412.0|ENU27:007:ETS1|C57BL/6NCrlAnu-Ets1/AnuApb|C57BL/6NCrlAnu-Ets1/AnuApb|Recessive|E26 avian leukemia oncogene 1, 5' domain|Ets1|Unknown|Ets-1, MGC:18571, p42Ets-1, p51Ets-1, Tpl1|MGI:95455|E26 avian leukemia oncogene 1, 5' domain; mutation 1, The Australian National University|Ets1|MGI:5563474|9|ENSMUSG00000032035|ENSMUST00000034534|Ets1-001|1001|1363|C to T|ENSMUSE00000537123|7|334|Proline to Leucine|||||TGCCCTGGCTGGCTACACAGGAAGTGGGCCGATCCAGCTGTGGCAGTTTCTTCTGGAATTA||||||||||||||Normal blood lymphocyte populations as measured by expression of following proteins: B220, CD3, C4, CD44, KLRG1, NK1.1, IgM, IgD by flow cytometry.||C57BL/6NCrlAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|23-Aug-2013|Cryopreserved sperm|29.0|0.0|Unknown||T cell, CD8, CD4, plasma cell|Yes| 7414.0|ENU23:005:ATG16L2:B6|C57BL/6NCrlAnu-Dclre1c/AnuApb|C57BL/6NCrlAnu-Dclre1c/AnuApb|Recessive|DNA cross-link repair 1C, PSO2 homolog (S. cerevisiae)|Dclre1c||9930121L06Rik, Art, Artemis|MGI:2441769||||2|ENSMUSG00000026648|ENSMUST00000061852|Dclre1c-001|284|371|T to A|ENSMUSE00001293954|4|95|Leucine to STOP|||||TGAAATTGAAACTCCTACGCAGATATCTTTAGTTGATGAGGCTTCGGGTGAGAAGGAAGAG||||||||||||||Lymphopenia||C57BL/6NCrlAnu|Yes|Unknown|Yes|Yes|Unknown|Yes|No|Unknown||||No|23-Aug-2013|Cryopreserved sperm|31.0|0.0|Unknown||T cell|Yes| 7413.0|ENU27:031:RAG1|C57BL/6NCrlAnu-Rag1/AnuApb|C57BL/6NCrlAnu-Rag1/AnuApb|Recessive|recombination activating gene 1|Rag1|Unknown|Rag-1|MGI:97848|recombination activating gene 1; mutation 1, The Australian National University|Rag1|MGI:5563427|2|ENSMUSG00000061311|ENSMUST00000078494|Rag1-001|2408|2502|A to C|ENSMUSE00000471535|2|803|Glutamic acid to Glycine|||||GCTTCACTGTGACATTGGCAATGCAGCTGAATTCTATAAGATTTTCCAGCTGGAGATAGGG||||||||||||||Lymphopenia||C57BL/6NCrlAnu|Yes|Unknown|Yes|Yes|Unknown|Yes|No|Unknown||||No|23-Aug-2013|Cryopreserved sperm|19.0|0.0|Unknown||T cell, B cell|Yes| 7418.0|ENU22::NFATc2|C57BL/6NCrlAnu-Nfatc2/AnuApb|C57BL/6NCrlAnu-Nfatc2/AnuApb|Recessive|nuclear factor of activated T cells, cytoplasmic, calcineurin dependent 2|Nfatc2|Unknown|NFAT1, NFAT1-D, NFATp|MGI:102463|nuclear factor of activated T cells, cytoplasmic, calcineurin dependent 2|Nfatc2|MGI:5563447|2|ENSMUSG00000027544|ENSMUST00000109184|Nfatc2-001|2283|2457|A to T|ENSMUSE00001264777|9|761|Proline to Arginine|||||GCCCTCTACCAGAGAAGCAAGAGCCTGAGTCCCGGCCTGCTGGGCTACCAGCAGCCGTCCC||||||||||||||Normal blood lymphocyte populations as measured by expression of following proteins: B220, CD3, CD4, CD44, KLRG1, NK1.1, IgM, IgD by flow cytometry.||C57BL/6NCrlAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|23-Aug-2013|Cryopreserved sperm|16.0|0.0|Unknown|||Yes| 7417.0|ENU27:043:ZFP644|C57BL/6NCrlAnu-Zfp644/AnuApb|C57BL/6NCrlAnu-Zfp644/AnuApb|Recessive|zinc finger protein 644|Zfp644|Unknown|1110068L01Rik, BM-005, D5Ertd689e, mKIAA1221, Zep-2|MGI:1277212|zinc finger protein 644; mutation 1, The Australian National University|Zfp644|MGI:5563394|5|ENSMUSG00000049606|ENSMUST00000112698|Zfp644-201||||||||106638637|2|||GCAAATCTACATTTTTGTTTTCCATTTTCTAGACTAAAGGTGTTAAATGATCTTGCCAAC||||||||||||||Normal blood lymphocyte populations as measured by expression of following proteins: B220, CD3, CD4, CD44, KLRG1, NK1.1, IgM, IgD by flow cytometry.||C57BL/6NCrlAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|23-Aug-2013|Cryopreserved sperm|16.0|0.0|Unknown|||Yes| 7416.0|ENU26:029:WDR89:B6|C57BL/6NCrlAnu-Wdr89/AnuApb|C57BL/6NCrlAnu-Wdr89/AnuApb|Recessive|WD repeat domain 89|Wdr89|Unknown|2600001A11Rik|MGI:1919588|WD repeat domain 89; mutation 1, The Australian National University|Wdr89|MGI:5563398|12|ENSMUSG00000045690|ENSMUST00000062370|Wdr89-201|428|524|A to T|ENSMUSE00000368540|2|143|Leucine to STOP|||||TGCAGAGAAAGTTGACGAGGATGCATTGTTGGTATTTTGGGATGCAAGGTTCACATCTCAG||||||||||||||Normal blood lymphocyte populations phenotype as measured by flow cytometry screen.Parameters tested-Expression of following proteins: B220, CD3, C4, CD44, KLRG1, NK1.1, IgM, IgD.||C57BL/6NCrlAnu|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||G3||No|23-Aug-2013|Cryopreserved sperm|15.0|0.0|Unknown|||Yes| 7618.0|SVS7 -/-|C57BL/6-Pate4||Semi-dominant|Prostate and Testes Expressed 4 (PATE4)|Pate4|Nil|9530004K16Rik, Pate-B, Svs7, SVS VII|MGI:1930790||||9|||||||||||||||||||||||||||||Display osteopenia - reduced bone volume in the femur and tibia at 3 months as assessed by microcomputed tomography.|Normal|C57BL/6J|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|11-Mar-2014|Cryopreserved sperm|50.0|0.0|Unknown|||No| 7427.0||SJL/J-Ank1/Apb|SJL/J-Ank1|Dominant|ankyrin 1, erythroid|Ank1|Unknown|Ank-1, pale|MGI:88024|ankyrin 1, erythroid; ASAM142817|Ank1||8|ENSMUSG00000031543|ENSMUST00000121802|Ank1-004|2992|3246|C to T|ENSMUSE00001296345|27|998|Glutamine to STOP|||||CTCGCATCACCTGCCGCCTCGTTAAGCCGCAGAAGCTGAACACGCCACCCCCACTGGCTGA||||||||||||||Pre and Perinatal mortality with Jaundice, enlarge spleen and fragmented red blood cells|Heterozygous mice display a microcytic anaemia with increase osmotic fragility and splenomegaly. |SJL/J|No|No|Yes|No|No|Yes|No|Good||||No|27-Aug-2013|Cryopreserved sperm|50.0|0.0|Yes|Hereditary spherocytosis|Hereditary spherocytosis, Malaria resistance, microcytosis, ENU|Yes| 7419.0|ENU27:G3|ANU:ENU27:G3||Recessive||||||||||||||||||||||||||||||||||||||Unknown|Unknown|C57BL/6NCrlAnu|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown|2|||No|26-Aug-2013|Cryopreserved sperm|150.0|0.0|Unknown||ENU, mutagenesis, screen, random|Yes| 7423.0||SJL/ASAM||Dominant|CXADR-like membrane protein|Clmp|Reduced||MGI:1918816||||9||||||||||Unknown to Unknown|||||||||||||||||||Unknown|The mice displays an harmonious growth retardation phenotype without other gross abrnomalities. The mice are viable and fertile.|SJL/J|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Good|3|||No|27-Aug-2013|Cryopreserved sperm|40.0|0.0|Unknown||growth retardation, ENU|Yes| 6624.0|TG2KI.B6|C57BL/6-Tgm2||Semi-dominant|transglutaminase 2, C polypeptide|Tgm2||G[a]h, protein-glutamine gamma-glutamyltransferase, TG C, TG2, TGase2, tissue transglutaminase, tTG, tTGas|MGI:98731||||2|||||||||||||||||||||||||||||||C57BL/6|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|19-Oct-2011||0.0|0.0|Unknown||Transgluatminase, Gh, G-protein, cross-linking|Yes| 7425.0||B6/Mrit-MRI95318|B6/Mrit-MRI95318|Dominant|unknown||Unknown||||||Unknown|||||||||||||||||||||||||||||Unknown|Heterozygous mice display an harmonious and transient growth retardation|C57BL/6|No|No|Yes|No|No|Yes|No|Good||||No|27-Aug-2013|Cryopreserved sperm|50.0|0.0|Unknown||growth retardation, ENU|Yes| 7426.0||B6/Mrit-MRI109059|B6/Mrit-MRI109059|Dominant|unknown||Unknown||||||Unknown|||||||||||||||||||||||||||||Unknown|Heterozygous mice display a growth retardation phenotype|C57BL/6|No|No|Yes|No|No|Yes|No|Good||||No|27-Aug-2013|Cryopreserved sperm|50.0|0.0|Unknown||growth retardation, ENU|Yes| 7422.0||SJL/J-Tfrc/Apb||Dominant|transferrin receptor|Tfrc|Reduced|2610028K12Rik, CD71, E430033M20Rik, Mtvr1, Mtvr-1, p90, TfR1, Trfr|MGI:98822||Tfrc/Apb||9|ENSMUSG00000022797|ENSMUST00000023486|Tfrc-001|676|816|A to G|ENSMUSE00000130499|6|226|Lysine to Glutamic acid|||||AGTCTCCCGAGGGTTATGTGGCATTCAGTAAACCTACAGAAGTTTCTGGTAAACTGGTCCA||||||||||||||Prenatal mortality (E15) with severe anaemia and fragmented red blood cells|Heterozygous mice display a microcytic anaemia with decrease osmotic fragility.|SJL/J|No|No|Yes|No|No|Yes|No|Good|5|||No|27-Aug-2013|Cryopreserved sperm|60.0|0.0|Yes|thalassaemia|red blood cells, microcytosis, anaemia, thalassaemia, ENU|Yes| 7424.0|Grhl2 flox|B6.129S1-Grhl2/Marp||Recessive|grainyhead-like 2 (Drosophila)|Grhl2|Normal|0610015A08Rik, BOM, Tcfcp2l3|MGI:2182543|grainyhead-like 2 (Drosophila); targeted mutation 3.1, Stephen M Jane|Grhl2|MGI:2182543|15|||||||||||||||||||||||||||||Normal|Normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Excellent|||fl/fl x fl/fl|No|27-Aug-2013||0.0|0.0|No|||Possibly| 7421.0||SJL/Mrit-TfrcApb||Dominant|transferrin receptor|Tfrc|Reduced|2610028K12Rik, CD71, E430033M20Rik, Mtvr1, Mtvr-1, p90, TfR1, Trfr|MGI:98822||||16|||||||||||||||||||||||||||||Prenatal mortality (E15) with severe anaemia and fragmented red blood cells|Heterozygous mice display a microcytic anaemia with decrease osmotic fragility.|SJL/J|No|No|Yes|No|No|Yes|No|Good|4|||No|27-Aug-2013|Cryopreserved sperm|50.0|0.0|Yes|thalassaemia|red blood cells, microcytosis, anaemia, thalassaemia, ENU|Yes| 6590.0|NOD.H2Z|NZO.NOD/Lt-(D17Mit61-H2-D)/Arc||Recessive|||||||||||||||||||||||||||||DNA segment, Chr 17, Massachusetts Institute of Technology 61|D17Mit61|||MGI:90852||||17|As per background strain||NZO|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|10|||No|29-Sep-2011|Embryo|0.0|0.0|Yes|Type 2 diabetes|diabetes, obesity, MHC, autoimmunity|Possibly| 6590.0|NOD.H2Z|NZO.NOD/Lt-(D17Mit61-H2-D)/Arc||Recessive|||||||||||||||||||||||||||||histocompatibility 2, D region|H2-D|||MGI:1933561||||17|As per background strain||NZO|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|10|||No|29-Sep-2011|Embryo|||Yes|Type 2 diabetes|diabetes, obesity, MHC, autoimmunity|Possibly| 6589.0|BALB/c-2|Nod/Lt.C-Idd5 Idd1 Ubash3a/Arc||Recessive|||||||||||||||||||||||||||||insulin dependent diabetes susceptibility 5|Idd5||Idd-5|MGI:96407|insulin dependent diabetes susceptibility 5; BALB/c|Idd5||1|As per background strain.||NOD/Lt|Yes|Yes|Yes|Yes|Yes|Yes|No|Excellent|3|||No|29-Sep-2011|Embryo|0.0|0.0|Yes|Type 1 diabetes|T1D, GWAS, diabetes|Possibly| 6589.0|BALB/c-2|Nod/Lt.C-Idd5 Idd1 Ubash3a/Arc||Recessive|||||||||||||||||||||||||||||insulin dependent diabetes susceptibility 1|Idd1||Idd-1|MGI:96400|insulin dependent diabetes susceptibility 1; BALB/c|Idd1||17|As per background strain.||NOD/Lt|Yes|Yes|Yes|Yes|Yes|Yes|No|Excellent|3|||No|29-Sep-2011|Embryo|||Yes|Type 1 diabetes|T1D, GWAS, diabetes|Possibly| 6589.0|BALB/c-2|Nod/Lt.C-Idd5 Idd1 Ubash3a/Arc||Recessive|||||||||||||||||||||||||||||ubiquitin associated and SH3 domain containing, A|Ubash3a||Sts-2, TULA|MGI:1926074|rs48725557-C|Ubash3a||17|As per background strain.||NOD/Lt|Yes|Yes|Yes|Yes|Yes|Yes|No|Excellent|3|||No|29-Sep-2011|Embryo|||Yes|Type 1 diabetes|T1D, GWAS, diabetes|Possibly| 7429.0|GHSR-eGFP|Swiss-Tg(Ghsr-EGFP)KZ65Gsat/Apb||Dominant||||||||||||||||||||||||||transgene insertion KZ65, GENSAT Project at Rockefeller University|GHSR|||||||||||Normal|Normal|Swiss|No|No|Yes|No|No|Yes|No|Good||||No|02-Sep-2013|Cryopreserved sperm|50.0|0.0|Unknown||GHSR, GFP|Possibly| 7692.0|Rag2-fl|C57BL/6-Rag2/JAusb||Recessive|recombination activating gene 2|Rag2|Normal|Rag-2|MGI:97849|recombination activating gene 2; targeted mutation 1, University of Cologne|Rag2|MGI:2654906|2|||||||||||||||||||||||||||||Normal|Normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|22-May-2014||0.0|0.0|Unknown||B cell, follicular|Yes| 7428.0|Spi6 conditional KO clone 8F|C57BL/6J-SerpinB98F/PibMarpApb||Dominant|serine (or cysteine) peptidase inhibitor, clade B, member 9|Serpinb9||ovalbumin, PI-9, Spi6|MGI:106603||||13|||||||||||||||||||||||||||||Normal|Normal|C57BL/6J|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|02-Sep-2013|Cryopreserved sperm|50.0|0.0|Unknown|||Yes| 8720.0|Tlr9 KO|B6.129-Tlr9/AnuApb||Recessive|toll-like receptor 9|Tlr9|Nil||MGI:1932389|toll-like receptor 9; targeted mutation 1, Shizuo Akira|Tlr9|MGI:2660562|9|||||||||||||||||||||||||||||Tlr9 KO mice have:Abnormal immune system physiology:*Response to LPS and CpG is completely abrogated. Impaired NK cell cytolysis: *No NK cell activation is observed following infection with L. infantum. Decreased interferon-alpha secretion: *Following infection with Leishmania baziliensis. *However, secretion could be restored by treatment with GU-rich ssRNA, a TLR7 ligand. Decreased interferon-beta secretion: *Following infection with Leishmania baziliensis. *However, secretion could be restored by treatment with GU-rich ssRNA, a TLR7 ligand. Decreased interleukin-12b secretion: *Following infection with attenuated yellow fever vaccine 17D (YF-17D), dendritic cells produce less IL-12p40 relative to wild-type mice. *Unlike in wild-type mice, IL-12p40 production from dendritic cells following infection with Leishmania infantum is indetectable. Decreased tumor necrosis factor secretion: *Following treatment with PbA(Plasmodium bergbei ANKA)-parasitized erythrocytes or LPS-stimulation, TNF secretion is reduced. Decreased susceptibility to experimental autoimmune encephalomyelitis: *Myelin oligodendrocyte glycoprotein injection results in delayed onset of disease, 17.9 days after injection rather than 15.9 days as in controls. *Fewer infiltrating foci in the spinal cord. Abnormal response to infection: *Following treatment with PbA (Plasmodium bergbei ANKA)-parasitized erythrocytes, mice have a partially decreased immune response in terms of TNF secretion and response to CpG. Decreased susceptibility to parasitic infection: *Resistant to cerebral malaria. *Reduced accumulation of hemozoin. *Less upregulation of TNF-alpha in Plasmodium infection.|Normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|Yes|Good|>10||heterozygote mating|No|30-May-2019|Cryopreserved sperm|72.0|0.0|Yes|||Yes| 6603.0|BXD-45|BXD45/RwwJArc||Recessive||||||||||||||||||||||||||||||||||||||Normal|Normal|C57BL/6J x DBA/2|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|||brother x sister|No|04-Oct-2011|Embryo|0.0|0.0|Unknown|||Possibly| 6610.0|BXD-22|BXD22/TyJArc||Recessive||||||||||||||||||||||||||||||||||||||Normal|Normal|C57BL/6J x DBA/2|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|||brother x sister|No|04-Oct-2011|Embryo|0.0|0.0|Unknown|||Possibly| 5058.0|Cauli ; ENU12B6:C3H:003|B6;C3H-Ift140/AnuApb|B6;C3H-Ift140/AnuApb|Recessive|intraflagellar transport 140 homolog (Chlamydomonas)|Ift140||mKIAA0590, Tce5, Wdtc2 |MGI:2146906 |cauli|Ift140|MGI:4458412|17|ENSMUSG00000024169|ENSMUST00000024983|Ift140-001|2564|3109|T to A|ENSMUSE00000551541|19|855|Isoleucine to Lysine|||||ACTGGAAGCCAGAGTGGCCATGCTGGCCATACAGCTGGGCATGCTGGAGGAGGCAGAACAA|Yes|||||||||||||Phenotype found in 13.5 dpc embryo. Phenotype is exencephaly, hind limb polydactyly, forelimbs have a mixture of polydactyly and oligodactyly and midfacial cleft.|Normal|C57BL/6 x C3H|No|No|Yes|No|No|Yes|No|Good||||No|02-May-2007|Cryopreserved sperm|60.0|0.0|Unknown||polydactyly, exencephaly, cleft, embryonic lethal, ENU|No| 7433.0|OG2tg|B6;CBA-Tg(Pou5F1-EGFP)2Mnn/Apb||Recessive||||||||||||||||||||||||||transgene insertion 2, Jeff Mann|promoter and distal enhancer of the POU domain, class 5, transcription factor 1, (Pou5fl)|||||||||||Viable, fertile, normal|Viable, fertile, normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|16-Sep-2013|Cryopreserved sperm|50.0|0.0|Unknown|||No| 5423.0|203.2 ; cTnI-G203S.2|C57BL/6-Tg(Myh6-TNNI3*G203S)2Chs/Apb||Dominant||||||||||||||||||||||||||transgene insertion 2, Christopher Semsarian|cardiac specific mouse αMHC promoter (alpha myosin heavy chain)|48% of endogenous||||||||||Unknown|Mice develop cardiac phenotype - hypertrophic cardiomyopathy. Onset age dependent upon the amount of transgene protein expressed.|C57BL/6|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Excellent|||Transgenic x non-transgenic sibs|No|08-Feb-2011|Cryopreserved sperm|45.0|0.0|Yes|Hypertrophic cardiomyopathy (HCM) is a primary disorder of the myocardium characterized by cardiac hypertrophy. The clinical course of HCM is variable, with inter- and intra-familial variations ranging from benign asymptomatic disease to a malignant phenotype with a high risk of cardiac failure or sudden cardiac death.|Hypertrophy, Cardiomyopathy, Calcium, Troponin I gene|Yes| 7434.0|Mink|B6.129S6-Kcne1/Apb||Dominant|potassium voltage-gated channel, Isk-related subfamily, member 1|Kcne1|Nil|Isk, MinK, nmf190|MGI:96673|potassium voltage-gated channel, Isk-related subfamily, member 1; targeted mutation 1, Dan M Roden|Kcne1|MGI:3040614|16|||||||||||||||||||||||||||||Lethal|Normal,fertile, viable|C57BL/6|No|No|Yes|No|No|Yes|No|Good||||No|16-Sep-2013|Cryopreserved sperm|50.0|0.0|Unknown||congenital long-QT syndrome, cardiac myocytes|No| 7437.0||C3;SJL/Mrit-MRI16436|C3;SJL/Mrit-MRI16436|Dominant|unknown||Unknown||||||Unknown|||||||||||||||||||||||||||||Unknown|Heterozygous mice display a slight growth retardation phenotype|SJL/J|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|19-Sep-2013|Cryopreserved sperm|50.0|0.0|Unknown||growth retardation, ENU|Yes| 7441.0|ENU24:011:Ngf:B6|C57BL/6NCrlAnu-Ngf/Apb||Recessive|nerve growth factor|Ngf|Unknown||MGI:97321|mutation 1, The Australian National University|Ngf||3|ENSMUSG00000027859|ENSMUST00000106925|Ngf-202|548|646|A to G|ENSMUSE00001274982|4|183|Histidine to Arginine|||||CCATGGTACAATCCCTTTCAACAGGACTCACCGGAGCAAGCGCTCATCCACCCACCCAGTC||||||||||||||Unknown||C57BL/6NCrlAnu|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|19-Sep-2013||0.0|0.0|Unknown||ENU|Yes| 6622.0|APN 118|C57BL/6N-Slc13a4/Marp||Recessive|solute carrier family 13 (sodium/sulfate symporters), member 4 |Slc13a4 |Unknown|9630060C05Rik, SUT-1, SUT1 |MGI:2442367 | solute carrier family 13 (sodium/sulfate symporters), member 4; targeted mutation 1a, Wellcome Trust Sanger Institute |Slc13a4tm1a(EUCOMM)Wtsi|MGI:4441655|6||||||||||||||||Yes|||||||||||||Unknown - Not bred to homozygocity |Normal |C57BL/6N|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|14-Oct-2011|Cryopreserved sperm|50.0|0.0|Unknown||ES cell|Yes| 6613.0|APN 114|CPT1c||Recessive|carnitine palmitoyltransferase 1c |Cpt1c ||9630004I06Rik, CPT I-C |MGI:2446526 ||||7|||||||||||||||||||||||||||||Unknown|Normal|C57BL/6J|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Excellent||||No|11-Oct-2011|Cryopreserved sperm|50.0|0.0|Unknown|||Possibly| 7431.0|APN 371|C57BL/6N-A Katna1MarpApb||Recessive|katanin p60 (ATPase-containing) subunit A1|Katna1 |||MGI:1344353 |katanin p60 (ATPase-containing) subunit A1; targeted mutation 1a, Wellcome Trust Sanger Institute |Katna1tm1a(KOMP)Wtsi|MGI:4458514|10|||||||||||||||||||||||||||||Unknown|Normal|C57Bl/6N|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|05-Sep-2013|Cryopreserved sperm|30.0|0.0|Unknown|||Possibly| 7619.0|R26 MUT-Hoxa1 ki|C57BL/6-Gt(ROSA)26Sor||Semi-dominant|gene trap ROSA 26, Philippe Soriano|Gt(ROSA)26Sor|Unknown|beta geo, Gtrgeo26, Gtrosa26, R26, ROSA26|MGI:104735|gene trap ROSA 26, Philippe Soriano; targeted mutation 3237, TaconicArtemis|Gt(ROSA)26Sor||6|||||||||||||||||||||||||||||Unknown|Unknown|C57BL/6|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Excellent||||No|18-Mar-2014|Cryopreserved sperm|50.0|0.0|Unknown|||Possibly| 7436.0||C3;SJL/Mrit-MRI16932|C3;SJL/Mrit-MRI16932|Dominant|unknown||Unknown||||||Unknown|||||||||||||||||||||||||||||Unknown|Heterozygous mice display a slight growth retardation phenotype|SJL/J|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|19-Sep-2013|Cryopreserved sperm|60.0|0.0|Unknown||growth retardation, ENU|Yes| 7438.0||C3;SJL/Mrit-MRI12512|C3;SJL/Mrit-MRI12512|Dominant|unknown||Unknown||||||Unknown|||||||||||||||||||||||||||||Unknown|Heterozygous mice display a slight growth retardation phenotype|SJL/J|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|19-Sep-2013|Cryopreserved sperm|50.0|0.0|Unknown||growth retardation, ENU|Yes| 7439.0||C3;SJL/Mrit-MRI9417|C3;SJL/Mrit-MRI9417|Dominant|unknown||Unknown||||||Unknown|||||||||||||||||||||||||||||Unknown|Heterozygous mice display a slight growth retardation phenotype|SJL/J|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|19-Sep-2013|Cryopreserved sperm|60.0|0.0|Unknown||growth retardation, ENU|Yes| 7440.0||C3;SJL/Mrit-MRI9434|C3;SJL/Mrit-MRI9434|Dominant|unknown||Unknown||||||Unknown|||||||||||||||||||||||||||||Unknown|Heterozygous mice display a slight growth retardation phenotype|SJL/J|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|19-Sep-2013|Cryopreserved sperm|50.0|0.0|Unknown||growth retardation, ENU|Yes| 7442.0|ENU22:SCIN:B6|C57BL/6NCrlANu-Scin/Apb||Recessive|Scinderin|SCIN|Unknown|adseverin|MGI:1306794|scinderin; mutation 1, The Australian National University|Scin|MGI:5570658|12|ENSMUSG00000002565|ENSMUST00000002640|Scin-001|1375|1495|G to T|ENSMUSE00000106304|10|459|Glutamine to Lysine|||||AACTGACCATGTCCGCGTTTCTGACTGTCCAGTTGGACCGGTCCCTTGGAGGGCAGGCTGT|Unknown|||||||||||||Unknown|Unknown|C57BL/6NCrlAnu|Yes|Unknown|Yes|Yes|Unknown|Yes|No|Unknown||G4||No|20-Sep-2013|Cryopreserved sperm|66.0|0.0|Unknown||ENU, random, mutagenesis, screen|Possibly| 7620.0||SJL/ASAM||Dominant|unknown|unknown|Reduced||||||Unknown|||||||||||||||||||||||||||||Unknown|Normal|SJL/J|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Good|5|||No|20-Mar-2014|Cryopreserved sperm|50.0|0.0|Unknown||ENU|Yes| 4798.0|ENU:G1 library|WEHI:ENU:G1||Dominant||||||||||||||||||||||||||||||||||||||Random induced point mutations.Library. Sperm and DNA stored||C57BL/6 x C3H x BALB/c ?|Yes|Yes|Yes|Yes|Yes|Yes|No|Excellent||||No|06-Sep-2009|Cryopreserved sperm|89736.0|0.0|Unknown||ENU, G1, next generation sequencing|Yes| 7326.0||SJL-Tfrc/Apb||Dominant|transferrin receptor|Tfrc||2610028K12Rik, CD71, E430033M20Rik, Mtvr1, Mtvr-1, p90, TfR1, Trfr|MGI:98822||Tfrc||16|ENSMUSG00000022797|ENSMUST00000023486|Tfrc-001|905|1045|A to T|ENSMUSE00001238795|8|302|Histidine to Leucine|||||TGTTGAGGCAGACCTTGCACTCTTTGGACATGCTCATCTAGGAACTGGTGATCCATACACA||||||||||||||Homozygous mice are not viable.|Microcytosis associated with erythrocytosis and normochromia|SJL/J|No|No|Yes|No|No|Yes|No|Good||||No|23-Apr-2013|Cryopreserved sperm|45.0|0.0|Unknown||microcytosis, ENU, transferrin|Yes| 7379.0|hairloss|C57BL/6-Frem2/Apb||Dominant|Fras1 related extracellular matrix protein 2|Frem2||6030440P17Rik, 8430406N05Rik, b2b1562Clo, my, ne|MGI:2444465||Frem2||3|ENSMUSG00000037016|ENSMUST00000091137|Frem2-201|3652|3923|A to T|ENSMUSE00000517528|1|1218|Isoleucine to Phenylalanine|||||ACATTCCCAGGGATGATCTAACGTTTACTATTACCCGGTTTCCAACTCACGGTCATGTCAT||||||||||||||The homozygous mice displays a patchy fur loss at 6 weeks old over the body without specific localisation and without specific phenotypic abnormalities.|The heterozygous mice displays a patchy fur loss at 6 weeks old over the body without specific localisation and without specific phenotypic abnormalities.|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|18-Jul-2013|Cryopreserved sperm|45.0|0.0|Unknown||Dermatology, Coat, patchy fur, ENU|Yes| 7452.0|Ghsr KO|C57BL/6-Ghsr/MarpApb||Dominant|Growth hormone secretagogue receptor|Ghsr|Nil|C530020I22Rik|MGI:2441906||||3|||||||||||||||||||||||||||||Normal|Normal|C57BL/6J|Yes|Yes|Yes|Yes|Yes|Yes|No|Excellent||||Yes|08-Oct-2013|Cryopreserved sperm|37.0|0.0|Unknown||growth hormone, homeostasis|No| 6807.0|Larry|SJL/Mrit-Krt25/MriApb||Dominant|keratin 25|Krt25||4631426H08Rik, mIRSa1|MGI:1918060||Krt25||11|||||||||||||||||||||||||||||Curly coat and curly whiskers |Curly coat and curly whiskers |SJL|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|01-Feb-2012|Cryopreserved sperm|70.0|0.0|Unknown||Coat, wavy, curly, ENU|Yes| 7446.0|ENU29:G2|ANU:ENU29:G2||Recessive|Unknown|Unknown|||||||Unknown|||||||||||||||||||||||||||||Unknown|Unknown|C57BL/6NCrlAnu|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown|1|||No|24-Sep-2013|Cryopreserved sperm|2355.0|40.0|Unknown||ENU, mutagenesis, screen, random|Yes| 7443.0||C3;SJL/Mrit-MRI9414|C3;SJL/Mrit-MRI9414|Dominant|unknown||Unknown||||||Unknown|||||||||||||||||||||||||||||Unknown|Heterozygous mice display a slight increase growth phenotype|SJL/J|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Good||||No|23-Sep-2013|Cryopreserved sperm|70.0|0.0|Unknown||growth, ENU|Yes| 7444.0||C3;SJL/Mrit-MRI24650|C3;SJL/Mrit-MRI24650|Dominant|unknown||Unknown||||||Unknown|||||||||||||||||||||||||||||Unknown|Heterozygous mice display a slight increase growth phenotype|SJL/J|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Good||||No|23-Sep-2013|Cryopreserved sperm|50.0|0.0|Unknown||growth, ENU|Yes| 7449.0|IL-10R flox|STOCK Il10ra/WehiAnuApb||Dominant|interleukin 10 receptor, alpha|Il10ra|Normal|CDw210, Il10r, mIL-10R|MGI:96538|interleukin 10 receptor, alpha; targeted mutation 1.1, Robert S Jack|Il10ra|MGI:4437317|9|||||||||||||||||||||||||||||Normal||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|02-Oct-2013|Cryopreserved sperm|57.0|0.0|Unknown||colitis, LPS, T cell, macrophage|Yes| 7448.0|WEHI:G1:Snrnp48|STOCK Snrnp48/WehiApb||Recessive|small nuclear ribonucleoprotein 48 (U11/U12)|Snrnp48|Unknown|1110050F08Rik, 6530403A03Rik|MGI:1915047|mutation 1, Walter and Eliza Hall Institute|m1||13|ENSMUSG00000021431|ENSMUST00000091641|Snrnp48-201|794|828|A to G|ENSMUSE00000117800|7|265|Aspartic acid to Glycine|||||CTGGCAGGAAGAGCAGGGGAGAGCAGGAGACGCTGCTGAGAAGAATGAAGAAAGGCGGTCA||||||||||||||Unknown||C57BL/6NCrlAnu|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|26-Sep-2013||0.0|0.0|Unknown||ENU|Yes| 7451.0|hPlg1|B6.SJL/J-Tg(Alb-PLG/EGFP)||Dominant||||||||||||||||||||||||||human plasminogen|murine albumin (Alb)|17%||||||||||NA|Normal|C57BL/6|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Good|||Plg trans +ve x Plg trans +ve |No|08-Oct-2013||0.0|0.0|No||Plasminogen, fibrinolysis|Yes| 6642.0||ENU23FoxRag:B6:G1||Recessive|Unknown||||||||Unknown|||||||||||||||||||||||||||||Unknown||C57BL/6|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|03-Nov-2011|Cryopreserved sperm|10.0|0.0|Unknown||ENU|No| 7192.0||ENU17WT049a||Recessive|Unknown|Unknown|||||||Unknown|||||||||||||||||||||||||||||Mice exhibit increased levels of ALT in the serum following administration of Acetaminophen.|NA|C57BL/6JAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|unknown|unknown|affected by affacted or unaffected by affected|No|05-Nov-2012|Cryopreserved sperm|40.0|0.0|Unknown||ENU|Possibly| 7456.0|myo|C57BL/6-Gulo/MriApb|C57BL/6-Gulo|Recessive|Gulonolactone (L-) oxidase|Gulo|Unknown|L-gulono-gamma-lactone oxidase, MGC:29968, MGC:37793, MGC:37880, sfx|MGI:1353434||||14|ENSMUSG00000034450|ENSMUST00000059970|Gulo-201||||||||65990379|10|||ACAGCTGCTACATGAACATCATTATGTACAGGTGAAAGCTCTCTGCAGGGTGTGGGGTGT||||||||||||||Homozygous mice displays an impaired growth and mobility at 7 weeks old, especially on the extremities. This impaired growth is reversed with high protein diet content |Heterozygous mice are normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|14-Oct-2013|Cryopreserved sperm|50.0|0.0|Yes||myopathy, growth, ENU|Yes| 7454.0|GRP78+/-|C57BL/6NTac-Hspa5||Recessive|heat shock protein 5|Hspa5|Unknown|78kDa, baffled, Bip, D2Wsu141e, D2Wsu17e, Grp78, Hsce70, mBiP, Sez7, XAP-1 antigen|MGI:95835|heat shock protein 5; targeted mutation 1, Velocigene|Hspa5|MGI:4399453|2|||||||||||||||||||||||||||||Lethal|Unknown. Analagous mice developed by A Lee are haploinsufficent at HSPA5 and exibit recued ER stress responses|C57BL/6NTac|No|No|Yes|No|No|Yes|No|Excellent||||No|09-Oct-2013||0.0|0.0|No|||Yes| 7458.0|Ripply2null|ICR;B6CB(Cg)-Ripply2/Rbrc||Recessive|ripply2 homolog (zebrafish)|Ripply2|Nil|C030002E08Rik, LOC382089|MGI:2685968|targeted mutation 1, Yumiko Saga|Ripply2|MGI:3758856|9||||||||||Unknown to Unknown||||||No|||||||||||||Null pups die perinatally with vertebal segmentation defects.|None|C57BL/6|No|No|Yes|No|No|Yes|No|Good|3|0|Rippl2null +/- (heterozygous) mated with C57BL/6|No|22-Oct-2013|Cryopreserved sperm|50.0|0.0|Yes|Spondylocostal dysostosis|Ripply2, Somitogenesis, Mesp2, Notch signalling|No| 6648.0|APN 141|C57BL/6N-1110008L16Rik/Marp||Recessive|protein only RNase P catalytic subunit|Prorp|Unknown||MGI:1913382 |RIKEN cDNA 1110008L16 gene; gene trap IST12983B7, Texas A&M Institute for Genomic Medicine |Gt(IST12983B7)Tigm|MGI:4105973|12||||||||||Unknown to Unknown||||||Yes|||||||||||||Unknown - Not bred to homozygocity |Normal |C57BL/6N|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|22-Nov-2011|Cryopreserved sperm|50.0|0.0|Unknown||ES cell|Yes| 7453.0|Ampd3|C57BL/6N-Ampd3/AnuApb||Recessive|adenosine monophosphate deaminase 3|Ampd3|||MGI:1096344|adenosine monophosphate deaminase 3; targeted mutation 2a, Wellcome Trust Sanger Institute|Ampd3|MGI:4362154|7|||||||||||||||||||||||||||||Unknown|||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|08-Oct-2013|Cryopreserved sperm|50.0|0.0|Unknown|||Yes| 10390.0|C57BL/6NTac-Heatr3 tm1c(EUCOMM)Hmgu/IcsOrlAnu.C57BL/6J-TgTal1-cre/ERT1/JrgAnu |C57BL/6NTac-Heatr3 Tg(Tal1-cre/ERT1)42-056Jrg/Anu ||Dominant|HEAT repeat containing 3|Heatr3|||MGI:2444491|HEAT repeat containing 3; targeted mutation 1c, Helmholtz Zentrum Muenchen GmbH|Heatr3||8|ENSMUSG00000031657||||||||||||||||transgene insertion 42-056, Joachim R Gothert||||||||||||Normal (until treated with tamoxifen to induce Cre expression).|Normal (until treated with tamoxifen to induce Cre expression).|C57Bl/6N|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|10-Dec-2023|Cryopreserved sperm|54.0|0.0|Unknown|||No| 7459.0|Mesp2neo|B6.Cg-Mesp2||Recessive|mesoderm posterior 2|Mesp2|Nil|bHLHc6|MGI:1096325|mesoderm posterior 2; targeted mutation 13, Yumiko Saga|Mesp2|MGI:3715268|7||||||||||||||||No|||||||||||||Null pups die perinatally with vertebal segmentation defects.|None|C57BL/6|No|No|Yes|No|No|Yes|No|Good|10|0|Mesp2neo +/- (heterozygous) mated with C57BL/6|No|22-Oct-2013|Cryopreserved sperm|50.0|0.0|Unknown|Spondylocostal dysostosis|Mesp2, Somitogenesis, Notch signalling|No| 5521.0|F/F x Tlr2; gp130Y757F x Tlr2|B6;129(Cg)-Il6st Tlr2/MarpApb||Dominant|interleukin 6 signal transducer|Il6st|Unknown|CD130, D13Ertd699e, gp130|MGI:96560|interleukin 6 signal transducer; targeted mutation 1, Matthias Ernst|Il6st|MGI:2388478|13||||||||||||||||Yes|||||||||||||Mice develop gastric and inflammation and tumours, as well as splenomegaly and lymphadenopathy.|If the mice are heterozygous for the gp130 knock-in mutation (F+) then the mice appear normal. |C57BL/6|Yes|No|Yes|Yes|Yes|Yes|No|Good|10||heterozogous x homozygous|No|10-Jun-2011|Cryopreserved sperm|50.0|0.0|Yes|Gastric cancer|gastric, cancer, gp130, tlr|No| 5521.0|F/F x Tlr2; gp130Y757F x Tlr2|B6;129(Cg)-Il6st Tlr2/MarpApb||Dominant|toll-like receptor 2|Tlr2|Nil|Ly105|MGI:1346060|toll-like receptor 2; targeted mutation 1, Shizuo Akira|Tlr2|MGI:2178675|3||||||||||||||||No|||||||||||||Mice develop gastric and inflammation and tumours, as well as splenomegaly and lymphadenopathy.|If the mice are heterozygous for the gp130 knock-in mutation (F+) then the mice appear normal. |C57BL/6|Yes|No|Yes|Yes|Yes|Yes|No|Good|10||heterozogous x homozygous|No|10-Jun-2011|Cryopreserved sperm|||Yes|Gastric cancer|gastric, cancer, gp130, tlr|No| 7460.0|Mesp2null|B6.Cg-Mesp2/Rbrc||Recessive|mesoderm posterior 2|Mesp2|Nil|bHLHc6|MGI:1096325|mesoderm posterior 2; targeted mutation 13, Yumiko Saga|Mesp2|MGI:3715271|7||||||||||||||||No|||||||||||||Null pups die perinatally with vertebal segmentation defects.|None|C57BL/6|No|No|Yes|No|No|Yes|No|Good|10|0|Mesp2null +/- (heterozygous) mated with C57BL/6|No|22-Oct-2013|Cryopreserved sperm|50.0|0.0|Unknown|Spondylocostal dysostosis|Mesp2, Somitogenesis, Notch signalling|No| 7924.0|Rsp19 D:R26 M2-rtTa|C57BL/6-Col1a1 Gt(ROSA)26Sor/AnuApb||Recessive|collagen, type I, alpha 1|Col1a1||Col1a-1, Cola1, Cola-1, Mov-13|MGI:88467|collagen, type I, alpha 1; targeted mutation 2, Stefan Karlsson|Col1a1|MGI:5304755|11|||||||||||||||||||||||||||||Normal without doxycycline treatment.Premature death:• most mice die within 2 months following doxycycline treatment.Macrocytosis:• seven weeks after doxycycline treatment.Thrombocytosis:• two weeks after doxycycline treatmentDecreased hematopoietic cell number.Decreased erythrocyte cell number:• two and seven weeks after doxycycline treatmentDecreased neutrophil cell number:• seven weeks after doxycycline treatment.Thrombocytopenia:• seven weeks after doxycycline treatment.Decreased lymphocyte cell number:• two and seven weeks after doxycycline treatment.Reticulocytopenia:• two weeks after doxycycline treatmentPostnatal growth retardation:• following doxycycline treatment|Normal without doxycycline treatment.mortality/agingN • unlike homozygous mice, heterozygotes survive at least 3 months following doxycycline treatmentAbnormal bone marrow cell morphology/development:• decrease in the frequency of bipotential megakaryocytic-erythroid cells and preGM/GMP progenitor cells at 7 weeks after doxycycline treatment.Decreased bone marrow cell number:• by 10 days after doxycycline treatment• absolute numbers of all hematopoietic stem and progenitor cells are reduced at 7 weeks after doxycycline treatment.Decreased megakaryocyte cell number:• seven weeks after doxycycline treatment.Abnormal proerythroblast morphology:• decrease in the frequency or proerythroblasts in the bone marrow by 10 days after doxycycline treatment.Macrocytosis:• seven weeks after doxycycline treatmentThrombocytosis:• two weeks after doxycycline treatmentDecreased hematopoietic cell number.Decreased erythrocyte cell number:• two and seven weeks after doxycycline treatmentDecreased lymphocyte cell number:• two and seven weeks after doxycycline treatmentReticulocytopenia:• two weeks after doxycycline treatmentAbnormal bone marrow cell physiology:• preMegE and preCFU-E/CFU-E progenitors show impaired proliferation and increased apoptosis following doxycycline treatmentPostnatal growth retardation:• following doxycycline treatment• less pronounced than in homozygous mice|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|||Females Rps19 Het/R26 M2-rtTA Hom x Male Rps19 Het/R26 M2-rtTA Hom|No|19-Jun-2015|Cryopreserved sperm|107.0|0.0|Yes|Diamond-Blackfan anemia|Macrocytosis, Thrombocytosis, Thrombocytopaenia|Yes| 7924.0|Rsp19 D:R26 M2-rtTa|C57BL/6-Col1a1 Gt(ROSA)26Sor/AnuApb||Recessive|gene trap ROSA 26, Philippe Soriano|Gt(ROSA)26Sor||beta geo, Gtrgeo26, Gtrosa26, R26, ROSA26, Thumpd3as1|MGI:104735|gene trap ROSA 26, Philippe Soriano; targeted mutation 1, Rudolf Jaenisch|Gt(ROSA)26Sor|MGI:3702294|6|||||||||||||||||||||||||||||Normal without doxycycline treatment.Premature death:• most mice die within 2 months following doxycycline treatment.Macrocytosis:• seven weeks after doxycycline treatment.Thrombocytosis:• two weeks after doxycycline treatmentDecreased hematopoietic cell number.Decreased erythrocyte cell number:• two and seven weeks after doxycycline treatmentDecreased neutrophil cell number:• seven weeks after doxycycline treatment.Thrombocytopenia:• seven weeks after doxycycline treatment.Decreased lymphocyte cell number:• two and seven weeks after doxycycline treatment.Reticulocytopenia:• two weeks after doxycycline treatmentPostnatal growth retardation:• following doxycycline treatment|Normal without doxycycline treatment.mortality/agingN • unlike homozygous mice, heterozygotes survive at least 3 months following doxycycline treatmentAbnormal bone marrow cell morphology/development:• decrease in the frequency of bipotential megakaryocytic-erythroid cells and preGM/GMP progenitor cells at 7 weeks after doxycycline treatment.Decreased bone marrow cell number:• by 10 days after doxycycline treatment• absolute numbers of all hematopoietic stem and progenitor cells are reduced at 7 weeks after doxycycline treatment.Decreased megakaryocyte cell number:• seven weeks after doxycycline treatment.Abnormal proerythroblast morphology:• decrease in the frequency or proerythroblasts in the bone marrow by 10 days after doxycycline treatment.Macrocytosis:• seven weeks after doxycycline treatmentThrombocytosis:• two weeks after doxycycline treatmentDecreased hematopoietic cell number.Decreased erythrocyte cell number:• two and seven weeks after doxycycline treatmentDecreased lymphocyte cell number:• two and seven weeks after doxycycline treatmentReticulocytopenia:• two weeks after doxycycline treatmentAbnormal bone marrow cell physiology:• preMegE and preCFU-E/CFU-E progenitors show impaired proliferation and increased apoptosis following doxycycline treatmentPostnatal growth retardation:• following doxycycline treatment• less pronounced than in homozygous mice|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|||Females Rps19 Het/R26 M2-rtTA Hom x Male Rps19 Het/R26 M2-rtTA Hom|No|19-Jun-2015|Cryopreserved sperm|||Yes|Diamond-Blackfan anemia|Macrocytosis, Thrombocytosis, Thrombocytopaenia|Yes| 7463.0|gp130Y757F/gp130Y757F x ApoE-/- x Stat3-/+|B6.Cg-Apoe Il6st Stat3/MarpApb||Recessive|interleukin 6 signal transducer|Il6st|Normal|5133400A03Rik, CD130, D13Ertd699e, gp130|MGI:96560|interleukin 6 signal transducer; targeted mutation 1, Matthias Ernst|Il6st|MGI:2388478|13|||||||||||||||||||||||||||||Homozygous Stat3 mice are not viable. They are embryonic lethal.Mild gastric tumourigenesis and emphysema|Normal|C57L/6|No|No|Unknown|No|No|Unknown|No|Unknown||||No|25-Oct-2013|Cryopreserved sperm|50.0|0.0|Unknown||signal transduction, tumourigenesis|Yes| 7463.0|gp130Y757F/gp130Y757F x ApoE-/- x Stat3-/+|B6.Cg-Apoe Il6st Stat3/MarpApb||Recessive|signal transducer and activator of transcription 3|Stat3|Nil|1110034C02Rik, Aprf|MGI:103038|signal transducer and activator of transcription 3; targeted mutation 1, Shizuo Akira|Stat3|MGI:1926814|11|||||||||||||||||||||||||||||Homozygous Stat3 mice are not viable. They are embryonic lethal.Mild gastric tumourigenesis and emphysema|Normal|C57L/6|No|No|Unknown|No|No|Unknown|No|Unknown||||No|25-Oct-2013|Cryopreserved sperm|||Unknown||signal transduction, tumourigenesis|Yes| 7463.0|gp130Y757F/gp130Y757F x ApoE-/- x Stat3-/+|B6.Cg-Apoe Il6st Stat3/MarpApb||Recessive|apolipoprotein E|Apoe|Nil||MGI:88057|apolipoprotein E; targeted mutation 1, University of North Carolina|Apoe|MGI:1857129|7|||||||||||||||||||||||||||||Homozygous Stat3 mice are not viable. They are embryonic lethal.Mild gastric tumourigenesis and emphysema|Normal|C57L/6|No|No|Unknown|No|No|Unknown|No|Unknown||||No|25-Oct-2013|Cryopreserved sperm|||Unknown||signal transduction, tumourigenesis|Yes| 7510.0|APN 394|C57BL/6N-A Abca12MarpApb||Recessive| ATP-binding cassette, sub-family A (ABC1), member 12|Abca12 |||MGI:2676312 |ATP-binding cassette, sub-family A (ABC1), member 12; targeted mutation 1a, Helmholtz Zentrum Muenchen GmbHmutation|Abca12tm1a(EUCOMM)Hmgu|MGI:4941545|1|||||||||||||||||||||||||||||Unknown|Normal|C57Bl/6N|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|20-Nov-2013|Cryopreserved sperm|50.0|0.0|Unknown|||Possibly| 10387.0|hF10alb|C57BL/6J-F10em1(alb_hF10)MAGEC||Recessive|coagulation factor X|F10||AI194738, Cf10, fX|MGI:103107||||8|ENSMUSG00000031444||||||||||||||||||||||||||||Unknown|Normal|C57Bl/6J|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|01-Dec-2023|Cryopreserved sperm|40.0|0.0|Unknown|||Possibly| 7465.0|ENU30:G2|ANU:ENU30:G2||Recessive|Unknown|Unknown|||||||Unknown|||||||||||||||||||||||||||||Unknown|Unknown|C57BL/6NCrlAnu|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown|1|||No|29-Oct-2013|Cryopreserved sperm|2569.0|0.0|Unknown||ENU, mutagenesis, screen, random|Yes| 7462.0|BATGal|B6.D2-Tg(BAT-lacZ)3Picc/VccriApb||Dominant||||||||||||||||||||||||||transgene insertion 3, Stefano Piccolo|Seven TCF/LEF-binding sites fused upstream of a 0.13-kb fragment containing the minimal promoter–TATA box of the gene siamois|||||||||||Normal phenotype, expresses LacZ reporting Wnt signalling.Beta-galactosidase expression is initially detectable at E6 in posterior side of proximal epiblast and is observed in the posterior primitive streak and node at gastrulation, progressing to the paraxial mesoderm and notochord.|Normal phenotype, expresses LacZ reporting Wnt signalling|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|10|0|BATGal +/- (hemizygous) mated with C57BL/6|No|22-Oct-2013|Cryopreserved sperm|80.0|0.0|Unknown|Spondylocostal dysostosis|Wnt signalling, LacZ|No| 10388.0|mhF8kohF9ki|C57BL/6J-F8em1(MAGEC) x C57BL/6J-F9em1(hF9)MAGEC||X-linked|coagulation factor VIII|F8||Cf8|MGI:88383||||X|ENSMUSG00000031196 ||||||||||||||||||||||||||||Display mild haemophilia with a propensity for bruising.|Normal|C57Bl/6J|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|01-Dec-2023|Embryo|0.0|459.0|Unknown|||Possibly| 10388.0|mhF8kohF9ki|C57BL/6J-F8em1(MAGEC) x C57BL/6J-F9em1(hF9)MAGEC||X-linked|coagulation factor IX|F9||Cf9|MGI:88384||||X|||||||||||||||||||||||||||||Display mild haemophilia with a propensity for bruising.|Normal|C57Bl/6J|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|01-Dec-2023|Embryo|||Unknown|||Possibly| 7466.0|ENU22:MED28:G1|C57BL/6NCrlAnu-Med28/AnuApb||Recessive|mediator of RNA polymerase II transcription, subunit 28 homolog (yeast)|Med28||1500003D12Rik, Eg1, magicin|MGI:1914249|mediator complex subunit 28; mutation 1, The Australian National University|Med28|MGI:5570703|5|ENSMUSG00000015804|ENSMUST00000156481|Med28-001|275|380|A to G|ENSMUSE00001257470|3|92|Glutamic acid to Glycine|||||GAAGTTTTTGGACATTGCAAGACAGACAGAATGTTTTTTCCTACAAAAAAGGTTGCAGTTA|Unknown|||||||||||||Unknown|Unknown|C57BL/6NCrlAnu|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Good||1||No|29-Oct-2013|Cryopreserved sperm|16.0|0.0|Unknown||ENU, random, mutagenesis, screen|Yes| 7455.0|APN376A|C57Bl/6NTac-Mlxipl/MarpApb||Recessive|MLX interacting protein-like|Mlxipl|Unknown|bHLHd14, ChREBP, Wbscr14, WS-bHLH |MGI:1927999|MLX interacting protein-like; targeted mutation 1, Velocigene |Mlxipltm1(KOMP)Vlcg |MGI:5051293|5|||||||||||||||||||||||||||||Unknown|Normal|C57Bl6N|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Good||||No|10-Oct-2013|Cryopreserved sperm|50.0|0.0|Unknown|||Possibly| 7468.0|Des lpr|B10.BR.(Cg)-H2 Fas Rag1 Tg(TcraKB5.C20,TcrbKB5.C20)10395Arnd/Apb||Recessive|Fas (TNF receptor superfamily member 6)|Fas|Nil|APO-1, CD95, TNFR6, Tnfrsf6|MGI:95484|Fas (TNF receptor superfamily member 6); lymphoproliferation|Fas|MGI:1856334|19||||||||||||||||Yes|transgene insertion 10395, Bernd Arnold|||histocompatibility-2, MHC|H2||H-2, MHC-II|MGI:95894|histocompatibility-2, MHC; k variant|H2|MGI:3579322|17|Normal |Normal|B10.BR|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|10|||Yes|29-Oct-2013|Cryopreserved sperm|50.0|0.0|No||T cell, Fas, CD8, TCR|Yes| 7468.0|Des lpr|B10.BR.(Cg)-H2 Fas Rag1 Tg(TcraKB5.C20,TcrbKB5.C20)10395Arnd/Apb||Recessive|recombination activating gene 1|Rag1|Normal|Rag-1|MGI:97848|recombination activating gene 1; targeted mutation 1, Peter Mombaerts|Rag1|MGI:1857241|2|||||||||||||||||||||||||||||Normal |Normal|B10.BR|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|10|||Yes|29-Oct-2013|Cryopreserved sperm|||No||T cell, Fas, CD8, TCR|Yes| 7470.0|GzmB Cre|STOCK Gt(ROSA)26Sor Tg(Gzmb-cre/ERT2)1Dtf/MarpApb||Dominant|gene trap ROSA 26, Philippe Soriano|Gt(ROSA)26Sor||beta geo, Gtrgeo26, Gtrosa26, R26, ROSA26|MGI:104735|gene trap ROSA 26, Philippe Soriano; targeted mutation 1, Frank Costantini|Gt(ROSA)26Sor|MGI:2449038|6|||||||||||||||||transgene insertion 1, Douglas T Fearon|granzyme B|||||||||||Normal|Normal|C57BL/6J|Yes|Yes|Yes|Yes|Yes|Yes|No|Excellent|10|||No|07-Nov-2013|Cryopreserved sperm|50.0|0.0|Unknown||T cell, CD8, granzyme B, infection|Yes| 7469.0|ENU12B6:020:G4|ANU:ENU12B6:020:G4||Recessive|Unknown|Unknown|||||||Unknown|||||||||||||||||||||||||||||Unknown|Unknown|C57BL/6JSfdAnu|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Good||||No|31-Oct-2013|Cryopreserved sperm|11.0|0.0|Unknown||ENU|Possibly| 7473.0|MNABko:Cre_neg|C57BL/6-Rc3h2/AnuApb|C57BL/6-Rc3h2/Anu|Recessive|ring finger and CCCH-type zinc finger domains 2|Rc3h2|||MGI:2442789|ring finger and CCCH-type zinc finger domains 2; targeted mutation 1.1, Carola Vinuesa|Rc3h2|MGI:5508926|2|||||||||||||||||||||||||||||Normal||C57BL/6JAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|11-Nov-2013|Cryopreserved sperm|29.0|0.0|Unknown||Roquin, T Cell, ICOS, interferon, RING|Yes| 7472.0|Maspin KO|C57BL/6J-SerpinB5/PibMarpApb||Dominant|serine (or cysteine) peptidase inhibitor, clade B, member 5|Serpinb5||1110036M19Rik, Maspin, ovalbumin, Spi7|MGI:109579|serine (or cysteine) peptidase inhibitor, clade B, member 5; targeted mutation 1.1, Phillip I Bird|Serpinb5|MGI:5484764|1|ENSMUSG00000067006 |||||||||Unknown to Unknown|||||||||||||||||||Unknown|Unknown|C57BL/6J|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|11-Nov-2013|Cryopreserved sperm|50.0|0.0|Unknown|||Yes| 7477.0|Gaia Momme D27|FVB/N-Pbrm1 Tg(HBA1-Gfp)1Ew/Apb||Semi-dominant|polybromo 1|Pbrm1|Unknown|2310032M22Rik, 2610016F04Rik, BAF180, Pb1|MGI:1923998|polybromo 1; modifier of murine metastable epialleles, D27|Pbrm1|MGI:5515370|14||||||||||Unknown to Unknown||||||Yes|transgene insertion 1, Emma Whitelaw|human alpha-globin promoter and enhancer region|||||||||||Mutant homozygous mice die before birth. Postnatal lethality: * Hetrozygous animals survive to weaning * normal litter size at birth||FVB/NJ|No|No|Yes|No|No|Yes|No|Good|||MommeD27<+/->;Tg(Hba1-Gfp)3Ew x Tg(Hba1-Gfp)3Ew|No|13-Nov-2013|Cryopreserved sperm|49.0|0.0|Unknown||epigenetics, suppressor of variegation, ENU|Yes| 6762.0|SBmut9|NOD/Lt-Tn(sb-pTrans-SA-IRESLacZ-CAG-GFP-SD:Neo)9TCB/Apb|TCB|Semi-dominant||||||||||||||||||||||||||pTrans-SA-IRESLacZ-CAG-GFP-SD:Neo||||||||||||Unknown|Unknown|NOD/Lt|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|14-Dec-2011|Cryopreserved sperm|50.0|0.0|Unknown||sleeping beauty|No| 6762.0|SBmut9|NOD/Lt-Tn(sb-pTrans-SA-IRESLacZ-CAG-GFP-SD:Neo)9TCB/Apb|TCB|Semi-dominant||||||||||||||||||||||||||pRP-1345|proximal protamine 1 (Prm-1) promoter|||||||||||Unknown|Unknown|NOD/Lt|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|14-Dec-2011|Cryopreserved sperm|||Unknown||sleeping beauty|No| 7471.0|square head|C57BL/6-Pfas/Apb||Dominant|phosphoribosylformylglycinamidine synthase (FGAR amidotransferase)|Pfas|Unknown|4432409B16Rik, Sofa|MGI:2684864||||11|ENSMUSG00000020899|ENSMUST00000021282|Pfas-001|2099|2192|T to C|ENSMUSE00001246828|18|700|Lysine to Proline|||||TGTTGCCCAACAGCAGTGTGTCGGACCCCTGCAGACTCCTCTGGCTGATGTGGCTGTTGTA||||||||||||||Unknown|Heterozygous mice displays a short snout, domed cranium and a decreased body weight.|C57BL/6|No|No|Yes|No|No|Yes|No|Poor||||No|07-Nov-2013|Cryopreserved sperm|40.0|0.0|Unknown||craniofacial, snout face, ENU|Yes| 7474.0|MNABko:Cre_pos|C57BL/6-Rc3h2/AnuApb|C57BL/6-Rc3h2/Anu|Recessive|ring finger and CCCH-type zinc finger domains 2|Rc3h2|||MGI:2442789|ring finger and CCCH-type zinc finger domains 2; targeted mutation 1.2, Carola Vinuesa|Rc3h2|MGI:5508928|2|||||||||||||||||||||||||||||Immune system phenotype:• homozygotes are viable and do not over express ICOS• effector and memory CD4+ cells, T follicular helper cells all normal• germinal centers all normalIncreased macrophage cytokine production:• increased portion of macrophage producing TNF||C57BL/6JAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|11-Nov-2013|Cryopreserved sperm|47.0|0.0|Unknown||Roquin, T Cell, ICOS, interferon, RING|Yes| 7478.0|Line 3C|C57BL/6J-Tg(HBA1-Gfp)1Ew/Apb||Semi-dominant||||||||||||||||||||||||||transgene insertion 1, Emma Whitelaw|human alpha-globin promoter and enhancer region.|||||||||||Normal|Normal|C57BL/6J |Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|13-Nov-2013|Cryopreserved sperm|30.0|0.0|Unknown||epigenetics, suppressor of variegation|Yes| 5548.0|Smg1|B6;129P2-Smg1/QimrApb||Semi-dominant|SMG1|SMG1|Reduced|mKIAA0421; 2610207I05Rik; 5430435M13Rik; C130002K18Rik |MGI:1919742 |SMG1 homolog, phosphatidylinositol 3-kinase-related kinase (C. elegans); gene trap AG0297, Wellcome Trust Sanger Institute|Smg1|MGI:3876748|7|||||||||||||||||||||||||||||Knockout is early embryonic lethal.|Heterozygous mice have increased cancer susceptibility.|C57BL/6J x 129P2/Sv|No|No|Yes|No|No|Yes|No|Good||34|Hetrezygotes x Heterozygotes|No|08-Aug-2011|Cryopreserved sperm|50.0|0.0|Yes|model of spontaneous cancer development associated with aging.|nonsense mediated decay, DNA damage, cancer |Possibly| 7483.0|Vav1KO/B6|B6.129S2-Vav1/AnuApb||Recessive|vav 1 oncogene|Vav1|Nil||MGI:98923|vav 1 oncogene; targeted mutation 1, Victor L J Tybulewicz|Vav1|MGI:2387838|17|||||||||||||||||||||||||||||Abnormal negative T cell selection:• deletion of CD4+ cells expressing Vbeta3, 5, and 11 is less than in wild-type mice suggesting impaired negative selection.Abnormal T cell number:• large decrease of single "+" cellsIncreased double-negative T cell number.Increased DN2 thymocyte number.Increased DN3 thymocyte number.Decreased double-positive T cell number.Abnormal immune system physiology.Abnormal CD8-positive T cell physiology:• reduced ability of CD8+ cells to form conjugates with antigen presenting cells.Abnormal interleukin-2 secretion.||C57BL/6|Yes|Yes|Unknown|Yes|Yes|Yes|No|Unknown||||No|14-Nov-2013|Cryopreserved sperm|29.0|0.0|Unknown||T cell, GTP, selection, thymocyte, Rho|Yes| 7484.0|Clock Mel|CBA;B6-Clock/Apb||Semi-dominant|circadian locomotor output cycles kaput|Clock||5330400M04Rik, bHLHe8, KAT13D, mKIAA0334|MGI:99698|circadian locomotor output cycles kaput; Clock|Clock|MGI:1861634|5|||||||||||||||||||||||||||||The mutant animals displays an altered period of rhythmicity of wheel running activity in constant darkness (approx 27 hours), followed by arrythmicity after an extended period.|The heterozygote displays a slightly longer period of behavioural rhythmicity in constant darkness (approx 24.5 hours).|CBA|Yes|Yes|Yes|Yes|Yes|Yes|No|Poor|4|0|Maintain mutant and wild type as separate lines.|No|14-Nov-2013|Cryopreserved sperm|50.0|0.0|Unknown||circadian, clock|No| 7485.0|WinSlpi|B6.129P2-Muc2 Slpi/Apb|UTAS|Recessive|mucin 2|Muc2|Unknown||MGI:1339364|mucin 2; winnie|Muc2|MGI:3614806|7|||||||||||||||||||||||||||||No explicit phenotype, normal|Normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|14-Nov-2013|Cryopreserved sperm|50.0|0.0|Unknown||endoplasmic reticulum , stress, mucin, colitis|No| 7485.0|WinSlpi|B6.129P2-Muc2 Slpi/Apb|UTAS|Recessive|secretory leukocyte peptidase inhibitor|Slpi|Nil||MGI:109297|secretory leukocyte peptidase inhibitor; targeted mutation 1, Toshihiro Nukiwa|Slpi|MGI:2652666|2|||||||||||||||||||||||||||||No explicit phenotype, normal|Normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|14-Nov-2013|Cryopreserved sperm|||Unknown||endoplasmic reticulum , stress, mucin, colitis|No| 7475.0|Momme D28|FVB/NJ-Rlf Tg(Hba1-Gfp)1Ew/Apb||Recessive|rearranged L-myc fusion sequence|Rlf|Reduced||MGI:1924705|rearranged L-myc fusion sequence; modifier of murine metastable epialleles, D28|Rlf|MGI:5515366|4||||||||||Unknown to Unknown||||||Yes|transgene insertion 1, Emma Whitelaw|human alpha-globin promoter and enhancer region|11 copies||||||||||Homozygous die|Normal|FVB/NJ|No|No|Yes|No|No|Yes|No|Good||||No|12-Nov-2013|Cryopreserved sperm|20.0|0.0|Unknown||ENU|Yes| 5399.0|FVB x FVB.B6 ; Dirc-2|FVB/N;B6-Dircq2/ArcApb||Dominant||||||||||||||||||||||||||||||||||||||As per parental strain.Once injected with Alloxan mice are resistant to becoming diabetic (check via urine glucose or blood monitor), these mice do not show nephropathy and retinopathy disease consistent with the human conditions as compared to the B6;FVB/N-Dirc-2 strain. |As per parental strain.|FVB/N|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|10|5|Hom x Hom|No|31-Jan-2011|Embryo|0.0|0.0|Yes|Once injected with Alloxan mice become diabetic (check via urine glucose or blood monitor), these mice show nephropathy and retinopathy disease consistent with the human conditions. |diabetic complications, retinopathy, nephropathy|Yes| 7127.0|Ig1|FVB/N-Tg(Myl1-Igf1)1Nros/Ausb||Dominant||||||||||||||||||||||||||transgene insertion 1, Nadia Rosenthal|keletal muscle-specific regulatory elements from the rat myosin light chain (MLC)-1/3 |restricted to skeletal muscle and predominated in muscles enriched in fast fibers, such as the triceps or gastrocnemius.||||||||||Enlarged skeletal muscles especially in the forearms.||FVB/N|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|02-Nov-2012||0.0|0.0|Unknown||muscle, growth factor, hypertrophy|Possibly| 8725.0|ACAD10KO|C57BL/6-Acad10/Apb||Recessive|Acyl-CoA Dehydrogenase Family Member 10|Acad10||2410021P16Rik|MGI:1919235||||5|||||||||||||||||||||||||||||Normal as far as initial experiments have shown|Normal as far as initial experiments have shown|C57BL/6J|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|05-Jun-2019|Cryopreserved sperm|50.0|0.0|Unknown|||Yes| 7874.0|Kmt2d𝚫2|C5BL/6-Kmt2d/MegaAusb||Recessive|lysine (K)-specific methyltransferase 2D|Kmt2d|Unknown|C430014K11Rik, Mll2, Mll4|MGI:2682319||||15|||||||||||||||||||||||||||||Unknown|Unknown|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|16-Apr-2015||0.0|0.0|Unknown|||Yes| 7488.0|Rag1-D708A|B6.129-Rag1 Tg(Rag1*D708A)/Ausb||Recessive|recombination activating gene 1|Rag1|Nil|Rag-1|MGI:97848|recombination activating gene 1; targeted mutation 1, Peter Mombaerts|Rag1|MGI:1857241|2|||||||||||||||||transgene insertion 1, David Schatz||||||||||||Express Rag1 protein. Protein able to bind to DNA but lacks catalytic activity.Phenotype is similar to Rag1 KO.Exhibit blocks at pro-B and pro-T stages of lymphocyte development equivalent to Rag1 KO.Expression of D708A does not support lymphocyte development as does not support V(D)J recombination.||C57BL/6|Yes|Yes|Unknown|Yes|Yes|Yes|No|Unknown||||No|18-Nov-2013||0.0|0.0|Unknown||T cell, B cell, development, V(D)J|Yes| 7489.0|Prf KO|C57BL/6-Prf1/Ausb|C57BL/6-Prf1/Ausb|Recessive|perforin 1 (pore forming protein)|Prf1|Nil|perforin, Pfn, Pfp, Prf-1|MGI:97551|targeted mutation 1, Sandoz Pharmaceutical|Prf1|MGI:1857235|10|||||||||||||||||||||||||||||Homozygous null mice exhibit increased susceptibility to viral infection and defective cytotoxic T cell cytolysis and NK cell cytolysis.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|18-Nov-2013||0.0|0.0|Unknown||cytotoxic T cell, CD8, Natural Killer cell, cytolysis, infection|Yes| 7492.0|PRLRfx|B6.Cg-Prlr/Ausb||Recessive|prolactin receptor|Prlr|Unknown||MGI:97763||||15|||||||||||||||||||||||||||||Normal||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|19-Nov-2013||0.0|0.0|Unknown||receptor, signalling, Cre recombinase|Yes| 4524.0||C57BL/6-Socs1 Tg(Lck-cre)157Jxm/Apb||Recessive|suppressor of cytokine signaling 1|socs1|Nil|Cish1, Cish7, JAB, JAK-binding protein, JAK2-binding protein, SOCS-1, SSI-1, STAT-induced STAT inhibitor 1|MGI:1354910|targeted mutation 3, Walter and Eliza Hall Institute of Medical Research|Socs1|MGI:2656917|16||||||||||Unknown to Unknown||||||Yes|transgene insertion I57, Jamey Marth|lymphocyte protein tyrosine kinase (Lck)|||||||||||Enhanced differentiation of thymocytes toward CD8+ T cells. Thymus hyperplasia.Enlarged lymph nodes||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Poor||||No|27-Feb-2009|Cryopreserved sperm|95.0|0.0|Unknown||cytokine signalling, T cell, thymus, hyperplasia|Yes| 7509.0|GDF9cre|C57BL/6-Tg(Gdf9-cre)5092Coo/JAusb||Dominant||||||||||||||||||||||||||transgene insertion 5092, Austin J Cooney|Gdf9 ; growth differentiation factor 9|||||||||||Cre recombinase was expressed in postnatal ovaries, but not in heart, liver, spleen, kidney, and brain.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|19-Nov-2013||0.0|0.0|Unknown||Cre recombinase, Oocyte, early embryonic development, folliculogenesis|Yes| 7503.0|Arwen|C57BL/6-Tg(Elf5V5-rtTA2-cre/ERT2)/Ausb ??||Dominant||||||||||||||||||||||||||Cre recombinase|E74-like factor 5 ??|||||||||||Unknown||C57BL/6|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|19-Nov-2013||0.0|0.0|Unknown||Cre recombinase, inducible|Yes| 7505.0|A2BRKO|B6.129-Adora2b/?Ausb||Recessive|adenosine A2b receptor|Adora2b||A2b, A2BAR, A2BR, A2b, Rs, AA2BR|MGI:99403|Unknown|||11|||||||||||||||||||||||||||||Unknown||C57BL/6|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|19-Nov-2013||0.0|0.0|Unknown|||Yes| 7507.0|Nrg1T3|C57BL/5NTac-Tg(Nrg1)Xen/TacAusb||Dominant||||||||||||||||||||||||||neuregulin 1||||||||||||Overexpression of Nrg1 in forebrain.||C57L/6NTac|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|19-Nov-2013||0.0|0.0|Unknown||neuregulin|Yes| 7508.0|rag1-cre|129S/SvEv-Rag1/WehiAusb|129S/SvEv-Rag1/WehiAusb|Dominant|recombination activating gene 1|Rag1||Rag-1|MGI:97848|recombination activating gene 1; targeted mutation 1, Terence H Rabbitts|Rag1|MGI:3584018|2|||||||||||||||||||||||||||||Abnormal lymphopoiesis:* fail to develop lymphocytes||129/SvEv|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|19-Nov-2013||0.0|0.0|Unknown||T cell, B cell, lymphocyte|Yes| 5116.0|ENU11B6-C3H:005 ; bfb|B6;C3H-Fras1/AnuApb|B6;C3H-Fras1/AnuApb|Recessive|Fraser syndrome 1 homolog (human)|Fras1|Unknown|bl, E130113P14Rik, mKIAA1500|MGI:2385368|Fraser syndrome 1 homolog (human); blood filled blisters|Fras1|MGI:5463442|5|ENSMUSG00000034687|ENSMUST00000036019|Fras1-201|10762|11620|T to C|ENSMUSE00000318929|69|3588|Serine to Proline|||||AGCTCTTGTGGAGTGCTCAGACATTTGATTCTCCTCATCAACTCTGGCGAGCCACGAGCTC|Yes|||||||||||||Embryonic lethal.Cleft secondary palate:• at E18.5Eyelids open at birth:• at E18.5Bleb• blood filled blisters on the head and feet at E13.5.Preaxial polydactyly:• at E18.5Absent kidney:• at E18.5Cleft secondary palate:• at E18.5||C57BL/6|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|11-May-2010|Cryopreserved sperm|50.0|0.0|Unknown||ENU, blebs, adhesion, Fraser syndrome|Yes| 5209.0|MIP-GFP|C57BL/6-Tg(Ins1-EGFP)1Hara/Arc|C57BL/6-Tg(Ins1-EGFP)1Hara/Arc|Dominant||||||||||||||||||||||||||transgene insertion 1, Manami Hara|mouse insulin 1 promoter|high, restricted to pancreatic islet beta cells|||||||||||Transgenic mice develop normally and exhibit glucose tolerance and pancreatic insulin levels similar to those of controls. Histological analysis reveals normal islet architecture and coexpression of insulin and EGFP.GFP expression in pancreatic islet beta cells. |C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Excellent|10|7|Hom x Hom|No|23-Aug-2010||0.0|0.0|No||pacreas, beta cell, insulin, GFP|Yes| 3941.0|C3H.MOLD|C3H.M.domesticus-Oas1b/Arc|C3H.M.domesticus-Oas1b/Arc|Dominant|2'-5' oligoadenylate synthetase 1B|Oas1b|Normal|Flavivirus resistance, Flv, L1, Mmu-L1, Oias-2, Oias2, Wnv|MGI:97430|flavivirus resistance|Oas1b|MGI:1857800|5||||||||||||||||No|||||||||||||Flv Phenotype – Resistance to infections by Flaviviruses.Tlr4 Phenotype – Toll 4 receptor is responsive to LPS injection.|Flv Phenotype – dominant phenotype, heterozygotes are resistant to infection.Tlr4 phenotype is dominant and heterozygous mice show responsiveness to LPS.|C3H/HeJARC|Yes|Yes|Yes|Yes|Yes|Yes|No|Poor|11||brother x sister|No|17-Oct-2008||0.0|0.0|Unknown||Flavivirus resistance, Lipopolysaccharide (LPS), Toll like receptor|Yes| 5378.0|Cdk4/Nras|FVB.Cg-Cdk4 Tg(Tyr-NRAS*Q61K)1Bee/Arc|FVB;Cg-Cdk4 Tg(Tyr-NRAS*Q61K)1Bee/Arc|Dominant|cyclin-dependent kinase 4|Cdk4|Normal|Crk3, p34/cdk4|MGI:88357|cyclin-dependent kinase 4; targeted mutation 1.1, Mariano Barbacid|Cdk4|MGI:2154521|10||||||||||||||||Yes|transgene insertion 1, Friedrich Beemann|tyrosinase|Directed towards melanocyte lineage||||||||||The Cdk4 mice are mice are indistinguishable from wt visually. Tyr-Nras mice have thin hair, probably smaller body, possibly smaller eyes - or sometimes enlarged eyes. Only the compound genotype develops melanoma. The Tyr-Nras transgene needs to be in a heterozygous state. The phenotype much more severe in Nras homozygotes.||FVB|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|3|||No|04-Jan-2011||0.0|0.0|Unknown||melanoma, metastasis|Possibly| 5469.0|ENU12B6-C3/H:C3H:022|B6;C3H-Lig1/AnuApb||Recessive|ligase I, DNA, ATP-dependent|Lig1|Unknown|LigI, mLigI|MGI:101789|ligase I, DNA, ATP-dependent; mutation 1, The Australian National University|Lig1|MGI:5510743|7|ENSMUSG00000056394|ENSMUST00000148471|Lig-001|1798|2054|A to T|ENSMUSE00000537286|19|600|Isoleucine to Phenylalanine|||||TACATGTTCTGGAAGGTGGAGAAGTGAAGATCTTCAGCAGGAACCAGGAAGACAACACAGG|Yes|||||||||||||Embryonic lethality. Embryos at E13.5 exhibit a pale, orange liver with failure of definitive erythropoiesis|Normal|C57BL/6J X C3H|No|No|Yes|No|No|Yes|Yes|Good||3|het x het|No|24-Mar-2011|Cryopreserved sperm|45.0|0.0|Unknown||embryonic, erythropoiesis, ENU, anaemia|Yes| 5462.0|Str ; Stretcher|C.Cg-Ndrg1/Arc|C.Cg-Ndrg1/Arc|Recessive|N-myc downstream regulated gene 1|Ndrg1|Reduced|CAP43, CMT4D, DRG1, Ndr1, Ndrl, PROXY1, TDD5, Tdd5 |1341799|N-myc downstream regulated gene 1; stretcher|Ndrg1|MGI:5009138|15||||||||||||||||Yes|||||||||||||Progressive peripheral neuropathy,tremor and the characteristic stretching of the hind-limbs and clasping when suspended, are seen from 5 weeks of age. The mice become progressively more severely affected until by 15 to 20 weeks they are very disabled, being not only weak but unable to control their hind legs which show severe flacid paralysis and highly abnormal positioning. The hind-legs muscles atrophy and the mice weigh less than their normal siblings. Clinically, the mice seem to stabilize after about 30 weeks of age and do not deteriorate further. |Normal|BALB/c|Yes|Unknown|Yes|Yes|Unknown|Yes|No|Excellent||||No|07-Mar-2011||0.0|0.0|Yes|hereditary motor and sensory neuropathy-Lom (HMSNL) shows features of Schwann-cell dysfunction and a concomitant early axonal involvement, suggesting that impaired axon-glia interactions play a major role in its pathogenesis. |recessive, neuropathy, schann cell, axon, peripheral nerve|Yes| 3338.0|Cbfa2t3|C57BL/6-Cbfa2t3/Apb||Semi-dominant|core-binding factor, runt domain, alpha subunit 2, translocated to, 3 (human)|Cbfa2t3|Normal|ETO-2, Eto2, MTGR2|MGI:1338013||||8||||||||||||||||Yes|||||||||||||Normal|Normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|4|||No|20-Jun-2008|Cryopreserved sperm|59.0|0.0|No||leukaemia / leukemia, translocation, breast, transcription|Yes| 7173.0|ApoDtgAPP|B6.Cg-Tg(APOD) Tg(APPswePSEN1dE9)85Dbo/JAusb||Recessive||||||||||||||||||||||||||transgene insertion 85, David R Borchelt||||||||||||Double mutation associated with early-onset of Alzheimer's disease.||C57BL/6|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|02-Nov-2012||0.0|0.0|Unknown|||Possibly| 7173.0|ApoDtgAPP|B6.Cg-Tg(APOD) Tg(APPswePSEN1dE9)85Dbo/JAusb||Recessive||||||||||||||||||||||||||human Apolipoprotein D||||||||||||Double mutation associated with early-onset of Alzheimer's disease.||C57BL/6|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|02-Nov-2012||||Unknown|||Possibly| 6660.0|Mozart|B6.129P2-Msi2/Ausb||Dominant|Musashi homolog 2 (Drosophila) |Msi2|Normal|msi2h, Musashi2 |MGI:1923876|Musashi homolog 2 (Drosophila); gene trap E035H03, German Gene Trap Consortium|Msi2|MGI:3893933|11|||||||||||||||||||||||||||||Partial prenatal lethality:*Half of expected mice die prior to birth.Abnormal fertility/fecundity:*Mice are infertile when crossed to each other.*However, mice fertile when mated to wild-type mice.Hematopoietic system phenotype:*Mice exhibit normal numbers of platelets. Decreased erythrocyte cell number: *In young and old mice. Decreased leukocyte cell number: *Circulating in old mice. Decreased B cell number: *In the spleen. *2.5- to 5-fold in the blood of old mice. Decreased immature B cell number: *In old mice. Decreased pre-B cell number: *In young and old mice. Decreased mature B cell number: *In young and old mice. Decreased CD4-positive T cell number: *In the thymus. Decreased CD8-positive T cell number: *In the thymus. Decreased double-negative T cell number: *In the thymus. Decreased DN2 thymocyte number: *In the thymus. Decreased DN3 thymocyte number: *In the thymus. Decreased double-positive T cell number: *In the thymus. Decreased granulocyte number: *In the spleen. *In the bone marrow of young and old mice. *2-fold in the blood of old mice. Decreased macrophage cell number: *In the spleen. *In the bone marrow of old mice. *2-fold in the blood of old mice. Abnormal myeloid leukocyte morphology: *Young and old mice exhibit decreased myeloid lineage cells compared with wild-type mice. Abnormal bone marrow cell morphology/development: *Megakaryocyte-erythroid progenitors and erythroblasts are slightly decreased compared to in wild-type. Decreased common myeloid progenitor cell number: *Old mice exhibit decreased common myeloid progenitors (CMPs) and granulocyte macrophage progenitors (GMPs) compared with wild-type mice. Decreased double-negative T cell number: *In the thymus. Decreased DN2 thymocyte number: *In the thymus. Decreased DN3 thymocyte number: *In the thymus. Decreased double-positive T cell number: *In the thymus. Abnormal common lymphocyte progenitor cell morphology: *Young mice exhibit decreased common lymphocyte progenitor cells compared with wild-type mice. Decreased hematopoietic stem cell number: *Mice exhibit reduced numbers of primitive hematopoietic, intermediate progenitors, lymphoid myeloid primed multipotent progenitors (LMPPs; in young and old mice), and short term hematopoietic stem cells (in old mice) compared with wild-type mice. *However, mice exhibit normal numbers of long term hematopoietic stem cells. Small spleen Spleen hypoplasia Small thymus Thymus hypoplasia Abnormal hematopoietic stem cell physiology: *Hematopoietic stem cells exhibit a slight decreased in cells in the S-G2/M phase compared with wild-type cells. *In bone marrow transplantation assays, hematopoietic stem cells exhibit reduced repopulation capacity compared with wild-type cells. *However, apoptosis rates are not significantly different.Decreased body weight||C57BL/6|Yes|No|Yes|Yes|No|Yes|No|Unknown||||No|02-Dec-2011||0.0|0.0|Unknown||Msi2, HSCs|Yes| 5467.0|D6|B6.129/Sv-Ccbp2/Apb||Recessive|chemokine binding protein 2|Ccbp2|Nil|CCR10, CCR9, Cmkbr9, D6|MGI:1891697|chemokine binding protein 2; targeted mutation 1, Gerard J Graham|Ccbp2|MGI:3623613|9||||||||||||||||Yes|||||||||||||Increased inflammatory response: * subcutaneous injection of complete Freund's adjuvant (CFA) produces a granuloma-like lesion in homozygotes by 3 days post injection and 18 of 28 mutants develop grade 2 or higher lesions by 7 days post injection versus 2 of 28 wild-type mice * at the site of CFA injection increased necrosis, angiogenesis and leukocyte infiltration are seen * 3 days after CFA injection increase lymph node cellularity is seen in homozygotes compared to wild-type mice; however 7 days after injection wild-type contralateral lymph nodes display hyperplasia which is not seen in homozygotes.Dermatitis: * 24 hours after a single exposure of dorsal skin to 12-O-tetradecanoylphorbol-13-acetate (TPA) beta-chemokine levels remain elevated suggesting a defect in post-inflammatory clearance. * after 3 daily applications of TPA homozygotes develop a psoriasis-like skin lesion that is characterized by skin thickening, basal and suprabasal epidermal hyperproliferation, severe epidermal acanthosis, parakeratosis, hyperkeratosis, extensive growth of convoluted blood vessels, and a dense inflammatory cell infiltrate that includes high numbers of T cells * this TPA-induced inflammatory skin lesion persists for 6 to 10 days. * injection of TNF neutralizing antibodies, depletion of CD4+ and CD8+ T cells, or blockage of mast cell degranulation can prevent development of the TPA-induced psoriaform lesion.||129/Sv x C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|22-Mar-2011|Cryopreserved sperm|50.0|0.0|Unknown||dermatitis|Yes| 5315.0|BALB.SHIP-1 knockout|C.129P2(B6)-Inpp5d/JAcbdLudApb|C.129P2(B6)-Inpp5d/JAcbdLudApb|Recessive|inositol polyphosphate-5-phosphatase D|Inpp5d|Nil|s-SHIP, SHIP, SHIP-1, SHIP1, Src homology 2 domain-containing inositol-5-phosphatase|MGI:107357|inositol polyphosphate-5-phosphatase D; targeted mutation 1, Dan Dumont|Inpp5d|MGI:1861956|1||||||||||||||||No|||||||||||||Young mice are apparently healthy, and do not develop inflammatory lung disease, unlike mixed genetic background or C57BL/6 background SHIP-1<-/-> mice. |No obvious disease is apparent in SHIP-1<+/-> mice, even at 12 months of age.|BALB/c|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|7|||No|10-Nov-2010|Cryopreserved sperm|50.0|0.0|Unknown||phosphorylation, phosphatase, PI3'K, inflammatory lung disease, myeloid hyperplasia, signal transduction|Yes| 6658.0|Mahler|TgMsi2(transgenic lactate dehydrogenase C4-Musashi2/Ausb||Recessive||LdHC4|||MGI:1923876||||Unknown|||||||||||||||||||||||||||||Homozygous exhibit subfertility or infertiity.||Mixed - mice|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|02-Dec-2011|Embryo|0.0|0.0|Unknown|||Possibly| 7490.0|Cre/6N|C57BL/6NTac-Gt(ROSA)26Sor/Ausb|C57BL/6NTac-Gt(ROSA)26Sor/Ausb|Dominant|gene trap ROSA 26, Philippe Soriano|Gt(ROSA)26Sor|Unknown|beta geo, Gtrgeo26, Gtrosa26, R26, ROSA26|MGI:104735|gene trap ROSA 26, Philippe Soriano; targeted mutation 16, TaconicArtemis|Gt(ROSA)26Sor|MGI:3839354|6|||||||||||||||||||||||||||||Normal|Normal|C57BL/6N|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|4|||No|18-Nov-2013||0.0|0.0|Unknown||Cre recombinase, deleter, ROSA26|Yes| 6553.0|Fgf2Δ|B6.129P2-Fgf2/JAusb|B6.129P2-Fgf2/JAusb|Recessive|fibroblast growth factor 2|Fgf2|Nil|bFGF, Fgf-2, Fgfb|MGI:95516|fibroblast growth factor 2; targeted mutation 1, Thomas Doetschman|Fgf2|MGI:1857458|3|||||||||||||||||||||||||||||Abnormal vascular endothelial cell migration:*Following de-endothelialization and treatment with 17beta-Estradiol (E2), mice fail to re-endothelialize the site of injury unlike wild-type mice.*Endothelial precursor cell migration in response to E2 is disrupted.||129/B6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown||Fibroblast growth factor 2, Vascular tone|Yes| 6445.0|GEM?|B6.Cg-Gem/?Ausb||Recessive||GEM||||||||||||||||||||||||||||||||||||||C57BL6|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown|||Possibly| 6702.0|Gt2|B6.D2-Tg(ACTA1-Gtfird2)30Hrd/Ausb|B6.D2-Tg(ACTA1-Gtfird2)30Hrd/Ausb|Recessive||Gt2|||||||Unknown|||||||||||||||||||||||||||||Muscle weakness,reduced body weight.||B6D2|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|02-Dec-2011||0.0|0.0|Unknown|||Possibly| 6813.0|B6.hCD55.Tg.EA|CBA.B6-Tg(H2-K-CD55)/SvhmApb||Dominant||||||||||||||||||||||||||human CD55 Antigen|murine class 1 H2-K|moderate to high||||||||||Normal|Normal|C57BL/6|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Good|14|||No|08-Feb-2012|Cryopreserved sperm|50.0|0.0|Unknown|||Possibly| 125.0|Ceres ; MM4|C57BL/6SfdAnu-Tg(IghelM)Ccg/AnuApb|C57BL/6SfdAnu-Tg(IghelM)Ccg/AnuApb|Dominant||||||||||||||||||||||||||transgene insertion 4, Christopher C Goodnow|Controlled by normal promoter|low, transgene H and L chains are cointergrated and driven under their normal elements||||||||||||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|06-Feb-2006|Cryopreserved sperm|37.0|0.0|No||IgM, Hen Egg Lysozyme, B cell, receptor, Immunoglobulin|Yes| 6556.0|G2FCtg|G2f x CAMcre||Recessive||G2,CAM|||||||Unknown|||||||||||||||||||||||||||||||Mixed - mice|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011|Embryo|0.0|0.0|Unknown|||Possibly| 6699.0|Ga1|B6.Cg-Gad1/Ausb||Dominant|glutamic acid decarboxylase 1|Gad1|Normal|EP10, Gad-1, GAD25, GAD44, GAD67, Z49976 |MGI:95632 |glutamic acid decarboxylase 1; targeted mutation 1, Nobuaki Tamamaki|Gad1|MGI:3590300|2|||||||||||||||||||||||||||||||C57BL/6|No|Unknown|Yes|No|Unknown|Yes|No|Unknown||||No|02-Dec-2011||0.0|0.0|Unknown||Gamma-aminobutyric acid (GABA), Calretinin (CR), Parvalbumin (PV), Somatostatin (SS), GFP|Yes| 5248.0|Lyn STAT6 double knockout ; BALB.Lyn-/-STAT6-/-|C.Cg-Lyn Stat6/Apb||Recessive|Yamaguchi sarcoma viral (v-yes-1) oncogene homolog|Lyn|Nil|Hck-2|MGI:96892|Yamaguchi sarcoma viral (v-yes-1) oncogene homolog; targeted mutation 1, Ashley R Dunn|Lyn|MGI:2157129|4||||||||||||||||No|||||||||||||Mice develop exaggerated autoimmune disease compared with Lyn<-/-> mice.At a time-point where Lyn(-/-) mice showed only mild autoimmune disease, Lyn(-/-)STAT6(-/-) mice had maximal titres of IgG and IgA auto-Abs, impaired renal function, myeloid expansion and a highly activated T cell compartment. Remarkably, low level IgE auto-Abs but not IgG1 auto-Abs were a feature of some aged Lyn(-/-) STAT6(-/-) mice. Furthermore, aged Lyn(-/-)STAT6(-/-) mice showed dramatically increased levels of serum IgE but minimal IgG1, suggesting that class-switching to IgE can occur in the absence of an IgG1 intermediate.|Not defined|BALB/c|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|19-Oct-2010|Cryopreserved sperm|50.0|0.0|Unknown||B cell, src family, kinase, signal transduction, autoimmunity, lymphocyte|Yes| 5248.0|Lyn STAT6 double knockout ; BALB.Lyn-/-STAT6-/-|C.Cg-Lyn Stat6/Apb||Recessive|signal transducer and activator of transcription 6|Stat6|Nil||MGI:103034|signal transducer and activator of transcription 6; targeted mutation 1, Shizuo Akira|Stat6|MGI:2386746|10||||||||||||||||No|||||||||||||Mice develop exaggerated autoimmune disease compared with Lyn<-/-> mice.At a time-point where Lyn(-/-) mice showed only mild autoimmune disease, Lyn(-/-)STAT6(-/-) mice had maximal titres of IgG and IgA auto-Abs, impaired renal function, myeloid expansion and a highly activated T cell compartment. Remarkably, low level IgE auto-Abs but not IgG1 auto-Abs were a feature of some aged Lyn(-/-) STAT6(-/-) mice. Furthermore, aged Lyn(-/-)STAT6(-/-) mice showed dramatically increased levels of serum IgE but minimal IgG1, suggesting that class-switching to IgE can occur in the absence of an IgG1 intermediate.|Not defined|BALB/c|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|19-Oct-2010|Cryopreserved sperm|||Unknown||B cell, src family, kinase, signal transduction, autoimmunity, lymphocyte|Yes| 6857.0|ENU15NIH85a ; enid|C57BL/6JAnu-Sppl2a/AnuApb|C57BL/6JAnu-Sppl2a/AnuApb|Recessive|signal peptide peptidase like 2A|Sppl2a|Unknown|2010106G01Rik, C130089K23Rik|MGI:1913802 |signal peptide peptidase like 2A; mutation 1, The Australian National University|Sppl2a|MGI:5432126|2|ENSMUSG00000027366|ENSMUST00000028844|2010106G01Rik-001||||||||126746052|7|||ATTCATAGGATGCCATGTGGACAGTGCACGTACGTATCTGTTAGCCTATGATGCAATTAG||||||||||||||Decreased number of B cells.Very low expression of IgD on the IgM subset of mature B cells.25-fold less serum IgM.6-fold less serum IgG1.Almost no specific antibody was made after immunization with formalin-inactivated and heat-killed Bordetella pertussis and alum-precipitated chicken gamma globulin (CGG) coupled to p-azobenzenearsonate (ABA) hapten or after immunization with the T-independent antigen 4-hydroxy-3-nitrophenylacetyl-Ficoll (NP-Ficoll.Normal numbers of pro-B, pre-B, and immature B cells, and normal cell surface IgM and normal onset of IgD expression among the IgM T1 subset.Mature IgD<+>IgM recirculating B cells were selectively decreased in the bone marrow and had very low surface IgD. In the spleen, the T1 subset of recent bone marrow emigrants (CD93<+>IgMCD23<−>) was present in normal numbers and expressed levels of surface IgM comparable with controls.Subsequent maturational stages of T2, T3, and mature CD93<−>IgM B cells were 20-fold reduced, whereas the mature marginal zone B cell subset was decreased 200-fold. Immunofluorescent staining of spleen sections showed that the residual B cells in SPPL2A-deficient mice nevertheless localized normally in primary follicles.Sppl2a<−/−> mice had fewer CD11c<+> DCs as the result of only 12% of normal numbers in the CD4<+> and the CD4<−>CD8<−> double-negative (DN) DC subsets, whereas CD8<+> and plasmacytoid DCs were present at normal and increased numbers, respectively. Less CD11c and CD8 was present on the B220<−>CD8<+> DCs in Sppl2a<−/−> animals.|Normal|C57BL/6JAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||G7||No|15-Mar-2012|Cryopreserved sperm|67.0|0.0|Unknown||lymphocyte, B cell, IgD, ENU, immunoglobulin|No| 78.0|Thunder|C57BL/6JSfdAnu-Hnrnpll/AnuApb|C57BL/6JSfdAnu-Hnrnpll/AnuApb|Recessive|heterogeneous nuclear ribonucleoprotein L-like|Hnrpll|Nil||MGI:1919942|heterogeneous nuclear ribonucleoprotein L-like; thunder|Hnrpll|MGI:3707008|17|ENSMUSG00000024095|ENSMUST00000061331|Hnrpll-201|407|683|T to A|ENSMUSE00000138333|2|136|Valine to Aspartic acid|||||TGTCCATGTTCGAGGGCTCTGTGAATCTGTTGTGGAAGCTGACCTTGTGGAGGCACTGGAG|Yes|||||||||||||Low T cell numbers which are hyperactivated. By flow cytometric staining of blood, initially detected a strain with CD4 T cells decreased to 25% of wild-type. Further analysis revealed entirely normal thymic development and single positive cells, but a marked reduction in the number of peripheral T cells especially naïve CD4 and CD8 cells, and poor survival of thunder T cells upon adoptive transfer. During this analysis, it was found that thunder thymocytes stain with the RA3-6B2 antibody that selectively recognizes the CD45RABC B220 isoform normally restricted to B cells. Staining with antibodies to CD45RA, B or C showed a 50-fold increase in staining on all thymocytes and peripheral T cells, as well as macrophages and dendritic cells, so that the staining intensity matched that on B cells. Amplification of cDNA with primers spanning CD45 exons 4-6 showed a dramatic increase in the inclusion of these exons in thymocyte CD45 mRNA, establishing that the thunder mutation interferes with the normal CD45 exon 4-6 silencing process.||C57BL/6JSfdAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Poor||||No|06-Feb-2006|Cryopreserved sperm|48.0|0.0|Unknown||T cell, B cell, lymphocyte, CD45, ENU, NIH|Yes| 74.0|theoden ; ENU4AT:050 |STOCK H2 Fas/AnuApb|STOCK H2 Fas/AnuApb|Recessive|Fas (TNF receptor superfamily member 6)|Fas|Nil|APO-1, CD95, TNFR6, Tnfrsf6|MGI:95484|theoden|Fas|MGI:4455060|19|ENSMUSG00000024778|ENSMUST00000025691|Fas-201|416|422|G to A|ENSMUSE00000144910|4|139|Cysteine to Tyrosine|||||CTACTGCGATTCTCCTGGCTGTGAACACTGTGTTCGCTGCGCCTCGTGTGAACATGGAACC|Yes||||histocompatibility-2, MHC|H2||H-2, MHC-II|MGI:95894|histocompatibility-2, MHC; k2 variant|H2|MGI:4936842|17|Antinuclear autoantibodies, lymphadenopathy.||C57BL/6JStdAnu x C57BL/10.Cg-H2|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|20-Apr-2004|Cryopreserved sperm|44.0|0.0|Unknown||B cell, T cell, lymphadenopathy, ENU, Wellcome Trust|Yes| 8731.0|Foxo1flox:Mb1CreERT2:B1-8:Tomato|B6.129-Cd79a Foxo1 Igh Gt(ROSA)26Sor/AnuApb||Recessive|forkhead box O1|Foxo1|Normal|Afxh, FKHR, Fkhr1, Foxo1a|MGI:1890077|forkhead box O1; targeted mutation 1, Richard A Flavell|Foxo1|MGI:3840910|3|||||||||||||||||||||||||||||Normal||C57BL/6J|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|12-Jun-2019|Cryopreserved sperm|36.0|0.0|Unknown||T cell, transcription|Yes| 8731.0|Foxo1flox:Mb1CreERT2:B1-8:Tomato|B6.129-Cd79a Foxo1 Igh Gt(ROSA)26Sor/AnuApb||Recessive|CD79A antigen (immunoglobulin-associated alpha)|Cd79a||Cd79a, Iga, Igalpha, Ig alpha, Ig-alpha, Ly54, Ly-54, mb-1|MGI:101774|CD79A antigen (immunoglobulin-associated alpha); targeted mutation 3, Michael Reth|Cd79a|MGI:5568505|7|||||||||||||||||||||||||||||Normal||C57BL/6J|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|12-Jun-2019|Cryopreserved sperm|||Unknown||T cell, transcription|Yes| 8731.0|Foxo1flox:Mb1CreERT2:B1-8:Tomato|B6.129-Cd79a Foxo1 Igh Gt(ROSA)26Sor/AnuApb||Recessive|immunoglobulin heavy chain complex|Igh|||MGI:96442|immunoglobulin heavy chain complex; targeted mutation 1, Michel C Nussenzweig|Igh|MGI:3712224|12|||||||||||||||||||||||||||||Normal||C57BL/6J|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|12-Jun-2019|Cryopreserved sperm|||Unknown||T cell, transcription|Yes| 8731.0|Foxo1flox:Mb1CreERT2:B1-8:Tomato|B6.129-Cd79a Foxo1 Igh Gt(ROSA)26Sor/AnuApb||Recessive|gene trap ROSA 26, Philippe Soriano|Gt(ROSA)26Sor||beta geo, Gtrgeo26, Gtrosa26, R26, ROSA26 |MGI:104735|gene trap ROSA 26, Philippe Soriano; targeted mutation 9, Hongkui Zeng|Gt(ROSA)26Sor|MGI:3809523|6|||||||||||||||||||||||||||||Normal||C57BL/6J|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|12-Jun-2019|Cryopreserved sperm|||Unknown||T cell, transcription|Yes| 10399.0| Dicer floxed:GtROSA |B6(Cg)-Dicer Gt(ROSA)26Sor/Anu||Dominant|dicer 1, ribonuclease type III|Dicer1|||MGI:2177178 |dicer 1, ribonuclease type III; targeted mutation 1, Brian D Harfe|Dicer |MGI:3589208|12|ENSMUSG00000041415|ENSMUST00000041987|||||||||||||||gene trap ROSA 26, Philippe Soriano||||||||||||Prone to seizures, handle gently and with hood light off.|Normal|C57Bl/6N|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|20-Dec-2023|Cryopreserved sperm|33.0|0.0|Unknown|||Possibly| 10393.0|gBT-1|C57BL/6-Tg(TcraHsv2.3,TcrbHsv2.3)L118-1Cbn/AnuApb||Dominant||||||||||||||||||||||||||transgene insertion L118-1, Frank Carbone||||||||||||Normal|Normal|Congenic B6 - B6Ncrl.SJL CD45.1|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|20-Dec-2023||0.0|0.0|Unknown|||Possibly| 2455.0|anubis|CBA/CaJAnu-Cd83/AnuApb|CBA/CaJAnu-Cd83/AnuApb|Recessive|CD83 antigen|Cd83|Unknown||MGI:1328316|anubis|Cd83|MGI:3819968|13|ENSMUSG00000015396|ENSMUST00000015540|Cd83-201||||||||43895078|4|||TTCTACCTGACACTCATCATTTTCACCTGCGTAAGTGTCTGGTCAAAGCACCTGTTGCTG|Yes|||||||||||||Fewer CD4 T cells in peripheral blood or in thymus. Decreased cell surface expression of MHC II and CD86 on dendritic cells and B cells. Antinuclear autoantibodies (homogeneous nuclear) although this was incompletely penetrant on B6 background and absent on CBAxB6 background and may or may not be linked to CD4 cell deficiency. ||CBA/CaJAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|14-Jan-2008|Cryopreserved sperm|35.0|0.0|Unknown||T cell, CD4, B cell, MHC II, ENU, Wellcome Trust|Yes| 4523.0|batface|BALB/c-Ctnnb1/HAnuApb||Recessive|catenin (cadherin associated protein), beta 1|Ctnnb1|Unknown|beta catenin, beta-catenin, Catnb|MGI:88276|catenin (cadherin associated protein), beta 1; batface|Ctnnb1|MGI:2656734|9|ENSMUSG00000006932|ENSMUST00000007130|Ctnnb1-001|1958|2245|C to A|ENSMUSE00001277189|12|653|Threonine to Lysine|||||ACTCCACTCCAGGAATGAAGGCGTGGCAACATACGCAGCTGCTGTCCTATTCCGAATGTCT|Yes|||||||||||||Homozygous null embryos show anterior-posterior axis formation anomalies, but develop to E 7. Multiple conditional mutations have shown defects in distinct stem cell types that result in proliferation defects, such as intestinal polyps, brain and spinalcord size anomalies, etc.|Craniofacial defects|BALB/c|No|No|Yes|No|No|Yes|No|Good|10||Het male x wt Balb/c female|No|27-Feb-2009|Cryopreserved sperm|90.0|0.0|Unknown||embryonic lethal, ENU, craniofacial, forebrain, exencephaly|Yes| 3686.0|Thoth ; ENU9B6:064a|C57BL/6JSfdAnu-Cd4/AnuApb|C57BL/6JSfdAnu-Cd4/AnuApb|Recessive|CD4 antigen|Cd4|Unknown|L3T4, Ly-4|MGI:88335|CD4 antigen; thoth|Cd4|MGI:4819162|6|ENSMUSG00000023274|ENSMUST00000024044|Cd4-001||||||||124823158|3|||CAGGGCACCTCAACTTCTTTTGTATGGCTTCGATTTGCAGGAGGTTCGCCTTCGCAGTTT|Yes|||||||||||||No CD4<+> T cells in thymus or periphery||C57BL/6JAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||4|affected x affected or affected x B6|No|26-Aug-2008|Cryopreserved sperm|55.0|0.0|Unknown||T cell, CD4, ENU, NIH, Wellcome Trust|Yes| 28.0|Armadillo|STOCK H2 Dsg4/AnuApb|STOCK H2 Dsg4/AnuApb|Recessive|desmoglein 4|Dsg4|Unknown|CDHF13, lah|MGI:2661061|armadillo|Dsg4|MGI:3846150|18||||||||||||||||No||||histocompatibility-2, MHC|H2||H-2, MHC-II|MGI:95894|histocompatibility-2, MHC; k2 variant|H2|MGI:4936842|17|Hairless and wrinkly. The Armadillo mice have a very short hair coat all over the body. The short hair is most pronounced on the extremities, eg. Ears, tail, muzzle and limbs up to the hock and elbow, and ventrally. The hair dorsally looks more normal, but it appears to lack guard hairs. This appearance is possibly due to breakage of all hair follicles causing an overall shorter appearance to the coat. The skin also appears slightly hyperaemic (reddened), but this could just be due to less hair coverage. The affected mice appear to have no whiskers and are also smaller than normal littermates. On histology, the most obvious feature is generalised epidermal hyperplasia. The affected mice also have an "onion bulb" appearance to the base of the hair follicle. Above this is an area of bright orange/pink staining which suggests premature cornification of the hair shaft and adjacent inner root sheath. Some mice had a mild neutrophilic infiltrate into the dermis and some mice had focal pink swellings of the hair fibres. The hair follicle produced is abnormal and prone to breakage resulting in short hair. ||C57BL/6JSfdAnu x B10.BR-H2|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||6|Affected male by unaffected female|No|06-Feb-2006|Cryopreserved sperm|87.0|0.0|Unknown||Hair, Coat, Epidermis, follicle, ENU|Yes| 90.0|Willow|C57BL/6JSfdAnu-Jak3/AnuApb|C57BL/6JSfdAnu-Jak3/AnuApb|Recessive|Janus kinase 3|Jak3|Nil||MGI:99928|willow|Jak3|MGI:3611885|8|ENSMUSG00000031805|ENSMUST00000051995|Jak3-001|2474|2771|G to T|ENSMUSE00000213233|18|825|Glycine to Valine|||||GAGACACCTTAAGTACATCTCTTTGCTGGGCAAGGGCAACTTTGGCAGCGTGGAGCTGTGC|No|||||||||||||Lymphopenia due to reduction of both Thy1.2⁺ and B220⁺ cellsReduced numbers of CD8⁺ cellsB cell block in transition from pro-pre B cells; Develop autoimmune inflammatory bowel disease associated with diarrhoea and prolapse. Homozygotes have reduced life span.? SCID phenotype.||C57BL/6JSfdAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Poor||||No|06-Feb-2006|Cryopreserved sperm|80.0|0.0|Unknown||B cell, T cell, maturation, lymphopenia, ENU|Yes| 7583.0|ENU26:008:Klotho|C57BL/6NCrlAnu-Kl/AnuApb|C57BL/6NCrlAnu-Kl/AnuApb|Recessive|klotho|Kl||alpha-kl|MGI:1101771|klotho; mutation 1, The Australian National University|Kl|MGI:5563457|5|ENSMUSG00000058488|ENSMUST00000078856|Kl-201|984|1094|G to A|ENSMUSE00000191090|2|328|Tryptophan to STOP|||||CAGAAGTCTCTTGACTTTGTGCTAGGCTGGTTTGCCAAACCCATATTTATTGATGGCGACT||||||||||||||MacropathologyThe mouse displayed moderate dehydration and respiratory distress before euthanasia. Loops of small intestine were noted in the thoracic cavity upon opening of the thoracic cavity indicating the presence of a diaphragmatic hernia. The spleen was very small and the kidneys were bronze. No masses were noted on thepaws at necropsy.HistopathologyBrain, salivary gland, liver, oesophagus, ileum, caecum, colon, pancreas, lung – unremarkable.KidneyThe kidney displays severe mineralisation of the cortex. The areas of mineralisation are multifocal to coalescingand involve the tubular tissues as well as blood vessel walls. There is golden pigment present in the medullarytubules and collecting ducts.DuodenumThe lamina propria of the duodenum is effaced by the presence of large amounts of mineralisation.HeartThe heart displays severe multifocal mineralisation of the aorta and large blood vessels. In addition, there issevere mineralisation of tracheal cartilage rings and submucosa (still attached to heart).StomachThe glandular stomach displays severe dilatation of occasional gastric glands with necrotic cellular content aswell as fragments of calcium. In addition, severe mineralisation of all small blood vessels and the entiresubmucosa of the glandular stomach is apparent. Furthermore, moderate mineralisation of the smooth muscleof the tunica muscularis is also evident.SpleenThe spleen indicates an immunocompromised phenotype with a complete absence of periarteriolar lymphoidsheaths. Minimal haemopoiesis is evident in the red pulp.PawsThere is evidence of small, focal areas of mineralisation in the dermal tissue, connective tissue as well asadjacent to the bone. The bones display moderate medullary haemorrhage and lack of trabeculae which maybe related to excessive bone destruction resulting in hypercalcaemia.DiagnosisSevere, chronic, multifocal mineralisation of glandular stomach, kidney, aorta, duodenum, trachea,dermis/connective tissue of paws.Minimal splenic haemopoiesis and absence of periarteriolar lymphoid sheaths.||C57BL/6NCrlAnu|Yes|Unknown|Yes|Yes|Unknown|Yes|No|Unknown||||No|05-Feb-2014|Cryopreserved sperm|29.0|0.0|Unknown||calcification|Yes| 5375.0|anubis|B6;CB-Cd83/AnuApb|B6;CB-Cd83/AnuApb|Recessive|CD83 antigen|Cd83|Unknown||MGI:1328316|anubis|Cd83|MGI:3819968|13|ENSMUSG00000015396|ENSMUST00000015540|Cd83-201||||||||43895078|4|||TTCTACCTGACACTCATCATTTTCACCTGCGTAAGTGTCTGGTCAAAGCACCTGTTGCTG|Yes|||||||||||||Fewer CD4 T cells in peripheral blood or in thymus. Decreased cell surface expression of MHC II and CD86 on dendritic cells and B cells. Antinuclear autoantibodies (homogeneous nuclear) although this was incompletely penetrant on B6 background and absent on CBAxB6 background and may or may not be linked to CD4 cell deficiency. ||C57BL/6JAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|22-Dec-2010|Cryopreserved sperm|18.0|0.0|Unknown||T cell, CD4, B cell, MHC II, ENU, Wellcome Trust|Yes| 5237.0|Warpy ; ENU15embryo:006 ; Marawarpina|C57BL/6JAnu-Dzip1l/AnuApb|C57BL/6JAnu-Dzip1l/AnuApb|Recessive|DAZ interacting protein 1-like|Dzip1l|||MGI:1919757|DAZ interacting protein 1-like; Warpy|Dzip1l|MGI:5563494|9|ENSMUSG00000037784|ENSMUST00000078367|Dzip-1l-001|1123|1326|C to T|ENSMUSE00000325142|8|375|Glutamine to STOP|||||TGTCTCAGGACCAGAAGAAAGCAGCTGCCCAGTCTCAGCGCCATATCAATGCCCTCCGTGC|Yes|||||||||||||Polydactlyly and craniofacial dismorphology in embryos at e14.5.Extra digits on each limb some have 6 some have 7) and there is a craniofacial dismorphology (the front of the head protrudes, the eye position is changed and there is a mandible malformation.|Normal|C57BL/6JAnu|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Excellent||G1||No|12-Oct-2010|Cryopreserved sperm|98.0|0.0|Unknown||polydactyly, ENU|No| 4498.0|primurus, ENU7B6:079|C57BL/6JAnu-Dock8/AnuApb|C57BL/6JAnu-Dock8/AnuApb|Recessive|dedicator of cytokinesis 8|Dock8|Unknown||MGI:1921396|primurus|Dock8|MGI:3835421|19|ENSMUSG00000052085|ENSMUST00000025831|Dock8-201|5479|5601|T to C|ENSMUSE00000145941|42|1827|Serine to Proline|||||AACCCGCAATCACGAAGCTCCCGGAGATCTCACATAGACTAGAGGGATTTTATGGCCAGTG|Yes|||||||||||||Defective antibody response to immunization: failure to sustain antibody formation, undergo affinity maturation or to mount heightened recall (memory) response upon booster immunization. DOCK8-mutant B cells were unable to form marginal zone B cells or to persist in germinal centers and undergo affinity maturation. Dock8 mutations disrupted accumulation of the integrin ligand ICAM-1 in the B cell immunological synapse but did not alter other aspects of B cell antigen receptor signaling.||C57BL/6JAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|25-Feb-2009|Cryopreserved sperm|62.0|0.0|Unknown||memory, antibody, immunization, ENU, Wellcome Trust, B cell, GTP|Yes| 7674.0|ENU25:036:DDX21|C57BL/6NCrlAnu-Ddx21/AnuApb|C57BL/6NCrlAnu-Ddx21/AnuApb|Recessive|DEAD (Asp-Glu-Ala-Asp) box polypeptide 21|Ddx21|Unknown|D10Ertd645e, D10Wsu42e, RH II/Gu, RH-II/Gualpha|MGI:1860494|DEAD (Asp-Glu-Ala-Asp) box polypeptide 21; mutation 1, The Australian National University|Ddx21|MGI:5563491|10|ENSMUSG00000020075|ENSMUST00000045866|Ddx21-201|577|661|C to A|||193|Glutamic acid to STOP|||||AGCTGAAGAATGGACTCTCCCAACCTTCCGAAGAAGAGGTAGACATTCCTAAGCCCAAGAA||||||||||||||Embryonic lethal|Normal blood lymphocyte populations as measured by expression of following proteins: B220, CD3, CD4, CD44, KLRG1, NK1.1, IgM, IgD measured by flow cytometry.|C57BL/6NCrlAnu|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||G5|Het x Het|No|08-May-2014|Cryopreserved sperm|26.0|0.0|Unknown||ENU, embryonic lethal|Yes| 2164.0|Delficio ; ENU8F:005|B6;CBA-Clcn1/AnuApb|B6;CBA-Clcn1/AnuApb|Recessive|chloride channel 1|Clcn1|Unknown|Clc-1, Clc1, nmf310, NMF355, nmf355, SMCC1|MGI:88417|chloride channel 1; mutation 1, The Australian National University|Clcn1|MGI:5563496|6|ENSMUSG00000029862|ENSMUST00000031894|Clcn1-201|99|181|C to A|ENSMUSE00000712505|1|32|Tyrosine to STOP|||||TACATGCCCTTTGAACATTGTACCAGCTACGGACTGCCCTCAGAGAATGGGGGCCTTCAGC|Yes|||||||||||||Progressive hindlimb weakness and ataxia with stiff gait. Develops sensory deficits and shows periods of increased muscular tone/tetany.||C57BL/6JSfdAnu x CBA/H|Yes|No|Yes|Yes|No|Yes|No|Poor||4|Het x Het|No|15-Oct-2007|Cryopreserved sperm|52.0|0.0|Unknown||Ataxia, weakness, hind limb, muscle, ENU|Yes| 7549.0|ENU24:048:Dennd5b|C57BL/6NCrlAnu-Dennd5b/AnuApb|C57BL/6NCrlAnu-Dennd5b/AnuApb|Recessive|DENN/MADD domain containing 5B|Dennd5b||9330160C06Rik, D030011O10Rik|MGI:2444273|DENN/MADD domain containing 5B; mutation 1, The Australian National University|Dennd5b|MGI:5563480|6|ENSMUSG00000030313|ENSMUST00000111557|Dennd5b-001|2344|2715|A to G|ENSMUSE00000898644|10|782|Cysteine to Arginine|||||TGGAAGAAAACACCTTGATCGCCAGCCTGTGTGACCTACTGGAGAGGATATGGAGCCACGG||||||||||||||Normal blood lymphocyte populations as measured by expression of following proteins: B220, CD3, CD4, CD44, KLRG1, NK1.1, IgM, IgD by flow cytometry.|Normal blood lymphocyte populations as measured by expression of following proteins: B220, CD3, CD4, CD44, KLRG1, NK1.1, IgM, IgD by flow cytometry.|C57BL/6NCrlAnu|Yes|Unknown|Yes|Yes|Unknown|Yes|No|Unknown||G5||No|19-Dec-2013|Cryopreserved sperm|46.0|0.0|Unknown||ENU|Yes| 5530.0|ENU16WT:029|C57BL/6JAnu-Inpp5d/AnuApb|C57BL/6JAnu-Inpp5d/AnuApb|Recessive|inositol polyphosphate-5-phosphatase D|Inpp5d|Unknown|s-SHIP, SHIP, SHIP-1, SHIP1, Src homology 2 domain-containing inositol-5-phosphatase|MGI:107357|inositol polyphosphate-5-phosphatase D; mutation 1, The Australian National University|Inpp5d|MGI:5563462|1|ENSMUSG00000026288|ENSMUST00000169754|Inpp5d-001|1411|1588|T to C|ENSMUSE00000157571|12|471|Serine to Proline|||||AGAAGGAGTGGCTGGAGCTACTCAGGCACTCCCTGCAAGAAGTCACCAGCATGACATTTAA||||||||||||||Animals begin to show signs of ill health between 7 and 12 weeks of age. Examination by pathologist of an affected animal gave the following report:1.Intra-alveolar acidophilic macrophage pneumonia with scattered microhaemorrhages. A superimposed recent suppurative bronchiolar pneumonia with microabscesses and early bronchitis.2.Histiocytic (B cell) Lymphoma involving mediastinal lymph nodes, lung, spleen and small intestine.3.The micromorphological changes in the lymphoid tissues were examined by three Veterinary Histopathologists and by consensus there was agreement that there was a histiocytic B cell type of lymphoma involving nodes, lung, small intestine and spleen (minimally).|Macroscopically normal. Detailed pathology not performed.|C57BL/6JAnu|No|Unknown|Yes|No|Unknown|Yes|No|Good|||Het x Het|No|06-Jul-2011|Cryopreserved sperm|31.0|0.0|No||ENU, pneumonia, macrophage|Yes| 5070.0|Warmflash|C57BL/6J-Flt3/BtlrAnuApb|C57BL/6J-Flt3/BtlrAnuApb|Recessive|FMS-like tyrosine kinase 3|Flt3|Unknown|CD135, Flk-2, Flk2, Flt-3, wmfl|MGI:95559|FMS-like tyrosine kinase 3; mutation 1, Bruce Beutler|Flt3|MGI:3628823|5|ENSMUSG00000042817|ENSMUST00000049324|Flt3-001||||||||147367088|8|||AATATCTAATTTGTAAATTTCCTTTTTACAGAAAAAGGGTTTATAAACGCTACCAGCTCG|Yes|||||||||||||Susceptible to Mouse cytomegalovirus (MCMV) at a dose of 1x10<5> PFU.Decreased dendritic cell number: conventional DCs are reduced in bone marrow and spleen.Decreased plasmacytoid dendritic cell number: both the number and percentage of pDCs are reduced in bone marrow and spleen.Decreased NK cell number: splenic NK cells are reduced in percentage and number, bone marrow NK cells are only moderately reduced.Decreased splenocyte number: spleens and lymph nodes are consistently smaller and show reduced cellularity.Small lymph nodes.Abnormal dendritic, marcophage and NK cell physiology.Decreased body weight.||C57BL/6J|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|25-Mar-2010|Cryopreserved sperm|50.0|0.0|Unknown||infection, MCMV, ENU, dendritic cell, marcophage, NK cell, ENU|Yes| 7584.0|Eeyore C57BL/6J|C57BL/6J-Muc2/AnuUqApb||Recessive|Mucin 2|Muc2|Unknown||MGI:1339364|mucin 2; eeyore|Muc2|MGI:5471473|7|ENSMUSG00000025515|ENSMUST00000026590|Muc2-201|5038|5038|T to C|ENSMUSE00000526021|32|1680|Serine to Proline|||||TAGAAGCCAAGATCTCCTACAATGGCCTTTCTTTCTCCATCCGGCTGCCCTACAAACTGTT|No|||||||||||||Intestinal inflammation. Spontaneous diarrhoea and colitis, compromised barrier function, hypersusceptible to dextran sulfate colitis, deficiency of goblet cells, goblet cell apoptosis, endoplasmic reticulum stress, misfolding of mucin-2.|Minor histological changes in the intestinal tract only, no disease phenotype|C57BL/6J|Yes|Yes|Yes|Yes|Yes|Yes|No|Poor|11|0|heterozygous x heterozygous|No|12-Feb-2014|Cryopreserved sperm|50.0|0.0|Yes|Inflammatory bowel disease|diarrhoea, inflammatory bowel disease, colitis, ENU, mucus, malabsorption|Yes| 7552.0|ENU25:011:Gdpd3:B6|C57BL/6NCrlAnu-Gdpd3/AnuApb|C57BL/6NCrlAnu-Gdpd3/AnuApb|Recessive|glycerophosphodiester phosphodiesterase domain containing 3|Gdpd3|Unknown|1110015E22Rik|MGI:1915866|glycerophosphodiester phosphodiesterase domain containing 3; mutation 1, The Australian National University|Gdpd3|MGI:5563465|7|ENSMUSG00000030703|ENSMUST00000032944|Gdpd3-201|354|411|C to A|ENSMUSE00000202169|4|118|Tyrosine to STOP|||||CCCCTCTACAAGGAAGAGTTGGAAATTTACTTCTCACCAGGCCATTTTGCCCACGGGTCAG||||||||||||||Normal blood lymphocyte populations as measured by expression of following proteins: B220, CD3, CD4, CD44, KLRG1, NK1.1, IgM, IgD by flow cytometry.|Normal blood lymphocyte populations as measured by expression of following proteins: B220, CD3, CD4, CD44, KLRG1, NK1.1, IgM, IgD by flow cytometry.|C57BL/6NCrlAnu|Yes|Unknown|Yes|Yes|Unknown|Yes|No|Poor||G4||No|19-Dec-2013|Cryopreserved sperm|56.0|0.0|Unknown||ENU|Yes| 5151.0|BOOREANA:::B6 ; Ped11.28 ; ENU11B6:028|C57BL/6JAnu-Myb/AnuApb||Recessive|myeloblastosis oncogene|Myb|Unknown|c-myb|MGI:97249|myeloblastosis oncogene; booreana|Myb|MGI:4867909|10|ENSMUSG00000019982|ENSMUST00000020156|Myb-201|923|1189|A to G|ENSMUSE00000644654|8|308|Glutamic acid to Glycine|||||GGAGTTGCTCCTGATGTCAACAGAGAACGAGCTGAAGGGACAGCAGGCATTACCAACACAG|Yes|||||||||||||E14.5 embryo:15x increase in platelet numbers2x increase in stem cells in foetal liver.Increase in primitive RBCDecrease in definitive RBCIncrease in haemopoietic progenitor cellsPups are born and survive to adulthood. Adults display a 5x increase in platelet numbers|Normal|C57BL/6JAnu|Yes|Unknown|Yes|Yes|Unknown|Yes|No|Unknown||||No|11-Jun-2010|Cryopreserved sperm|55.0|0.0|Unknown||haemopoiesis, stem cell, platelet, differentiation, transcription factor, proliferation, ENU|Yes| 5206.0|theoden ; ENU4AT:050 |STOCK H2/H2 Fas/AnuApb|STOCK H2/H2 Fas/AnuApb|Recessive|Fas (TNF receptor superfamily member 6)|Fas|Nil|APO-1, CD95, TNFR6, Tnfrsf6|MGI:95484|theoden|Fas|MGI:4455060|19|ENSMUSG00000024778|ENSMUST00000025691|Fas-201|416|422|G to A|ENSMUSE00000144910|4|139|Cysteine to Tyrosine|||||CTACTGCGATTCTCCTGGCTGTGAACACTGTGTTCGCTGCGCCTCGTGTGAACATGGAACC|Yes||||Histocompatibility-2, MHC|H2||H-2, MHC-II|MGI:95894|histocompatibility-2, MHC; k variant|H2|MGI:3579322|17|Antinuclear autoantibodies, lymphadenopathy.||C57BL/6JStdAnu x C57BL/10.Cg-H2|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|16-Aug-2010|Cryopreserved sperm|19.0|0.0|Unknown||B cell, T cell, lymphadenopathy, ENU, Wellcome Trust|Yes| 2377.0|Pengu, ENU8B6:075|C57BL/6Apb-Gdf5/AnuApb|C57BL/6Apb-Gdf5/AnuApb|Recessive|growth differentiation factor 5|Gdf5|Unknown|bp, brp, cartilage-derived morphogenetic protein-1, CDMP-1|MGI:95688|growth differentiation factor 5; pengu|Gdf5|MGI:3847115|2|ENSMUSG00000038259|ENSMUST00000040162|Gdf5-001|2|314|T to C|ENSMUSE00000323175|1|1|Methionine to Threonine|||||ATGAGACTCCCCAAACTCCTCACTCTTTTGCTG|No|||||||||||||Limb deformity. Four shortened limbs with angular deformity, most pronounced in hindlimbs||C57BL/6|Yes|No|Yes|Yes|No|Yes|No|Good||||No|14-Dec-2007|Cryopreserved sperm|53.0|0.0|Unknown||Limb, deformity, Brachypodism, Feet, ENU|Yes| 157.0|Lochy|C57BL/6JSfdAnu-Ptprc/AnuApb|C57BL/6JSfdAnu-Ptprc/AnuApb|Recessive|Protein tyrosine phosphatase, receptor type, C|Ptprc|Nil|B220, CD45, CD45R, Ly-5|MGI:97810|Lochy|Ptprc|MGI:3611894|1|ENSMUSG00000026395|ENSMUST00000027645|Ptprc-201||||||||139980367|20|||TCCATAAATGACTGTTCTCTTTGTGTGTTTTGATCAGGGCTTCAAGGAACCCAGGAAATA|Yes|||||||||||||Decreased expression of CD45 on CD19⁺ B cellsloc/loc mice have normal numbers of B cellsCell intrinsic defectSlightly reduced levels of IgM⁺IgD⁻, IgM⁺IgD⁺ and IgD⁺CD21⁺ cellsReduced levels of B220loCD19⁺ cells but normal levels of B220⁺CD19⁺ in bone marrow3 fold decrease in DP thymocytes10 fold decrease in CD4 SP thymocytes5 fold decrease in CD8 SP thymocytesDP thymocytes had 2.5 fold increase in expression of CD4 and CD8, cell intrinsic Co-receptor expression on SP T cells was increased 1.5 foldDramatic decrease in CD8⁺CD44lo/med cellsTCRβ is up-regulated on DP thymocytes and down regulated on mature T cells. CD5 is down-regulated on DP thymocytes and up-regulated on peripheral T cells.Decrease in DP thymocytes is not cell intrinsicDecrease in SP thymocytes is cell intrinsicThe decrease of CD69 and CD5 on thymocytes in thymus was cell intrinsicNo CD45 protein visually detected by Western blottingInhibition of DN cells progressing to DPBlock preventing DP thymocytes maturing to SP T cells attributed to defective thymic selectionDecrease in peripheral T cellsReduction in naïve CD8+ T cells and shift to activated/memory CD8⁺ T cell phenotypeLack of TCRβhi and CD69⁺ cells in thymus-implies defect in TCR signalling for positive selection||C57BL/6JSfdAnu|Yes|Yes|Yes|Yes|Yes|Yes|Yes|Excellent||7||No|06-Mar-2006|Cryopreserved sperm|75.0|0.0|Unknown||CD45, T cell, B cell, CD8, lymphocyte, ENU|Yes| 82.0|Tiny, ENU4AT:013 |STOCK Lig4/AnuApb|STOCK Lig4/AnuApb|Recessive|ligase IV, DNA, ATP-dependent|Lig4|Reduced|DNA ligase IV, ligase IV|MGI:1335098|tiny|Lig4|MGI:3714783|8|ENSMUSG00000049717|ENSMUST00000095476|Lig4-201|863|1161|A to G|ENSMUSE00000610685|2|288|Tyrosine to Cysteine|||||CATGCAGATGCACAAAGATGGCGCGCTGTACCGGTACTTCTCCAGAAACGGTTACAACTAT|No|||||||||||||Animal model for human LIGIV Syndrome. Small stature. Severe combined immune deficiency. Hypogammaglobulinemia, no antibody response to immunization, very few circulating B or T cells. Hemopoiesis defect. Hypoplastic anemia, hemopoietic stem cells unable to transplant, poorly proliferative in tissue culture, unable to compete with transplanted wild-type hemopoietic stem cells even in the absence of any conditioning regime. Non-homologous end-joining DNA repair defect. Reduced DNA ligase IV protein levels and enzymatic activity. Western blot and immunofluorescent analysis of extracts from homozygous mutant mouse embryonic fibroblasts (MEFs) reveal 5-fold reduction in the protein level. Although the mutant protein complexes stably with XRCC4, in vivo adenylation activity is reduced 10-fold in mutant versus wild type MEFs.||C57BL/6JSfdAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|28-Apr-2004|Cryopreserved sperm|18.0|0.0|Yes||T cell, CD8, severe combined immunodeficiency, DNA repair, ENU, Wellcome Trust|Yes| 2441.0|Kenny ; ENU9CAT:040|C57BL/6JAnu-Muc2/AnuApb||Recessive|mucin 2|Muc2|Unknown||MGI:1339364|kenny|Muc2|MGI:4820425|7|ENSMUSG00000025515|ENSMUST00000026590|Muc2-202|4187|4192|C to A|ENSMUSE00000519387|31|1396|Serine to STOP|||||AATGGAATACTGTACTCCTTCAACTATCTCACCTACAACTTCAACAACAACCTTGTCTACC|No|||||||||||||Diarrhoea.Multiple plaques on GIT and lymphomegaly.Other mutants homozygote for a point mutation have soft feces at weaning and develop diarrhea associated with malapsorption syndrome. Homozygous null mutants pass blood in their feces at 6 months, and 65% of null mutants have intestinal tumors at 1 year.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|14-Jan-2008|Cryopreserved sperm|11.0|0.0|Unknown||malabsorption, colon, goblet cells, diarrhoea, ENU|Yes| 8743.0|ASD696:Thunderbird|C57BL/6NCrlAnu-Ifne/AnuApb||Recessive|interferon epsilon|Ifne||Ifne1, Ifnt1|MGI:2667156|Ifne, endonuclease-mediated mutation 2, Australian National University|Ifne||4||||||||||Unknown to Unknown|||||||||||||||||||Unknown|Unknown|C57BL/6NCrlAnu|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|28-Jun-2019|Cryopreserved sperm|44.0|0.0|Unknown|||Yes| 4512.0|bata ;ENU8B6:058|C57BL/6JSfdAnu-Pnp/AnuApb||Recessive|purine-nucleoside phosphorylase|Pnp||Np, Np-1, Np-2, Pnp, Pnp1|MGI:97365|bata|Pnp|MGI:5468722|14|ENSMUSG00000021871|ENSMUST00000048615|Pnp-001|644|925|A to T|ENSMUSE00000617134|5|215|Aspartic acid to Valine|||||GAGTCGTCTGCTAAAGATGCTGGGGGCAGATGCTGTTGGCATGAGCACAGTCCCAGAAGTT|Yes|||||||||||||Decreased anti-IgM B cell proliferation in vitro, age-dependent increase in CD44hi ICOShi CD4 cells and decrease in marginal zone B cells.||C57BL/6JSfdAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|26-Feb-2009|Cryopreserved sperm|89.0|0.0|Unknown||B cell, T cell, ENU, Wellcome Trust|Yes| 45.0|Jasmine|C57BL/6JSfdAnu-Tap2/AnuApb|C57BL/6JSfdAnu-Tap2/AnuApb|Recessive|transporter 2, ATP-binding cassette, sub-family B (MDR/TAP)|Tap2|Normal|ABC18, Abcb3, Ham-2, HAM2, Ham2, MTP2, PSF-2, PSF2, RING11, Tap-2, Y1|MGI:98484|jasmine|Tap2|MGI:3611893|17|ENSMUSG00000024339|ENSMUST00000025197|Tap2-001|874|1292|A to C|ENSMUSE00000141074|5|292|Threonine to Proline|||||TCTTCATGCTCCAGGTATCGCCCCGACTCACCTTCCTCTCCCTGCTGGACCTGCCCCTCAC|Yes|||||||||||||No CD8⁺ T cells.Normal CD4⁺ and B cells||C57BL/6JSfdAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|06-Feb-2006|Cryopreserved sperm|117.0|0.0|Yes|Bare Lymphocyte syndrome type 1|Tap2, T cell, CD8, CD4, ENU, Tap1, Bare Lymphocyte syndrome type 1|Yes| 7553.0|ENU25:021:MAP4K1:B6|C57BL/6NCrlAnu-Map4k1/AnuApb|C57BL/6NCrlAnu-Map4k1/AnuApb|Recessive|mitogen-activated protein kinase kinase kinase kinase 1|Map4k1|Unknown|Hpk1|MGI:1346882|mitogen-activated protein kinase kinase kinase kinase 1; mutation 1, The Australian National University|Map4k1|MGI:5563448|7|ENSMUSG00000037337|ENSMUST00000085835|Map4k1-201|400|502|A to G|ENSMUSE00000473624|6|134|Isoleucine to Leucine|||||GACTGGCCTACCTGCATTCAGAGAAGAAGATACATCGAGACATCAAGGGAGCCAACATCCT||||||||||||||Normal blood lymphocyte populations as measured by expression of following proteins: B220, CD3, CD4, CD44, KLRG1, NK1.1, IgM, IgD by flow cytometry.|Normal blood lymphocyte populations as measured by expression of following proteins: B220, CD3, CD4, CD44, KLRG1, NK1.1, IgM, IgD by flow cytometry.|C57BL/6NCrlAnu|Yes|Unknown|Yes|Yes|Unknown|Yes|No|Unknown||G4||No|19-Dec-2013|Cryopreserved sperm|26.0|0.0|Unknown||ENU|Yes| 59.0|Nessy|C57BL/6JSfdAnu-Ncaph2/AnuApb |C57BL/6JSfdAnu-Ncaph2/AnuApb |Recessive|non-SMC condensin II complex, subunit H2|Ncaph2|Unknown|Kleisin beta|MGI:1289164|nessy|Ncaph2|MGI:3710093|15|ENSMUSG00000008690|ENSMUST00000074552|Ncaph2-001|44|144|T to A|ENSMUSE00000504356|1|15|Isoleucine to Asparagine|||||GGTGCGCTTTGCTCACCTCTTGCAGCCCATCCGGGATCTCACTAAGAACTGGGAGGTGGAC|Yes|||||||||||||The nessy mouse has a defect in T lymphocyte development that decreases circulating T cell numbers, increases their expression of the activation/memory marker CD44, and dramatically decreases the numbers of CD4(+)CD8(+) thymocytes and their immediate DN4 precursors. Thymic T cell differentiation defect at DN-DP transition, low peripheral T cell numbers, remaining cells all CD44high, Two fold more gd T cells, Defect resembles mice with exaggerated TCR signalling due to defects in c-cbl and slap proteins and defects in cbl plus cbl-b. No defect in B cells. Homozygotes grow at normal rate, size and are fertile. Intrinsic to T cells.Despite the ubiquitous expression and role of condensins, kleisin beta(nes/nes) mice were viable, fertile, and showed no defects even in the parallel pathway of B cell lymphocyte differentiation. ||C57BL/6JSfdAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|06-Feb-2006|Cryopreserved sperm|79.0|0.0|Unknown||T cell, lymphocyte, condensin, differentiation, ENU|Yes| 4.0|San Roque|C57BL/6JSfdAnu-Rc3h1/AnuApb |C57BL/6JSfdAnu-Rc3h1/AnuApb|Recessive|RING CCCH (C3H) domains 1|Rc3h1|Unknown|Roquin|MGI:2685397|sanroque|Rc3h1|MGI:3581675|1|ENSMUSG00000040423|ENSMUST00000035911|Rc3h1-201|596|981|T to G|ENSMUSE00000536751|5|199|Methionine to Arginine|||||TAGGGGCTGCCAGTTCCTTGGACCAGCGATGCAGGAGGAAGCTCTGAAGCTGGTCTTGCTG|Yes|||||||||||||Spontaneous autoimmune disease. Systemic lupus erythematosus. Anti-nuclear autoantibodies (ANA), hypergammaglobulinemia, autoimmune nephritis, lymphadenopathy, increased numbers of CD44high activated memory T cells, increased numbers of T follicular helper cells, spontaneous germinal centres, CD28-independent activation of T cells. Increased ICOS mRNA and protein expression on T cells, defect in micro-RNA (mir) inhibition of mRNA stability.|Low penetrance in hets|C57BL/6JSfdAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|28-Nov-2005|Cryopreserved sperm|155.0|20.0|Yes||Systemic lupus erythematosus (SLE), autoimmunity, T cell, ubiquitin ligase, Wellcome Trust, ENU, lymphadenopathy|Yes| 4118.0|Wobbly ; ENU9B6:046a|C57BL/6JSfdAnu-Elp6/AnuApb|C57BL/6JSfdAnu-Elp6/AnuApb|Recessive|elongator acetyltransferase complex subunit |Elp6|Unknown|2610001P13Rik, 2610002I17Rik, Tmem103|MGI:1919349|elongator acetyltransferase complex subunit ; mutation 1, The Australian National University|Elp6|MGI:5563405|11|||||||||||||||||||||||||||||Affected mice have uncoordinated movement. Video available.Fertility of affecteds is unknown.||C57BL/6JSfdAnu|Yes|Unknown|Yes|Yes|Unknown|Yes|No|Unknown||5||No|05-Dec-2008|Cryopreserved sperm|42.0|0.0|Unknown||Motion, Movement, Shaky, wobble, ENU, ataxia|Yes| 6.0|Face|C57BL/6JSfdAnu-Stat1/AnuApb|C57BL/6JSfdAnu-Stat1/AnuApb|Recessive|signal transducer and activator of transcription 1|Stat1|Unknown|STAT-1|MGI:103063|face|Stat1|MGI:3611892|1|ENSMUSG00000026104|ENSMUST00000070968|Stat1-201|1978|2329|T to A|ENSMUSE00000630003|22|660|Methionine to Lysine|||||TCCCAGATATTATTCGCAACTACAAAGTCATGGCTGCCGAGAACATACCAGAGAATCCCCT|Yes|||||||||||||Diminished Th1 antibody formation upon immunization with heat-killed Bordetella pertussis bacilli. Increase proportion of CD44hi activated/memory T cells in a subset of animals and increased IgE.||C57BL/6JSfdAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Poor||16|hom x hom|No|28-Nov-2005|Cryopreserved sperm|140.0|0.0|Unknown||T cell, hypergammaglobulinaemia, B cell, ENU, Wellcome Trust|Yes| 64.0|Fragile red (redburst, fred, snow), ENU5WT:027 |STOCK H2 Steap3/AnuApb|STOCK H2 Steap3/AnuApb|Recessive|STEAP family member 3|Steap3|Nil|pHyde|MGI:1915678|fragile-red|Steap3|MGI:3758911|1|ENSMUSG00000026389|||862|1292|T to C|ENSMUSE00000158639|4|288|Tyrosine to Histidine|||||CTGCGCTTCAGCTGCGGAGGGGGACCAAGTACCAGCGCTTCCCAGACTGGCTGGACCACTG|Yes||||histocompatibility-2, MHC|H2||H-2, MHC-II|MGI:95894|histocompatibility-2, MHC; k2 variant|H2|MGI:3579322|17|Hypochromic microcytic anemia, erythrocyte poikilocytosis, defect in iron transport, defect in endosomal targeting to acidified endosomes.Mutation disrupts the endosomal targeting motif of the Steap3 protein.||C57BL/6JSfdAnu x B10.BR-H2|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|28-Apr-2004|Cryopreserved sperm|28.0|0.0|Unknown||anaemia, erythrocyte, endosome, ENU, Wellcome Trust, red blood cell|Yes| 4505.0|Duane ; ENU6NIHB:019|C57BL/6JSfdAnu-Tbx21/AnuApb|C57BL/6JSfdAnu-Tbx21/AnuApb|Recessive|T-box 21|Tbx21|Reduced|T-bet, Tblym, TBT1|MGI:1888984|T-box 21; Duane|Tbx21|MGI:4367995|11|ENSMUSG00000001444|ENSMUST00000001484|Tbx21-001||||||||96962921|2|||CTGGTCGATACTTGACAATAAGGTTAACTGTCCACAGGGAACCGCTTATATGTCCACCCA|Yes|||||||||||||Defective antibody response to immunization: failure to mount a normal Th1 polarized IgG2c antibody response to heat killed B pertussis bacteria. Few circulating NK cells.Decreased NK cell number: the percent of NK cells in the blood, spleen, and liver is lower than in wild-type mice.Increased NK cell number:* the frequency of NK cells in the peripheral lymph nodes and bone marrow is increased compared to in wild-type mice.* NK cells accumulate in lymph nodes due to defective egression.Absent NK T cells: mice exhibit a near complete absence of invariant natural killer T cells unlike in wild-type mice.Abnormal NK cell differentiation:* NK cells exhibit an immature phenotype unlike in wild-type mice.* NK cells accumulate in lymph nodes due to defective egression.* in reconstitution experiments, derived NK cells accumulate in the peripheral lymph nodes due to defective egression.||C57BL/6JAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|26-Feb-2009|Cryopreserved sperm|70.0|0.0|Unknown||antibody, B cell, NK cell, ENU, Wellcome Trust, Natural Killer cell (NK), T cell, lymphocyte|Yes| 7658.0|ENU17Ch14:KLHL6|C57BL/6JAnu-Klhl6/AnuApb|C57BL/6JAnu-Klhl6/AnuApb|Recessive|kelch-like 6|Klhl6|||MGI:2686922|kelch-like 6; mutation 1, The Australian National University|Klhl6|MGI:5563461|16|ENSMUSG00000043008|ENSMUST00000058839|Klhl6-001|799|834|C to T|ENSMUSE00000346330|3|267|Tryptophan to STOP|||||AGAATGTGCGTTTACCACTTCTGGATCCGTGGTACTTCGTGGAGATGGTTGAAGCAGACCC||||||||||||||Reduced numbers of B cells, increased numbers of immature B cells and reduced numbers of mature B cells.|Normal|C57BL/6JAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||G7||No|11-Apr-2014|Cryopreserved sperm|26.0|0.0|Unknown||B cell, lymphocyte, ENU|No| 7664.0|APN 436|C57BL/6N-A Katnal2/MarpApb||Recessive|katanin p60 subunit A-like 2|Katnal2 |||MGI:1924234|katanin p60 subunit A-like 2; targeted mutation 1a, Wellcome Trust Sanger Institute|Katnal2|MGI:4842422|18|||||||||||||||||||||||||||||Unknown|Normal|C57BL/6N|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|15-Apr-2014|Cryopreserved sperm|40.0|0.0|Unknown|||Possibly| 123.0|CD40L -/- TCR|B10JAnu.Cg-H2 Cd40lg Tg(TcrHEL3A9)1Mmd/AnuApb|B10JAnu.Cg-H2 Cd40lg Tg(TcrHEL3A9)1Mmd/AnuApb|Recessive|CD40 ligand|Cd40lg|Nil|CD154, Cd40L, gp39, HIGM1, IMD3, Ly-62, T-BAM, Tnfsf5|MGI:88337|targeted mutation 1, Richard A Flavell|Cd40lg|MGI:2182733|X||||||||||||||||No|transgene insertion 1, Mark M Davis|TCR|||||||||||Homozygous mice display: - immune system, lymphoid development/B lymphocyte defects: - B cells failed to undergo isotype switching - failed to produce germinal centers in spleen in response to T-dependent antigens - reduced serum immunoglobulin concentrations (IgG1, IgG2a, IgG2b, IgG3), at 12 weeks of age, but not at 6 weeks of age - decreased IgM response to T-dependent antigens - failed to produce antigen-specific IgG1 after immunization - immune system, no defect detected: - no alterations in B or T lymphocyte development - T lymphocytes responded normally to mitogen stimulation - B lymphocytes had normal responses to T-independent antigens||C57BL/10J|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||16||No|06-Feb-2006|Cryopreserved sperm|150.0|0.0|No||B cell, T cell, immunoglobulin, germinal centre|Yes| 7621.0|EGFL6 His Siamese|C57BL/6J-Tg(CMV-Egfl6/His)||Dominant||||||||||||||||||||||||||EGF-like-domain, multiple 6|cytomegalovirus (CMV)|||||||||||Generally the EGFL6 transgenic mice appear normal and have not displayed any adverse effects due to genetic modifications. |Unknown|C57BL/6J|Yes|Yes|Unknown|Yes|Yes|Unknown|No|Good||||No|24-Mar-2014|Cryopreserved sperm|50.0|0.0|Unknown|||Possibly| 126.0|Charles ; ML5|C57BL/6JSfdAnu-Tg(ML5sHEL)5Ccg/AnuApb|C57BL/6JSfdAnu-Tg(ML5sHEL)5Ccg/AnuApb|Dominant||||||||||||||||||||||||||transgene insertion 5, Christopher C Goodnow|metallothionein I|high||||||||||Mice express a soluble form of hen egg lysozyme, levels are higher than similar strain C57BL/6-Tg(ML4sHEL)5Ccg/J.||C57BL/6JSfdAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||22|sib x sib|No|06-Feb-2006|Cryopreserved sperm|150.0|0.0|Yes||Hen egg lysozyme (HEL), autoimmunity, T cell, B cell, tolerance|Yes| 131.0|Guildenstern ; MD2|C57BL/6JSfdAnu-Tg(IghelMD2)Ccg/AnuApb|C57BL/6JSfdAnu-Tg(IghelMD2)Ccg/AnuApb|Dominant||||||||||||||||||||||||||Heavy chain trangene for anti-HEL IgM and IgD.|normal control elements and mRNA splicing|||||||||||B cells express chimeric Ig molecule of extracellular domain of IgM and intracellular domains of IgD. Ig has affinity for Hen Egg Lysozyme||C57BL/6JAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||2|sib x sib|No|06-Feb-2006|Cryopreserved sperm|20.0|0.0|No||Hen Egg Lysozyme (HEL), immunoglobulin, lymphocyte, T cell, B cell|Yes| 117.0|Carrie ; GM2|C57BL/6JSfdAnu-Tg(IghelMG)Ccg/AnuApb|C57BL/6JSfdAnu-Tg(IghelMG)Ccg/AnuApb|Dominant||||||||||||||||||||||||||transgene insertion 2, Christopher C Goodnow||low||||||||||B cells express immunoglobulin specific for Hen Egg Lysozyme.||C57BL/6JAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||21|Ig+ male x B6 female|No|06-Feb-2006|Cryopreserved sperm|36.0|0.0|No||Hen Egg Lysozyme, IgM, IgG, autoimmunity, tolerance, B cell|Yes| 113.0|Bcl-2 :B6:Ly5a|B6.Cg-Ptprc Tg(BCL2)22Wehi/WehiAnuApb|B6.Cg-Ptprc Tg(BCL2)22Wehi/WehiAnuApb|Recessive||||||||||||||||||||||||||transgene insertion 22, Walter and Eliza Hall Institute of Medical Research ; human Bcl-2|IgH enhancer and SV40 promoter|primarily expresses Bcl-2 in B cells (as opposed to Bcl-2-36 which is T and B and Bcl-2-25 which is T only)|protein tyrosine phosphatase, receptor type, C|Ptprc||B220, CD45, Ly-5, Lyt-4, T200|MGI:97810|protein tyrosine phosphatase, receptor type, C; a variant|Ptprc|MGI:4819849|1|During an immune response, hypermutation of immunoglobulin genes in B cells proliferating within germinal centres (GCs) generates variant antibodies that react with higher affinity against either foreign or self antigens. Several experiments suggest that self-reactive B cells may be censored at this stage of the immune response, but the rarity of these cells and the dynamic nature of GC reactions have prevented direct analysis. We have developed a new approach to visualize the fate of antigen-specific B cells during GC reactions by seeding an ongoing immune response with lysozyme-specific B cells from immunoglobulin-gene transgenic animals. Administration of soluble antigen at the peak of the GC response rapidly eliminates lysozyme-specific GC B cells in two waves of apoptosis, one within the GC and a second in cells that have redistributed to lymphoid zones that are rich in T cells. Elimination of these cells is inhibited by constitutive expression of the follicular lymphoma proto-oncogene bcl-2. These findings reveal censoring steps that may normally prevent affinity maturation of autoantibodies to systemic autoantigens, and might be used by pathogenic microorganisms or in clinical strategies to interfere with antibody responses.||C57BL/6|Yes|No|Yes|Yes|Yes|Yes|No|Good|18||B6Ly5a x Bcl-2Tg|No|06-Feb-2006|Cryopreserved sperm|150.0|0.0|No||B cell, germinal centre, selection, Bcl-2, autoimmunity|Yes| 114.0|Bcl-6 -/-|B6.129-Bcl6/AnuApb|B6.129-Bcl6/AnuApb|Recessive|B-cell leukemia/lymphoma 6|Bcl-6|Nil|Bcl5|MGI:107187|targeted mutation 1, Louis M Staudt|Bcl6|MGI:2158439|16||||||||||||||||No|||||||||||||Homozygous null mutants develop myocarditis and pulmonary vasculitis, show impaired germinal center formation in the spleen, and display T helper 2 cell hyperimmune responsiveness. Mice frequently die before reaching maturation.|||Yes|Yes|Yes|Yes|Yes|Yes|No|Poor||||No|06-Feb-2006|Cryopreserved sperm|100.0|0.0|Unknown||myocarditits, T cell, hyperimmune responsive, germinal centre|Yes| 160.0||B6.129P2-Cited1/Apb|B6.129P2-Cited1/Apb|X-linked|Cbp/p300-interacting transactivator with Glu/Asp-rich carboxy-terminal domian 1|Cited1|Nil|Msg1, ER154|MGI:108023|Cited1 targeted mutation 1, Sally L Dunwoodie|Cited1|MGI:3028946|X||||||||||||||||No|||||||||||||Results in impaired embryonic growth and survival due to defects in trophoblast and placental development.|Male hemizygotes have the same phenotype as the female homozygotes. Female heterzygotes have a variable phenotype depending on which parent the Cited1 allele is inherited from. Heterozygous females with paternally inherited Cited1 have no placental phenotype, whereas heterozygous females with maternally inherited Cited1 have the same placental phenotype as homozygotes|C57BL/6|No|No|Yes|No|No|No|No|Good|7|9|Cited1/Y x +/Cited1|No|08-Mar-2006|Cryopreserved sperm|125.0|0.0|Yes||Cited1, placenta, growth restriction, embryonic, placenta|Yes| 112.0|BALB/b-CMV1r|C.B6-Klra8 H2/AnuApb|C.B6-Klra8 H2/AnuApb|Dominant|killer cell lectin-like receptor, subfamily A, member 8|Klra8|Normal|Cmv-1, Cmv1, Ly49H, Ly49h, Ly49u<129>|MGI:102968|cytomegalovirus resistance 1, resistant|Klra8|MGI:2387148|6||||||||||||||||Yes||||histocompatibility-2, MHC|H2||H-2, MHC-II|MGI:95894|histocompatibility-2, MHC; b variant|H2|MGI:3579319|17|The Klra8 gene from C57BL/6 has been recombined into the genome of Balb/c mice. The H2 locus of C57BL/6 has also been recombined into this BALB/c. Mice expressing Klra8 are resistant to CMV infection compared to BALB/c H2 and BALB/c H2 controls.||BALB/c|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|06-Feb-2006|Cryopreserved sperm|110.0|0.0|No||cytomegalovirus, lymphocyte, natural killer cell, resistance, infection|Yes| 143.0||Porthos||Dominant||||||||||||||||||||||||||Genomic IgG anti-HEL H + L||low copy||||||||||||C57BL/5 x B10.BR|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|06-Feb-2006|Cryopreserved sperm|72.0|0.0|No||Hen Egg Lysozyme, autoimmunity, T cell, B cell|Yes| 166.0|Cited|B6;129S4-Cited1/Apb|B6;129S4-Cited1/Apb|X-linked|Cbp/p300-interacting transactivator with Glu/Asp-rich carboxy-terminal domain 1|Cited1|Nil|Msg1|MGI:108023|targeted mutation 1, Finian Martin|Cited1|MGI:3623213|X||||||||||||||||Yes|||||||||||||Results in retarded mammary ductal growth at puberty.|Females have no overt phenotype|C57BL/6|No|No|No|Yes|Yes|Yes|No|Good|3|11|Cited1/Y x +/Cited1|No|15-Apr-2006|Cryopreserved sperm|135.0|0.0|Unknown||Cited1, mammary gland, Wnt inhibitor, placenta|Yes| 169.0|Adamts1 knockout|B6.129-Adamts1/Apb|B6.129-Adamts1/Apb|Recessive|a disintegrin-like and metallopeptidse (reprolysin type) with thrombospondin type 1 motif, 1|Adamts1|Nil|ADAM-TS1, ADAMTS, C3-C5, METH1|MGI:109249|targeted mutation 1, Melanie A Pritchard|B6.129-Adamts1|MGI:3574351|16||||||||||||||||No|||||||||||||perinatal lethality: the expected Mendelian ratio of null mice was present on the day preceding birth but only 55% remained on the day after birth. postnatal lethality: of those surviving after day 1, most survived to adulthood with 40% surviving at time of weaning.abnormal kidney morphology: the day following birth, pups showed a shrinkage of both layers of the kidney and an enlarged caliceal space, however kidneys were normal at E18.5.abnormal kidney cortex: saw a reduction of the width of the cortex in homozygous nulls on the days before and after birthabnormal kidney medulla morphology: saw a reduction of the width of the medulla in homozygous nulls on the days before and after birth.decreased ovulation frequency: release of oocytes from the follicles was reduced by 70% resulting in a decreased number of oocytes in the oviducts and the number of implantation sites was reduced by 43%, however females have a normal uterus and estrous cycle. Several oocytes were found to be trapped in the corpora lutea after ovulation.reduced female fertility: 38% of females give birth to pups after plug formation. The pregnancy rate was decreased during gestation at a greater rate (83% at E4.5 to 50% at E15.5) compared with wildtype (100% at E4.5 to 83% at E15.5), suggesting a loss of embryos as pregnancy progressed.decreased litter size||C57BL/6|No|No|Yes|No|No|Yes|No|Good|10||het x het OR Het male x WT female OR Het female x WT male|No|15-Apr-2006|Cryopreserved sperm|55.0|0.0|Unknown||fertility, kidney, angiogenesis, urogenital, ovulation|Yes| 167.0|Bean Knockout|C57BL/6-Bean1/Apb|C57BL/6-Bean1/Apb|Recessive|brain expressed, associated with Nedd4|Bean1|Nil||MGI:1929597|targeted mutation 1, Sharad Kumar|Bean1|MGI:5605284|8||||||||||||||||Yes|||||||||||||None detected so far|None|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|||Hom x Hom|Yes|15-Apr-2006|Cryopreserved sperm|40.0|0.0|Unknown||WW domain, PY motif, Nedd4, ubiquitin ligase|Yes| 164.0|C2NX1f|129/Sv-Cited2/Apb|129/Sv-Cited2/Apb|Recessive|Cbp/p300-interacting transactivator, with Glu/Asp-rich carboxy-terminal domain, 2|Cited2|Unknown|ER154-like, Mrg1, Msg2, p35srj|MGI:1306784|targeted mutation 1, Sally L Dunwoodie|Cited2|MGI:3696061|10||||||||||||||||Yes|||||||||||||Mice homozygous for the conditional allele of Cited2 are viable and no phenotype has been observed.|No Phenotype|129S1/Sv|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|3|0|Heterozygous mice are backcrossed into 129X1/SvJ to increase health as ES origin is not as viable|No|15-Apr-2006|Cryopreserved sperm|90.0|0.0|Yes||Cited2, heart, placenta, left-right axis|Yes| 165.0|C2B6∆|B6.129P2-Cited2/Apb|B6.129P2-Cited2/Apb|Recessive|Cbp/p300-interacting transactivator, with Glu/Asp-rich carboxy-terminal domain, 2|Cited2|Nil|ER154-like, Mrg1, Msg2, p35srj|MGI:1306784|targeted mutation 1, Juan Pedro Martinez Barbera|Cited2|MGI:2176158|10||||||||||||||||No|||||||||||||Embryos die during gestation (~E15.5). Heart, left-right axis, neural tube, adrenal gland and placental defects.|None|C57BL/6|No|No|No|No|No|Yes|No|Good|10|4|C2B6∆ +/- (heterozygous) mated with C57BL/6|No|15-Apr-2006|Cryopreserved sperm|130.0|0.0|Yes||Cited2, heart, placenta, left-right axis|Yes| 5412.0|NOD.IL-12SV x IL-12KO|NOD/Lt-IL12b Tg(IL12B)HJ15-3Gem/ArcApb||Recessive|interleukin 12b|Il12b|Unknown|IL-12 p40, Il-12b, Il-12p40, IL-23 subunit p40|MGI:96540|interleukin 12b; targeted mutation 1, Jeanne Magram|Il12b|MGI:1857201|11||||||||||||||||Yes|human interleukin 12b||over-expression||||||||||Unknown.||NOD/Lt|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|10|||No|03-Feb-2011|Embryo|0.0|0.0|Yes|“In Caucasian-American Families the IL-12p40 locus has recently been shown to be associated with type 1 diabetes. A number of susceptibility genes have been mapped to chromosomal regions in both mouse and humans using genome-scanning techniques. However, identification of the specific genes has been difficult because the contribution of each gene is usually very small. The analysis of candidate genes has been a very fruitful approach in the studies of type 1 diabetes susceptibility genes. For example, the first two type 1 diabetes genes, type 1 diabetes1 (HLA) and type 1 diabetes2 (INS), were both identified by the candidate gene approach. Recently, an association between type 1 diabetes and IL-12p40 was reported. Interleukin (IL)-12 is known to induce Th1-cell differentiation and cytokine production. A link between type 1 diabetes and IL12 is also suggested in NOD mice, BB rats, and humans. There is also a correlation between the expression of IL-12 and the destruction of insulin-producing cells in the course of disease progression in NOD mice. Administration of IL-12 to young NOD mice accelerates diabetes, which correlates with a higher production of interferon-γ (IFN-γ) and a lower production of IL-4.” (Diabetes, 2002, She et. al.)|delayed type hypersensitivity, T cell, interferon gamma, autoimmunity|Yes| 10398.0|Tap1/Tap2 KO:Tg(hTAP1/hTAP2)|C57BL/6J-Tap1/Tap2 Tg(hTAP1/hTAP2)/MarpAnu||Recessive|TAP complex|Tap1/Tap2|||||||Unknown|||||||||||||||||HumanTap1Tap2||||||||||||Normal|Normal|C57Bl/6N|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|20-Dec-2023|Cryopreserved sperm|54.0|0.0|Unknown|||Possibly| 260.0||C57BL/10ScSn-Dmd/ArcAnuApb||X-linked|dystrophin, muscular dystrophy|Dmd|Unknown|Dp427, Duchenne muscular dystrophy, mdx, pke, X-linked muscular dystrophy|MGI:94909|X linked muscular dystrophy|Dmd|MGI:1856328|X||||||||||||||||No|||||||||||||Abnormal muscle morphology.dilated sarcoplasmic reticulum.Abnormal skeletal muscle fiber morphology: * development of electron-dense bodies in the mitochondria resulting in swelling and degenerating mitochondria, and disruption of the plasmalemma basal lamina. * the normal myofibrillar architecture of bands and lines disappears and myofilaments disintegrate and become misaligned.Increased variability of skeletal muscle fiber size: variable muscle fiber size; progressive starting at 3 weeks of age.Skeletal muscle fibrosis: exhibit mild muscle fibrosis, however there is no replacement of lost muscle by fat cells.Skeletal muscle necrosis: progressive starting at 9 weeks of age.Muscle degeneration: progressive starting at 3 weeks of age.Abnormal muscle physiology: increased intracellular sodium concentration in muscle; increased severity with age.Muscular atrophy: progressive starting at 3 weeks of age.Dystrophic muscle.Myopathy: progressive degenerative myopathy; increased severity with age.Abnormal circulating enzyme level: exhibit elevated blood levels of muscle creatine kinase and pyruvate kinase.Reduced female fertility: slight reduction in fertility.||C57BL/10ScSn|Yes|Yes|Yes|Yes|Yes|Yes|Yes|Unknown||||No|30-Apr-2006|Cryopreserved sperm|40.0|0.0|Yes||Muscular dystrophy, Duchenne Type, muscle, necrosis, degeneration|Yes| 263.0|eotaxin -/-|C.129S6-Ccl11/Apb|C.129S6-Ccl11/Apb|Recessive|chemokine (C-C motif) ligand 11|Ccl11|Nil|eotaxin, Scya11|MGI:103576|targeted mutation 1, Marc E Rothenberg|Ccl11|MGI:2384435|11|||||||||||||||||||||||||||||Abnormal immune system physiology* mutant mice have markedly fewer eosinophils in the jejunum than do wild-type controls||BALB/c|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|30-Apr-2006|Cryopreserved sperm|100.0|0.0|Unknown||eosinophils, chemokine, infection, C-C, inflammation, recruitment|Yes| 267.0|B6.gA-/-|C57BL/6-Gzma/AnuApb||Recessive|granzyme A|Gzma|Nil|BLT esterase, Ctla-3, Ctla3, H factor, Hanukah factor, Hf, SE1, serine esterase 1, TSP-1, TSP1|MGI:109266|targeted mutation 1, Markus M Simon|Gzma|MGI:2449926|13||||||||||||||||No|||||||||||||Tumorigenesis * homozygotes control growth of syngeneic tumors (s.c. inoculation of H-2b MC57G fibrosarcoma) as efficiently as wild-type miceHematopoietic system phenotype * homozygotes are viable, fertile, and display normal hematopoiesis relative to wild-type mice* in mutant spleens, the numbers of CD4+ and CD8+ T cells, macrophages, NK cells and B cells fall within normal ranges* the frequencies of CD4+ and CD8+ T cells responding to H-2 alloantigens in primary mixed lymphocyte cultures (MLC) with proliferation are also within normal rangesImmune system phenotype* in vitro- and ex vivo-derived cytotoxic T cells and NK cells from mutant mice induce specific target cell membrane disruption, DNA fragmentation, and apoptosis as efficiently as wild-type cells * homozygotes control infections with lymphocytic choriomeningitis (LCM) virus and L. monocytogenes as efficiently as wild-type mice * homozygotes develop a normal contact hypersensitivity (CHS) response (based on increase in ear thickness) to trinitrophenyl (TNP) relative to wild-type mice ||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|30-Apr-2006|Cryopreserved sperm|50.0|0.0|Unknown||Cytotoxic T Cell, Natural Killer Calls, Serine Proteinase|Yes| 268.0|B6.gAB-/-|B6.Cg-Gzma Gzmb/Apb|B6.Cg-Gzma Gzmb/Apb|Recessive|granzyme A|Gzma|Unknown|BLT esterase, Ctla-3, Ctla3, H factor, Hanukah factor, Hf, SE1, serine esterase 1, TSP-1, TSP1|MGI:109266|targeted mutation 1, Markus M Simon|Gzma|MGI:2449926|13||||||||||||||||Yes|||||||||||||Increased sensitivity to induced morbidity/mortality * WNV-infected double homozygotes start to die at day 10 post-infection (p.i.); wild-type mice die between 10-13 days p.i.* 70% of WNV-infected double homozygotes versus 29% of wild-type succumb to encephalitis by day 16 p.i.Immune system phenotype * double homozygotes develop a normal contact hypersensitivity (CHS) response (based on increase in ear thickness) to trinitrophenyl (TNP) relative to wild-type miceIncreased susceptibility to parasitic infection:* decreased clearance and survival after infection with Trypanosoma cruziIncreased susceptibility to viral infection:* double homozygotes display increased susceptibility to West Nile flavivirus (WNV) infection relative to wild-type* double mutants show a higher level of infectious virus in brain relative to wild-type or Prf1tm1Sdz mice at the same time point||C57BL/6|Yes|No|Yes|Yes|Yes|Yes|No|Unknown|||Brother x Sister|No|30-Apr-2006|Cryopreserved sperm|39.0|0.0|Unknown||T Cell, Cytotoxic, Serine Proteinase, Natural Killer Calls, Infection|Yes| 268.0|B6.gAB-/-|B6.Cg-Gzma Gzmb/Apb|B6.Cg-Gzma Gzmb/Apb|Recessive|granzyme B|Gzmb|Nil|CCP-1/C11, CCP1, Ctla-1, Ctla1|MGI:109267|targeted mutation 1, Timothy J Ley|Gzmb|MGI:1857156|14|||||||||||||||||||||||||||||Increased sensitivity to induced morbidity/mortality * WNV-infected double homozygotes start to die at day 10 post-infection (p.i.); wild-type mice die between 10-13 days p.i.* 70% of WNV-infected double homozygotes versus 29% of wild-type succumb to encephalitis by day 16 p.i.Immune system phenotype * double homozygotes develop a normal contact hypersensitivity (CHS) response (based on increase in ear thickness) to trinitrophenyl (TNP) relative to wild-type miceIncreased susceptibility to parasitic infection:* decreased clearance and survival after infection with Trypanosoma cruziIncreased susceptibility to viral infection:* double homozygotes display increased susceptibility to West Nile flavivirus (WNV) infection relative to wild-type* double mutants show a higher level of infectious virus in brain relative to wild-type or Prf1tm1Sdz mice at the same time point||C57BL/6|Yes|No|Yes|Yes|Yes|Yes|No|Unknown|||Brother x Sister|No|30-Apr-2006|Cryopreserved sperm|||Unknown||T Cell, Cytotoxic, Serine Proteinase, Natural Killer Calls, Infection|Yes| 2462.0||B6.CBA-Tg(hGMCSF-2CK1)1200/AnuApb||Dominant|||||||||Unknown||||||||||||||||Yes|human GMCSF (GM-CSF)|human GM-CSF promoter and enhancer (10.5kb)|||||||||||Express human GM-CSF. hGM-CSF detected in serum by ELISA. Murine GM-CSF used as internal control.|||Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|16-Jan-2008|Cryopreserved sperm|30.0|0.0|Unknown||T cell, lymphocyte, transcription, chromatin remodelling, NF-kappaB|Yes| 270.0|gB -/-|C57BL/6-Gzmb/Apb||Recessive|granzyme B|Gzmb|Nil|CCP-1/C11, CCP1, Ctla-1, Ctla1|MGI:109267|targeted mutation 1, Timothy J Ley|Gzmb|MGI:1857156|14||||||||||||||||No|||||||||||||Homozygous mutant mice develop normally, with normal lymphopoiesis and hematopoiesis. However, CTLs from mutant mice are unable to induce rapid fragmentation of DNA and apoptosis in target cells; with long incubation, fragmentation is partially and cell lysis completely rescued (J:23560). Natural killer (NK) cells also release granzyme-bearing granules, and rapid cytoxicity by these cells is dependent on granzyme B. Granzyme B independent mechanisms of cytotoxicity exist, since CTLs from null homozygotes can lyse target cells after extended incubation, but these mechanism are not active in null mutant NK cells (J:28160).specific activity of caspase 3 executioner protease in cytoplasm of CTLs is decreaseddefective cytotoxic T cell cytolysis (J:23560)cytotoxic T lymphocytes (CTLs) defective in ability to induce rapid DNA fragmentation and apoptosis in allogeneic target cellswith long incubation, fragmentation is partially and cell lysis completely rescuednormal activation and proliferation of cytotoxic T lymphocytes (CTLs) in mixed lymphocyte cultures (MLCs)defective NK cell cytolysis (J:113213)impaired ability of NK cells to induce DNA fragmenting but normal ability to induce membrane damage||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|30-Apr-2006|Cryopreserved sperm|90.0|0.0|Unknown||Fas, natural killer cell, cytotoxic T cell|Yes| 341.0|EphA1-/- hPLAP|B6;129-Epha1/Apb|B6;129-Epha1/Apb|Recessive|Eph receptor A1|Epha1|Nil|5730453L17Rik, Eph, Esk|MGI:107381|targeted mutation 1, Shannon L Duffy|Epha1|MGI:3822370|6||||||||||||||||Yes|internal ribosome entry site - human placental alkaline phosphatase|endogenous EphA1|Restricted to epithelial tissue||||||||||Vaginal inflammation:mice exhibit inflammation of the vaginal mucosa secondary to hydrometrocolpos.Endometrium inflammation:mice exhibit endometrium inflammation secondary to hydrometrocolpos.Dilated uterine horn:mice exhibit dilated, attenuated uterine horns secondary to hydrometrocolposEnlarged uterus:mice exhibit an enlarged uterus due to an accumulation of clear uterine fluid (hydrometrocolpos).Increased uterus weight:Vagina atresia:18% of mice exhibit a failure of vaginal openingdespite normal estrogen receptor expression, beta-estradiol treatment fails to induce precocious vaginal opening in P12 mice unlike in wild-type mice and vaginal opening can not be induced by likewise treating affected adult mice.Hydrometrocolpos:mice exhibit inflammation of the vaginal mucosa and endometrium with dilated, attenuated uterine horns secondary to hydrometrocolposFemale infertility:female mice affected by hydrometrocolpos are sterileKinked tail:up to 80% of mice exhibit a kinky tail due to incorrectly positioned caudal vertebraeDistended abdomen:in some mice due to an enlarged uterusAbnormal response/metabolism to endogenous compounds:treatment with beta-estradiol fails to induce apoptosis in the lower genital tract and precocious vaginal opening unlike in wild-type mice.|Normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|3|5|Homozygous knockout crossed with homozygous knockout or C57BL/6 wildtype|No|22-Sep-2006|Cryopreserved sperm|40.0|0.0|No||Eph, Receptor Tyrosine Kinase, ephrin, epithelium, uterus, tail, hydrometrocolpos|Yes| 344.0|B7C bb|C57BL/6-Tg(SERPINC1-CD86)/Apb||Dominant||||||||||||||||||||||||||murine CD86|human anti-thrombin III (SERPINC1)+ regulatory intronic sequences of MHC class II|low on 15% of hepatocytes||||||||||Expression of CD86 on 15% of hepatocytes. Expression elsewhere has not been reported.|Expression of CD86 on 15% of hepatocytes. Expression elsewhere has not been reported.|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|10|15|B7Cbb x B7Cbb|No|22-Sep-2006|Cryopreserved sperm|40.0|0.0|Unknown||costimulation, hepatocytes, T cells, liver, T cell activation, Hepatocellular carcinoma, Hepatitis C virus (HCV)|Yes| 345.0|Human GM-CSF|NOD.Cg-Prkdc Tg(hGM-CSF)8KHsr/Apb||Recessive|protein kinase, DNA activated, catalytic polypeptide|Prkdc||DNAPDcs, DNA-PK, DNA-PKcs, DOXNPH, dxnph, slip, XRCC7|MGI:104779|protein kinase, DNA activated, catalytic polypeptide; severe combined immunodeficiency|Prkdc|MGI:1857113|16||||||||||Unknown to Unknown||||||No|human granulocyte-macrophage colony stimulating factor |murine T Cell Receptor (TCR) enhancer and H2-K promoter|High||||||||||Unable to maintain colony in homozygous state|Normal|NOD/SCID|Yes|No|Yes|Yes|No|Yes|No|Excellent|20|0|Purchased NOD/SCID mated with transgenic mouse from colony to maintain colony|No|25-Sep-2006|Cryopreserved sperm|85.0|0.0|No||cytokine secreting, GM-CSF, immunodeficient, chronic myelomonocytic leukaemia (CMML), engraftment|Yes| 347.0|C2f|B6;129S1-Cited2/Apb|B6;129S1-Cited2/Apb|Semi-dominant|Cbp/p300-interacting transactivator, with Glu/Asp-rich carboxy-terminal|Cited2|Nil|ER154-like, Mrg1, Msg2, p35srj|MGI:1306784|targeted mutation 1.1, Sally L Dunwoodie|Cited2|MGI:3696062|10||||||||||Unknown to Unknown||||||Yes|||||||||||||Mice homozygous for the conditional allele of Cited2 are viable and no phenotype has been observed.|Normal|75% C57BL/6, 25% 129S1/Sv|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|2|2|Homozygous sib-matings to propagate the line in the homozygous state|No|25-Sep-2006|Cryopreserved sperm|106.0|0.0|Yes||Cited2, heart, placenta, left-right axis|Yes| 282.0||129/Sv-Ifngr/Apb||Recessive|interferon gamma receptor 1|Ifngr1|Unknown|CD119, Ifgr, IFN-gamma R, Ifngr, INF-g receptor, Nktar|MGI:107655|targeted mutation 1, Michel Aguet|Ifngr1|MGI:1857286|10||||||||||Unknown to Unknown||||||Yes|||||||||||||abnormal immunoglobulin level:levels of IgG2a and IgG2b neutralizing antibodies are reduced relative to controls after secondary infection with Ectromelia virusincreased susceptibility to viral infection:slightly more susceptible to MCMV viral infection than controls increased susceptibility to Ectromelia virus 100% mortality by day 6-12 after primary infection infectionelevated virus titers in all organs tested after primary infection but much improved after secondary infectionssurvive secondary infections ||129|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|02-May-2006|Cryopreserved sperm|100.0|0.0|Unknown||infection, interleukin, splenocyte|Yes| 283.0||129/Sv-Irf1/Apb|129/Sv-Irf1|Recessive|interferon regulatory factor 1|Irf1|Unknown|Irf-1|MGI:96590|targeted mutation 1, Charles Weissmann|Irf1|MGI:2429553|11||||||||||||||||Yes|||||||||||||Immune systemabnormal T cell proliferation:higher background proliferation rateshyperproliferation requires higher MOGp35-55 peptide concentrations as a stimulusabnormal cytokine level:lower expression of lymphotoxin alpha and lymphotoxin beta after stimulation with anti-CD3 antibody or with MOGp35-55 peptidedecreased circulating interferon-gamma level:levels are reduced relative to controls after stimulation with anti-CD3 antibody or with MOGp35-55 peptideabnormal circulating interleukin-10 level:detectable levels after stimulation with anti-CD3 antibody or with MOGp35-55 peptideincreased circulating interleukin-13 level:after stimulation with anti-CD3 antibody or with MOGp35-55 peptideabnormal circulating interleukin-4 level:detectable levels after stimulation with anti-CD3 antibody or with MOGp35-55 peptideincreased circulating interleukin-5 level:after stimulation with anti-CD3 antibody or with MOGp35-55 peptideincreased circulating interleukin-6 level:after stimulation with anti-CD3 antibody or with MOGp35-55 peptidedecreased susceptibility to experimental autoimmune encephalomyelitis:develop an attenuated disease after injection with MOGp35-55disease onset delayed about 4 daysHematopoietic systemabnormal T cell proliferation:higher background proliferation rateshyperproliferation requires higher MOGp35-55 peptide concentrations as a stimulusHomeostasis/metabolismAbnormal cytokine level:lower expression of lymphotoxin alpha and lymphotoxin beta after stimulation with anti-CD3 antibody or with MOGp35-55 peptidedecreased circulating interferon-gamma level:levels are reduced relative to controls after stimulation with anti-CD3 antibody or with MOGp35-55 peptideabnormal circulating interleukin-10 level:detectable levels after stimulation with anti-CD3 antibody or with MOGp35-55 peptideincreased circulating interleukin-13 level:after stimulation with anti-CD3 antibody or with MOGp35-55 peptideabnormal circulating interleukin-4 level:detectable levels after stimulation with anti-CD3 antibody or with MOGp35-55 peptideincreased circulating interleukin-5 level:after stimulation with anti-CD3 antibody or with MOGp35-55 peptideincreased circulating interleukin-6 level:after stimulation with anti-CD3 antibody or with MOGp35-55 peptide||129/Sv|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|||Brother x Sister|No|02-May-2006|Cryopreserved sperm|135.0|0.0|Unknown||interferon, T cell, CD4, CD8, iNOS|Yes| 290.0||C.CBA-Tg(CD2-IL5)5C2Ldt/Apb [cc]|C.CBA-Tg(CD2-IL5)5C2Ldt/Apb [cc]|Dominant||||||||||||||||||||||||||transgene insertion 5C2, Lindsay A Dent|the dominant control region (DCR) of the gene encoding human CD2|High - 49 Copies||||||||||Constitutive expression of the IL5 gene is sufficient to induce lifelong high-level eosinophilia. Northern blotanalysis identified 11,5 mRNA in the thymus, Peyer's patches, and subcutaneous (pooled inguinal and axillary) lymph nodes. No IL5 mRNA was detected in liver, heart, brain, or skeletal muscle tissues from transgenics, nor in any tissues from normal littermates. Do not maintain as homozygotes. While this is apparently possible, survival of homozygotes likely to be lower.|Appear normal with peripheral blood eosinophilia and increased numbers of eosinophils in the spleen (with splenomegaly), bone marrow. Heterozygous BALB/c and C57BL/6 IL-5 Tg2 mice are resistant to methylcholanthrene-induced carcinogenesis - see Simson, L, et al., 2007, Regulation of carcinogenesis by IL-5 and CCL11: a potential role for eosinophils in tumor immune surveillance. J. Immunol., 178:4222-4229.|Balb/c|No|No|Yes|No|No|Yes|No|Excellent|20||Transgenic male with wild type female|No|03-May-2006|Cryopreserved sperm|135.0|0.0|Yes||eosinophil, immune surveillance, resistance to helminthic parasites, asthma, allergy|Yes| 6638.0|Circling ; ENU18PiDTau_ TBx1|STOCK Tbx1 Tg(Thy1-MAPT*K369I)K3Gotz/AnuApb||Dominant|T-box 1|Tbx1|||MGI:98493|T-box 1; enu37|Tbx1|MGI:5490246|16|||||||||||||||||transgene insertion K3, Jurgen Gotz|Thy1|neuron specific||||||||||Unknown|Head tilt:• head tilting and weavingBidirectional circling|C57BL/6|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Good||||No|02-Nov-2011|Cryopreserved sperm|18.0|0.0|Yes|Frontotemporal dementia (FTD)|Pick's disease, Parkinsonism, Frontotemporal dementia (FTD)|Yes| 338.0|Activin Beta C+ FL2|C57BL/6-Tg(ACTIVIN-β{C})3Grb/Apb||Semi-dominant|||||||||Unknown||||||||||||||||No|human activin beta C|CMV|Greater than 20 copies, mRNA upregulated at least 3 fold in tissues assessed to date||||||||||Essenitally normal at gross level, male fertility decreased from 10 weeks (decreased sperm production and litter size), liver disease (mild fibrosis) from 14 weeks, prostate hyperplasia from 20 weeks.|Essenitally normal at gross level, male fertility decreased from 14 weeks (decreased sperm production and litter size), liver disease (mild fibrosis), prostate hyperplasia from 25 weeks.|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|Yes|Good||3|het x wt OR het x het|No|20-Sep-2006|Cryopreserved sperm|55.0|0.0|Unknown||activin, inhibin, prostate, testis, liver|Yes| 1494.0|B6.C1q-/-|B6;129S-C1qa/Apb|B6;129S-C1qa/Apb|Recessive|complement component 1, q subcomponent, alpha polypeptide|C1qa|Nil|C1q|MGI:88223|complement component 1, q subcomponent, alpha polypeptide; targeted mutation 1, Mark J Walport|C1qa|MGI:2158701|4||||||||||||||||No|||||||||||||Premature death: 15% die at 4 - 6 months of ageIncreased anti-nuclear antigen antibody level:* mutants develop high titers of anti-nuclear antibodiesIncreased anti-histone antibody level.Glomerulonephritis:* Background Sensitivity: severe proliferative crescentic glomerulonephritis evident in 27% mice.* Background Sensitivity: striking feature is presence of multiple apoptotic bodies in diseased glomeruli.* among mutants without glomerulonephritis, significantly greater numbers of glomerular apoptotic bodies are seen than in controls.Increased susceptibility to bacterial infection:* animals challenged with virulent pneumococci develop bacteremia and pneumonia after passive immunization with human IgG1 or human IgG2 unlike wild-type mice that are protected after immunization.||C57BL/6 x 129|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|03-Jul-2007|Cryopreserved sperm|136.0|0.0|Unknown||glomerulonephritis, autoimmunity, anti-nuclear antibodies, infection|Yes| 1502.0||C57BL/6NTac-IL15/AnuApb||Recessive|interleukin 15|Il15|Nil|IL-15|MGI:103014|targeted mutation 1, Immunex Research and Development Corporation|Il15|MGI:2136897|8||||||||||||||||Yes|||||||||||||Mice homozygous for disruptions of this gene have normal life spans but display a variety of immune system abnormalities and maternal placental defects.These mutant mice lack NK cells and have marked reductions in memory CD8+ T cells, NK 1.1 T cells and Thy-CD8a intraepithelial lymphocytes. Mice are unable to mount a protective immune response to challenge with vaccinia virus.Abnormal immune system morphology.Abnormal dendritic cell morphology/development:* lower numbers of splenic dendritc cells after Plasmodium chabaudi infection.Abnormal lymphocyte morphology/development:* Intestinal intraepithelial lymphocytes maturing outside of the thymus greatly reduced in numbers.Abnormal CD8+ T cell morphology/development:* two fold reduction in numbers of CD8 single positive cells in spleen and lymph nodes.Abnormal NK cell morphology/development:* reduced numbers of natural killer cells in thymus liver and spleen.* absent in uterusSmall lymph nodes: peripheral lymph nodes significantly lower in weight.Abnormal immune system physiology:Defective NK cell cytolysis: significantly reduced cytolytic activityabnormal immune serum protein physiology.Decreased immunoglobulin concentration:* lower levels of malaria specific antibodies producedlower levels of total immune globulin.Decreased IgG level: decreased levels of IgG1, IgG2a, IgG2b, and IgG3 after Plasmodium infection.Decreased IgM level: after plasmodium infection.Abnormal cytokine physiology.Abnormal interferon physiology: reduced production of IFN gamma by NK cells.Abnormal interleukin physiology:* reduced Il12 production by dendritic cells after Plasmodium infection.Altered susceptibility to infection.Decreased susceptibility to bacterial infection.* Improved survival after infection with Listeria monocytogenesincreased susceptibility to parasitic infection.* parasitemia higher but only minor effect on mortalityincreased susceptibility to viral infection.* dead by day 9 after Vaccinia infection* very susceptible to HSV-2 infectionDecreased susceptibility to type IV hypersensitivity reaction: no contact hypersensitivity* T mediated effects delayed but not B cell activation or antibody production.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|5||brother x sister mating|No|04-Jul-2007|Cryopreserved sperm|110.0|0.0|Unknown||T cell, infection, Natural killer cell, memory|Yes| 1604.0|agouti viable yellow (Avy)|B6;C3-A/Apb|B6;C3-A|Dominant|nonagouti|a|Reduced|agouti, agouti signal protein, As, ASP|MGI:87853|viable yellow|A|MGI:1855930|2||||||||||||||||No|||||||||||||Agouti acts in the hair follicles, primarily affecting the relative amount and distribution of yellow pigment (phaeomelanin) and black pigment (eumelanin) in hairs of the coat. This strain has abnormal coat colour. Affects coat colour and body weight: A/A mice exhibit a varied coat colour ranging from clear yellow, through mottling with dark patches, to a completely agouti-like coat. The degree of yellow coat colour correlates with the severity of adult-onset obesity. A larger proportion of homozygotes than heterozygotes are clear yellow.|Affects coat colour and body weight: A/a mice exhibit a varied coat colour ranging from clear yellow, through mottling with dark patches, to a completely agouti-like coat. The degree of yellow coat colour correlates with the severity of adult-onset obesity.|C57BL/6 x C3H|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|3||C57BL6/J a/a X C57BL6/J Avy/a and select transmission of Avy allele by coat colour inspection|No|11-Jul-2007|Cryopreserved sperm|114.0|0.0|Unknown||coat colour, agouti, yellow, obesity|Yes| 4838.0|Speedy|ENU7B6:044||Recessive|Unknown||Unknown||||||13|||||||||||||||||||||||||||||Circling in both directions, hyperactive in response to stimulation (cage changing, moving cage, walking past cage). Possible histological phenotype in brain as assessed by APN Histopathology and Organ Pathology.|Normal|C57BL/6 x C57BL/10|Yes|No|Yes|Yes|No|Yes|No|Unknown||||No|24-Sep-2009|Cryopreserved sperm|15.0|0.0|Unknown||circling, hyperactive, ENU|Yes| 1514.0|eNOS -/-|B6.129S4-Nos3/AnuApb|B6.129S4-Nos3/AnuApb|Recessive|nitric oxide synthase 3, endothelial cell|Nos3|Nil|2310065A03Rik, ecNOS, eNOS, Nos-3|MGI:97362|targeted mutation 1, Paul L Huang|Nos3|MGI:2150145|5||||||||||||||||Yes|||||||||||||Homozygotes for targeted null mutations exhibit reduced survival, hypertension, inhibited basal vasodilation, insulin resistance, fewer mitochondria, reduced heart rate, impaired ovulation and, in some, shortened limbs. ||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Poor||||No|04-Jul-2007|Cryopreserved sperm|150.0|0.0|Unknown||oocytes, limb, gonadotrophin, hypertension|Yes| 631.0|Pkr KO|B6;129-Eif2ak2/Apb|B6;129-Eif2ak2/Apb|Recessive|eukaryotic translation initiation factor 2-alpha kinase 2|Eif2ak2|Nil|dsRNA-activated kinase, eIF-2 alpha, eIF-2 alpha, Eif2ak2, IFN- type I-induced and dsRNA-activated kinase, IFN-induced and double-stranded RNA-activated kinase, Pkr, Prkr, Tik|MGI:1353449|targeted mutation 1, Charles Weissmann|Eif2ak2|MGI:2182566|17||||||||||||||||Yes|||||||||||||Mice homozygous for disruptions in this gene display altered susceptibility to viral infection. Enlarged lymph nodes. Altered susceptibility to viral infection.increased T cell proliferation.Proliferative responses of both CD4+ and CD8+ T-cells from sensitized mice is somewhat increasedabnormal inflammatory mediator physiology.A 2 fold increase in Il4 production by CD44+ cellsincreased susceptibility to viral infection.Susceptibility to encephalomyocarditis virus testedresponse to infection and survival were similar to control mice; however, pretreatment of mice with IFNgamma failed to improve survival as it did in controlsincreased susceptibility to type IV hypersensitivity reaction. Exaggerated response to challenge after presensitization in contact hypersensitivity testeffect can be transferred to naive mice using CD8+ cells from sensitized mice.|Normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|Yes|Excellent|||Hom x Hom|No|25-Apr-2007|Cryopreserved sperm|96.0|0.0|No||T cell, stimulation, viral infection, hypersensitivity, proliferation|Yes| 637.0|Human GM-CSF transgenic 8L|NOD.Cg-Prkdc Tg(hGM-CSF)8LHsr/Apb||Dominant|||||||||Unknown||||||||||||||||No|human granulocyte-macrophage colony stimulating factor (GM-CSF)|murine TCR enhancer and H2-K promoter|high expression||||||||||Unable to breed Hom x Hom|Normal|NOD/SCID|Yes|No|Yes|Yes|No|Yes|No|Excellent|20|0||No|25-Apr-2007|Cryopreserved sperm|35.0|0.0|No||cytokine secreting, GM-CSF, immunodeficient, chronic myelomonocytic leukaemia (CMML), engraftment|Yes| 633.0|Elvis|NOD.129-Tg(Csf2rb) Csf2rb1 Csf2rb Prkdc/Apb||Dominant|colony stimulating factor 2 receptor, beta 1, low-affinity (granulocyte-macrophage)|Csf2rb1|Nil|AIC2B, Bc, beta c, CDw131, common beta chain, Il3r, Il3rb1, Il5rb|MGI:1339759|targeted mutation 1, C Glenn Begley|Csf2rb1|MGI:2181245|15||||||||||||||||Yes|colony stimulating factor 2 receptor, beta 1, low-affinity (granulocyte-macrophage)||High||||||||||None detected|Normal|NOD/SCID|Yes|Yes|Yes|Yes|Yes|Yes|No|Excellent|||Matings of 2 transgenic non-sibling mice|Yes|25-Apr-2007|Cryopreserved sperm|65.0|0.0|No||murine beta chain, GM-CSF, receptor, phosphorylation, signal transduction|Yes| 633.0|Elvis|NOD.129-Tg(Csf2rb) Csf2rb1 Csf2rb Prkdc/Apb||Dominant|colony stimulating factor 2 receptor, beta, low-affinity (granulocyte-macrophage)|Csf2rb|Nil|AIC2B, Bc, beta c, CDw131, common beta chain, Csf2rb1, Il3r, Il3rb1, Il5rb|MGI:1339759|targeted mutation 1, Clare L Scott|Csf2rb|MGI:3653883|15|||||||||||||||||||||||||||||None detected|Normal|NOD/SCID|Yes|Yes|Yes|Yes|Yes|Yes|No|Excellent|||Matings of 2 transgenic non-sibling mice|Yes|25-Apr-2007|Cryopreserved sperm|||No||murine beta chain, GM-CSF, receptor, phosphorylation, signal transduction|Yes| 633.0|Elvis|NOD.129-Tg(Csf2rb) Csf2rb1 Csf2rb Prkdc/Apb||Dominant|protein kinase, DNA activated, catalytic polypeptide|Prkdc||DNA-PK, DNA-PKcs, DNAPDcs, slip, XRCC7|MGI:104779|severe combined immunodeficiency|Prkdc|MGI:1857113|16|||||||||||||||||||||||||||||None detected|Normal|NOD/SCID|Yes|Yes|Yes|Yes|Yes|Yes|No|Excellent|||Matings of 2 transgenic non-sibling mice|Yes|25-Apr-2007|Cryopreserved sperm|||No||murine beta chain, GM-CSF, receptor, phosphorylation, signal transduction|Yes| 778.0|MPDtg|C57BL/6-Tg(Ckm-hPDGF-BB)/Apb||Dominant||||||||||||||||||||||||||human platelet derived growth factor receptor b|a mouse muscle creatine kinase 6.5-kb enhancer/promoter/first intron segment|||||||||||Transgenic mice that specifically express the PDGF receptor in skeletal muscle. In these mice, PDGF stimulated glucose transport into skeletal muscle in vitro and in vivo. The degree of glucose uptake in vivo reached ∼60% of that by insulin injection in skeletal muscle, but blood glucose levels were not decreased by PDGF in these mice. ||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|18-May-2007|Cryopreserved sperm|50.0|0.0|Unknown||platelet derived growth factor receptor (PDGFR), receptor, transgene, membrane, insulin, glucose, skeletal muscle|Yes| 1357.0|ATM-ΔSR1|B6.129T2(FVB)-Atm/Apb|B6.129T2(FVB)-Atm/Apb|Semi-dominant|ataxia telangiectasia mutated homolog (human)|Atm|Normal|C030026E19Rik|MGI:107202|targeted mutation 1, Martin F Lavin|Atm|MGI:2181756|9||||||||||||||||Yes|||||||||||||Premature death: 50% mortality by 40 weeks of ageDecreased body size: smaller size persists through adulthoodPostnatal growth retardation: 20% growth reduction in males and 18% reduction in females from birth to 45 days of age.Increased tumor incidence: mice dying after 40 weeks of age usually have tumors that are not thymic lymphomasThymic lymphoma: found in all mice dying before 40 weeks, diverse cell types involved, spongy tumors with a high proportion of cells undergoing apoptosisAbnormal immune system cell morphology: occasional increase in thymocyte size.Abnormal T lymphocyte development: lymph node T cells are primarily at early stages of development.Increased double-negative T cell count: occurs at randomAbnormal effector T cell morphology/development: randomly observed increases in single positive T cells.Decreased thymocyte number: 10% reduction in thymocytes, 30-50% reduction in thymocytes expressing alpha and beta T cell receptors or CD3.Abnormal immune system organ morphology:enlarged spleen: usually found in mice dying after 40 weeks of age.small spleen: in mice under 40 weeks of agesmall thymussmall lymph nodesAbnormal chromosome morphology: 3 fold increase in radiation induced chromosomal aberrations.Increased cellular sensitivity to ionizing radiation: increased sensitivity of thymocytes and splenocytes to ionizing radiation.Seminiferous tubule degeneration: tubules disruptedAbnormal testis development: poorly developedAbnormal gametogenesis:abnormal oogenesis: disrupted, lack of maturing follicles and oocytes.Abnormal spermatogenesis: disrupted spermatogenesis, degenerating spermatocytes, loss of spermatidsNervous system phenotype: no gross neuronal degeneration at time points between 2 and 16 months of age.Abnormal Purkinje cell morphology: survival of Purkinje cells in culture less than 60% of controls at 4 days and about 40% at 10 day, survival of cultured cells improves if cultured with cerebellar astroglial cells, develop simpler dendritic arboritization with reduced secondary branching, nitroxide free radicals improve survival and arborizationSeminiferous tubule degeneration: tubules disrupted|Increased tumor incidence: average age at onset 18.6 months, varying tumor types including dermatoid cystsadenoma: 13% of totalleukemia: 5% of totallymphoma:24% of totalovary tumor: 8% of totalsarcoma: 32% of total, half of sarcomas are in Mammary glands|C57BL/6|Yes|No|Yes|Yes|No|Yes|Yes|Unknown|6|||No|22-Jun-2007|Cryopreserved sperm|100.0|0.0|Yes||ataxia telangiectasia, lymphoma, T cell, spermatogenesis, thymocyte|Yes| 651.0|Aromatase knockout|FVB.129S6(B6)-Cyp19a1/Apb|FVB.129S6(B6)-Cyp19a1/Apb|Recessive|cytochrome P450, family 19, subfamily a, polypeptide 1|Cyp19a1|Nil|Ar, ArKO, aromatase, Cyp19, Int-5, Int5, p450arom|MGI:88587|targeted mutation 1, Evan R Simpson|Cyp19a1|MGI:2154536|9||||||||||||||||No|||||||||||||Abnormal coat color At 3 weeks of age, both males and females exhibit Dull coatAdipose tissueAbnormal fat pad Females exhibited a 50% to 80% increase in mammary fat pad weightAbnormal gonadal fat pad Males and females exhibited a 50% and 50% to 80% increase in gonadal fat pad weight, respectivelyendocrine/exocrine glandsAbnormal ovary morphology The ovaries of mice on a soy free diet exhibited seminiferous tubule-like structures throughout 80% of ovaries, hemorrhagic cysts, and age dependent increase in collagen deposition of collagen in constrast, animals fed a soy diet did not display Sertoli-like cells in follicles absent corpora lutea impaired ovarian folliculogenesis though ovaries contained numerous follicles with abundant granulosa cells, antrum formation was arrested before ovulationno corpora leuteaabnormal prostate morphology increase in combined prostate/urinary bladder weightincreased seminal gland weight increased weight of seminal vescicles, putatively due to an increased volume of secretions rather than due to structural changesabnormal seminiferous tubule morphologydecrease in the volume of epitheliumin contrast to Esr1tm1Ksk homozygotes, no decrease in luminal volumedecreased testis weight reduction in weight, 1 year of agehomeostasis/metabolismincreased circulating follicle stimulating hormone level female FSH levels were elevated 3- to 4-fold relative to wild type femalesincreased circulating luteinizing hormone level female LH levels were elevated 2- to 10-fold relative to wild type femalesLH levels were also increased in male miceincreased circulating testosterone level female testosterone level was increased to ~10 times the level in wild type femalesmale testosterone levels varied though they were in general increased relative to those of control malesreproductive systemabnormal reproductive system morphologyabnormal female reproductive anatomy abnormal ovary morphologythe ovaries of mice on a soy free diet exhibited seminiferous tubule-like structures throughout 80% of ovaries, hemorrhagic cysts, and age dependent increase in collagen deposition of collagen in constrast, animals fed a soy diet did not display Sertoli-like cells in follicles absent corpora lutea impaired ovarian folliculogenesis though ovaries contained numerous follicles with abundant granulosa cells, antrum formation was arrested before ovulationno corpora leuteaabnormal uterus development underdeveloped uterus observed at 12 to 14 weeks of age3-fold enlargement of the clitoral gland relative to that of wild typeabnormal labium morphologylabial folds do not developabnormal spermiogenesisnormal at 4.5 months of agedysfunction evident at 1 year of agespermatids did not complete elongation and spermiationdegenerating round spermatidsabnormal prostate morphology increase in combined prostate/urinary bladder weightincreased seminal gland weight increased weight of seminal vescicles, putatively due to an increased volume of secretions rather than due to structural changesabnormal seminiferous tubule morphologydecrease in the volume of epitheliumin contrast to Esr1tm1Ksk homozygotes, no decrease in luminal volumedecreased testis weight reduction in weight, 1 year of ageabnormal primary sex determinationon a soy free diet, the ovaries develop cells that possess structural and functional characteristics of testicular interstitial (Leydig) cells and of seminiferous tubule-like structures lined with Sertoli cellsthe development of testicular tissue was postponed and reduced with estrogen replacementfemale infertilitymale infertilityprogressive infertility developing between 4.5 months and 1 year of age||FVB/N|Yes|No|Yes|Yes|No|Yes|Yes|Unknown|12||Het x Het|No|25-Apr-2007|Cryopreserved sperm|90.0|0.0|Unknown||Cyp19, reproductive system, adipose, cholesterol, sperm|Yes| 696.0|PrlΔ|STOCK Prl/Apb|STOCK Prl/Apb|Recessive|prolactin|Prl|Nil|Prl, Prl1a1|MGI:97762|targeted mutation 1, Nelson D Horseman|Prl|MGI:1934021|13||||||||||||||||Yes|||||||||||||Homozygous null female mice have irregular oestrus cycles and are infertile. Defects of the pituitary gland include hyperplasia, which progresses to adenoma, and impaired secretion.Abnormal branching of the mammary ductal tree:* ductal system comprises an extended branching network but devoid of terminal and lateral lobulationDecreased prolactin level: * in the pituitaryDecreased circulating prolactin level Failure of embryo implantation Abnormal mammary gland morphology Abnormal branching of the mammary ductal tree:* ductal system comprises an extended branching network but devoid of terminal and lateral lobulationAbnormal estrous cycle: * a consistent pattern of cycling was not established.||Unknown|Yes|No|Yes|Yes|Yes|Yes|No|Unknown|||HET x HET to maintain colony, KO male x HET female to produce more KOs|No|01-May-2007|Cryopreserved sperm|95.0|0.0|Unknown||eostrous cycle (estrous), infertility, pituitary gland, hyperplasia, mammary gland, duct, lobe|Yes| 5419.0|IL21 KO NOD|NOD.129-IL21/Apb||Recessive|interleukin 21|Il21|Nil||MGI:1890474|targeted mutation 1, Lexicon Genetics|Il21|MGI:3528994|3||||||||||||||||No|||||||||||||Protected from diabetes on NOD background.Decreased germinal center B cell number:* the percentage of GC B cells that make up the total B cell population in the spleen of immunized mice is reduced by two-thirdsAbnormal CD4-positive T cell morphology:* the percentage of follicular T helper cells (defined as CXCR5+ICOS+CD4+ T cells) is reduced by a third.Abnormal spleen germinal center morphology:* the number of actively proliferating T cells found within GC is reduced 3- to 4- fold.* the percentage of follicular T helper cells (defined as CXCR5+ICOS+CD4+ T cells) is reduced by a third.Decreased spleen germinal center number:* there is a paucity of GC in the spleen of mice after immunization with sheep red blood cells (SRBC).Decreased CD4-positive T cell number:* Il-17+ CD4+ cells are absent from lamina propria and spleen in mutants.Abnormal T cell differentiation:* when naive TH cells are subjected to TH17 differentiation, a deficit in generation of Il-17-producing cells is observed with an increased number of Foxp3+ cells compared to wild-type.* one week after immunization with MOG peptide in CFA, restimulation of spleen cells with TPA or MOG peptide results in production of almost no Il-17 producing cells, showing impaired TH17 differentiation.Abnormal gamma-delta T cell morphology:*lamina propria and splenic TCRgd+ T cells show <10-fold decrease in Il-17-expressing cells compared to wild-type cells.Abnormal interleukin level:* CNS-infiltrating and splenic CD4+ T cells produce interferon gamma, in contrast to CD4+ T cells from controls which produce predominantly Il-17.|Normal|NOD|Yes|Yes|Yes|Yes|Yes|Yes|No|Excellent|10|0|intercross hets to derive homozygous for experiments|No|04-Feb-2011|Cryopreserved sperm|60.0|0.0|Unknown||interleukin, Immunoglobulin, B cell, T cell, CD4, germinal centre, IL17|Yes| 1526.0|B6.LMP2-/-|B6.129P2-Psmb9/AnuApb||Recessive|proteasome (prosome, macropain) subunit, beta type 9 (large multifunctional peptidase 2)|Psmb9|Nil|Lmp-2, Lmp2|MGI:1346526|targeted mutation 1, Susumu Tonegawa|Psmb9|MGI:2152729|17||||||||||||||||Yes|||||||||||||Mice homozygous for disruptions in this gene have a grossly normal phenotype but suffer from increased susceptibility to some viruses and have an increased risk of tumor development.Decreased CD8-positive T cell number:* by 36% in blood* by 22% in spleen* by 49% in thymusAbnormal CD8-positive, alpha-beta cytotoxic T cell morphology :* 5-6 fold lower levels of cytotoxic T lymphocyte precursors after infection with influenza A virus but not Sendai virusAbnormal immune system physiology:* splenic lymphoblasts and peritoneal exudates cells are less efficient stimulators of CD8+ T cells.Increased susceptibility to viral infection:* 5-6 fold lower levels of cytotoxic T lymphocyte precursors after infection with influenza A virus but not Sendai virus.||C57BL/6 x 129S2|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|||Brother x Sister|No|05-Jul-2007|Cryopreserved sperm|150.0|0.0|Unknown||T cell, CD8, tumour, viral infection, cytotoxic|Yes| 1527.0||B6.129S2-Tap1/AnuApb||Recessive|transporter 1, ATP-binding cassette, sub-family B (MDR/TAP)|Tap1|Nil|Abcb2, Ham-1, Ham1, MTP1, PSF-1, RING4, TAP, Tap-1|MGI:98483|targeted mutation 1, Philip Ashton-Rickardt|Tap1|MGI:1857253|17||||||||||||||||No|||||||||||||Mice homozygous for targeted mutations that inactivate the gene are deficient in antigen presentation, surface class I antigens, and CD4-8+ T cells. absent CD4-8+ cells (J:3524)decreased double-negative T cell count (J:3524)exhibit a 30-40 fold reduction in CD4-CD8- T cells in spleen, blood and lymph nodes, but not thymusabnormal dendritic cell antigen presentation (J:112436)mutant bone marrow-derived dendritic cells (BM-DC) treated with ovalbumin-immune complexes (OVA-IC) do not present the MHC class I-restricted epitope after OVA-IC internalizationdecreased level of surface class I molecules (J:3524)splenocytes exhibit little or no H2-Kb or -Db surface expression, however, at lower temperatures (26C) surface expression is increaseddefective intracellular transport of class I molecules (J:3524)class I Kb and Db molecules have little heavy chain sialylation indicating an impaired delivery to trans Golgihematopoietic systemabsent CD4-8+ cells (J:3524)decreased double-negative T cell count (J:3524)exhibit a 30-40 fold reduction in CD4-CD8- T cells in spleen, blood and lymph nodes, but not thymus||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|05-Jul-2007|Cryopreserved sperm|140.0|0.0|Unknown||T cell, MHC, antigen presentation, dendritic cell, CD8, CD4|Yes| 1535.0|IL-4 -/- IL-13 -/-|BALB/c-Il4/Il13/AnuApb||Recessive|interleukin 4|Il4|Nil|Il-4|MGI:96556|targeted mutation 3, Andrew NJ McKenzie|Il4/Il13|MGI:3038244|11||||||||||||||||Yes|||||||||||||Using a pulmonary granuloma model, induced with Schistosoma mansoni eggs, eosinophil infiltration, immunoglobulin E, and IL-5 production are abolished only in the combined absence of both cytokines. Furthermore, IL-4/13-deficient animals are severely impaired in their ability to expel the gastrointestinal nematode Nippostrongylus brasiliensis. Unexpectedly, N. brasiliensis-infected IL-4/13-deficient mice developed elevated IL-5 and eosinophilia, indicating that compensatory mechanisms exist for the expression of IL-5, although serum IgE remained undetectable. IL-4/13-deficient mice default to a Th1-like phenotype characterized by the expression of interferon gamma and the production of IgG2a and IgG2b.Decreased IgE level:less antigen-specific IgE is made compared to controls during an induced airway hyperresponsiveness model.Increased IgG2a level:more antigen-specific IgG2a is made compared to controls during an induced airway hyperresponsiveness modelDecreased interferon-gamma secretion:lymphocytes from mice sensitized and challenged with OVA produce less IFN-gamma than controlsDecreased interleukin-13 secretion:lymphocytes fail to produce IL-13Abnormal interleukin-4 secretion:lymphocytes fail to produce IL-4Decreased interleukin-5 secretion:lymphocytes from mice sensitized and challenged with OVA produce less IL-5 than controlsDecreased susceptibility to autoimmune disorder:mice fail to develop airway hyperresponsiveness after first being sensitized and challenged with OVA peptidein these mice, inflammation with eosinophil infiltrates occurs in the airways but there is a conspicuous absence of mucosal production.||Balb/c|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|05-Jul-2007|Cryopreserved sperm|150.0|0.0|Unknown||T cell, CD4, dendritic cell, interferon, asthma, IgE|Yes| 1535.0|IL-4 -/- IL-13 -/-|BALB/c-Il4/Il13/AnuApb||Recessive|interleukin 13|Il13|Unknown|Il-13|MGI:96541|targeted mutation 3, Andrew NJ McKenzie|Il4/Il13|MGI:3038244|11|||||||||||||||||||||||||||||Using a pulmonary granuloma model, induced with Schistosoma mansoni eggs, eosinophil infiltration, immunoglobulin E, and IL-5 production are abolished only in the combined absence of both cytokines. Furthermore, IL-4/13-deficient animals are severely impaired in their ability to expel the gastrointestinal nematode Nippostrongylus brasiliensis. Unexpectedly, N. brasiliensis-infected IL-4/13-deficient mice developed elevated IL-5 and eosinophilia, indicating that compensatory mechanisms exist for the expression of IL-5, although serum IgE remained undetectable. IL-4/13-deficient mice default to a Th1-like phenotype characterized by the expression of interferon gamma and the production of IgG2a and IgG2b.Decreased IgE level:less antigen-specific IgE is made compared to controls during an induced airway hyperresponsiveness model.Increased IgG2a level:more antigen-specific IgG2a is made compared to controls during an induced airway hyperresponsiveness modelDecreased interferon-gamma secretion:lymphocytes from mice sensitized and challenged with OVA produce less IFN-gamma than controlsDecreased interleukin-13 secretion:lymphocytes fail to produce IL-13Abnormal interleukin-4 secretion:lymphocytes fail to produce IL-4Decreased interleukin-5 secretion:lymphocytes from mice sensitized and challenged with OVA produce less IL-5 than controlsDecreased susceptibility to autoimmune disorder:mice fail to develop airway hyperresponsiveness after first being sensitized and challenged with OVA peptidein these mice, inflammation with eosinophil infiltrates occurs in the airways but there is a conspicuous absence of mucosal production.||Balb/c|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|05-Jul-2007|Cryopreserved sperm|||Unknown||T cell, CD4, dendritic cell, interferon, asthma, IgE|Yes| 7875.0|Kmt2d𝚫1|C5BL/6-Kmt2d/MegaAusb||Recessive|lysine (K)-specific methyltransferase 2D|Kmt2d|Unknown|C430014K11Rik, Mll2, Mll4|MGI:2682319||||15|||||||||||||||||||||||||||||Unknown|Unknown|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|16-Apr-2015||0.0|0.0|Unknown|||Yes| 8744.0|ASD572:Shn-2 KO:AIRE KO|B6.Cg-Aire Hivep2/AnuApb||Recessive|autoimmune regulator (autoimmune polyendocrinopathy candidiasis ectodermal dystrophy)|Aire|Nil||MGI:1338803|autoimmune regulator (autoimmune polyendocrinopathy candidiasis ectodermal dystrophy); targeted mutation 1, Leena Peltonen|Aire|MGI:2182940|10|||||||||||||||||||||||||||||unknown|unknown|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|02-Jul-2019|Cryopreserved sperm|55.0|0.0|Unknown|||Yes| 8744.0|ASD572:Shn-2 KO:AIRE KO|B6.Cg-Aire Hivep2/AnuApb||Recessive|human immunodeficiency virus type I enhancer binding protein 2|Hivep2|Nil|Gm20114, MIBP1, Schnurri-2, Shn-2|MGI:1338076|human immunodeficiency virus type I enhancer binding protein 2; targeted mutation 1, Shunsuke Ishii|Hivep2|MGI:2182914|10|||||||||||||||||||||||||||||unknown|unknown|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|02-Jul-2019|Cryopreserved sperm|||Unknown|||Yes| 1929.0|Balb/C Stat6-/- N10|C.129P2-Stat6/AnuApb|C.129P2-Stat6/AnuApb|Recessive|signal transducer and activator of transcription 6|Stat6|Nil|stat6-|MGI:103034|signal transducer and activator of transcription 6; targeted mutation 1, Shizuo Akira|Stat6|MGI:2386746|10||||||||||||||||No|||||||||||||Skin inflammation:* mice exhibit mild dermal infiltration of inflammatory cells.* few CD4+ cells infiltrate the perioral dermis and epidermis.Acanthosis: sight.Decreased B cell proliferation:* B cell proliferation in response to anti-IgM plus IL-4 is impaired.* however, B cell proliferation in response to LPS is normal.Decreased T cell proliferation:* thymocyte proliferation in response to TPA is impaired.* however, thymocyte proliferate in response to other stimuli.Decreased IgE level: IgE levels are lower than in wild-type mice following infection with N. brasiliensis.Decreased IgG1 level: IgG1 levels are 16-fold lower than in wild-type mice and following infection with N. brasiliensis they are 10-fold lower than in infected wild-type mice.Increased IgA level: IgA levels are slightly increased following infection with N. brasiliensis.Increased IgG level: IgG2 and IgG3 levels are slightly increased following infection with N. brasiliensis.Abnormal T-helper 2 physiology: mice fail to produce increased levels of Th2 cytokines in response to infection with N. brasiliensis.||BALB/c|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|23-Aug-2007|Cryopreserved sperm|63.0|0.0|Unknown||T cell, IL-4, signal transduction, lymphocyte, B cell|Yes| 1945.0|CBA/H. IL5 -/-|CBA/H.B6-Il5/AnuApb||Recessive|interleukin 5|Il5|Nil|Il-5|MGI:96557|targeted mutation 1, Manfred A Kopf|Il5|MGI:1861948|11||||||||||||||||Yes|||||||||||||Homozygotes for a targeted null mutation exhibit loss of normal airway hyperreactivity resulting from aeroallergen challenge, reduced numbers of CD5+ B cells in the peritoneal cavity at 2 weeks, and some altered responses to schistosomiasis infection. Mice appear normal. They have normal basal levels of eosinophils but in response to parasite infections or aeroallergen challenge, numbers do not increase. Further, resistance to some phases of helminthic infections may be impaired. Decreased airway responsiveness: airways of aeroallergen-challenged knockout mice lose hyperresponsiveness to methacholine.Increased neutrophil cell number: after aerosolized OVA challenge, knockout mice have increased levels of neutrophils in BALF compared to unchallenged animals.Increased lymphocyte cell number: after aerosolized OVA challenge, knockout mice have increased levels of lymphocytes in BALF compared to unchallenged animals but the increase is less pronounced than in wild type mice.Abnormal interferon physiology: in mesenteric lymph nodes in culture, there is a marked increase in IFNG production in knockouts compared to wild type after restimulation with mitogen or SEA.Granulomatous inflammation:* pulmonary granulomas that form in knockout mice in response to schistosome eggs are almost completely devoid of eosinophils compared to granulomas in wild type mice; the average size of granulomas in knockout mice are 40% smaller than those of wild type.* there is a 20-25% increase in numbers of macrophages associated with granulomas in knockouts compared with wild type; with acute or chronic parasite infection, the numbers of both fibroblasts and macrophages nearly double in knockout animals compared to wild type.Liver fibrosis: hepatic fibrosis is significantly reduced in knockouts with acute or chronic helminth parasite infection.Increased eosinophil cell number: knockout mice infected with parasites do not show eosinophil counts above baseline values, while 35-week old controls develop eosinophilia in the blood, bone marrow and peritoneal cavity.||CBA/H|Yes|Yes|Yes|Yes|Yes|Yes|No|Excellent|20||IL5-/- male mated with IL5-/- female|No|01-Sep-2007|Cryopreserved sperm|140.0|0.0|Unknown||infection, T cell, B cell, CD5, eosinophil|Yes| 1626.0|C2X1f|129X1;129S1-Cited2/Apb|129X1;129S1-Cited2/Apb|Recessive|Cbp/p300-interacting transactivator, with Glu/Asp-rich carboxy-terminal domain, 2|Cited2|Normal|ER154-like, Mrg1, Msg2, p35srj|MGI:1306784|targeted mutation 1.1, Sally L Dunwoodie|Cited2|MGI:3696062|10||||||||||||||||No|||||||||||||Normal|None|129X1/SvJ|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|3|0|Backcrossed into 129X1/SvJ to increase health as ES origin is not as viable.|No|16-Jul-2007|Cryopreserved sperm|200.0|0.0|Yes||Cited2, heart, placenta, left-right axis|Yes| 2465.0||B6.CBA-Tg(hGMCSF-2CK1)91/AnuApb||Dominant|||||||||Unknown||||||||||||||||No|human GMCSF (GM-CSF)|human GM-CSF promoter and enhancer (10.5kb)|||||||||||Express human GM-CSF. hGM-CSF detected in serum by ELISA. Murine GM-CSF used as internal control.||C57BL/6 x CBA|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|16-Jan-2008|Cryopreserved sperm|30.0|0.0|No||T cell, lymphocyte, transcription, chromatin remodelling, NF-kappaB|Yes| 1635.0|Itsn1-L knockout|129/Sv-Itsn1/Apb|129/Sv-Itsn1/Apb|Recessive|intersectin 1 (SH3 domain protein 1A)|Itsn1|Reduced|Eh domain, SH3 domain regulator of endocytosis 1, EHSH1, Ese1, Intersectin-L, Sh3p17|MGI:1338069|intersectin 1 (SH3 domain protein 1A); targeted mutation 2.1, Melanie A Pritchard|Itsn1|MGI:3812035|16||||||||||||||||Yes|||||||||||||Some homozygotes are runty after birth compared to the wildtype and die before weaning age. Otherwise they can catch up with the wildtype|No overt phenotype|129Sv|Yes|Yes|Yes|Yes|Yes|Yes|No|Poor|||Het x het|No|17-Jul-2007|Cryopreserved sperm|36.0|0.0|Yes|Alzheimer’s disease and Down syndrome|Alzheimer's disease, Down Syndrome, endocytosis, endosome, neuron|Yes| 1636.0|Lefty2-Cre ; L2Cre (Ninnag)|B6.Cg-Tg(Lefty2-cre)21bHmd/Apb|B6.Cg-Tg(Lefty2-cre)21bHmd/Apb|Dominant||||||||||||||||||||||||||transgene insertion 21b, Hiroshi Hamada|3.0kb upstream region of murine Lefty2 gene|High||||||||||No overt phenotype|Expresses Cre-recombinase in mesoderm of 8.5dpc embryos.The promoter specifically directed cre expression in the epiblast and its derivatives between E5.5 and E8.0.|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|6||Transgenic x wildtype|No|17-Jul-2007|Cryopreserved sperm|100.0|0.0|Unknown||Mesoderm, left-right, transcription, Nodal|Yes| 1637.0|NDE-Cre|C57BL/6-Tg(Nodal-cre)16Hmd/Apb|C57BL/6-Tg(Nodal-cre)16Hmd/Apb|Dominant||||||||||||||||||||||||||transgene insertion 16, Hiroshi Hamada|Two tandem copies of the NDE enhancer element from Nodal genes upstream region (0.7kb each) ligated upstream of heat shock promoter|Weak initially in node ~LB stage. Becomes stronger as embryos age ie quiet strong at 4 somites|||||||||||Expresses Cre-recombinase in node at LB/EHF stage.|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Poor|6||Transgenic x wildtype|No|17-Jul-2007|Cryopreserved sperm|140.0|0.0|Unknown||Nodal, left-right, Heat shock Protein, Mesoderm|Yes| 1927.0|S1 SuprMam/09:S2Balb/Balb Hom::G4|B6.BALB/c-SuprMam1 SuprMam2/AnuApb||Recessive|||||||||Unknown||||||||||||||||Yes|||||||||||||Mice are more susceptible to mammary tumours.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|6|||No|23-Aug-2007|Cryopreserved sperm|100.0|0.0|Unknown||mammary, tumour, DMBT1, p53, modifier|Yes| 2355.0|Patel|B6.129S2-Cd28 Tg(TcrLCMV)327Sdz Tcra/AnuApb||Recessive|CD28 antigen|CD28|Nil|Tcr alpha, Tcralpha|MGI:88327|targeted mutation 1, Tak Mak|Cd28|MGI:1857150|1||||||||||||||||Yes|transgene insertion 327, Birgit Ledermann||High||||||||||Homozygous mutation of this CD28 results in impairment of some T cell responses and decreased basal immunoglobulin levels. Mutant animals have reduced T helper cell activity and impaired T cell response to lectins, but cytotoxic T cells can still be induced||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|11-Dec-2007|Cryopreserved sperm|25.0|0.0|Unknown||T cell, immunoglobulin, receptor|Yes| 2355.0|Patel|B6.129S2-Cd28 Tg(TcrLCMV)327Sdz Tcra/AnuApb||Recessive|T-cell receptor alpha chain|Tcra|Unknown|Tcr alpha, Tcralpha|MGI:98553|targeted mutation 1, Peter Mombaerts|Tcra|MGI:1857255|14|||||||||||||||||||||||||||||Homozygous mutation of this CD28 results in impairment of some T cell responses and decreased basal immunoglobulin levels. Mutant animals have reduced T helper cell activity and impaired T cell response to lectins, but cytotoxic T cells can still be induced||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|11-Dec-2007|Cryopreserved sperm|||Unknown||T cell, immunoglobulin, receptor|Yes| 2390.0|Light Knockout|B6.129-Tnfsf14/AnuApb||Recessive|tumor necrosis factor (ligand) superfamily, member 14|Tnfsf14|Nil|HVEM-L, LIGHT|MGI:1355317|tumor necrosis factor (ligand) superfamily, member 14; targeted mutation 1, Klaus Pfeffer|Tnfsf14|MGI:2671122|17||||||||||||||||No|||||||||||||Develop intact lymphoid organs.Abnormal immune system physiology.The knockout provides in vivo evidence for a cooperative role forLIGHT and Lymphotoxin in lymphoid organogenesis and indicates important costimulatory functions for LIGHT in T cell activation.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|Yes|Unknown||||No|19-Dec-2007|Cryopreserved sperm|130.0|0.0|No||T cell, lymphotoxin, lymphocyte, CD28, activation|Yes| 8746.0|ASD873:Pear:XB3bpins|C57BL/6NCrlAnu-Xbp1/AnuApb||Recessive|X-box binding protein 1|Xbp1|Unknown|D11Ertd39e, TREB5, TREB-5, XBP-1|MGI:98970|Xbp1, endonuclease-mediated mutation 2, Australian National University|Xbp1||11||||||||||Unknown to Unknown|||||||||||||||||||Unknown|Unknown|C57BL/6NCrlAnu|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|02-Jul-2019|Cryopreserved sperm|55.0|0.0|Unknown|||Yes| 1952.0|BALB/c.Zeta|BALB/c-Gstz1/AnuApb||Recessive|glutathione transferase zeta 1 (maleylacetoacetate isomerase)|Gstz1|Nil|maleylacetoacetate isomerase|MGI:1341859|glutathione transferase zeta 1 (maleylacetoacetate isomerase); targeted mutation 1, Philip G Board|Gstz1|MGI:3050206|12||||||||||||||||No|||||||||||||Increased sensitivity to induced morbidity/mortality: 3% phenylalanine in the water is lethal to young homozygotes, less than 28 days old, but not to older homozygotes, greater than 66 days old.Premature death: several mutants died after 1 year of age from heart pathologies.Dystrophic cardiac calcinosis:* in some mutants over 1 year of age calcification of the myocardium in the right atrium and/or ventricle is seen* calcification is also seen in 3 of 8 young mutants that died after 3% phenylalanine exposure.Cellular necrosis:* in some mutants over 1 year of age myocyte necrosis is seen* myocyte necrosis is also seen in 2 of 8 young mutants that died after 3% phenylalanine exposure.Decreased body weight: male homozygotes weigh slightly less than wild-type or heterozygous males.Weight loss: 3% phenylalanine in the water results in greater weight loss and growth restriction in male homozygotes compared to wild-type mice.Decreased leukocyte cell number: 3% phenylalanine in the water results in decreased total white cell counts in mutants but not in wild-type mice.Decreased spleen weight: * spleen weight is significantly decreased in female homozygotes and tends to be decreased in male homozygotes compared to wild-type mice.* 3% phenylalanine in the water results in a dramatic decrease in spleen weight in homozygotes with reduction in both white and red pulp, but an increase in spleen weight in wild-type mice.Chronic inflammation: in some mutants over 1 year of age chronic inflammation is seen in the heart.Liver inflammation: at 6 weeks and 6 months of age multifocal hepatitis is seen.Abnormal hepatocyte morphology: large pleomorphic mitochondria are seen in hepatocytes from mutants.Increased liver weight: on a normal diet liver weight is greater in homozygotes compared to wild-type mice.Hepatic necrosis:* at 6 months of age 3 of 7 homozygotes show hepatocyte necrosis.* 3 out of 8 homozygotes that died after 3% phenylalanine exposure displayed hepatocyte necrosis.Hepatic steatosis: 5 out of 8 homozygotes that died after 3% phenylalanine exposure displayed macrovesicular steatosis.Increased kidney weight:* kidney weight is greater in homozygotes compared to wild-type mice.* 3% phenylalanine in the water results in an increase in kidney weight in homozygotes but not in wild-type mice.||BALB/c |Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|03-Sep-2007|Cryopreserved sperm|50.0|0.0|Yes||GST, maleylacetoacetate, maleylacetone (MA) and succinylacetone, phenylalanine and tyrosine, Keap1/Nrf2 pathway, oxidative stress, inflammation, glutathione transferase|Yes| 5427.0|203.3 ; cTnI-G203S.3|C57BL/6-Tg(Myh6-TNNI3*G203S)3Chs/Apb||Dominant||||||||||||||||||||||||||transgene insertion 3, Christopher Semsarian|cardiac specific mouse αMHC promoter (alpha myosin heavy chain)|58% of endogenous||||||||||Unknown|Mice develop cardiac phenotype - hypertrophic cardiomyopathy. Onset age dependent upon the amount of transgene protein expressed.|C57BL/6|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Excellent||17|Transgenic x non-transgenic sibs|No|10-Feb-2011|Cryopreserved sperm|36.0|0.0|Yes|Hypertrophic cardiomyopathy (HCM) is a primary disorder of the myocardium characterized by cardiac hypertrophy. The clinical course of HCM is variable, with inter- and intra-familial variations ranging from benign asymptomatic disease to a malignant phenotype with a high risk of cardiac failure or sudden cardiac death.|Hypertrophy, Cardiomyopathy, Calcium, Troponin I gene|Yes| 2397.0|Zap70 knockout|B6;129X1-Zap70/AnuApb|B6;129X1-Zap70/AnuApb|Recessive|zeta-chain (TCR) associated protein kinase|Zap70|Nil|Srk, TZK, ZAP-70|MGI:99613|targeted mutation 1, Arthur Weiss|Zap70|MGI:2176252|1||||||||||||||||No|||||||||||||Abnormal T cell differentiation:* the number of dendritic epidermal T cells is reduced and those cells present lack the characteristic dendritic extensions.* few intestinal intraepithelial lymphocytes express gamma delta or alpha beta T cell receptors.Arrested T cell differentiation: arrest at the double positive stageAbnormal splenic cell ratio: spleens are composed of mostly B cells.Abnormal lymph node cell ratio:* lymph nodes contain mostly B cells and a significant percentage of CD3+ (but CD4- and CD8-) cells which are primarily gamma delta T cells.* the percentage of gamma delta T cells is increased but the absolute number of these cell is similar to wild-type.||C57BL/6 x 129X1|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|20-Dec-2007|Cryopreserved sperm|20.0|0.0|No||T cell, lymphocyte, B cell, lymph node, spleen, differentiation|Yes| 2476.0|Toll 3 Receptor, Pkr double KO|B6.129-Tlr3 Eif2ak2/MarpApb||Recessive|toll-like receptor 3|Tlr3|Nil|2310047A08Rik, 4732414G15Rik, dsRNA-activated kinase, eIF-2 alpha, eIF-2 alpha, Eif2ak2, IFN- type I-induced and dsRNA-activated kinase, IFN-induced and double-stranded RNA-activated kinase, Pkr, Prkr, Tik|MGI:2156367|toll-like receptor 3; targeted mutation 1, Richard A Flavell|Tlr3|MGI:2653138|8||||||||||||||||Yes|||||||||||||Splenomegaly developing between 8 and 10 weeks of agewas observed in tlr3<-/-> and tlr3<-/-> pkr<-/-> mice.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|Yes|Excellent|||Hom x Hom|No|18-Jan-2008|Cryopreserved sperm|100.0|0.0|Unknown||viral infection, hypersensitivity, T cell, stimulation, proliferation|Yes| 2476.0|Toll 3 Receptor, Pkr double KO|B6.129-Tlr3 Eif2ak2/MarpApb||Recessive|eukaryotic translation initiation factor 2-alpha kinase 2|Eif2ak2|Nil|2310047A08Rik, 4732414G15Rik, dsRNA-activated kinase, eIF-2 alpha, eIF-2 alpha, IFN- type I-induced and dsRNA-activated kinase, IFN-induced and double-stranded RNA-activated kinase, Pkr, Prkr, Tik|MGI:1353449|eukaryotic translation initiation factor 2-alpha kinase 2; targeted mutation 1, Charles Weissmann|Eif2ak2|MGI:2182566|17|||||||||||||||||||||||||||||Splenomegaly developing between 8 and 10 weeks of agewas observed in tlr3<-/-> and tlr3<-/-> pkr<-/-> mice.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|Yes|Excellent|||Hom x Hom|No|18-Jan-2008|Cryopreserved sperm|||Unknown||viral infection, hypersensitivity, T cell, stimulation, proliferation|Yes| 5431.0|Funky|STOCK Ndufs4/DrthApb|STOCK-Ndufs4/Drth|Recessive|NADH dehydrogenase (ubiquinone) Fe-S protein 4|Ndufs4|Reduced|C1-18k|MGI:1343135|funky|Ndufs4|MGI:4942335|13||||||||||||||||Yes|||||||||||||Homozygous mice initially present with fur loss around postnatal day 14, which regrows in the next hair cycle. They show reduced growth and several behavioural abnormalities that appear from postnatal week five, such as tilting of the head, walking in circles and twisting of the body when suspended by the tail. Due to progressively wobbly gait and general deterioration in physical condition, all homozygous mice have to be euthanased around postnatal week eight in compliance with ethical guidelines.|Appears indistinguishable from Wild-Type|C57BL/6|Yes|Unknown|Yes|Yes|Unknown|Yes|No|Poor|unknown||het X het|No|14-Feb-2011|Cryopreserved sperm|49.0|0.0|Yes|Mitochondrial Disease; Leigh Syndrome|Mitochondria, Oxidative Phosphorylation, Complex I|Possibly| 2352.0|Tg (F5 TCR)|B6.SJL-PtprcPep3 Tg(CD2-TcraF5,CD2-TcrbF5)1Kio/AnuApb||Recessive|protein tyrosine phosphatase, receptor type, C|Ptprc|Unknown|B220, CD45, CD45 antigen, Cd45, Ly-5, Lyt-4, T200, lymphocyte antigen 5|Ptprc|Ptprc|||1||||||||||||||||Yes|transgene insertion 1, Dimitris Kioussis|CD2 minigene|||||||||||Transgenic mice have TCRs recognizing, in the context of D, a peptide of the influenza virus A/NT/60/68 nucleoprotein [NP-(366-379)]. ||SJL/JxC57BL/10|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|11-Dec-2007|Cryopreserved sperm|80.0|0.0|No||T cell, B cell, phosphatase, cell growth, transplant|Yes| 2352.0|Tg (F5 TCR)|B6.SJL-PtprcPep3 Tg(CD2-TcraF5,CD2-TcrbF5)1Kio/AnuApb||Recessive|peptidase C|Pepc|Unknown|Dip-1, Pep-3, Pep3|MGI:97541|Pepc|||1|||||||||||||||||||||||||||||Transgenic mice have TCRs recognizing, in the context of D, a peptide of the influenza virus A/NT/60/68 nucleoprotein [NP-(366-379)]. ||SJL/JxC57BL/10|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|11-Dec-2007|Cryopreserved sperm|||No||T cell, B cell, phosphatase, cell growth, transplant|Yes| 2398.0|Activin Beta C ++ FL2|C57BL/6-Tg(ACTIVIN-β{C})2Grb/Apb||Recessive|||||||||Unknown||||||||||||||||No|human activin betaC|CMV|High||||||||||No gross external abnormalities evident, male sub-fertile (narrow window of fertility 7-9 weeks), limited pups resulting from matings, infertile from around 9 weeks. |No gross external abnormalities evident, male sub-fertile (window of fertility 7-14 weeks), decreased litter size, infertile from around 15 weeks. |C57BL/6|Yes|Yes|Yes|Yes|No|Yes|Yes|Poor|||Het x Het or Het x WT|No|20-Dec-2007|Cryopreserved sperm|90.0|0.0|Unknown||activin, inhibin, prostate, testis, liver|Yes| 2418.0|Gz alpha knockout|C57BL/6JAnu-Gnaz/AnuApb|C57BL/6JAnu-Gnaz/AnuApb|Recessive|guanine nucleotide binding protein, alpha z subunit|Gnaz|Nil|Gz|MGI:95780|guanine nucleotide binding protein, alpha z subunit; targeted mutation 1, I A Hendry|Gnaz|MGI:3575007|10||||||||||||||||No|||||||||||||Decreased sensitivity to xenobiotic induced morbidity/mortality:* morphine treated homozygotes are able to tolerate higher morphine doses compared to wild-type mice (LD50 of 800 mg/kg compared to 700 mg/kg for wild-type).* however no significant difference in the serum levels of morphine or its metabolites is seen.Decreased chemically-elicited antinociception:* in previously unexposed female homozygotes reduced analgesia at low morphine doses is seen, a similar but not significant effect was seen in males.* with repeated morphine doses mutants develop tolerance faster than wild-type mice.* acute morphine administration induces the same degree of antinociception; however homozygotes develop tolerance to morphine more rapidly compared to wild-type mice in the hot and cold plate tests.* spinal mechanisms of morphine tolerance are normalReduced fertility: litters from homozygous parents on the C57BL/6 background had increased mortality that was not seen in litters from heterozygous or mixed strain parents.Decreased body weight:* body weight is normal at birth but homozygotes gain less weight and males and females are 22% and 27% smaller than their wild-type littermates at 2 - 3 weeks of age.* After 3 weeks of age homozygotes gain weight more rapidly and the body weight difference is gone by 2 - 3 months of age.|Abnormal chemically-elicited antinociception: with repeated morphine doses heterozygotes develop tolerance faster than wild-type mice but not as quickly as homozygous mutants.Decreased sensitivity to xenobiotic induced morbidity/mortality: morphine treated homozygotes are able to tolerate higher morphine doses compared to wild-type mice (LD50 of 750 mg/kg compared to 700 mg/kg for wild-type).|C57BL/6jAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Poor|20|||No|09-Jan-2008|Cryopreserved sperm|109.0|0.0|Unknown||G-protein, Tolerance, Feeding Behaviour, xenobiotic, morphine|Yes| 8360.0|ASD866|C57BL/6NCrlAnu:Orange||Dominant||||||||||||||||||||||||||||||||||||||Normal|||Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|04-Dec-2017||0.0|0.0|Unknown|||Yes| 2474.0||B6.129-Bmi1/WehiApb||Recessive|Bmi1 polycomb ring finger oncogene|Bmi1|Nil|Bmi-1, Bmi1, Pcgf4|MGI:88174|targeted mutation 1, Anton Berns|Bmi1|MGI:1857632|2||||||||||||||||Yes|||||||||||||Homozygous null mutants display decreased hematopoietic cell number, immune deficiency, neurological abnormalities, and posterior transformation, while transgenic overexpressing mice show an opposite dose-dependent anterior transformation of vertebral identity.Postnatal lethality.|Vertebral transformation||No|No|Yes|No|No|Yes|No|Poor||||No|18-Jan-2008|Cryopreserved sperm|150.0|0.0|Unknown||Proliferation, Ataxia, Sporadic seizures, posterior transformation, anteroposterior axis|Yes| 2475.0|Mel18|B6;129-Pcgf2RbrcApb||Recessive|polycomb group ring finger 2|Pcgf2|Unknown|mel-18, Mel18, Rnf110, Zfp144|MGI:99161|polycomb group ring finger 2; targeted mutation 1, Haruhiko Koseki|Pcgf2|MGI:1857633|11||||||||||||||||Yes|||||||||||||Homozygous null mutants exhibit multiple abnormalities of the axial skeleton (including homeotic transformations), grow markedly slower, and die either perinatally or between 3-6 weeks of age depending on genetic background.||C57BL/6|No|No|Yes|No|No|Yes|No|Unknown||||No|18-Jan-2008|Cryopreserved sperm|140.0|0.0|Unknown||growth retardation, Ataxia, posterior transformation, anteroposterior axis|Yes| 2732.0|-0.9E3CreERT line 90|C57BL/6-Tg(Tal1-cre/ERT)90Jame/Apb|C57BL/6-Tg(Tal1-cre/ERT)90Jame/Apb|Semi-dominant||||||||||||||||||||||||||transgene insertion 90, J Anke M van Eekelen|-0.9E3 neural enhancer/promoter of the Stem Cell Leukemia (Scl/tal1) gene|Moderate expression of creERT in Scl expressing neurons of the CNS||||||||||Normal|Normal|C57BL/6J|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|5||-0.9E3CreERT line 90 x C57BL/6J|No|06-Feb-2008|Cryopreserved sperm|89.0|0.0|No||Cre/loxP, tamoxifen inducibility, neurogenesis, transcription factor , conditional gene deletion|Yes| 2733.0|-0.9E3CreERT line 145B|C57BL/6-Tg(Tal1-cre/ERT)145BJame/Apb||Semi-dominant||||||||||||||||||||||||||transgene insertion 145B, J Anke M van Eekelen|-0.9E3 neural enhancer/promoter of the Stem Cell Leukemia (Scl/tal1) gene|Moderate expression of creERT in Scl expressing neurons of the CNS||||||||||Normal|Normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|4||-0.9E3CreERT line 145B x C57BL/6J|No|06-Feb-2008|Cryopreserved sperm|70.0|0.0|No||Cre/loxP, tamoxifen inducibility, neurogenesis, transcription factor, conditional gene deletion|Yes| 2734.0|-0.9E3CreERT line 145A|C57BL/6-Tg(Tal1-cre/ERT)145AJame/Apb|C57BL/6-Tg(Tal1-cre/ERT)145AJame/Apb|Semi-dominant||||||||||||||||||||||||||transgene insertion 145A, J Anke M van Eekelen|-0.9E3 neural enhancer/promoter of the Stem Cell Leukemia (Scl/tal1) gene|Moderate expression of creERT in Scl expressing neurons of the CNS||||||||||Normal|Normal|C57BL/6J|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|5||-0.9E3CreERT line 145A x C57BL/6J|No|06-Feb-2008|Cryopreserved sperm|65.0|0.0|No||Cre/loxP, conditional gene deletion, tamoxifen inducibility, neurogenesis, transcription factor|Yes| 8750.0|Gsdmd KO|C57BL/6N-Gsdmd/GneAnu||Recessive|gasdermin D|Gsdmd||1810036L03Rik, DF5L, Dfna5l, Gsdmdc1, M2-4|MGI:1916396|gasdermin D; endonuclease-mediated mutation 1, Genentech|Gsdmd|MGI:6259809|15|||||||||||||||||||||||||||||||C57BL/6N|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|09-Jul-2019||0.0|0.0|Unknown||Caspase-11, infection|Yes| 7790.0||C57BL/6NCrlAnu-Prdm1/AnuApb|C57BL/6NCrlAnu-Prdm1/AnuApb|Recessive|PR domain containing 1, with ZNF domain|Prdm1||b2b1765Clo, Blimp1, Blimp-1, PRDI-BF1|MGI:99655|Prdm1; mutation 1, Australian National University|Prdm1||10||||||A to T||||Unknown to Unknown|||||||||||||||||||Absence of B and T cells|Small reduction in %B cells and increased CD44 expression on B cells|C57BL/6NCrlAnu|Yes|Unknown|Yes|Yes|Unknown|Yes|No|Unknown||||No|19-Nov-2014|Cryopreserved sperm|40.0|0.0|Unknown||T cell, B cell, Cd44|Yes| 2746.0|BALB/c.Flii 1.5F ; FIN|BALB/c-Flii/AnuApb|BALB/c-Flii/AnuApb|Recessive|flightless I homolog (Drosophila)|Flii|Nil|Fli1, Fliih|MGI:1342286|targeted mutation 1, Hugh D Campbell|Flii|MGI:2179825|11||||||||||||||||Yes|||||||||||||Embryonic lethality at implantation: no embryos are recovered after E5.5; embryos develop normally until cellularization, the development arrests before completion of gastrulation blastocysts initiate uterine implantation but embryos fail to develop. embryonic growth arrest: development arrests during gastrulation|Enhanced wound healing: 3 days after a 1 cm full-thickness incision was made in the dorsal skin, surface wound area measurements show smaller, more contracted wounds than in wild-type mice. Length of neoepidermis is significantly greater in mutant animals, and percentage or re-epithelialization of wounds is greater at 5 days after wounding. By day 7, healing is comparable in mutants and wild-type|BALB/c|No|No|Yes|No|No|Yes|No|Good|10|11|Het male x wt female|No|10-Feb-2008|Cryopreserved sperm|150.0|0.0|Yes||cell migration, embryonic lethal, wound repair, gelsolin, gastrulation|Yes| 2763.0|BALB/c.Flii 2.1A|BALB/c-Flii/3AnuApb|BALB/c-Flii/3AnuApb|Recessive|flightless I homolog (Drosophila)|Flii|Nil|Fli1, Fliih|MGI:1342286|targeted mutation 1, Hugh D Campbell|Flii|MGI:2179825|11||||||||||||||||Yes|||||||||||||Embryonic lethality at implantation: no embryos are recovered after E5.5; embryos develop normally until cellularization, the development arrests before completion of gastrulation blastocysts initiate uterine implantation but embryos fail to develop. embryonic growth arrest: development arrests during gastrulation|Enhanced wound healing: 3 days after a 1 cm full-thickness incision was made in the dorsal skin, surface wound area measurements show smaller, more contracted wounds than in wild-type mice. Length of neoepidermis is significantly greater in mutant animals, and percentage or re-epithelialization of wounds is greater at 5 days after wounding. By day 7, healing is comparable in mutants and wild-type|BALB/c|No|No|Yes|No|No|Yes|No|Good|10|11|Het male x WT female|No|14-Feb-2008|Cryopreserved sperm|150.0|0.0|No||gelsolin, embryonic lethal, wound repair, cell migration, gastrulation|Yes| 2766.0|BALB/c.Flii<+/+> FLII ; FIC|BALB/c-Tg(FLII)1Hdc/AnuApb|BALB/c-Tg(FLII)1Hdc|Dominant||||||||||||||||||||||||||transgene insertion 1, Hugh D Campbell|human flightless promoer|||||||||||Ubiquitous expression of human Flightless gene.|Normal|BALB/c|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||1|Hom x Hom|No|15-Feb-2008|Cryopreserved sperm|150.0|0.0|Unknown||human Flightless, wound repair, cellular proliferation, cell migration, gelsolin|Yes| 2772.0|BALB/c.Flii<+/+> FLII ; FIT|BALB/c-Tg(FLII)2Hdc/AnuApb|BALB/c-Tg(FLII)2Hdc|Dominant||||||||||||||||||||||||||Human Flightless gene|Human Flightless|||||||||||Ubiquitous expression of human Flightless protein||BALB/c|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|5||Het x wt BALB/c|No|16-Feb-2008|Cryopreserved sperm|80.0|0.0|Unknown||human flightless, wound repair, cellular proliferation, cell migration, gelsolin|Yes| 2776.0|Balb/c-hK14FLII 18|BALB/c-Tg(hK14-FLII)18/AnuApb||Dominant|||||||||Unknown||||||||||||||||Yes|Human Flightless|Human Keratin 14|||||||||||Not bred to homozygous state|Normal|BALB/C|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|5||Het FLII transgenic x WT BALB/c|No|16-Feb-2008|Cryopreserved sperm|45.0|0.0|Unknown||human, skin, enhancer, keratin|Yes| 2779.0|C57BL/6.hK14-FLII 5|C57BL/6-Tg(hK14-FLII)5/AnuApb||Dominant|||||||||Unknown||||||||||||||||Yes|Human Flightless|Human Keratin 14|||||||||||Not bred to Homozygous state|Normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|5||Het FLII transgenic x WT C57BL/6|No|16-Feb-2008|Cryopreserved sperm|60.0|0.0|Unknown||human, keratin, skin, enhancer|Yes| 2782.0|C57BL/6.Flii 1.5F|B6.C-Flii/AnuApb|B6.C-Flii/AnuApb|Recessive|flightless I homolog (Drosophila)|Flii|Nil|Fli1, Fliih|MGI:1342286|targeted mutation 1, Hugh D Campbell|Flii|MGI:2179825|11||||||||||||||||Yes|||||||||||||Embryonic lethality at implantation: no embryos are recovered after E5.5; embryos develop normally until cellularization, the development arrests before completion of gastrulation blastocysts initiate uterine implantation but embryos fail to develop. embryonic growth arrest: development arrests during gastrulation|Enhanced wound healing: 3 days after a 1 cm full-thickness incision was made in the dorsal skin, surface wound area measurements show smaller, more contracted wounds than in wild-type mice. Length of neoepidermis is significantly greater in mutant animals, and percentage or re-epithelialization of wounds is greater at 5 days after wounding. By day 7, healing is comparable in mutants and wild-type.|C57BL/6|No|No|Yes|No|No|Yes|No|Good|10|11|Het male x WT female|No|16-Feb-2008|Cryopreserved sperm|75.0|0.0|Unknown||embryonic lethal, gelsolin, wound repair, egg cylinder, gastrulation|Yes| 3324.0|TGM2 floxed|B6;129S1-Tgm2/Apb|B6;129S1-Tgm2/Apb|Recessive|transglutaminase 2, C polypeptide|Tgm2|Normal|G[a]h, protein-glutamine gamma-glutamyltransferase, TG C, TG2, tissue transglutaminase, tTG, tTGas|MGI:98731|targeted mutation 1, Robert M Graham|Tgm2|MGI:3525256|2||||||||||||||||Yes|||||||||||||Normal|Normal|129S1/Sv x C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|10||Hom x Hom|No|15-Jun-2008|Cryopreserved sperm|138.0|0.0|Unknown||Transgluatminase, Gh, G-protein, cross-linking|Yes| 3341.0|CBA/Ca Tg(IL5)C1|CBA/Ca-Tg(CD2-Il5)5C1Ldt/Apb [cc]|CBA/Ca-Tg(CD2-Il5)5C1Ldt/Apb [cc]|Recessive||||||||||||||||||||||||||transgene insertion 5C1, Lindsay A Dent|dominant controlling region (DCR), to approx. 2.1kb, 3' of the genomic sequence of the human CD2 gene|8 copies||||||||||Do not maintain as homozygotes. While this is apparently possible, survival of homozygotes likely to be lower.|Appear normal with peripheral blood eosinophilia and increased numbers of eosinophils in the spleen (with splenomegaly), bone marrow.Heterozygous BALB/c and C57BL/6 IL-5 Tg2 mice are resistant to methylcholanthrene-induced carcinogenesis - see Simson, L, et al., 2007, Regulation of carcinogenesis by IL-5 and CCL11: a potential role for eosinophils in tumor immune surveillance. J. Immunol., 178:4222-4229.|CBA/Ca|No|No|Yes|No|No|Yes|No|Excellent|||Tg male wild type female|No|20-Jun-2008|Cryopreserved sperm|150.0|0.0|Yes||eosinophil, asthma, resistance to helminthic parasites, allergy, immune surveillance|Yes| 3342.0|CBA/Ca Tg(IL5)C2|CBA/Ca-Tg(CD2-Il5)5C2Ldt/Apb [cc]|CBA/Ca-Tg(CD2-Il5)5C2Ldt/Apb [cc]|Dominant||||||||||||||||||||||||||transgene insertion 5C2, Lindsay A Dent|Dominant controlling region (DCR), to approx. 2.1kb, 3' of the genomic sequence of the human CD2 gene|49 copies. The DCR drives thymocyte and T cell specific expression.||||||||||Do not maintain as homozygotes. While this is apparently possible, survival of homozygotes likely to be lower.|Appear normal with peripheral blood eosinophilia and increased numbers of eosinophils in the spleen (with splenomegaly), bone marrow. Heterozygous BALB/c and C57BL/6 IL-5 Tg2 mice are resistant to methylcholanthrene-induced carcinogenesis - see Simson, L, et al., 2007, Regulation of carcinogenesis by IL-5 and CCL11: a potential role for eosinophils in tumor immune surveillance. J. Immunol., 178:4222-4229.|CBA/Ca|No|No|Yes|No|No|Yes|No|Excellent|||Tg male wild type female|No|20-Jun-2008|Cryopreserved sperm|150.0|0.0|Yes||eosinophil, asthma, resistance to helminthic parasites, allergy, immune surveillance|Yes| 8751.0|Db|B6-Lepr/AnuApb||Recessive|leptin receptor|Lepr||Leprb, LEPROT, leptin receptor gene-related protein, Modb1, obese-like, obl, Obr, OB-RGRP|MGI:104993|leptin receptor; diabetes|Lepr|MGI:1856009|4|||||||||||||||||||||||||||||ObesityDiabetes||C57BL/6|Yes|No|Yes|Yes|No|Yes|No|Unknown||||No|17-Jul-2019|Cryopreserved sperm|55.0|0.0|Unknown|||Yes| 3314.0|P301L tau ; pR5|C57BL/6-Tg(Thy1-MAPT)183Gotz/Apb||Recessive||||||||||||||||||||||||||transgene insertion 183, Jurgen Gotz|murine Thy1|High in the hippocampus, fornix fimbriae, amygdala, spinal cord, and cortex|||||||||||Transgene expression high in brain, low in spinalcord. No altered physical phenotype.Tangle formation|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|10||T6 x C57BL/6|No|09-Jun-2008|Cryopreserved sperm|20.0|0.0|Yes||memory impairment, Alzheimer’s disease, tangles, phosphorylation, amygdala, tau, microtubule-associated protein tau|Yes| 3926.0|K5-crePR1 , K5cre*PR1 ; K5S|BALB/c-Tg(KRT5-cre*/PGR)1Der/AnuApb||Dominant||||||||||||||||||||||||||Cre recombinase, mutant; Cre* fused to a deletion mutant of the human progesterone receptor (PR)|bovine keratin 5|Normal to high, restricted to keratinocytes||||||||||To activate or inactivate conditional alleles in murine stratified epithelia, a novel system has been developed. It is based on the generation of transgenic mice that express an inducible Cre recombinase under the control of a promoter specific for stratified epithelia. The inducible features of Cre were achieved by fusing Cre to a deletion mutant of the human progesterone receptor (PR), which fails to bind progesterone but can be activated by progesterone antagonists, such as RU486. This fusion protein (CrePR1) is sequestered in the cytoplasm. After activation with RU486, CrePR1 translocates to the nucleus, where it mediates the excision of DNA sequences flanked by LoxP sites. Mice generated express CrePR1 under the control of the K5 which is expressed in the basal cells of stratified epithelia ||Balb/c|Yes|Yes|Yes|Yes|Yes|Yes|No|Excellent|4||Backcross to balb/c|No|14-Oct-2008|Cryopreserved sperm|86.0|0.0|Unknown||RU486, codon optimised Cre, modified Cre, keratin, inducible|Yes| 3945.0|MommeD3|FVB/N-MommeD3 Tg(HBA1-Gfp)1Ew/Apb||Semi-dominant|||Unknown|||modifiers of murine metastable epiallele D3|MommeD3|MGI:3586550|11||||||||||||||||Yes|transgene insertion 3 Emma Whitelaw|human alpha-globin promoter and enhancer region|||||||||||Homozygous embryonic lethality around 10.5 dpc|Percentage of cells expressing the GFP transgene (Line3) is increased (suppressor of variegation). Heterozygotes are slightly smaller than wild-types at weaning.|FVB/NJ|No|No|Yes|No|No|Yes|No|Good|||MommeD3<+/->;Tg(Hba1-Gfp)3Ew x Tg(Hba1-Gfp)3Ew|No|17-Oct-2008|Cryopreserved sperm|60.0|0.0|Unknown||epigenetics, suppressor of variegation, modifier, ENU|Yes| 4185.0||C57BL/6-CD151/Apb||Recessive|Cd151 antigen|Cd151|Nil|PETA-3, SFA-1, Tspan24|MGI:1096360|targeted mutation 1, Leonie K Ashman|Cd151|MGI:3050539|7||||||||||||||||Yes|||||||||||||abnormal cell migration: keratinocyte migration is significantly impaired hematopoietic system: abnormal T cell proliferation, a significant increase in proliferation of activated T cells is seen. Abnormal bone marrow cell number: a slight but significant increase in the number of immature myeloid lineage cells and corresponding decrease in lymphocyte numbers is seen.homeostasis/metabolism: increased bleeding time- a small but significant increase in mean tail bleeding time and a 3 fold increase in the volume of blood lost is seen||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|19-Dec-2008|Cryopreserved sperm|100.0|0.0|Unknown||epithelium, integrin, fibroblast, wound, migration|Yes| 4196.0||NOD.129P2/Ola-Csf2/WehiApb|NOD.129P2/Ola-Csf2/WehiApb|Recessive|colony stimulating factor 2 (granulocyte-macrophage)|Csf2|Nil|Csfgm, Gm-CSf, MGI-IGM|MGI:1339752|targeted mutation 1, Ashley R Dunn|Csf2|MGI:1930997|11||||||||||||||||Yes|||||||||||||These mice may develop diabetes beginning at around 12 weeks of age. When these mice are used for incidence curves, the longest they are kept alive is 300 days.Mice develop pulmonary pathology from 10 weeks onwards. They are more susceptible to lung infections caused by bacterial or fungal organisms.|Phenotype as for wild type NOD/Lt mice- develop type 1 diabetes starting around 12-15 weeks of age|NOD/Lt|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|16|2|sib x sib|No|20-Dec-2008|Cryopreserved sperm|135.0|0.0|Yes||Macrophage, haematopoiesis|Yes| 3392.0|C3H.PRI-Flv; C3H/Rv|C3.PRI-Oas1b/ArcApb|C3.PRI-Oas1b/ArcApb|Dominant|2'-5' oligoadenylate synthetase 1B|Oas1b|Normal|Flavivirus resistance, Flv, L1, Mmu-L1, Oias-2, Oias2, Wnv|MGI:97430|flavivirus resistance|Oas1b|MGI:1857800|5||||||||||||||||No|||||||||||||Decreased susceptibility to viral infection: viral replication was inhibited in mice from resistant strains upon innoculation with the following viruses: Yellow Fever, Dengue Fever, West Nile Fever, Japanese Encephalitis, St. Louis Encephalitis, Russian Spring Summer Encephalities. Flv Phenotpye:- resistance to infections by Flaviviruses. Tlr4 Phenotpye:- Toll 4 receptor is responsive to LPS infection. Diht Phenotpye:- an increased hypothermia response as measured by a drop in core temperature following peripheral administration of a dopamine agonist.|Flv Phenotpye:- dominant phenotype, heterozygotes are resistant to infection. Tlr4 Phenotpye:- dominant phenotype, heterzygotes show responsiveness to LPS. Diht Phenotpye:- dominant and dopamine-induced hypothermia in heterozygotes show the high responder phenotype.|C3.PRI.Oas1b|Yes|Yes|Yes|Yes|Yes|Yes|No|Poor||12|brother x sister|No|11-Jul-2008|Cryopreserved sperm|145.0|0.0|Unknown||dopamine, flavivirus resistance, apomorphine, hypothermia, lipopolysaccharide (LPS)|Yes| 3393.0|C3H.PRI-Hyp|C3.PRI-Diht/ArcApb|C3.PRI-Diht/ArcApb|Recessive|||Normal|||dopamine-induced hypothermia; C3.PRI|Diht|MGI:3586688|5||||||||||||||||No|||||||||||||High dopamine-induced hypothermia characterised in Dihrt/Diht (Diht x Diht) homozygous mice|High dopamine-induced hypothermia characterised in Dihrt/Diht (Diht x Diht) heterozygous mice|C3H/HeJARC|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||8|brother x sister|No|11-Jul-2008|Cryopreserved sperm|150.0|0.0|Unknown||dopamine, flavivirus resistance, apomorphine, hypothermia, lipopolysaccharide (LPS)|Yes| 3395.0|C3H/HeJARC|C3H/HeJArcApb|C3H/HeJArcApb|Recessive|2'-5' oligoadenylate synthetase 1B|Oas1b|Normal|Flavivirus resistance, Flv, L1, Mmu-L1, Oias-2, Oias2, Wnv|MGI:97430|2'-5' oligoadenylate synthetase 1B; flavivirus susceptibility|Oas1b|MGI:2181524|5||||||||||||||||Yes|||||||||||||Flv phenotype:- Susceptible to infections by Flaviviruses. Tlr4 Phenotype:- responsiveness of Toll 4 Receptor to LPS infection. Diht Phenotype:- a decreased hypothermia response as measured by drop in core temperature following the peripheral administration of a dopamine agonist|Flv Phenotype:- recessive phenotype, hets are resistant to infection by Flaviviruses. Tlr4 phenotype:- is dominant and heterozygous mice show responsiveness to LPS.Diht phenotype is recessive and dopamine-induced hypothermia in heterozygotes show the high responder type.|C3H/HeJArc|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||16|brother x sister|No|11-Jul-2008|Cryopreserved sperm|150.0|0.0|Unknown||dopamine, flavivirus resistance, apomorphine, hypothermia, lipopolysaccharide (LPS)|Yes| 3395.0|C3H/HeJARC|C3H/HeJArcApb|C3H/HeJArcApb|Recessive|dopamine-induced hypothermia|Diht|Unknown||MGI:3033372|C3H/HeJArc|Diht|MGI:3586687|5|||||||||||||||||||||||||||||Flv phenotype:- Susceptible to infections by Flaviviruses. Tlr4 Phenotype:- responsiveness of Toll 4 Receptor to LPS infection. Diht Phenotype:- a decreased hypothermia response as measured by drop in core temperature following the peripheral administration of a dopamine agonist|Flv Phenotype:- recessive phenotype, hets are resistant to infection by Flaviviruses. Tlr4 phenotype:- is dominant and heterozygous mice show responsiveness to LPS.Diht phenotype is recessive and dopamine-induced hypothermia in heterozygotes show the high responder type.|C3H/HeJArc|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||16|brother x sister|No|11-Jul-2008|Cryopreserved sperm|||Unknown||dopamine, flavivirus resistance, apomorphine, hypothermia, lipopolysaccharide (LPS)|Yes| 3395.0|C3H/HeJARC|C3H/HeJArcApb|C3H/HeJArcApb|Recessive|toll-like receptor 4|Tlr4||lipopolysaccharide response, Lps, Rasl2-8|MGI:96824|toll-like receptor 4; wild type revertant|Tlr4|MGI:4943781|4||||||||||||||||Yes|||||||||||||Flv phenotype:- Susceptible to infections by Flaviviruses. Tlr4 Phenotype:- responsiveness of Toll 4 Receptor to LPS infection. Diht Phenotype:- a decreased hypothermia response as measured by drop in core temperature following the peripheral administration of a dopamine agonist|Flv Phenotype:- recessive phenotype, hets are resistant to infection by Flaviviruses. Tlr4 phenotype:- is dominant and heterozygous mice show responsiveness to LPS.Diht phenotype is recessive and dopamine-induced hypothermia in heterozygotes show the high responder type.|C3H/HeJArc|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||16|brother x sister|No|11-Jul-2008|Cryopreserved sperm|||Unknown||dopamine, flavivirus resistance, apomorphine, hypothermia, lipopolysaccharide (LPS)|Yes| 5435.0|Funky|B6.Cg-Ndufs4/DrthApb|B6.Cg-Ndufs4/Drth|Recessive|NADH dehydrogenase (ubiquinone) Fe-S protein 4|Ndufs4|Reduced|C1-18k|MGI:1343135|funky|Ndufs4|MGI:4942335|13||||||||||||||||Yes|||||||||||||Homozygous mice initially present with fur loss around postnatal day 14, which regrows in the next hair cycle. They show reduced growth and several behavioural abnormalities that appear from postnatal week five, such as tilting of the head, walking in circles and twisting of the body when suspended by the tail. Due to progressively wobbly gait and general deterioration in physical condition, all homozygous mice have to be euthanased around postnatal week eight in compliance with ethical guidelines.|Appears indistinguishable from Wild-Type|C57BL/6|Yes|Unknown|Yes|Yes|Unknown|Yes|No|Poor|10||het X het|No|15-Feb-2011|Cryopreserved sperm|73.0|0.0|Yes|Mitochondrial Disease; Leigh Syndrome|Mitochondria, Oxidative Phosphorylation, Complex I|Possibly| 4184.0||C57BL/6-CD151/Apb||Recessive|CD151 antigen|Cd151|Normal|PETA-3, SFA-1, Tspan24|MGI:1096360||||7||||||||||||||||Yes|||||||||||||Normal|Normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|19-Dec-2008|Cryopreserved sperm|106.0|0.0|Unknown||tetraspanin, integrin, wound repair, cell migration, angiogenesis|Yes| 4197.0|NOD-Tg(IE-Igrp)44Wehi/J|NOD-Tg(H2-Ea-G6pc2)44Tkay/Apb||Dominant||||||||||||||||||||||||||glucose-6-phosphatase, catalytic, 2. The ∆G6pc2 transgene has a mutation in the dominant epitope of G6pc2 (G6pc2206-214).|1.8-kb fragment encoding nucleotides -1,903 through -39 of the 5' flanking sequence of the MHC Class II gene, H2-Ea (k allele)||||||||||||Type 1 Diabetes with same incidence as NOD/Lt control or littermate control mice. Mice do not develop T cell responses to the beta cell autoantigen G6pc2.|NOD/Lt|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|||Transgene positive males were then backcrossed to NOD/LtJ females.|No|20-Dec-2008|Cryopreserved sperm|140.0|0.0|Yes||Tolerance, Autoimmunity, Autoantigen|Yes| 4444.0|GSTkappa -/-|BALB/c-Gstk1/AnuApb||Recessive|glutathione S-transferase kappa 1|Gstk1|Unknown||MGI:1923513|glutathione S-transferase kappa 1; targeted mutation 1, Philip G Board|Gstk1|MGI:5294676|6||||||||||||||||Yes|||||||||||||Abnormal survival:• male mice exhibit a different shaped survival curve compared with wild-type mice• over 1 year, fewer male mice die of heart pathologies compared with wild-type mice• however, female mice exhibit normal survival curvePremature death:• at 6 months, male mice exhibit increased death due to kidney or urinary tract pathologies compared with wild-type miceIncreased testis weight.Rrenal/urinary system phenotype: • kidney tubules are normalIncreased urine micro albumin level• microalbuminuria at 12 and 26 weeks of age• dexamethasone treatment does not improve albumin to creatinine levels• however, microalbuminuria is the same as in wild-type mice at 45 to 48 weeks of ageUrethritis:• urethra inflammed in mice that die of kidney or urinary tract pathologiesUrinary bladder inflammation:• in mice that die of kidney or urinary tract pathologiesPodocyte foot process effacement:• in male and female mice at 5 to 6 months of ageAbnormal renal glomerulus basement membrane morphology:• at 3 months, glomerular basement membrane changes include laminations, splits, subepithelial protrusions, and lucent areasAbnormal renal glomerulus morphology:• at 3 months, male and female mice develop glomerular nephropathy with glomerular basement membrane changes• dexamethasone treatment does not improve abnormal glomerulus morphologyGlomerulonephritis.Increased kidney weight.Distended urinary bladder:• in mice that die of kidney or urinary tract pathologiesUrinary bladder obstruction:• in mice that die of kidney or urinary tract pathologiesDecreased circulating triglyceride level:• at 25 weeks of age but not in older miceDecreased adiponectin level:• slightlyIncreased urine micro albumin level:• microalbuminuria at 12 and 26 weeks of age• dexamethasone treatment does not improve albumin to creatinine levels• however, microalbuminuria is the same as in wild-type mice at 45 to 48 weeks of age.Decreased spleen red pulp amount:• at 25 weeks of age but not in older miceUrethritis:• urethra inflammed in mice that die of kidney or urinary tract pathologiesUrinary bladder inflammation:• in mice that die of kidney or urinary tract pathologiesCellular phenotype: • mice exhibit little or no oxidative stressIncreased testis weight.||BALB/c|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|||Hom x Hom|No|19-Feb-2009|Cryopreserved sperm|100.0|0.0|Unknown||Mitochondria, antioxidant, enzyme, glomerular nephropathy, kidney|No| 4449.0||C57BL/6-Gpx4/Apb||Dominant|glutathione peroxidase 4|Gpx4|Reduced|mtPHGPx, PHGPx, phospholipid hydroperoxide glutathione peroxidase, snGPx, sperm nuclei glutathione peroxidase|MGI:104767|targeted mutation 1, Tomas A Prolla|Gpx4|MGI:2651590|10||||||||||||||||No|||||||||||||Lethality/Prenatal-PerinatalEmbryonic lethality before somite formation * embryos die around E7.5Embryogenesis*Failure to gastrulate*Abnormal triploblastic development|Normal|C57BL/6|No|No|Yes|No|No|Yes|No|Good||||No|20-Feb-2009|Cryopreserved sperm|100.0|0.0|Unknown||glutathione peroxidase, oxidative stress, lipoperoides|Yes| 4454.0||C57BL/6-Tg(CD2-IL5)5C2Ldt/AnuApb||Dominant||||||||||||||||||||||||||transgene insertion 5C2, Lindsay A Dent|the dominant control region (DCR) of the gene encoding human CD2|High - 49 Copies||||||||||Constitutive expression of the IL5 gene is sufficient to induce lifelong high-level eosinophilia. Northern blot analysis identified 11,5 mRNA in the thymus, Peyer's patches, and subcutaneous (pooled inguinal and axillary) lymph nodes. No IL5 mRNA was detected in liver, heart, brain, or skeletal muscle tissues from transgenics, nor in any tissues from normal littermates. Do not maintain as homozygotes. While this is apparently possible, survival of homozygotes likely to be lower. These mice appeared macroscopically normal apart from splenomegaly. Eosinophils were at least 65- and 265-fold higher in blood from transgenics, relative to normal littermates, and approximately two- or sevenfold more numerous relative to blood from mice infected with the helminth Mesocestoides corti. Much more modest increases in blood neutrophil, lymphocyte, and monocyte numbers were noted in transgenics, relative to normal littermates (less than threefold). Thus IL-5 in vivo is relatively specific for the eosinophil lineage. Large numbers of eosinophils were present in spleen, bone marrow, and peritoneal exudate, and were highest in the line with the greatest transgene copy number. Eosinophilia was also noted in histological sections of transgenic lungs, Peyer's patches, mesenteric lymph nodes, and gut lamina propria but not in other tissues examined. IL-5 was detected in the sera of transgenics at levels comparable to those seen in sera from parasite-infected animals.|Appear normal with peripheral blood eosinophilia and increased numbers of eosinophils in the spleen (with splenomegaly), bone marrow. Heterozygous BALB/c and C57BL/6 IL-5 Tg2 mice are resistant to methylcholanthrene-induced carcinogenesis - see Simson, L, et al., 2007, Regulation of carcinogenesis by IL-5 and CCL11: a potential role for eosinophils in tumor immune surveillance. J. Immunol., 178:4222-4229.|C57BL/6|No|No|Yes|No|No|Yes|No|Unknown|||Transgenic male with wild type female|No|20-Feb-2009|Cryopreserved sperm|50.0|0.0|Unknown||eosinophil, immune surveillance, resistance to helminthic parasites, asthma, allergy|Yes| 4467.0||C57BL/6-H2-K1 H2-D1/AnuApb||Recessive|histocompatibility 2, K1, K region|H2-K1|Nil|H-2K|MGI:95904|targeted mutation 1, Beatrice Perarnau|H2-K1|MGI:1931444|17||||||||||||||||Yes|||||||||||||The double knockout mice are virtually devoid of Class Ia cell surface molecules. 90% reduction in peripheral CD8<+> T cells without Vβ diversity alteration. Double knockout mice survived intracranial infection by lymphocytic choriomeningitis virus.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|10|2|sib x sib|No|22-Feb-2009|Cryopreserved sperm|150.0|0.0|Unknown||T cell, CD8, Presentation, Major histocompatibility complex (MHC), viral infection|Yes| 4467.0||C57BL/6-H2-K1 H2-D1/AnuApb||Recessive|histocompatibility 2, D region locus 1|H2-D1|Unknown|H-2D|MGI:95896|targeted mutation 1, Beatrice Perarnau|H2-D1|MGI:1931445|17|||||||||||||||||||||||||||||The double knockout mice are virtually devoid of Class Ia cell surface molecules. 90% reduction in peripheral CD8<+> T cells without Vβ diversity alteration. Double knockout mice survived intracranial infection by lymphocytic choriomeningitis virus.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|10|2|sib x sib|No|22-Feb-2009|Cryopreserved sperm|||Unknown||T cell, CD8, Presentation, Major histocompatibility complex (MHC), viral infection|Yes| 4596.0|NOD.scid H-2K homozygous|NOD-Prkdc Tg(H2K)1Rms/MarpApb||Dominant|protein kinase, DNA activated, catalytic polypeptide|Prkdc|Unknown|DNA-PK, DNA-PKcs, DNAPDcs, slip, XRCC7|MGI:104779|severe combined immunodeficiency|Prkdc|MGI:1857113|16||||||||||||||||Yes|transgene insertion 1, Robyn M Slattery|MHC Class I|||||||||||Decreased T and B cells.||NOD-Prkdc|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|13-Mar-2009|Cryopreserved sperm|100.0|0.0|Yes|Type I diabetes|MHC, autoimmunity, diabetes, T cell, autoimmune|Yes| 4469.0|FVB/n-Tg(GFAP-hGFP-S56T)|FVB/n-Tg(GFAPGFP)14Mes/AnuApb||Dominant||||||||||||||||||||||||||transgene insertion 14, Albee Messing|astrocyte specific glial fibrillary, glial fibrillary acidic protein (Gfap)|||||||||||Bright fluorescence was observed in the cell bodiesand processes of unfixed or fixed astrocytes, using both whole mount and brain slice preparations, from multiple areas of thecentral nervous system. However, in contrast to GFAP–lacZ transgenics, retinal Muller cells expressed the GFP transgene inresponse to degeneration of neighboring photoreceptors. These data indicate that the 2.2-kb hGFAP promoter contains sufficientregulatory elements to direct expression in Muller cells, and that GFP is a suitable reporter gene for use in living preparationsof the mammalian nervous system.||FVB/N|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|22-Feb-2009|Cryopreserved sperm|130.0|0.0|Unknown||GFP, neuron, photoreceptor, astrocyte|Yes| 5443.0|NODGrzA|NOD.B6-Gzma/LtJApb||Dominant|granzyme A|Gzma|Nil|BLT esterase, Ctla-3, Ctla3, H factor, Hanukah factor, Hf, SE1, serine esterase 1, TSP-1, TSP1|MGI:109266|granzyme A; targeted mutation 1, Markus M Simon|Gzma|MGI:2449926|13||||||||||||||||No|||||||||||||Mice are healthy and develop normally, but develop diabetes at a slightly accelerated rate compared to NOD/Lt mice.|Mice are healthy and develop normally, but will develop diabetes similar to NOD/Lt mice.|NOD/Lt|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|11|5|Sister X Brother|Yes|23-Feb-2011|Cryopreserved sperm|50.0|0.0|No||Cytotoxic T lymphocytes, Granzymes, Type 1 Diabetes, Apoptosis, Pancreatic beta cell|Possibly| 5506.0|Brca1 floxed|B6.Cg-Brca1/Apb||Recessive|breast cancer 1|Brca1|Normal||MGI:104537|breast cancer 1; targeted mutation 2, Chu-Xia Deng|Brca1|MGI:1931238|11||||||||||||||||No|||||||||||||Normal|Normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|12-May-2011|Cryopreserved sperm|50.0|0.0|Unknown||epithelium, mammary, breast|Yes| 5540.0|Circletail|B6.Cg-Scrib/MarpApb||Semi-dominant|scribbled homolog (Drosophila)|Scrib|Reduced|Circletail|MGI:2145950|scribbled homolog (Drosophila); circletail|Scrib|MGI:1889322|15|||||||||||||||||||||||||||||Mice homozygous for this spontaneous mutation develop severe neural tube defects and die at birth. In it's most severe form, the neural tube fails to initiate Closure 1 (craniorachischichisis). Heterozygotes, predominantly males, often exhibit a looping or kinked tail. This strain may used to research neural tube defects. |Heterozygotes, predominantly males, often exhibit a looping or kinked tail. |C57BL/6|No|No|Yes|No|No|Yes|No|Good|||wildtype x heterzygote|No|18-Jul-2011|Cryopreserved sperm|50.0|0.0|No||planar cell polarity, neural tube|No| 4530.0|B6.129-163C Del Neo|B6.129-Ryr1/AnuApb||Recessive|ryanodine receptor 1, skeletal muscle|Ryr1|Unknown|calcium release channel isoform 1, Ryr, skrr|MGI:99659|ryanodine receptor 1, skeletal muscle; targeted mutation 2.1, Paul D Allen|Ryr1|MGI:4887389|7||||||||||||||||Yes|||||||||||||Embryonic lethal, E17-18|Fulminant malignant hyperthermia episodes in R163C heterozygous mice after exposure to 1.25–1.75% halothane or an ambient temperature of 42°C characterized by increased rectal temperature, respiratory rate, and inspiratory effort, with significant blood biochemical changes indicating metabolic acidosis, ending in death and hyperacute rigor mortis; (3) intraperitoneal pretreatment with dantrolene provided 100% protection from the halothane-triggered fulminant malignant hyperthermia episode; (4) significantly increased sensitivity (decreased effective concentration causing 50% of the maximal response) of R163C heterozygous and homozygous myotubes to caffeine, 4-chloro-m-cresol, and K-induced depolarization; (5) R163C heterozygous and homozygous myotubes have a significantly increased resting intracellular Ca2 concentration compared with wild type; (6) R163C heterozygous sarcoplasmic reticulum membranes have a twofold higher affinity (Kd =35.4 nM) for [3H]ryanodine binding compared with wild type (Kd= 80.1 nM) and a diminished inhibitory regulation by Mg2.|C57BL/6|No|No|Yes|No|No|Yes|No|Unknown|4|||No|27-Feb-2009|Cryopreserved sperm|70.0|0.0|Unknown||hyperthermia, muscle, sarcoplasmic reticulum, myotubules|Yes| 4533.0|Drasic -/-|B6.129-Asic3/Apb||Recessive|acid-sensing (proton-gated) ion channel 3|Asic3|Unknown|Accn3, DRASIC|MGI:2159339|acid-sensing (proton-gated) ion channel 3; targeted mutation 1, Michael J Welsh |Asic3|MGI:2429689|5||||||||||||||||Yes|||||||||||||Homozygotes for targeted null mutations exhibit reduced latency to onset of pain responses, increased sensitivity to light touch, but decreased sensitivity to noxious pinch and responses of acid- and noxious heat-sensitive nociceptors. Hyperglasia- at site of injury (carrageenan-induced inflammation), mice showed increased sensitivity to mechanical stimuli, but not to noxious thermal stimulus. Responses to somatosensory stimuli under normal conditions were similar to wild-type littermates||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|27-Feb-2009|Cryopreserved sperm|100.0|0.0|Unknown||cation channel, visceral afferents, mechanosensation, touch sensation|No| 4580.0|Gld:kk|B10.BR-H2 Fasl/JAnuApb||Recessive|Fas ligand (TNF superfamily, member 6)|Fasl|Unknown|APT1LG1, CD178, CD95L, Fas-L, Tnfsf6|MGI:99255|generalized lymphoproliferative disease|Fasl|MGI:1856384|1||||||||||||||||Yes||||histocompatibility-2, MHC|H2||H-2, MHC-II|MGI:95894|histocompatibility-2, MHC; k variant|H2|MGI:3579322|17|homeostasis/metabolismabnormal interleukin level (J:8267)stimulation with concanavalin A does not induce cells to produce Il2immune systemabnormal T cell morphology (J:8267)lymph node cells (T cell origin) are abnormal; cells are Ly-2-/L3T4-/surface Ig-abnormal T cell proliferation (J:8267)cells do not proliferate in response to stimulation with alloantigensabnormal interleukin level (J:8267)stimulation with concanavalin A does not induce cells to produce Il2abnormal T cell physiology (J:8267)cells do not generate CTL in response to stimulation with alloantigens||B10.BR|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|08-Mar-2009|Cryopreserved sperm|100.0|0.0|Unknown||T cell, lymphocyte, splenomegaly , lymphoadenopathy, autoimmunity, antinuclear antibodies|Yes| 4595.0|REKO|C57BL/6-Ren1/Apb||Recessive|renin 1 structural|Ren1|Nil|Ren, Ren-1, Ren-A, Ren1c, Ren1d, Rn-1, Rnr|MGI:97898|targeted mutation 1, Brian J Morris|Ren1|MGI:3699140|1||||||||||||||||No|||||||||||||Abnormal renal tubule morphology; decreased renal glomerular filtration rate; decreased diastolic blood pressure; decreased mean arterial blood pressure; hypotension increased heart rate; increased circulating creatinine level; locomotor activity is 35% lower than in wild-type; chronic in vivo stimulus (low salt/enalapril) leads to blunted renin response |Not determined|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|13-Mar-2009|Cryopreserved sperm|100.0|0.0|Unknown||enhancer, blood pressure, low sodium diet, hypotension|Yes| 4742.0|San Roque:CBA|CBA;B6-Rc3h1/AnuApb|CBA;B6-Rc3h1/AnuApb|Recessive|Ring finger and CCCH-type zinc finger domains 1|Rc3h1|Unknown|roquin|MGI:2685397|sanroque|Rc3h1|MGI:3581675|1||||||||||Unknown to Unknown||||||Yes|||||||||||||Spontaneous autoimmune disease. Systemic lupus erythematosus. Anti-nuclear autoantibodies (ANA), hypergammaglobulinemia, autoimmune nephritis, lymphadenopathy, increased numbers of CD44high activated memory T cells, increased numbers of T follicular helper cells, spontaneous germinal centres, CD28-independent activation of T cells. Increased ICOS mRNA and protein expression on T cells, defect in micro-RNA (mir) inhibition of mRNA stability.|Low penetrance of disease phenotype in Hets|CBA x C57BL/6|Yes|No|Yes|Yes|No|Yes|No|Unknown||7||No|27-Apr-2009|Cryopreserved sperm|5.0|0.0|Yes||Systemic lupus erythematosus (SLE), autoimmunity, T cell, ubiquitin ligase, Wellcome Trust|Yes| 4785.0|Line3|FVB-Tg(HBA1-GFP)3Ew/Apb||Dominant|||Increased||||||Unknown||||||||||||||||No|transgene insertion 3, Emma Whitelaw|α-Globin (-570 to +37) (4.1kb of enhancer)|36 copies||||||||||Fluorescence in erythrocytes can be observed by FACS or fluorescent microscopy. The allele is subject to variegation.|Fluorescence in erythrocytes can be observed by FACS or fluorescent microscopy. The allele is subject to variegation|FVB|Yes|Yes|Yes|Yes|Yes|Yes|No|Poor|||Hom x Hom|No|06-Sep-2009|Cryopreserved sperm|150.0|0.0|No||Metastable epiallele, Transgene silencing, Green fluorescent protein|Yes| 4862.0||C57BL/6-Tg(ICAM2-huCD59)/Apb||Dominant||||||||||||||||||||||||||human CD59 |ICAM2|endothelial cells and neutrophils||||||||||Expression of membrane bound human CD59 on endothelial cells and neutrophils.|Expression of membrane bound human CD59 on endothelial cells and neutrophils.|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|24-Sep-2009|Cryopreserved sperm|70.0|0.0|Unknown||complement, heart, endothelial, ischemia, reperfusion, xenotransplantation|Yes| 4700.0|NOD-Tg(IE-Insll)1Wehi/J (NODPI)|NOD-Tg(H2-Ea-Ins2)1Wehi/WehiApb||Dominant||||||||||||||||||||||||||transgene insertion 1, Walter and Eliza Hall Institute|MHC Class II gene H2-Ea (k allele|spleen and thymus of transgenic NOD/LtWehi mice||||||||||The mononuclear cell infiltration of the islets (insulitis) is almost completely absent, and diabetes is prevented in these transgenic NOD mice. The mononuclear cell infiltration of the salivary glands (sialitis) and immune responses to ovalbumin (OVA) are not altered, indicating that the protective effect of the transgene is specific for islet pathology and not due to general immunosuppression. |Mice do not develop T1D when compared with NOD/Lt control or littermate control mice. Mice do not develop T cell responses to the beta cell autoantigen proinsulin.|NOD|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|07-Apr-2009|Cryopreserved sperm|150.0|0.0|Yes||Autoimmunity, Tolerance, Insulin, Autoantigen|Yes| 4729.0|Louise2|B6;B10.BR-H2 Tg(TLK2mHEL)2Ccg/AnuApb|B6;B10.BR-H2 Tg(TLK2mHEL)2Ccg/AnuApb|Dominant||||||||||||||||||||||||||transgene insertion 2, Christopher C Goodnow|rat thyroglobulin|expression limited to thyroid|histocompatibility-2, MHC|H2||H-2, MHC-II|MGI:95894|histocompatibility-2, MHC; k variant|H2|MGI:3579322|17|Express low levels of membrane bound HEL in thyroid. Low serum levels of HEL detected.||B10.Cg-H2 x C57BL/6JSfdAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|10|7|sib x sib|No|17-Apr-2009|Cryopreserved sperm|150.0|0.0|No||autoimmunity, B cell, tolerance, Hen egg lysozyme (HEL), T cell|Yes| 4756.0|NOD eGFP|STOCK Tg(CAG-EGFP)1Osb/MarpApb||Dominant||||||||||||||||||||||||||transgene insertion 1, Research Institute for Microbial Diseases, Osaka University|chicken beta-actin promoter and CMV intermediate early enhancer|||||||||||Transgenic mice were uniformly green with the exception of hair and red blood cells. The brain, liver, kidney, adrenal gland and testis, lung, muscle, heart, intestine, and adipose tissue, thymus, spleen and testicular cells of all transgenic mouse lines were naturally green when irradiated with excitation light.||NOD x C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|30-Apr-2009|Cryopreserved sperm|135.0|0.0|Unknown||GFP, expression|Yes| 4769.0|C57BL/6J.i-K|C57BL/6-H2-K1/AnuApb||Recessive|histocompatibility 2, K1, K region|H2-K1|Unknown|H2-K1tm1Bpe|MGI:95904|targeted mutation 1, Beatrice Perarnau|H2-K1|MGI:1931444|17||||||||||||||||Yes|||||||||||||increased CD4-positive T cell number: numbers increase in parallel to decrease in CD8+ cells.decreased CD8-positive T cell number: 30-50% reduction of single positive CD8<+> peripheral T cells.Abnormal susceptibility to viral infections||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|10|2|Sib x sib|No|06-May-2009|Cryopreserved sperm|150.0|0.0|No||T cell, CD8, Presentation, Major histocompatibility complex (MHC)|Yes| 4786.0|Blades|C.129-IL5 Eotaxin/AnuApb||Recessive|interleukin 5|Il5|Unknown|Il-5|MGI:96557|targeted mutation 1, Manfred A Kopf|Il5|MGI:1861948|11||||||||||||||||Yes|||||||||||||Unknown||BALB/c|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|10|||No|06-Sep-2009|Cryopreserved sperm|125.0|0.0|Unknown||eosinophil, chemokine, asthma, B cell, infection|Yes| 4786.0|Blades|C.129-IL5 Eotaxin/AnuApb||Recessive|chemokine (C-C motif) ligand 11|Ccl11|Unknown|eotaxin, Scya11|MGI:103576|targeted mutation 1, Marc E Rothenberg|Ccl11|MGI:2384435|11||||||||||Unknown to Unknown|||||||||||||||||||Unknown||BALB/c|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|10|||No|06-Sep-2009|Cryopreserved sperm|||Unknown||eosinophil, chemokine, asthma, B cell, infection|Yes| 5451.0|HOM.NOD.407|NOD.Cg-H2-K Tg(RIP2-Bcl2)407Wehi/LtJApb||Dominant|histocompatibility 2, K region|H2-K|Unknown||MGI:3040519|histocompatibility 2, K region; b haplotype mutation 1|H2-K|MGI:3618114|17|||||||||||||||||human B-cell leukemia/lymphoma 2|rat insulin promoter 2 (RIP)|||||||||||Homozygous NOD.407 mice get non-immune diabetes starting at weaning age. Males remain diabetic but females recover after about 100 days of age. They do not need insulin to remain healthy but should be monitored and killed if unwell|Mice develop type 1 diabetes at the same incidence as NOD/Lt mice|NOD/Lt|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|10|20|Sister X Brother|No|02-Mar-2011|Cryopreserved sperm|50.0|0.0|Yes|Type 1 diabetes|Pancreatic beta cell, Type 1 Diabetes, Apoptosis, Bcl2, cytokines|Possibly| 4878.0|B6.Rag1.KO|C57BL/6-Rag1/ArcStvApb||Recessive|recombination activating gene 1|Rag1|Nil|Rag-1|MGI:97848|targeted mutation 1, Peter Mombaerts|Rag1|MGI:1857241|2||||||||||||||||No|||||||||||||Homozygotes for targeted null mutations exhibit arrested development of T and B cell maturation at the CD4-8- thymocyte or B220+/CD43+pro-B cell stage due to inability to undergo V(D)J recombination.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|28-Sep-2009|Cryopreserved sperm|93.0|0.0|Unknown||T cell, B cell, eosinophil, inflammation, interferon|Yes| 4897.0|B6-Lym1|B6.C-Nfkb2/SviApb||Recessive|nuclear factor of kappa light polypeptide gene enhancer in B-cells 2, p49/p100|Nfkb2|Unknown|NF kappaB2, p52|MGI:1099800|Lym1|Lym1||19|||||||||||||||||||||||||||||Increased circulating lymphocytes.A comprehensive histopathological analysis of these mice, however, revealed an absence of peripheral LN (inguinal, brachial, axillary, cervical) and Peyer’s patches. Mesenteric LN were present, but were reduced in size and cellularity.presence of inflammatory cell infiltrates in the lung and liver.The number of mature recirculating B cells was significantly reduced.Nfkb2 bone marrow was almost completely unresponsive to RANKL with osteoclast formation <0.5% of that seen with wt.Mild osteopetrosis, with significantly increased trabecular bone volume|The ability of Nfkb2 cells to form osteoclasts in response to RANKL stimulation was significantly reduced|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|8|||No|09-Oct-2009|Cryopreserved sperm|70.0|0.0|Unknown||noncanonical, p52, signal transduction, lymph node, osteopetrosis, B cell|Yes| 5454.0|Phc2|C57BL/6-Phc2/WehiApb||Recessive|polyhomeotic-like 2 (Drosophila)|Phc2|Nil|Edr2, Mph2|MGI:1860454|polyhomeotic-like 2 (Drosophila); targeted mutation 1, Haruhiko Koseki|Phc2|MGI:3586989|4|||||||||||||||||||||||||||||Minor skeletal abnormalities. Female infertilityAbnormal axial skeleton morphology: * all homozygotes have at least a few alterations to the axial skeleton characteristic of posterior transformations; however, the skull is similar to wild-type. * an ectopic bone floats between the occipital bones and the first cervical vertebra.Abnormal rib morphology.Increased rib number: ectopic ribs are associated with C7 in 67% of homozygotes.Rib fusion: C7 ectopic ribs are imperfect and fused to the middle part of the first ribs; the rest of the ribs are perfect and directly associated with the cranially shifted sternum.Abnormal sternum morphology: the sternum is shifted cranially.Asymmetric rib-sternum attachment: the 7th rib pair are detached from the sternum and the 13th rib pair are missing or floating.Fusion of atlas and odontoid process: the odontoid process is fused to the first cervical vertebra (C1).Split cervical atlas: the dorsal part of the C1 is often bifurcated.Split cervical axis: the dorsal part of C2 is often bifurcated.Vertebral transformation: the thoracolumbar and lumbosacral boundaries are shifted anteriorly.Thoracic vertebral transformation: a prominent spinous process normally associated with the second thoracic vertebra (T2) is associated with T1 in all homozygotes.Cervical vertebral transformation: in the lateral view C2 resembles C3.Decreased cell proliferation: MEFs grow more slowly and stop dividing earlier.|Normal|C57BL/6|Yes|No|Yes|Yes|Yes|Yes|No|Good|10||Het x WT or Het x Het or Hom male x Het or WT female|No|03-Mar-2011|Cryopreserved sperm|60.0|0.0|Unknown||Polycomb group proteins, polycomb repressive complex 1, Hox, skeleton, Cdkn2a|Yes| 5468.0|gpx1 ko|C57BL/6J-Gpx1/MarpApb||Recessive|glutathione peroxidase 1|Gpx1|Nil|cellular GPx, CGPx, Gpx, GPx-1, GSHPx-1|MGI:104887|glutathione peroxidase 1; targeted mutation 1, Ismail Kola|Gpx1|MGI:2388705|9|||||||||||||||||||||||||||||It is reported that the mice exhibit no overt behavioural, physiological, reproductive or developmental defects. However, these animals have deficient responses to oxidative stress caused by brain injury and by myocardial infarction.|Normal|C57BL/6J|Yes|Yes|Yes|Yes|Yes|Yes|No|Excellent||||No|23-Mar-2011|Cryopreserved sperm|50.0|0.0|Unknown||antioxidant, oxidative stress, ischemia / reperfusion|Yes| 10370.0|CCDC89PM|C57BL/6J-Ccdc89em2MAGEC||Dominant|Coiled-Coil Domain-Containing Protein 89|CCDC89|Unknown||MGI:1917304||||11|ENSMUSG00000044362 ||||||||||||||||||||||||||||Sub-fertile|Normal|C57Bl/6J|Yes|Yes|Yes|Yes|Yes|Yes|Yes|Good||||No|12-Oct-2023|Cryopreserved sperm|90.0|0.0|Unknown|||Possibly| 4901.0|Yaa|C57BL/6-Yaa<+>/JAnuApb||Dominant|accelerated autoimmunity and lymphoproliferation transposition|Yaa|Unknown|Tp(X;Y)1Ekw|MGI:99140|accelerated autoimmunity and lymphoproliferation|Yaa|MGI:1856277|Y||||||||||||||||Yes|||||||||||||Mutant males have accelerated autoimmunity, lymphoproliferation, splenomegaly, hemolytic anemia, hypergammaglobulinemia and glomerulonephritis. The syndrome is strain-dependent, requiring presence of certain autosomal allelic combinations.Males have premature death - half the life span of females.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|09-Oct-2009|Cryopreserved sperm|79.0|0.0|Unknown||Monocytes, T cell, lymphoma, glomerulonephritis, autoantibody, splenomegaly|Yes| 4902.0||BALB/c-Il4/MelbApb||Recessive|interleukin 4|Il4|Unknown|IgG1, Il-4|MGI:96556|targeted mutation 2, Nancy Noben-Trauth|Il4|MGI:1857195|11||||||||||||||||No|||||||||||||decreased IgG:IgG1 response to immunization with the protein antigen OVA is severely impairedabnormal T helper 2 physiology:homozygotes display impaired pulmonary granuloma formation in response to schistosome egg immunizationeosinophil infiltration is impaired in response to schistosome egg immunization||BALB/c|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|09-Oct-2009|Cryopreserved sperm|150.0|0.0|Unknown||infection, inflammation, immunoglobulin, lymphocyte|Yes| 5484.0|MPSIIIA-GFP|B6.Cg-Sgsh Tg(UBC-GFP)30Scha/JApb||Recessive|N-sulfoglucosamine sulfohydrolase (sulfamidase)|Sgsh|Reduced|sulphamidase|MGI:1350341|N-sulfoglucosamine sulfohydrolase (sulfamidase); mucopolysaccharidosis IIIA|Sgsh|MGI:2151181|11||||||||||||||||Yes|transgene insertion 30, Brian Schaefer|Human ubiquitin C|Increased||||||||||The phenotype of the mice has not been fully characterised but is expected to be similar to MPS IIIA mice that do not express the GFP gene (Crawley et al (2006) Brain Research 1104:1-17). Newborn MPS IIIA-GFP mice are no different to their unaffected counterparts. It is not until around 10 weeks of age that we begin to see increased aggression in MPS IIIA-GFP males.|Normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|||Homozygous x homozygous|No|15-Apr-2011|Cryopreserved sperm|50.0|0.0|Yes|Progressive neurodegenerative condition|Sanfilippo, Mucopolysaccharidosis, GFP|Possibly| 7683.0|TG2KI.B6|B6.Cg-Tgm2/Apb|MGI:5521582|Recessive|transglutaminase 2, C polypeptide|Tgm2|Normal|G[a]h, protein-glutamine gamma-glutamyltransferase, TG C, TG2, tissue transglutaminase, tTG, tTGas|MGI:98731|targeted mutation 2.1, Robert M Graham|Tgm2|MGI:5521582|2||||||||||||||||No|||||||||||||Normal|Normal|C57BL/6J|Yes|Yes|Yes|Yes|Yes|Yes|No|Excellent|Maintained on C57BL/6J|N/A|Het x het matings|No|15-May-2014|Cryopreserved sperm|50.0|0.0|Unknown||transgluatminase, Gh, G-protein, cross linking, constitutively-active|Yes| 7682.0|TG2KI.129T2|129.B6(Cg)-Tgm2/Apb|MGI:5521582|Recessive|transglutaminase 2, C polypeptide|Tgm2|Normal|G[a]h, protein-glutamine gamma-glutamyltransferase, TG C, TG2, tissue transglutaminase, tTG, tTGas|MGI:98731|targeted mutation 2.1, Robert M Graham|Tgm2|MGI:5521582|2||||||||||||||||No|||||||||||||Normal|Normal|129T2|Yes|Yes|Yes|Yes|Yes|Yes|No|Excellent|10 generations back-crossed to 129T2/SvImsJ|N/A|Het x het matings|No|15-May-2014|Cryopreserved sperm|50.0|0.0|Unknown||transgluatminase, Gh, G-protein, cross linking, constitutively-active|Yes| 8759.0|ENU46:072:Casp1|C57BL/6NCrlAnu-Casp1/AnuApb||Recessive|caspase 1|Casp1|Unknown|Caspase-1, ICE, Il1bc, interleukin 1 beta-converting enzyme|MGI:96544||||9|||||||||||||||||||||||||||||Unknown||C57BL/6NCrlAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|01-Aug-2019|Cryopreserved sperm|56.0|0.0|Unknown||Caspase|Yes| 4913.0|VASP|C57BL/6-Vasp/Apb||Recessive|vasodilator-stimulated phosphoprotein|Vasp|Nil||MGI:109268|targeted mutation 1, Michael Zimmer|Vasp|MGI:1858032|7|||||||||||||||||||||||||||||Haematopoietic system phenotype:homozygotes show no differences in platelet number in total blood and platelet-rich plasma relative to wild-type littermatesIncreased megakaryocyte cell number:homozygotes display a moderate megakaryocyte hyperplasia in bone marrow and spleenAbnormal platelet activation:upon stimulation of platelet-rich plasma with 0.5 units/ml of thrombin, mutant platelets show a 2-fold increase in surface expression of P-selectin and fibrinogen binding relative to wild-type platelets, indicating enhanced agonist-induced platelet activation.unexpectedly, preincubation with the cAMP-elevating prostaglandin E1 completely abolished thrombin-induced fibrinogen binding and P-selectin expression, as well as platelet aggregation, in both wild-type and homozygous mutant platelets.||C57BL/6`|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|||Hom x Hom, Hom x Het|No|16-Oct-2009|Cryopreserved sperm|90.0|0.0|Unknown||cAMP, kinase, platelet, megakaryocytes, profilin|Yes| 4914.0|EphA1-/- hPLAP|B6;129/Sv-Epha1/Apb|B6;129/Sv-Epha1/Apb|Recessive|Eph receptor A1|Epha1|Nil|5730453L17Rik, Eph, Esk|MGI:107381|targeted mutation 1, Shannon L Duffy|Epha1|MGI:3822370|6||||||||||||||||Yes|internal ribosome entry site - human placental alkaline phosphatase|endogenous EphA1|Restricted to epithelial tissue||||||||||Vaginal inflammation:mice exhibit inflammation of the vaginal mucosa secondary to hydrometrocolpos.Endometrium inflammation:mice exhibit endometrium inflammation secondary to hydrometrocolpos.Dilated uterine horn:mice exhibit dilated, attenuated uterine horns secondary to hydrometrocolposEnlarged uterus:mice exhibit an enlarged uterus due to an accumulation of clear uterine fluid (hydrometrocolpos).Increased uterus weight:Vagina atresia:18% of mice exhibit a failure of vaginal openingdespite normal estrogen receptor expression, beta-estradiol treatment fails to induce precocious vaginal opening in P12 mice unlike in wild-type mice and vaginal opening can not be induced by likewise treating affected adult mice.Hydrometrocolpos:mice exhibit inflammation of the vaginal mucosa and endometrium with dilated, attenuated uterine horns secondary to hydrometrocolposFemale infertility:female mice affected by hydrometrocolpos are sterileKinked tail:up to 80% of mice exhibit a kinky tail due to incorrectly positioned caudal vertebraeDistended abdomen:in some mice due to an enlarged uterusAbnormal response/metabolism to endogenous compounds:treatment with beta-estradiol fails to induce apoptosis in the lower genital tract and precocious vaginal opening unlike in wild-type mice.|Normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|3|5|Homozygous knockout crossed with homozygous knockout or C57BL/6 wildtype|No|16-Oct-2009|Cryopreserved sperm|300.0|0.0|No||Eph, Receptor Tyrosine Kinase, ephrin, epithelium, uterus, tail, hydrometrocolpos|Yes| 4916.0|IL-4ra -/-|BALB/c-IL4ra/AnuApb||Recessive|interleukin 4 receptor, alpha|Il4ra|Unknown|CD124, IL-4 receptor alpha chain, Il4r|MGI:105367|targeted mutation 1, Leonard Shultz|Il4ra|MGI:1861951|7|||||||||||||||||||||||||||||Abnormal microglial cell morphology:microglial cells fail to express the cell marker Ym1 (Chi3l3)Decreased IgE level:lower circulating levels of IgE in normal and bacterial infected miceDecreased IgG1 level:lower circulating levels in normal and bacterial infected miceIncreased IgG2a levelAbnormal T-helper 2 physiology:mice are unable to mount an effective Th2 response to N. brasiliensis bacteria as determined by Th2 cyotkine production by T cellsDecreased interleukin-10 secretion:decrease production by T cells from mice infected with N. brasiliensis bacteriaDecreased interleukin-4 secretion:decrease production of IL-4 by T cells from mice infected with N. brasiliensis bacteriaDecreased interleukin-5 secretion:decrease production of IL-5 by T cells from mice infected with N. brasiliensis bacteria||BALB/c|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|16-Oct-2009|Cryopreserved sperm|100.0|0.0|Unknown||T cell, signal transduction, TH2, infection, IL10, parasite, CD4|Yes| 4921.0|Kinks|NOD.129/Sv-Tg(Csf2rb) Csf2rb Csf2rb Prkdc/Apb||Dominant|colony stimulating factor 2 receptor, beta 1, low-affinity (granulocyte-macrophage)|Csf2rb1|Nil|AIC2B, Bc, beta c, CDw131, common beta chain, Il3r, Il3rb1, Il5rb|MGI:1339759|targeted mutation 1, C Glenn Begley|Csf2rb|MGI:2181245|15||||||||||||||||Yes|colony stimulating factor 2 receptor, beta 1, low-affinity (granulocyte-macrophage)||High||||||||||None detected|Normal|NOD/SCID|Yes|Yes|Yes|Yes|Yes|Yes|No|Excellent|||Matings of 2 transgenic non-sibling mice|Yes|22-Oct-2009|Cryopreserved sperm|110.0|0.0|No||murine beta chain, GM-CSF, receptor, phosphorylation, signal transduction|Yes| 4921.0|Kinks|NOD.129/Sv-Tg(Csf2rb) Csf2rb Csf2rb Prkdc/Apb||Dominant|colony stimulating factor 2 receptor, beta, low-affinity (granulocyte-macrophage)|Csf2rb|Nil|AIC2B, Bc, beta c, CDw131, common beta chain, Csf2rb1, Il3r, Il3rb1, Il5rb|MGI:1339759|targeted mutation 1, Clare L Scott|Csf2rb|MGI:3653883|15|||||||||||||||||||||||||||||None detected|Normal|NOD/SCID|Yes|Yes|Yes|Yes|Yes|Yes|No|Excellent|||Matings of 2 transgenic non-sibling mice|Yes|22-Oct-2009|Cryopreserved sperm|||No||murine beta chain, GM-CSF, receptor, phosphorylation, signal transduction|Yes| 4921.0|Kinks|NOD.129/Sv-Tg(Csf2rb) Csf2rb Csf2rb Prkdc/Apb||Dominant|protein kinase, DNA activated, catalytic polypeptide|Prkdc||DNA-PK, DNA-PKcs, DNAPDcs, slip, XRCC7|MGI:104779|severe combined immunodeficiency|Prkdc|MGI:1857113|16|||||||||||||||||||||||||||||None detected|Normal|NOD/SCID|Yes|Yes|Yes|Yes|Yes|Yes|No|Excellent|||Matings of 2 transgenic non-sibling mice|Yes|22-Oct-2009|Cryopreserved sperm|||No||murine beta chain, GM-CSF, receptor, phosphorylation, signal transduction|Yes| 4940.0|Linie 659|Swiss-Tg(tPA-LacZ)659/MarpApb||Dominant||||||||||||||||||||||||||Beta-galactosidase|9.5kb of human t-PA gene promoter|||||||||||Normal.Expression of LacZ in brain. Very high expression in hippocampus, dentate gyrus and cortex.||Swiss white|Yes|Yes|Yes|Yes|Yes|Yes|No|Excellent|||Tg Het x WT Swiss white|No|04-Dec-2009|Cryopreserved sperm|40.0|0.0|No||tissue type plasminogen activator, brain, hippocampus, medial habenula, dentate gyrus|Yes| 4955.0|BALB/c. IL5 -/-; Lynagh|C.B6-Il5/AnuApb||Recessive|interleukin 5|Il5|Nil|Il-5|MGI:96557|targeted mutation 1, Manfred A Kopf|Il5|MGI:1861948|11||||||||||||||||Yes|||||||||||||Homozygotes for a targeted null mutation exhibit loss of normal airway hyperreactivity resulting from aeroallergen challenge, reduced numbers of CD5+ B cells in the peritoneal cavity at 2 weeks, and some altered responses to schistosomiasis infection. Mice appear normal. They have normal basal levels of eosinophils but in response to parasite infections or aeroallergen challenge, numbers do not increase. Further, resistance to some phases of helminthic infections may be impaired. Decreased airway responsiveness: airways of aeroallergen-challenged knockout mice lose hyperresponsiveness to methacholine.Increased neutrophil cell number: after aerosolized OVA challenge, knockout mice have increased levels of neutrophils in BALF compared to unchallenged animals.Increased lymphocyte cell number: after aerosolized OVA challenge, knockout mice have increased levels of lymphocytes in BALF compared to unchallenged animals but the increase is less pronounced than in wild type mice.Abnormal interferon physiology: in mesenteric lymph nodes in culture, there is a marked increase in IFNG production in knockouts compared to wild type after restimulation with mitogen or SEA.Granulomatous inflammation:* pulmonary granulomas that form in knockout mice in response to schistosome eggs are almost completely devoid of eosinophils compared to granulomas in wild type mice; the average size of granulomas in knockout mice are 40% smaller than those of wild type.* there is a 20-25% increase in numbers of macrophages associated with granulomas in knockouts compared with wild type; with acute or chronic parasite infection, the numbers of both fibroblasts and macrophages nearly double in knockout animals compared to wild type.Liver fibrosis: hepatic fibrosis is significantly reduced in knockouts with acute or chronic helminth parasite infection.Increased eosinophil cell number: knockout mice infected with parasites do not show eosinophil counts above baseline values, while 35-week old controls develop eosinophilia in the blood, bone marrow and peritoneal cavity.||BALB/c|Yes|Yes|Yes|Yes|Yes|Yes|No|Excellent|20||IL5-/- male mated with IL5-/- female|No|14-Dec-2009|Cryopreserved sperm|100.0|0.0|Unknown||infection, T cell, B cell, CD5, eosinophil|Yes| 5042.0|PRlacZ|B6.129S7/SvEvBrd-Pgr/Apb||Recessive|progesterone receptor|Pgr|Unknown|NR3C3, PR, PR-A, PR-B|MGI:97567|progesterone receptor; targeted mutation 1, John P Lydon|Pgr|MGI:3032652|9||||||||||||||||No|||||||||||||Abnormal sexual interaction: females did not exhibit sexual behavior.Abnormal female reproductive system morphology.Abnormal mammary gland development.Absent corpus luteum.Uterus hyperplasia.Abnormal reproductive system physiology.Abnormal ovulation: ovulation could not be stimulated with exogenous hormones.Female infertility.|Normal|129S7/SvEvBrd x C57BL/6|Yes|No|Yes|Yes|Yes|Yes|No|Unknown||||No|22-Feb-2010|Cryopreserved sperm|96.0|0.0|Unknown||Progesterone, mammary, receptor, luminal epithelial, ducts|Yes| 5127.0|Aire KO|B10.Br(Cg)-Aire/AnuApb||Recessive|autoimmune regulator (autoimmune polyendocrinopathy candidiasis ectodermal dystrophy)|Aire|Nil||MGI:1338803|autoimmune regulator (autoimmune polyendocrinopathy candidiasis ectodermal dystrophy); targeted mutation 1, Leena Peltonen|Aire|MGI:2182940|10||||||||||||||||No|||||||||||||Targeted mutations that inactivate the gene result in immune system dysfunction characterized by multiorgan lymphocytic infiltration and circulating autoantibodies.Absent adrenal gland: absence of the adrenal glands is seen with incomplete penetrance; however, the thyroid and pancreas are normal.Abnormal T cell morphology: the TCR-Vbeta repertoire is altered in peripheral T cells.Increased T cell proliferation: immunization with hen egg lysozyme antigen results in a 4-5-fold increase in proliferating response of peripheral T cells, with mutants showing twice as many T cells in the lymph nodes than controls.Thymus atrophy: thymic atrophy is seen in 2 of 14 mutants.Increased autoantibody level: 73% of homozygous mice generated autoantibodies against at least one of the organs (liver, testis, pancreas and adrenal gland) tested and 40% of mice contain autoantibodies against two or more of the organs.Liver inflammation: 50% of mutants exhibit accumulation of lymphocytes in periportal regions.Infertility: 85% of male or female mutants fail to produce any litters.||129 x C57BL/6 x C57BL/10.Br|Yes|No|Yes|Yes|No|Yes|No|Poor||||No|19-May-2010|Cryopreserved sperm|50.0|0.0|Yes|Autoimmune polyendocrinopathy syndrome type 1|autoimmunity, clonal deletion, T cell, tolerance|Yes| 5065.0|Zic5 V504G: C3H/HeH|C3H.C-Zic5/AnuApb||Recessive|Zinc finger protein of the cerebellum 5|Zic5|Unknown|odd-paired related, Opr|MGI:1929518||||14||||||||||||||||Yes|||||||||||||Viable and fertile|Viable and fertile|C3H/HeH|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|10||Homozygote male paired with homozygote female|No|25-Mar-2010|Cryopreserved sperm|40.0|0.0|Unknown||zinc finger, ENU|Yes| 4959.0|K5-crePR1 , K5crePR1 ; K5C|C(Cg)-Tg(KRT5-cre/PGR)1Der/AnuApb||Dominant||||||||||||||||||||||||||transgene insertion 1, Dennis R Roop|bovine keratin 5|||||||||||To activate or inactivate conditional alleles in murine stratified epithelia, a novel system has been developed. It is based on the generation of transgenic mice that express an inducible Cre recombinase under the control of a promoter specific for stratified epithelia. The inducible features of Cre were achieved by fusing Cre to a deletion mutant of the human progesterone receptor (PR), which fails to bind progesterone but can be activated by progesterone antagonists, such as RU486. This fusion protein (CrePR1) is sequestered in the cytoplasm. After activation with RU486, CrePR1 translocates to the nucleus, where it mediates the excision of DNA sequences flanked by LoxP sites. Mice generated express CrePR1 under the control of the K5 which is expressed in the basal cells of stratified epithelia||BALB/c|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|10|||No|12-Jan-2010|Cryopreserved sperm|138.0|0.0|Unknown||RU486, keratin, inducible, receptor|Yes| 4961.0|B6 Stat6-/- N10|B6(Cg)-Stat6/AnuApb||Recessive|signal transducer and activator of transcription 6|Stat6|Nil|stat6-|MGI:103034|signal transducer and activator of transcription 6; targeted mutation 1, Shizuo Akira|Stat6|MGI:2386746|10||||||||||||||||No|||||||||||||Skin inflammation:* mice exhibit mild dermal infiltration of inflammatory cells.* few CD4+ cells infiltrate the perioral dermis and epidermis.Acanthosis: sight.Decreased B cell proliferation:* B cell proliferation in response to anti-IgM plus IL-4 is impaired.* however, B cell proliferation in response to LPS is normal.Decreased T cell proliferation:* thymocyte proliferation in response to TPA is impaired.* however, thymocyte proliferate in response to other stimuli.Decreased IgE level: IgE levels are lower than in wild-type mice following infection with N. brasiliensis.Decreased IgG1 level: IgG1 levels are 16-fold lower than in wild-type mice and following infection with N. brasiliensis they are 10-fold lower than in infected wild-type mice.Increased IgA level: IgA levels are slightly increased following infection with N. brasiliensis.Increased IgG level: IgG2 and IgG3 levels are slightly increased following infection with N. brasiliensis.Abnormal T-helper 2 physiology: mice fail to produce increased levels of Th2 cytokines in response to infection with N. brasiliensis.||C57BL/6 x BALB/c|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|13-Jan-2010|Cryopreserved sperm|100.0|0.0|Unknown||T cell, IL-4, signal transduction, lymphocyte, B cell|Yes| 4970.0|B6.Flii 1.5F|B6;C-Flii/AnuApb|B6;C-Flii/AnuApb|Recessive|flightless I homolog (Drosophila)|Flii|Nil|Fli1, Fliih|MGI:1342286|targeted mutation 1, Hugh D Campbell|Flii|MGI:2179825|11||||||||||||||||Yes|||||||||||||Embryonic lethality at implantation: no embryos are recovered after E5.5; embryos develop normally until cellularization, the development arrests before completion of gastrulation blastocysts initiate uterine implantation but embryos fail to develop. embryonic growth arrest: development arrests during gastrulation|Enhanced wound healing: 3 days after a 1 cm full-thickness incision was made in the dorsal skin, surface wound area measurements show smaller, more contracted wounds than in wild-type mice. Length of neoepidermis is significantly greater in mutant animals, and percentage or re-epithelialization of wounds is greater at 5 days after wounding. By day 7, healing is comparable in mutants and wild-type|C57BL/6|No|No|Yes|No|No|Yes|No|Good|4||Het male x wt female|No|15-Jan-2010|Cryopreserved sperm|40.0|0.0|Yes||cell migration, embryonic lethal, wound repair, gelsolin, gastrulation|Yes| 4966.0|pGL3(-1501bp)CYP27B1 promotor-luciferase reporter|B6;CBA-Tg(Cyp27B1-Luc)/Apb||Dominant||||||||||||||||||||||||||luciferase|1.5kb human CYP27B1|||||||||||Strain not maintained in homozygous state|Luciferase activity are observed in a variety of tissues which is driven by the human 1501 bp CYP27B1 flanking sequence. The level of luciferase activity can vary depending on age and treatment. No other phenotype is observed.|CBA x C57BL/6|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Good|||Het x WT|No|15-Jan-2010|Cryopreserved sperm|100.0|0.0|No||Vitamin D, 25-Hydroxyvitamin D 1-hydroylase|Yes| 5137.0|A7|C57BL/6-Tg(Tcra149.42)Cbn/JWehiApb||Dominant||||||||||||||||||||||||||transgene insertion Tcra149.42, Francis R Carbone|H-2Kb|||||||||||Homozygous mice exhibit an increased incidence of seizures so mice are maintained as heterozygous.|The majority of CD8 T cells express the trangenic Va2 T cell receptor.|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||greater than 30|brother-sister|No|26-May-2010|Cryopreserved sperm|50.0|0.0|No||TCR tansgenic, cytotoxic T lymphocytes, T cell repertoire|Yes| 4987.0|BYAC|B6.SJL-Tg(YACA201F4)/Apb||Dominant||||||||||||||||||||||||||human β-globin locus|β-globin|||||||||||Transgenic human β-globin locus expression was limited to spleen and blood.To establish the pattern of expression of the transgenichuman β-globin locus during development, RNA was analyzedby primer extension. At day 8.5, the first human gene expressed was the foetal γ-globin gene. In day 10.5 yolk sac, the percentage of γ-globin mRNA decreased, while theε-globin mRNA level increased, and this trend continued on day 11.5. At day 12.5, expression of the ε-globin gene hadlargely been switched off. There is an abrupt shift to β-globingene expression that exceeds the level of γ-globin mRNA.Human β-globin expression continued to increase at day 14.5as the dominant globin mRNA. Quantitation by Phosphorlmageranalysis revealed that the ratio of adult mouse toadult human β-globin gene activity per gene copy was 1.35.Thus, the expression level of the single, integrated humanβ-globin locus was comparable to that of the endogenousmurine β-globin locus. The pattern of ε- and β-globin geneactivity followed the expression of the mouse embryonic andadult genes, respectively. However, expression ofthe humanγ-globin gene preceded ε-globin gene expression at day 8.5and persisted throughout the fetal stage. In adult transgenicanimals, low-level human fetal gene expression was occasionally detected. This may be a consequence of theextreme erythroid hyperplasia observed after treatment withphenylhydrazine.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|28-Jan-2010|Cryopreserved sperm|100.0|0.0|No||erythrocyte, red blood cell, globin, YAC, yeast artificial chromosome|Yes| 4990.0|EPO IL5tg1|C.129/Ola-Epx Tg(CD2-IL5)5C2Ldt/AnuApb||Dominant|eosinophil peroxidase|Epx|Nil|EPO|MGI:107569|eosinophil peroxidase; targeted mutation 1, Nancy A Lee|Epx|MGI:2182952|11||||||||||||||||Yes|transgene insertion 5C2, Lindsay A Dent|the dominant control region (DCR) of the gene encoding human CD2|High - 49 Copies||||||||||Constitutive expression of the IL5 gene is sufficient to induce lifelong high-level eosinophilia. Northern blotanalysis identified 11,5 mRNA in the thymus, Peyer's patches, and subcutaneous (pooled inguinal and axillary) lymph nodes. No IL5 mRNA was detected in liver, heart, brain, or skeletal muscle tissues from transgenics, nor in any tissues from normal littermates. Do not maintain as homozygotes. While this is apparently possible, survival of homozygotes likely to be lower.|Appear normal with peripheral blood eosinophilia and increased numbers of eosinophils in the spleen (with splenomegaly), bone marrow. Heterozygous BALB/c and C57BL/6 IL-5 Tg2 mice are resistant to methylcholanthrene-induced carcinogenesis - see Simson, L, et al., 2007, Regulation of carcinogenesis by IL-5 and CCL11: a potential role for eosinophils in tumor immune surveillance. J. Immunol., 178:4222-4229.|BALB/c x 129|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Excellent||||No|28-Jan-2010|Cryopreserved sperm|105.0|0.0|Yes||eosinophil, immune surveillance, resistance to helminthic parasites, asthma, allergy|Yes| 4991.0|Lps2|C57BL/6-Ticam1/BtlrAnuApb|C57BL/6-Ticam1/BtlrAnuApb|Recessive|toll-like receptor adaptor molecule 1|Ticam1||TICAM-1, Trif|MGI:2147032|toll-like receptor adaptor molecule 1; lipopolysaccharide 2|Ticam1|MGI:2679794|17|||||||||||||||||||||||||||||Abnormal cytokine secretion:* cytokine secretion induced by naked polyI:C is severely impaired by 5- to 10-fold.* however, secretion induced by transfected polyI:C is unaffectedDecreased susceptibility to endotoxin shock: though some mice became ill and died after intraperitoneal LPS injection, the survival rate was significantly greater than that of wild-type.Increased susceptibility to viral infection: no production of type I interferons in response to mouse cytomegalovirus (mCMV).||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|28-Jan-2010|Cryopreserved sperm|58.0|0.0|Unknown||ENU, Toll like receptor, LPS, endotoxin, MyD88, cytokine|No| 4899.0||129-Actn3/Apb||Recessive|actinin alpha 3|Actn3|Nil||MGI:99678|targeted mutation 1, Kathryn N North|Actn3|MGI:3760255|19|||||||||||||||||||||||||||||Abnormal skeletal muscle morphology: fast muscle fibers exhibit an increase in mitochondria density compared to wild-type.Abnormal muscle physiology: fast muscle fibers exhibit more staining for two markers of aerobic metabolism (NADH-tetrazolium reductase and succinate dehydroganse) compared to wild-type mice.Fast muscle metabolism is shifted from anaerobic to aerobic as determined by pyruvate metabolism enzyme activity, however, the increase in oxidative enzyme activity does not result in the loss of fast muscle fibers.Increased aerobic running capacity: when run until exhaustion, mice run 33% further than wild-type mice when run until exhaustion.||129|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|09-Oct-2009|Cryopreserved sperm|140.0|0.0|Unknown||Muscle, mitochondria, skeletal, twitch, endurance|Yes| 5157.0|LacZ1 ; Tg(ACTA1-Tnni1(USE)-(nls)lacZ)27BHrd|B6;D2-Tg(ACTA1-lacZ)27BHrd/AusbApb|Hrd|Dominant||||||||||||||||||||||||||Tg(ACTA1-lacZ)27BHrd|Human Skeletal Actin |Skeletal muscle-specific expression of nuclear localised b-galactosidase in differentiated muscle fibres driven by the human -skeletal actin promoter + the upstream enhancer of the rat troponin I slow. Predominant expression in skeletal muscle (soleus>EDL); might have expression in the heart.||||||||||Normal|Normal|C57BL/6J x DB2|Yes|Yes|Yes|Yes|Yes|Yes|No|Excellent|>20||Heterozygote males crossed with C57BL/6J females|No|17-Jun-2010|Cryopreserved sperm|50.0|0.0|Unknown||LacZ reporter gene, Transgenic Mouse, Skeletal Actin, Mouse Skeletal Muscle, Mouse Muscle transplantation|No| 7786.0|Dynll-KO|C57BL/6-Dynll1/StvApb||Dominant|dynein light chain LC8-type 1|Dynll1|Nil|8kDa LC, DLC8, Dnclc1, Pin|MGI:1861457|dynein light chain LC8-type 1; germline knockout 1.2, Jorg Heierhorst|Dynll1||5||||||||||Unknown to Unknown||||||Yes|||||||||||||Embryonic Lethal|Normal|C57BL/6|No|No|Yes|No|No|Yes|No|Excellent||||No|17-Nov-2014|Cryopreserved sperm|50.0|0.0|Unknown||Dynll-1, ASCIZ|Possibly| 5167.0|Idd5A|NOD.B6-Idd5A/ArcApb||Dominant||||||||||||||||||||||||||||||||||||||As per the parental strain (NOD/Lt).Delayed onset of Type 1 diabetes.||NOD/Lt|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|||Hom x Hom|No|29-Jun-2010|Embryo|0.0|0.0|Yes|All of these 4 strains are derived from the Non Obese Diabetes (NOD) model where we have bred a small section of the protective mouse (C57BL/6) into the Idd locus. This generated 4 congenic mouse strains that have enabled us to evaluate the effectiveness of a protective allele in a known Type 1 Diabetic region in the NOD/Lt mouse.||Yes| 5225.0|FvbN Adamts1 null|FVB/N-Adamts1/Apb|FVB/N-Adamts1/Apb|Recessive|a disintegrin-like and metallopeptidse (reprolysin type) with thrombospondin type 1 motif, 1|Adamts1|Nil|ADAM-TS1, ADAMTS, C3-C5, METH1|MGI:109249|targeted mutation 1, Melanie A Pritchard|B6.129-Adamts1|MGI:3574351|16||||||||||||||||No|||||||||||||Female sub-fertility. Reduced nubers of ovulated oocytes and reduced litter size of homozygous nulls compared to heterozygous or wildtype littermates|Unknown|FVB/N|No|No|Yes|Yes|Yes|Yes|No|Good|8|8|het x het OR Het male x WT female OR Het female x WT male|No|01-Oct-2010|Cryopreserved sperm|50.0|0.0|Unknown||fertility, ovulation, angiogenesis, urogenital|Possibly| 10401.0|mPfCSP|C57BL/6J-Gt(ROSA)26Sortm1.1(LPfCSPrev-mCherry)Anu/Ozg||Dominant|Plasmodium falciparum circumsporozoite protein|PfCSP|||||||Unknown|||||||||||||||||||||||||||||ubiquitous Plasmodium falciparum circumsporozoite protein (PfCSP) expression in cellular membrane |ubiquitous Plasmodium falciparum circumsporozoite protein expression in cellular membrane |C57Bl/6J|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|31-Jan-2024|Cryopreserved sperm|40.0|0.0|Unknown|||Possibly| 5066.0|Zic5 V504G: C57BL/6|B6(Cg)-Zic5/AnuApb||Recessive|Zinc finger protein of the cerebellum 5|Zic5|Unknown|odd-paired related, Opr|MGI:1929518||||14||||||||||||||||Yes|||||||||||||Viable and fertile|Viable and fertile|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|5||Homozygote male paired with homozygote female|No|25-Mar-2010|Cryopreserved sperm|50.0|0.0|Unknown||zinc finger, ENU|Yes| 5131.0|Delta 358 ; Tie2DeltaCx40.358|B6;CBA-Tg(Tie2-Gja5)/AnuApb||Dominant|gap junction protein, alpha 5|Gja5|Increased|connexin 40, Cx40, Gja-5|MGI:95716||||Unknown|||||||||||||||||dominant negative of Cx40|Tie2 endothelial specific|||||||||||Unknown|Mild Hypertension|N3 B6|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Good|2|||No|24-May-2010|Cryopreserved sperm|50.0|0.0|Yes|hypertension|connexins, hypertension, gap junctions|Possibly| 5146.0|Aire KO|B6.129-Aire/AnuApb||Recessive|autoimmune regulator (autoimmune polyendocrinopathy candidiasis ectodermal dystrophy)|Aire|Nil||MGI:1338803|autoimmune regulator (autoimmune polyendocrinopathy candidiasis ectodermal dystrophy); targeted mutation 1, Leena Peltonen|Aire|MGI:2182940|10||||||||||||||||No|||||||||||||Targeted mutations that inactivate the gene result in immune system dysfunction characterized by multiorgan lymphocytic infiltration and circulating autoantibodies.Absent adrenal gland: absence of the adrenal glands is seen with incomplete penetrance; however, the thyroid and pancreas are normal.Abnormal T cell morphology: the TCR-Vbeta repertoire is altered in peripheral T cells.Increased T cell proliferation: immunization with hen egg lysozyme antigen results in a 4-5-fold increase in proliferating response of peripheral T cells, with mutants showing twice as many T cells in the lymph nodes than controls.Thymus atrophy: thymic atrophy is seen in 2 of 14 mutants.Increased autoantibody level: 73% of homozygous mice generated autoantibodies against at least one of the organs (liver, testis, pancreas and adrenal gland) tested and 40% of mice contain autoantibodies against two or more of the organs.Liver inflammation: 50% of mutants exhibit accumulation of lymphocytes in periportal regions.Infertility: 85% of male or female mutants fail to produce any litters.||C57BL/6|Yes|No|Yes|Yes|No|Yes|No|Poor||||No|02-Jun-2010|Cryopreserved sperm|50.0|0.0|Yes|Autoimmune polyendocrinopathy syndrome type 1|autoimmunity, clonal deletion, T cell, tolerance|Yes| 5160.0|NODCD19cre|NOD.129-Cd19/MarpApb||Dominant|CD19 antigen|Cd19|Nil||MGI:88319|CD19 antigen; targeted mutation 1, University of Cologne|Cd19|MGI:1931143|7||||||||||Unknown to Unknown|||||||||||||||||||No CD19 expression.Decreased B-1 B cell number: reduced numbers of B1 cells (Cd23-, IgM hi, IgD lo).Abnormal B cell differentiation.Absent spleen germinal center: failure of germinal center formation.Abnormal B cell physiology: impaired B cell response to T cell dependent antigens; mutants exhibit a decreased hapten-specific antibody response by an NP-chicken-gamma-globulin conjugate.Abnormal immunoglobulin level: failure of affinity maturation of serum antibodies.Decreased IgE level.Decreased IgG1 level: absence of high-affinity NP-specific IgG1 antibody following immunization with NP-chicken-gamma-globulin conjugate.Decreased IgM level: reduction in serum IgM.|Mice express Cre recombinase under the control of Cd19 promoter, B cell specific.|NOD|Yes|Yes|Yes|Yes|Yes|Yes|No|Poor|>10|||No|28-Jun-2010|Cryopreserved sperm|50.0|0.0|Unknown||Cd19, B cell, Cre recombinase|Possibly| 5217.0|Ku70 null 129/SvJ|129/SvJ-Xrcc6/AnuApb||Recessive|X-ray repair complementing defective repair in Chinese hamster cells 6|Xrcc6|Nil|G22p1, Ku p70, Ku70|MGI:95606|X-ray repair complementing defective repair in Chinese hamster cells 6; targeted mutation 1, Frederick W Alt|Xrcc6|MGI:2179954|15||||||||||||||||No|||||||||||||Smaller than littermate controls (about 50% reduction in size). Ku70 null male and females are infertile; they also have impaired T cell development with 1% developing thymic or T cell lymphomas by >9 mths.|Normal|129/SvJ|Yes|No|Yes|Yes|No|Yes|Yes|Poor|||Ku70 het to Ku70 het crossings required|No|14-Sep-2010|Cryopreserved sperm|140.0|0.0|Yes||T cell, hepatocyte, hepatocellular carcinoma (HCC), DNA-dependent protein kinase (DNA-PK), repair, T cell, immunoglobulin, V(D)J, lymphocyte|Possibly| 5219.0|Lyn|B6;129S1/Sv-Lyn/LudApb|B6;129S1/Sv-Lyn/LudApb|Dominant|Yamaguchi sarcoma viral (v-yes-1) oncogene homolog|Lyn|Reduced|Hck-2|MGI:96892|Yamaguchi sarcoma viral (v-yes-1) oncogene homolog; targeted mutation 1, Margaret Hibbs|Lyn|MGI:2157016|4||||||||||||||||Yes|||||||||||||The mice carry a gene-targeted gain-of-function mutation in the Lyn tyrosine kinase. The mice display a severe diminution of mature B cells but have increased numbers of B1a B cells. Their B cells display marked down-regulation of surface IgM, Ig-beta, CD19, CD21 and CD22, and they are poorly responsive to B cell receptor cross-linking. With age, the mice develop antibody-mediated autoimmune disease. Due to the dominant nature of the gain-of-function Lyn mutation, Lyn-expressing cells from Lyn mice show hyper-phosphorylation of many signaling proteins.Increased neutrophil cell number: in the spleen and peripheral blood.Decreased spleen weight: unlike Lyn null mice, mice do not develop age-dependent splenomegaly and spleen weight are modestly lower than in wild-type mice.|Lyn<+/up> mice show a reduction in numbers of B cells and Lyn-expressing cells show hyper-phosphorylation of many signaling proteins.|C57BL/6 x 129|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|16-Sep-2010|Cryopreserved sperm|50.0|0.0|Yes||phophatase, signal transduction, myeloid, neutrophil, tyrosine, src family, B cell, lymphocyte|Possibly| 5165.0|WA2|NOD/Lt-Idd11/ArcApb||Dominant||||||||||||||||||||||||||||||||||||||As per background strain.This mouse model appears to get diabetes earlier than the NOD/Lt mouse that is the background of the WA2 strain. Given we have introduced C57BL/6 mouse region into the NOD/Lt we expected to see a protection against T1D in this strain. So we feel this strain is very helpful in understanding the epigenetic effect of Type 1 Diabetes. It appears it is not enough to change the gene locus involved in T1D, but there are other factor affecting the C57BL/6 genes we have introduced. We believe that the same genes in the NOD/Lt strain now behave differently when there is a C57BL/6 stretch of DNA in a small region of Chromosome 4.|As per background strain.|NOD/Lt|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|||Hom x Hom|No|29-Jun-2010|Embryo|0.0|0.0|Yes|Type I Diabetes|Type I Diabetes, acceleration|Yes| 10389.0|Ubf2 KO - Ubtf8/9 fusion|C57BL/6NCrlAnu-Ubtf/ANU||Dominant|upstream binding transcription factor, RNA polymerase I|Ubtf||Tcfubf, UBF, UBF1 |MGI:98512||||11|||||||||||||||||||||||||||||can be runty and pale extremities|Unknown|C57Bl/6N|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Good||||No|07-Dec-2023|Cryopreserved sperm|54.0|0.0|Unknown|||Possibly| 228.0||EYFP||Dominant||||||||||||||||||||||||||Yellow Fluorescent Protein||||||||||||Mice that are homozygous for the transgenic insert are viable, fertile, normal in size and do not display any gross physical or behavioural abnormalities. All tissues from hemizygous animals display fluorescence in all cell types under appropriate lighting conditions. Homozygotes fluoresce with twice the intensity of the hemizygotes. Notable exceptions to this phenotype are erythrocytes and adipocytes in with fluorescence is negligible or absent. Coat colour expected from breeding: albino|||Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|25-Apr-2006||0.0|0.0|Unknown||EYFP|Yes| 5557.0|T16; IL1RA T16OX|B6;CBA-Tg(Il1rn)1Dih/AnuApb||Dominant||||||||||||||||||||||||||transgene insertion 1, David Hirsh|IL1RA promoter|||||||||||Increased circulating interleukin-1 level: serum IL-1 levels are higher following lipopolysaccharide (LPS) endotoxin challenge.Decreased susceptibility to endotoxin shock: less susceptible to lipopolysaccharide (LPS) endotoxin challenge.Increased susceptibility to bacterial infection: more susceptible to experimental Listeria monocytogenes infection.|Abnormal angiogenesis: reduced angiogenesis observed in stromal keratitis caused by herpes simplex virus (HSV) ocular infection, reduced vascular endothelial growth factor (VEGF) and vascular endothelial growth factor receptor 2 (VEGFR-2) levels.Decreased circulating interleukin-6 level: reduced IL-6 levels in response to stromal keratitis caused by herpes simplex virus (HSV) ocular infection.Abnormal circulating serum amyloid protein level: 30% decrease in serum amyloid P levels after subcutaneous turpentine administration.Decreased susceptibility to endotoxin shock: less susceptible to lipopolysaccharide (LPS) endotoxin challenge, hemizygotes exhibit an intermediate phenotype when compared to wild-type and homozygous.Decreased inflammatory response: reduced polymorphonuclear leukocyte infiltration in response to stromal keratitis caused by herpes simplex virus (HSV) ocular infection.Decreased susceptibility to viral infection: severity of stromal keratitis caused by herpes simplex virus (HSV) ocular infection is diminished.Increased susceptibility to bacterial infection: more susceptible to experimental Listeria monocytogenes infection, hemizygotes exhibit an intermediate phenotype when compared to wild-type and homozygous.|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|Unknown|2 since arrival at ANU||No|12-Aug-2011|Cryopreserved sperm|95.0|0.0|Unknown||IL1, infection, interleukin, LPS, endotoxin, infection, cytokine|Possibly| 5562.0|S100-EGFP|B6;D2-Tg(S100B-EGFP)/Apb||Dominant||||||||||||||||||||||||||Enhanced Green Fluorescence Protein|-1669/+3106 sequence of the murine S100B|||||||||||NormalS100B promoter drives expression of eGFP.From embryonic day 13 onward, EGFP expression was targeted to selected neuroepithelial, glial, and neuronal cells, indicating that cell-specific expression of S100B is regulated at the transcriptional level during development. In adult mice, the highest level of EGFP expression was found in ependymocytes; astrocytes; and spinal, medullar, pontine, and deep cerebellar S100B neurons.|Normal|C57BL/6N|Yes|Yes|Yes|Yes|Yes|Yes|No|Poor|||homozygote x homozygote|No|16-Aug-2011|Cryopreserved sperm|60.0|0.0|No||S100B promoter, EGFP reporter mice, nervous system, glial cells, brain|Possibly| 5560.0|Leptin; Ob|B6;129/Sv-Lep/JAnuApb||Semi-dominant|leptin|Lep|Nil||MGI:104663|leptin; obese|Lep|MGI:1856424|6|||||||||||||||||||||||||||||Homozygotes are obese, hyperphagic, have low activity, high metabolic efficiency, impaired thermogenesis, infertility and short lifespan in addition to varying other abnormalities. Strain background affects severity and course of diabetes.|Heterozygotes survive fasting longer than control mice.|C57BL/6 x 129/Sv|Yes|No|Yes|Yes|No|Yes|No|Unknown||||No|12-Aug-2011|Cryopreserved sperm|45.0|0.0|Yes|Morbid obesity|obesity, lipid, adipose|Possibly| 5168.0|Idd5C|NOD.B6-Idd5C/ArcApb||Dominant||||||||||||||||||||||||||||||||||||||As per the parental strain (NOD/Lt).Type I diabetes onset same as NOD/Lt.||NOD/Lt|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|||Hom x Hom|No|29-Jun-2010|Embryo|0.0|0.0|Yes|All of these 4 strains are derived from the Non Obese Diabetes (NOD) model where we have bred a small section of the protective mouse (C57BL/6) into the Idd locus. This generated 4 congenic mouse strains that have enabled us to evaluate the effectiveness of a protective allele in a known Type 1 Diabetic region in the NOD/Lt mouse.||Yes| 5223.0|C57.Lyn up/up|B6.129-Lyn/LudApb||Semi-dominant|Yamaguchi sarcoma viral (v-yes-1) oncogene homolog|Lyn|Reduced|Hck-2|MGI:96892|Yamaguchi sarcoma viral (v-yes-1) oncogene homolog; targeted mutation 1, Margaret Hibbs|Lyn|MGI:2157016|4||||||||||||||||Yes|||||||||||||The mice carry a gene-targeted gain-of-function mutation in the Lyn tyrosine kinase. The mice display a severe diminution of mature B cells but have increased numbers of B1a B cells. Their B cells display marked down-regulation of surface IgM, Ig-beta, CD19, CD21 and CD22, and they are poorly responsive to B cell receptor cross-linking. With age, the mice develop antibody-mediated autoimmune disease. Due to the dominant nature of the gain-of-function Lyn mutation, Lyn-expressing cells from Lyn mice show hyper-phosphorylation of many signaling proteins.Increased neutrophil cell number: in the spleen and peripheral blood.Decreased spleen weight: unlike Lyn null mice, mice do not develop age-dependent splenomegaly and spleen weight are modestly lower than in wild-type mice.|Lyn<+/up> mice show a reduction in numbers of B cells and Lyn-expressing cells show hyper-phosphorylation of many signaling proteins.|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|10||Het female x Hom male|No|30-Sep-2010|Cryopreserved sperm|50.0|0.0|Unknown||B cell, signal transduction, phosphorylation, src family, mlymphocyte|Yes| 5577.0|∆SRI |C.129T2-Atm/QimrApb||Recessive|ataxia telangiectasia mutated homolog (human)|Atm|Reduced|C030026E19RIK|MGI:107202|ataxia telangiectasia mutated homolog (human); targeted mutation 1, Martin F Lavin|Atm|MGI:2181756|9|||||||||||||||||||||||||||||Premature death: 50% mortality by 40 weeks of age Decreased body size: smaller size persists through adulthood Postnatal growth retardation: 20% growth reduction in males and 18% reduction in females from birth to 45 days of age. Increased tumor incidence: mice dying after 40 weeks of age usually have tumors that are not thymic lymphomas Thymic lymphoma: found in all mice dying before 40 weeks, diverse cell types involved, spongy tumors with a high proportion of cells undergoing apoptosis Abnormal immune system cell morphology: occasional increase in thymocyte size. Abnormal T lymphocyte development: lymph node T cells are primarily at early stages of development. Increased double-negative T cell count: occurs at random Abnormal effector T cell morphology/development: randomly observed increases in single positive T cells. Decreased thymocyte number: 10% reduction in thymocytes, 30-50% reduction in thymocytes expressing alpha and beta T cell receptors or CD3. Abnormal immune system organ morphology: enlarged spleen: usually found in mice dying after 40 weeks of age. small spleen: in mice under 40 weeks of age small thymus small lymph nodes Abnormal chromosome morphology: 3 fold increase in radiation induced chromosomal aberrations. Increased cellular sensitivity to ionizing radiation: increased sensitivity of thymocytes and splenocytes to ionizing radiation. Seminiferous tubule degeneration: tubules disrupted Abnormal testis development: poorly developed Abnormal gametogenesis: abnormal oogenesis: disrupted, lack of maturing follicles and oocytes. Abnormal spermatogenesis: disrupted spermatogenesis, degenerating spermatocytes, loss of spermatids Nervous system phenotype: no gross neuronal degeneration at time points between 2 and 16 months of age. Abnormal Purkinje cell morphology: survival of Purkinje cells in culture less than 60% of controls at 4 days and about 40% at 10 day, survival of cultured cells improves if cultured with cerebellar astroglial cells, develop simpler dendritic arboritization with reduced secondary branching, nitroxide free radicals improve survival and arborization Seminiferous tubule degeneration: tubules disrupted|Increased tumor incidence: average age at onset 18.6 months, varying tumor types including dermatoid cysts adenoma: 13% of total leukemia: 5% of total lymphoma:24% of total ovary tumor: 8% of total sarcoma: 32% of total, half of sarcomas are in Mammary glands|BALB/c|Yes|No|Yes|Yes|No|Yes|No|Good|22|14|Hetrezygotes x Heterozygotes|Yes|05-Sep-2011|Cryopreserved sperm|47.0|0.0|Yes|A-T is characterized by immunodeficiency, neurological abnormalities and a |ataxia telangiectasia , T cell , spermatogenesis, thymocyte, lymphoma |Possibly| 6030.0|Robo2Cond|B.129-Robo2/Apb||Recessive|roundabout homolog 2 (Drosophila)|Robo2||2600013A04Rik, 9430089E08Rik, D230004I22Rik, mKIAA1568|MGI:1890110|roundabout homolog 2 (Drosophila); targeted mutation 1, Richard Maas|Robo2|MGI:3759447|16|||||||||||||||||||||||||||||Normal|Normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|13-Sep-2011|Cryopreserved sperm|50.0|0.0|Unknown||slit|Possibly| 6635.0|Cd11c-DTR/EGFP|C.FVB-Tg(Itgax-DTR/EGFP)57Lan/MarpApb||Dominant||||||||||||||||||||||||||transgene insertion 57, Richard A Lang|mouse Itgax promoter (CD11c)|||||||||||Immune system phenotype: conventional T cell, macrophages, B cell, NK cell, and NK T cell numbers are unaffected by treatment with diphtheria toxin.Decreased dendritic cell number: 24 hours after treatment with diphtheria toxin, spleens and livers are depleted of dendritic cells.Decreased circulating interferon-gamma level: following treatment with diphtheria toxin, little IFN-gamma in alpha-GalCer-injected mice and no IFN-gamma in alpha-C-GalCer-injected mice was detected unlike in transgenic mice not treated with diphtheria toxin.Decreased circulating interleukin-12 level: following treatment with diphtheria toxin and stimulation with alpha-GalCer or alpha-C-GalCer, virtually no serum IL-12 was detected unlike in transgenic mice not treated with diphtheria toxin.Abnormal NK cell physiology: following treatment with diphtheria toxin and stimulation with alpha-GalCer, only 2% at 6 hours and 4% at 12 hours post-treatment of liver or spleen NK cells stain positive for IFN-gamma compared to 20% to 23% and 13% to 16%, respectively, of cells from transgenic mice not treated with diphtheria toxin.Decreased interferon-gamma secretion: following treatment with diphtheria toxin and stimulation with alpha-GalCer, only 2% at 6 hours and 4% at 12 hours post-treatment of liver or spleen NK cells stain positive for IFN-gamma compared to 20% to 23% and 13% to 16%, respectively, of cells from transgenic mice not treated with diphtheria toxin.||BALB/c|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|20-Oct-2011|Cryopreserved sperm|50.0|0.0|Unknown||CD11c, dendritic cell, CD8, T cell|Yes| 5229.0|Ripk2tm1Flv|C57BL/6-Ripk2/Apb||Recessive|receptor (TNFRSF)-interacting serine-threonine kinase 2|Ripk2||CARD3, CARDIAK, CCK, D4Bwg0615e, RICK, RIP2|MGI:1891456|receptor (TNFRSF)-interacting serine-threonine kinase 2; targeted mutation 1, Richard A Flavell|Ripk2|MGI:2660793|4||||||||||||||||No|||||||||||||Abnormal macrophage physiology: * bone marrow derived macrophages produce less IL-6 and TNF when cultured in the presence of L. monocytogenes * in macrophages pre-treated with TLR ligands (i.e. "tolerized"), macrophages produce significantly less inflammatory cytokines upon incubation with L. monocytogenes than controls that were LPS pre-treatedDecreased interleukin-6 secretion: * bone marrow derived macrophages secrete half the amount of IL-6 as wild-type controls in response to culturing with L. monocytogenes * IL-6 secretion is 22% that of controls when macrophages are pre-treated with LPS prior to L. monocytogenes incubation * bone marrow derived macrophages fail to produce IL-6 when pre-treated with LPS prior to NOD2 stimulationDecreased tumor necrosis factor secretion: * bone marrow derived macrophages secrete 61% TNF as wild-type controls in response to culturing with L. monocytogenes * IL-6 secretion is about 20% that of controls when macrophages are pre-treated with LPS or LTA prior to L. monocytogenes incubation * bone marrow derived macrophages fail to produce TNF when pre-treated with LPS prior to NOD2 stimulation|Unknown|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|05-Oct-2010|Cryopreserved sperm|50.0|0.0|Unknown||Nod1, adaptive, signal transduction|Yes| 8765.0|F8 KO (72B)|C57BL/6-F8/72BCslApb||Recessive|coagulation factor VIII|F8|Nil|Cf8, Cf-8, Factor VIII, FVIII|MGI:88383||||X||||||||||Unknown to Unknown|||||||||||||||||||Mice are haemophilic as they are deficient in the clotting factor, FVIII.|Mice may be haemophilic.|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|09-Aug-2019|Cryopreserved sperm|50.0|0.0|Unknown|||Yes| 8774.0|F9 human KI, mouse KO (202A)|C57BL/6-F9/202ACslApb||Recessive|coagulation factor IX|F9||Cf9, Cf-9|MGI:88384||||X|||||||||||||||||||||||||||||Mice may exhibit haemophilia B - it is unknown to what degree the human F9 clotting factor compensates.|Mice may exhibit haemophilia B - it is unknown to what degree the human F9 clotting factor compensates.|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|09-Aug-2019|Cryopreserved sperm|50.0|0.0|Unknown||Haemophilia|Yes| 8004.0|Hes7|C57BL/6-Hes7/KagDunwApb||Recessive|hairy and enhancer of split 7 (Drosophila)|Hes7|Unknown|bHLHb37|MGI:2135679|hairy and enhancer of split 7 (Drosophila); targeted mutation 1, Ryoichiro Kageyama|Hes7|MGI:2652222|11|||||||||||||||||||||||||||||Complete neonatal lethality• most died within a few hours of birth, apparently from respiratory failureAbnormal somite developmentAbnormal left-right axis symmetry of the somites:• loss of left-right axis somite symmetryAbnormal dorsal-ventral polarity of the somites:• disrupted anterior-posterior polarity of the somitesAbnormal somite shape:• somites were irregular in both size and shape, and the boundaries between somites were less clearAbnormal somite size:• somites were irregular in both size and shape, and the boundaries between somites were less clearIncomplete somite formation:• abnormal segmentation|Some mice have a vertebral defect|C57BL/6J|No|Unknown|Unknown|No|Unknown|Unknown|No|Good||||No|08-Dec-2015||0.0|0.0|Unknown||Scoliosis, presomitic mesoderm, Somites|Possibly| 7686.0|DBH-GFP|B6.Cg-Tg(DBH-tauGFP)17/RbrcAnu||Dominant||||||||||||||||||||||||||Tg(DBH-tauGFP)17 |human dopamine beta hydroxylase|||||||||||These transgenic mice express a fusion gene of bovine tau protein and GFP under the control of the human DBH promoter in typical noradrenergic and adrenergic cell groups. Line 17 and 36 were generated. The expression level of Tg in each line was following order: 17 > 36 (developer's information). ||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|20|||No|22-May-2014|Cryopreserved sperm|48.0|0.0|Unknown||GFP, T cell|Yes| 7696.0|Spi6 conditional KO clone 1D|C57BL/6J-SerpinB91D/PibMarpApb||Dominant|serine (or cysteine) peptidase inhibitor, clade B, member 9|Serpinb9||ovalbumin, PI-9, Spi6|MGI:106603||||13|||||||||||||||||||||||||||||Normal|Normal|C57BL/6J|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|09-Jun-2014|Cryopreserved sperm|50.0|0.0|Unknown|||Yes| 6767.0|580s/TVA |STOCK Apc Tg(Gpa33-TVA)#Ern/LudApb||Dominant|adenomatosis polyposis coli|Apc|Reduced|CC1, Min|MGI:88039|adenomatosis polyposis coli; targeted mutation 1, Tetsuo Noda|Apc|MGI:1857966|18|||||||||||||||||transgenic insertion 1, Matthias Ernst|glycoprotein A33 (transmembrane)|||||||||||Liver tumours will develop in animals 18 months or older|Liver tumours will develop in animals 18 months or older|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|16-Dec-2011|Cryopreserved sperm|50.0|0.0|Unknown|||Yes| 6873.0|A1A2f|C57BL/6-Acaca Acacb/AusbApb|C57BL/6-Acaca Acacb/Ausb|Dominant|acetyl-Coenzyme A carboxylase alpha|Acaca|Normal|A530025K05Rik, Acac, Acc1, acetyl-CoA carboxylase, LOC327983|MGI:108451|acetyl-Coenzyme A carboxylase alpha; targeted mutation 1, David E James|Acaca|MGI:5618483|11||||||||||Unknown to Unknown|||||||||||||||||||Normal|Normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|17-Apr-2012|Cryopreserved sperm|50.0|0.0|No||ACC1, ACC2, Flox, adipose|Yes| 6873.0|A1A2f|C57BL/6-Acaca Acacb/AusbApb|C57BL/6-Acaca Acacb/Ausb|Dominant|acetyl-Coenzyme A carboxylase beta|Acacb|Normal|Acc2, Accb|MGI:2140940|acetyl-Coenzyme A carboxylase beta; targeted mutation 1.1, David James| Acacb|MGI:4430244|5||||||||||Unknown to Unknown|||||||||||||||||||Normal|Normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|17-Apr-2012|Cryopreserved sperm|||No||ACC1, ACC2, Flox, adipose|Yes| 243.0||B6.129P2-Apoe/Arc||Recessive|apolipoprotein E|Apoe|Nil||MGI:88057|targeted mutation 1, University of North Carolina|Apoe|MGI:1857129|7||||||||||||||||No|||||||||||||premature death (J:73202)35% dead by 18 monthscardiovascular systemincreased heart weight (J:108154)at 13 months, homozygotes show a 23% increase in heart weight relative to wild type mice (186 ? 7.1 vs. 151 ? 2.5 mg)cardiac hypertrophy (J:108154)at 13 months, homozygotes show a 59% increase in heart weight-to-body weight ratio relative to wild type miceabnormal aorta morphology (J:101576)at 24 weeks of age, homozygotes fed a normal diet (but not similarly-fed C57BL/6J control mice) show obvious atherosclerotic lesions in the aortic sinus and ascending aortathe number of atherosclerotic lesions in aortic sinus and ascending aorta is significantly increased in homozygotes fed an atherosclerotic diet vs a normal dietendothelial nitric oxide synthase (eNOS) in mutant aortic wall is distinctly reducedabnormal spiral modiolar artery morphology (J:101576)homozygotes fed an atherosclerotic diet develop atherosclerotic alterations in the spiral modiolar artery (SMA)in contrast, no such changes are detected in the SMA of homozygotes fed a normal dietspiral modiolar artery stenosis (J:101576)lumen stenosis of the spiral modiolar artery in the cochlea is exacerbated by an atherosclerotic diet relative to a normal dietarteriosclerosis (J:108154)homozygotes exhibit a 13% increase in aortic pulse-wave velocity (PWV) relative to wild type mice (428 ? 14.5 cm/s vs 379 ? 10.1 cm/s), indicating increased arterial stiffness and reduced vascular elasticityatherosclerotic lesions (J:73202, J:108154, J:97385, J:101576)advanced atherosclerotic lesions (J:73202)at 13 months, homozygotes display atherosclerotic lesions extending from the carotid arteries, heart, and aorta down to the renal arteries and the iliac bifurcation (J:108154)lesions are most severe in the proximal aorta and at the bifurcation of carotid arteries; the proximal carotid arteries are relatively free of lesions (J:108154)regular exercise does not reduce atherosclerotic lesion formation in homozygotes, as shown by a comparable % oil red-O staining of whole aortas from sedentary and exercised mutant mice (J:97385)at 24 weeks of age, homozygotes fed a normal diet (but not similarly-fed C57BL/6J control mice) show obvious atherosclerotic lesions in the aortic sinus and ascending aorta (J:101576)the number of atherosclerotic lesions in aortic sinus and ascending aorta is significantly increased in homozygotes fed an atherosclerotic diet vs a normal diet (J:101576)plaques in the luminal surface of the aorta are significantly larger in atherosclerotic diet homozygotes than in normal diet homozygotes (J:101576)increased susceptibility to atherosclerosis (J:101576)severity of atherosclerosis is 2-fold and 99-fold higher in atherosclerotic diet homozygotes than in normal diet homozygotes and C57BL/6J control mice, respectivelyvascular stenosis (J:101576)vascular stenosis is significantly increased in homozygotes fed an atherosclerotic diet vs a normal dietabnormal blood flow velocity (J:108154)anesthetized homozygotes show significantly increased transaortic blood velocities relative to wild type mice with peak aortic velocity at 133.4 ? 7.8 cm/s vs 89.2 ? 5.8 cm/s, and mean aortic velocity at 35.9 ? 2.7 vs 22.0 ? 1.6 cm/s, respectivelyin addition, anesthetized homozygotes show significantly increased transmitral blood velocities relative to wild type mice with peak mitral velocities at 92 ? 7.2 cm/s vs 47.2 ? 5.3 cm/s, and mean mitral velocities at 20.6 ? 1.7 vs 11.4 ? 1.3 cm/s, respectivelyno significant differences in heart rate, peak aortic acceleration or ejection time are observed in the conscious or anesthetized state, when normalized to body weighthowever, homozygotes show alterations in aortic arch acceleration suggestive of increased peripheral wave reflectionsincreased cardiac output (J:108154)under anesthesia, homozygotes exhibit elevated flow velocities suggesting elevated cardiac outputabnormal cardiac stroke volume (J:108154)under anesthesia, homozygotes appear to exhibit significantly increased stroke volumedecreased systemic vascular resistance (J:108154)under anesthesia, homozygotes appear to exhibit significantly reduced peripheral vascular resistance and compliance in the presence of normal blood pressuresabnormal blood-brain barrier function (J:69455)impairment of blood-brain barrier (BBB) functionimpairment of blood-nerve barrier (BNB) functiondecreased vasodilation (J:101576)homozygotes fed a normal or atherosclerotic diet show severely impaired endothelium-dependent relaxation to acetylcholine in aortic rings relative to age-matched C57BL/6J control micehomeostasis/metabolismabnormal circulating homocysteine level (J:73202)decreased plasma total homocysteine levelsdecreased circulating glucose level (J:73202)in plasmaabnormal circulating cholesterol level (J:73202)decreased HDL/total cholesterol ratiodecreased HDL/LDL ratioincreased circulating cholesterol level (J:73202, J:97385, J:101576)increasing with age (J:73202)exercise (15 or 60 min/day swim) causes no significant changes in total cholesterol levels among homozygotes or wild type mice relative to sedentary, genotype-matched controls (J:97385)on a normal diet, homozygotes display significantly increased plasma total cholesterol (TC) levels relative to C57BL/6J control mice (J:101576)on an atherosclerotic diet, homozygotes show a further significant increase in plasma TC levels relative to homozygotes on a normal diet (J:101576)increased circulating LDL cholesterol level (J:101576)on a normal diet, homozygotes display significantly increased plasma LDL cholesterol levels relative to C57BL/6J control miceon an atherosclerotic diet, homozygotes show a further significant increase in plasma LDL levels relative to homozygotes on a normal dietincreased circulating VLDL cholesterol level (J:101576)on a normal diet, homozygotes display significantly increased plasma VLDL cholesterol levels relative to C57BL/6J control miceon an atherosclerotic diet, homozygotes show a further significant increase in plasma VLDL cholesterol levels relative to homozygotes on a normal diethyperlipidemia (J:101576)homozygotes develop hyperlipidemia; however, HDL cholesterol levels, body weight and blood glucose remain unchanged relative to C57BL/6J control mice on a normal diet, with no further differences noted on an atheroscletoric dietincreased circulating triglyceride level (J:73202, J:101576)in plasma (J:73202)on a normal diet, homozygotes display significantly increased plasma triglyceride levels relative to C57BL/6J control mice (J:101576)on an atherosclerotic diet, homozygotes show a further significant increase in plasma triglyceride levels relative to homozygotes on a normal diet (J:101576)skin/coat/nailsskin lesions (J:73202)eruptive xanthomas on shoulder and back areas with lipids and extracellular matix as the predominant componentsgrowth/sizedecreased body weight (J:108154)at 13 months, homozygotes show a 22% reduction in body weight relative to wild type mice (34.5 ? 0.9 vs. 44.5 ? 1.1 g)hematopoietic systemdecreased hematocrit (J:108154)at 13 months, awake, unanesthetized homozygotes display slightly but significantly reduced hematocrits ( 11%) relative to wild type mice at 41.7 ? 1.1% vs 46.6 ? 0.4%; in contrast, systolic blood pressures remain unaffected (140 ? 7.6 mmHg vs 136 ? 7.4 mmHg)cellularoxidative stress (J:97385)regular exercise fails to reduce endogenous oxidant load and mitochondrial damage in hypercholesterolemic mutant micein contrast, regular exercise results in reduced mitochondrial damage and oxidant load and increased SOD2 and adenine nucleotide translocator activities in normocholesterolemic control micehearing/vestibular/earabnormal cochlea morphology (J:101576)endothelial nitric oxide synthase (eNOS) in mutant cochlea is distinctly reducedabnormal basilar membrane (J:101576)on an atherosclerotic diet, homozygotes display a sclerosed and atrophic basilar membraneorgan of Corti degeneration (J:101576)at 24 weeks, homozygotes fed a normal diet show significant degeneration of the organ of Corti in the basal turn while the middle turn is relatively normaldegeneration of the organ of Corti is excerbated by an atherosclerotic diet, with complete loss noted in the basal turn in some animalscochlear inner hair cell degeneration (J:101576)at 24 weeks, homozygotes fed a normal diet show almost complete loss of IHCs in the basal turn and some IHC loss in the middle turnIHC loss at the base turn is exacerbated by an atherosclerotic dietcochlear outer hair cell degeneration (J:101576)at 24 weeks, homozygotes fed a normal diet show almost complete loss of OHCs in the basal turn and some OHC loss in the middle turnOHC loss at the base turn is exacerbated by an atherosclerotic dietabnormal stria vascularis (J:101576)on an atherosclerotic diet, homozygotes display a sclerosed and atrophic stria vascularisabnormal tectorial membrane morphology (J:101576)on an atherosclerotic diet, homozygotes display a sclerosed and atrophic tectorial membranedecreased brainstem auditory evoked potential (J:101576)at 10 weeks, homozygotes fed a normal diet display higher ABR thresholds than C57BL/6J control mice at all test frequencies, with more hearing loss noted at 32 kHz; by 24 weeks, further hearing loss is detected at all test stimuli levelshomozygotes fed an atherosclerotic diet show higher ABR thresholds than homozygotes fed a normal dietdeafness (J:101576)homozygotes fed a normal diet display hearing loss esp. at high frequencies as compared with C57BL/6J control micea high positive correlation between ABR thresholds at 16 and 8 kHz, or click and atherosclerotic lesions, and atherosclerotic plaque area of the aorta, and plasma total choelsterol levels is observed in both normal diet and high-fat diet homozygotesnervous systemabnormal blood-brain barrier function (J:69455)impairment of blood-brain barrier (BBB) functionimpairment of blood-nerve barrier (BNB) functioncochlear inner hair cell degeneration (J:101576)at 24 weeks, homozygotes fed a normal diet show almost complete loss of IHCs in the basal turn and some IHC loss in the middle turnIHC loss at the base turn is exacerbated by an atherosclerotic dietcochlear outer hair cell degeneration (J:101576)at 24 weeks, homozygotes fed a normal diet show almost complete loss of OHCs in the basal turn and some OHC loss in the middle turnOHC loss at the base turn is exacerbated by an atherosclerotic dietcochlear ganglion degeneration (J:101576)at 24 weeks, homozygotes fed a normal diet show a reduced number of spiral ganglion cells in the basal turn of the cochlealoss of ganglion cells is excerbated by an atherosclerotic diet||C57BL/6 x 129|Yes|Yes|Yes|Yes|Yes|Yes|No|Poor||||No|25-Apr-2006||0.0|0.0|Unknown||aorta, artery, arteriosclerosis, glucose, cochlear|Yes| 8771.0|F9 human KI, mouse KO (165C) |C57BL/6-F9/165CCslApb||Recessive|coagulation factor IX|F9|Nil|Cf9, Cf-9|MGI:88384||||X|||||||||||||||||||||||||||||Mice may exhibit haemophilia B - it is unknown to what degree the human F9 clotting factor compensates.|Mice may exhibit haemophilia B - it is unknown to what degree the human F9 clotting factor compensates.|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|09-Aug-2019||0.0|0.0|Unknown||Haemophilia|Yes| 7691.0|zDC-DTR|B6(Cg)-Zbtb46/JAusb||Recessive|zinc finger and BTB domain containing 46|Zbtb46||2610019F01Rik, 4933406L05Rik, Btbd4|MGI:1919397|zinc finger and BTB domain containing 46; targeted mutation 1, Michel C Nussenzweig|Zbtb46|MGI:5444842|2||||||||||||||||||||||||||||||Immune system phenotype:Normal:• diphtheria-treated bone marrow chimeras exhibit normal numbers of NK cells and splenic red pulp macrophages• diphtheria toxin-treated chimeras infected with L. monocytogenes exhibit normal numbers of activated monocytes compared with control mice• diphtheria-treated mice exhibit normal numbers of F4/80+ red pulp macrophages, CD169+ marginal zone macrophages and lymph node subscapular sinus macrophagesDecreased dendritic cell number:• absence of classical dendritic cells in diphtheria toxin-treated bone marrow chimeras• partial loss of CD11chiMHCII+ dendritic cells of the small intestine lamina propria of diphtheria toxin-treated bone marrow chimeras• reduced Lin-CD11chi classical dendritic cells in diphtheria-treated T. gondii-infected bone marrow chimeras• however, plasmacytoid cell numbers are normal in diphtheria toxin-treated bone marrow chimerasIncreased monocyte cell number:• small increase in diphtheria toxin-treated bone marrow chimerasincreased neutrophil cell number• diphtheria toxin-treated bone marrow chimeras exhibit increased numbers of splenic Ly6G+ neutrophils compared with controlsabnormal T-helper 1 physiology• reduced IFNgamma+ CD3+CD4+ T cells in diphtheria toxin-treated bone marrow chimeras immunized with either alpha-DEC-205-GAGp24 or alpha-Treml4-GAGp24, or infected with T. gondiiabnormal memory T cell physiology• diphtheria toxin-treated bone marrow chimeras exhibit reduced antitumor memory response compared with control mice that is not as severe as in Tg(Itgax-DTR/EGFP)57Lan hemizygotesAbnormal response to infection:• diphtheria toxin-treated chimeras infected with L. monocytogenes exhibit fewer activated monocytes compared with control mice• mice treated with diphtheria toxin and LPS fail to accumulate CD11c+MHCII+CD14+DEC-205- and CD11c+MHCII+DC-SIGN/CD209+CD14+ cells in the skin lymph nodes unlike control mice• however, diphtheria toxin-treated chimeras infected with L. monocytogenes exhibit normal numbers of activated monocytes compared with control miceIncreased susceptibility to parasitic infection:• diphtheria toxin-treated mice infected with T. gondii exhibit decreased IFNgamma+ CD3+CD4+ T cells and increased parasitic burden compared with controls that is not as severe as in Tg(Itgax-DTR/EGFP)57Lan hemizygotes.|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|22-May-2014||0.0|0.0|Unknown||Dendritic cell, infection, diphtheria toxin, CD11c|Yes| 7028.0|MKB ; Met-Kb|STOCK-Aire Tg(sMt1-H2-K)/ArcApb||Recessive|autoimmune regulator (autoimmune polyendocrinopathy candidiasis ectodermal dystrophy)|Aire|||MGI:1338803|autoimmune regulator (autoimmune polyendocrinopathy candidiasis ectodermal dystrophy); targeted mutation 1, Part Peterson|Aire|MGI:3722595|10|||||||||||||||||mouse H2-K (MHC class I)|Sheep metallothionein promoter|variable and slightly lower than wild type H2-K. Expression can be induced with Zinc||||||||||Normal|Normal|B10.BR|Yes|Yes|Yes|Yes|Yes|Yes|No|Excellent|more than 10|||Yes|25-Jul-2012|Cryopreserved sperm|50.0|0.0|No||tolerance, liver, CD8 T cells, MHC class I, autoimmunity|Possibly| 7033.0|TFF-Cre/PIK3flox|STOCK Pik3ca Tg(Tff1-CreERT2/Tff2-CreERT2)/LudApb||Dominant|phosphatidylinositol 3-kinase, catalytic, alpha polypeptide|Pik3ca|Normal|6330412C24Rik, caPI3K, p110alpha|MGI:1206581|phosphatidylinositol 3-kinase, catalytic, alpha polypeptide; targeted mutation 1.1, Wayne A Phillips|Pik3ca|MGI:5427579|3|||||||||||||||||trefoil1/2|Tff1/Tff2|||||||||||Tumour formation in the stomach after Cre activation by tamoxifen.|Unknown|Mixed|No|Unknown|Yes|No|Unknown|Yes|No|Unknown||||No|30-Jul-2012|Cryopreserved sperm|50.0|0.0|Unknown|||Possibly| 7777.0|ORX/Arch ; Orexin/archaerhodopsin-3|STOCK Tg(HRCT-Arch)#Ahky||Dominant||||||||||||||||||||||||||archaerhodopsin-3|Homo sapiens prepro-orexin (HRCT, hypocretin)|||||||||||Normal|Normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|30-Oct-2014|Cryopreserved sperm|50.0|0.0|Unknown|||Yes| 7778.0|ORX/tTA|B6.Cg-Tg(HCRT-tTA)#Ahky||Dominant||||||||||||||||||||||||||transgene insertion, Akihiro Yamanaka|Homo sapiens prepro-orexin|||||||||||Normal|Normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|30-Oct-2014|Cryopreserved sperm|50.0|0.0|Unknown|||Yes| 298.0||129P1/ReJ-Lama2||Recessive|laminin, alpha 2|Lama2|Unknown|mer, merosin, nmf417|MGI:99912|dystrophia muscularis|Lama2|MGI:1856026|10||||||||||||||||No|||||||||||||This mutation arose spontaneously in the 129/Re inbred strain at The Jackson Laboratory in 1951. Homozygotes are deficient in merosin (J:18187). Partial restoration of the ability to express Lama2 can be achieved by transplantation of a primary muscle cell culture (J:32227). Lama2dy homozygotes are characterized by progressive weakness and paralysis beginning at about 3 1/2 weeks of age. The hindlimbs are affected first, later the axial and forelimb musculature. Death usually occurs before 6 months of age, and the mice are usually sterile (J:13125). Skeletal muscle shows degenerative changes with proliferation of sarcolemmal nuclei, increase in amount of interstitial tissue, and size variation among individual muscle fibers (J:13125). In the dorsal and ventral roots of the peripheral nerves, both spinal and cranial, Schwann cells fail to separate and ensheathe axons so that groups of closely apposed naked axons, normally seen only in early stages, persist into adulthood (J:5331). At birth there is a deficiency of Schwann cells in the spinal roots, but many undifferentiated cells are present which are probably uncommitted Schwann cells that can differentiate when transplanted to a normal environment (J:12727). In the rest of the peripheral nervous system, the basement membrane of Schwann cells is interrupted by gaps (J:5565), the internodal gap in the nodes of Ranvier is lengthened (J:5866, J:6188), and there is delayed onset of myelination with fewer myelinated axons and shorter internode length (J:12730). There is reduced conduction velocity in spinal roots and peripheral nerves (J:5948) and evidence of defective axonal transport in the sciatic nerve (J:5709, J:5906). It is probable that the myelination defects of the peripheral nerves are due to an intrinsic defect in the dystrophic Schwann cells but the evidence from transplantation experiments, chimeras, and cell cultures is somewhat conflicting (J:30709, J:5580, J:5904, J:7618). There is some evidence for defective myelination in the central nervous system also (J:7911). In culture, myogenic cells from homozygous Lama2dy mice develop muscle properties just as well as cells from control mice (J:5909) and there is no peripheral block of neuromuscular transmission (J:5851, J:5922). Muscle of Lama2dy homozygous mice transplanted into normal hosts is indistinguishable from transplanted control muscle by 100 days (J:8221). There is an extensive literature on morphological and biochemical defects in Lama2dy/Lama2dy muscle.||129|Yes|Unknown|Yes|Yes|Unknown|Yes|No|Unknown||||No|03-May-2006||0.0|0.0|Yes||muscular dystrophy, ataxia, degeneration|Yes| 8772.0|F9 human KI, mouse KO (195A)|C57BL/6-F9/195ACslApb||Recessive|coagulation factor IX|F9|Nil|Cf9, Cf-9|MGI:88384||||X|||||||||||||||||||||||||||||Mice may exhibit haemophilia B - it is unknown to what degree the human F9 clotting factor compensates.|Mice may exhibit haemophilia B - it is unknown to what degree the human F9 clotting factor compensates.|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|09-Aug-2019|Cryopreserved sperm|50.0|0.0|Unknown||Haemophilia|Yes| 8773.0|F9 human KI, mouse KO (195B)|C57BL/6-F9/195BCslApb||Recessive|coagulation factor IX|F9|Nil|Cf9, Cf-9|MGI:88384||||X|||||||||||||||||||||||||||||Mice may exhibit haemophilia B - it is unknown to what degree the human F9 clotting factor compensates.|Mice may exhibit haemophilia B - it is unknown to what degree the human F9 clotting factor compensates.|C57BL/6|Yes|Yes|Yes|Yes|Yes|Unknown|No|Unknown||||No|09-Aug-2019|Cryopreserved sperm|40.0|0.0|Unknown||Haemophilia|Yes| 259.0||C57BL/10pd-Kit||Semi-dominant|kit oncogene|Kit|Normal|belly-spot, c-KIT, CD117, Dominant white spotting, Steel Factor Receptor, Tr-kit|MGI:96677|fertile dominant spotting|Kit|MGI:1856261|5||||||||||||||||No|||||||||||||lethality/postnatalpostnatal lethality (J:6187)some loss by 2 weeks of age due to chronic macrocytic anemiapigmentationdiluted coat color (J:6187)typical dilution of pigmented areas not observedirregular coat pigmentation (J:6187)extensive depigmented areas lacking a defined patternhematopoietic systemmacrocytic anemia (J:6187)decreased mast cell number (J:27513)immune systemdecreased mast cell number (J:27513)reproductive systemreproductive system phenotype (J:6187)no abnormal reproducitve system phenotypes detectedskin/coat/nailsdiluted coat color (J:6187)typical dilution of pigmented areas not observedirregular coat pigmentation (J:6187)extensive depigmented areas lacking a defined pattern|KitW-f/Kit+ C3H/HePaspigmentationnon-pigmented tail tip (J:6187)diluted coat color (J:27513)typical dilution of pigmented areas not observed on strain of origin but is noted on C57BL/6 backgroundbelly spot (J:6187)sharply demarcated but variable in size, sometimes reduced to a few hairspresence is background sensitivehead spot (J:6187)sharply demarcated but variable in size, sometimes reduced to a few hairspresence is background sensitivehematopoietic systemmacrocytic anemia (J:6187)limbs/digits/tailnon-pigmented tail tip (J:6187)skin/coat/nailsnon-pigmented tail tip (J:6187)diluted coat color (J:27513)typical dilution of pigmented areas not observed on strain of origin but is noted on C57BL/6 backgroundbelly spot (J:6187)sharply demarcated but variable in size, sometimes reduced to a few hairspresence is background sensitivehead spot (J:6187)sharply demarcated but variable in size, sometimes reduced to a few hairspresence is background sensitive|C57BL/10|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|30-Apr-2006||0.0|0.0|Unknown||c-kit, coat, migration, mast cell, stem cell, white spotting|Yes| 330.0|tx|DL-Atp7b||Recessive|ATPase, Cu++ transporting, beta polypeptide|Atp7b|Unknown|Atp7a, Wilson protein, WND|MGI:103297|toxic milk|Atp7b|MGI:1856220|8||||||||||||||||Yes|||||||||||||Postnatal lethality:mice die at about 14 days of ageseverity of defects depends on genetic background (less severe on a mixes C57BL/6 background) and maternal age (decreasing severity with increasing maternal age)however, fostering with wild-type dams reverses many defects depending on the age of onset of fosteringReduced female fertility:older female mice exhibit decreased fertility compared to wild-type miceAbnormal mineral level: mice exhibit an increase in zinc the brain, liver and muscle.Abnormal copper level: mice exhibit an increase copper accumulation in the kidney, spleen, brain, muscle, serum and red blood cells.Decreased circulating copper level.Decreased liver copper level: in postnatal miceIncreased liver copper level: in adult mice.Liver cirrhosis.Tremors and ataxia.Decreased body weight: mice reach their maximal weight at day 9 (70% of wild-type) and exhibit weight loss until their death.Postnatal growth retardation: apparent within a day or two after birth.However, fostering with wild-type dams reverses many defects depending on the age of onset of fostering.Diluted coat colour and hypopigmentation.Curly whiskers and disheveled coat.||DL|Yes|No|Yes|Yes|No|Yes|No|Unknown||||No|05-May-2006||0.0|0.0|Yes|Wilson's disease|Wilson disease, milk, copper, transporter, ATPase|Yes| 1503.0|B6.IL-12-/-|B6.129-IL12b/AnuApb||Recessive|interleukin 12b|Il12b|Unknown|IL-12 p40, Il-12b, Il-12p40, IL-23 subunit p40|MGI:96540|interleukin 12b; targeted mutation 1, Jeanne Magram|Il12b|MGI:1857201|11||||||||||||||||Yes|||||||||||||Decreased circulating interferon-gamma level:* serum levels of IFNG in LPS-injected mice are only 17 +/- 5% of LPS-induced controls.Abnormal macrophage physiology:* fewer than expected macrophages in the dermis of carcinogen treated skin.Abnormal granulocyte physiology:* fewer than expected granulocytes in the dermis of carcinogen treated skin.Abnormal lymphocyte physiology:* lymph node cells from keyhole limpet hemocyanin (KLH) immunized mice are severely impaired in their ability to produce IFNG when cultured with KLH; however, their production of IL4 is increased.Abnormal NK cell physiology:* mean NK lytic activity is about 66% of controls; however when cultured with IL2 lytic activity is similar to controls.Abnormal CD8-positive T cell physiology:* dramatic increase in the number of cytotoxic CD8+ cells in the dermis and epidermis of carcinogen treated skin.Decreased interleukin-17 secretion:* barely detectable levels of IL17 in the skin after carcinogen treatment unlike wild-type mice which express high levels of IL17.Increased susceptibility to bacterial infection:* vaccination does not produce a protective response to M. tuberculosis.Decreased susceptibility to type IV hypersensitivity reaction:* specific foot pad swelling 48 hours after challenge with methylated bovine serum albumin is inhibited by 47 +/- 3% compared to wild-type mice; however, cytotoxic T lymphocyte responses are similar to wild-type.Decreased incidence of chemically-induced tumors:* resistant to induction of papillomas compared to wild-type mice after treatment with DMBA and TPA in a 2 step skin carcinogenesis protocol.* however, there is an increase in the incidence of tumors following intradermal challenge with PDV squamous carcinoma cells.Abnormal CD4-positive T cell physiology:* 75 days after infection Ifng mRNA expression in CD4+ cells is more than 50-fold lower than in wild-type.* 75 days after infection Il4 mRNA expression in CD4+ cells is 100-fold higher than in wild-type.* draining lymph node cells in L. major infected mice produce significantly more IL4 compared to IFNG in contrast to wild-type mice which express more IFNG than IL4.||C57BL/6 x 129S1|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|04-Jul-2007|Cryopreserved sperm|150.0|0.0|Unknown||delayed type hypersensitivity, T cell, Natural killer cell ; NK cell, interferon, granulocyte|Yes| 822.0|CD40L KO|B6.129-Cd40lg||Semi-dominant|CD40 ligand|Cd40lg|Nil|CD154, Cd40L, gp39, HIGM1, IMD3, Ly-62, T-BAM, Tnfsf5|MGI:88337|targeted mutation 1, Immunex|Cd40lg|MGI:1857145|X||||||||||||||||Yes||||||||||||||Immune system phenotype:* serum IgM and IgG3 levels are more or less normal at all ages.Abnormal immune system organ morphology.Absent spleen germinal center:* failure to form germinal centers.Abnormal lymph node morphology.Lymph node hypoplasia:* about 1/3 that of controls while overall T and B cell numbers are normal.Absent lymph node germinal center:* failure to form germinal centers in inguinal lymph nodes although primary follicle formation is normal.Abnormal immune system physiology.Abnormal class switch recombination.Decreased immunoglobulin level.Decreased IgA level.Decreased IgE level: undetectableDecreased IgG1 level.Decreased IgG2b level.Abnormal antigen presentation:* unable to mount a secondary response to TNP-KLH antigen (T cell dependent).* T cell independent responses are normal as is isotype switching for these antigens.|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|21-May-2007||0.0|0.0|Unknown||T cell, CD8, CD4, Thymus, thymocyte|Yes| 1363.0|IL2 KO|B6.129-IL2/Wehi||Recessive|interleukin 2|Il2|Nil|IL-2|MGI:96548|targeted mutation 1, Ivan Horak|Il2|MGI:1857191|3||||||||||||||||No|||||||||||||Homozygous null mutants develop adult onset autoimmune disease, with 50% mortality by 9 weeks due to hemolytic anemia. Survivors develop inflammatory bowl disease/colitis. Immune system dysregulation and CD4+ T-cell overproduction may be responsible. Impaired CD4 T cell function and reduced natural killer cell activity.Immune system phenotype:* bone marrow chimeras (mutant bone marrow in Rag2-deficient hosts) do not develop a wasting autoimmune disease compared to the lethal disease that develops with Il2ratm1Dw bone marrow chimeras.Increased T cell number.Increased CD4-positive T cell number:* activated T cell numbers fail to decrease to normal levels after immunization with staphylococcal enterotoxin, indicating a problem with peripheral deletion.* Increased CD8-positive T cell number:* activated T cell numbers decrease with slower kinetics than wild-type mice after after immunization with staphylococcal enterotoxin.Increased activated T cell number:* higher numbers due to less sensitivity to Fas-mediated cell death (apoptosis).Increased T cell proliferation:* T cells continue to respond to antigen instead of going into anergy during secondary stimulation with antigens.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|22-Jun-2007||0.0|0.0|Unknown||T cell, lymphocyte, autoimmunity, CD4, inflammatory bowel disease|Yes| 1364.0|ICOSΔ|C57BL/6-Icos/Ausb||Recessive|inducible T-cell co-stimulator|Icos|Nil||MGI:1858745|inducible T-cell co-stimulator; targeted mutation 1, Tak Mak|Icos|MGI:2445839|1||||||||||||||||No|||||||||||||Mice homozygous for disruptions in this gene show reduced basal IgG1 levels and impaired interactions between T and B cells. T cell dependent B cell isotype switching was impaired as well. Size and mean number of germinal centers severely reduced. Fewer T cells producing IL4IFN-gamma production unaffected.Abnormal spleen morphology.Decreased spleen germinal center number: the mean number of germinal centers is severely reduced.Decreased spleen germinal center size:* the size of the germinal centers is severely reducedAbnormal immune system physiology: interactions between T and B cells were impaired.Abnormal B cell physiology:* B cell proliferation normal.* no impairment in T-cell independent response and B cell development was normal.Abnormal class switch recombination:* B cell isotype switching was impaired in both primary and secondary T-cell dependent B cell response.Decreased IgE level: after stimulation with T-cell dependent antigen.Decreased IgG1 level: IgG1 only immunoglobulin significantly reduced in amount.Abnormal T cell physiology:* fewer T cells producing IL4* IFN-gamma production unaffectedDecreased T cell proliferation:* impaired early stage T-cell proliferation to some stimuli, however, T cell development was unaffected.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|22-Jun-2007||0.0|0.0|Unknown||T cell, B cell, germinal centre, immunoglobulin, proliferation|Yes| 8777.0||ASD937:Pomegranate:87||Recessive|blicr ||||||||Unknown|||||||||||||||||||||||||||||unknown|unknown|C57BL/6NCrlAnu|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|12-Aug-2019|Cryopreserved sperm|11.0|0.0|Unknown|||Yes| 1729.0|Grid2 Lc|B6.CBA-Grid2/Wehi||Semi-dominant|glutamate receptor, ionotropic, delta 2|Grid2|Unknown|B230104L07Rik, GluRdelta2, tpr|MGI:95813|lurcher|Grid2|MGI:1857337|6||||||||||||||||No|||||||||||||Neonatal lethality: mice are dead or dying within the first 12 hours after birth.Abnormal hindbrain morphology:* there is a general loss of neurons between E15.5 and birthAbnormal cerebellum development: conspicuous absence of Purkinje cells.Abnormal trigeminal motor nucleus morphology:* there is a conspicuous absence of large neurons* beginning at E15.5 large numbers of pyknotic cells are evident and an obvious increase in the number of pyknotic neurons in E16.5 mice is evident.* results in loss of muscle control required for suckling* abnormalities occur after its formation.|Reduced linear vestibular evoked potential:* elevated threshold and reduced amplitudesAtaxia: due to progressive loss of Purkinje cellsPurkinje cell degeneration: occurs within the first three weeks of life.|C57BL/6 x CBA|No|No|Yes|No|No|Yes|No|Unknown||||No|01-Aug-2007||0.0|0.0|Unknown||Purkinje, degeneration, ataxia, neuron, muscle|Yes| 1749.0||B6.129-Il2rg/Wehi||X-linked|interleukin 2 receptor, gamma chain|Il2rg|Nil|[g]c, CD132, common cytokine receptor gamma chain, common gamma chain, gamma C receptor, gamma(c)|MGI:96551|targeted mutation 1, Warren J Leonard|Il2rg|MGI:1857455|X||||||||||||||||No|||||||||||||Mice homozygous for the Il2rg targeted mutation are viable and fertile. Mutant mice have hypoplastic thymuses with a 10-fold reduction in the absolute number of lymphocytes. They have a limited number of mature splenic B and T cells, lack NK cells and Peyer's patches, and development of gut-associated intraepithelial lymphocytes is diminished. In vitro studies show defects in NK activity, IL4-directed Ig class switching of thymocytes, and thymocyte mitogenic responses. Decreased myeloid dendritic cell number: the proportion and absolute number of CD11c+ dendritic cells is decreased in the spleen.Abnormal splenic cell ratio:* reduced numbers of splenocytes* decrease in the proportion and absolute number of CD11c+ dendritic cells in the spleen.Abnormal dendritic cell physiology:* in culture, dendritic cells are resistant to cytokine withdrawal-induced apoptosis.* bone marrow-derived dendritic cells overproduce IL12 and IL10.||C57BL/6 x 129|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|02-Aug-2007||0.0|0.0|Unknown||interleukin, common chain receptor, T cell, Lymphocyte, NK cell|Yes| 1778.0|Bax Knockout|C57BL/6-Bax/Wehi||Recessive|Bcl2-associated X protein|Bax|Nil||MGI:99702|BCL2-associated X protein; targeted mutation 1, Stanley J Korsmeyer|Bax|MGI:1857429|7||||||||||||||||Yes|||||||||||||Mice homozygous for the Bax mutation are viable but display lineage-specific aberrations in cell death. Thymocytes and B cells from homozygous mutant mice display hyperplasia. Ovaries contain unusual atretic follicles with excess granulosa cells while Bax-deficient males are infertile. There is an accumulation of atypical premeiotic germ cells and no mature haploid sperm found in seminiferous tubules. Multinucleated giant cells and dysplastic cells accompany massive cell death.Grey fur.||C57BL/6|Yes|Yes|Yes|Yes|No|Yes|Yes|Unknown|8|||No|03-Aug-2007||0.0|0.0|Unknown||Spermatogenesis, Follicles, Thymocyte, Germ cell, Bcl-2, T cell, hyperplasia, B cell|Yes| 1813.0|Ghrhr Knockout|Un-Ghrhr/Wehi||Recessive|growth hormone releasing hormone receptor|Ghrhr|Nil|Ghrfr|MGI:95710|little|Ghrhr|MGI:1856425|6||||||||||||||||Yes|||||||||||||Homozygotes for a spontaneous null mutation exhibit reduced growth from 2 weeks of age, impaired growth hormone synthesis and release, obesity, decreased bone mass, reduced fertility in males, impaired first lactations, and extended life span.|||Yes|Yes|Yes|Yes|Yes|Yes|Yes|Unknown||||No|06-Aug-2007||0.0|0.0|Unknown||Growth Hormone, Dwarf, Pituitary gland, Adipose, Prolactin|Yes| 1845.0||B6.129P2(B6)-IL10/Wehi||Recessive|interleukin 10|Il10|Nil|cytokine synthesis inhibitory factor, IL-10|MGI:96537|interleukin 10; targeted mutation 1, University of Cologne|Il10|MGI:1857199|1||||||||||||||||Yes|||||||||||||Homozygotes for a targeted null mutation exhibit retarded growth, anemia, chronic enterocolitis, a high incidence of colorectal adenocarcinomas, and altered responses to various infectious organisms such as Mycobacterium bovis and Leishmania donovani. Intestinal problems are far less severe (local inflammation of the proximal colon) in a pathogen-free environment. Lymphoctye development and antibody responses are normal in homozygous mutant mice. For a more detailed description please refer to the JAX Notes Fall 1997 article. Homozygotes may be small, possibly anemic and may develop inflammatory bowel disease. ||C57BL/6 x 129|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|10-Aug-2007||0.0|0.0|Unknown||T cell, Macrophage, Enterocolitis, Growth retardation, Mucosal hyperplasia|Yes| 7825.0|MICki|C57BL/6-Gdf15/Ausb||Recessive|growth differentiation factor 15|Gdf15||macrophage inhibiting cytokine-1, MIC-1, NAG-1|MGI:1346047||||8|||||||||||||||||||||||||||||Normal||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|04-Jan-2015||0.0|0.0|Unknown|||Yes| 1847.0||B6By.Cg-Sd Mcoln3 Krt25/JWehi||Semi-dominant|mucolipin 3|Mcoln3|Unknown|6720490O21Rik, TRPML3, Va, varitint-waddler|MGI:1890500|mucolipin 3; varitint waddler Jackson|Mcoln3|MGI:1856231|3||||||||||||||||Yes|||||||||||||Homozygotes are white with small patches of color and show severe behavioral abnormalities, poor postnatal viability and are nearly infertile.|Heterozygotes show normal/diluted/white hair patches, circling, hyperactivity, deafness, and reduced fertility.||Yes|No|Yes|Yes|No|Yes|Yes|Unknown||||No|10-Aug-2007||0.0|0.0|Unknown||Behaviour, pigmenatation, body size, circling, deaf, coat|Yes| 1847.0||B6By.Cg-Sd Mcoln3 Krt25/JWehi||Semi-dominant|keratin 25|Krt25|Normal|mIRSa1|MGI:1918060|keratin 25; rex|Krt25|MGI:1856137|11|||||||||||||||||||||||||||||Homozygotes are white with small patches of color and show severe behavioral abnormalities, poor postnatal viability and are nearly infertile.|Heterozygotes show normal/diluted/white hair patches, circling, hyperactivity, deafness, and reduced fertility.||Yes|No|Yes|Yes|No|Yes|Yes|Unknown||||No|10-Aug-2007||||Unknown||Behaviour, pigmenatation, body size, circling, deaf, coat|Yes| 1847.0||B6By.Cg-Sd Mcoln3 Krt25/JWehi||Semi-dominant|Danforth's short tail|Sd|Unknown||MGI:98265|Danforth's short tail|Sd|MGI:1857746|2|||||||||||||||||||||||||||||Homozygotes are white with small patches of color and show severe behavioral abnormalities, poor postnatal viability and are nearly infertile.|Heterozygotes show normal/diluted/white hair patches, circling, hyperactivity, deafness, and reduced fertility.||Yes|No|Yes|Yes|No|Yes|Yes|Unknown||||No|10-Aug-2007||||Unknown||Behaviour, pigmenatation, body size, circling, deaf, coat|Yes| 1928.0|Kit-W|C57BL/6J-Kit/HNihrJaeBsmJAnuApb||Recessive|kit oncogene|Kit|Nil|belly-spot, c-KIT, CD117, Dominant white spotting, Steel Factor Receptor, Tr-kit|MGI:96677|kit oncogene; sash|Kit|MGI:1856265|5||||||||||||||||Yes|||||||||||||Abnormal coat/hair pigmentation: the coat is white except for small patches on or near the ears and, infrequently, at the base of the tail.Absent coat pigmentation: classic black eyes and white coat.Abnormal hematopoiesis.Abnormal erythrocyte cell number.Decreased erythrocyte cell number: on this background,lower than normal mean hematocrit values were found but did not manifest as an anemia.Decreased mast cell number: mice are described as being mast cell deficient.|Variable body spotting: appears as a distinctive broad white sash|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|10|||No|23-Aug-2007|Cryopreserved sperm|105.0|0.0|Unknown||tyrosine kinase receptor, melanocyte, proto-oncogene, pigmentation, mast cell|Yes| 1931.0||B6.129S4-C3/JAnuApb|B6.129S4-C3/JAnuApb|Recessive|complement component 3|C3|Nil|acylation stimulating protein, complement factor 3, Plp|MGI:88227|complement component 3; targeted mutation 1, Michael C Carroll|C3|MGI:1861799|17||||||||||||||||No|||||||||||||Immuno-compromised. Mice homozygous for the C3 (complement component C3) targeted mutation are viable and fertile. Homozygous mutants exhibit an increased susceptibility to lethal infection by Group B streptococci. Reductions in peritoneal mast cell degranulation, production of tumor necrosis factor alpha, neutrophil infiltration and bacterial clearance have also been reported in these mice. Homozygotes also demonstrate a profound defect in antibody response to T cell dependent antigens. They show a diminished level of peanut agglutin+ germinal centers and a failure in isotype switching despite normal B cell signalling in vitro. ||C57BL/6 x 129|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|23-Aug-2007|Cryopreserved sperm|184.0|0.0|Unknown||Neutrophil, Mast cell, Bacterial infection, complement, T cell|Yes| 1956.0|available from Animal Resources Centre - www.arc.wa.gov.au|129X1/SvJ||Dominant||||||||||||||||||||||||||||||||||||||Inbred albino. Most other substrains carry the white-bellied agouti gene AW though only a subset have the agouti pattern as many carry albino or chinchilla and/or the pink-eyed dilution gene, p, which is derived from Asian mice of the Mus musculus type (see also strains SJL, P/J and FS/Ei).|||Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|04-Sep-2007||0.0|0.0|No|||Yes| 3545.0||C57BL/6.Cg-Kitl Krt71/JWehi||Semi-dominant|kit ligand|Kitl|Unknown|b, grizzle-belly, Mgf, SF, Sl, SLF, Steel, Steel factor, stem cell factor|MGI:96974|kit ligand; steel |Kitl|MGI:1856161|10||||||||||||||||Yes|||||||||||||The severity of the phenotypic effects of the steel alleles is correlated with the degree of alteration in the gene. The multiple steel mutations (KitlSl) behave in a semidominant fashion and cause deficiencies in pigment cells, germ cells, and blood cells paralleling those caused by the Kit locus mutations (dominant spotting alleles). Most of the alleles at steel locus cause severe anemia in utero and death by 15 to 16 days of gestation in homozygous mutant mice. However, compounds of two steel mutants (e.g. KitlSl/KitlSl-d are viable, black-eyed white, are usually sterile in one or both sexes, and have severe macrocytic anemia. Primordial germ cells are absent in the nonviable steel homozygotes and severely reduced in steel heterozygotes. Mast cells are virtually absent in skin and other tissues of steel mutant mice. Tumors tend to develop in germ-cell-deficient ovaries with advancing age. Krt71 mice have waved or curly hair / vibrissae|Heterozygous steel mice have a diluted coat color with a small amount of white spotting, are viable and fertile, and may have a slight macrocytic anemia.|C57BL/6By|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|30-Jul-2008||0.0|0.0|Unknown||white spotting, c-kit, fur / coat, melanocyte, mast cell|Yes| 3545.0||C57BL/6.Cg-Kitl Krt71/JWehi||Semi-dominant|keratin 71|Krt71|Unknown|Ca, Cu, Krt2-6g, mK6irs, mK6irs1|MGI:1861586|keratin 71; caracul|Krt71|MGI:1855990|15|||||||||||||||||||||||||||||The severity of the phenotypic effects of the steel alleles is correlated with the degree of alteration in the gene. The multiple steel mutations (KitlSl) behave in a semidominant fashion and cause deficiencies in pigment cells, germ cells, and blood cells paralleling those caused by the Kit locus mutations (dominant spotting alleles). Most of the alleles at steel locus cause severe anemia in utero and death by 15 to 16 days of gestation in homozygous mutant mice. However, compounds of two steel mutants (e.g. KitlSl/KitlSl-d are viable, black-eyed white, are usually sterile in one or both sexes, and have severe macrocytic anemia. Primordial germ cells are absent in the nonviable steel homozygotes and severely reduced in steel heterozygotes. Mast cells are virtually absent in skin and other tissues of steel mutant mice. Tumors tend to develop in germ-cell-deficient ovaries with advancing age. Krt71 mice have waved or curly hair / vibrissae|Heterozygous steel mice have a diluted coat color with a small amount of white spotting, are viable and fertile, and may have a slight macrocytic anemia.|C57BL/6By|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|30-Jul-2008||||Unknown||white spotting, c-kit, fur / coat, melanocyte, mast cell|Yes| 1957.0|available from Animal Resources Centre - www.arc.wa.gov.au|A/JArc||Dominant||||||||||||||||||||||||||||||||||||||Moderate breeder, 0.9 young/female/wk., avg litter 4.4. High social dominance of males in competition for females. Intermediate life span up to approximately 600 days. High spontaneous incidence of lung adenomas and mammary tumours in breeding females. Incidence of nephritis and amyloidosis nearly 100% at 15 months. Congenital defects include cleft-lip/palate and polydactyly at a prevalence of up to 10%. Low aggression, low responder in general (activity, alcohol, anaesthetics, metabolism). High incidence of lung tumours in response to carcinogens. C5 deficient. The strain has a defect in its macrophage function resembling the mutant lps.|||Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||Yes|04-Sep-2007||0.0|0.0|No|||Yes| 1964.0|available from Animal Resources Centre - www.arc.wa.gov.au|DBA/1JArc||Dominant|Inbred grey: (Dilute brown): a, Tyrp1, Myo5a, H-2||Unknown||||||Unknown||||||||||||||||No|||||||||||||Poor breeding performance (0.4 young /female/ week). Litter size average 4.4. Life span of males short (487 days), longer in females (686 days). High incidence of mammary tumours in unfostered mice (90% in breeding females, 60% in virgin females). Low incidence of tumours in males. High incidence of chronic degenerative lesions in heart muscle of old animals. Normal C5.|||Yes|Yes|Yes|Yes|Yes|Yes|No|Poor||||Yes|04-Sep-2007||0.0|0.0|Unknown|||Yes| 1965.0|available from Animal Resources Centre - www.arc.wa.gov.au|DBA/2JArc||Dominant|Inbred grey (Dilute Brown): a, Tyrp1, Myo5a, H-2||Unknown||||||Unknown||||||||||||||||No|||||||||||||Poor breeding performance 0.5 young/female/wk., average litter 4.5. High incidence of sterility. Moderate life span (males and females 2 years). Moderate to high mammary tumour incidence in unfostered mice (70% in breeding females and 50% in virgin females). High incidence of spontaneous calcification of the heart muscle, up to 90% in older mice. Fairly docile, low blood pressure, high RBC count. Males susceptible to chloroform fumes.Susceptible to audiogenic seizures (begins at 2 weeks, peaks at 3 weeks, gradually declines with age). Recommended host for fibrosarcoma SaD2, lymphatic leukaemia P1534, mammary adenocarcinoma CaD2. Hybrids involving DBA/2 are often used as hosts of transplantable leukaemia L1210, melanoma S91 and MOPC myeloma. C5 deficient. This strain has been embryo rederived using enrofloxacin treated egg donor dams.|||Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||Yes|04-Sep-2007||0.0|0.0|No|||Yes| 1966.0|available from Animal Resources Centre - www.arc.wa.gov.au|FVB/NJ||Dominant|Inbred albino. A, Tyr, Pde6b, H-2||Unknown||||||Unknown||||||||||||||||No|||||||||||||Useful for production of transgenic mice as fertilised eggs contain large and prominent pronuclei which facilitates the microinjections of DNA. Large litters.|||Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|04-Sep-2007|Cryopreserved sperm|12.0|0.0|No|||Yes| 1967.0|available from Animal Resources Centre - www.arc.wa.gov.au|NOD/LtJ (Non-obese diabetic)||Dominant|Inbred albino: A, Tyr, Cdh23, H-2g<7>||Unknown||||||Unknown||||||||||||||||Yes|||||||||||||General Information: Lt refers to Leiter, the holder of the strain at Jackson Laboratory. Originally derived from outbred Jcl:ICR mice by selection for spontaneous development of insulin-dependent diabetes due to insulitis under polygenetic control. Diabetes occurs from 90 to 120 days with a higher incidence in females (80%) than males (10-70%). Incidence in males is influenced by environmental factors including pathogens. This is an inverse relationship ie. there is a higher incidence in germfree animals than conventional animals. Immunosuppressive agents that suppress T-cell activity prevents the development of overt diabetes. Mice free from diabetes by 1 year are prone to develop follicle centre cell lymphomas. (Reference: Immunodeficient rodents A guide to their immunobiology, husbandry and use. National Academy Press, Washington, 1989). Females produce 4 to 5 litters before becoming diabetic. Litter size 7 to 14. C5 deficient.|||Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||Yes|04-Sep-2007||0.0|0.0|No|||Yes| 2331.0|B6.SJL ; Live stock available at Animal Resources Centre|B6.SJL-Ptprc Pepc/BoyJAnuApb|B6.SJL-Ptprc Pepc/BoyJAnuApb|Dominant|||||||||||||||||||||||||||||protein tyrosine phosphatase, receptor type, C|Ptprc||B220, CD45, CD45 antigen, Cd45, Ly-5, Lyt-4, T200, lymphocyte antigen 5|MGI:97810|protein tyrosine phosphatase, receptor type, C; a variant|Ptprc|MGI:4819849|1|||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|04-Dec-2007|Cryopreserved sperm|20.0|0.0|Unknown||transplant, Ly-5|Yes| 2331.0|B6.SJL ; Live stock available at Animal Resources Centre|B6.SJL-Ptprc Pepc/BoyJAnuApb|B6.SJL-Ptprc Pepc/BoyJAnuApb|Dominant|||||||||||||||||||||||||||||peptidase C|Pepc||Dip-1, Pep-3, Pep3|MGI:97541|peptidase C; b variant|Pepc|MGI:4819861|1|||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|04-Dec-2007|Cryopreserved sperm|||Unknown||transplant, Ly-5|Yes| 2471.0|Cbx2|C.129P2-Cbx2/JWehiApb|C.129P2-Cbx2/JWehiApb|Dominant|chromobox homolog 2 (Drosophila Pc class)|Cbx2|Nil|M33|MGI:88289|chromobox homolog 2 (Drosophila Pc class); targeted mutation 1, Centre d'Immunologie de Marseille Luminy|Cbx2|MGI:1857631|11||||||||||||||||No|||||||||||||Mutations cause malformations of the axial skeletal, reduced viability, poor growth and male to female sex reversal.Postnatal lethality:* 50% die within a few hours of birth* 90% are dead within 4 weeks.Abnormal body weight: a few days after birth pups weigh one fourth of littermate control weight. Mice homozygous for the targeted mutation show greatly retarded growth, premature death, homeotic transformations of the axial skeleton, sternal and limb malformations and arrested T cell development. Null mice show an aggravation of the skeletal malformations when treated to retinoic acid at embryonic day 7.5.||BALB/c |No|No|Yes|No|No|Yes|No|Good|20||Het x WT|No|18-Jan-2008|Cryopreserved sperm|150.0|0.0|Unknown||Growth Defects, Skeletal defects, Polycomb group protein, T cell, differentiation|Yes| 3404.0|ACT-mOVA-II|C57BL/6-Tg(CAG-OVA)916Jen||Dominant||||||||||||||||||||||||||transgene insertion 916, Marc K Jenkins|chicken β-actin|||||||||||Ubiquitously express membrane bound chicken ovalbumin under the control of chicken β-actin promoter. Breed less well than hets||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|13-Jul-2008||0.0|0.0|Unknown||Autoimmunity, T cell, ovalbumin, membrane|Yes| 3410.0|IL-6 KO|B6.129-Il6/Wehi||Recessive|interleukin 6|Il6|Nil|Il-6|MGI:96559|targeted mutation 1, Manfred Kopf|Il6|MGI:1857197|5||||||||||||||||No|||||||||||||Homozygous null mutants show impaired immune response to pathogens, decreased T cell numbers and resistance to plasma cell neoplasia. They are defective in wound healing and liver regeneration and show increased emotionality and high bone turnover rate.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|14-Jul-2008|Cryopreserved sperm|40.0|0.0|Unknown||T cell, infection, lipopolysaccharide (LPS), macrophage, osteoclast|Yes| 3424.0|8.3 NOD|NOD-Tg(TcraTcrbNY8.3)1Pesa/Wehi||Dominant||||||||||||||||||||||||||transgene insertion 1, Pere Santamaria|TCR||||||||||||Pancreas inflammation:* insulitis at 3 weeks less than in controls* insulitis at 6 weeks of age significantly greater than in controlsIncreased circulating glucose level:* diabetes develops in 26% (males) to 33% (females) of mice* diabetes slow to develop and moderate.|NOD|Yes|No|Yes|Yes|No|Yes|No|Unknown|6|||No|15-Jul-2008||0.0|0.0|Yes||Diabetes Mellitus, Insulin-Dependent; IDDM, T cell, receptor (TCR), autoimmunity, cytotoxic|Yes| 4945.0|EIIa-cre|B6.FVB-Tg(EIIa-cre)C5379Lmgd/JApb||Dominant||||||||||||||||||||||||||transgene insertion C5379, Laboratory of Mammalian Genes and Development, Heiner Westphal|adenovirus EIIa promoter||||||||||||Normal.|C57BL/6|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|04-Dec-2009|Cryopreserved sperm|97.0|0.0|Unknown||adenovirus, embryo, Cre recombinase|Yes| 3431.0|Nodal|C57BL/6-Nodal/Wehi||Recessive|nodal|Nodal|Nil|Tg.413d|MGI:97359|targeted mutation 1, Elizabeth J Robertson|Nodal|MGI:2180793|10||||||||||||||||No|lacZ (Beta-galactosidase)|endogenous|||||||||||Embryonic lethal at gastrulation|Normal|C57BL/6|No|No|Yes|No|No|Yes|No|Unknown||||No|15-Jul-2008||0.0|0.0|Unknown||primitive streak, gastrulation, left-right body axis, mesoderm cells|Yes| 3495.0||C3.MRL-Fas/JWehi||Recessive|Fas (TNF receptor superfamily member 6)|Fas|Unknown|APO-1, CD95, TNFR6, Tnfrsf6|MGI:95484|lymphoproliferation|Fas|MGI:1856334|19||||||||||||||||Yes|||||||||||||Description: Suffer from an automimmune disease. The can show clinical symptoms from 3 months of age and by 12 months, 60% should be showing signs of ilness. They may also suffer from kidney disease and arthritis. Animals should be checked reguarly for enlarged Lymph nodes in the neck, arm and groin areas - scruff the animal to do t his and feel for the pressure of lumps. Don't discard if mice develop lumps- this is normal. Mice homozygous for the lymphoproliferation spontaneous mutation (Faslpr) show systemic autoimmunity, massive lymphadenopathy associated with proliferation of aberrant T cells, arthritis, and immune complex glomerulonephrosis. Onset and severity of symptoms is dependent on genetic background, with the original MRL/MpJ background being most severely affected beginning about 8 weeks of age. Females die at an average age of 17 weeks of age and males at 22 weeks. This mouse is a model for systemic lupus erythematosus-like autoimmune syndromes. This strain is homozygous for the retinal degeneration allele Pde6b. ||C3H x MRL/Mp|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|24-Jul-2008||0.0|0.0|Unknown||Systemic Lupus Erythematosus (SLE), Autoimmune Lymphoproliferative Syndrome (ALPS), lymphoproliferation, autoimmunity, T cell|Yes| 3520.0|NOD.Idd11D|NOD.B6-Idd11/Wehi||Recessive|||Unknown|||insulin dependent diabetes susceptibility 11; C57BL/6|Idd11|MGI:3036811|4||||||||||||||||Yes|||||||||||||Non obese diabetic (NOD) mice exhibit a susceptibility to Spontaneous development of type 1 diabetes. It is best to best to begin monitoring development of glycosuria at weekly intervals starting at 10 wks of age. Use of the strains generated defines the IDD region to between D4Mit72 ad D4Mit203||NOD|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|10|||No|28-Jul-2008||0.0|0.0|Unknown||insulin, non obese, diabetic, NOD|Yes| 3534.0||C57BL/6-KD/JWehi||Recessive|histocompatibility-2, MHC|H2|Nil|H-2, MHC-II|MGI:95894||||17||||||||||||||||Yes|||||||||||||The homozygous H-2Kb and H-2Db double targeted mutation mice are virtually devoid of Class Ia cell surface molecules and exibit a 90% reduction in the total number of CD8ab+ peripheral lymphocytes in spite of increased expression of specific Class Ib lymphocytes.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|10|||No|29-Jul-2008||0.0|0.0|Unknown||MHC, T cell, cytotoxic, presentation, vaccine|Yes| 3543.0||B6.FVB-Tg(Itgax-DTR/EGFP)57Lan/JWehi||Dominant||||||||||||||||||||||||||transgene insertion 57, Richard A Lang|Mouse Itgax (integrin alpha X) promoter (CD11c)|High - 20 copies|||||||||||These transgenic mice have a diphtheria toxin (DT) inducible system that transiently depletes dendritic cells. All CD8+ and CD8- dendritic cells in the spleen fluoresce and are DT sensitive. Rapid reduction of Itgax+ dendritic cell number induced by intraperitoneal injection of DT persists for 2 days, after which the cell population gradually recovers. Repeated DT induction is lethal to the mouse. |FVB|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|30-Jul-2008||0.0|0.0|Unknown||Dendritic cell, infection, diphtheria toxin, Cytotoxic T lymphocytes (CTL), T cell|Yes| 7780.0|ENU31:G3|ANU:ENU31:G3||Recessive|Unknown||||||||Unknown||||||||||||||||Unknown|||||||||||||Unknown|Unknown|C57BL/6NCrlAnu|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||1||No|07-Nov-2014|Cryopreserved sperm|308.0|0.0|Unknown||ENU, random, mutagenesis, screen|Yes| 3576.0||BALB/c-Tg(CMV-cre)1Cgn/JWehi||Dominant||||||||||||||||||||||||||transgene insertion 1, University of Cologne |human cytomegalovirus minimal promoter|||||||||||In this transgenic strain, deletion of loxP-flanked genes occurs in all tissues, including germ cells. The Cre gene in this strain is under the transcriptional control of a human cytomegalovirus minimal promoter and is likely to be expressed before implantation during early embryogenesis. It also appears to be X-linked since transgene transmission through males is restricted to female offspring.||BALB/c|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|04-Aug-2008||0.0|0.0|Unknown||Cre recombinase, CMV, deleter|Yes| 4464.0|D/N|CBA-Tmc1/JAnuApb||Recessive|transmembrane channel-like gene family 1|Tmc1|Unknown|dn , Beethoven, Bth|MGI:2151016|deafness|Tmc1|MGI:1856845|19||||||||||||||||Yes|||||||||||||Mutant mice are characterized by progressive degeneration of the cochlear inner hair cells and concomitant deafness. Profound congenital deafness.||CBA|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|22-Feb-2009|Cryopreserved sperm|150.0|0.0|Yes||deafness, hair, sodium channel, neuron, cochlear|Yes| 4548.0||B6.129-Phc1/JWehiApb||Recessive|polyhomeotic-like 1 (Drosophila)|Phc1|Nil|Edr1, Mph1, Rae-28, rae28|MGI:103248|targeted mutation 1, Osaka University Medical School|Phc1|MGI:1857629|1||||||||||||||||Yes|||||||||||||Perinatal lethality* mutants are alive at E17.5 but do not survive birthCraniofacialAbnormal occipital bone morphology * an ectopic arch is associated with the occipital bonesAbnormal sphenoid bone morphology * the sphenoid is partially splitAbnormal presphenoid bone morphology * the center of the presphenoid is not ossifiedcleft palate SkeletonAbnormal occipital bone morphology *an ectopic arch is associated with the occipital bonesAbnormal sphenoid bone morphology * the sphenoid is partially splitAbnormal presphenoid bone morphology* the center of the presphenoid is not ossifiedAbnormal vertebrae morphology * changes in the vertebral column are similar to those in Phc2tm1HkoDigestive/alimentary systemcleft palate ||C57BL/6|No|No|Yes|No|No|Yes|No|Good|10||Het x WT|No|02-Mar-2009|Cryopreserved sperm|100.0|0.0|Unknown||Polycomb group proteins, skeletal defects, polycomb repressive complex 1|Yes| 4801.0||DBA-Kit/J||Semi-dominant|kit oncogene|Kit|Normal|belly-spot, c-KIT, CD117, Dominant white spotting, Steel Factor Receptor, Tr-kit|MGI:96677|fertile dominant spotting|Kit|MGI:1856261|5||||||||||||||||No|||||||||||||lethality/postnatalpostnatal lethality (J:6187)some loss by 2 weeks of age due to chronic macrocytic anemiapigmentationdiluted coat color (J:6187)typical dilution of pigmented areas not observedirregular coat pigmentation (J:6187)extensive depigmented areas lacking a defined patternhematopoietic systemmacrocytic anemia (J:6187)decreased mast cell number (J:27513)immune systemdecreased mast cell number (J:27513)reproductive systemreproductive system phenotype (J:6187)no abnormal reproducitve system phenotypes detectedskin/coat/nailsdiluted coat color (J:6187)typical dilution of pigmented areas not observedirregular coat pigmentation (J:6187)extensive depigmented areas lacking a defined pattern|KitW-f/Kit+ C3H/HePaspigmentationnon-pigmented tail tip (J:6187)diluted coat color (J:27513)typical dilution of pigmented areas not observed on strain of origin but is noted on C57BL/6 backgroundbelly spot (J:6187)sharply demarcated but variable in size, sometimes reduced to a few hairspresence is background sensitivehead spot (J:6187)sharply demarcated but variable in size, sometimes reduced to a few hairspresence is background sensitivehematopoietic systemmacrocytic anemia (J:6187)limbs/digits/tailnon-pigmented tail tip (J:6187)skin/coat/nailsnon-pigmented tail tip (J:6187)diluted coat color (J:27513)typical dilution of pigmented areas not observed on strain of origin but is noted on C57BL/6 backgroundbelly spot (J:6187)sharply demarcated but variable in size, sometimes reduced to a few hairspresence is background sensitivehead spot (J:6187)sharply demarcated but variable in size, sometimes reduced to a few hairspresence is background sensitive|DBA|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|23-Sep-2009||0.0|0.0|Unknown||c-kit, coat, migration, mast cell, stem cell, white spotting|Yes| 4890.0|eNOS-/-|B6.129-Nos3/JMarpApb||Dominant|nitric oxide synthase 3, endothelial cell|Nos3|Nil|ecNOS, eNOS, Nos-3|MGI:97362|targeted mutation 1, University of North Carolina|Nos3|MGI:1857229|5|||||||||||||||||||||||||||||eNOS-/- mice are deficient in endothelial nitric oxide (NO) synthase which produces NO. eNOS-/- animals do not display alterations in behaviour, reproduction or development. Animals develop mild hypertension, have an elevated plasma renin concentration and a lower heart rate. Mice also exhibit insulin resistance at the level of the liver and peripheral tissues and females have a slightly lower body weight (~7.5%) as compared with wild-types. Although eNOS knockout mice are viable, litter sizes are small and offspring have minor congenital cardiac abnormalites. Studies have indicated homozygous offspring have a high rate of neonatal mortality due to abnormalities in lung development. |eNOS+/- mice are normotensive and do not display alterations in behaviour, reproduction or development. Mice display some evidence of impaired vascular NO production with attenuated endothelium-dependent vasorelaxation in carotid arteries and enhanced pulmonary vasoconstrictor responses to hypoxia.|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|12||Hom x Hom|No|28-Sep-2009|Cryopreserved sperm|100.0|0.0|Yes|Hypertension|endothelial, nitric oxide, synthase|Yes| 4956.0|OT2.CD45.1|B6.Cg-Ptprc Tg(TcraTcrb)425Cbn/AnuApb||Dominant||||||||||||||||||||||||||transgene insertion 425, Frank Carbone|||protein tyrosine phosphatase, receptor type, C|Ptprc||220, CD45, Ly-5, Lyt-4, T200|MGI:97810|protein tyrosine phosphatase, receptor type, C; a variant|Ptprc|MGI:4819849|1|Homozygous mice are viable and fertile. In these mice there is a four-fold increase in the CD4 to CD8 peripheral T-cell ratio, and lymph node T-cells demonstrate a dose-dependent proliferative response to the specific ovalbumin ligand.T cells express T cell receptor specific for chicken ovalalbumin residues 323 - 339 in the context of H2-Ab1 (I-A)Transgenic mice express the mouse alpha-chain and beta-chain T-cell receptor that pairs with the CD4 coreceptor and is specific for chicken ovalbumin 323-339 in the context of I-A b. Homozygous transgenic mice are viable and fertile. In these mice there is a four-fold increase in the CD4 to CD8 peripheral T-cell ratio, and lymph node T-cells demonstrate a dose-dependent proliferative response to the specific ovalbumin ligand.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|18-Dec-2009|Cryopreserved sperm|80.0|0.0|Unknown||receptor (TCR), CD4, ovalbumin, thymic selection, B cell receptor|Yes| 5035.0|NDL2-5|FVB/N-Tg(MMTV-Erbb2*)NDL2-5Mul/JAusbApb||Dominant||||||||||||||||||||||||||transgene insertion NDL2-5, William J Muller|mouse mammary tumor virus LTR||||||||||||Females from several independent lines develop multiple mammary tumors that frequently metastasize to the lung. Tumor progression in these strains was associated with elevated levels of tyrosine-phosphorylated Neu and ErbB-3. |FVB/N|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|22-Feb-2010|Cryopreserved sperm|100.0|0.0|Yes|Mammary tumourigenesis|Mammary, neu, ErbB-2, tumourigenesis, signal transduction|Yes| 5041.0|ICAM-1 null|B6.129S7-Icam1/JApb||Recessive|intercellular adhesion molecule 1|Icam1|Normal|CD54, Icam-1, Ly-47, MALA-2, MGC:6195|MGI:96392|intercellular adhesion molecule 1; targeted mutation 1, Baylor College of Medicine|Icam1|MGI:1857183|9||||||||||||||||No|||||||||||||Increased body weight: mice are ~20% heavier than wild-type or Sell mutant mice.Increased lymphocyte cell number: number of circulating lymphocytes is increased over wild-type (47% of wild-type number).Increased eosinophil cell number: increased significantly compared to wild-type (178% of wild-type).Increased neutrophil cell number: * 4-5 fold increase in numbers of circulating neutrophils. * number of circulating neutrophils is increased over wild-type (190% of wild-type number).Increased monocyte cell number: number of circulating monocytes is increased over wild-type (223% of wild-type number).Abnormal leukocyte migration: Streptococcus pneumoniae induced peritonitis reduced neutrophil emigration into peritoneum by 64% after 4 hours.Abnormal cellular extravasation: 2 hours after thioglycollate-induced peritonitis, neutrophil entry into peritoneum is significantly inhibited by 61% compared to wild-type.Abnormal leukocyte rolling: * Tnfa (TNFalpha) treatment increases leukocyte rolling flux fraction slightly compared to wild-type. * rolling velocities of leukocytes are slightly greater compared to wild-type mice at times <30 minutes after surgery; >60 minutes after surgery-induced inflammation, rolling velocities are significantly faster than wild-type (58 vs 38 um/second). * similar results on rolling velocity are observed with Tnfa-activated rolling as induced by surgical trauma.Decreased susceptibility to endotoxin shock: * following treatment with a lethal dose of LPS, mice succumb after 10 hours compared to wild-type mice that succumb after 8 hours. * mice only develop mild liver injury in response to low doses of LPS at 8 hours that does not worsen compared to wild-type mice that exhibit liver severe injury at 6 hours.Increased tumor growth/size: when injected with melanoma cells, mice exhibit a 2.6 fold increase in tumor volume on day 14 compared to wild-type mice.Decreased angiogenesis: in a disk angiogenesis assay, no increase in capillary density in response to Vegfa is observed in the dermal vasculature overlying implanted disks, whereas wild-type mice show a clear increase in capillary density in response to Vegfa.Abnormal cell physiology: endothelial cells show attenuated chemotactic response to Vegfa in transwell chemotactic assays compared with wild-type control cells.Abnormal cell migration.Abnormal nitric oxide homeostasis: in endothelial cell culture, Vegf-dependent and basal nitric oxide production is attenuated relative to wild-type cells.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|22-Feb-2010|Cryopreserved sperm|70.0|0.0|Unknown||migration, leukocyte, neutrophil, lymphocyte, eosinophil, angiogenesis|Yes| 5119.0|Ednrb s/sl|B6.C3H-Ednrb/J||Recessive|endothelin receptor type B|Ednrb|Nil|ETb, ETR-b, Sox10m1|MGI:102720|endothelin receptor type B; piebald lethal|Ednrb|MGI:1856149|14|||||||||||||||||||||||||||||Postnatal lethality: * most usually die by 15 days of age * some live to breed but die between 3 and 15 months of ageAbnormal coat/hair pigmentation.Absent coat pigmentation: mice are white-coated with small patches of pigmented hair about the eyes,ears and tail.Megacolon: * distal four sections of the colon are aganglionic * grossly evident via markedly distended colon in weaning age or older mice.Abnormal enteric ganglia morphology: deficiency of ganglion cells of the myenteric plexus of the lower colon.||C57BL/6|No|No|Yes|No|No|Yes|No|Unknown||||No|12-May-2010||0.0|0.0|Yes|Hirschsprung Disease, Susceptibility to, 1; HSCR1 OMIM ID: 142623|neuron, pigmentation, coat, piebald, lethal, cholinergic, migration, neural crest|Yes| 5489.0||CBACaJ;129S-Chrna9/J||Recessive|cholinergic receptor, nicotinic, alpha polypeptide 9|Chrna9|Nil|Acra9, Gm8311|MGI:1202403|cholinergic receptor, nicotinic, alpha polypeptide 9; targeted mutation 1, Belen Elgoyhen and Douglas E Vetter|Chrna9|MGI:2158742|5||||||||||||||||Yes|||||||||||||Hearing/vestibular/ear phenotype: * homozygotes are viable with a normal Preyer's reflex and no gross deficits in balance or movement. * no structural abnormalities in cochlear hair cells, supporting cells or spiral ganglion neurons are observed. * in addition, development and position of the olivocochlear bundle remains unchanged. * in vitro, mutant apical OHCs exhibit normal electromotility in response to a 100-Hz sinusoidal voltage command relative to wild-type OHCs.Abnormal cochlear IHC efferent innervation pattern: * unlike wild-type mice, homozygotes appear to lack a sparse plexus of efferent terminals in close apposition to the IHC somata * however, a dense plexus of terminals is still present below the IHCs.Abnormal cochlear OHC efferent innervation pattern: * most efferent terminals under mutant OHCs occur as large singlets rather than as clusters of roughly equal-size terminals * most mutant OHCs are contacted by only one terminal (66.7%) and very few by >2 terminals, whereas 61.8% of wild-type OHCs are contacted by two terminals.Abnormal cochlear nerve compound action potential: * at 6-24 weeks, homozygotes fail to show suppression of compound action potential (CAP) amplitudes during efferent fiber activation by olivocochlear (OC) shocks * however, in the absence of crossing OC bundle electrical stimulation, homozygotes display normal CAP thresholds at 16 kHz relative to wild-type mice * also, at 4-9 weeks, homozygotes show normal mean CAP threshold curves over the entire range of mouse hearing (between 1.7 and 50 kHz) relative to 129S6/SvEvTac control mice.Abnormal distortion product otoacoustic emission: * homozygotes fail to show suppression of distortion product otoacoustic emissions (DPOAEs) during efferent fiber activation by olivocochlear (OC) shocks * however, in the absence of OC bundle electrical stimulation, homozygotes display normal DPOAEs relative to wild-type mice.||129S1/Sv x CBA/CaJ|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|21-Apr-2011||0.0|0.0|Unknown||cholinergic receptor, cochlear, hearing, ear, CNS, efferent fibres|Possibly| 6595.0|BXD-11|BXD11/TyJArc||Recessive||||||||||||||||||||||||||||||||||||||Normal|Normal|C57BL/6J x DBA/2|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|||brother x sister|No|04-Oct-2011|Embryo|0.0|0.0|Unknown|||Possibly| 6600.0|BXD-28|BXD28/TyJArc||Recessive||||||||||||||||||||||||||||||||||||||Normal|Normal|C57BL/6J x DBA/2|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|||brother x sister|No|04-Oct-2011|Embryo|0.0|0.0|Unknown|||Possibly| 6602.0|BXD-32|BXD32/TyJArc||Recessive||||||||||||||||||||||||||||||||||||||Normal|Normal|C57BL/6J x DBA/2|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|||brother x sister|No|04-Oct-2011|Embryo|0.0|0.0|Unknown|||Possibly| 6606.0|BXD-66|BXD66/RwwJArc||Recessive||||||||||||||||||||||||||||||||||||||Normal|Normal|C57BL/6J x DBA/2|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|||brother x sister|No|04-Oct-2011|Embryo|0.0|0.0|Unknown|||Possibly| 6607.0|BXD-73|BXD73/RwwJArc||Recessive||||||||||||||||||||||||||||||||||||||Normal|Normal|C57BL/6J x DBA/2|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|||brother x sister|No|04-Oct-2011|Embryo|0.0|0.0|Unknown|||Possibly| 7785.0|ENU31:027|ANU:ENU31:027||Recessive|Unknown||||||||Unknown|||||||||||||||||||||||||||||Unknown|Unknown|C57BL/6NCrlAnu|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Poor||||No|13-Nov-2014||0.0|0.0|Unknown||ENU|Yes| 6836.0|SIRT3|129-Sirt3/JAusb||Recessive|sirtuin 3 (silent mating type information regulation 2, homolog) 3 (S. cerevisiae) |Sirt3 ||2310003L23Rik, Sir2l3 |MGI:1927665 |sirtuin 3 (silent mating type information regulation 2, homolog) 3 (S. cerevisiae); targeted mutation 1.1, Frederick W Alt |Sirt3tm1.1Fwa |MGI:3769234|7|ENSMUSG00000025486||||||||||||||||||||||||||||Mice are phenotypically normal with unremarkable metabolism and adaptive thermogenesis. They develop an exaggerated increase in liver and bloood lipids when challenged with a long-term high-fat diet. |Normal|129|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|||Homozygous x Homozygous|No|02-Mar-2012||0.0|0.0|Unknown||Hypoglycemia, ATP, Mitochondria, Fatty acid, cardiovascular, steatosis|Yes| 7020.0|CXCR5tg OT2; CXCR5tg OTII|B6;129-Il21r Tg(Lck-Cxcr5)Cys Tg(TcraTcrb)425Cbn/JAusbApb||Dominant|interleukin 21 receptor|Il21r|Nil|NILR|MGI:1890475|interleukin 21 receptor; targeted mutation 1, Warren J Leonard|Il21r|MGI:2446509|7|||||||||||||||||transgene insertion 425, Frank Carbone||||||||||||Homozygous mice are viable and fertile. In OTIItg mice there is a four-fold increase in the CD4 to CD8 peripheral T-cell ratio, and lymph node T-cells demonstrate a dose-dependent proliferative response to the specific ovalbumin ligand.T cells express T cell receptor specific for chicken ovalalbumin residues 323 - 339 in the context of H2-Ab1 (I-A)Transgenic mice express the mouse alpha-chain and beta-chain T-cell receptor that pairs with the CD4 coreceptor and is specific for chicken ovalbumin 323-339 in the context of I-A b. CXCR5tg mice express CXCR5 in naive T cells and in mature B cells. IL-21R knockout mice show a mild reduction in IgG1 isotype antibodies in response to infection or vaccination.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|17-Jul-2012|Cryopreserved sperm|50.0|0.0|Unknown||receptor (TCR), CD4, ovalbumin, thymic selection, CXCR5, IL-21R|Possibly| 7020.0|CXCR5tg OT2; CXCR5tg OTII|B6;129-Il21r Tg(Lck-Cxcr5)Cys Tg(TcraTcrb)425Cbn/JAusbApb||Dominant||||||||||||||||||||||||||chemokine (C-X-C motif) receptor 5|lymphocyte protein tyrosine kinase|||||||||||Homozygous mice are viable and fertile. In OTIItg mice there is a four-fold increase in the CD4 to CD8 peripheral T-cell ratio, and lymph node T-cells demonstrate a dose-dependent proliferative response to the specific ovalbumin ligand.T cells express T cell receptor specific for chicken ovalalbumin residues 323 - 339 in the context of H2-Ab1 (I-A)Transgenic mice express the mouse alpha-chain and beta-chain T-cell receptor that pairs with the CD4 coreceptor and is specific for chicken ovalbumin 323-339 in the context of I-A b. CXCR5tg mice express CXCR5 in naive T cells and in mature B cells. IL-21R knockout mice show a mild reduction in IgG1 isotype antibodies in response to infection or vaccination.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|17-Jul-2012|Cryopreserved sperm|||Unknown||receptor (TCR), CD4, ovalbumin, thymic selection, CXCR5, IL-21R|Possibly| 7184.0|FceRI?|B6.129S2(Cg)-Fcer1a/JAusb||Recessive||Fcer1a|||MGI:95494||||Unknown|||||||||||||||||||||||||||||Mice homozygous for a knock-out allele exhibit abnormal mast cell physiology and altered susceptibility to type I hypersensitivity reaction. Mice homozygous for another knock-out allele display altered development of allergic airway inflammation and airway hyperresponsiveness.||C57BL/6|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|02-Nov-2012||0.0|0.0|Unknown|||Possibly| 7185.0|LRKK2|B6;C3-Tg(PDGFB-LRRK2*G2019S)340Djmo/JAusb|B6;C3-Tg(PDGFB-LRRK2*G2019S)340Djmo/JAusb|Dominant||G2019S-LRRK2|||MGI:4950671||||Unknown|||||||||||||||||||||||||||||These tg mice display progressive nigral dopaminergic degeneration, in addition to reduced complexity of cultured midbrain dopaminergic neurons.Also exhibit enhanced dopamine turnover in the olfatory bulb, as well as autophagic and mitochondrial abnormal.||C57BL/6J x C3H/HeJ F1|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|02-Nov-2012||0.0|0.0|Unknown|||Possibly| 7789.0||C57BL/6JAnu-Elovl3/AnuApb|C57BL/6JAnu-Elovl3/AnuApb|Recessive|elongation of very long chain fatty acids (FEN1/Elo2, SUR4/Elo3, yeast)-like 3|Elovl3|Unknown|Cig30, CIN-2|MGI:1195976|Elovl3; mutation 1, Australian National University|Elovl3||19|ENSMUSG00000038754|ENSMUST00000043739|Elovl3-001|545|718|T to A|ENSMUSE00000380471|4|182|Methionine to Lysine|||||GACCATGAACTTTGGCGTCCATTCTGTCATGTACACTTACTACACTATGAAGGCTGCCAAA||||||||||||||Hom mice have sparse fur and can been phenotyped at weaning||C57BL/6JAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|19-Nov-2014|Cryopreserved sperm|51.0|0.0|Unknown|||Yes| 8363.0|ASD867|BALB/cNCrlAnu:Yellow||Dominant|||||||||||||||||||||||||||||||||||||||||Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|04-Dec-2017||0.0|869.0|Unknown|||No| 7547.0|Dhcr24 KO|B6.129S5-Dhcr24/SbpaJAnuApb|B6.129S5-Dhcr24/SbpaJAnu|Recessive|24-dehydrocholesterol reductase|Dhcr24|Nil|2310076D10Rik, 3-beta-hydroxysterol delta-24 reductase, 5830417J06Rik, mKIAA0018, seladin-1|MGI:1922004|24-dehydrocholesterol reductase; targeted mutation 1, Lexicon Genetics|Dhcr24|MGI:3027024|4|||||||||||||||||||||||||||||Dhcr24-/- mice die on day 1 after birth with severe skin deficiencies.Partial prenatal lethality:• the number of mice born was less than expected by Mendelian ratios.Decreased subcutaneous adipose tissue amount.Abnormal mesenteric fat pad morphology:• decreased stores of mesenteric fatDecreased body size:• approximately 25% smaller than wild-typeDecreased body weight:• whereas female mice reached normal weight by 4 to 5 weeks of age, male mice did not.Postnatal growth retardationAbnormal circulating cholesterol level:• desmosterols accounted for approximately 99% of sterols• tissue levels of cholesterol were nearly completely ablatedDecreased circulating cholesterol level:• plasma contained nearly no cholesterolTesticular atrophy.Male and female infertility.||C57BL/6J|No|No|Yes|No|No|Yes|No|Unknown|14|||No|18-Dec-2013||0.0|0.0|Unknown||embryonic lethal, skin, cholesterol, epidermis, keratinocytes|Yes| 7705.0|MerCreMer|B6.FVB(129)-Tg(Myh6-cre/Esr1*)1Jmk/JVccrApb||Dominant||||||||||||||||||||||||||transgene insertion 1, Jeffery D Molkentin|mouse cardiac-specific alpha-myosin heavy chain|heart||||||||||The advent of conditional and tissue-specific recombination systems in gene-targeted or transgenic mice has permitted an assessment of single gene function in a temporally regulated and cell-specific manner. Here we generated transgenic mice expressing a tamoxifen-inducible Cre recombinase protein fused to two mutant estrogen-receptor ligand-binding domains (MerCreMer) under the control of the alpha-myosin heavy chain promoter. These transgenic mice were crossed with the ROSA26 lacZ-flox-targeted mice to examine Cre recombinase activity and the fidelity of the system. The data demonstrate essentially no Cre-mediated recombination in the embryonic, neonatal, or adult heart in the absence of inducing agent but >80% recombination after only four tamoxifen injections. Expression of the MerCreMer fusion protein within the adult heart did not affect cardiac performance, cellular architecture, or expression of hypertrophic marker genes, demonstrating that the transgene-encoded protein is relatively innocuous. In summary, MerCreMer transgenic mice represent a tool for temporally regulated inactivation of any loxP-targeted gene within the developing and adult heart or for specifically directing recombination and expression of a loxP-inactivated cardiac transgene in the heart.|The advent of conditional and tissue-specific recombination systems in gene-targeted or transgenic mice has permitted an assessment of single gene function in a temporally regulated and cell-specific manner. Here we generated transgenic mice expressing a tamoxifen-inducible Cre recombinase protein fused to two mutant estrogen-receptor ligand-binding domains (MerCreMer) under the control of the alpha-myosin heavy chain promoter. These transgenic mice were crossed with the ROSA26 lacZ-flox-targeted mice to examine Cre recombinase activity and the fidelity of the system. The data demonstrate essentially no Cre-mediated recombination in the embryonic, neonatal, or adult heart in the absence of inducing agent but >80% recombination after only four tamoxifen injections. Expression of the MerCreMer fusion protein within the adult heart did not affect cardiac performance, cellular architecture, or expression of hypertrophic marker genes, demonstrating that the transgene-encoded protein is relatively innocuous. In summary, MerCreMer transgenic mice represent a tool for temporally regulated inactivation of any loxP-targeted gene within the developing and adult heart or for specifically directing recombination and expression of a loxP-inactivated cardiac transgene in the heart.|C57BL/6J|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|10|10|hom x hom|No|25-Jun-2014|Cryopreserved sperm|40.0|0.0|No|||Yes| 7775.0|MyD88 knockout|B6.129P2(SJL)-Myd88/JMarpApb||Recessive|myeloid differentiation primary response gene 88|Myd88|Nil||MGI:108005|myeloid differentiation primary response gene 88; targeted mutation 1.1, Anthony L DeFranco|Myd88|MGI:4421295|9|||||||||||||||||||||||||||||Homozygous mice are viable and fertile. The Myd88-deficient allele encodes a deletion of exon 3 of the myeloid differentiation primary response gene 88 gene. MYD88 is a cytosolic adapter protein that plays a central role in the innate and adaptive immune response. MyD88 signaling is required to limit bacterial burden and prolong survival during infection. Myd88-deficiency is associated with a number of immune system abnormalities, as well as hematopoietic system, molecular signaling, and apoptotic abnormalities. These mice have increased susceptibility to bacterial and viral infection and should be maintained in a specific pathogen free environment.|Normal|C57BL/6J|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|3||homo x homo|No|24-Oct-2014|Cryopreserved sperm|80.0|0.0|Unknown||IL12a, MyD88, Ifnar1|Yes| 7242.0|DMP-1-Cre Recql4|C57BL/6-Recql4 Gt(ROSA)26Sor Tg(Dmp1-Cre)1Jqfe/Apb||Dominant|gene trap ROSA 26, Philippe Soriano|Gt(ROSA)26Sor||beta geo, Gtrgeo26, Gtrosa26, R26, ROSA26, Thumpd3as1|MGI:104735|gene trap ROSA 26, Philippe Soriano; targeted mutation 1, Frank Costantini|Gt(ROSA)26Sor|MGI:2449038|6|||||||||||||||||transgene insertion 1, Jian Q Feng|Dmp1|odontoblast||||||||||Homozygous animals are normal, fertile and viable (floxed line with eYFP reporter of cre activity)|Normal, fertile and viable (floxed line with eYFP reporter of cre activity)|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|generated on pure C57Bl/6 so not backcrossed. Only maintained on C57||homozygous R26eYFP Recql4fl/fl in breeding|No|06-Dec-2012|Cryopreserved sperm|30.0|0.0|Yes|Rothmund-Thomson Syndrome|Recql4, R26eYFP, Rothmund-Thomson Syndrome|Possibly| 7242.0|DMP-1-Cre Recql4|C57BL/6-Recql4 Gt(ROSA)26Sor Tg(Dmp1-Cre)1Jqfe/Apb||Dominant|RecQ protein-like 4|Recql4 |Unknown||MGI:1931028|RecQ protein-like 4; targeted mutation 1.1, TaconicArtemis|Recql4|MGI:5645319|15|||||||||||||||||||||||||||||Homozygous animals are normal, fertile and viable (floxed line with eYFP reporter of cre activity)|Normal, fertile and viable (floxed line with eYFP reporter of cre activity)|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|generated on pure C57Bl/6 so not backcrossed. Only maintained on C57||homozygous R26eYFP Recql4fl/fl in breeding|No|06-Dec-2012|Cryopreserved sperm|||Yes|Rothmund-Thomson Syndrome|Recql4, R26eYFP, Rothmund-Thomson Syndrome|Possibly| 7787.0|Dynll-SHH|C57BL/6-Dynll1 Shh/StvApb||Dominant|dynein light chain LC8-type 1|Dynll1|Normal|8kDa LC, DLC8, Dnclc1, Pin|MGI:1861457|dynein light chain LC8-type 1; targeted mutation 1.1, Jorg Heierhorst|Dynll1||5||||||||||||||||Yes|||||||||||||Normal|Normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Excellent||||No|17-Nov-2014|Cryopreserved sperm|50.0|0.0|Unknown||Dynll-1, ASCIZ, SHH|Possibly| 7787.0|Dynll-SHH|C57BL/6-Dynll1 Shh/StvApb||Dominant|sonic hedgehog|Shh||Hhg1, Hx, Hxl3, M100081|MGI:98297|sonic hedgehog; targeted mutation 1, Clifford J Tabin|Shh|MGI:3053959|5|||||||||||||||||||||||||||||Normal|Normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Excellent||||No|17-Nov-2014|Cryopreserved sperm|||Unknown||Dynll-1, ASCIZ, SHH|Possibly| 7794.0|MPEG1 targeted KO clone 7F|C57BL/6J-Mpeg17F/PibMarpApb||Dominant|macrophage expressed gene 1|Mpeg1||Mpg-1, MPS1|MGI:1333743||||19|||||||||||||||||||||||||||||Unknown|Unknown|C57BL/6J|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Excellent||||No|25-Nov-2014|Cryopreserved sperm|50.0|0.0|Unknown|||Possibly| 8780.0|Tph2-GFP|CD1.FVB/N-Tg(Tph2-EGFP)LO210Gsat/Apb||Dominant||||||||||||||||||||||||||transgene insertion LO210, GENSAT Project at Rockefeller University|Tph2|||||||||||GFP expressed in Tph2-expressing cells. No other phenotype abnormalities. Breeding not great as Homs|GFP expressed in Tph2-expressing cells. No other phenotype abnormalities. prefer maintain line as hets for breeding.|Crl:CD1(ICR) |Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|19-Aug-2019|Cryopreserved sperm|50.0|0.0|Unknown|||Yes| 7796.0|Tiger ; Cx40Tg|B6.CBA-Tg(Tie2-Gja5/EGFP)1/AnuApb||Dominant||||||||||||||||||||||||||transgene insertion 1, |endothelial-specific receptor tyrosine kinase; Tie2, Tek||||||||||||Expression of Cx40 (Gja5) at endothelial gap junctions.Arteries from Cx40Tg mice were significantly more sensitiveto the vasodilator, calcitonin gene related peptide (CGRP), thanwild-type or Cx40T202STg arteries.There was no difference among the genotypes in the sensitivityto phenylephrine (PE) or the total vascular tone achievedat 70 mm Hg (Figure III in the online-only Data Supplement).However, the maximum constriction to PE was significantlygreater in Cx40Tg arteries than in Cx40T202STg and wild typearteries.|C57BL/6JAnu|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown|8|||No|25-Nov-2014|Cryopreserved sperm|49.0|0.0|Unknown||arterial dysfunction, connexin40, endothelium, myogenic response, stiffness|Yes| 7793.0|LMN|B6.129S1(Cg)-Lmna/VccriApb||Dominant|lamin A|Lmna|Nil|Dhe, lamin A/C|MGI:96794|lamin A; targeted mutation 1, Colin L Stewart|Lmna|MGI:2177930|3|||||||||||||||||||||||||||||Lethal by 6-8weeks.Postnatal growth retardation.Muscle weakness.Small seminiferous tubules.Small testis.Azoospermia: spermatids and spermatozoa are largely absentArrest of male meiosis: * increased frequency of leptotene and zygotene spermatocytes and decreased frequency of pachytene and diplotene spermatocytes resulting from arrest and apoptosis of spermatocytes during the pachytene stage * unpaired chromosomes and/or improperly paired sex chromosomes and failure to progress through prophase I are seen * however, oogenesis in females is normal.|Viable, fertile.Abnormal nucleus morphology: in many MEFs, nuclei appear elongated but distribution of nuclear envelope proteins is normal except for increased levels of cytoplasmic emerin.|C57BL/6|No|Unknown|Yes|No|Unknown|Yes|No|Good|Backcrossed to C57BL/6 since 2009|None since 2009|LMN het male x BL6 female|No|21-Nov-2014|Cryopreserved sperm|70.0|0.0|Unknown||muscular dystrophy, membrane, interphase, spermatogenesis|Yes| 7788.0||C57BL/6JAnu-Scd1/AnuApb|C57BL/6JAnu-Scd1/AnuApb|Recessive|stearoyl-Coenzyme A desaturase 1|Scd1||SCD, Scd-1, stearoyl-CoA desaturase|MGI:98239||||19|ENSMUSG00000037071|ENSMUST00000041331|Scd1-201||||||||||||||||||||||||||Hom mice have sparse fur and can been phenotyped at weaning||C57BL/6JAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|19-Nov-2014|Cryopreserved sperm|50.0|0.0|Unknown|||Yes| 7791.0||C57BL/6NCrlAnu-Nck/AnuApb|C57BL/6NCrlAnu-Nck/AnuApb|Recessive|non-catalytic region of tyrosine kinase adaptor protein 1|Nck1|Unknown|6330586M15Rik, D230010O13Rik, Nck|MGI:109601||||9|||||||||||||||||||||||||||||Increased IgM expression on mature B cells||C57BL/6NCrlAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|19-Nov-2014|Cryopreserved sperm|30.0|0.0|Unknown||B cell, IgM|Yes| 7795.0|CAG-KD:ER; MMTV-Cre|C57BL/6-Hprt Tg(MMTV-Cre)/Apb||X-linked|hypoxanthine guanine phosphoribosyl transferase|Hprt|Normal||MGI:96217||||X||||||||||||||||||MMTV|||||||||||Normal|Normal|C57BL/6|Yes|Yes|Unknown|Yes|Yes|Unknown|No|Good|5|||No|25-Nov-2014|Cryopreserved sperm|50.0|0.0|No|||Possibly| 7797.0|Favola ; Cx40T202STg ; DeltaF|B6.CBA-Tg(Tie2-Gja5*T202S/EGFP)1/AnuApb||Dominant||||||||||||||||||||||||||transgene insertion 1, |endothelial-specific receptor tyrosine kinase; Tie2, Tek||||||||||||Expression of mutant form of Cx40 (Gja5) (amino acid substitution T202S at endothelial gap junctions.Body weight, blood pressure and heart rate are normal.Expression of transgene results in significant decrease in Cx37 expression.Endothelial Cx40T202S expression enhances myogenic activation and impairs endothelium-derived hyperpolarization (EDH) in mesenteric resistance arteries.Endothelial Cx40T202S expression increases stiffness of mesenteric resistance arteries. |C57BL/6JAnu|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown|8|||No|25-Nov-2014|Cryopreserved sperm|63.0|0.0|Unknown||arterial dysfunction, connexin40, endothelium, myogenic response, stiffness|Yes| 7798.0|DeltaG ; Cx40T152ATg|C57BL/6JAnu-Tg(Tie2-Gja5*T152A/EGFP)1/AnuApb||Dominant||||||||||||||||||||||||||transgene insertion 1, |endothelial-specific receptor tyrosine kinase; Tie2, Tek|||||||||||||C57BL/6JAnu|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown|8|||No|25-Nov-2014|Cryopreserved sperm|48.0|0.0|Unknown||arterial dysfunction, connexin40, endothelium, myogenic response, stiffness|Yes| 7805.0|DBC2 / DBC3 knockout|C57BL/6-Brinp2 Brinp3/PibMarpApb||Recessive|bone morphogenic protein/retinoic acid inducible neural-specific 2|Brinp2|Nil|6430517E21Rik, Fam5b, mKIAA1747|MGI:2443333|bone morphogenic protein/retinoic acid inducible neural-specific 2; targeted mutation 1.1, Phillip I Bird|Brinp2|MGI:5604615|1||||||||||||||||Yes|||||||||||||DBC2 and DBC3 mice show behavioral phenotypes similar to DBC3 knockout mice. * Reduced anxiety in the elevated plus maze* Reduction in sociability. ||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Poor|||From homozygous breeding|Yes|08-Dec-2014|Cryopreserved sperm|50.0|0.0|Unknown||Brinp3, Brinp2|Yes| 7805.0|DBC2 / DBC3 knockout|C57BL/6-Brinp2 Brinp3/PibMarpApb||Recessive|bone morphogenetic protein/retinoic acid inducible neural specific 3|Brinp3||B830045N13Rik, Fam5c|MGI:2443035|bone morphogenetic protein/retinoic acid inducible neural specific 3; targeted mutation 1.1, Phillip I Bird|Brinp3|MGI:5604620|1|||||||||||||||||||||||||||||DBC2 and DBC3 mice show behavioral phenotypes similar to DBC3 knockout mice. * Reduced anxiety in the elevated plus maze* Reduction in sociability. ||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Poor|||From homozygous breeding|Yes|08-Dec-2014|Cryopreserved sperm|||Unknown||Brinp3, Brinp2|Yes| 7810.0|R26CreER RARaRARg R26eYFP|B6.Cg-Gt(ROSA)26Sor RARa RARg Gt(ROSA)26Sor/Apb||Recessive|retinoic acid receptor, alpha|Rara|Nil|RARalpha1, RAR alpha 1|MGI:97856|retinoic acid receptor, alpha; targeted mutation 1, Pierre Chambon|Rara|MGI:1857622|11|||||||||||||||||transgene insertion 1, Douglas T Fearon|granzyme B|||||||||||In absence of tamoxifen cells are wildtype, when treated with tamoxifen loss of the vitamin A receptors, RARa and RARg occur, causing different phenotypes in distinct cell types.|Unknown|C57BL/6|Yes|Unknown|Unknown|Yes|Unknown|Unknown|No|Excellent|At least 10|||No|10-Dec-2014||0.0|0.0|Unknown|||Possibly| 7810.0|R26CreER RARaRARg R26eYFP|B6.Cg-Gt(ROSA)26Sor RARa RARg Gt(ROSA)26Sor/Apb||Recessive|gene trap ROSA 26, Philippe Soriano|Gt(ROSA)26Sor|Nil|beta geo, Gtrgeo26, Gtrosa26, R26, ROSA26|MGI:104735|gene trap ROSA 26, Philippe Soriano; targeted mutation 1, Frank Costantini|Gt(ROSA)26Sor|MGI:2449038|6|||||||||||||||||||||||||||||In absence of tamoxifen cells are wildtype, when treated with tamoxifen loss of the vitamin A receptors, RARa and RARg occur, causing different phenotypes in distinct cell types.|Unknown|C57BL/6|Yes|Unknown|Unknown|Yes|Unknown|Unknown|No|Excellent|At least 10|||No|10-Dec-2014||||Unknown|||Possibly| 7810.0|R26CreER RARaRARg R26eYFP|B6.Cg-Gt(ROSA)26Sor RARa RARg Gt(ROSA)26Sor/Apb||Recessive|gene trap ROSA 26, Philippe Soriano|Gt(ROSA)26Sor||beta geo, Gtrgeo26, Gtrosa26, R26, ROSA26|MGI:104735|gene trap ROSA 26, Philippe Soriano; targeted mutation 1, Tyler Jacks|Gt(ROSA)26Sor|MGI:3699244|6|||||||||||||||||||||||||||||In absence of tamoxifen cells are wildtype, when treated with tamoxifen loss of the vitamin A receptors, RARa and RARg occur, causing different phenotypes in distinct cell types.|Unknown|C57BL/6|Yes|Unknown|Unknown|Yes|Unknown|Unknown|No|Excellent|At least 10|||No|10-Dec-2014||||Unknown|||Possibly| 7810.0|R26CreER RARaRARg R26eYFP|B6.Cg-Gt(ROSA)26Sor RARa RARg Gt(ROSA)26Sor/Apb||Recessive|gene trap ROSA 26, Philippe Soriano|Gt(ROSA)26Sor||beta geo, Gtrgeo26, Gtrosa26, R26, ROSA26|MGI:104735|gene trap ROSA 26, Philippe Soriano; targeted mutation 1, Frank Costantini|Gt(ROSA)26Sor|MGI:2449038|6|||||||||||||||||||||||||||||In absence of tamoxifen cells are wildtype, when treated with tamoxifen loss of the vitamin A receptors, RARa and RARg occur, causing different phenotypes in distinct cell types.|Unknown|C57BL/6|Yes|Unknown|Unknown|Yes|Unknown|Unknown|No|Excellent|At least 10|||No|10-Dec-2014||||Unknown|||Possibly| 7806.0|DBC2 knockout|C57BL/6-Brinp2/PibMarpApb||Recessive|bone morphogenic protein/retinoic acid inducible neural-specific 2|Brinp2||6430517E21Rik, Fam5b, mKIAA1747|MGI:2443333|bone morphogenic protein/retinoic acid inducible neural-specific 2; targeted mutation 1.1, Phillip I Bird|Brinp2|MGI:5604615|1|||||||||||||||||||||||||||||Hyperactive.Mice have normal short-term memory, olfactory responses, pre-pulse inhibition, and motor learning.|Normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|||From hetrozygous breeding|No|08-Dec-2014|Cryopreserved sperm|50.0|0.0|Unknown|||Yes| 7803.0|p16f|C57BL/6-Cdkn2a/Apb||Recessive|cyclin-dependent kinase inhibitor 2A|Cdkn2a|Unknown|Arf, ARF-INK4a, Ink4a/Arf, INK4a-ARF, MTS1, p16, p16INK4a, p19ARF, p19, Pctr1|MGI:104738|cyclin-dependent kinase inhibitor 2A; targeted mutation 2.1, Norman E Sharpless|Cdkn2a|MGI:4835008|4|||||||||||||||||||||||||||||Normal|Normal|C57BL6/J|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|26-Nov-2014|Cryopreserved sperm|60.0|0.0|Unknown||melanoma, melanocyte, Ras|Possibly| 7807.0|ENU28:020:Usp37|C57BL/6NCrlAnu-Usp37/AnuApb|C57BL/6NCrlAnu-Usp37/AnuApb|Recessive|ubiquitin specific peptidase 37|Usp37|Unknown|4932415L06Rik, C330008N13Rik|MGI:2442483|ubiquitin specific peptidase 37; mutation 1, The Australian National University|Usp37|MGI:5648437|1|ENSMUSG00000033364|ENSMUST00000189257|Usp37-001|187|560|G to A|ENSMUSE00000393309|5|63|Arginine to STOP|||||TAAGTCATAACATTAAAAATGTGGTACTACGACCCAGTGGAATAAAACAAAGCCGCCTAAT||||||||||||||Embryonic lethal||C57BL/6NCrlAnu|No|No|Yes|No|No|Yes|No|Unknown||||No|08-Dec-2014|Cryopreserved sperm|51.0|0.0|Unknown||ENU, embryonic lethal|Yes| 7802.0| 14CreER|B6.CD1-Tg(KRT14-cre/ERT)20Efu/MarpApb||Recessive||||||||||||||||||||||||||transgene insertion 20, Elaine Fuchs|human keratin 14 (KRT14) promoter|||||||||||skin lesions, increased skin squamous cell carcinoma incidence, hyperkerotosis, parakerotosis, reddish skin, scaly skin||C57BL/6J|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|0|6||No|26-Nov-2014|Cryopreserved sperm|50.0|0.0|No||Keratin 76, tight junctions, CLDN1, inflammation, skin|Possibly| 7809.0|ENU26:042:Depdc5:B6:G4|C57BL/6NCrlAnu-Depdc5/AnuApb|C57BL/6NCrlAnu-Depdc5/AnuApb|Recessive|DEP domain containing 5|Depdc5|Unknown||MGI:2141101|DEP domain containing 5; mutation 1, The Australian National University|Depdc5|MGI:5648440|5|ENSMUSG00000037426|ENSMUST00000087897|Depdc5-001|510|979|G to T|ENSMUSE00000246481|10|170|Methionine to Isoleucine|||||AGGGTGGTGTTCCGTTCTACGTCGGCTATGGTTTACATATTTATTCAGATGAGCTGTGAAA||||||||||||||Unknown|Unknown|C57BL/6NCrlAnu|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown|1|3|Het x het |No|09-Dec-2014|Cryopreserved sperm|50.0|0.0|Unknown||ENU, mutagenesis, screen, random, Depdc5|Possibly| 9358.0||B6.C-H2-Kbm1 B6.129(Cg), B6.FVB(129), B10.BR (DBA-2) Gt(ROSA)26Sortm4(ACTB-tdTomato,-EGFP)Luo/J Tg(Alb1-cre)1Dlr/J Tg(Alb-H2-Kb)/Apb||Dominant|gene trap ROSA 26, Philippe Soriano|Gt(ROSA)26Sor|||MGI:104735|Gt(ROSA)26Sortm4(ACTB-tdTomato,-EGFP)|||6||||||||||||||||| Alb1-cre, Alb-H2-Kb|Albumin|||||||||||These mice result from the cross of 4 different mouse lines:mT/mG mice (From JAX labs Stock No. 007676)express ROSAmT/mG, a cell membrane-targeted, two-color fluorescent Cre-reporter allele. Prior to Cre recombination, cell membrane-localized tdTomato (mT) fluorescence expression is widespread in cells/tissues. Cre recombinase expressing cells (and future cell lineages derived from these cells) have cell membrane-localized EGFP (mG) fluorescence expression replacing the red fluorescence. Alb1-cre mice express a Cre recombinase transgene under control of Alb promoter/enhancer elements, thus restricted CoRe expression in all hepatocytes (Cre expression is also detected in the biliary epithelial cells in this mouse line). Alb-Kb mice express a transgenic H-2Kb under the control of the mouse albumin promoter, thus restricting H-2Kb expression to hepatocytes. Mice have been backcrossed and maintained on the H-2Kbm1 background |In these mice, all cells but hepatocytes and biliary epithelial cells express membrane tomato (red) while hepatocytes and bile ducts are GFP+ (green). H-2Kb expression is restricted to Hepatocytes. |C57Bl/6N|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|16-Mar-2022|Cryopreserved sperm|50.0|0.0|Unknown|||Possibly| 7256.0|APN275|C57BL/6N(Ag)-Katnb1MarpApb||Recessive|katanin p80 (WD40-containing) subunit B 1|Katnb1 ||2410003J24Rik, KAT |MGI:1921437 |katanin p80 (WD40-containing) subunit B 1; targeted mutation 1a, Helmholtz Zentrum Muenchen GmbH |Katnb1tm1a(EUCOMM)Hmgu|MGI:4436305|8|||||||||||||||||||||||||||||Unknown|Normal|C57Bl/6N|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|15-Jan-2013|Cryopreserved sperm|30.0|0.0|Unknown|||Possibly| 7808.0|ENU28:011:Etaa1|C57BL/6NCrlAnu-Etaa1/AnuApb|C57BL/6NCrlAnu-Etaa1/AnuApb|Recessive|Ewing tumor-associated antigen 1|Etaa1|Unknown|5730466H23Rik|MGI:1915395|Ewing tumor-associated antigen 1; mutation 1, Australian National University|Etaa1|MGI:6343404|11|ENSMUSG00000016984|ENSMUST00000076661|Etaa1-001||||||||17952576|2|||TCAAAATTCTCCAATGACAAAGCAGTTAGGTAATCTGTTGTTATTTTTATGTGGGTAGGT||||||||||||||Poor response to immunisation.Partial embryonic lethality||C57BL/6NCrlAnu|Yes|Unknown|Yes|Yes|Unknown|Yes|No|Unknown||||No|08-Dec-2014|Cryopreserved sperm|91.0|0.0|Unknown||ENU|Yes| 7814.0|SGSH Flox|C57Bl/6-Sgsh/LdruApb|ldru|Recessive|N-sulfoglucosamine sulfohydrolase (sulfamidase)|Sgsh|Normal|4632406A19Rik, sulphamidase|MGI:1350341||||11|||||||||||||||||||||||||||||Normal|Normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|0|6|brother X sister|No|15-Dec-2014|Cryopreserved sperm|50.0|0.0|Unknown||Flox, SGSH|Possibly| 7817.0|Transgenic Control|C57BL/6-Sgsh/LrduApb|ldru|Recessive|N-sulfoglucosamine sulfohydrolase (sulfamidase)|Sgsh|Unknown|4632406A19Rik, sulphamidase|MGI:1350341||||11|||||||||||||||||||||||||||||Expected to be normal|Expected to be normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|0|6|brother X sister|No|15-Dec-2014|Cryopreserved sperm|85.0|0.0|Unknown|||Possibly| 7781.0|203.4 ; cTnI-G203S.4|C57BL/6-Tg(Myh6-TNNI3*G203S)4Chs/Apb|MGI:3690014|Dominant||||||||||||||||||||||||||transgene insertion 4, Christopher Semsarian|cardiac specific mouse αMHC promoter (alpha myosin heavy chain)|83% of endogenous||||||||||Unknown|Mice develop cardiac phenotype - hypertrophic cardiomyopathy by 21 weeks of age. Left ventricular hypertrophy was observed on echocardiography, it was associated with a significant 4-fold increase in RNA markers of hypertrophy, ANF and BNP. Myocyte hypertrophy, myofiber disarray and interstitial fibrosis were observed. |C57BL/6|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Excellent||21|Transgenic x non-transgenic sibs|No|11-Nov-2014|Cryopreserved sperm|60.0|0.0|Yes|Hypertrophic cardiomyopathy (HCM) is a primary disorder of the myocardium characterized by cardiac hypertrophy. The clinical course of HCM is variable, with inter- and intra-familial variations ranging from benign asymptomatic disease to a malignant phenotype with a high risk of cardiac failure or sudden cardiac death.|Hypertrophy, Cardiomyopathy, Calcium, Troponin I gene|Yes| 7801.0|Krt76 tm1c x K14CreER|B6(Cg)-Krt76Tg(KRT14-Cre/ER)20Efu/MarpApb||Recessive|keratin 76|Krt76|Nil|2310001L23Rik|MGI:1924305||||15|||||||||||||||||transgene insertion 20, Elaine Fuchs|human keratin 14 (KRT14) promoter|||||||||||Unkempt, dull coats and smaller body size, scaling of skin of the tail, abnormal paw pad hyperpigmentation |Abnormal sebaceous gland morphology, abnormal hair cycle, abnormal epidermis stratum basale morphology, hyperkerotosis, parakerotosis|C57BL/6J|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|0|6||No|26-Nov-2014|Cryopreserved sperm|50.0|0.0|No||Keratin 76, tight junctions, CLDN1, inflammation, skin|Possibly| 8788.0|R26-CreER Srsf2 P95H/+ Tet2fl/fl|B6-Srsf2 Tet2 Gt(ROSA)26Sor/Apb||Recessive|serine/arginine-rich splicing factor 2|Srsf2||D11Wsu175e, MRF-1, SC35, Sfrs10, Sfrs2|MGI:98284|serine and arginine-rich splicing factor 2; targeted mutation 2874.1, TaconicArtemis|Srsf2|MGI:7408195|11|||||||||||||||||||||||||||||normal - require tamoxifen treatment to induce Cre activity and gene modification|normal - require tamoxifen treatment to induce Cre activity and gene modification|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|06-Sep-2019|Cryopreserved sperm|20.0|0.0|Yes|myelodysplastic syndromes (MDS) and MDS/myeloproliferative neoplasms (MPN||Yes| 8788.0|R26-CreER Srsf2 P95H/+ Tet2fl/fl|B6-Srsf2 Tet2 Gt(ROSA)26Sor/Apb||Recessive|tet methylcytosine dioxygenase 2|Tet2||Ayu17-449, E130014J05Rik, mKIAA1546|MGI:2443298|tet methylcytosine dioxygenase 2; targeted mutation 1.1, Iannis Aifantis|Tet2|MGI:5141120|3|||||||||||||||||||||||||||||normal - require tamoxifen treatment to induce Cre activity and gene modification|normal - require tamoxifen treatment to induce Cre activity and gene modification|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|06-Sep-2019|Cryopreserved sperm|||Yes|myelodysplastic syndromes (MDS) and MDS/myeloproliferative neoplasms (MPN||Yes| 8788.0|R26-CreER Srsf2 P95H/+ Tet2fl/fl|B6-Srsf2 Tet2 Gt(ROSA)26Sor/Apb||Recessive|gene trap ROSA 26, Philippe Soriano|Gt(ROSA)26Sor||beta geo, Gtrgeo26, Gtrosa26, R26, ROSA26, Thumpd3as1|MGI:104735|gene trap ROSA 26, Philippe Soriano; targeted mutation 1, Frank Costantini|Gt(ROSA)26Sor|MGI:2449038|6|||||||||||||||||||||||||||||normal - require tamoxifen treatment to induce Cre activity and gene modification|normal - require tamoxifen treatment to induce Cre activity and gene modification|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|06-Sep-2019|Cryopreserved sperm|||Yes|myelodysplastic syndromes (MDS) and MDS/myeloproliferative neoplasms (MPN||Yes| 7811.0|MIP 1alpha|B6.129P2-Ccl3/J||Recessive|chemokine (C-C motif) ligand 3|Ccl3|Nil|CCL3, G0S19-1, LD78alpha, macrophage inflammatory protein-1alpha, Mip1a, MIP1-(a), MIP-1alpha, MIP-1 alpha, MIP1-alpha, Scya3|MGI:98260|chemokine (C-C motif) ligand 3; targeted mutation 1, University of North Carolina|Ccl3|MGI:1857243|11|||||||||||||||||||||||||||||Mice homozygous for the Ccl3 (chemokine [C-C motif] ligand 3) (also known as macrophage inflammatory protein 1a, Mip1a or Scya3) knock-out mutation are viable and fertile. Homozygous mutant mice are resistant to Coxsakievirus-induced myocarditis. Mutant mice infected with influenza virus show reduced pneumonitis and delayed clearance of virus. There are no overt hematopoietic abnormalities. Bone remodeling induced by mechanical loading during orthodontic tooth movement was significantly decreased in Ccl3tm1Unc mice. Compared to wild-type mice liver fibrosis was reduced upon treatment with either carbon tetrachloride or methionine- and choline-deficient diets to induce fibrosis. Melanoma growth is augmented and lung metastasis is enhanced in these knock-out mice. With renal cell carcinoma, however, the number of metastasis foci in the lung is reduced, and intra-tumoral neovascularization, an indispensable process for metastasis, is attenuated in these gene-deficient mice. These mice can be useful in studies of chemokine receptors in inflammatory diseases.|Unknown|C57BL/6J|Yes|Yes|Unknown|Yes|Yes|Unknown|No|Good||13|Brother x sister|No|10-Dec-2014|Cryopreserved sperm|49.0|0.0|Unknown||Ccl3, Mip1a, virus, infection|No| 7819.0|Ctss KO:MHC II KO|B6NCrl;129-Ctss H2/AnuApb||Recessive|cathepsin S|Ctss|Nil|Cat S|MGI:107341|cathepsin S; targeted mutation 1, Harold A Chapman|Ctss|MGI:2182133|3||||||||||||||||Yes|||||||||||||Defective CD4 T cell response and humoral responses, but no overt immunodeficiency. Homozygous null mice are resistant to the development of experimental autoimmune myasthenia gravis and showed reduced T and B cell responses to acetylcholine receptor.||C57BL/6NCrlAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|03-Jan-2015|Cryopreserved sperm|10.0|0.0|Unknown||T cell, MHC class II, cysteine proteinase, Humoral resposne, arthritis, germinal centre|Yes| 7819.0|Ctss KO:MHC II KO|B6NCrl;129-Ctss H2/AnuApb||Recessive|histocompatibility-2, MHC|H2||H-2, MHC-II|MGI:95894|histocompatibility-2, MHC; targeted deletion, H2 complex|H2|MGI:2658725|17|||||||||||||||||||||||||||||Defective CD4 T cell response and humoral responses, but no overt immunodeficiency. Homozygous null mice are resistant to the development of experimental autoimmune myasthenia gravis and showed reduced T and B cell responses to acetylcholine receptor.||C57BL/6NCrlAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|03-Jan-2015|Cryopreserved sperm|||Unknown||T cell, MHC class II, cysteine proteinase, Humoral resposne, arthritis, germinal centre|Yes| 7822.0|ENU15NIH:085:a:B6:BC8|B6(Cg)-Sppl2a/AnuApb|B6(Cg)-Sppl2a/AnuApb|Recessive|signal peptide peptidase like 2A|Sppl2a|Unknown|2010106G01Rik, C130089K23Rik|MGI:1913802 |signal peptide peptidase like 2A; mutation 1, The Australian National University|Sppl2a|MGI:5432126|2|ENSMUSG00000027366|ENSMUST00000028844|2010106G01Rik-001||||||||126746052|7|||ATTCATAGGATGCCATGTGGACAGTGCACGTACGTATCTGTTAGCCTATGATGCAATTAG||||||||||||||Decreased number of B cells.Very low expression of IgD on the IgM subset of mature B cells.25-fold less serum IgM.6-fold less serum IgG1.Almost no specific antibody was made after immunization with formalin-inactivated and heat-killed Bordetella pertussis and alum-precipitated chicken gamma globulin (CGG) coupled to p-azobenzenearsonate (ABA) hapten or after immunization with the T-independent antigen 4-hydroxy-3-nitrophenylacetyl-Ficoll (NP-Ficoll.Normal numbers of pro-B, pre-B, and immature B cells, and normal cell surface IgM and normal onset of IgD expression among the IgM T1 subset.Mature IgD<+>IgM recirculating B cells were selectively decreased in the bone marrow and had very low surface IgD. In the spleen, the T1 subset of recent bone marrow emigrants (CD93<+>IgMCD23<−>) was present in normal numbers and expressed levels of surface IgM comparable with controls.Subsequent maturational stages of T2, T3, and mature CD93<−>IgM B cells were 20-fold reduced, whereas the mature marginal zone B cell subset was decreased 200-fold. Immunofluorescent staining of spleen sections showed that the residual B cells in SPPL2A-deficient mice nevertheless localized normally in primary follicles.Sppl2a<−/−> mice had fewer CD11c<+> DCs as the result of only 12% of normal numbers in the CD4<+> and the CD4<−>CD8<−> double-negative (DN) DC subsets, whereas CD8<+> and plasmacytoid DCs were present at normal and increased numbers, respectively. Less CD11c and CD8 was present on the B220<−>CD8<+> DCs in Sppl2a<−/−> animals.|Normal|C57BL/6JAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|8|||No|03-Jan-2015|Cryopreserved sperm|55.0|0.0|Unknown||lymphocyte, B cell, IgD, ENU, immunoglobulin|No| 7824.0|Dimit; ENU13NIH:039ab|B6(Cg)-Ighd/AnuApb|B6(Cg)-Ighd/AnuApb|Recessive|immunoglobulin heavy constant delta|Ighd|Unknown|IgD|MGI:96447|dimit|Ighd|MGI:4819235|12|ENSMUSG00000076616|ENSMUST00000103424|Igh-5-201|241|241|T to A|ENSMUSE00000663372|1|74|Isoleucine to Lysine|||||CAGAACTGAACCTCAACCACACTTGCACCATAAATAAACCCAAAAGGAAAGAAAAACCTTT|Yes|||||||||||||Shifted IgD expression measured by flow cytometry||C57BL/JAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|03-Jan-2015||0.0|0.0|Unknown||IgD, immunoglobulin, B cell, ENU, NIH|Yes| 7820.0| ENU15NIH:085:CD74KO:MHCIIKO:G3|C57BL/6JAnu-Cd74 H2 Sppl2a/AnuApb||Recessive|signal peptide peptidase like 2A|Sppl2a|Unknown|2010106G01Rik, C130089K23Rik|MGI:1913802 |signal peptide peptidase like 2A; mutation 1, The Australian National University|Sppl2a|MGI:5432126|2|ENSMUSG00000027366|ENSMUST00000028844|2010106G01Rik-001||||||||126746052|7|||ATTCATAGGATGCCATGTGGACAGTGCACGTACGTATCTGTTAGCCTATGATGCAATTAG|||||||||||||||Normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|03-Jan-2015|Cryopreserved sperm|20.0|0.0|Unknown||lymphocyte, B cell, IgD, ENU, immunoglobulin|Possibly| 7820.0| ENU15NIH:085:CD74KO:MHCIIKO:G3|C57BL/6JAnu-Cd74 H2 Sppl2a/AnuApb||Recessive|CD74 antigen (invariant polypeptide of major histocompatibility complex, class II antigen-associated)|Cd74|Nil|CLIP, Ii|MGI:96534|CD74 antigen (invariant polypeptide of major histocompatibility complex, class II antigen-associated); targeted mutation 1, Elizabeth Bikoff|Cd74|MGI:1927530|18||||||||||||||||||||||||||||||Normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|03-Jan-2015|Cryopreserved sperm|||Unknown||lymphocyte, B cell, IgD, ENU, immunoglobulin|Possibly| 7820.0| ENU15NIH:085:CD74KO:MHCIIKO:G3|C57BL/6JAnu-Cd74 H2 Sppl2a/AnuApb||Recessive|histocompatibility-2, MHC|H2|Nil|H-2, MHC-II|MGI:95894|histocompatibility-2, MHC; targeted deletion, H2 complex|H2|MGI:2658725|17||||||||||||||||||||||||||||||Normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|03-Jan-2015|Cryopreserved sperm|||Unknown||lymphocyte, B cell, IgD, ENU, immunoglobulin|Possibly| 7821.0|ENU15NIH:085:Cd19-cre:Ikk2ca-Tg:G2|C57BL/6JAnu-Cd19 Gt(ROSA)26Sor Sppl2a/AnuApb||Recessive|signal peptide peptidase like 2A|Sppl2a|Unknown|2010106G01Rik, C130089K23Rik|MGI:1913802 |signal peptide peptidase like 2A; mutation 1, The Australian National University|Sppl2a|MGI:5432126|2|ENSMUSG00000027366|ENSMUST00000028844|2010106G01Rik-001||||||||126746052|7|||ATTCATAGGATGCCATGTGGACAGTGCACGTACGTATCTGTTAGCCTATGATGCAATTAG|||||||||||||||Normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|03-Jan-2015|Cryopreserved sperm|10.0|0.0|Unknown||lymphocyte, B cell, IgD, ENU, immunoglobulin|Possibly| 7821.0|ENU15NIH:085:Cd19-cre:Ikk2ca-Tg:G2|C57BL/6JAnu-Cd19 Gt(ROSA)26Sor Sppl2a/AnuApb||Recessive|CD19 antigen|Cd19|||MGI:88319|targeted mutation 1, University of Cologne|Cd19|MGI:1931143|7||||||||||||||||||||||||||||||Normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|03-Jan-2015|Cryopreserved sperm|||Unknown||lymphocyte, B cell, IgD, ENU, immunoglobulin|Possibly| 7821.0|ENU15NIH:085:Cd19-cre:Ikk2ca-Tg:G2|C57BL/6JAnu-Cd19 Gt(ROSA)26Sor Sppl2a/AnuApb||Recessive|gene trap ROSA 26, Philippe Soriano|Gt(ROSA)26Sor||beta geo, Gtrgeo26, Gtrosa26, R26, ROSA26|MGI:104735|gene trap ROSA 26, Philippe Soriano; targeted mutation 4, Klaus Rajewsky|Gt(ROSA)26Sor|MGI:3687199|6||||||||||||||||||||||||||||||Normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|03-Jan-2015|Cryopreserved sperm|||Unknown||lymphocyte, B cell, IgD, ENU, immunoglobulin|Possibly| 7827.0|Otop1|B6.Cg-Otop1/JAusb||Recessive|otopetrin 1|Otop1|Unknown|A530025J20Rik, tlt|MGI:2388363|otopetrin 1; tilted|Otop|MGI:1856638|5|||||||||||||||||||||||||||||Impaired swimming:• when dropped into a tank of water, most homozygous mice spiral immediately downward and require rescuing• a small number of homozygotes could keep the nose but not the tail out of water; a few others could sometimes find the water surface but occasionally required rescuingHead tilt:• observed in 50-75% of homozygous miceHearing/vestibular/ear phenotype:Normal:• mice do not appear to have any hearing loss; ABR threshold determination shows similar levels compared to controls for all sound pressure levels tested• histological analysis shows a grossly normal appearance of the middle ear and the bony and membranous labyrinths• the sensory epithelia and otoconial membranes appear similar to controls; the otolithic membrane is visible over the surface of the maculae and there is no significant difference in the density of hair cells in the saccular and utricular maculae• the cochlear duct, including the sensory and supporting cells, cochlear nerve fibers and the tectorial membrane all appear similar to controlsAbsent otoliths:• complete absence of otoconia from the saccule and the utricle is observed at 3-5 weeks of age as well as E17.5 and newborn homozygous mice• in the rare mice that show a partial ability to swim, either otoconia are completely absent, or one or more giant otoconia are seen in the sacculeAbsent linear vestibular evoked potential:• absent vestibular nerve compund action potentials in response to linear acceleration at 9 and 16 pulses/sAbnormal vestibular ganglion morphology:• morphometric analysis of the total vestibular ganglion volume and total cellular volume shows that mutants have reduced levels and developed slower than controls in the first 12 days of postnatal life||C57BL/6J|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|04-Jan-2015||0.0|0.0|Unknown||Balance, head, vestibular|Possibly| 9053.0|R26-LSL-Adar1p110|C57BL/6-Gt(ROSA)26Sor/CwaApb ||Recessive|gene trap ROSA 26, Philippe Soriano|Gt(ROSA)26Sor||Gtrgeo26, Gtrosa26, R26, ROSA26|MGI:104735|C57BL/6-Gt(ROSA)26Sor/CwaApb|||6||||||||||Unknown to Unknown|||||||Adenosine Deaminase RNA specific|R26 endogenous|Moderate to low||||||||||Normal - Lox-stop-lox KI of Adar1p110 into Rosa26 locus; requires Cre to express|Normal - Lox-stop-lox KI of Adar1p110 into Rosa26 locus; requires Cre to express|C57Bl/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|Unknown||Unknown|No|06-Aug-2020|Cryopreserved sperm|40.0|0.0|No||Adenosine Deaminase RNA specific, Stress, anti-apoptotic, p110|No| 7830.0|MH2-403|FVB-Tg(tetO7-hCMVmin-aMHCR403Q)1Rmgr/VccriApb||Dominant||||||||||||||||||||||||||tetO7-hCMVmin-aMHCR403Q|tetO7-hCMVmin|||||||||||Unknown|Normal|FVB/n|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Excellent|more than 10|N/A|FVB/n female x hemizygous MH2-403 male|No|13-Jan-2015|Cryopreserved sperm|70.0|0.0|Unknown|||Possibly| 8785.0|Ap2a2 floxed|C57BL/6N-Ap2a2/MarpApb||Recessive|adaptor-related protein complex 2, alpha 2 subunit|Ap2a2||2410074K14Rik, Adtab, alpha-adaptin C, alpha-C adaptin, L25|MGI:101920||||7|||||||||||||||||||||||||||||Although Ap2a2 deletion had onlyminor effects on glycaemic control, it led to substantial impairment in b-adrenergic activation of lipolysis, as evidencedby a loss of cAMPresponse,PKAactivation, andglycerol/fattyacidrelease. These differenceswere related to increased cell surface localization of the b2- and b3-ARs. Lipolytic defects were accompanied by impaired WY-mediated loss of fat mass and whole-body fat oxidation.|Normal|C57BL/6N|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|06-Sep-2019|Cryopreserved sperm|50.0|0.0|Unknown||Lipolysis, adipose, PPARα|Yes| 7831.0|tTA|FVB.Cg-Tg(Myh6-tTA)6Smbf/VccriApb||Dominant||||||||||||||||||||||||||transgene insertion 6, Section of Myocardial Biology - Fishman Lab|rat Myh6 promoter|||||||||||Unknown|Normal|FVB/n|Unknown|Unknown|Yes|Unknown|Unknown|Unknown|No|Excellent|more than 10|N/A|FVB/n male x hemizygous tTA female|No|13-Jan-2015|Cryopreserved sperm|50.0|0.0|Unknown||tet|Possibly| 7832.0|C57BL/6-Nabp2-KO|C57BL/6J-Nabp2/QimrApb|Already registered |Recessive|nucleic acid binding protein 2|Nabp2|Nil|Ssb1; Obfc2b, 2610036N15Rik|MGI:1917167|Nuceic Acid Binding Protein 2; targeted mutation 1.2; Kum Kum Khanna|Nabp2-tm1.2Kkha|MGI:5502335|10|||||||||||||||||||||||||||||Homozygous Nabp2-/- offspring die perinatally from respiratory distress at birth due to aberrant ossification of the ribcage. Nabp2-/- embryos also exhibit skeletal malformations of the craniofacial skeleton, limb outgrowth defects and oligodactyly of the hindlimb. |Heterozygotes are viable and fertile. |C57BL/6|No|No|Yes|No|No|Yes|No|Good|||Heterozygous X Heterzyous or Heterozygous x Wild-type|No|15-Jan-2015|Cryopreserved sperm|50.0|0.0|Unknown||SSB, DNA repair, Skeletal Development|Yes| 7834.0|Il15 KO|B6(Cg)-IL15/AnuApb||Recessive|interleukin 15|Il15|Nil|IL-15|MGI:103014|targeted mutation 1, Immunex Research and Development Corporation|Il15|MGI:2136897|8||||||||||||||||Yes|||||||||||||Mice homozygous for disruptions of this gene have normal life spans but display a variety of immune system abnormalities and maternal placental defects.These mutant mice lack NK cells and have marked reductions in memory CD8+ T cells, NK 1.1 T cells and Thy-CD8a intraepithelial lymphocytes. Mice are unable to mount a protective immune response to challenge with vaccinia virus.Abnormal immune system morphology.Abnormal dendritic cell morphology/development:* lower numbers of splenic dendritc cells after Plasmodium chabaudi infection.Abnormal lymphocyte morphology/development:* Intestinal intraepithelial lymphocytes maturing outside of the thymus greatly reduced in numbers.Abnormal CD8+ T cell morphology/development:* two fold reduction in numbers of CD8 single positive cells in spleen and lymph nodes.Abnormal NK cell morphology/development:* reduced numbers of natural killer cells in thymus liver and spleen.* absent in uterusSmall lymph nodes: peripheral lymph nodes significantly lower in weight.Abnormal immune system physiology:Defective NK cell cytolysis: significantly reduced cytolytic activityabnormal immune serum protein physiology.Decreased immunoglobulin concentration:* lower levels of malaria specific antibodies producedlower levels of total immune globulin.Decreased IgG level: decreased levels of IgG1, IgG2a, IgG2b, and IgG3 after Plasmodium infection.Decreased IgM level: after plasmodium infection.Abnormal cytokine physiology.Abnormal interferon physiology: reduced production of IFN gamma by NK cells.Abnormal interleukin physiology:* reduced Il12 production by dendritic cells after Plasmodium infection.Altered susceptibility to infection.Decreased susceptibility to bacterial infection.* Improved survival after infection with Listeria monocytogenesincreased susceptibility to parasitic infection.* parasitemia higher but only minor effect on mortalityincreased susceptibility to viral infection.* dead by day 9 after Vaccinia infection* very susceptible to HSV-2 infectionDecreased susceptibility to type IV hypersensitivity reaction: no contact hypersensitivity* T mediated effects delayed but not B cell activation or antibody production.||C57BL/6NCrlAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|5||brother x sister mating|No|25-Jan-2015|Cryopreserved sperm|22.0|0.0|Unknown||T cell, infection, Natural killer cell, memory|Yes| 7833.0||C57BL/6-Klf5/Apb||Dominant|Kruppel-like factor 5|Klf5||4930520J07Rik, Bteb2, CKLF, IKLF|MGI:1338056||||14|||||||||||||||||||||||||||||Normal|Normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|10|||No|23-Jan-2015|Cryopreserved sperm|80.0|0.0|No||signal transduction, proliferation|No| 7836.0|Louise:TCR:Ly5a::N12|C57BL/6JSfdAnu-Tg(TLK2mHEL)2Ccg TCR:Ly5a::N12 /AnuApb||Dominant||||||||||||||||||||||||||transgene insertion 2, Christopher C Goodnow|rat thyroglobulin|expression limited to thyroid|Ly5a||||||||Unknown|Express low levels of membrane bound HEL in thyroid. Low serum levels of HEL detected.||C57BL/6JStdAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||5|sib x sib|No|25-Jan-2015|Cryopreserved sperm|22.0|0.0|Unknown||autoimmunity, B cell, tolerance, Hen egg lysozyme (HEL), T cell|Yes| 7836.0|Louise:TCR:Ly5a::N12|C57BL/6JSfdAnu-Tg(TLK2mHEL)2Ccg TCR:Ly5a::N12 /AnuApb||Dominant||||||||||||||||||||||||||tcr||||||||||||Express low levels of membrane bound HEL in thyroid. Low serum levels of HEL detected.||C57BL/6JStdAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||5|sib x sib|No|25-Jan-2015|Cryopreserved sperm|||Unknown||autoimmunity, B cell, tolerance, Hen egg lysozyme (HEL), T cell|Yes| 7837.0|Vavbcl69|C57BL/6-Tg(Vav-BCL2)1Jad/WehiAnuApb||Semi-dominant||||||||||||||||||||||||||transgene insertion 1, Jerry M Adams|mouse Vav promoter|Overexpression||||||||||Abnormal lymphocyte cell number:*The ratio of CD4 cells per B cell is 25% to 50% lower than in wild-type mice. Increased B cell number: *5-fold higher in the spleen at 18 weeks. Increased T cell number: *Mice exhibit higher splenic T cell numbers than in wild-type and Tg(BCL2)22Wehi or Tg(BCL2)36Wehi mice. Increased CD4-positive T cell number: *The increase in CD4+ T cells is greater than the increase in CD8+ T cells. Increased CD8-positive T cell number: *The increase in CD4+ T cells is greater than the increase in CD8+ T cells.Abnormal class switch recombination:*The total number of B cells that undergo class switching is 50-fold higher than in wild-type mice.Abnormal somatic hypermutation frequency:*22 of 23 clones isolated from class-switching cells harbor on average about 6 somatic mutations compared to in wild-type cells where no mutations are found.Enlarged spleenAbnormal spleen germinal center morphology:*Mice exhibit a larger pool of cycling B cells with a germinal center phenotype than in wild-type mice.*At 18 weeks, mice exhibit an increased in germinal center size and number compared to in wild-type mice.*However, expansion of germinal centers is dependent on CD4 T cell help. Increased spleen germinal center number: *At 18 weeks. Increased spleen germinal center size: *At 18 weeks.Enlarged lymph nodesGlomerulonephritis:*At 40 weeks, 15% to 25% of mice develop autoimmune glomerulonephritis.Increased tumor incidence:*12% of mice develop plasma cell tumors. Increased lymphoma incidence: *Less than 10% of mice develop lymphoblastic lymphomas. B cell derived lymphoma: *Less than 10% of mice develop large cell B lymphomas. Follicular lymphoma: *At 18 months, 37% to 50% of mice develop monoclonal follicular lymphoma. Increased histiocytic sarcoma incidence: *In less than 10% of mice. Thymic lymphoma: *In less than 10% of mice.Abnormal renal glomerular capsule:*Bowman epithelium proliferates to form crescents in the most advanced cases.Abnormal renal glomerulus morphology:*Mice develop hypercellular glomeruli that contain amorphous, eosinophilic deposits.*Most capillaries are no longer patent.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|25-Jan-2015|Cryopreserved sperm|66.0|0.0|Unknown||Bcl-2, Hematopoietic system|Yes| 7838.0||VavBcl2:CD11c-DTR:::F1||Semi-dominant||||||||||||||||||||||||||transgene insertion 1, Jerry M Adams|mouse Vav promoter|Overexpression||||||||||Abnormal lymphocyte cell number:*The ratio of CD4 cells per B cell is 25% to 50% lower than in wild-type mice. Increased B cell number: *5-fold higher in the spleen at 18 weeks. Increased T cell number: *Mice exhibit higher splenic T cell numbers than in wild-type and Tg(BCL2)22Wehi or Tg(BCL2)36Wehi mice. Increased CD4-positive T cell number: *The increase in CD4+ T cells is greater than the increase in CD8+ T cells. Increased CD8-positive T cell number: *The increase in CD4+ T cells is greater than the increase in CD8+ T cells.Abnormal class switch recombination:*The total number of B cells that undergo class switching is 50-fold higher than in wild-type mice.Abnormal somatic hypermutation frequency:*22 of 23 clones isolated from class-switching cells harbor on average about 6 somatic mutations compared to in wild-type cells where no mutations are found.Enlarged spleenAbnormal spleen germinal center morphology:*Mice exhibit a larger pool of cycling B cells with a germinal center phenotype than in wild-type mice.*At 18 weeks, mice exhibit an increased in germinal center size and number compared to in wild-type mice.*However, expansion of germinal centers is dependent on CD4 T cell help. Increased spleen germinal center number: *At 18 weeks. Increased spleen germinal center size: *At 18 weeks.Enlarged lymph nodesGlomerulonephritis:*At 40 weeks, 15% to 25% of mice develop autoimmune glomerulonephritis.Increased tumor incidence:*12% of mice develop plasma cell tumors. Increased lymphoma incidence: *Less than 10% of mice develop lymphoblastic lymphomas. B cell derived lymphoma: *Less than 10% of mice develop large cell B lymphomas. Follicular lymphoma: *At 18 months, 37% to 50% of mice develop monoclonal follicular lymphoma. Increased histiocytic sarcoma incidence: *In less than 10% of mice. Thymic lymphoma: *In less than 10% of mice.Abnormal renal glomerular capsule:*Bowman epithelium proliferates to form crescents in the most advanced cases.Abnormal renal glomerulus morphology:*Mice develop hypercellular glomeruli that contain amorphous, eosinophilic deposits.*Most capillaries are no longer patent.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|25-Jan-2015|Cryopreserved sperm|33.0|0.0|Unknown||Bcl-2, Hematopoietic system|Yes| 7838.0||VavBcl2:CD11c-DTR:::F1||Semi-dominant||||||||||||||||||||||||||CD11c -DTR||||||||||||Abnormal lymphocyte cell number:*The ratio of CD4 cells per B cell is 25% to 50% lower than in wild-type mice. Increased B cell number: *5-fold higher in the spleen at 18 weeks. Increased T cell number: *Mice exhibit higher splenic T cell numbers than in wild-type and Tg(BCL2)22Wehi or Tg(BCL2)36Wehi mice. Increased CD4-positive T cell number: *The increase in CD4+ T cells is greater than the increase in CD8+ T cells. Increased CD8-positive T cell number: *The increase in CD4+ T cells is greater than the increase in CD8+ T cells.Abnormal class switch recombination:*The total number of B cells that undergo class switching is 50-fold higher than in wild-type mice.Abnormal somatic hypermutation frequency:*22 of 23 clones isolated from class-switching cells harbor on average about 6 somatic mutations compared to in wild-type cells where no mutations are found.Enlarged spleenAbnormal spleen germinal center morphology:*Mice exhibit a larger pool of cycling B cells with a germinal center phenotype than in wild-type mice.*At 18 weeks, mice exhibit an increased in germinal center size and number compared to in wild-type mice.*However, expansion of germinal centers is dependent on CD4 T cell help. Increased spleen germinal center number: *At 18 weeks. Increased spleen germinal center size: *At 18 weeks.Enlarged lymph nodesGlomerulonephritis:*At 40 weeks, 15% to 25% of mice develop autoimmune glomerulonephritis.Increased tumor incidence:*12% of mice develop plasma cell tumors. Increased lymphoma incidence: *Less than 10% of mice develop lymphoblastic lymphomas. B cell derived lymphoma: *Less than 10% of mice develop large cell B lymphomas. Follicular lymphoma: *At 18 months, 37% to 50% of mice develop monoclonal follicular lymphoma. Increased histiocytic sarcoma incidence: *In less than 10% of mice. Thymic lymphoma: *In less than 10% of mice.Abnormal renal glomerular capsule:*Bowman epithelium proliferates to form crescents in the most advanced cases.Abnormal renal glomerulus morphology:*Mice develop hypercellular glomeruli that contain amorphous, eosinophilic deposits.*Most capillaries are no longer patent.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|25-Jan-2015|Cryopreserved sperm|||Unknown||Bcl-2, Hematopoietic system|Yes| 7835.0|Foxp3-gfp:kk:TCR:N12|B6.B10.BR-H2 Foxp3 Tg(TcrHEL3A9)1Mmd/AnuApb||Recessive|forkhead box P3|Foxp3|Normal|JM2, scurfin|MGI:1891436|targeted mutation 2, Alexander Y Rudensky|Foxp3|MGI:3574964|X||||||||||||||||No|transgene insertion 1, Mark M Davis|||histocompatibility-2, MHC|H2||H-2, MHC-II|MGI:95894|Histocompatibility-2, MHC; k variant|H2|MGI:3579322|17|Normal. Cells expressing FoxP3 fluoresce green, predominantly T cells.T cell express T cell receptor alpha and beta (Tcra and Tcrb, respectively) chains from the hen egg lysozyme (HEL)-specific T cell hybridoma 3A9||129 x C57BL/6 x C57BL10.BR|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|25-Jan-2015|Cryopreserved sperm|23.0|0.0|Unknown||T cell, IL-2, GFP, transcription factor|Yes| 7828.0|TetO ET/TC, B6-tetO-ChR2/ETTC KI |B6.Cg-Actb ||Dominant|actin, beta|Actb||Actx, A-X actin-like protein, beta-actin, E430023M04Rik|MGI:87904||||5|||||||||||||||||||||||||||||Normal|Normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|07-Jan-2015|Cryopreserved sperm|50.0|0.0|Unknown||Channelrhodopsin2, MCH neuron|Yes| 7842.0|Foxo1-flox|B6.129-Foxo1/AnuApb||Recessive|forkhead box O1|Foxo1|Normal|Afxh, FKHR, Fkhr1, Foxo1a|MGI:1890077|forkhead box O1; targeted mutation 1, Richard A Flavell|Foxo1|MGI:3840910|3|||||||||||||||||||||||||||||Normal||C57BL/6JAnu|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|05-Feb-2015|Cryopreserved sperm|22.0|0.0|Unknown||T cell, transcription|Possibly| 7845.0|Foxp3-gfp:kk:N12|B6.B10.BR-H2 Foxp3/AnuApb||Recessive|forkhead box P3|Foxp3|Normal|JM2, scurfin|MGI:1891436|targeted mutation 2, Alexander Y Rudensky|Foxp3|MGI:3574964|X||||||||||||||||No||||histocompatibility-2, MHC|H2||H-2, MHC-II|MGI:95894|histocompatibility-2, MHC; k variant|H2|MGI:3579322|17|Normal. Cells expressing FoxP3 fluoresce green, predominantly T cells||129 x C57BL/6 x C57BL10.BR|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|19-Feb-2015|Cryopreserved sperm|66.0|0.0|Unknown||T cell, IL-2, GFP, transcription factor|Yes| 7841.0|ENU32:G3|ANU:ENU32:G3||Recessive|Unknown||||||||Unknown||||||||||||||||Unknown|||||||||||||Unknown|Unknown|C57BL/6NCrlAnu|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||1||No|02-Feb-2015|Cryopreserved sperm|296.0|0.0|Unknown||ENU, random, mutagenesis, screen|Yes| 7843.0|CD11c-DTR|B6.Cg-Tg(Itgax-DTR/EGFP)57Lan/AnuApb||Semi-dominant||||||||||||||||||||||||||transgene insertion 57, Richard A Lang|mouse Itgax promoter (CD11c)|||||||||||||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|16-Feb-2015|Cryopreserved sperm|33.0|0.0|Unknown||Cytotoxic T lymphocytes (CTL) , Dentritic cells|Yes| 8787.0|hScl-CreER R26eYFP Srsf2P95H/+|B6-Srsf2 Gt(ROSA)26Sor Tg(Tal1-cre/ERT)42-056Jrg/Apb||Recessive|serine/arginine-rich splicing factor 2|Srsf2||D11Wsu175e, MRF-1, SC35, Sfrs10, Sfrs2|MGI:98284|serine and arginine-rich splicing factor 2; targeted mutation 2874.1, TaconicArtemis|Srsf2|MGI:7408195|11|||||||||||||||||transgene insertion 42-056, Joachim R Gothert||||||||||||"normal" - requires tamoxifen treatment to induce Srsf2 mutation to heterozygosity|"normal" - requires tamoxifen treatment to induce Srsf2 mutation to heterozygosity|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|06-Sep-2019|Cryopreserved sperm|41.0|0.0|Yes|myelodysplastic syndromes (MDS) and MDS/myeloproliferative neoplasms (MPN)||Yes| 8787.0|hScl-CreER R26eYFP Srsf2P95H/+|B6-Srsf2 Gt(ROSA)26Sor Tg(Tal1-cre/ERT)42-056Jrg/Apb||Recessive|gene trap ROSA 26, Philippe Soriano|Gt(ROSA)26Sor|Unknown|beta geo, Gtrgeo26, Gtrosa26, R26, ROSA26, Thumpd3as1|MGI:104735|gene trap ROSA 26, Philippe Soriano; targeted mutation 1, Frank Costantini|Gt(ROSA)26Sor|MGI:2449038|6|||||||||||||||||||||||||||||"normal" - requires tamoxifen treatment to induce Srsf2 mutation to heterozygosity|"normal" - requires tamoxifen treatment to induce Srsf2 mutation to heterozygosity|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|06-Sep-2019|Cryopreserved sperm|||Yes|myelodysplastic syndromes (MDS) and MDS/myeloproliferative neoplasms (MPN)||Yes| 7844.0|gzmK ko|B6(Cg)-Gzmk Tg(CMV-Cre)/MarpApb||Recessive|Granzyme K|Gzmk|Reduced||MGI:1298232||||13|||||||||||||||||transgene insertion 1, University of Cologne||||||||||||unknown|unknown|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|17-Feb-2015|Cryopreserved sperm|77.0|0.0|Unknown|||Possibly| 7847.0|Foxp3-gfp:kk:Arjuna:N12|B6.B10.BR-H2 Foxp3 Tg(ILK3mHEL)3Ccg/AnuApb||Recessive|forkhead box P3|Foxp3|Normal|JM2, scurfin|MGI:1891436|targeted mutation 2, Alexander Y Rudensky|Foxp3|MGI:3574964|X||||||||||||||||No|transgene insertion 3, Christopher C Goodnow|Rat insulin promoter|Expression of the inserted sequence specifically to pancreatic islet beta cells|histocompatibility-2, MHC|H2||H-2, MHC-II|MGI:95894|histocompatibility-2, MHC; k variant|H2|MGI:3579322|17|Normal. Cells expressing FoxP3 fluoresce green, predominantly T cells.Islet cells express HEL on cell surface.||129 x C57BL/6 x C57BL10.BR|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|19-Feb-2015||0.0|0.0|Unknown||T cell, IL-2, GFP, transcription factor|Yes| 4713.0|Rolex/C57|B6.129-Hccs/MarpApb||X-linked|holocytochrome c synthetase|Hccs|Unknown||MGI:106911|targeted mutation 1, Timothy C Cox|Hccs|MGI:3826866|X||||||||||||||||Yes|||||||||||||NormalHomozygous female or hemizygous males for a conditional allele activated in the heart exhibit fetal lethality associated with abnormal fetal cardiomyocyte morphology and physiology.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|08-Apr-2009|Cryopreserved sperm|100.0|0.0|Unknown||cardiac, midgestation, mitochondria|Yes| 4868.0|FxyC57|B6.129-Mid1/MarpApb||X-linked|midline 1|Mid1|Nil|61B3-R, DXHXS1141, Fxy, Trim18|MGI:1100537|midline 1; targeted mutation 1, Alan Ashworth|Mid1|MGI:5562687|X|||||||||||||||||||||||||||||Viable. Reduced / delayed fertility. Litter size may be slightly reduced. No other phenotype described as yet.Abnormal axon morphology:• axon length and branch number are increased in cultured cortical neurons• callosal axons grow further into the contralateral hemisphere at P4• at P14, axon distribution in the corpus callosum is disturbed with a greater number of axon terminals, with a wider distribution in both the S1 and S2 regions• broader distribution of the contralateral axon projection pattern in the corpus callosumEmbryogenesis phenotype:• no obvious midline defects, unlike in Opitz Syndrome patients|Breeder pairs often only litter down after 3 months together, if they litter down at all. Around 1 in 3 produce litters.|C57BL/6|Yes|Yes|Yes|Unknown|Unknown|Yes|No|Unknown||||No|25-Sep-2009|Cryopreserved sperm|75.0|0.0|Yes|Opitz GBBB syndrome|X-linked, craniofacial, cleft lip|Yes| 7359.0|ENU23 15 NIP7|C57BL/6NCrlAnu-Nip7/AnuApb|C57BL/6NCrlAnu-Nip7/AnuApb|Recessive|nuclear import 7 homolog (S. cerevisiae)|NIP7|Unknown|1110017C15Rik, 6330509M23Rik |MGI:1913414|nuclear import 7 homolog (S. cerevisiae); mutation 1, The Australian National University|Nip7|MGI:5563445|8|ENSMUSG00000031917|ENSMUST00000034392|Nip7-201|134|192|A to G|ENSMUSE00000214640|2|45|Tyrosine to Cysteine|||||CTGTTTCCGGCTGCACAACGACCGAGTGTACTATGTGAGTGAGATGATGCTGAAGCTGGCC||||||||||||||Homozygous mutation appears lethal|Heterozygous mice appear normal and healthy|C57BL/6NCrlAnu|No|No|Yes|No|No|Yes|No|Good|none|Generation 4|HET x HET|No|20-Jun-2013|Cryopreserved sperm|36.0|0.0|Unknown||lethal, embryo, ENU|Yes| 7851.0|ENU34:G1|ANU:ENU34:G1||Recessive|Unknown||||||||Unknown||||||||||||||||Unknown|||||||||||||Unknown|Unknown|C57BL/6NCrlAnu|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||1||No|04-Mar-2015|Cryopreserved sperm|1963.0|41.0|Unknown||ENU, random, mutagenesis, screen|Yes| 7852.0|ENU34:G2|ANU:ENU34:G2||Recessive|Unknown||||||||Unknown||||||||||||||||Unknown|||||||||||||Unknown|Unknown|C57BL/6NCrlAnu|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||1||No|04-Mar-2015|Cryopreserved sperm|6300.0|0.0|Unknown||ENU, random, mutagenesis, screen|Yes| 8784.0|R26-LSL-Adar1 Za|C57BL/6-Gt(ROSA)26Sor/CwaApb||Recessive|gene trap ROSA 26, Philippe Soriano|Gt(ROSA)26Sor||beta geo, Gtrgeo26, Gtrosa26, R26, ROSA26, Thumpd3as1|MGI:104735||Gt(ROSA)26Sor||6|||||||||||||||||||||||||||||normal (requires Cre to express Adar1 cDNA)|Normal (requires Cre to express Adar1 cDNA)|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|04-Sep-2019|Cryopreserved sperm|60.0|0.0|Unknown|||Yes| 7856.0|ENU30:057|C57BL/6NCrlANu-Pik3ap1/AnuApb||Recessive|phosphoinositide-3-kinase adaptor protein 1|Pik3ap1|Unknown|1810044J04Rik, BCAP|MGI:1933177|mutation 1, Australian National University|Pik3ap1||19|ENSMUSG00000025017|ENSMUST00000059672|Pik3ap1-201|1094|1195|G to A|ENSMUSE00000147300|7|365|Alanine to Valine|||||GCTGCTCACCTGTCCAGGGGCTCTCCAGGCCTACAGTGTAGCCAACAAGCACGGCCACTAT||||||||||||||High IgM expression on mature B cells||C57BL/6NCrlAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|05-Mar-2015|Cryopreserved sperm|55.0|0.0|Unknown||B cell, IgM|Yes| 7853.0|Thunder|B6(Cg)-Bcl2l11 Hnrnpll/AnuApb|B6(Cg)-Bcl2l11 Hnrnpll/AnuApb|Recessive|heterogeneous nuclear ribonucleoprotein L-like|Hnrpll|Nil||MGI:1919942|heterogeneous nuclear ribonucleoprotein L-like; thunder|Hnrpll|MGI:3707008|17|ENSMUSG00000024095|ENSMUST00000061331|Hnrpll-201|407|683|T to A|ENSMUSE00000138333|2|136|Valine to Aspartic acid|||||TGTCCATGTTCGAGGGCTCTGTGAATCTGTTGTGGAAGCTGACCTTGTGGAGGCACTGGAG|Yes|||||||||||||Unknown||C57BL/6JAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Poor|10|7||No|05-Mar-2015|Cryopreserved sperm|44.0|0.0|Unknown||T cell, B cell, lymphocyte, CD45, ENU, Bim|Yes| 7853.0|Thunder|B6(Cg)-Bcl2l11 Hnrnpll/AnuApb|B6(Cg)-Bcl2l11 Hnrnpll/AnuApb|Recessive|BCL2-like 11 (apoptosis facilitator)|Bcl2l11||1500006F24Rik, Bim, Bod|MGI:1197519|BCL2-like 11 (apoptosis facilitator); targeted mutation 1.1, Andreas Strasser|Bcl2l11|MGI:2156498|2|||||||||||||||||||||||||||||Unknown||C57BL/6JAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Poor|10|7||No|05-Mar-2015|Cryopreserved sperm|||Unknown||T cell, B cell, lymphocyte, CD45, ENU, Bim|Yes| 8789.0||B6.Cg-Mcc/Ausb||Recessive|mutated in colorectal cancers|Mcc||D18Ertd451e|MGI:96930||||Unknown|||||||||||||||||||||||||||||Normal viability. MCC whole body knockout mice are expected to develop a DNA repair defect in the inflamed tissue after induction of chronic inflammation, such as colitis, that can lead to cancer development.|Normal viability. MCC whole body heterozygous mice may have an attenuated phenotype compared to homozygous mice.|C57BL/6J|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|08-Sep-2019|Cryopreserved sperm|50.0|0.0|Unknown||DNA damage, colorectal|Yes| 7869.0||ENU18Flt3-ITD:G1(24)||Recessive|FMS-like tyrosine kinase 3|Flt3||CD135, Flk2, Flk-2, Flt-3, wmfl|MGI:95559|FMS-like tyrosine kinase 3; targeted mutation 1, D Gilliland|Flt3|MGI:3763385|5|||||||||||||||||||||||||||||Accelerated onset of AML compared to control FLT3-ITD mice.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Poor||||No|09-Apr-2015||0.0|0.0|Yes|Myelomonocytic Leukaemia|AML, myeloid, lymphocyte, CML, ENU|Yes| 7869.0||ENU18Flt3-ITD:G1(24)||Recessive|Unknown||||||||Unknown|||||||||||||||||||||||||||||Accelerated onset of AML compared to control FLT3-ITD mice.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Poor||||No|09-Apr-2015||||Yes|Myelomonocytic Leukaemia|AML, myeloid, lymphocyte, CML, ENU|Yes| 10407.0|Wheat|C57BL/6CrlAnu-5(Gbp8-Gbp4-Gbp9)em1Anu||Recessive|guanylate-binding protein 8|Gbp8|||MGI:1923324||||5|ENSMUSG00000034438||||||||||||||||||||||||||||Normal|Normal||Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Good||||No|07-Mar-2024|Cryopreserved sperm|39.0|0.0|Unknown|||Possibly| 10407.0|Wheat|C57BL/6CrlAnu-5(Gbp8-Gbp4-Gbp9)em1Anu||Recessive|guanylate binding protein 4|Gbp4|||MGI:97072||||5|ENSMUSG00000079363||||||||||||||||||||||||||||Normal|Normal||Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Good||||No|07-Mar-2024|Cryopreserved sperm|||Unknown|||Possibly| 10407.0|Wheat|C57BL/6CrlAnu-5(Gbp8-Gbp4-Gbp9)em1Anu||Recessive|guanylate-binding protein 9|Gbp9|||MGI:3605620||||5|ENSMUSG00000029298 ||||||||||||||||||||||||||||Normal|Normal||Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Good||||No|07-Mar-2024|Cryopreserved sperm|||Unknown|||Possibly| 7858.0|ENU15NIH:085:CD74KO|C57BL/6JAnu-Cd74 Sppl2a/AnuApb||Recessive|signal peptide peptidase like 2A|Sppl2a|Unknown|2010106G01Rik, C130089K23Rik|MGI:1913802 |signal peptide peptidase like 2A; mutation 1, The Australian National University|Sppl2a|MGI:5432126|2|ENSMUSG00000027366|ENSMUST00000028844|2010106G01Rik-001||||||||126746052|7|||ATTCATAGGATGCCATGTGGACAGTGCACGTACGTATCTGTTAGCCTATGATGCAATTAG|||||||||||||||Normal|C57BL/6JAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|10-Mar-2015|Cryopreserved sperm|22.0|0.0|Unknown||lymphocyte, B cell, IgD, ENU, immunoglobulin|Yes| 7858.0|ENU15NIH:085:CD74KO|C57BL/6JAnu-Cd74 Sppl2a/AnuApb||Recessive|CD74 antigen (invariant polypeptide of major histocompatibility complex, class II antigen-associated)|Cd74|Nil|CLIP, Ii|MGI:96534|CD74 antigen (invariant polypeptide of major histocompatibility complex, class II antigen-associated); targeted mutation 1, Elizabeth Bikoff|Cd74|MGI:1927530|18||||||||||||||||||||||||||||||Normal|C57BL/6JAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|10-Mar-2015|Cryopreserved sperm|||Unknown||lymphocyte, B cell, IgD, ENU, immunoglobulin|Yes| 7859.0|ASD146:C57BL/6NTac:IL15 tm1imx:C57BL/6NCrl:N12|B6(Cg)-IL15/AnuApb||Recessive|interleukin 15|Il15|Nil|IL-15|MGI:103014|targeted mutation 1, Immunex Research and Development Corporation|Il15|MGI:2136897|8||||||||||||||||Yes|||||||||||||Mice homozygous for disruptions of this gene have normal life spans but display a variety of immune system abnormalities and maternal placental defects.These mutant mice lack NK cells and have marked reductions in memory CD8+ T cells, NK 1.1 T cells and Thy-CD8a intraepithelial lymphocytes. Mice are unable to mount a protective immune response to challenge with vaccinia virus.Abnormal immune system morphology.Abnormal dendritic cell morphology/development:* lower numbers of splenic dendritc cells after Plasmodium chabaudi infection.Abnormal lymphocyte morphology/development:* Intestinal intraepithelial lymphocytes maturing outside of the thymus greatly reduced in numbers.Abnormal CD8+ T cell morphology/development:* two fold reduction in numbers of CD8 single positive cells in spleen and lymph nodes.Abnormal NK cell morphology/development:* reduced numbers of natural killer cells in thymus liver and spleen.* absent in uterusSmall lymph nodes: peripheral lymph nodes significantly lower in weight.Abnormal immune system physiology:Defective NK cell cytolysis: significantly reduced cytolytic activityabnormal immune serum protein physiology.Decreased immunoglobulin concentration:* lower levels of malaria specific antibodies producedlower levels of total immune globulin.Decreased IgG level: decreased levels of IgG1, IgG2a, IgG2b, and IgG3 after Plasmodium infection.Decreased IgM level: after plasmodium infection.Abnormal cytokine physiology.Abnormal interferon physiology: reduced production of IFN gamma by NK cells.Abnormal interleukin physiology:* reduced Il12 production by dendritic cells after Plasmodium infection.Altered susceptibility to infection.Decreased susceptibility to bacterial infection.* Improved survival after infection with Listeria monocytogenesincreased susceptibility to parasitic infection.* parasitemia higher but only minor effect on mortalityincreased susceptibility to viral infection.* dead by day 9 after Vaccinia infection* very susceptible to HSV-2 infectionDecreased susceptibility to type IV hypersensitivity reaction: no contact hypersensitivity* T mediated effects delayed but not B cell activation or antibody production.||C57BL/6NCrlAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|12||brother x sister mating|No|17-Mar-2015|Cryopreserved sperm|48.0|0.0|Unknown||T cell, infection, Natural killer cell, memory|Yes| 7862.0|ENU26:034:Shroom3:B6:G3|C57BL/6NCrlAnu-Shroom3/AnuApb||Recessive|shroom family member 3|Shroom3|Unknown|D5Ertd287e, Shrm, Shrm3|MGI:1351655|Shroom3; mutation 1, Australian National University|Shroom3||5||||||||||Unknown to Unknown|||||||||||||||||||Unknown|Unknown|C57BL/6NCrlAnu|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown|1|||No|25-Mar-2015|Cryopreserved sperm|88.0|0.0|Unknown||ENU, mutagenesis, screen, random|Yes| 7863.0|TauKO|B6.129X1-Mapt/J||Recessive|microtubule-associated protein tau|Mapt|Nil|Mtapt, Tau|MGI:97180|microtubule-associated protein tau; targeted mutation 1, Hana N Dawson|Mapt|MGI:2385630|11|||||||||||||||||||||||||||||Same as wildtype|Same as wildtype|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|25-Mar-2015||0.0|0.0|Unknown||Tau, neuronal|Possibly| 7864.0|ENU18::B6|C57BL/6JAnu-Gsdmd/AnuApb||Recessive|gasdermin D|Gsdmd|Unknown|1810036L03Rik, DF5L, Dfna5l, Gsdmdc1, M2-4|MGI:1916396||||15||||||||||||||||Unknown|||||||||||||Unknown|Unknown|C57BL/6JAnu|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||1||No|01-Apr-2015|Cryopreserved sperm|87.0|0.0|Unknown||ENU, random, mutagenesis, screen|Possibly| 1236.0|Pinky ; ENU8C:027|B6JSfdAnu;CBA(Cg)-Zbtb16/AnuApb|B6JSfdAnu;CBA(Cg)-Zbtb16/AnuApb|Recessive|zinc finger and BTB domain containing 16|Zbtb16|Unknown|Green's luxoid, PLZF, Zfp145|MGI:103222|pinky|Zbtb16|MGI:4462277|9|ENSMUSG00000066687|ENSMUST00000093852|Zbtb16-201|210|457|T to A|ENSMUSE00000584531|2|70|Tyrosine to STOP|||||ATCCTCTTCCACCGAAACAGCCAGCACTATACTCTAGACTTCCTCTCGCCAAAAACCTTCC|Yes|||||||||||||Limb deformity. Shortening and angular deformity of hindlimbs with extra digits present in some cases. Deformity affects mouse mobility. Previously described homozygous mutants exhibit abnormal anterior-posterior patterning, with skeletal abnormalities of the limb, especially the hindlimb, and homeotic transformations of anterior skeletal elements into posterior structures. Males develop infertility due to loss of germline cells with age.||C57Bl6JSfdAnu x CBA/HAnu|Yes|No|Yes|Yes|No|Yes|Yes|Good|1 to B6JSfdAnu, 1x CBH/CaJ|||No|15-Jun-2007|Cryopreserved sperm|175.0|0.0|Unknown||limb, deformity, extra digit, anterior-posterior patterning, ENU|Yes| 7867.0|tetO-ChR2(C128S), tetO-ChR2 BAC Tg, B6-tetO-ChR2/YFP Tg|B6(Cg)-Tg(tetO-ChR2*C128S/EYFP)1Kftnk||Dominant||||||||||||||||||||||||||Channelrhodopsin-2 (C128S)|E. coli Tetracycline operator, CMV minimal promotor, rabbit Beta globin intron |||||||||||Normal|Normal|C57BL/6|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Excellent||over 20|hemizygous transgenic x non-transgenic (wild type) sibs|No|09-Apr-2015|Cryopreserved sperm|50.0|0.0|Unknown||tetO-system, light, channel|Yes| 9359.0||B6.C-H2-Kbm1 B6.129(Cg), B6.FVB(129), B10.BR (DBA-2) Gt(ROSA)26Sortm4<(ACTB-tdTomato,-EGFP)Luo/J> Tg<(Alb1-cre)1Dlr/J>Tg<(Alb-H2-Kb)>/Apb||Semi-dominant| ROSA, |||||Gt(ROSA)26Sortm4(ACTB-tdTomato,-EGFP)|||Unknown||||||||||||||||| Alb1-cre, Alb-H2-Kb|Albumin|||||||||||These mice result from the cross of 4 different mouse lines:mT/mG mice (From JAX labs Stock No. 007676)express ROSAmT/mG, a cell membrane-targeted, two-color fluorescent Cre-reporter allele. Prior to Cre recombination, cell membrane-localized tdTomato (mT) fluorescence expression is widespread in cells/tissues. Cre recombinase expressing cells (and future cell lineages derived from these cells) have cell membrane-localized EGFP (mG) fluorescence expression replacing the red fluorescence. Alb1-cre mice express a Cre recombinase transgene under control of Alb promoter/enhancer elements, thus restricted CoRe expression in all hepatocytes (Cre expression is also detected in the biliary epithelial cells in this mouse line). Alb-Kb mice express a transgenic H-2Kb under the control of the mouse albumin promoter, thus restricting H-2Kb expression to hepatocytes. Mice have been backcrossed and maintained on the H-2Kbm1 background |In these mice, all cells but hepatocytes and biliary epithelial cells express membrane tomato (red) while hepatocytes and bile ducts are GFP+ (green). H-2Kb expression is restricted to Hepatocytes. |C57Bl/6N|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|17-Mar-2022||0.0|0.0|Unknown|||Possibly| 7868.0||ENU18Flt3-ITD:G1||Recessive|FMS-like tyrosine kinase 3|Flt3||CD135, Flk2, Flk-2, Flt-3, wmfl|MGI:95559|FMS-like tyrosine kinase 3; targeted mutation 1, D Gilliland|Flt3|MGI:3763385|5|||||||||||||||||||||||||||||Accelerated onset of AML compared to control FLT3-ITD mice.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Poor||||No|09-Apr-2015|Cryopreserved sperm|40.0|0.0|Yes|Myelomonocytic Leukaemia|AML, myeloid, lymphocyte, CML, ENU|Yes| 7868.0||ENU18Flt3-ITD:G1||Recessive|Unknown||||||||Unknown|||||||||||||||||||||||||||||Accelerated onset of AML compared to control FLT3-ITD mice.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Poor||||No|09-Apr-2015|Cryopreserved sperm|||Yes|Myelomonocytic Leukaemia|AML, myeloid, lymphocyte, CML, ENU|Yes| 10412.0||C57BL/6-Ddx5/DunwApb||Dominant|DEAD-Box Helicase 5 |Ddx5||Hlr1|MGI:105037|Ddx5|||11|||||||||||||||||||||||||||||Mice homozygous for the knock-in allele may have heart defects or craniofacial defects|Heterozygous mice are likely to be normal.|C57Bl/6J|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|12-Mar-2024|Cryopreserved sperm|54.0|0.0|Unknown|||No| 8790.0|Slc1a5:Eif2ak4|C57BL/6NCrlAnu-Eif2ak4 Slc1a5/AnuApb||Recessive|eukaryotic translation initiation factor 2 alpha kinase 4|Eif2ak4|Unknown|GCN2|MGI:1353427|Eif2ak4; mutation 1, Australian National University|Eif2ak4||2||||||||||Unknown to Unknown|||||||||||||||||||Unknown||C57BL/6NCrlAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|17-Sep-2019|Cryopreserved sperm|22.0|0.0|Unknown||ENU|Yes| 8790.0|Slc1a5:Eif2ak4|C57BL/6NCrlAnu-Eif2ak4 Slc1a5/AnuApb||Recessive|solute carrier family 1 (neutral amino acid transporter), member 5|Slc1a5|Unknown|ASCT2|MGI:105305|Slc1a5; mutation 1, Australian National University|Slc1a5||7||||||||||Unknown to Unknown|||||||||||||||||||Unknown||C57BL/6NCrlAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|17-Sep-2019|Cryopreserved sperm|||Unknown||ENU|Yes| 7876.0|Pik3cd𝚫|C57BL/6-Pik3cd/MegoAusb||Recessive|phosphatidylinositol 3-kinase catalytic delta polypeptide|Pik3cd|Unknown|2410099E07Rik, 2610208K16Rik, p110delta|MGI:1098211||||4|||||||||||||||||||||||||||||Unknown|Unknown|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|16-Apr-2015||0.0|0.0|Unknown||B cell, T cell|Yes| 7877.0|TCRHEL3A9|STOCK TgTg(TcrHEL3A9)1Mmd/JAusb||Dominant||||||||||||||||||||||||||transgene insertion 1, Mark M Davis||||||||||||Expresses T Cell receptor specific for hen egg lysozyme (HEL).|Expresses T Cell receptor specific for hen egg lysozyme (HEL).|Unknown|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|16-Apr-2015||0.0|0.0|Unknown||T cell, receptor, HEL|Yes| 10411.0||C57BL/6-Pcsk6||Dominant|Proprotein Convertase Subtilisin/Kexin Type 6 |Pcsk6||PACE4, SPC4|MGI:102897|Pcsk6|||7|||||||||||||||||||||||||||||Mice homozygous for the His490Tyr change may have heart defects and die as a result|Heterozygous mice are unlikely to be affected|C57Bl/6J|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|12-Mar-2024|Cryopreserved sperm|53.0|0.0|Unknown|||No| 7881.0|C57BL/6-Nabp-Floxed|C57BL/6J-Nabp2||Recessive|nucleic acid binding protein 2|Nabp2|Normal|2610036N15Rik, Nabp2, Obfc2b|MGI:1917167|nucleic acid binding protein 2; targeted mutation 1.1, Kum Kum Khanna|Nabp2|MGI:5502334|10|||||||||||||||||||||||||||||Viable and Fertile|Viable and Fertile|C57BL/6J|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|21-Apr-2015|Cryopreserved sperm|50.0|0.0|Unknown||Single-stranded binding protein, DNA repair, DNA damage, Skeletogenesis|Possibly| 7879.0|Spotty|STOCK Tg(tetO-HIST1H2BJ/GFP)47Efu/JAusb||Dominant||||||||||||||||||||||||||transgene insertion 47, Elaine Fuchs|tetracycline-responsive promoter element (TRE) and cytomegalovirus regulatory elements (mCMV)|||||||||||Normal|Normal|Mixed|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|16-Apr-2015||0.0|0.0|Unknown|||Yes| 7880.0|Blue-uteri|FVB.129S4(B6)-Gt(ROSA)26Sor/JAusb||Recessive|gene trap ROSA 26, Philippe Soriano|Gt(ROSA)26Sor|Unknown|beta geo, Gtrgeo26, Gtrosa26, R26, ROSA26|MGI:104735|gene trap ROSA 26, Philippe Soriano; targeted mutation 1, Philippe Soriano|Gt(ROSA)26Sor|MGI:1861932|6||||||||||Unknown to Unknown|||||||||||||||||||No abnormal phenotype observed|No abnormal phenotype observed|FVB/N|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|16-Apr-2015||0.0|0.0|Unknown||LacZ, Rosa|Yes| 7882.0|C57BL/6-Nabp1-floxed|STOCK Nabp1/KkhaApb|STOCK Nabp1/KkhaApb|Recessive|nucleic acid binding protein 1|Nabp1|Normal|Nbp1, Obfc2a, Ssb2|MGI:1923258|nucleic acid binding protein 1; targeted mutation 1, Kum Kum Khanna|Nabp1|MGI:5644720|1||||||||||Unknown to Unknown|||||||||||||||||||Viable and Fertile|Viable and Fertile|C57BL/6J|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|21-Apr-2015|Cryopreserved sperm|50.0|0.0|Unknown||Single-stranded binding protein, DNA repair, DNA damage|Possibly| 7883.0|C57BL/6-Nabp1-floxed strain 2|STOCK Nabp1/2KkhaApb||Recessive|nucleic acid binding protein 1|Nabp1|Normal|Nbp1, Obfc2a, Ssb2|MGI:1923258|targeted mutation 1, Kum Kum Khanna|Nabp||1|||||||||||||||||||||||||||||Viable and Fertile|Viable and Fertile|C57BL/6J|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|21-Apr-2015|Cryopreserved sperm|50.0|0.0|Unknown||Single-stranded binding protein, DNA repair, DNA damage|Possibly| 7884.0|C57BL/6-Nabp1-KO strain 1|STOCK Nabp1/KkhaApb||Recessive|nucleic acid binding protein 1|Nabp1|Normal|Nbp1, Obfc2a, Ssb2|MGI:1923258|targeted mutation 1.1, Kum Kum Khanna|Nabp|MGI:5644800|1||||||||||Unknown to Unknown|||||||||||||||||||Viable and Fertile|Viable and Fertile|C57BL/6J|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|||homozygous x homozygous|No|21-Apr-2015|Cryopreserved sperm|50.0|0.0|Unknown||Single-stranded binding protein, DNA repair, DNA damage|Possibly| 7872.0|Sppl2a KO2 conditional|B6.Cg-Sppl2a Tg(ACTFLPe)9205Dym/2MarpAnuApb||Recessive|signal peptide peptidase like 2A|Sppl2a|Unknown|2010106G01Rik, C130089K23Rik|MGI:1913802|signal peptide peptidase like 2A; targeted mutation 1a, Helmholtz Zentrum Muenchen GmbH|Sppl2a|MGI:4887673|2|||||||||||||||||transgene insertion 9205, Susan Dymecki|ACTB, actin, beta, human|The FLPe recombinase variant exhibits enhanced thermostability with recombination activity being 4X and 10X that of wildtype FLP at 37°C and 40°C, respectively||||||||||Normal|Normal|C57BL/6NCrlAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|16-Apr-2015|Cryopreserved sperm|33.0|0.0|Unknown||Conditional|Possibly| 7885.0|C57BL/6-Nabp1-KO strain 2|STOCK Nabp1/2KkhaApb||Recessive|nucleic acid binding protein 1|Nabp1|Normal|Nbp1, Obfc2a, Ssb2|MGI:1923258|targeted mutation 1.1, Kum Kum Khanna|Nabp||1|||||||||||||||||||||||||||||Viable and Fertile|Viable and Fertile|C57BL/6J|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|||homozygous x homozygous|No|21-Apr-2015||0.0|0.0|Unknown||Single-stranded binding protein, DNA repair, DNA damage|Possibly| 7106.0|Nude|B6.B10.BR-Foxn1/WehiAnuApb||Recessive|forkhead box N1|Foxn1|Unknown|D11Bhm185e, Hfh11, whn|MGI:102949|nude|Foxn1|MGI:1856108|11||||||||||||||||Yes|||||||||||||Postnatal lethality:some mice die within 1 week of birth55% mortality within 2 weeksPremature death:100% mortality by 25 weeksDecreased body size and weight.Postnatal growth retardation.Abnormal T cell differentiation.Athymia.Abnormal cell-mediated immunity.Abnormal liver morphology:liver lobes were atrophied and covered with red scarsvariable degrees of severity, typically increasing with age at time of death.Small ovaryCoiled sperm flagellum: many sperm had coiled tailsAbnormal estrous cycle: many females exhibited continuous dioestrus and metaoestrus phasesFemale infertility: severely reduced fertilityReduced male fertility.Asthenozoospermia.Nude: sparse hair growth around 5 weeks of agein some mice, cephalo-caudal migration of an irregular band of short sparse hairThin skin:reduction in skin thickness at 3 weeks of age, corresponding to the catagen stage of normal skinAbsent vibrissae: absent at birthShort and wavy vibrissae: older mice show repeated growth and loss of short and wavy vibrissae.|Same as wild-type|B10.BR|Yes|Yes|Yes|Yes|Yes|Yes|Yes|Poor|4|0|Male hom x female het if possible|No|16-Oct-2012|Cryopreserved sperm|36.0|0.0|Unknown||hair loss, T cell, thymus, body size / mass, growth retardation, alopecia, keratin|Yes| 5531.0|Woodrat|C57BL/6J-Mbtps1/BtlrAnuApb||Recessive|membrane-bound transcription factor peptidase, site 1|Mbtps1|Normal|0610038M03Rik; AV003995; site-1 protease, S1P; subtilisin/kexin isozyme-1, SKI-1; mKIAA0091; membrane-bound transcription factor protease, site 1|MGI:1927235|membrane-bound transcription factor peptidase, site 1; woodrat|Mbtps1|MGI:3652524|8|ENSMUSG00000031835|ENSMUST00000098362|Mbtps1-202|1487|2075|A to G|ENSMUSE00000319486|13|496|Tyrosine to Cysteine|||||TAGCTACATCGACCTGACTGAGTGTCCCTACATGTGGCCCTACTGCTCCCAGCCTATCTAC||||||||||||||The woodrat (wrt) phenotype was identified as a visible recessive variant among G3 mice homozygous for mutations induced by ENU. Homozygous woodrat mice exhibit coat hypopigmentation beginning on postnatal day 8, which progresses with time so that by 4 weeks of age wrt/wrt coats are composed of both white and black hairs, varying in pigment content along the length of each hair shaft. Adult wrt/wrt mice have a more homogeneous coat composed of hairs with a white base and a grey/brown tip|Compound heterozygosity for a null mutation (a gene trap allele) and the wrt allele (Mbtps1wrt/trap) results in embryonic lethality, while 53% and 54% of the expected numbers of Mbtps1+/trap or Mbtps1wrt/wrt mice, respectively, survive to term. Because a single copy of the gene (Mbtps1+/trap) is associated with diminished survival to term and causes no visible phenotype, while Mbtps1wrt/wrt is associated with about the same impairment of survival to term but does cause a visible phenotype, it is inferred that the wrt allele encodes a protein with ≤50% of wild type activity. In addition, it appears that the survival threshold likely falls between 25% and 50% of wild type enzyme activity levels.|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|unknown|unknown||No|06-Jul-2011|Cryopreserved sperm|50.0|0.0|Unknown||ENU, colitis, endoplasmic reticulum|Possibly| 7684.0|Thunder|B6(Cg)-Hnrnpll/AnuApb|B6(Cg)-Hnrnpll/AnuApb|Recessive|heterogeneous nuclear ribonucleoprotein L-like|Hnrpll|Nil||MGI:1919942|heterogeneous nuclear ribonucleoprotein L-like; thunder|Hnrpll|MGI:3707008|17|ENSMUSG00000024095|ENSMUST00000061331|Hnrpll-201|407|683|T to A|ENSMUSE00000138333|2|136|Valine to Aspartic acid|||||TGTCCATGTTCGAGGGCTCTGTGAATCTGTTGTGGAAGCTGACCTTGTGGAGGCACTGGAG|Yes|||||||||||||Low T cell numbers which are hyperactivated. By flow cytometric staining of blood, initially detected a strain with CD4 T cells decreased to 25% of wild-type. Further analysis revealed entirely normal thymic development and single positive cells, but a marked reduction in the number of peripheral T cells especially naïve CD4 and CD8 cells, and poor survival of thunder T cells upon adoptive transfer. During this analysis, it was found that thunder thymocytes stain with the RA3-6B2 antibody that selectively recognizes the CD45RABC B220 isoform normally restricted to B cells. Staining with antibodies to CD45RA, B or C showed a 50-fold increase in staining on all thymocytes and peripheral T cells, as well as macrophages and dendritic cells, so that the staining intensity matched that on B cells. Amplification of cDNA with primers spanning CD45 exons 4-6 showed a dramatic increase in the inclusion of these exons in thymocyte CD45 mRNA, establishing that the thunder mutation interferes with the normal CD45 exon 4-6 silencing process.||C57BL/6JAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Poor|10|7||No|16-May-2014|Cryopreserved sperm|40.0|0.0|Unknown||T cell, B cell, lymphocyte, CD45, ENU, NIH|Yes| 8794.0|Tpbeta - Transgenic|C57BL/6-Tg(Tp beta)/Apb||Dominant||||||||||||||||||||||||||Tb beta||||||||||||Unknown|Unknown||Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|17-Sep-2019|Cryopreserved sperm|50.0|0.0|Unknown|||Yes| 7702.0|Mot|B6.Cg-Rabl2a/MarpApb||Recessive|RAB, member of RAS oncogene family-like 2A|Rabl2a|||MGI:1915958|RAB, member of RAS oncogene family-like 2; mot|Rabl2|MGI:5469381|15|ENSMUSG00000022621|ENSMUST00000023294|Rabl2a-201|218|311|A to G|ENSMUSE00000128937|5|73|Aspartic acid to Glycine|||||CACAGTAGACGGCAAGACGATCCTTGTGGACTTCTGGGATACAGCAGGCCAGGAGCGGTTC|Yes|||||||||||||Male InfertilityDecreased testis weightOligozoospermiaShort sperm flagellumAsthenozoospermia:• low total motility and minimal progressive motility• however, ultrastructure is normal||C57BL/6|Yes|Yes|Yes|Yes|No|Yes|No|Poor|15|||No|13-Jun-2014|Cryopreserved sperm|50.0|0.0|Yes|Male Infertility|ENU, fertility, sperm|No| 7545.0|Jnk2 KO|B6.129-Mapk9/JAnuApb|B6.129-Mapk9/JAnuApb|Recessive|mitogen-activated protein kinase 9|Mapk9|Nil|JNK2, JNK/SAPK alpha, Prkm9|MGI:1346862|mitogen-activated protein kinase 9; targeted mutation 1, Richard Flavell|Mapk9|MGI:2176243|11|||||||||||||||||||||||||||||Abnormal keratinocyte morphology:• exhibit greater number of keratinocyte stem cells in skinAbnormal keratinocyte differentiation:• keratohyalin granules, markers of epidermal differentiation, are increased in the stratum granulosumEpidermal hyperplasia:• keratinocyte hyperplasia, resulting in an increased number of epithelial cell layersThick epidermis.Abnormal liver physiology:• exhibit protection from galactosamine/lipopolysaccharide (GalN/LPS)-induced liver injury, showing decreased injury, mortality, and blockage of the TNF death pathway and mitochondrial death pathway (decrease in Bid cleavage, mitochondrial translocation, and cytochrome c release)||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|13-Dec-2013|Cryopreserved sperm|60.0|0.0|Unknown||CD4, T cell, interferon|Yes| 10408.0||C57BL/6-Ipo7-A209V/DunwApb||Recessive|Importin 7 |Ipo7|||MGI:2152414|Ipo7 A209V |||7|ENSMUSG00000066232 ||||||||||||||||||||||||||||Phenotypes may include Brain and heart defects and scoliosis in the heterozygous or homozygous state. May also be lethal in the homozygous state.|Phenotypes may include Brain and heart defects and scoliosis in the heterozygous or homozygous state.||Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|12-Mar-2024|Cryopreserved sperm|55.0|0.0|Unknown|||No| 7562.0|Spi6 KO|C57BL/6J-SerpinB9/MarpApb||Dominant|serine (or cysteine) peptidase inhibitor, clade B, member 9|Serpinb9|Nil|ovalbumin, PI-9, Spi6|MGI:106603||||13|||||||||||||||||||||||||||||Increased apoptosis:• apoptosis is increased in LCMV- and LM-specific CTLs in mutantsAbnormal CD8-positive, alpha-beta cytotoxic T cell morphology:• upon infection with LCMV Armstrong or a strain of Listeria monocytogenes (LM), numbers of LCMV-specific CTLs are reduced 5-fold and LM-specific CTLs are reduced 9-fold compared to control B6 mice.• frequency of CTLs devoid of Gsmb granules is 3 times greater than in controls; number of Gzmb granules per CTL is 2-fold lower than in controls.Abnormal cytotoxic T cell physiology:• apoptosis is increased in LCMV- and LM-specific CTLs in mutants.Defective cytotoxic T cell cytolysis:• deficit in CTL activity is observed in ex vivo activity assay over course of LCMV infection; on day 10, activity is decrease 6-fold compared to controls.Abnormal enzyme/ coenzyme level:• caspase 3 in cytoplasm is increased.Abnormal enzyme/coenzyme activity:• GranzymeB activity is significantly increased in cytoplasm of mutants compared to controls.|Normal|C57BL/6J|Yes|Yes|Yes|Yes|Yes|Yes|No|Excellent||||No|07-Jan-2014|Cryopreserved sperm|50.0|0.0|Unknown||T cell, CD8, dendritic cell, MHC I, cross-priming|Possibly| 6865.0||Emergency||Recessive|||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|26-Mar-2012||0.0|0.0|Unknown|||No| 10409.0||C57BL/6-Prmt5/DunwApb||Recessive|Protein Arginine N-Methyltransferase 5|Prmt5||Jbp1, Skb1|MGI:1351645|Prmt5|||14|ENSMUSG00000023110 ||||||||||||||||||||||||||||Mice homozygous for the knock-in allele may have heart defects or craniofacial defects.|Heterozygous mice are likely to be normal|C57Bl/6J|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|12-Mar-2024|Cryopreserved sperm|50.0|0.0|Unknown|||Possibly| 10362.0|C57BL/6NCrlAnu-Nlrp3/Anu|ENU26-Nlrp3||Recessive|NLR family, pyrin domain containing 3|Nlrp3||Cias1, cryopyrin, Mmig1, NALP3, Pypaf1|MGI:2653833||Nlrp3||11|||||||||||||||||||||||||||||healthy|healthy|C57Bl/6N|Yes|Yes|Yes|Yes|Yes|Yes|No|Excellent||||No|20-Sep-2023|Cryopreserved sperm|55.0|0.0|Unknown|||No| 4456.0||B6;C-Gstz1/AnuApb||Recessive|glutathione transferase zeta 1 (maleylacetoacetate isomerase)|Gstz1|Nil|maleylacetoacetate isomerase|MGI:1341859|targeted mutation 1, Philip G Board|Gstz1|MGI:3050206|12||||||||||||||||No|||||||||||||Increased sensitivity to induced Morbidity/Mortality * 3% phenylalanine in the water is lethal to young homozygotes, less than 28 days old, but not to older homozygotes, greater than 66 days oldpremature death * several mutants died after 1 year of age from heart pathologiesDystrophic cardiac calcinosis* in some mutants over 1 year of age Calcification of the myocardium in the right atrium and/or ventricle is seen* calcification is also seen in 3 of 8 young mutants that died after 3% phenylalanine exposurecellular necrosis* in some mutants over 1 year of age myocyte necrosis is seen* myocyte necrosis is also seen in 2 of 8 young mutants that died after 3% phenylalanine exposureDecreased leukocyte cell number* 3% phenylalanine in the water results in decreased total white cell counts in mutants but not in wild-type micedecreased spleen weight * spleen weight is significantly decreased in female homozygotes and tends to be decreased in male homozygotes compared to wild-type mice* 3% phenylalanine in the water results in a dramatic decrease in spleen weight in homozygotes with reduction in both white and red pulp, but an increase in spleen weight in wild-type micechronic inflammation* in some mutants over 1 year of age chronic inflammation is seen in the heartliver inflammation* at 6 weeks and 6 months of age multifocal hepatitis is seenLiver inflammation* at 6 weeks and 6 months of age multifocal hepatitis is seenAbnormal hepatocyte morphology* large pleomorphic mitochondria are seen in hepatocytes from mutantsIncreased liver weight* on a normal diet liver weight is greater in homozygotes compared to wild-type miceHepatic necrosis* at 6 months of age 3 of 7 homozygotes show hepatocyte necrosis* 3 out of 8 homozygotes that died after 3% phenylalanine exposure displayed hepatocyte necrosisHepatic steatosis * 5 out of 8 homozygotes that died after 3% phenylalanine exposure displayed macrovesicular steatosis||C57BL/6 x BALB/c|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|20-Feb-2009|Cryopreserved sperm|149.0|0.0|Unknown||GST, maleylacetoacetate, maleylacetone (MA) and succinylacetone, phenylalanine and tyrosine, Keap1/Nrf2 pathway, Oxidative stress|Yes| 10392.0|Wt/Rosa26:D3|C57Bl/6-Rosa26-delta(D3muc)/Apb||Semi-dominant|mucin 2|Muc2|||MGI:1339364 ||||7|ENSMUSG00000025515 ||||||||||||||||gene trap ROSA 26, Philippe Soriano||||||||||||Normal|Normal|C57Bl/6J|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|20-Dec-2023|Cryopreserved sperm|22.0|0.0|Unknown|||No| 7813.0|FLPe|B6.Cg-Tg(ACTFLPe)9205Dym/J||Recessive||||||||||||||||||||||||||FLP1, FLP1 recombinase, Saccharomyces cerevisiae|ACTB, actin, beta, human|expression of the enhanced FLP1 recombinase variant (FLPe) is detected in a wide variety of tissues (spinal cord, heart, gonad, adrenal) as early as embryonic day 10.5||||||||||Normal|Normal|C57BL/6J|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||6|brother X sister|No|11-Dec-2014|Cryopreserved sperm|50.0|0.0|No||FLPe, deleter|No| 5450.0|WT1-GFP|C57BL/6-Wt1/MarpApb||Dominant|Wilms tumor 1 homolog|Wt1|Nil|Wt-1|MGI:98968|Wilms tumor 1 homolog; targeted mutation 1, Naoki Hosen|Wt1|MGI:3721102|11||||||||||||||||Yes|Green fluorescent protein|WT1|||||||||||Embryonic lethal. Fetuses day around E10 from heart defect.|Heterozygotes express green fluorescent protein wherever WT1 is expressed. Otherwise phenotype is normal|C57BL/6-CD45.2|No|No|Yes|No|No|Yes|No|Poor||||No|02-Mar-2011|Cryopreserved sperm|50.0|0.0|No||Wilms tumour, GFP, neural, urogenital, kidney|Yes| 7049.0|Sftpc-/- 129|129/Sv-Sftpc/MarpApb||Recessive|surfactant associated protein C|Sftpc|Nil|pro-SpC, Sftp2, Sftp-2, SP-C|MGI:109517|surfactant associated protein C; targeted mutation 1, Stephan W Glasser|Sftpc|MGI:2387813|14|||||||||||||||||||||||||||||The lungs of the SP-C (−/−) mice lack detectable mature SP-C or precursor SP-C (proSP-C). In the absence of detectable SP-C, these mice survive and grow normally with no adverse effects on health, reproduction, or pulmonary function. SP-B mRNA levels and the level of SP-A, SP-B, and SP-D proteins were unaltered in the alveolar lavage of SP-C (−/−) mice. Both SP-C and SP-B are hydrophobic peptides that dramatically enhance surface activity of surfactant phospholipids. The survival of the SP-C (−/−) mice in the absence of the mature active SP-C peptide indicates that SP-C is not required for the surface properties of the alveolar phospholipid films required for respiratory function in vivo. However, subtle abnormalities in lung mechanics and the instability of SP-C (−/−) surfactant at low bubble size support the importance of SP-C in surfactant function at low lung volumes such as that seen in respiratory distress syndrome in adults and preterm infants. The present findings in the SP-C (−/−) mice are distinct from results reported for SP-B gene-targeted mice and infants with hereditary SP-B deficiency, wherein severe respiratory failure occurs at birth (15, 19). In the SP-B (−/−) mice and human infants with hereditary SP-B deficiency, the mature form of SP-C was absent or diminished and an aberrant form of proSP-C was detected.|Normal|129/Sv|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|>20|||No|13-Aug-2012|Cryopreserved sperm|40.0|0.0|Yes|Interstitial Pneumonitis, Desquamative, Familial; DIP|lung, alveolar, surfactant, respiratory|Possibly| 7622.0|Shiraz KO ; SCN1B C121W|C57BL/6J-Scn1b/Apb||Dominant|sodium channel, voltage-gated, type I, beta|Scn1b|Normal||MGI:98247|sodium channel, voltage-gated, type I, beta; targeted mutation 1.1, Bionomics Limited|Scn1b|MGI:4829975|7|||||||||||||||||||||||||||||Seizures:• spontaneous and heat-inducedenvironmentally induced seizures.• when exposed to a stream of warm air, mice exhibit febrile seizures (including behavioral arrest, facial automatisms, and early epileptiform discharges localized to the hippocampus) unlike similarly treated wild-type mice• febrile seizures rapidly evolve into tonic-clonic seizures unlike in wild-type mice• mice exhibit febrile seizures at lower temperatures than wild-type miceTonic-clonic seizures:• febrile seizures rapidly evolve into tonic-clonic seizures unlike in wild-type miceAbnormal brain wave pattern.Postnatal growth retardation.Tremors: • severe|Environmentally induced seizures:• when exposed to a stream of warm air, mice exhibit febrile seizures (including behavioral arrest, facial automatisms, and early epileptiform discharges localized to the hippocampus) unlike similarly treated wild-type mice• mice exhibit febrile seizures at lower temperatures than wild-type miceAbnormal nervous system electrophysiology:• average burst duration in subicular pyramidal neurons is lengthened compared to in wild-type cells• neurons exhibit axonal hyperexcitability, increased spike gain, and increased burst firing compared with wild-type cells• however, total burst events and frequency of action potentials within bursts is normalAbnormal action potential:• the number of action potentials (APs) per bursts is increased compared to in wild-type mice• neurons begin firing APs at lower drive currents compared to in wild-type mice• the threshold for AP initiation is more negative than in wild-type cells• the amplitude of first APs is higher than in wild-type cells• the AP half-width is decreased compared to in wild-type cells• however, the frequency of action potentials within bursts is normal|C57BL/6J|Yes|No|Yes|Unknown|Unknown|Unknown|No|Unknown||||No|24-Mar-2014|Cryopreserved sperm|50.0|0.0|Yes|Generalized Epilepsy with Febrile Seizures Plus, Type 1; GEFSP1|epilepsy, seizure, axon, sodium channel, di-sulphide|Yes| 7623.0|RQ/B6 ; GABRG2 R43Q|B6.129-Gabrg2/Apb||Dominant|gamma-aminobutyric acid (GABA) A receptor, subunit gamma 2|Gabrg2|Reduced||MGI:95623|gamma-aminobutyric acid (GABA) A receptor, subunit gamma 2; targeted mutation 1, Steven Petrou|Gabrg2|MGI:3764923|11|||||||||||||||||||||||||||||Partial perinatal lethality:• mice are rarely bornComplete postnatal lethality:• mice that are born die before P19Tremors:• mice that are born exhibit a severe tremorAbnormal gait:• mice that are born have altered gaitsAbnormal brain wave pattern:• mice lack normal brain rhythms|Mice heterozygous for the mutation demonstrated behavioral arrest associated with 6-to 7-Hz spike-and-wave discharges, which are blocked by ethosuximide, a first-line treatment for absence epilepsy in man. Seizures in the mouse showed an abrupt onset at around age 20 days corresponding to the childhood nature of this disease. Reduced cell surface expression of gamma2(R43Q) was seen in heterozygous mice in the absence of any change in alpha1 subunit surface expression|C57BL/6J|No|No|Yes|No|No|Yes|No|Unknown|8|||No|24-Mar-2014|Cryopreserved sperm|60.0|0.0|Yes|childhood absence epilepsy|Epilepsy, febrile, seizure, R43Q|Yes| 7518.0|HA-TetO (4)|C57BL/6-Tg(tetO-CYP19A1)4/MarpApb||Dominant||||||||||||||||||||||||||Human Aromatase ; human cytochrome P450, family 19, subfamily a, polypeptide 1|TetO|||||||||||None; no phenotype|None; no phenotype|C57BL/6J|No|Yes|Unknown|No|Yes|Unknown|No|Unknown||||No|29-Nov-2013|Cryopreserved sperm|50.0|0.0|Unknown||aromatase|Yes| 2783.0|C57BL/6.OCIL-KO|B6(Cg)-Clec2d/Apb|B6(Cg)-Clec2d/Apb|Recessive|C-type lectin domain family 2, member d|Clec2d|Unknown|Clr-b, Clrb, Ocil|MGI:2135589|targeted mutation 1.1, Matthew T Gillespie|Clec2d|MGI:3826396|6||||||||||||||||Yes|||||||||||||The mice show no overt phenotype. The bone phenotype (as analysed by bone histomorphometry) is mild "osteopenia" or a low bone mass due to a high bone turnover(caused by increased numbers of osteoclasts).|Not examined|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|5|9|Hom x Hom|Yes|16-Feb-2008|Cryopreserved sperm|98.0|0.0|Unknown||c-type lectin, osteoclast, bone remodelling, natural killer cell|Yes| 10410.0||C57BL/6-Ipo7/DunwApb||Dominant|Importin 7|Ipo7||Imp7, RanBP7|MGI:2152414|Ipo7|||7|ENSMUSG00000066232 ||||||||||||||||||||||||||||Embryonic lethal|Heterozygous knock-out mice are viable but are reported to have abnormal eye, skin, trachea, lymph nodes and spleen morphology.|C57Bl/6J|No|No|Unknown|No|No|Unknown|No|Unknown||||No|12-Mar-2024|Cryopreserved sperm|55.0|0.0|Unknown|||No| 5497.0|PAF|C57BL/6-Ptafr/Apb||Recessive|platelet-activating factor receptor|Ptafr||PAF receptor, PAFR|MGI:106066|platelet-activating factor receptor; targeted mutation 1, Takao Shimizu|Ptafr|MGI:3036770|4||||||||||||||||No|||||||||||||Normal.Increased susceptibility to type I hypersensitivity reaction: * homozygous mutants have a marked reduction in systemic anaphylactic symptoms when challenged with ovalbumin (OVA) * compared to controls, homozygous mice did not develop anaphylactic hypotension, anaphylactic tachycardia followed by bradycardia nor do they develop any anaphylaxis dependent changes in the lungs or suffer lethal affects in response to antigen challenge * homozygous mutants do respond normally to endotoxins and develop endotoixc shock at the same level as controls.Decreased inflammatory response: inflammatory response to S. venezuelensis worm infection is lower at 7 days after infection as indicated by lower numbers of eosinophils and globlet cells in tissue and diminished cytokine production, with a reduction in the production of Th2 cytokines (IL-4, IL-5, and IL-10) in the small intestine and by specific antigen-stimulated spleen or MLN cells.Increased susceptibility to parasitic infection: while the fecundity of the worm, Strongyloides venezuelensis, is decreased in mutant mice, overall elimination is delayed.||C57BL/6|Yes|Yes|Unknown|Yes|Yes|Unknown|No|Good||||No|04-May-2011|Cryopreserved sperm|50.0|0.0|Unknown||anaphylaxis, sperm, endotoxin|Possibly| 7891.0|ENU19:Mapt:B6|C57BL/6JAnu-Mapt/AnuApb||Recessive|microtubule-associated protein tau|Mapt|Nil|Mtapt, Tau|MGI:97180|Mapt; mutation 1, Australian National University|Mapt||11||||||||||Unknown to Unknown|||||||||||||||||||||C57BL/6JAnu|No|No|Yes|No|No|Yes|No|Unknown||||No|11-May-2015|Cryopreserved sperm|44.0|0.0|Unknown||Tau, neuronal|Yes| 7887.0||SJL-MRI156922||Dominant|Unknown||Unknown||||||Unknown|||||||||||||||||||||||||||||none|Small red cells|SJL|No|No|Yes|No|No|Yes|No|Unknown||||No|30-Apr-2015|Cryopreserved sperm|55.0|0.0|Unknown|||Yes| 7888.0|Bim Knockout|B6.129-Bcl2l11/WehiAnuApb||Recessive|BCL2-like 11 (apoptosis facilitator)|Bcl2l11|Nil|1500006F24Rik, Bim, Bod|MGI:1197519|BCL2-like 11 (apoptosis facilitator); targeted mutation 1.1, Andreas Strasser|Bcl2l11|MGI:2156498|2||||||||||||||||Yes|||||||||||||Increased numbers of lymphoid and myeloid cells. Spleen and lymph nodes are 2-3-fold bigger than in wt. Sternum is sticking out. Bim-/- females are bad mothers and should not be used for breeding unless necessary. Bim -/-: blood - increased lymphocytes (B + T cells), granulocytes & monocytes. - decreased platelets - Increased serum Ig. Thymus - fewer pre T cells. Age 1 year - lymphadenopathy - 55% -/-, 35% +/- mice sick with kidney disease or cardiac infarction/vasculitis. Fewer -/- females born. When born, often have poorly formed reproductive organs. -/- have protruding sternum. ||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|10|||No|08-May-2015|Cryopreserved sperm|92.0|0.0|Unknown||T cell, B cell, Lymphoid, Myeloid, Sternum|Yes| 10413.0||C57BL/6-Wdr90em1Dunw/DunwApb||Dominant|WD Repeat Domain 90 |Wdr90|||MGI:1921267|Wdr90|||17|||||||||||||||||||||||||||||Mice homozygous for the null allele may have heart defects|Heterozygous mice are unlikely to be affected|C57Bl/6J|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|12-Mar-2024|Cryopreserved sperm|53.0|0.0|Unknown|||No| 7193.0|CAG-Flpe|C57BL/6NTac-Tg(CAG-Flpe)2Arte/Ausb||Dominant||||||||||||||||||||||||||transgene insertion 2, TaconicArtemis|chicken--actin promoter and an hCMV immediate early enhancer (CAG)|||||||||||Ubiquitous expression of FLPe recombinase.|Ubiquitous expression of FLPe recombinase.|C57BL/6NTac|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|05-Nov-2012||0.0|0.0|Unknown||recombinase|Yes| 7152.0|Ikk1FL|C57BL/6-Chuk/Ausb||Recessive||IKK1|||MGI:3714160|||||||||||||||||||||||||||||||||||C57BL/6|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|02-Nov-2012||0.0|0.0|Unknown|||Possibly| 7502.0|KI-Rag2/EGFP|129S6/SvEVTac-Rag2/FwaAusb||Dominant|recombination activating gene 2|Rag2|Normal|Rag-2|MGI:97849|recombination activating gene 2; targeted mutation 2, Frederick W Alt|Rag2|MGI:3623131|2|||||||||||||||||||||||||||||No abnormal phenotype detected:• homozygotes produce Rag2 protein capable of V(D)J recombination and exhibit normal lymphocyte development; mice are used to analyze Rag2 expression in primary and peripheral lymphoid tissues||129S6/SvEvTac|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|19-Nov-2013||0.0|0.0|Unknown||GFP, B cell, T cell, IgM|Yes| 10404.0|C57BL/6NCrlAnu-Nlrp1a/Anu|ENU55:208:Nlrp1a:B6:||Recessive|NLR family, pyrin domain containing 1A|Nlrp1a||Nalp1a|MGI:2684861|Nlrp1a|||11|ENSMUSG00000069830||||||||||||||||||||||||||||Unknown|unknown|C57Bl/6N|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|05-Feb-2024|Cryopreserved sperm|53.0|0.0|Unknown|||Possibly| 6736.0|Klf1KOBALB/c|BALB/c-Klf1/Ausb||Dominant|Kruppel-like factor 1 (erythroid)|Klf1|Normal|Eklf, Nan |MGI:1342771|Kruppel-like factor 1 (erythroid); targeted mutation 1, National Institute of Medical Research|Klf1|MGI:1857557|8|||||||||||||||||||||||||||||Complete embryonic lethality during organogenesis:*Homozygotes die of rapid, fatal anemia at ~E14 after switching of embryonic hematopoiesis to the fetal liver.Abnormal erythropoiesis:*Homozygotes display a defect in the late steps of differentiation of mature erythroid progenitors. Decreased hemoglobin content: *At E14.5, mutant fetal livers contain no hemoglobin. Anemia: *By E14.5, homozygotes are severely anemic. Erythroblastosis: *At E12.5, homozygotes exhibit erythroblastosis.Impaired hematopoiesis:*Homozygotes exhibit defective hematopoiesis in fetal liver.*Enucleated erythrocytes are formed but do not contain the full complement of hemoglobin.Small liver:*At E12.5, homozygotes display significant growth retardation of the fetal liver.*However, a normal number of colony-forming cells are detected in early fetal liver, indicating that the progenitor cell compartment is unaffected.Pale liver:*At E12,5 and E13.5, homozygotes exhibit pale livers that lack their full complement of hemoglobin.||BALB/c|No|No|Yes|No|No|Yes|No|Unknown||||No|02-Dec-2011||0.0|0.0|Unknown||Erythroid Krüppel-like factor (EKLF), ES cells, Haematopoiesis|Yes| 7892.0||ENU24:045:unknown||Recessive|||||||||Unknown|||||||||||||||||||||||||||||Incidental phenotype of lower CD44 MFI on CD4 T cells (inheritence unclear)||C57BL/6NCrlAnu|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|15-May-2015|Cryopreserved sperm|33.0|0.0|Unknown||ENU, CD4, T cell, CD44|Yes| 7504.0|Lig4-Y288C|B6(Cg)-Lig4/ApbAusb|B6(Cg)-Lig4/ApbAusb|Recessive|ligase IV, DNA, ATP-dependent|Lig4|Reduced|DNA ligase IV, ligase IV|MGI:1335098|tiny|Lig4|MGI:3584400|8|ENSMUSG00000049717|ENSMUST00000095476|Lig4-201|863|1161|A to G|ENSMUSE00000610685|2|288|Tyrosine to Cysteine|||||CATGCAGATGCACAAAGATGGCGCGCTGTACCGGTACTTCTCCAGAAACGGTTACAACTAT|No|||||||||||||Animal model for human LIGIV Syndrome. Small stature. Severe combined immune deficiency. Hypogammaglobulinemia, no antibody response to immunization, very few circulating B or T cells. Hemopoiesis defect. Hypoplastic anemia, hemopoietic stem cells unable to transplant, poorly proliferative in tissue culture, unable to compete with transplanted wild-type hemopoietic stem cells even in the absence of any conditioning regime. Non-homologous end-joining DNA repair defect. Reduced DNA ligase IV protein levels and enzymatic activity. Western blot and immunofluorescent analysis of extracts from homozygous mutant mouse embryonic fibroblasts (MEFs) reveal 5-fold reduction in the protein level. Although the mutant protein complexes stably with XRCC4, in vivo adenylation activity is reduced 10-fold in mutant versus wild type MEFs.||C57BL/6JAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|19-Nov-2013||0.0|0.0|Yes||T cell, CD8, severe combined immunodeficiency, DNA repair, ENU|Yes| 9378.0|Dnas1L3 (27)|C57Bl/6N-Dnas1L3 <(27)>/Apb||Semi-dominant|Dnas1L3||||||||Unknown|||||||||||||||||||||||||||||Unknown|Unknown|C57Bl/6N|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|05-May-2022|Cryopreserved sperm|51.0|0.0|Unknown|||Possibly| 8799.0|ENU46:136:P2rx7|C57BL/6NCrlAnu-P2rx7/AnuApb||Recessive|purinergic receptor P2X, ligand-gated ion channel, 7|P2rx7||P2X(7), P2X7R, P2X7 receptor|MGI:1339957||||5|||||||||||||||||||||||||||||Unknown||C57BL/6NCrlAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|04-Oct-2019|Cryopreserved sperm|106.0|0.0|Unknown||ENU|Yes| 7898.0|ENU22:Stat4|C57BL/6JAnu-Stat4/AnuApb||Recessive|signal transducer and activator of transcription 4|Stat4|||MGI:103062|Stat4; mutation 1, Australian National University|Stat4||1||||||||||Unknown to Unknown|||||||||||||||||||Unknown||C57BL/6JAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|27-May-2015|Cryopreserved sperm|54.0|0.0|Unknown||signal transduction, T cell, NK cell|Yes| 7900.0|L3mbtl1 KO|B6.129-L3mbtl1/Marp||Recessive|l(3)mbt-like (Drosophila)|L3mbtl1|Nil|L3MBTL1|MGI:2676663|l(3)mbt-like (Drosophila); targeted mutation 1.1, Hanno Hock|L3mbtl1|MGI:4840260|2|||||||||||||||||||||||||||||Normal||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|27-May-2015|Cryopreserved sperm|50.0|0.0|Unknown||methylation, brain|Yes| 7901.0|Cd19-cre|C57BL/6JAnu-Cd19/AnuApb||Recessive|CD19 antigen|Cd19|||MGI:88319|targeted mutation 1, University of Cologne|Cd19|MGI:1931143|7||||||||||||||||||||||||||||||Normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|01-Jun-2015|Cryopreserved sperm|44.0|0.0|Unknown||Cre recombinase, CD19|No| 7897.0|"p75-AD" mouse|129(Cg)-Ngfr Tg(APPSWE)2576Kha/Apb||Dominant|nerve growth factor receptor (TNFR superfamily, member 16)|Ngfr|Reduced|LNGFR, p75, p75 neurotrophin receptor, p75NGFR, p75NTR, Tnfrsf16|MGI:97323|nerve growth factor receptor (TNFR superfamily, member 16); targeted mutation 1, Rudolf Jaenisch|Ngfr|MGI:1857226|11|||||||||||||||||transgene insertion 2576, Karen Hsiao Ashe|Hamster Prion protein promoter|medium to high||||||||||Develop plaque in brain from 6-8 months of age. Cognitive performance is normal due to reduced p75 expression|Normal|129Sv|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|20 or more|20|p75 null homozygotes mated to APP transgenic heterozygotes|No|26-May-2015|Cryopreserved sperm|49.0|0.0|Yes|Alzheimers Disease|dementa, p75NTR, nerve growth factor|Possibly| 7899.0|Ptprt KO|B6.129P2-Ptprt/Marp||Recessive|protein tyrosine phosphatase, receptor type, T|Ptprt|Unknown||MGI:1321152|protein tyrosine phosphatase, receptor type, T; targeted mutation 1, Zhenghe Wang|Ptprt|MGI:4437410|2|||||||||||||||||||||||||||||Increased incidence of tumors by chemical induction:• 17 of the 20 homozygous mice develop visible colon tumors induced by azoxymethane, compared with none develop tumor in wild-type miceIncreased colonic adenoma incidence• 17 of the 20 homozygous mice develop visible colon adenomas induced by azoxymethane• average 1.5 tumors per mouse• highly proliferative dysplastic cells as indicated by Ki-67 immunohistochemistry staining||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|27-May-2015||0.0|0.0|Unknown||Tyrosine, Phosphatase|Yes| 9381.0|ENU55:G2|ANU:ENU55:G2||Recessive|Unknown||||||||Unknown||||||||||||||||Unknown|||||||||||||Unknown|Unknown|C57BL/6JAnu|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||1||No|11-May-2022|Cryopreserved sperm|87.0|0.0|Unknown||ENU, random, mutagenesis, screen|Yes| 7906.0|ENUProx1-GFP|ENUProx1-GFP||Recessive|||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|12-Jun-2015|Cryopreserved sperm|175.0|0.0|Unknown||Prox1-GFP, GFP, ENU|No| 8800.0|ENU46:270:P2rx7|C57BL/6NCrlAnu-P2rx7/AnuApb||Recessive|purinergic receptor P2X, ligand-gated ion channel, 7|P2rx7||P2X(7), P2X7R, P2X7 receptor|MGI:1339957||||5|||||||||||||||||||||||||||||Unknown||C57BL/6NCrlAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|04-Oct-2019|Cryopreserved sperm|88.0|0.0|Unknown||ENU|Yes| 8801.0|ENU46:269:Stat2|C57BL/6NCrlAnu-Stat2/AnuApb||Recessive|signal transducer and activator of transcription 2|Stat2|Unknown|1600010G07Rik|MGI:103039||||10|||||||||||||||||||||||||||||Unknown||C57BL/6NCrlAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|04-Oct-2019|Cryopreserved sperm|47.0|0.0|Unknown||ENU|Yes| 7894.0|ENU32:047:Ikzf1|C57BL/6NCrlAnu-Ikzf1/AnuApb||Recessive|IKAROS family zinc finger 1|Ikzf1||5832432G11Rik, Ikaros, LyF-1, Zfpn1a1|MGI:1342540||||11|ENSMUSG00000018654|ENSMUST00000076700|Ikzf1-201|395|665|T to C|ENSMUSE00000330373|4|132|Leucine to Proline||||||Unknown|||||||||||||Low B cells in peripheral blood in HOM. |HETS may have a subtle phenotype of a small increase in CD44 MFI on CD4s|C57BL/6NCrlAnu|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||1||No|15-May-2015|Cryopreserved sperm|55.0|0.0|Unknown||ENU, B cell, CD44, T cell, CD4|Yes| 7912.0|Rictor fl|B6.129-Rictor/Anu||Recessive|RPTOR independent companion of MTOR, complex 2|Rictor|Unknown|4921505C17Rik, 6030405M08Rik, D530039E11Rik|MGI:1926007|RPTOR independent companion of MTOR, complex 2; targeted mutation 1.1, Kun-Liang Guan|Rictor|MGI:5448837|15|||||||||||||||||||||||||||||Normal||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|18-Jun-2015||0.0|0.0|Unknown||mTOR|Yes| 7908.0||SJL/ASAM||Dominant|unknown|unknown|Reduced||||||Unknown|||||||||||||||||||||||||||||Unknown|The mice displays a normal phenotype.|SJL/J|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Good||||No|16-Jun-2015|Cryopreserved sperm|22.0|0.0|Unknown|||Yes| 7909.0||SJL/ASAM||Dominant|unknown|unknown|Reduced||||||Unknown|||||||||||||||||||||||||||||Unknown|The mice displays a normal phenotype.|SJL/J|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Good||||No|16-Jun-2015|Cryopreserved sperm|34.0|0.0|Unknown|||Yes| 7910.0|CAG-rtTA3|B6(Cg).129-Tg(CAG-rtTA3)#Slowe/Anu||Dominant||||||||||||||||||||||||||transgene insertion, Scott Lowe|cytomegalovirus (CMV) early enhancer element and chicken beta-actin||||||||||||Ubiquitous expression of Cre recombinase|C57BL/6N|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|5|||No|18-Jun-2015|Cryopreserved sperm|54.0|0.0|Unknown||Cre recombinase|Yes| 7914.0|iCre Rictor fl|B6.129-Rictor Tg(UBC-cre/ERT2)1Ejb/Anu||Recessive|RPTOR independent companion of MTOR, complex 2|Rictor|Unknown|4921505C17Rik, 6030405M08Rik, D530039E11Rik|MGI:1926007|RPTOR independent companion of MTOR, complex 2; targeted mutation 1.1, Kun-Liang Guan|Rictor|MGI:5448837|15|||||||||||||||||transgene insertion 1, Eric J Brown|Human ubiquitin C (UBC) promoter|||||||||||Unknown||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|8|||No|18-Jun-2015|Cryopreserved sperm|107.0|0.0|Unknown||mTOR, inducible, Cre recombinase|Yes| 8797.0|Osteopontin null|B6.129S7-Spp1/Apb||Recessive|secreted phosphoprotein 1|Spp1||2ar, 44kDa bone phosphoprotein, Apl-1, BNSP, bone sialoprotein 1, ETA-1, minopontin, OP, Opn, Opnl, osteopontin, osteopontin-like protein, Ric, Spp-1|MGI:98389|secreted phosphoprotein 1; targeted mutation 1, Susan R Rittling|Spp1|MGI:1932084|5|||||||||||||||||||||||||||||Mortality/aging:N • homozygotes are viable, fertile and overtly normal with no significant differences in lactation, growth development, or organ and tissue histologyDecreased osteoclast cell number:• fewer osteoclasts accumulate at the site of an implanted bone disc compared to in similarly treated wild-type mice.Increased osteoclast cell number:• homozygotes exhibit a 3-fold increase in osteoclast number relative to wild-type mice; ovariectomy does not increase the number of osteoclasts significantly• in vitro, several-fold more osteoclasts are generated in co-culture systems with wild-type calvarial osteoblast cells by using spleen cells (3- to 13-fold) or bone marrow cells (~2- to 4-fold) from homozygous mutant mice compared with wild-type mice.Abnormal osteoclast physiology:• in contrast to wild-type mice, homozygotes are resistant to ovariectomy-induced bone resorption despite a comparable reduction in uterine weight (25-30%)• ovariectomized homozygotes exhibit a 12% reduction in trabecular bone volume in the absence of increased bone formation, whereas ovariectomized wild-type mice show a 58% reduction in trabecular bone volume along with a 73% increase in bone formation• bone resorption and osteoclast formation induced by PTH in cultured mouse calvariae are absent in calvariae from homozygous mutant miceDecreased interferon-gamma secretion:• following treatment with polyvinyl pyrrolidone, mice exhibit a 90% reduction in IL12 production compared with in similarly treated wild-type mice• splenocytes from L. monocytogenes infected mice produce less IFN-gamma when restimulated with heat-killed bacteria compared with similarly treated wild-type miceIncreased interleukin-10 secretion:• draining lymph node cells from HSV-1-infected mice produce increased IL10 compared with cells from similarly treated wild-type mice.Decreased interleukin-12 secretion:• following treatment with polyvinyl pyrrolidone, mice exhibit a 95% reduction in IL12 production compared with in similarly treated wild-type mice• draining lymph node cells and splenocytes from HSV-1-infected mice produce decreased IL12 compared with cells from similarly treated wild-type mice.Increased interleukin-4 secretion:• draining lymph node cells from HSV-1-infected mice produce increased IL4 compared with cells from similarly treated wild-type mice.Abnormal inflammatory response:• mice treated with polyvinyl pyrrolidone fail to exhibit a granulomatous response unlike similarly treated wild-type miceDecreased susceptibility to type IV hypersensitivity reaction:• mice infected with HSV-1 do not display a tuberculin-type delayed-type hypersensitivity when challenged with HSV-1 unlike similarly treated wild-type miceAbnormal response to infection:• clearance of Listeria monocytogenes is defective compared to in similarly treated wild-type mice• splenocytes from L. monocytogenes infected mice produce less IFN-gamma when restimulated with heat-killed bacteria compared with similarly treated wild-type miceDecreased susceptibility to viral infection:• mice infected with HSV-1 do not display a tuberculin-type delayed-type hypersensitivity when challenged with HSV-1 unlike similarly treated wild-type mice• corneal HSV-1 infection fails to trigger herpes simplex keratitis unlike in similarly treated wild-type mice|Normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|01-Oct-2019|Cryopreserved sperm|33.0|0.0|Unknown|||Yes| 7904.0|Astn2 KO|C57BL/6-Astn2/Marp|MGI:5636645|Recessive|Astrotactin 2|Astn2|Nil|1d8, Astnl|MGI:1889277|Astrotactin 2, endonuclease mutation 1, Phillip I Bird|Astn2|MGI:5636645|4||||||||||Unknown to Unknown|||||||||||||||||||Unknown|Unknown|C57BL/6|Yes|Unknown|Yes|Yes|Unknown|Yes|No|Good||||No|12-Jun-2015|Cryopreserved sperm|50.0|0.0|Unknown||Astrotactin, membrane attack complex / perforin domain, MACPF|Possibly| 7913.0|iCre|B6.129-Tg(UBC-cre/ERT2)1Ejb/Anu||Dominant||||||||||||||||||||||||||transgene insertion 1, Eric J Brown|human ubiquitin C (UBC) promoter||||||||||||Mice display tamoxifen-inducible Cre activity in all tissue types. |C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|18-Jun-2015|Cryopreserved sperm|55.0|0.0|Unknown||Cre recombinase, inducible, tamoxifen|Yes| 7917.0|Vav-cre|C57BL/6-Tg(Vav1-Cre)1Awr/WehiAnu||Dominant||||||||||||||||||||||||||transgene insertion 1, Andrew W Roberts|Vav1|Haemopoietic||||||||||Normal|Normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|18-Jun-2015|Cryopreserved sperm|75.0|0.0|Unknown||Cre recombinase|Yes| 7918.0|Mb1-cre|B6.C-Cd79a/Anu||Dominant|CD79A antigen (immunoglobulin-associated alpha)|Cd79a||Cd79a, Iga, Igalpha, Ig alpha, Ig-alpha, Ly54, Ly-54, mb-1|MGI:101774|CD79A antigen (immunoglobulin-associated alpha); targeted mutation 1, Michael Reth|Cd79a|MGI:3687451|7||||||||||||||||||||||||||||||Normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|19-Jun-2015|Cryopreserved sperm|154.0|0.0|Unknown||B cell, Cre recombinase|Yes| 7919.0|Ubf fl|STOCK Ubtf/Anu||Recessive|upstream binding transcription factor, RNA polymerase I|Ubtf||A930005G04Rik, Tcfubf, UBF, UBF1|MGI:98512|upstream binding transcription factor, RNA polymerase I; targeted mutation 1.1, Tom Moss|Ubtf|MGI:5708602|11||||||||||Unknown to Unknown|||||||||||||||||||Normal|||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|19-Jun-2015|Cryopreserved sperm|66.0|0.0|Unknown||RNA polymerase, rRNA|Yes| 7921.0|Pad4 KO|B6.Cg-Padi4/KmowAnu||Recessive|peptidyl arginine deiminase, type IV|Padi4|Nil|Pad4, PAD type IV, Pdi4|MGI:1338898|peptidyl arginine deiminase, type IV; targeted mutation 1.1, Kerri A Mowen|Padi4|MGI:5285854|4|||||||||||||||||||||||||||||Abnormal neutrophil physiology:• neutrophils lack histone deimination unlike wild-type cellsdecreased susceptibility to viral infection• influenza-infected mice exhibit decreased weight loss compared with similarly treated wild-type mice• however, influenza-infected mice exhibit normal survival, neutrophil recruitment into the lung, lung viral titers, and pro-inflammatory cytokine levelsDecreased susceptibility to weight loss:• influenza-infected mice exhibit decreased weight loss compared with similarly treated wild-type mice||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|19-Jun-2015|Cryopreserved sperm|55.0|0.0|Unknown||Infection, neutrophil, extracellular traps|Yes| 7915.0|TiF1a fl|B6.129-Rrn3/Anuapb||Recessive|RRN3 RNA polymerase I transcription factor homolog (yeast)|Rrn3||E130302O19Rik, TIF-1A|MGI:1925255|RRN3 RNA polymerase I transcription factor homolog (yeast); targeted mutation 1.1, Ingrid Grummt|Rrn3|MGI:3584035|16|||||||||||||||||||||||||||||Normal|Normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|11|||No|18-Jun-2015|Cryopreserved sperm|105.0|0.0|Unknown||rRNA, p53, cell cycle|Yes| 7920.0|VCE ER/Stop YFP:VAV-CreER|C57BL/-Tg(Vav1-cre/ERT)1Wehi/WehiAnu||Dominant||||||||||||||||||||||||||Vav1-cre/ERT|||||||||||||Normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|19-Jun-2015|Cryopreserved sperm|109.0|0.0|Unknown||Cre recombinase, inducible, tamoxifen|Yes| 7923.0|RORgt|B6.129-Rorc/WehiAnu||Dominant|RAR-related orphan receptor gamma|Rorc||RORgamma, Thor, thymus orphan receptor|MGI:104856|RAR-related orphan receptor gamma; targeted mutation 2, Dan R Littman|Rorc|MGI:3026635|3|||||||||||||||||||||||||||||Increased thymocyte apoptosis:• isolated thymocytes undergo apoptosis in culture within 2-3 hours compared to controls that survive for more than 5 hoursdecreased double-negative T cell number• numbers of intestinal alpha beta T cells including CD4-CD8- cells are significantly reducedDecreased double-positive T cell number:• fewer double-positive T cells (30-50% that of wild-type)decreased NK cell number• the percentage and absolute numbers of the Ncr(NKp46)+CD127+NK1.1- subset of intestinal natural killer cells is strongly decreased compared to controls• however, the number of NK1.1+ subset of intestinal natural killer cells is normalAbnormal CD4-positive, alpha-beta intraepithelial T cell morphology:• numbers of intestinal alpha beta T cells including CD4+ cells are significantly reducedAbnormal CD8 positive, alpha-beta intraepithelial T cell morphology:• numbers of intestinal alpha beta T cells including CD8alpha-beta+ and CD8alpha-alpha+ cells are significantly reducedAbnormal gut-associated lymphoid tissue morphology• absence of lymphoid tissue inducer (LTi) cells• intestinal cryptopatches and isolated lymphoid follicles are absentAbsent Peyer's patchesAbsent lymph nodes:• mice lack all lymph nodesAbnormal lymph organ development:• absence of lymphoid tissue inducer (LTi) cells||C57BL/6|Yes|Unknown|Yes|Yes|Unknown|Yes|No|Unknown||||No|19-Jun-2015|Cryopreserved sperm|30.0|0.0|Unknown||Lymph node, Peyer's patches|Yes| 7925.0|Il22-DY|C57BL/6NTac-Tg(Il22-DY)01Stsc/Anu||Recessive|interleukin 22|Il22||IL-22, Iltif, IL-TIF|MGI:1355307||||10|||||||||||||||||||||||||||||Reporter for IL22 cytokine expression, no pathological phenotype||C57BL/6N|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|19-Jun-2015|Cryopreserved sperm|21.0|0.0|Unknown||Cytokine|Yes| 7926.0|2A10gHC|C57BL/6-Tg(IgH2A10)1Anu/Anu||Dominant||||||||||||||||||||||||||2A10||||||||||||||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|19-Jun-2015|Cryopreserved sperm|46.0|0.0|Unknown||Infection|Yes| 7930.0|A23.Foxp3-DTR|BALB/c(Cg)-Foxp3 Tg(TcraA23,TcrbA23)#Ird/IrdApb||Dominant|forkhead box P3|Foxp3||JM2, scurfin|MGI:1891436|forkhead box P3; targeted mutation 3, Alexander Y Rudensky|Foxp3|MGI:3698131|X|||||||||||||||||A23 T cell reeptor|T cell receptor|||||||||||Restricted T cell receptor usage due to TCR transgene. |As above|BALB/c|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|22-Jun-2015|Cryopreserved sperm|50.0|0.0|Unknown||autoimmune gastritis, autoimmune disease, T cell receptor, Treg cells, regulatory T cell|Possibly| 7927.0|Mdm2 S6 Mx1-Cre |B6(Cg).129(Cg)-Mdm2 Rps6 Tg(Mx1-Cre)1Cgn/JAnu||Recessive|transformed mouse 3T3 cell double minute 2|Mdm2||1700007J15Rik, Mdm-2|MGI:96952|transformed mouse 3T3 cell double minute 2; targeted mutation 1.1, Yangping Zhang|Mdm2|MGI:4836988|10|||||||||||||||||transgene insertion 1, University of Cologne|Mx1|||||||||||Unknown||C57BL/6J|Yes|Unknown|Yes|Yes|Unknown|Yes|No|Unknown||||No|19-Jun-2015|Cryopreserved sperm|54.0|0.0|Unknown|||Yes| 7927.0|Mdm2 S6 Mx1-Cre |B6(Cg).129(Cg)-Mdm2 Rps6 Tg(Mx1-Cre)1Cgn/JAnu||Recessive|ribosomal protein S6|Rps6|Normal|S6R|MGI:98159|ribosomal protein S6; targeted mutation 1, George Thomas|Rps6|MGI:2387471|4|||||||||||||||||||||||||||||Unknown||C57BL/6J|Yes|Unknown|Yes|Yes|Unknown|Yes|No|Unknown||||No|19-Jun-2015|Cryopreserved sperm|||Unknown|||Yes| 7929.0|A23.IEβ|BALB/c-Tg(H2-Ea-Atp4b) Tg(TcraA23,TcrbA23)#Ird/Ird||Dominant||||||||||||||||||||||||||H⁺/K⁺ ATPase β subunit ; ATPase, H+/K+ exchanging, beta polypeptide|MHC I-E|||||||||||Restricted T cell receptor usage due to TCR transgene. Resistant to autoimmune gastritis|As above|BALB/c|Yes|Yes|Yes|Unknown|Unknown|Unknown|No|Unknown||||No|22-Jun-2015|Cryopreserved sperm|50.0|0.0|Unknown||autoimmune gastritis, autoimmune disease, T cell receptor, Thymus|Possibly| 7929.0|A23.IEβ|BALB/c-Tg(H2-Ea-Atp4b) Tg(TcraA23,TcrbA23)#Ird/Ird||Dominant||||||||||||||||||||||||||A23 T cell reeptor|T cell receptor|||||||||||Restricted T cell receptor usage due to TCR transgene. Resistant to autoimmune gastritis|As above|BALB/c|Yes|Yes|Yes|Unknown|Unknown|Unknown|No|Unknown||||No|22-Jun-2015|Cryopreserved sperm|||Unknown||autoimmune gastritis, autoimmune disease, T cell receptor, Thymus|Possibly| 7933.0|Solox Med |B6.CBA-Ifnar2 Tg(sIfnar2)1Pjh/Marp||Recessive|interferon (alpha and beta) receptor 2 |Ifnar2|Nil|Ifnar-2 |MGI:1098243|interferon (alpha and beta) receptor 2; targeted mutation 1, Paul J Hertzog|Ifnar2|MGI:2680693|16|||||||||||||||||soluble type I interferon (alpha and beta) receptor 2a overexpressing|Endogenous|Medium||||||||||Normal|Normal|B6/CBA|Yes|Yes|Yes|Yes|Yes|Yes|No|Poor||||No|24-Jun-2015|Cryopreserved sperm|50.0|0.0|Unknown||soluble, cytokine, interferon|Possibly| 7935.0|ENU26:037:Pkhd1:B6:|C57BL/6NCrlAnu-Pkhd1/AnuApb||Recessive|polycystic kidney and hepatic disease 1|Pkhd1|Unknown|FPC, tigmin|MGI:2155808|Pkhd1; mutation 1, Australian National University|Pkhd1||1|ENSMUSG00000043760|ENSMUST00000088448|Pkhd1-001|823|1059|A to T|ENSMUSE00000630693|38|275|Isoleucine to Phenylalanine|||||AAGTTGGGAGCCTTGGGGGAAGAACGGACATCATCATTACGGGAGATTTCTTTGACCCTTC||||||||||||||Unknown|Unknown|C57BL/6NCrlAnu|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|26-Jun-2015|Cryopreserved sperm|44.0|0.0|Unknown||ENU, mutagenesis, screen, random|Possibly| 7936.0|ENU18:Recql4::B6|C57BL/6JAnu-Recql4/AnuApb||Recessive|RecQ protein-like 4|Recql4|Unknown||MGI:1931028|Recql4; mutation 1, Australian National University|Recql4||15|ENSMUSG00000033762|ENSMUST00000036852|Recql4-201|1039|1122|G to A|ENSMUSE00000237138|5|347|Arginine to STOP|||||CAGCTTCCCTAGACAGAGGGAACTATATTCGACTCAACATGAAAAACAAACGCTTTGTACG|Unknown|||||||||||||Unknown|Unknown|C57BL/6JAnu|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|26-Jun-2015|Cryopreserved sperm|44.0|0.0|Unknown||ENU, random, mutagenesis, screen|Possibly| 7932.0|Ampd3 KO|C57BL/6N-Ampd3 Tg(CMV-cre)1Cgn/AnuApb||Recessive|adenosine monophosphate deaminase 3|Ampd3|||MGI:1096344|adenosine monophosphate deaminase 3; targeted mutation 2a, Wellcome Trust Sanger Institute|Ampd3||7|||||||||||||||||transgene insertion 1, University of Cologne|Cytomegalovirus (CMV) early enhancer element and chicken beta-actin|||||||||||Unknown||C57BL/6NCrlAnu|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|22-Jun-2015||0.0|0.0|Unknown|||Yes| 7938.0|ENU31:016 B6|C57BL/6NCrlAnu-Gfi1/AnuApb||Recessive|growth factor independent 1|Gfi1|Unknown|Gfi-1, Pal1, Pal-1|MGI:103170||||5|ENSMUSG00000029275|ENSMUST00000065478|Gfi1-201||||||||107723722|2|||GGAGACCGTGCCTGCGCCGGGCAGAGCAGGTGCGAAGCGCGCAGAGGCCGGGTAGGGCAG||||||||||||||Activated CD8 T cells in blood.|Normal|C57BL/6NCrlAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|26-Jun-2015|Cryopreserved sperm|43.0|0.0|Unknown||T cell, CD8, ENU|Yes| 7939.0|ENU31:104:Mll2:b6|C57BL/6NCrlAnu-Kmt2d/AnuApb||Recessive|lysine (K)-specific methyltransferase 2D|Kmt2d|Unknown|C430014K11Rik, Mll2, Mll4|MGI:2682319||||15|ENSMUSG00000048154|ENSMUST00000023741|Kmt2d-001|16445|16673|A to T|ENSMUSE00000268270|52|5482|Isoleucine to Asparagine|||||||||||||||||||Embryonic Lethal|Normal|C57BL/6NCrlAnu|No|No|Yes|No|No|Yes|No|Unknown||||No|26-Jun-2015|Cryopreserved sperm|55.0|0.0|Unknown||ENU, embryonic lethal|Yes| 7931.0|B6.SJL|B6.SJL-Ptprc/AnuApb||Recessive|||||||||||||||||||||||||||||protein tyrosine phosphatase receptor type C|Ptprc |||MGI:97810|protein tyrosine phosphatase receptor type C; a variant|Ptprc|MGI:4819849|1|T cells express the Ptprc allele instead of Ptprc allele usually carried by Lymphocytes isolated from C57BL/6 mice.||C57BL/6J|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|22-Jun-2015|Cryopreserved sperm|21.0|0.0|Unknown||Ly5a|Yes| 7941.0|Kaos|B6.Cg-Lrguk/MarpApb||Recessive|leucine-rich repeats and guanylate kinase domain containing|Lrguk|Unknown||MGI:1921604||||6|ENSMUSG00000056215|ENSMUST00000070189|Lrguk-001|1582|1591|C to T|ENSMUSE00000459708|14|528|Arginine to STOP|||||GAAGTTTGAAATATTCTTATTTTGAGCCTCGATATATCTTGGTGGTGCCTATGGACAAGGA|Yes|||||||||||||Male infertility. ||C57BL/6J|Yes|Yes|Yes|Yes|No|Yes|No|Poor|13|||No|26-Jun-2015|Cryopreserved sperm|50.0|0.0|Yes|Male Infertility|ENU, fertility, sperm|Yes| 7934.0|ENU27:005:Cfh:B6|C57BL/6NCrlAnu-Cfh/AnuApb||Recessive|complement component factor h|Cfh|Unknown|Mud-1, Sas1, Sas-1|MGI:88385|Cfh; mutation 1, Australian National University|Cfh||1|ENSMUSG00000026365|ENSMUST00000111976|Cfh-201|3538|3673|A to G|ENSMUSE00001040918|21|1180|Tryptophan to Arginine|||||AGAAGACAATAACATGTAGAAATGGAAAGTGGTCTGAGCCACCAACATGCTTACATGCATG|Unknown|||||||||||||Unknown|Unknown|C57BL/6NCrlAnu|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Good||||No|26-Jun-2015|Cryopreserved sperm|55.0|0.0|Unknown||ENU, random, mutagenesis, screen|Possibly| 7942.0|ENU33:G3|ANU:ENU33:G3||Recessive|Unknown||||||||Unknown||||||||||||||||Unknown|||||||||||||Unknown|Unknown|C57BL/6NCrlAnu|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||1||No|02-Jul-2015|Cryopreserved sperm|111.0|0.0|Unknown||ENU, random, mutagenesis, screen|Yes| 7943.0|HNT Thy1.1|BALB/c-Thy1 Tg(Tcra,Tcrb)1Mcd/Wehi||Recessive||||||||||||||||||||||||||transgene insertion 1, Hugh O McDevitt|||thymus cell antigen 1, theta|Thy1||CD90, T25, theta, Thy-1, Thy1.1, Thy 1.2, Thy-1.2, Thy1.2|MGI:98747|thymus cell antigen 1, theta; a variant|Thy1|MGI:3579311|9|HNT-TCR mice express an I-A-restricted TCR specific for the HA peptide 126–138 (HNTngvtaacshe). TCR transgenics immunocompromised by having mono-specific TCR however in a clean environment mice do not show a phenotype different to B6.||BALB/c|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|09-Jul-2015|Cryopreserved sperm|33.0|0.0|Unknown||T cell, receptor (TCR), selection, tolerance, haemaglutanin|Yes| 4768.0|C57BL/6J.i-D|C57BL/6;129P2-H2-D1/AnuApb||Recessive|histocompatibility 2, D region locus 1|H2-D1|Nil|H2-D1|MGI:95896|targeted mutation 1, Beatrice Perarnau|H2-D1|MGI:1931445|17||||||||||||||||Yes|||||||||||||Mice lack H-2D molecule and are deficient in antigen presentation to CD8<+> T cells||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|10|2|sib x sib|No|06-May-2009|Cryopreserved sperm|90.0|0.0|No||T cell, CD8, presentation, Major histocompatibility complex (MHC)|Yes| 7944.0|Db -/-|B6.129P2-H2-D1/AnuApb||Recessive|histocompatibility 2, D region locus 1|H2-D1|Nil|H-2D|MGI:95896|histocompatibility 2, D region locus 1; targeted mutation 1, Beatrice Perarnau|H2-D1|MGI:1931445|17|||||||||||||||||||||||||||||||C57BL/6JAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|09-Jul-2015|Cryopreserved sperm|22.0|0.0|Unknown||H2|Yes| 7956.0|TetO ArchT, B6-tetO-ArchT/GFP Tg |C57BL/6-Tg(tetO-ArchT/EGFP)1Ahky ||Dominant||||||||||||||||||||||||||Archaerhodopsin-T (Halorubrum strain TP009) |E. coli Tetracycline operator, CMV minimal promotor, rabbit Beta globin intron |||||||||||Normal|Normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||over 20|hemizygous transgenic x non-transgenic (wild type) sibs|No|27-Jul-2015|Cryopreserved sperm|49.0|0.0|Unknown||tetO-system, light, Archaerhodopsin|Yes| 10403.0|Zeb2flox|B6;129(Cg)-Zeb2tm1.1Yhi||Recessive|zinc finger E-box binding homeobox 2|Zeb2||mKIAA0569, SIP1, Zfhx1b|MGI:1344407|zinc finger E-box binding homeobox 2; targeted mutation 1.2, Yujiro Higashi|Zeb2tm1.2Yhi|MGI:2387501|2|ENSMUSG00000026872 |ENSMUST00000028229|||||||||||||||||||||||||||Normal|Normal|C57Bl/6J|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|Backcross to C57BL/6Cr|||No|31-Jan-2024|Cryopreserved sperm|20.0|0.0|Unknown|||No| 10403.0|Zeb2flox|B6;129(Cg)-Zeb2tm1.1Yhi||Recessive|phage P1 loxP|loxP|||||||Unknown|||||||||||||||||||||||||||||Normal|Normal|C57Bl/6J|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|Backcross to C57BL/6Cr|||No|31-Jan-2024|Cryopreserved sperm|||Unknown|||No| 7946.0|ENU35:G1|ANU:ENU35:G1||Recessive|Unknown||||||||Unknown||||||||||||||||Unknown|||||||||||||Unknown|Unknown|C57BL/6NCrlAnu|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||1||No|21-Jul-2015|Cryopreserved sperm|2367.0|0.0|Unknown||ENU, random, mutagenesis, screen|Yes| 7948.0|ENU35:G2|ANU:ENU35:G2||Recessive|Unknown||||||||Unknown||||||||||||||||Unknown|||||||||||||Unknown|Unknown|C57BL/6NCrlAnu|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||1||No|23-Jul-2015|Cryopreserved sperm|2996.0|30.0|Unknown||ENU, random, mutagenesis, screen|Yes| 7949.0|ENU36:G1|ANU:ENU36:G1||Recessive|Unknown||||||||Unknown||||||||||||||||Unknown|||||||||||||Unknown|Unknown|C57BL/6NCrlAnu|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||1||No|23-Jul-2015|Cryopreserved sperm|2646.0|22.0|Unknown||ENU, random, mutagenesis, screen|Yes| 7950.0|ENU36:G2|ANU:ENU36:G2||Recessive|Unknown||||||||Unknown||||||||||||||||Unknown|||||||||||||Unknown|Unknown|C57BL/6NCrlAnu|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||1||No|23-Jul-2015|Cryopreserved sperm|2550.0|42.0|Unknown||ENU, random, mutagenesis, screen|Yes| 7848.0|alpha-synuclein knockout |B6;129X1-Snca/J||Recessive|synuclein, alpha (non A4 component of amyloid precursor)|Snca|Nil|alpha-Syn-; alpha-Synko|MGI:1277151|targeted mutation 1, Arnon Rosenthal|Snca|MGI:1888382|6|||||||||||||||||||||||||||||Homozygous null mice are viable, fertile, normal in size and do not display any gross abnormalities. No gene product (mRNA or protein) is detected in brain tissue. A wild-type complement of dopamine neurons, fibers and synaptic terminals is present and the overall brain architecture appears to be intact. They suffer from a reduction in total striatal dopamine and exhibit an attenuated locomotor response when given amphetamine. Normal dopamine release is observed upon stimulation of the nigrostriatal terminal with a single electrical pulse. When multiple stimuli are applied however, null mice exhibit an accelerated recovery of dopamine release. A similar acceleration is seen in wildtype mice in the presence of increased extracellular calcium. The phenotype observed in homozygous Snca-null mice suggests that Snca is an activity-dependent negative regulator of dopamine neurotransmission. |Unknown|B6;129X |Yes|Yes|Yes|Yes|Yes|Yes|No|Good||1|brother x sister|No|20-Feb-2015|Cryopreserved sperm|50.0|0.0|Yes|Parkinson's Disease|snca, dopamine, presynaptic, negative regulator|No| 7945.0|Elane KO|B6.129X1-Elane/J||Recessive|elastase, neutrophil expressed|Elane||Ela2, F430011M15Rik, NE, neutrophil elastase|MGI:2679229|elastase, neutrophil expressed; targeted mutation 1, Steven D Shapiro|Elane|MGI:2182771|10|||||||||||||||||||||||||||||Abnormal neutrophil physiology:• despite normal neutrophil recruitment, recognition and binding, neutrophils fail to degrade phagocytosed Klebsiella pneumoniae or Escherichia coli unlike in wild-type micedecreased susceptibility to bacterial infection induced Morbidity/mortality• mice are less susceptible to death induced by Gram positive Staphylococcus aureus infection compared to wild-type miceIncreased susceptibility to bacterial infection:• mice appear clinically worse than wild-type mice following infection with Gram negative Klebsiella pneumoniae or Escherichia coli• when infected with Klebsiella pneumoniae, mice exhibit signs of severe infection including ruffled fur, hunched posture, impaired ambulation and diarrhea unlike wild-type mice• despite normal neutrophil recruitment, recognition and binding, bacterial burden is greater than in wild-type mice following infection with Klebsiella pneumoniaeIncreased susceptibility to bacterial infection induced morbidity/mortality:• at 16 hours following infection with Gram negative Klebsiella pneumoniae, 50% of mice are dead unlike wild-type mice that do not display mortality due to infection at 16 hours• at 48 hours following infection with Klebsiella pneumoniae, all mice are dead unlike wild-type mice that display 50% mortalityDecreased physiological sensitivity to xenobiotic:• mice exhibit 59% protection from emphysema induced by a 6 month cigarette smoke exposure• following a 6 month exposure to cigarette smoke, mice exhibit fewer neutrophils and 60% less macrophages in bronchoalveolar lavage samples compared to wild-type mice||C57BL/6J|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|13-Jul-2015|Cryopreserved sperm|78.0|0.0|Unknown||Infection, Proteinase, Neutrophil|Yes| 7776.0|TnI.2; cTnIwt.2|C57BL/6-Tg(Myh6-TNNI3*wt)2Chs||Dominant||||||||||||||||||||||||||transgene insertion wild type 1, Christopher Semsarian|cardiac specific mouse αMHC promoter (alpha myosin heavy chain)|50% of endogenous (hemizygous)||||||||||Unknown|Indistinguishable from non-transgenic wild type C57BL/6 mice |C57BL/6|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Excellent||over 20|hemizygous transgenic x non-transgenic (wild type) sibs|No|29-Oct-2014|Cryopreserved sperm|50.0|0.0|Yes|Hypertrophic cardiomyopathy (HCM) is a primary disorder of the myocardium characterized by cardiac hypertrophy. The clinical course of HCM is variable, with inter- and intra-familial variations ranging from benign asymptomatic disease to a malignant phenotype with a high risk of cardiac failure or sudden cardiac death.|Hypertrophy, Cardiomyopathy, Calcium, Troponin I gene|Yes| 7895.0|HOM.bm1.407|B6-H2-K Tg(RIP1-Bcl2)407Wehi/J|WEHI|Dominant|histocompatibility 2, K region|H2-K|Unknown||MGI:3040519|histocompatibility 2, K region; b haplotype mutation 1|H2-K|MGI:3618114|17|||||||||||||||||human BCL2|rat insulin promoter|islet b cells||||||||||Normal|Normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|||Brother x sister and C57BL/6 x Positive|No|18-May-2015|Cryopreserved sperm|50.0|0.0|Unknown||pancreas, Bcl2, islet|No| 7782.0|203.4sv ; cTnI-G203S.4sv|129SvEv.B6-Tg(Myh6-TNNI3*G203S)4Chs/Apb||Dominant||||||||||||||||||||||||||transgene insertion 4, Christopher Semsarian|cardiac specific mouse αMHC promoter (alpha myosin heavy chain)|83% of endogenous||||||||||Unknown|Mice develop cardiac phenotype - hypertrophic cardiomyopathy by 21 weeks of age. Left ventricular hypertrophy was observed on echocardiography, it was associated with a significant 4-fold increase in RNA markers of hypertrophy, ANF and BNP. Myocyte hypertrophy, myofiber disarray and interstitial fibrosis were observed. |129SvEv|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Good|10|4|Transgenic x non-transgenic sibs|No|11-Nov-2014|Cryopreserved sperm|40.0|0.0|Yes|Hypertrophic cardiomyopathy (HCM) is a primary disorder of the myocardium characterized by cardiac hypertrophy. The clinical course of HCM is variable, with inter- and intra-familial variations ranging from benign asymptomatic disease to a malignant phenotype with a high risk of cardiac failure or sudden cardiac death.|Hypertrophy, Cardiomyopathy, Calcium, Troponin I gene|Yes| 7952.0|ENU30:065:Ddhd2:B6|C57BL/6NCrlAnu-Ddh2/AnuApb||Recessive|DDHD domain containing 2|Ddhd2||2010305K11Rik, SAMWD1|MGI:1919358|Ddh2; mutation 2, Australian National University|Ddh2||8|ENSMUSG00000061313|ENSMUST00000033975|Ddhd2-201|1685|1786|A to T|ENSMUSE00000637587|15|562|Leucine to STOP|||||ACACCATAAAGGCAGGAAGCGGATGCACTTAGAACTGAGAGAGGGCTTGACCAGGATGAGT||||||||||||||||C57BL/6NCrlAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|27-Jul-2015|Cryopreserved sperm|44.0|0.0|Unknown||ENU|Yes| 7953.0|ENU29:030:Polr3b:B6|C57BL/6NCrlAnu-Polr3b/AnuApb||Recessive|polymerase (RNA) III (DNA directed) polypeptide B|Polr3b||2700078H01Rik, A330032P03Rik, RPC2|MGI:1917678|Polr3b; mutation 1, Australian National University|Polr3b||10|ENSMUSG00000034453|ENSMUST00000077175|Polr3b-201|3365|3395|T to A|ENSMUSE00000514755|28|1122|Isoleucine to Asparagine|||||GCTCTTCCAGGAGTTACAGTCCATGAACATCATCCCCAGGCTGAAACTGGCCAAGTACAAC||||||||||||||||C57BL/6NCrlAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|27-Jul-2015|Cryopreserved sperm|48.0|0.0|Unknown||ENU|Yes| 7954.0|ENU30:078:Polr3b:B6|C57BL/6NCrlAnu-Polr3b/AnuApb||Recessive|polymerase (RNA) III (DNA directed) polypeptide B|Polr3b||2700078H01Rik, A330032P03Rik, RPC2|MGI:1917678|Polr3b; mutation 2, Australian National University|Polr3b||10|ENSMUSG00000034453|ENSMUST00000077175|Polr3b-201|283|313|A to T|ENSMUSE00000292314|5|95|Arginine to STOP|||||CTGATGTTGAAGAAAGCTTCAATGTAACTAGACCAGTGTCCCCTCATGAGTGCCGTCTGAG||||||||||||||||C57BL/6NCrlAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|27-Jul-2015|Cryopreserved sperm|55.0|0.0|Unknown||ENU|Yes| 10418.0|Tnfaip3 S254R |Tnfaip3S254R C57BL/6NCrl-Tnfaip3/Anu||Recessive|tumor necrosis factor, alpha-induced protein 3|Tnfaip3||zinc finger protein A20|MGI:1196377|Tnfaip3: endonuclease-mediated mutation 4, Australian National University|Tnfaip3/Anu||10|ENSMUSG00000019850||||||||||||||||||||||||||||unknown|unknown|C57Bl/6N|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|24-Apr-2024|Cryopreserved sperm|55.0|0.0|Unknown|||No| 10363.0|Irf5 KO (6)|C57BL/6NCrl-Irf5/Anu||Recessive|interferon regulatory factor 5|Irf5|Unknown|mirf5 |MGI:1350924 ||Irf5||6|ENSMUSG00000029771 |ENSMUST00000163511.7|||||||||||||||||||||||||||unknown|unknown|C57Bl/6N|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|26-Sep-2023|Cryopreserved sperm|11.0|0.0|Unknown|||Possibly| 7951.0|ENU30:033:Ddhd2:B6|C57BL/6NCrlAnu-Ddh2/AnuApb||Recessive|DDHD domain containing 2|Ddhd2||2010305K11Rik, SAMWD1|MGI:1919358|Ddh2; mutation 1, Australian National University|Ddh2||8|ENSMUSG00000061313|ENSMUST00000033975|Ddhd2-201|1499|1600|A to T|ENSMUSE00000637598|8|500|Methionine to Lysine|||||CTTCTTTGCCTTTGGCTCCCCCATCGGAATGTTTCTTACTGTCCGAGGGTTGAGAAGAATT||||||||||||||||C57BL/6NCrlAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||G4, G5|Het x Het|No|27-Jul-2015|Cryopreserved sperm|78.0|0.0|Unknown||ENU|Yes| 9386.0||C57Bl/6J-Prox1/Apb||Semi-dominant|Prox1||||| -11kb enhancer|||Unknown|||||||||||||||||LacZ|Hsp68|||||||||||Presence of the transgene drives LacZ expression, chiefly in lymphatic vessels and valves.|Presence of the transgene drives LacZ expression, chiefly in lymphatic vessels and valves.|C57Bl/6J|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|19-May-2022||0.0|0.0|Unknown|||Possibly| 7306.0|RIP-OVAhi|C57BL/6-Tg(Ins2-OVA)Wehi/WehiApb||Dominant||||||||||||||||||||||||||transgene insertion, Walter and Eliza Hall Institute of Medical Research|rat Ins2rat insulin 2|estimate 1ug/mg of pancreatic islet tissue||||||||||Normal. Mice express OVA in the pancreas beta cells. Protein can be detected by immunohistology.|Normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Excellent||>30|brother-sister or Tg x C57BL/6|No|05-Apr-2013|Cryopreserved sperm|50.0|0.0|No||pancreas, autoimmunity, ovalbumin|Yes| 7960.0|DC-SIGN|B6-Tg(Itgax-DC-SIGN)Litt/LittAnu||Dominant||||||||||||||||||||||||||DC-SIGN|CD11c; Itgax|||||||||||Decreased Pathology and Prolonged Survival of Human DC-SIGN Transgenic Mice during Mycobacterial Infection||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|10-Aug-2015|Cryopreserved sperm|115.0|0.0|Unknown||infection|Yes| 7675.0|ENU27:034:DZIP3:B6:G4|C57BL/6NCrlAnu-Dzip3/AnuApb|C57BL/6NCrlAnu-Dzip3/AnuApb|Recessive|DAZ interacting protein 3, zinc finger|Dzip3|Unknown|2310047C04Rik, 2A-HUB, 6430549P11Rik|MGI:1917433|DAZ interacting protein 3, zinc finger; mutation 1, The Australian National University|Dzip3|MGI:5563492|16|ENSMUSG00000064061|ENSMUST00000121869|Dzip3-001||||||||48935497|25|||ATGTTCGAAACAAGATTGCATTCCTCAGGGTAAGTTCTGAGTATACTTAATCAAAGTGGC||||||||||||||Embryonic lethal|Normal blood lymphocyte populations as measured by expression of following proteins: B220, CD3, CD4, CD44, KLRG1, NK1.1, IgM, IgD measured by flow cytometry.|C57BL/6NCrlAnu|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||G4|Het x Het|No|09-May-2014|Cryopreserved sperm|27.0|0.0|Unknown||ENU, embryonic lethal|Yes| 7959.0|Ghrelin|B6.129-Ghrl Mboat4/Marp||Dominant|ghrelin|Ghrl|Nil|2210006E23Rik, Ghr, m46, MTLRP, MTLRPAP|MGI:1930008||||6|||||||||||||||||||||||||||||Body weight, neuroprotection, blood glucose|unknown|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|10||het x het|No|05-Aug-2015||0.0|0.0|Unknown|||Possibly| 7959.0|Ghrelin|B6.129-Ghrl Mboat4/Marp||Dominant|membrane bound O-acyltransferase domain containing 4|Mboat4|Nil|GOAT|MGI:2685017||||8|||||||||||||||||||||||||||||Body weight, neuroprotection, blood glucose|unknown|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|10||het x het|No|05-Aug-2015||||Unknown|||Possibly| 7958.0|OVE-442|FVB/NJ-OVE442|SPPL-131|Recessive|RIKEN cDNA A630009H07 gene|A630009H07Rik|Unknown||MGI:2443964|||AK042353|8|||||||||||||||||sleeping beauty|alpha-crystalin|low - tissue specific||||||||||severe hypospadias, failure of urethral closure in males. Females are normal. |mice are wild type|FVB/NJ|Yes|No|Yes|Yes|No|Yes|Yes|Good|||het-het|No|30-Jul-2015||0.0|0.0|Yes|hypospadias|urogenital development, urethral closure|No| 7962.0||ENU32:085:B6||Recessive|Unknown||||||||Unknown|||||||||||||||||||||||||||||Unknown||C57BL/6NCrlAnu|Yes|Unknown|Yes|Yes|Unknown|Yes|No|Poor||||No|12-Aug-2015|Cryopreserved sperm|11.0|0.0|Unknown||ENU|Yes| 7812.0|CMV-Cre|B6.C-Tg(CMV-cre)1Cgn/J||X-linked||||||||||||||||||||||||||cre, cre recombinase, bacteriophage P1|CMV, cytomegalovirus, human|widespread expression, including germline||||||||||Normal|Normal|C57BL/6J|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||5|brother X sister|No|11-Dec-2014|Cryopreserved sperm|60.0|0.0|No||Cre recombinase, Knockout, CMV|No| 7961.0|ENU33:003:B6|C57BL/6NCrlAnu-Trex1/AnuApb||Recessive|three prime repair exonuclease 1|Trex1|Unknown||MGI:1328317||||9|||||||||||||||||||||||||||||Unknown||C57BL/6NCrlAnu|Yes|Unknown|Yes|Yes|Unknown|Yes|No|Poor||||No|12-Aug-2015|Cryopreserved sperm|44.0|0.0|Unknown||ENU|Yes| 7624.0|Gabrg2KO|STOCK Gabrg2/Apb||Recessive|gamma-aminobutyric acid (GABA) A receptor, subunit gamma 2|Gabrg2|Nil|GABAA-R, Gabrg-2, gamma2|MGI:95623|gamma-aminobutyric acid (GABA) A receptor, subunit gamma 2; targeted mutation 1, Bernhard Luscher|Gabrg2|MGI:2177608|11|||||||||||||||||||||||||||||Complete postnatal lethality:• most mice died within a few days of birth, although the animals had normal birth weight and peripheral organ structure• remainder of surviving mice failed to thrive and none survived beyond P18Impaired righting response.Limb grasping.Hyperactivity:• exceessive hyperactivity in body and limb movement following birth.Abnormal gait:• described as duck walkNervous system phenotype: no obvious alterations in brain cytoarchitecture in newborn mutant mice (J:28662)||DBA|No|No|Yes|No|No|Yes|No|Unknown||||No|24-Mar-2014|Cryopreserved sperm|70.0|0.0|Unknown||Epilepsy, benzodiazepine (BZ), GABAA receptor|Yes| 7907.0|STAT6DN|B6.129S2(C)-Stat6/J||Dominant|signal transducer and activator of transcription 6|Stat6|Nil||MGI:103034|signal transducer and activator of transcription 6; targeted mutation 1, Michael J Grusby|Stat6|MGI:1888385|10|||||||||||||||||||||||||||||Mice homozygous for the Stat6 mutation show a striking defect in the generation of Th2 cells. Lymphocytes are unable to respond to IL4 as measured in a variety of in vitro and in vivo assays. Stat6-deficient B cells do not produce IgE following in vivo immunization with anti-IgD. Mesenteric lymph node cells from STAT6-/- mice with colitis exhibited reduced secretion of IL-4, IL-5, IL-13, and IFN-gamma. They also show impaired Th2 differentiation and reduced airway response to allergen. With enhanced renal injury, Th1 and Th17 nephritogenic immune responses were increased in STAT6-/- mice while production of IL-5, a key Th2-associated cytokine, was decreased significantly.|Unknown|C57BL/6J|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|16-Jun-2015||0.0|0.0|Unknown||IL4, signal transduction, T cell, transcription factor|No| 7971.0|Srsf7-flox|B6;129-Srsf7/MarpApb||Recessive|serine/arginine-rich splicing factor 7|Srsf7||9430065L19Rik, 9G8, NX-96, Sfrs7|MGI:1926232||||17|||||||||||||||||||||||||||||Normal|Normal|C57BL/6 x 129|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|22-Sep-2015||0.0|0.0|No||LoxP|Possibly| 8768.0|F8 KO (84B)|C57BL/6-F8/84BCslApb||Recessive|coagulation factor VIII|F8||Cf8, Cf-8, Factor VIII, FVIII|MGI:88383||||X|||||||||||||||||||||||||||||Mice are haemophilic as they are deficient in the clotting factor, FVIII.|Mice may be haemophilic.|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|09-Aug-2019|Cryopreserved sperm|50.0|0.0|Unknown||Haemophilia|Yes| 5537.0|APN 75|C57BL/6N-Trim35/Marp||Recessive|tripartite motif-containing 35 |Trim35|Unknown|0710005M05Rik, A430106H13Rik, Hls5, Mair, mKIAA1098 |MGI:1914104 |tripartite motif-containing 35 ; targeted mutation 1, Velocigene|Trim35||14||||||||||||||||Yes|||||||||||||Unknown - Not bred to homozygocity |Normal |C57BL/6N|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|14-Jul-2011|Cryopreserved sperm|60.0|0.0|Unknown||ES cell|Yes| 7947.0|IL-38 KO|C57BL/6NMarp-Il1f10/Marp|Mnold|Recessive|interleukin 1 family, member 10|Il1f10|||MGI:2652548|interleukin 1 family, member 10; targeted mutation 1a, Wellcome Trust Sanger Institute|Il1f10|MGI:5008051|2|||||||||||||||||||||||||||||normal|normal|C57BL/6N|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|21-Jul-2015|Cryopreserved sperm|49.0|0.0|Unknown|||Possibly| 7963.0||NOD.Cg-Prkdc Il2rg/SzJAnuApb||Recessive|interleukin 2 receptor, gamma chain|Il2rg|Nil|[g]c, CD132, common cytokine receptor gamma chain, common gamma chain, gamma C receptor, gamma(c), gc |MGI:96551 |interleukin 2 receptor, gamma chain; targeted mutation 1, Warren J Leonard |Il2rgtm1|MGI:1857455|X|||||||||||||||||||||||||||||Premature death:*Median survival time is lengthened to between 59-95 weeks (median 89 weeks) in contrast to the shorter lifespan observed homozygous Prkdc controls.*The majority of autopsies indicate no evidence of lymphomas.Decreased leukocyte cell number:*Decrease in peripheral leukocytes at 10 weeks as compared to to Prkdc controls Decreased immature B cell number: *Flow cytometric analysis indicates that spleen cells exhibit a reduction in B220+ IgK- immature B cells in comparison to Prkdc controls Decreased mature B cell number: *Spleens are deficient in B220+ IgK+ B cells Decreased NK cell number: *Mice are deficient in cells expressing NK cell markers in comparison to Prkdc controls *Spleen cells from poly(I:C) stimulated 6-8 week old mice exhibit very low levels of NK cell cytotoxic activity Decreased CD4-positive T cell number: *Spleens are deficient in mature T cells Decreased CD8-positive T cell number: *Spleens are deficient in mature T cellsAbnormal immune system organ morphology:*Lymph tissues are severely depleted of lymphoid cells Abnormal spleen B cell follicle morphology: *Spleens do not have detectable follicles Abnormal splenic cell ratio: *Two fold reduction in nucleated spleen cell numbers in comparison to Prkdc controls Abnormal thymus morphology: *Thymus consists mostly of stromal cells with sporadic cyst structures Small lymph nodes: *Lymph nodes in the double mutant are markedly smaller than those of homozygous Prkdc mice Lymph node hypoplasia: *Lymph nodes are hypocellularDecreased immunoglobulin level:*No detectable immunoglobulin in mice at 394-426 days of ageAbnormal response to transplant:*Mice support CD34+ human stem cell engraftment at much higher levels than Prkdc controls*Human CD45+ cells comprise almost 50% of cells in the spleen, approximately 35% in bone marrow and thymus, and 6% in blood at 10 weeks post-engraftmentDecreased mean corpuscular volume:*Slight decrease in packed cell volume at 10 weeks as compared to to Prkdc controlsDecreased leukocyte cell number:*Decrease in peripheral leukocytes at 10 weeks as compared to to Prkdc controls Decreased immature B cell number: *Flow cytometric analysis indicates that spleen cells exhibit a reduction in B220+ IgK- immature B cells in comparison to Prkdc controls Decreased mature B cell number: *Spleens are deficient in B220+ IgK+ B cells Decreased NK cell number: *Mice are deficient in cells expressing NK cell markers in comparison to Prkdc controls *Spleen cells from poly(I:C) stimulated 6-8 week old mice exhibit very low levels of NK cell cytotoxic activity Decreased CD4-positive T cell number: *Spleens are deficient in mature T cells Decreased CD8-positive T cell number: *Spleens are deficient in mature T cellsAbnormal spleen B cell follicle morphology:*Spleens do not have detectable folliclesAbnormal splenic cell ratio:*Two fold reduction in nucleated spleen cell numbers in comparison to Prkdc controlsAbnormal thymus morphology:*Thymus consists mostly of stromal cells with sporadic cyst structuresIncreased cellular sensitivity to X-ray irradiation:*Mice do not survive doses above or equal to 400cGyDecreased incidence of ionizing radiation-induced tumors:*Mice irradiated with doses below 400cGy do not exhibit thymic lymphomas in contrast to homozygous Prkdc controlsAbnormal glucose homeostasis:*Streptozotocin-diabetic mice are not restored to euglycemia after receiving transplants of 1000 to 3000 IEQ, while 4000 IEQ transplant was successful in two long-term survivors Hyperglycemia: *Treptozotocin effectively induced hyperglycemia essentially equally in male and female mice at doses of 120to 160 mg/kg; some mice do not become hyperglycemic at all doses of streptozotocin administered||NOD|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|17-Aug-2015|Cryopreserved sperm|55.0|0.0|Unknown|||Yes| 7963.0||NOD.Cg-Prkdc Il2rg/SzJAnuApb||Recessive|protein kinase, DNA activated, catalytic polypeptide|Prkdc|Nil|DNA-PK, DNA-PKcs, DNAPDcs, DOXNPH, dxnph, slip, XRCC7|MGI:104779 |protein kinase, DNA activated, catalytic polypeptide; severe combined immunodeficiency |Prkdc|MGI:1857113|16|||||||||||||||||||||||||||||Premature death:*Median survival time is lengthened to between 59-95 weeks (median 89 weeks) in contrast to the shorter lifespan observed homozygous Prkdc controls.*The majority of autopsies indicate no evidence of lymphomas.Decreased leukocyte cell number:*Decrease in peripheral leukocytes at 10 weeks as compared to to Prkdc controls Decreased immature B cell number: *Flow cytometric analysis indicates that spleen cells exhibit a reduction in B220+ IgK- immature B cells in comparison to Prkdc controls Decreased mature B cell number: *Spleens are deficient in B220+ IgK+ B cells Decreased NK cell number: *Mice are deficient in cells expressing NK cell markers in comparison to Prkdc controls *Spleen cells from poly(I:C) stimulated 6-8 week old mice exhibit very low levels of NK cell cytotoxic activity Decreased CD4-positive T cell number: *Spleens are deficient in mature T cells Decreased CD8-positive T cell number: *Spleens are deficient in mature T cellsAbnormal immune system organ morphology:*Lymph tissues are severely depleted of lymphoid cells Abnormal spleen B cell follicle morphology: *Spleens do not have detectable follicles Abnormal splenic cell ratio: *Two fold reduction in nucleated spleen cell numbers in comparison to Prkdc controls Abnormal thymus morphology: *Thymus consists mostly of stromal cells with sporadic cyst structures Small lymph nodes: *Lymph nodes in the double mutant are markedly smaller than those of homozygous Prkdc mice Lymph node hypoplasia: *Lymph nodes are hypocellularDecreased immunoglobulin level:*No detectable immunoglobulin in mice at 394-426 days of ageAbnormal response to transplant:*Mice support CD34+ human stem cell engraftment at much higher levels than Prkdc controls*Human CD45+ cells comprise almost 50% of cells in the spleen, approximately 35% in bone marrow and thymus, and 6% in blood at 10 weeks post-engraftmentDecreased mean corpuscular volume:*Slight decrease in packed cell volume at 10 weeks as compared to to Prkdc controlsDecreased leukocyte cell number:*Decrease in peripheral leukocytes at 10 weeks as compared to to Prkdc controls Decreased immature B cell number: *Flow cytometric analysis indicates that spleen cells exhibit a reduction in B220+ IgK- immature B cells in comparison to Prkdc controls Decreased mature B cell number: *Spleens are deficient in B220+ IgK+ B cells Decreased NK cell number: *Mice are deficient in cells expressing NK cell markers in comparison to Prkdc controls *Spleen cells from poly(I:C) stimulated 6-8 week old mice exhibit very low levels of NK cell cytotoxic activity Decreased CD4-positive T cell number: *Spleens are deficient in mature T cells Decreased CD8-positive T cell number: *Spleens are deficient in mature T cellsAbnormal spleen B cell follicle morphology:*Spleens do not have detectable folliclesAbnormal splenic cell ratio:*Two fold reduction in nucleated spleen cell numbers in comparison to Prkdc controlsAbnormal thymus morphology:*Thymus consists mostly of stromal cells with sporadic cyst structuresIncreased cellular sensitivity to X-ray irradiation:*Mice do not survive doses above or equal to 400cGyDecreased incidence of ionizing radiation-induced tumors:*Mice irradiated with doses below 400cGy do not exhibit thymic lymphomas in contrast to homozygous Prkdc controlsAbnormal glucose homeostasis:*Streptozotocin-diabetic mice are not restored to euglycemia after receiving transplants of 1000 to 3000 IEQ, while 4000 IEQ transplant was successful in two long-term survivors Hyperglycemia: *Treptozotocin effectively induced hyperglycemia essentially equally in male and female mice at doses of 120to 160 mg/kg; some mice do not become hyperglycemic at all doses of streptozotocin administered||NOD|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|17-Aug-2015|Cryopreserved sperm|||Unknown|||Yes| 7850.0|MPS IIIB KO|B6.129S6-Naglu/J||Recessive|alpha-N-acetylglucosaminidase (Sanfilippo disease IIIB)|Naglu|Nil|MPS-IIIB; MPS3B; NAG; RGD1564228; UFHSD;|MGI Ref ID J:58950|Targeted mutation 1, Elizabeth F Neufeld|Naglu|MGI:1934018|11|||||||||||||||||||||||||||||At birth, homozygous null mice are viable, normal in size, and do not display any gross physical or behavioral abnormalities. The lysosomal enzyme alpha-N-acetylglucosaminidase (Naglu) is absent in all tissues. Large amounts of heparan sulfate accumulate in liver and kidney, and lesser amounts in other organs. At one month of age, vacuolated macrophages can be found in most tissues. Epithelial cells in kidney and neurons in some parts of the brain are also affected. The vacuolation becomes more prominent with age. At 4-5 months, the mice show abnormal behavior in an open field test. The life span is 8-12 months. Older animals may have urinary retention and difficulty walking and must be euthanized. The null mice were originally described as fertile, but their fertility has decreasd markedly with repeated back-crossing to an inbred strain. These mice are suitable for examining the pathophysiology of the Sanfilippo syndrome type B and for developing therapies for this lysosomal storage disorder.|Unknown|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||8|Brother x sister|No|27-Feb-2015|Cryopreserved sperm|50.0|0.0|Unknown||MPS IIIB, Knockout |No| 4515.0|Anaef ; ENU8B6:004|C57BL/6JSfdAnu-Rasgrp1/AnuApb|C57BL/6JSfdAnu-Rasgrp1/AnuApb|Recessive|RAS guanyl releasing protein 1|Rasgrp1|||MGI:1314635|RAS guanyl releasing protein 1; mutation 1, The Australian National University|Rasgrp1|MGI:4838027|2|ENSMUSG00000027347|ENSMUST00000102534|Rasgrp1-001|1555|1847|A to G|ENSMUSE00000295147|13|518|Arginine to Glycine|||||TGGACAAAGATAGGGAAGGCCTCATCAGCAGAGACGAGATCACGGCCTACTTCATGAGGGC||||||||||||||Subclinical autoimmune susceptibility. Antinuclear autoantibodies.Thymocyte selection in affected mice is mostly normal in vivo, although CD44 is overexpressed on naïve thymocytes and T cells in a T-cell-autonomous manner. ||C57BL6JSfdAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||9||No|26-Feb-2009|Cryopreserved sperm|56.0|0.0|Unknown||autoimmunity, Antinuclear antibodies (ANA), ENU, Wellcome Trust, T cell, signal transduction|Yes| 7964.0|ENU33:034|C57BL/6NCrlAnu-Fnip1/AnuApb||Recessive|folliculin interacting protein 1|Fnip1||A730024A03Rik, mKIAA1961|MGI:2444668|Fnip1; mutation 1, Australian National University|Fnip1||11|ENSMUSG00000035992|ENSMUST00000046835|Fnip1-001|228|326|T to A|ENSMUSE00000288119|3|76|Cysteine to STOP|||||AATGAGGACACATCAGTATCGAAGCTCTGTAATGATGCTCAAGTCAAGGTCTTTGGGAAGT||||||||||||||No B cells in peripheral blood as measured by flow cytometry.|Normal|C57BL/6NCrlAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||G4||No|02-Sep-2015|Cryopreserved sperm|46.0|0.0|Unknown||B cell|Yes| 7569.0|ENU14Yaa:032:b:-Yaa:G5|B6(SB)-Lyn/AnuApb|B6(SB)-Lyn/AnuApb|Recessive|Yamaguchi sarcoma viral (v-yes-1) oncogene homolog|Lyn||Hck-2|MGI:96892|Yamaguchi sarcoma viral (v-yes-1) oncogene homolog; mutation 1 Anu|Lyn|MGI:5563397|4|ENSMUSG00000042228|ENSMUST00000041377|Lyn-001||||||||3683632|9|||CTACATCATCACCGAGTTCATGGCTAAGGGTGAGTGGCATCACGAGTCTGTACCCCTAAA||||||||||||||Increased % immature B cells, and reduced % mature B cells (Almost no Mature B cells)||C57BL/6JAnu|Yes|Unknown|Yes|Yes|Unknown|Yes|No|Unknown||||No|17-Jan-2014|Cryopreserved sperm|10.0|0.0|Unknown||ENU, B cell, signal transduction|Possibly| 7889.0|alpha-syn X MPS IIIa Cg|B6.Cg;129X1-Sgsh Snca/J||Recessive|synuclein, alpha|Snca|Nil|alpha-Syn-; alpha-Synko;|MGI:1277151|targeted mutation 1, Arnon Rosenthal|Snca(tm1Rosl)|alpha-Syn-; alpha-Synko|6|||||||||||||||||||||||||||||Unknown|Unknown|C57BL/6|Yes|Yes|Unknown|Yes|Yes|Yes|No|Good|||brother x sister|No|11-May-2015|Cryopreserved sperm|50.0|0.0|Yes|||No| 7889.0|alpha-syn X MPS IIIa Cg|B6.Cg;129X1-Sgsh Snca/J||Recessive|N-sulfoglucosamine sulfohydrolase (sulfamidase)|Sgsh|Unknown|4632406A19Rik, sulphamidase|MGI:1350341|N-sulfoglucosamine sulfohydrolase (sulfamidase); mucopolysaccharidosis IIIA|Sgsh|MGI:2151181|11|||||||||||||||||||||||||||||Unknown|Unknown|C57BL/6|Yes|Yes|Unknown|Yes|Yes|Yes|No|Good|||brother x sister|No|11-May-2015|Cryopreserved sperm|||Yes|||No| 7083.0|Pinky ; ENU8C:027|B6(Cg).CBA-Zbtb16/AnuApb|B6.CBA-Zbtb16/AnuApb|Recessive|zinc finger and BTB domain containing 16|Zbtb16|Unknown|Green's luxoid, PLZF, Zfp145|MGI:103222|zinc finger and BTB domain containing 16; pinky|Zbtb16|MGI:4462277|9|ENSMUSG00000066687|ENSMUST00000093852|Zbtb16-201|210|457|T to A|ENSMUSE00000584531|2|70|Tyrosine to STOP|||||ATCCTCTTCCACCGAAACAGCCAGCACTATACTCTAGACTTCCTCTCGCCAAAAACCTTCC|Yes|||||||||||||Limb deformity. Shortening and angular deformity of hindlimbs with extra digits present in some cases. Deformity affects mouse mobility. Previously described homozygous mutants exhibit abnormal anterior-posterior patterning, with skeletal abnormalities of the limb, especially the hindlimb, and homeotic transformations of anterior skeletal elements into posterior structures. Males develop infertility due to loss of germline cells with age.||C57BL/6JAnu|Yes|Yes|Yes|Yes|Yes|Yes|Yes|Good|10|8||No|14-Sep-2012|Cryopreserved sperm|26.0|0.0|Unknown||limb, deformity, extra digit, anterior-posterior patterning, ENU|Yes| 7336.0|ENU17NIH:050b|C57BL/6JAnu-Zfp318/AnuApb|C57BL/6JAnu-Zfp318/AnuApb|Recessive|zinc finger protein 318|Zfp318|Unknown|2610034E08Rik, D530032D06Rik, TZF |MGI:1889348|zinc finger protein 318; mutation 1, The Australian National University|Zfp318|MGI:5563395|17|ENSMUSG00000015597|ENSMUST00000113481|Zfp318-001|4040|4148|T to C|ENSMUSE00000695799|10|1347|Isoleucine to Threonine|||||TGAAGTTGGAAAGGCAAAGCCCATCAAAATCAAGCTTTCTGGAAAAACTGTCATTGCACAC||||||||||||||Abolished IgD expression on marginal zone B cells, decreased IgD on follicular B cells, and increased IgM, but only slightly decreased the percentage of B cells and did not decrease expression of other maturation markers CD21, CD23, or CD62L.Gene is highly expressed in testis and male mice homozygous for a null allele seem to have reduced fertility.|Normal|C57BL/6JAnu|Yes|Unknown|Yes|Yes|Yes|Yes|No|Good|3|G7|Usually het x het but have used homozygous males|No|14-May-2013|Cryopreserved sperm|37.0|0.0|Unknown||B cell development, Follicular B cells, ENU|No| 7410.0|ENU26:020:Dock8:B6|C57BL/6NCrlAnu-Dock8/AnuApb|C57BL/6NCrlAnu-Dock8/AnuApb|Recessive|dedicator of cytokinesis 8|Dock8|Unknown|1200017A24Rik, 5830472H07Rik, A130095G14Rik|MGI:1921396|dedicator of cytokinesis 8; mutation 1, The Australian National University|Dock8|MGI:5563486|19|ENSMUSG00000052085|ENSMUST00000025831|Dock8-201|5656|5778|G to T|ENSMUSE00000145933|44|1886|Glutamic acid to STOP|||||ATGAGATGAAAGACCGGGTGACCTACTTCGAGAAGAATTTCAACCTCCGGAGGTTCATGTA||||||||||||||Peripheral blood shows reduced T cell numbers, activated CD8<+>T cells (high CD44 expression) and low IgM expression on mature B cells. No Marginal Zone B cells in spleen.Parameters measured by flow cytometry using antibodies against following antigens: B220, CD3, CD4, CD44, KLRG1, NK1.1, IgM, IgD|Normal blood lymphocyte populations as measured by expression of following proteins: B220, CD3, CD4, CD44, KLRG1, NK1.1, IgM, IgD by flow cytometry.|C57BL/6NCrlAnu|Yes|Unknown|Yes|Yes|Unknown|Yes|No|Unknown||G4|Het x Het|No|23-Aug-2013|Cryopreserved sperm|33.0|0.0|Unknown||T cell, B cell, antibody, ENU|Yes| 7415.0|ENU25:040:MAST4:B6|C57BL/6NCrlAnu-Mast4/AnuApb|C57BL/6NCrlAnu-Mast4/AnuApb|Recessive|microtubule associated serine/threonine kinase family member 4|Mast4|Unknown|4930420O11Rik, mKIAA0303|MGI:1918885|microtubule associated serine/threonine kinase family member 4; mutation 1, The Australian National University|Mast4|MGI:5563453|13|ENSMUSG00000034751|ENSMUST00000167058|Mast4-001|2176|2444|C to A|ENSMUSE00000483603|17|726|Glutamic acid to STOP|||||GATTAATGAGCATGACCACCAATCTCTATGAAGGCCACATAGAGAAGGACGCTCGAGAGTT||||||||||||||Malocclusion.Normal blood lymphocyte populations as measured by expression of following proteins: B220, CD3, C4, CD44, KLRG1, NK1.1, IgM, IgD by flow cytometry.||C57BL/6NCrlAnu|Yes|Unknown|Yes|Yes|Unknown|Yes|No|Unknown||G4||No|23-Aug-2013|Cryopreserved sperm|45.0|0.0|Unknown||malocclusion, ENU|Yes| 7558.0|ENU27:009:RASGRP1:B6|C57BL/6NCrlAnu-Rasgrp1/AnuApb|C57BL/6NCrlAnu-Rasgrp1/AnuApb|Recessive|RAS guanyl releasing protein 1|Rasgrp1|Unknown||MGI:1314635|RAS guanyl releasing protein 1; mutation 2, The Australian National University|Rasgrp1|MGI:5563430|2|ENSMUSG00000027347|ENSMUST00000102534|Rasgrp1-001|1976|2268|T to C|ENSMUSE00000295129|16|659|Lysine to Arginine|||||CATCATGCTCCTCGGAGTGTCCTCCCAGAAAATTTCAGTTCGGCTGAAGAGGACTGTTGCC||||||||||||||Normal blood lymphocyte populations as measured by expression of following proteins: B220, CD3, CD4, CD44, KLRG1, NK1.1, IgM, IgD by flow cytometry.|Normal blood lymphocyte populations as measured by expression of following proteins: B220, CD3, CD4, CD44, KLRG1, NK1.1, IgM, IgD by flow cytometry.|C57BL/6NCrlAnu|Yes|Unknown|Yes|Yes|Unknown|Yes|No|Unknown||G4||No|19-Dec-2013|Cryopreserved sperm|46.0|0.0|Unknown||ENU|Yes| 7559.0|ENU27:048:ATP10A:B6|C57BL/6NCrlAnu-Atp10a/AnuApb|C57BL/6NCrlAnu-Atp10a/AnuApb|Recessive|ATPase, class V, type 10A|Atp10a|Unknown|Atp10c, pfatp|MGI:1330809|ATPase, class V, type 10A; mutation 1, The Australian National University|Atp10a|MGI:5563515|7|ENSMUSG00000025324|ENSMUST00000168747|Atp10a-202|2716|2969|G to T|ENSMUSE00000149782|13|906|Aspartic acid to Tyrosine|||||CTGGCCTGCAGATTTGGGTTCTCACAGGTGACAAACAGGAAACAGCCATTAACATTGCATA||||||||||||||Normal blood lymphocyte populations as measured by expression of following proteins: B220, CD3, CD4, CD44, KLRG1, NK1.1, IgM, IgD by flow cytometry.|Normal blood lymphocyte populations as measured by expression of following proteins: B220, CD3, CD4, CD44, KLRG1, NK1.1, IgM, IgD by flow cytometry.|C57BL/6NCrlAnu|Yes|Unknown|Yes|Yes|Unknown|Yes|No|Unknown||G4||No|19-Dec-2013|Cryopreserved sperm|36.0|0.0|Unknown||ENU|Yes| 7977.0|Kaede Tg|B6.Cg-Tg(CAG-Kaede)#Kgwa/AusbAnuApb||Recessive||||||||||||||||||||||||||transgene insertion, Osami Kanagawa|Beta actin|||||||||||These mice expressed photoconvertible Kaede in all of the cell types analyzed with no abnormality in their growth and reproduction.|These mice expressed photoconvertible Kaede in all of the cell types analyzed with no abnormality in their growth and reproduction.|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|30-Sep-2015|Cryopreserved sperm|11.0|0.0|Unknown||fluorescence|Yes| 7965.0|ENU32:045|C57BL/6NCrlAnu-Galns/AnuApb||Recessive|galactosamine (N-acetyl)-6-sulfate sulfatase|Galns||N-acetylgalactosamine-6-sulfate sulfatase|MGI:1355303||||8|ENSMUSG00000015027|ENSMUST00000015171|Galns-201|176|325|A to G|ENSMUSE00000215107|2|59|Methionine to Threonine|||||TTCCAGAGAGACCCCAAATTTAGACCGGATGGCTGCAGAAGGGATGCTTTTCCCAAGCTTC||||||||||||||Low IgM expression on mature B cells in peripheral blood as measured by flow cytometry.|Normal|C57BL/6NCrlAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|02-Sep-2015|Cryopreserved sperm|36.0|0.0|Unknown||B cell, IgM, immunoglobulin|Yes| 7735.0|Duane ; ENU6NIHB:019|B6(Cg)-Tbx21/AnuApb|B6(Cg)-Tbx21/AnuApb|Recessive|T-box 21|Tbx21|Reduced|T-bet, Tblym, TBT1|MGI:1888984|T-box 21; Duane|Tbx21|MGI:4367995|11|ENSMUSG00000001444|ENSMUST00000001484|Tbx21-001||||||||96962921|2|||CTGGTCGATACTTGACAATAAGGTTAACTGTCCACAGGGAACCGCTTATATGTCCACCCA|Yes|||||||||||||Defective antibody response to immunization: failure to mount a normal Th1 polarized IgG2c antibody response to heat killed B pertussis bacteria. Few circulating NK cells.Decreased NK cell number: the percent of NK cells in the blood, spleen, and liver is lower than in wild-type mice.Increased NK cell number:* the frequency of NK cells in the peripheral lymph nodes and bone marrow is increased compared to in wild-type mice.* NK cells accumulate in lymph nodes due to defective egression.Absent NK T cells: mice exhibit a near complete absence of invariant natural killer T cells unlike in wild-type mice.Abnormal NK cell differentiation:* NK cells exhibit an immature phenotype unlike in wild-type mice.* NK cells accumulate in lymph nodes due to defective egression.* in reconstitution experiments, derived NK cells accumulate in the peripheral lymph nodes due to defective egression.||C57BL/6NCrlAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|4|G5N4|Het x Het ; Hom x Hom|No|06-Sep-2014|Cryopreserved sperm|14.0|64.0|Unknown||antibody, B cell, NK cell, ENU, Wellcome Trust, Natural Killer cell (NK), T cell, lymphocyte|Yes| 7967.0|GZMB-cre|B6.FVB-Tg(GZMB-cre)1Jcb/JWehiAnu||Dominant||||||||||||||||||||||||||transgene insertion 1, Joshy Jacob|human granzyme B|||||||||||Normal|Normal|C57L/6JWehi|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|10|||No|07-Sep-2015|Cryopreserved sperm|22.0|0.0|Unknown||Cre recombinase, T cell, CD8, granzyme|Yes| 7975.0|PP2A flox P|FVB.129S-Ppp2r1a/J||Recessive|protein phosphatase 2, regulatory subunit A, alpha|Ppp2r1a|Normal|6330556D22Rik, PP2A, PR65, protein phosphatase PP2A|MGI:1926334|protein phosphatase 2, regulatory subunit A, alpha; targeted mutation 1.1, Gernot Walter|Ppp2r1a|MGI:5287252|17|||||||||||||||||||||||||||||unknown|unknown|FVB and 129S6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|25-Sep-2015||0.0|0.0|Unknown||tumour suppressor, carcinoma|Yes| 7973.0||RBC10|RBC10|Dominant|Unknown||Unknown||||||Unknown|||||||||||||||||||||||||||||Unknown|Microcytosis|C57BL/6|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Good||||No|24-Sep-2015|Cryopreserved sperm|30.0|0.0|Unknown||ENU|No| 7974.0|Mst1r|C57BL/6-Gt(Rosa)26Sor/AnuApb||Dominant|gene trap ROSA 26, Philippe Soriano|Gt(ROSA)26Sor|Unknown|beta geo, Gtrgeo26, Gtrosa26, R26, ROSA26, Thumpd3as1|MGI:104735||||6||||||||||||||||No|||||||||||||Normal|Normal||Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||Yes|24-Sep-2015|Cryopreserved sperm|45.0|0.0|No||Cre recombinase, Mst1r|No| 7969.0|HSPE Tg x HIP-Cre|C57BL/6-Gt(ROSA)26Sor Tg(INS-cre)2Rms/AnuApb||Recessive|gene trap ROSA 26, Philippe Soriano|Gt(ROSA)26Sor||beta geo, Gtrgeo26, Gtrosa26, R26, ROSA26, Thumpd3as1|MGI:104735||||6|||||||||||||||||transgene insertion 2, Robyn M Slattery|human insulin promoter|||||||||||Unknown||C57BL/6|Yes|Unknown|Yes|Yes|Unknown|Yes|No|Unknown||||No|18-Sep-2015|Cryopreserved sperm|54.0|0.0|Unknown||heparanase, Cre recombinase|Yes| 7970.0|Srsf3-flox UBC-cre/ert|B6;129-Srsf3 Tg((UBC-cre/ERT2)1Ejb/MarpApb||Recessive|serine/arginine-rich splicing factor 3|Srsf3|Unknown|Sfrs3, X16|MGI:98285||||17|||||||||||||||||transgene insertion 1, Eric J Brow|human ubiquitin C (UBC) promoter|||||||||||No phenotype|No phenotype|C57BL/6 x 129|Yes|Yes|Yes|Yes|Yes|Yes|No|Excellent||||No|22-Sep-2015|Cryopreserved sperm|30.0|0.0|No||LoxP|Possibly| 7972.0|Tau KO|B6.129X1-Mapt/J ||Dominant|microtubule-associated protein tau|Mapt|Nil|Mtapt, Tau|MGI:97180|microtubule-associated protein tau; targeted mutation 1, Hana N Dawson|Mapt|MGI:2385630|11|||||||||||||||||||||||||||||Decreased susceptibility to pharmacologically induced seizures:• severity is reduced and seizure onset is delayed after pentylenetetrazole treatment compared to wild-type mice• mice are resistant to kainate-induced seizures over a larger range of doses than wild-type miceAbnormal axon extension:• neuronal cultures from E16 mice show less axonal extension than wild-type neurons; mutant neurons lag behind wild-type in development over initial 2 days in culture, then catch up, but total sum of minor processes/axonal lengths is less than wild-typeAbnormal dendrite morphology:• between 4 and 7 days in culture, total dendritic length of mutant neurons is less than in wild-type; after 7 days in culture, neurons still lag behind wild-type showing more developmental delay.|Decreased susceptibility to pharmacologically induced seizures:• severity is reduced and seizure onset is delayed after pentylenetetrazole treatment compared to wild-type mice• mice are resistant to kainate-induced seizures over a larger range of doses than wild-type mice|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Excellent||||Yes|24-Sep-2015||0.0|0.0|Unknown||Tau|Yes| 7980.0|Nrp2:Cre/dsRed|C57BL/6-Tg(Nrp2-cre/dsRed)||Dominant||||||||||||||||||||||||||Cre rcombinase fused to dsRed|Nrp2|||||||||||Normal|Normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|10|10|Male homozygous cross female homozygous|No|09-Oct-2015|Cryopreserved sperm|49.0|0.0|No||Neuropilin 2, Nrp2, Cre recombinase|Possibly| 7976.0|Ndfip1 flox|C57BL/6-Ndfip1/SestAnuApb||Recessive|Nedd4 family interacting protein 1|Ndfip1|Normal|0610010M22Rik|MGI:1929601|Nedd4 family interacting protein 1; targeted mutation 1, Seong-Seng Tan|Ndfip1|MGI:5313245|18|||||||||||||||||||||||||||||Normal|Normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|30-Sep-2015||0.0|0.0|Unknown||Nedd4, pten, ubiquitination|Yes| 7982.0|F/F:STAT3-SA , BJ33|B6.129-IL6st Stat3/MarpApb||Recessive|signal transducer and activator of transcription 3|Stat3|Unknown|1110034C02Rik, Aprf|MGI:103038|signal transducer and activator of transcription 3; targeted mutation 1, James E Darnell|Stat3|MGI:3028651|11||||||||||||||||No|||||||||||||||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|Yes|Good||||No|13-Oct-2015|Cryopreserved sperm|50.0|0.0|Unknown||signal transduction, JAK-STAT, cytokine, interferon, kinase, phosphorylation|Yes| 7982.0|F/F:STAT3-SA , BJ33|B6.129-IL6st Stat3/MarpApb||Recessive|interleukin 6 signal transducer|Il6st|Normal|CD130, D13Ertd699e, gp130|MGI:96560|interleukin 6 signal transducer; targeted mutation 1, Matthias Ernst|Il6st|MGI:2388478|13||||||||||||||||Yes|||||||||||||||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|Yes|Good||||No|13-Oct-2015|Cryopreserved sperm|||Unknown||signal transduction, JAK-STAT, cytokine, interferon, kinase, phosphorylation|Yes| 7599.0|TRAMP|B6;FVB/N-Tg(TRAMP)8247Ng/MarpApb||Dominant||||||||||||||||||||||||||transgene insertion 8247, Norman M Greenberg|rat probasin|prostate||||||||||Males develop prostate cancer from 10weeks, penetrance ~80% at 1yr of age|Males develop prostate cancer from 10weeks, penetrance ~80% at 1yr of age|C57BL/6J|Unknown|Unknown|Yes|No|No|No|Yes|Poor|||Heterozygous female crossed with wt male|No|19-Feb-2014|Cryopreserved sperm|60.0|0.0|Unknown||prostate, SV40, epithelium, androgen|Yes| 8806.0|ASD900:Dragonfruit:PH1bpins|C57BL/6NCrlAnu-Phrf1/AnuApb||Recessive|PHD and ring finger domains 1|Phrf1|Unknown||MGI:2141847||||7|||||||||||||||||||||||||||||Unknown|Unknown|C57BL/6NCrlAnu|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|21-Oct-2019||0.0|0.0|Unknown|||Yes| 7978.0|C3 ; Fgf10 c.505_507del CRISPR|C57BL/6J-Fgf10/MarpApb||Recessive|fibroblast growth factor 10|Fgf10|Unknown|AEY17, FGF-10, Gsfaey17 |MGI:1099809||||13|||||||||||||||||||||||||||||Unknown|Normal|C57BL/6J|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Good||||No|05-Oct-2015|Cryopreserved sperm|40.0|0.0|Unknown||CRISPR|Possibly| 10424.0|CD89Tgflx|B6-Tg(flox/cd89)227Ltku||Dominant|FCAR||||||||Unknown|||||||||||||||||LoxP-mCherry-Stop codon-LoxP-human CD89-IRES-GFP|CMV|||||||||||Normal|Normal|C57Bl/6J|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|03-May-2024|Cryopreserved sperm|50.0|0.0|Unknown|||No| 7516.0|PB-Tet|B6.FVB-Tg(Pbsn-rtTA*M2)42Xy/MarpApb|B6.FVB-Tg(Pbsn-rtTA*M2)42Xy/MarpApb|Dominant||||||||||||||||||||||||||transgene insertion 42, Xin Yuan|anterior prostate-specific rat promoter|||||||||||Prostate specific rtTA expression; no other phenotype |None/Unknown|C57BL/6J|No|Yes|Unknown|No|Yes|Unknown|No|Unknown||||No|29-Nov-2013|Cryopreserved sperm|60.0|0.0|Unknown||tetracycline, inducible|Possibly| 7512.0||Enu23:032:Hecr3 but not herc3||Recessive|Unknown||||||||Unknown|||||||||||||||||||||||||||||Jaw infectionNormal blood lymphocyte populations as measured by expression of following proteins: B220, CD3, CD4, CD44, KLRG1, NK1.1, IgM, IgD by flow cytometry.|Normal blood lymphocyte populations as measured by expression of following proteins: B220, CD3, CD4, CD44, KLRG1, NK1.1, IgM, IgD by flow cytometry.|C57BL/6NCrlAnu|Yes|Unknown|Yes|Yes|Unknown|Yes|No|Unknown||||No|21-Nov-2013|Cryopreserved sperm|31.0|0.0|Unknown||ENU|No| 7983.0|Foxn1|B6(Cg)-Foxn1/JAnu||Dominant|forkhead box N1|Foxn1|Normal|D11Bhm185e, Hfh11, whn|MGI:102949|forkhead box N1; targeted mutation 3, Nancy R Manley|Foxn1|MGI:3760775|11|||||||||||||||||||||||||||||Normal|Normal|C57BL/6J|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|23-Oct-2015|Cryopreserved sperm|21.0|0.0|Unknown||Cre recombinase|No| 7987.0|Trim33|FVB/N-Trim33/Ew||Recessive|Tripartite motif containing 33|Trim33|Reduced|8030451N04Rik, Ecto, ectodermin, mKIAA1113, Tif1g|MGI:2137357|Trim33|Trim33||3|||||||||||||||||transgene insertion 1, Emma Whitelaw|human alpha globin|high in erythrocytes||||||||||Embryonic Lethal|Normal|FVB|No|Unknown|Yes|No|Unknown|Yes|No|Excellent|At least 10||Dominant (heterozygous) mutants are crossed to FVB mice, both of which are also homozygous for the GFP transgene|No|29-Oct-2015||0.0|0.0|No||Trim33|Possibly| 7986.0|Recql4 R347*|C57BL/6JAnu-Recql4/AnuCrwApb||Recessive|RecQ protein-like 4|Recql4|Unknown||MGI:1931028|Recql4; mutation 2, Australian National University|Recql4||15|ENSMUSG00000033762|ENSMUST00000036852|Recql4-201|1039|1122|G to A|ENSMUSE00000237138|5|347|Arginine to STOP|||||CAGCTTCCCTAGACAGAGGGAACTATATTCGACTCAACATGAAAAACAAACGCTTTGTACG|Unknown|||||||||||||Unknown as none recovered at time of submission|Appear normal and fertile|C57BL/6JAnu|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Good|2 to C57BL/6|1|PM/+ to either PM/+ or WT|No|27-Oct-2015|Cryopreserved sperm|40.0|0.0|Yes|Rothmund-Thomson Syndrome|ENU, Recql4|Possibly| 7988.0|PTX3 knockout|B6.129-Ptx3||Semi-dominant|pentraxin related gene|Ptx3||pentraxin 3, TSG-14|MGI:104641|pentraxin related gene; targeted mutation 1, Alberto Mantovani|Ptx3|MGI:2675283|3|||||||||||||||||||||||||||||Reduced female fertility: • homozygotes display a severe defect in female fertilityLung inflammation:• lungs from Aspergillus fumigatus infected homozygotes display a massive inflammatory response, the presence of hyphae and numerous, mostly extracellular, conidia, relative to similarly infected wild-type controlsAbnormal T-helper 1 physiology:• upon challenge with Aspergillus fumigatus, homozygotes fail to develop an appropriate TH1-type response and display a cytokine profile skewed towards a TH2-type response, as revealed by reduced IFN-gamma and IL-12 levels and increased IL-4 levels in mutant lungsAbnormal macrophage physiology:• homozygotes exhibit defective recognition of Aspergillus fumigatus conidia by alveolar macrophagesImpaired macrophage phagocytosis:• in vitro, the ability of mutant alveolar macrophages to ingest and kill resting Aspergillus fumigatus conidia is impaired relative to wild-type macrophages|Normal.|C57BL/6|Yes|No|Yes|Yes|Yes|Yes|No|Good||||No|03-Nov-2015|Cryopreserved sperm|50.0|0.0|No|||No| 10415.0|TNFAIP3 KO|C57BL6/NCrl-Tnfaip3/Anu||Recessive|tumor necrosis factor, alpha-induced protein 3|Tnfaip3||zinc finger protein A20|MGI:1196377|Tnfaip3:endonuclease-mediated mutation 3, Australian National University|Tnfaip3/||10|ENSMUSG00000019850||||||||||||||||||||||||||||unknown|unknown|C57Bl/6N|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|08-Apr-2024|Cryopreserved sperm|50.0|0.0|Unknown|||No| 7993.0|Rag2|C.129S6-Rag2/UcApb|C.129S6-Rag2/UcApb|Recessive|recombination activating gene 2|Rag2|Normal|Rag-2|MGI:97849|recombination activating gene 2; targeted mutation 1, Frederick W Alt|Rag2|MGI:1858556|2|||||||||||||||||||||||||||||Homozygous mice exhibit total inability to initiate V(D)J rearrangement and fail to generate mature T or B lymphocytes.||BALB/c|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|18-Nov-2015|Cryopreserved sperm|50.0|0.0|Unknown||B cell, T cell, IgM|Yes| 8875.0|Mal fl|C57BL/6-Mal/PjhApb||Recessive|myelin and lymphocyte protein, T cell differentiation protein|Mal|Normal|VIP17|MGI:892970||||2|||||||||||||||||||||||||||||Normal||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|07-Mar-2020|Cryopreserved sperm|50.0|0.0|Unknown|||Yes| 7994.0|564Igi|B6.129S4-Igk Igh/TikAnu||Dominant|immunoglobulin kappa chain complex|Igk||kappa|MGI:96494|immunoglobulin kappa chain complex; targeted mutation 1, Thereza Imanishi-Kari|Igk|MGI:3687307|6|||||||||||||||||||||||||||||Glomerulonephritis:• mutant mice kidney changes consistent with those seen in mesangioproliferative glomerulonephropathies in humanAbnormal podocyte morphology:• mild basement membrane thickeningPodocyte foot process effacement• segmental epithelial cell foot process effacementAbnormal glomerular mesangium morphology:• expansion of the glomerular mesangium by increased mesangial cells, matrix, and numerous electron dense depositsMesangial cell hyperplasiaExpanded mesangial matrixSystemic Lupus Erythematosus; SLE||C57BL/6J|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|20|||No|19-Nov-2015|Cryopreserved sperm|32.0|0.0|Yes|Systemic Lupus Erythematosus; SLE|Immunoglobulin, autoimmunity, lupus|Yes| 7994.0|564Igi|B6.129S4-Igk Igh/TikAnu||Dominant|immunoglobulin heavy chain complex|Igh|||MGI:96442|immunoglobulin heavy chain complex; targeted mutation 1, Thereza Imanishi-Kari|Igh|MGI:3687305|12|||||||||||||||||||||||||||||Glomerulonephritis:• mutant mice kidney changes consistent with those seen in mesangioproliferative glomerulonephropathies in humanAbnormal podocyte morphology:• mild basement membrane thickeningPodocyte foot process effacement• segmental epithelial cell foot process effacementAbnormal glomerular mesangium morphology:• expansion of the glomerular mesangium by increased mesangial cells, matrix, and numerous electron dense depositsMesangial cell hyperplasiaExpanded mesangial matrixSystemic Lupus Erythematosus; SLE||C57BL/6J|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|20|||No|19-Nov-2015|Cryopreserved sperm|||Yes|Systemic Lupus Erythematosus; SLE|Immunoglobulin, autoimmunity, lupus|Yes| 7990.0|PEP-R619W 104|C57BL/6-Ptpn22/104MarpApb||Dominant|protein tyrosine phosphatase, non-receptor type 22 |Ptpn22|Unknown|70zpep, Ptpn8|MGI:107170||||3|||||||||||||||||||||||||||||Unknown|Unknown|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|04-Nov-2015|Cryopreserved sperm|50.0|0.0|Unknown|||Possibly| 7995.0|B6 control|C57BL/6NCrlAnu||Recessive|Not applicable||||||||Unknown|||||||||||||||||||||||||||||Normal||C57BL/6NCrlAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|20-Nov-2015|Cryopreserved sperm|63.0|315.0|Unknown||Control mouse|No| 7991.0|PEP-R619W 106 |C57BL/6-Ptpn22/106Marp ||Dominant|protein tyrosine phosphatase, non-receptor type 22 (lymphoid)|Ptpn22|Unknown|70zpep, Ptpn8|MGI:107170||||3|||||||||||||||||||||||||||||Unknown|Unknown|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|06-Nov-2015|Cryopreserved sperm|50.0|0.0|Unknown|||Possibly| 8001.0|Y-RFP ; Ddx3y_cl.330_RFP|129-Ddx3y/330KalpApb|Yrfp|Semi-dominant|DEAD (Asp-Glu-Ala-Asp) box polypeptide 3, Y-linked|Ddx3y|Normal||MGI:1349406||||Y|||||||||||||||||||||||||||||Normal|Most tissues express the mKate2 red fluorescent protein gene. There is some variation in expression between tissues.|129S1/Sv1mJ |Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|04-Dec-2015|Cryopreserved sperm|50.0|0.0|No||RFP|Yes| 10417.0|Tnfaip3S381A (1)|C57BL6/NCrl-Tnfaip3/AnuApb||Recessive|tumor necrosis factor, alpha-induced protein 3|Tnfaip3||zinc finger protein A20|MGI:1196377|Tnfaip3: endonuclease-mediated mutation 2, Australian National University|Tnfaip3||10|ENSMUSG00000019850||||||||||||||||||||||||||||unknown|unknown|C57Bl/6N|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|24-Apr-2024|Cryopreserved sperm|50.0|0.0|Unknown|||No| 7996.0|SMB|B6.129P2-Smg1||Dominant|SMG1 homolog, phosphatidylinositol 3-kinase-related kinase (C. elegans)|Smg1|Unknown|SMG-1, ATX|MGI:1919742|SMG1 homolog, phosphatidylinositol 3-kinase-related kinase (C. elegans); gene trap AG0297, Wellcome Trust Sanger Institute|Smug|MGI:3876748|7|||||||||||||||||||||||||||||Early embryonic lethal|Premature death:• due to high tumor incidenceIncreased tutor incidence:• in various organsIncreased lymphoma incidence:• predominantly B cell of follicular center originIncreased B cell derived lymphoma incidence:• of follicular center originIncreased lung adenocarcinoma incidence:• papillary adenocarcinoma in the lungAbnormal basicranium angle:• the angle formed by the plane of the mandible to the plane of the cranial base is decreased compared to in wild-type micePrognathiaAbnormal tooth morphology:• over-grownAbnormal tooth development:• producing over-grown teethIncreased body sizeIncreased body weightIncreased body lengthEnlarged spleenDecreased circulating interleukin-1 beta levelIncreased circulating interleukin-6 levelChronic inflammation:• low level inflammation that progresses to chronic inflammation• mainly in the kidney and lungEnlarged liverHepatic steatosisAbnormal kidney morphologyAbnormal basicranium angle:• the angle formed by the plane of the mandible to the plane of the cranial base is decreased compared to in wild-type mice|C57BL/6N|No|No|Yes|No|No|Yes|No|Good|20||Het x WT|No|20-Nov-2015|Cryopreserved sperm|50.0|0.0|Unknown|||Yes| 7998.0|PRLR|C57BL/6-Prlr||Semi-dominant|prolactin receptor |prlr||Pr-1, Prlr-rs1|MGI:97763||||15|||||||||||||||||||||||||||||Unknown|Unknown|C57BL/6J|Yes|Yes|Yes|No|Unknown|Yes|No|Unknown||||No|03-Dec-2015||0.0|0.0|Unknown|||No| 10421.0|Tyk2-2bpdel|C57BL/6NCrlAnu-Tyk2em2Anu/Anu||Recessive|tyrosine kinase 2|Tyk2||JTK1|MGI:1929470|Tyk2:endonuclease-mediated mutation 2, Australian National University|Tyk2||9|ENSMUSG00000032175|ENSMUST00000216874|||||||||||||||||||||||||||Normal|Normal|C57Bl/6N|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|02-May-2024|Cryopreserved sperm|53.0|0.0|Unknown|||No| 8005.0|Fgrf2|B6.129X1-Fgfr2/DunwApb||Recessive|fibroblast growth factor receptor 2|Fgfr2|Unknown|Bek, Fgfr-2, Fgfr7, Fgfr-7, KGFRTr, svs|MGI:95523|fibroblast growth factor receptor 2; targeted mutation 1, David M Ornitz|Fgfr2|MGI:3044679|7|||||||||||||||||||||||||||||Normal|Normal|C57BL/6J|Yes|Unknown|Yes|Yes|Unknown|Yes|No|Good||||No|08-Dec-2015|Cryopreserved sperm|49.0|0.0|Unknown|||Possibly| 8003.0|FcRn-|C.Cg-Fcgrt/DcrJApb||Dominant|Fc receptor, IgG, alpha chain transporter|Fcgrt|Nil|FcRn, neonatal Fc receptor|MGI:103017|Fc receptor, IgG, alpha chain transporter; targeted mutation 1, Derry C Roopenian|Fcgrt|MGI:3511510|7|||||||||||||||||||||||||||||Decreased circulating serum albumin, decreased circulating IgG, decreased IgG halflife, increased albumin/IgG catabolism, impaired IgG-mediated cross presentation, impaired IgG transcytosis, deminished perinatal maternal IgG transport, |Impaired|BALB/c|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|>9||Normal|No|08-Dec-2015|Cryopreserved sperm|90.0|0.0|Unknown||IgG receptor, IgG transcytosis, antigen presentation, neonatal Fc receptor|Possibly| 8006.0|FgfR1null|B6.129-FgfR1/DunwApb||Recessive|fibroblast growth factor receptor 1|Fgfr1|Unknown|Eask, Fgfr-1, FGFR-I, Flt-2, Hspy|MGI:95522|Fgfr1; targeted mutation 1.1, Sally Dunwoodie|FgfR1|MGI:2686864|Recessive||||||||||||||||||||||||||||||||||||||homozygous lethal|normal|C35BL6/J|No|No|Yes|No|No|Yes|No|Good||||No|09-Dec-2015||0.0|0.0|Unknown|||Possibly| 8002.0|PEP-Delta 87 |C57BL/6-Ptpn22MarpApb ||Recessive|protein tyrosine phosphatase, non-receptor type 22 (lymphoid)|Ptpn22|Unknown|70zpep, Ptpn8|MGI:107170||||3||||||||||||||||Yes|||||||||||||Unknown|Unknown|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|07-Dec-2015|Cryopreserved sperm|50.0|0.0|Unknown|||Possibly| 8013.0|Aicda fl|C57BL/6N(Cg)-Aicda/MarpAnuApb||Recessive|activation-induced cytidine deaminase|Aicda|Normal|Aid|MGI:1342279|activation-induced cytidine deaminase; targeted mutation 1a, Helmholtz Zentrum Muenchen GmbH|Aicda|MGI:4460367|6|||||||||||||||||||||||||||||Normal||C57BL/6N|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||4||No|17-Dec-2015|Cryopreserved sperm|80.0|0.0|Unknown||EuCOMM|Yes| 10394.0|GtROSA|B6.129-Gt(ROSA)26Sor/JWehiAnu||Recessive|gene trap ROSA 26, Philippe Soriano|Gt(ROSA)26Sor||R26, ROSA26|MGI:104735||||6|ENSMUSG00000086429||||||||||||||||GtROSA-Flox-Betagalactosidase||||||||||||Normal|Normal|C57Bl/6N|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Good||||No|20-Dec-2023|Cryopreserved sperm|50.0|0.0|Unknown|||No| 8010.0|Pax8 x TetOCre|B6.Cg-Tg(Pax8rtTA2S*M2)1Koes/J Tg(tetOcre)1Jaw/J||Dominant||||||||||||||||||||||||||transgene insertion 1, Robert Koesters|Pax8|||||||||||Normal|Normal|C57B/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|||double x double|Yes|14-Dec-2015|Cryopreserved sperm|50.0|0.0|Unknown|||Yes| 8010.0|Pax8 x TetOCre|B6.Cg-Tg(Pax8rtTA2S*M2)1Koes/J Tg(tetOcre)1Jaw/J||Dominant||||||||||||||||||||||||||transgene insertion 1, Jeffrey A Whitsett|CMV|||||||||||Normal|Normal|C57B/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|||double x double|Yes|14-Dec-2015|Cryopreserved sperm|||Unknown|||Yes| 4746.0|Rag:KK|B6.Cg-H2 Rag1/AnuApb||Recessive|recombination activating gene 1|Rag1|Unknown|Rag-1|MGI:97848|targeted mutation 1, Peter Mombaerts|Rag1|MGI:1857241|2||||||||||||||||Yes|||||||||||||Homozygotes for targeted null mutations exhibit arrested development of T and B cell maturation at the CD4-8- thymocyte or B220+/CD43+pro-B cell stage due to inability to undergo V(D)J recombination.||C57BL/10.BR x C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||18||No|27-Apr-2009|Cryopreserved sperm|205.0|0.0|Unknown||T cell, B cell, MHC, lymphocyte|Yes| 4746.0|Rag:KK|B6.Cg-H2 Rag1/AnuApb||Recessive|histocompatibility-2, MHC|H2||H-2, MHC-II|MGI:95894|histocompatibility-2, MHC; k variant|H2|MGI:3579322|17|||||||||||||||||||||||||||||Homozygotes for targeted null mutations exhibit arrested development of T and B cell maturation at the CD4-8- thymocyte or B220+/CD43+pro-B cell stage due to inability to undergo V(D)J recombination.||C57BL/10.BR x C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||18||No|27-Apr-2009|Cryopreserved sperm|||Unknown||T cell, B cell, MHC, lymphocyte|Yes| 8017.0|ENU37:G1|ANU:ENU37:G1||Recessive|Unknown||||||||Unknown||||||||||||||||Unknown|||||||||||||Unknown|Unknown|C57BL/6NCrlAnu|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||1||No|07-Jan-2016|Cryopreserved sperm|1249.0|0.0|Unknown||ENU, random, mutagenesis, screen|Yes| 8018.0|ENU37:G2|ANU:ENU37:G2||Recessive|Unknown||||||||Unknown||||||||||||||||Unknown|||||||||||||Unknown|Unknown|C57BL/6NCrlAnu|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||1||No|07-Jan-2016|Cryopreserved sperm|1599.0|0.0|Unknown||ENU, random, mutagenesis, screen|Yes| 8020.0|ICExiNOSxRKO/BL6|B6;129S2-Casp1 Ifngr1 Nos2/AnuApb||Recessive|caspase 1|Casp1|Nil|Caspase-1, ICE, Il1bc, interleukin 1 beta-converting enzyme|MGI:96544|caspase 1; targeted mutation 1, Tara Seshadri|Casp1|MGI:1927822|9|||||||||||||||||||||||||||||||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|Unknown||Hom X hom|No|09-Feb-2016|Cryopreserved sperm|43.0|0.0|Unknown|||Possibly| 8020.0|ICExiNOSxRKO/BL6|B6;129S2-Casp1 Ifngr1 Nos2/AnuApb||Recessive|interferon gamma receptor 1|Ifngr1||CD119, Ifgr, IFN-gammaR, IFN-gamma R, Ifngr, Nktar|MGI:107655|interferon gamma receptor 1; targeted mutation 1, Michel Aguet|Ifngr1|MGI:1857286|10|||||||||||||||||||||||||||||||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|Unknown||Hom X hom|No|09-Feb-2016|Cryopreserved sperm|||Unknown|||Possibly| 8020.0|ICExiNOSxRKO/BL6|B6;129S2-Casp1 Ifngr1 Nos2/AnuApb||Recessive|nitric oxide synthase 2, inducible|Nos2|Nil|iNOS, Nos-2, Nos2a, NOS-II|MGI:97361|nitric oxide synthase 2, inducible; targeted mutation 1, Merck Research Laboratory|Nos2|MGI:2158791|11|||||||||||||||||||||||||||||||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|Unknown||Hom X hom|No|09-Feb-2016|Cryopreserved sperm|||Unknown|||Possibly| 8007.0|Fgf8flox|B6.Cg-Fgf8/DunwApb||Recessive|fibroblast growth factor 8|Fgf8|Unknown|Aigf, Fgf-8|MGI:99604|fibroblast growth factor 8; targeted mutation 1, Anne M Moon|Fgf8|MGI:2686864|19|||||||||||||||||||||||||||||Normal|Normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|09-Dec-2015|Cryopreserved sperm|50.0|0.0|Unknown||Ectoderm, Endoderm|Possibly| 8014.0|HSA-GPX1-TG21|C57BL/6-Tg(ACTA1-Gpx1)21Ttig||Dominant||||||||||||||||||||||||||glutathione peroxidase 1|human skeletal apha actin|||||||||||Normal|Normal|C57BL/6J|Yes|Yes|Unknown|Yes|Yes|Unknown|No|Unknown||||No|21-Dec-2015|Cryopreserved sperm|60.0|0.0|Unknown|||Possibly| 10395.0|Rosa26:TdTomato|B6.Cg-Gt(ROSA)26Sor|MGI:3809524|6|ENSMUSG00000086429 ||||||||||||||||||||||||||||Normal|Normal|C57Bl/6N|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|20-Dec-2023|Cryopreserved sperm|62.0|0.0|Unknown|||No| 8021.0|Gstz1 KO|B6.C-Gstz1/AnuApb||Recessive|glutathione transferase zeta 1 (maleylacetoacetate isomerase)|Gstz1|Nil|maleylacetoacetate isomerase|MGI:1341859|targeted mutation 1, Philip G Board|Gstz1|MGI:3050206|12||||||||||||||||No|||||||||||||Increased sensitivity to induced Morbidity/Mortality * 3% phenylalanine in the water is lethal to young homozygotes, less than 28 days old, but not to older homozygotes, greater than 66 days oldpremature death * several mutants died after 1 year of age from heart pathologiesDystrophic cardiac calcinosis* in some mutants over 1 year of age Calcification of the myocardium in the right atrium and/or ventricle is seen* calcification is also seen in 3 of 8 young mutants that died after 3% phenylalanine exposurecellular necrosis* in some mutants over 1 year of age myocyte necrosis is seen* myocyte necrosis is also seen in 2 of 8 young mutants that died after 3% phenylalanine exposureDecreased leukocyte cell number* 3% phenylalanine in the water results in decreased total white cell counts in mutants but not in wild-type micedecreased spleen weight * spleen weight is significantly decreased in female homozygotes and tends to be decreased in male homozygotes compared to wild-type mice* 3% phenylalanine in the water results in a dramatic decrease in spleen weight in homozygotes with reduction in both white and red pulp, but an increase in spleen weight in wild-type micechronic inflammation* in some mutants over 1 year of age chronic inflammation is seen in the heartliver inflammation* at 6 weeks and 6 months of age multifocal hepatitis is seenLiver inflammation* at 6 weeks and 6 months of age multifocal hepatitis is seenAbnormal hepatocyte morphology* large pleomorphic mitochondria are seen in hepatocytes from mutantsIncreased liver weight* on a normal diet liver weight is greater in homozygotes compared to wild-type miceHepatic necrosis* at 6 months of age 3 of 7 homozygotes show hepatocyte necrosis* 3 out of 8 homozygotes that died after 3% phenylalanine exposure displayed hepatocyte necrosisHepatic steatosis * 5 out of 8 homozygotes that died after 3% phenylalanine exposure displayed macrovesicular steatosis||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|10-Feb-2016|Cryopreserved sperm|55.0|0.0|Unknown||GST, maleylacetoacetate, maleylacetone (MA) and succinylacetone, phenylalanine and tyrosine, Keap1/Nrf2 pathway, Oxidative stress|Yes| 8024.0|ENU26:Prpf40b|C57BL/6NCrlAnu-Prpf40b/Anu||Recessive|pre-mRNA processing factor 40B|Prpf40b|Unknown|2610317D23Rik|MGI:1925583|Prpf40b; mutation 1, Australian National University|Prpf40b||15|ENSMUSG00000023007|ENSMUST00000145482|Prpf40b-001|2570|2791|A to G|ENSMUSE00001300864|26|857|Glutamic acid to Glycine|||||CACGTCAGAAAGCGAGCTGAGTGAGGGGGAGCTGGAGAGGCGAAGGCGGACACTCCTACAG|||||||||||||||Normal|C57BL/6NCrlAnu|Unknown|Yes|Yes|Unknown|Yes|Yes|No|Unknown||||No|16-Feb-2016|Cryopreserved sperm|44.0|0.0|Unknown||ENU|Yes| 8026.0|Ndfip1 Gzmb-cre |B6.Cg-Ndfip1 Tg(GZMB-cre)1Jcb/AnuApb||Recessive|Nedd4 family interacting protein 1|Ndfip1|Normal|0610010M22Rik|MGI:1929601|Nedd4 family interacting protein 1; targeted mutation 1, Seong-Seng Tan|Ndfip1|MGI:5313245|18|||||||||||||||||transgene insertion 1, Joshy Jacob|human granzyme B|||||||||||Unknown|Normal|C57BL/6|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|19-Feb-2016|Cryopreserved sperm|31.0|0.0|Unknown||Nedd4, pten, ubiquitination|Yes| 8025.0|Roquin fl|B6.Cg-Rc3h1/Anu||Recessive|RING CCCH (C3H) domains 1|Rc3h1|Unknown|5730557L09Rik, roquin|MGI:2685397|RING CCCH (C3H) domains 1; targeted mutation 1.1, Carola Vinuesa|Rc3h1|MGI:5508920|1||||||||||||||||||||||||||||||No phenotypic analysis|C57BL/6|Yes|Yes|Yes|Yes|Yes|Unknown|No|Unknown||||No|16-Feb-2016||0.0|0.0|Unknown||T cell, arthritis, autoimmunity, mRNA, stress granules|Yes| 7652.0|RBL-1|SJL/J-Arhgap40 Rbl1/Marp||Semi-dominant|retinoblastoma-like 1 (p107)|Rbl1|Reduced|p107|MGI:103300||||2|||||||||||||||||||||||||||||Display macrocytosis|Mild macrocytosis|SJL/J|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|||homozygous intercrosses|No|08-Apr-2014|Cryopreserved sperm|50.0|0.0|Unknown||RBL1, Cell cycle, ENU|Possibly| 7652.0|RBL-1|SJL/J-Arhgap40 Rbl1/Marp||Semi-dominant|Rho GTPase activating protein 40|Arhgap40|Reduced||MGI:3649852||||2|||||||||||||||||||||||||||||Display macrocytosis|Mild macrocytosis|SJL/J|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|||homozygous intercrosses|No|08-Apr-2014|Cryopreserved sperm|||Unknown||RBL1, Cell cycle, ENU|Possibly| 8023.0|LysMcre|B6.129P2-Lyz2/JAusbAnu||Dominant|lysozyme 2|Lyz2|Normal|Lys, Lysm, Lyzs, Lzm, Lzm-s1, Lzp|MGI:96897|lysozyme 2; targeted mutation 1, Irmgard Forster|Lyz2|MGI:1934631|10|||||||||||||||||||||||||||||Unknown|Enlarged spleen:*Rare|C57BL/6|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|16-Feb-2016|Cryopreserved sperm|44.0|0.0|Unknown||Macrophage, Granulocyte, Conditional mutagenesis|Yes| 7653.0|RBC12|C57BL/6-Dnm2/WehiMarpApb||Dominant|Dynamin 2|Dnm2|Reduced|Dyn2|MGI:109547||||9|||||||||||||||||||||||||||||Lethal|Display microcytic anemia|C57BL/6|No|No|Yes|No|No|Yes|No|Good||10|heterozygous intercrosses|No|08-Apr-2014||0.0|0.0|Unknown||Dnm2, Endocytosis, ENU|Possibly| 8027.0|alphaMHC-Rln1|C57BL/6-Tg(Myh6-Rln1)1Nros/Marp||Dominant||||||||||||||||||||||||||relaxin 1 (Mus musculus) |Myh6 (alpha myosin heavy chain)|high||||||||||Unknown|Males are normal. Females have enlarged nipples and are prone to pseudopregnancy and have fertility issues. |C57BL/6|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Good|>50||use TG male and WT female|No|02-Mar-2016|Cryopreserved sperm|60.0|0.0|No|||Yes| 8028.0|ENU34:001:Zfp318|C57BL/6NCrlAnu-Zfp318/AnuApb||Recessive|zinc finger protein 318|Zfp318||2610034E08Rik, D530032D06Rik, TZF|MGI:1889348|Zfp318; mutation 2, Australian National University|Zfp318||17|ENSMUSG00000015597|ENSMUST00000113481|Zfp318-001|3301|3409|T to C|ENSMUSE00001294148|7|1101|Phenylalanine to Leucine|||||AAGACTGCAATACCACCTGTGGGACCATGTTTGACTTCTTCACCCATATGCACAATAAGAA||||||||||||||Increased expression of IgM and decreased expression of IgD on mature B cells||C57BL/6NCrlAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|17-Mar-2016|Cryopreserved sperm|44.0|0.0|Unknown||B cell, IgM, IgD|Yes| 8030.0|Hs2st1 fl|B6.129-Hs2st1/UcsdAnu||Recessive|heparan sulfate 2-O-sulfotransferase 1|Hs2st1|Normal|Hs2st, mKIAA0448|MGI:1346049|heparan sulfate 2-O-sulfotransferase 1; targeted mutation 1.1, Jeffrey D Esko|Hs2st1|MGI:4439161|3|||||||||||||||||||||||||||||Normal|Normal|C57BL/6J|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|>10|||No|24-Mar-2016|Cryopreserved sperm|33.0|0.0|Unknown||Heparan sulphate, sulfation, triglyceride|Yes| 8029.0|Ndst1 fl|B6.129-Ndst1/UcsdAnu||Recessive|N-deacetylase/N-sulfotransferase (heparan glucosaminyl) 1|Ndst1|Normal|1200015G06Rik, b2b2230Clo, glucosaminyl N-deacetylase/N-sulfotransferase 1, Hsst, Ndst-1|MGI:104719|N-deacetylase/N-sulfotransferase (heparan glucosaminyl) 1; targeted mutation 1, Jeffrey D Esko|Ndst1|MGI:3589211|18|||||||||||||||||||||||||||||Normal|Normal|C57BL/6J|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|>10|||No|24-Mar-2016|Cryopreserved sperm|57.0|0.0|Unknown||heparan sulphate, endothelial, chemokine, neutrophil|Yes| 7997.0|Osterix-Cre EphrinB2 fl|B6.Cg-Efnb2 Tg((Sp7-tTA,tetO-EGFP/cre)1Amc/StVApb||Semi-dominant|ephrin B2|Efnb2|Reduced|ELF-2, Epl5, Eplg5, Htk-L, Lerk5, LERK-5, NLERK-1|MGI:105097|ephrin B2; targeted mutation 1, David J Anderson|Efnb2|MGI:2176476|8|||||||||||||||||transgene insertion 1, Andrew P McMahon|Sp7|||||||||||Mice with an osteoblast-specific knockout of ephrinB2 have altered osteoblast differentiation and delayed bone mineralisation, causing their bones to have reduced stiffness. Their response to anabolic PTH treatment was altered. This is due to ephrinB2-deficient osteoblasts becoming more apoptotic, compared to cre +ve controls. |N/A|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|5|||No|27-Nov-2015|Cryopreserved sperm|50.0|0.0|Unknown||Osteoblast, Ephrin|Yes| 8032.0|CD11c-cre x Atg7|C57BL/6-Atg7 Tg(Itgax-cre)1-1Reiz/Wehi||Recessive|autophagy related 7|Atg7|Normal|1810013K23Rik, Apg7l|MGI:1921494|autophagy related 7; targeted mutation 1, Tomaki Chiba|Atg7|MGI:3587769|6|||||||||||||||||transgene insertion 1-1, Boris Reizis|mouse integrin alpha X (Cd11c)|||||||||||||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|31-Mar-2016|Cryopreserved sperm|10.0|0.0|Unknown||Dendritic cell, autophagy|Yes| 8816.0|AXDND1-571|C57BL/6-Axdnd1/MarpApb||Recessive|axonemal dynein light chain domain containing 1|Axdnd1|Unknown|9430070O13Rik, LOC381304|MGI:1924602||||1|||||||||||||||||||||||||||||Infertile|Unknown|C57/BL/6J|Yes|Unknown|Yes|Yes|No|Yes|No|Unknown||||No|21-Oct-2019|Cryopreserved sperm|50.0|0.0|Unknown||Infertility|Yes| 8031.0|Hs6st1 fl|B6.129-Hs6st1/WvcUcsdAnu||Recessive|heparan sulfate 6-O-sulfotransferase 1|Hs6st1|Normal|6)ST1|MGI:1354958|heparan sulfate 6-O-sulfotransferase 1; targeted mutation 1, Wellington V Cardoso|Hs6st1|MGI:3793786|1|||||||||||||||||||||||||||||Normal|Normal|C57BL/6J|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|>10|||No|24-Mar-2016|Cryopreserved sperm|57.0|0.0|Unknown||Heparan sulphate|Yes| 8037.0|FRG1|C57BL/6J-Tg(HSA-FRG1)/MarpApb|MARP|Dominant||||||||||||||||||||||||||human Fascioscapulohumeral muscular dystrophy gene 1|HSA|High||||||||||FRG1 transgenic mice represent a mouse model of the human muscle disease Facioscapulohumeral muscular dystrophy. The phenotype of FRG1 transgenic mice has been very well characterized (Sancisi et al., 2014. Am J Physiol Regul Integr, V306(2); R127-37), (Xynos et al., 2013. J Cell Sci, V126(10); 2236-45), (Gabellini et al., 2006. Nature, V439(7079); 973-7) and (Feeney and McGrath et al., 2015. PLoS One, V10(2): e0117665). The FRG1 transgenic mice develop muscle disease from 6 weeks of age affecting predominantly hindlimb muscles (tibialis anterior, quadriceps) as well as triceps and trapezius muscles. They display hindlimb weakness and spinal kyphosis. This muscle disease does not affect mobility, food intake or survival (Gabellini et al., 2006. Nature, V439(7079); 973-7).|FRG1 transgenic mice represent a mouse model of the human muscle disease Facioscapulohumeral muscular dystrophy. The phenotype of FRG1 transgenic mice has been very well characterized (Sancisi et al., 2014. Am J Physiol Regul Integr, V306(2); R127-37), (Xynos et al., 2013. J Cell Sci, V126(10); 2236-45), (Gabellini et al., 2006. Nature, V439(7079); 973-7) and (Feeney and McGrath et al., 2015. PLoS One, V10(2): e0117665). The FRG1 transgenic mice develop muscle disease from 6 weeks of age affecting predominantly hindlimb muscles (tibialis anterior, quadriceps) as well as triceps and trapezius muscles. They display hindlimb weakness and spinal kyphosis. This muscle disease does not affect mobility, food intake or survival (Gabellini et al., 2006. Nature, V439(7079); 973-7).|C57BL6/J|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|||Wild type females crossed with FRG1-transgenic males|No|05-Apr-2016|Cryopreserved sperm|50.0|0.0|Yes|Fascioscapulohumeral muscular dystrophy. Individuals with this type of muscular dystrophy develop muscle weakness in face, arms and torso.|FSHD, muscular dustrophy, muscle disease|Yes| 8818.0|hHER2|BALB/c-Tg(Wap-ERBB2)||Dominant||||||||||||||||||||||||||human erb-b2 receptor tyrosine kinase 2|whey acidic protein (Wap)|||||||||||BALB/c hHer2 +/+ is embryonic lethal|Heterozygous +/- BALB/c-Hher2 pups are viable. No overt phenotype|BALB/c|No|No|Yes|No|No|Yes|No|Unknown||||No|23-Oct-2019|Cryopreserved sperm|44.0|0.0|Unknown||Her-2|Yes| 8040.0|C57BL/6-TLR-4|B6;129P2-Tlr4|B6;129P2-Tlr4|Recessive|toll-like receptor 4|Tlr4|Nil|lipopolysaccharide response, Lps, Rasl2-8|MGI:96824|toll-like receptor 4; targeted mutation 1, Shizuo Akira|Tlr4|MGI:1860885|4||||||||||||||||Yes|||||||||||||Homozygotes for spontaneous or targeted mutations are hyporesponsive to bacterial lipopolysaccharide and more susceptible to infection by gram negative bacteria.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|07-Apr-2016|Cryopreserved sperm|54.0|82.0|Unknown||infection, T cell, inflammation, eosinophil, hyperresponsiveness|Yes| 8036.0|Nrp2:CreERT2/EGFP|C57BL/6-Tg(Nrp2-CreERT2/EGFP)#Qsch||Dominant||||||||||||||||||||||||||CreERT2 recombinase with IRES EGFP|Nrp2|low||||||||||Normal|Normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|10|10|Male homozygous cross female homozygous|No|05-Apr-2016|Cryopreserved sperm|49.0|0.0|No||Neuropilin 2, Nrp2, CreERT2 recombinase, EGFP|Possibly| 8042.0|gp130Y757F x sgp130Fc|B6.129- Il6st Tg(Hbb-sgp130Fc)/MarpApb||Recessive|interleukin 6 signal transducer|Il6st|Unknown|CD130, D13Ertd699e, gp130|MGI:96560|interleukin 6 signal transducer; targeted mutation 1, Matthias Ernst|Il6st|MGI:2388478|13||||||||||||||||Yes|soluble gp130 fused to Fc portion of IgG1|beta globin|||||||||||||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|10||heterozogous x homozygous|No|13-Apr-2016|Cryopreserved sperm|50.0|0.0|Yes||gp130|No| 8042.0|gp130Y757F x sgp130Fc|B6.129- Il6st Tg(Hbb-sgp130Fc)/MarpApb||Recessive|||Nil||||||1||||||||||||||||No|||||||||||||||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|10||heterozogous x homozygous|No|13-Apr-2016|Cryopreserved sperm|||Yes||gp130|No| 8041.0|Mir155 fl|C57BL/6-Mir155/J||Recessive|microRNA 155|Mir155|Normal|Mirn155, mmu-mir-155|MGI:2676840|microRNA 155; targeted mutation 1.1, Gwenn Garden|Mir155|MGI:5616592|16|||||||||||||||||||||||||||||Normal||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|11-Apr-2016|Cryopreserved sperm|60.0|0.0|Unknown||T cell, inflammation|Yes| 8034.0|ENU34:001:Relb|C57BL/6NCrlAnu-Relb/AnuApb||Recessive|avian reticuloendotheliosis viral (v-rel) oncogene related B|Relb|Unknown|shep|MGI:103289||||7|ENSMUSG00000002983|ENSMUST00000094762|Relb-001|842|1038|A to T|ENSMUSE00001216935|8|281|Leucine to Glutamine|||||||||||||||||||Activated T cells and dermatitis||C57BL/6NCrlAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|||Het x het|No|04-Apr-2016|Cryopreserved sperm|11.0|0.0|Unknown||ENU, T cell, dermatitis, autoimmunity|Yes| 8035.0|B6Bst2|B6.129-Bst2/Wehi||Recessive|bone marrow stromal cell antigen 2|Bst2||2310015I10Rik, Bst-2, C87040, GREG|MGI:1916800||||8|||||||||||||||||||||||||||||||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|04-Apr-2016|Cryopreserved sperm|30.0|0.0|Unknown|||Yes| 8038.0|NanogLacZ|C57BL/6J-Nanog/Lartf||Recessive|Nanog homeobox|Nanog|Nil|2410002E02Rik, ecat4, ENK|MGI:1919200|targeted mutation 1, Adam Hart|Nanog| |6||||||||||Unknown to Unknown||||||Yes|||||||||||||LethalHomozygous embryos fail at e5-6, due to a defect in epiblast development. Nanog is required for epiblast development.|None.Heterozygous males and females are normal and fertile and are generated in the expected medelian ratios.|C57BL/6J|No|No|Yes|No|No|Yes|No|Good|10+||backcross heterzgote males to C57BL/6 females|No|06-Apr-2016|Cryopreserved sperm|50.0|0.0|No||germline, spermatogenesis, stem cell|No| 5172.0|Mir146 -/-|C57BL/6-Mir146/BalAnuApb||Recessive|microRNA 146|Mir146|Nil|miR-146a, Mirn146, mmu-mir-146, mmu-mir-146a|MGI:2676831|microRNA 146; targeted mutation 1.1, David Baltimore|MIr146|MGI:4882045|11|||||||||||||||||||||||||||||Premature death:• mice become moribund by 18 to 22 months of ageAbnormal lymphopoiesis:• at 6 months, mice develop lympho- and myeloproliferative syndrome compared with wild-type mice• however, mice exhibit normal lymphoid cell numbers at 6 to 8 weeks and disease is not present in mice treated with an IFNgamma blockerMyeloid hyperplasia:• at 6 months, mice develop lympho- and myeloproliferative syndrome compared with wild-type mice• however, mice exhibit normal myeloid cell numbers at 6 to 8 weeks and disease is not present in mice treated with an IFNgamma blocker• chronic myeloproliferation and myelofibrosis in the bone marrowExtramedullary hematopoiesis:• in the spleenAnemia:Abnormal bone marrow cell morphology/development:• by 18 to 22 months, mice develop end-stage fibrosis or a hypercellular bone marrow and pale bone marrow unlike wild-type miceIncreased bone marrow cell number:• by 18 to 22 monthsDecreased erythrocyte cell number:Decreased hematocrit:Decreased hemoglobin contentThrombocytopenia:Increased regulatory T cell number:• in the periphery but not thymus• not rescued by treatment with an IFNgamma blockerDecreased leukocyte cell number:Decreased lymphocyte cell numberDecreased monocyte cell numberEnlarged spleen:• progressive starting at 5 to 6 months of age• 6 to 7 times on necropsyIncreased spleen weightAbnormal regulatory T cell physiology:• increased proliferation and suppressive function (measured by Th1 cytokine production)Increased T cell derived lymphoma incidence:• some mice develop lymphomas of B cell or mixed T and B cell lineage in the cervical lymph node, gastrointestinal tract, liver and kidneyIncreased B cell derived lymphoma incidence:• some mice develop lymphomas of B cell or mixed T and B cell lineage in the cervical lymph node, gastrointestinal tract, liver and kidney• some mice develop high-grade diffuse large B cell lymphoma with apoptotic bodies and atypical mitosisIncreased follicular lymphoma incidence:• low-grade in some miceIncreased myeloid sarcoma incidence:• in the spleen and occasionally in the liver and kidney• myeloid tumors are transplantable into immunocompromised miceIncreased spleen neoplasm incidence:• spleen tumors with myeloid sarcoma histology in many miceMyelofibrosis:• myelofibrosis in the bone marrow||C57BL/6J|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|02-Jul-2010|Cryopreserved sperm|93.0|0.0|Unknown||T cell, lymphoma, myeloproliferation|No| 8046.0|ENU36:G3|ANU:ENU36:G3||Recessive|Unknown||||||||Unknown||||||||||||||||Unknown|||||||||||||Unknown|Unknown|C57BL/6NCrlAnu|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||2||No|29-Apr-2016|Cryopreserved sperm|164.0|0.0|Unknown||ENU, random, mutagenesis, screen|Yes| 8043.0|B6:Thy1.1|B6.Cg-Thy1/AnuApb||Recessive|thymus cell antigen 1, theta|Thy1||CD90, T25, theta, Thy-1, Thy1.1, Thy 1.2, Thy-1.2, Thy1.2|MGI:98747|thymus cell antigen 1, theta; a variant|Thy1|MGI:3579311|9|||||||||||||||||||||||||||||Normal||C57BL/6JAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|15-Apr-2016|Cryopreserved sperm|55.0|0.0|Unknown||Thy1.1|Yes| 8047.0|B10|C57BL/10SnJAnu||Dominant|||||||||||||||||||||||||||||||||||||||||Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|01-May-2016|Cryopreserved sperm, Embryo|167.0|812.0|Unknown|||No| 8045.0|Ndufa10/C57|C57BL/6JAnu-Ndufa10/AnuUsa||Semi-dominant|NADH Dehydrogenase (Ubiquinone) 1 Alpha Subcomplex, 10|Ndufa10|Unknown|2900053E13Rik|MGI:1914523|Ndufa10: mutation 2, Australian National University|Ndufa10||1||||||||||Unknown to Unknown|||||||||||||||||||changes in blood compartment|changes in blood compartment|C57BL/6JAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|21-Apr-2016|Cryopreserved sperm|50.0|0.0|Unknown|||No| 8051.0|Thor:Del|Folr4:Del||Recessive|IZUMO1 receptor, JUNO|Izumo1r||0910001L11Rik, Folbp3, Folr4, Juno|MGI:1929185||||Unknown|||||||||||||||||||||||||||||Unknown|Unknown|C57BL/6NCrlAnu|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|23-May-2016|Cryopreserved sperm|44.0|0.0|Unknown||CRISPR|Yes| 4988.0|ATM 7271 T⇒G ; Adonis|C.B6-ATM ||Recessive|ataxia telangiectasia mutated homolog (human)|Atm|Normal|C030026E19Rik|MGI:107202|targeted mutation 1, Georgia Chenevix-Trench|ATM||9||||||||||Unknown to Unknown||||||No|||||||||||||Infertile. Increased sensitivity to ionizing radiation. Immune deficiencies. Increased susceptability to lymphoid tumours|Normal|BALB/c|Yes|No|Yes|Yes|No|Yes|Yes|Good|8|||No|28-Jan-2010|Cryopreserved sperm|163.0|0.0|Yes||ATM, cancer, Radiation, Breast|Possibly| 8052.0|Thor:Ins|Folr4:Ins||Recessive|IZUMO1 receptor, JUNO|Izumo1r||0910001L11Rik, Folbp3, Folr4, Juno|MGI:1929185||||Unknown|||||||||||||||||||||||||||||Unknown|Unknown|C57BL/6NCrlAnu|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|23-May-2016|Cryopreserved sperm|22.0|0.0|Unknown||CRISPR|Yes| 4874.0|B6.Myd88.KO|C57BL/6-Myd88/StVApb||Recessive|myeloid differentiation primary response gene 88|Myd88|Nil||MGI:108005|targeted mutation 1, Shizuo Akira|Myd88|MGI:2385681|9||||||||||||||||Yes|||||||||||||Increased apoptosis: 5 days after lung injury, mutants show significantly increased numbers of apoptotic lung epithelial and inflammatory cells.Abnormal response/metabolism to xenobiotics: knockout mice are more susceptible to bleomycin-induced lung injury.Abnormal dendritic cell morphology/development: increased numbers of dendritic cells in brains of mice infected with Plasmodium.Abnormal T cell physiology: induction of the antigen-specific CD8+ T-cell response by immunizing with soluble ovalbumin and TLR9 agonists, but not TLR2 and TLR6 agonists, was severely impaired.Abnormal macrophage physiology:* TNF production is impaired in thioglycollate-elicited macrophages treated with intact zymosan.* cytokine production by macrophages cultured with P. carinii cysts is reduced compared to wild type.Abnormal dendritic cell physiology: cytokine secretion elicited by zymosan or LPS is impaired.Abnormal inflammatory mediator physiology.Abnormal chemokine physiology: hyaluronan fragment-induced expression of chemokines by peritoneal macrophages is completely abolished in double knockout mice.Abnormal cytokine physiology: CpG-A or RNA polyuridylic acid induced production of interferon-alpha was abolished in plasmacytoid dendritic cells.Abnormal TNF physiology: less upregulation of TNF-alpha in Plasmodium infection.Abnormal cytokine secretion:* LPS-induced cytokine production by BMDCs is almost abolished compared to controls and Myd88-sufficient mutants.* after stimulation with zymosan, TNF and Il12 production are significantly reduced in Myd88-deficient animals.Abnormal interferon physiology: less up regulation of INF-gamma in Plasmodium infection.Abnormal interleukin physiology: less upregulation of IL-12b in Plasmodium infection.Altered susceptibility to infection:* decreased susceptibility to parasitic infection.* resistant to cerebral malaria but eventually die of extremely high parasitemia.Increased susceptibility to viral infection: increased susceptibility to encephalomyocarditis virus (EMCV) infection compared to wildtype.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|28-Sep-2009|Cryopreserved sperm|80.0|0.0|Unknown||T cell, Natural Killer, IL-18, IL-1 receptor, interferon|Yes| 8050.0|Tar mice; SPTB D1781R|SJL/JAnu-Sptb/AnuApb||Dominant|spectrin beta, erythrocytic|Sptb|Reduced|brain erythroid spectrin (235E), D330027P03Rik, LOC383567, spectrin R, Spnb1, Spnb-1|MGI:98387||||12|||||||||||||||||||||||||||||Low red blood cell count and increase osmotic fragility|Low red blood cell count and increase osmotic fragility|SJL/J|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|18-May-2016|Cryopreserved sperm|54.0|0.0|Unknown||Red blood cells, osmotic fragility|Yes| 8044.0|NanogLoxP|C57BL/6J-Nanog/Lartf||Recessive|Nanog homeobox|Nanog|Normal|2410002E02Rik, ecat4, ENK|MGI:1919200|targeted mutation 2, Adam Hart|Nanog| |6||||||||||Unknown to Unknown||||||Yes|||||||||||||Homozygous Nanog (LoxP/LoxP) mice are normal and fertile.|None.Heterozygous Nanog (LoxP/+) males and females are normal and fertile and are generated in the expected medelian ratios.|C57BL/6J|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|10+|10+|backcross heterzgote males to C57BL/6 females, or interbreed homozygotes|No|20-Apr-2016|Cryopreserved sperm|50.0|0.0|No||germline, spermatogenesis, stem cell|No| 7450.0|Lifr fl|B6NTac;B6N-Lifr/HTacAnuApb||Dominant|leukemia inhibitory factor receptor|Lifr|Normal|A230075M04Rik, soluble differentiation-stimulating factor receptor|MGI:96788|leukemia inhibitory factor receptor; targeted mutation 1a, Helmholtz Zentrum Muenchen GmbH|Lifr|MGI:4841519|15|||||||||||||||||||||||||||||Normal||C57BL/6NCrlAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|04-Oct-2013|Cryopreserved sperm|75.0|0.0|Unknown||receptor, growth|Yes| 8048.0|Gadd45a KO|B6.129-Gadd45a||Recessive|growth arrest and DNA-damage-inducible 45 alpha|Gadd45a|Nil|Ddit1|MGI:107799|growth arrest and DNA-damage-inducible 45 alpha; targeted mutation 1, Albert J Fornace|Gadd45a|MGI:2182720|6|||||||||||||||||||||||||||||Premature death:• homozygous mice begin to die after 7 months of age and the median life span of females is reduced to 16 months compared to about 22 months for wild-typeAbnormal cell nucleus morphology:• splenocytes and keratinocytes have 3 or more centrosomes per cell and many keratinocytes have asymmetric distribution of centrosomes during mitosis• most MEFs with extra centrosomes also have large, partially cleaved, bilobed nucleiAbnormal chromosome morphology:• chromosomal aberrations including double minutes, centromere fusions or end associations, chromatid deletions, and incomplete triradials and quadraradialsAbnormal chromosome number:• less than 40% of homozygous MEFs are diploid at passage 4 with the rest either tetraploid or aneuploid, unlike wild-type MEFs where about 70% of cells are diploid, 30% are tetraploid and no aneuploid cells are seen• at passage 11 no homozygous MEFs are diploid and over 60% are aneuploidAneuploidy:• at passage 4 some aneuploid cells are seen and by passage 11 over 60% of cells are aneuploid• about 2% of freshly isolated splenic lymphoblasts display aneuploidy while no aneuploid cells are found in wild-type miceAbnormal cell physiology:• retroviral transfection of homozygous MEFs with an activated ras allele produces obvious transformed foci and these cells are able to form colonies in soft agar, unlike wild-type MEFs where the introduction of 2 activated oncogenes is needed for transformation• the number of colonies produced in the soft agar assay is less than in transfected homozygous Trp53 null MEFs• however, when exposed to ionizing radiation or UV apoptosis is similar to wild-type unlike Trp53 null MEFsAbnormal mitosis:• some MEFs fail to fully condense all their chromatin at mitosis• IR induces a strong G1 delay similar to wild-type cells and unlike in Cdkn1a null cellsDecreased mitotic index:• when exposed to UV the dose dependent reduction in the mitotic index is decreased compared to wild-type cells; however, when exposed to ionizing radiation (IR), the reduction in mitotic index is similar to wild-type and IR or UV-induced apoptosis is similar to wild-type unlike Trp53 null MEFsIncreased fibroblast proliferation:• from passage 5-7 homozygous MEFs progressively grow more rapidly and attain higher saturation densities compared to wild-type cells; however at earlier passages growth is similar to wild-type• low passage MEFs have a plating efficiency of about 0.025% compared to 0.005% in wild-type cells, 1.6% in Trp53 null cells, 1.2% in Cdkn1a null cells, and up to 1.4% in Gadd45a Cdkn1a double null cellsIncreased kidney cell proliferation:• diffuse global mesangial proliferation involving 40 - 100% of glomeruli is seen in older homozygotesIncreased thymus weight:• thymus weight as a percent of body weight is increased about 70% compared to wild-typeAbnormal lymphopoiesis:• lymphoid hyperplasia is seen in the lymph nodes and spleen of 9 month old homozygotesIncreased T cell number:• the proportion of total T cells is increased in the spleen and lymph nodes compared to wild-type miceIncreased thymocyte number:• thymocyte number is increased but the distribution of thymocyte subpopulations is similar to wild-typeDecreased leukocyte cell number:• at 7-9 months of age 47% of homozygous females are leukopenic compared to 7% of wild-type miceDecreased basophil cell number.Decreased eosinophil cell number.Decreased lymphocyte cell number:• at 7-9 months of age 40% of homozygous females are lymphopenic compared to 7% of wild-type miceIncreased IgG1 level:• 2-fold increase in IgG1 and high levels of IgG2b and IgG3 anti-double stranded DNA antibodies at 7 - 9 months of ageIncreased IgM level:• 2-fold increase in IgM at 7 - 9 months of ageIncreased T cell proliferation:• the sensitivity of primary T cell activation by anti-CD3 is increased with a 3- to 10-fold leftward shift in the dose-response curve and the maximal proliferative response is about 2-fold more than in wild-type cells• however, proliferation in response to cytokines and T cell receptor independent proliferation is not increased compared to controlsIncreased autoantibody level.Increased anti-double stranded DNA antibody level:• after 7 months of age in female homozygotes the occurrence and titer of antibodies against double stranded DNA is increased compared to wild-type miceIncreased anti-histone antibody level:• after 7 months of age in female homozygotes the occurrence and titer of antibodies against histones is increased compared to wild-type miceIncreased anti-single stranded DNA antibody level:• after 7 months of age in female homozygotes the occurrence and titer of antibodies against single stranded DNA is increased compared to wild-type miceIncreased inflammatory response:• lymphocytic infiltrates are seen in the lung and salivary glands at 9 months of ageGlomerulonephritis:• some glomeruli contain inflammatory cells, nuclear debris, and mesangial cell interposition, mild dilation of the proximal tubules occurs, and mild to severe dense perivascular mononuclear cell infiltrates are seen suggesting autoimmune glomerulonphritis.Exencephaly:• about 8% of pups from homozygous crosses display exencephalyParturition failure:• about 50% of females fail to deliver their first litter resulting in death of the femaleIncreased incidence of tumors by ionizing radiation induction:• following gamma irradiation tumor latency is decreased, frequency is increased, and most of the tumors are lymphomas of thymic originIncreased kidney cell proliferation:• diffuse global mesangial proliferation involving 40 - 100% of glomeruli is seen in older homozygotesIncreased urine protein level:• 150 +/- 50 mg/dl of protein is seen in the urine of homozygous females suggesting chronic nephropathyGlomerulonephritis:• some glomeruli contain inflammatory cells, nuclear debris, and mesangial cell interposition, mild dilation of the proximal tubules occurs, and mild to severe dense perivascular mononuclear cell infiltrates are seen suggesting autoimmune glomerulonphritisMesangial cell hyperplasia:• diffuse global mesangial proliferation involving 40 - 100% of glomeruli is seen in older homozygotesMesangial cell interposition:• in some glomeruliDilated proximal convoluted tubules:• mild dilation of the proximal tubulesDecreased sensitivity to skin irradiation:• in newborn and adult homozygous mice acute UVB-induced epidermal apoptosis, erythema, and induction of subcorneal pustules or epidermal erosion is reduced• after UVB irradiation homozygous primary keratinocytes show an attenuated G1 arrest and a more pronounced reduction in G2 arrest compared to wild-type cells; however UVB-induced G1 and G2 arrest in dermal fibroblasts is similar to wild-type|Normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|11-May-2016|Cryopreserved sperm|50.0|0.0|Yes|Systemic Lupus Erythematosus; SLE||Possibly| 8049.0|Slc6a19 fl|C57BL/6-Slc6a19/MarpAnu||Recessive|solute carrier family 6 (neurotransmitter transporter), member 19|Slc6a19|Normal|4632401C08Rik, B<0>AT1|MGI:1921588||||13|||||||||||||||||||||||||||||Normal||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|11-May-2016|Cryopreserved sperm|94.0|0.0|Unknown|||Yes| 8054.0||SRB1 KO||Recessive|scavenger receptor class B, member 1|Scarb1|Unknown|Cd36l1, Chohd1, Chohd1, Cla-1, D5Ertd460e, Hdlq1, Hlb398, Srb1, SRBI, SR-BI|MGI:893578||||5|||||||||||||||||||||||||||||Unknown|||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|03-Jun-2016||0.0|0.0|Unknown|||Yes| 8065.0|ENU32:085|ENU32:085||Recessive|||Unknown||||||Unknown|||||||||||||||||||||||||||||Abnormal population of B220+ CD4+ cells.||C57BL/6NCrlAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||5||No|05-Jul-2016|Cryopreserved sperm|44.0|0.0|Unknown||T cell, lymphocyte, B cell|Yes| 8058.0|Mid1 Fxy|B6(Cg).129-Mid1/AnuApb||X-linked|midline 1|Mid1|Nil|61B3-R, DXHXS1141, Fxy, Trim18|MGI:1100537|midline 1; targeted mutation 1, Alan Ashworth|Mid1|MGI:5562687|X|||||||||||||||||||||||||||||Viable. Reduced / delayed fertility. Litter size may be slightly reduced. No other phenotype described as yet.Abnormal axon morphology:• axon length and branch number are increased in cultured cortical neurons• callosal axons grow further into the contralateral hemisphere at P4• at P14, axon distribution in the corpus callosum is disturbed with a greater number of axon terminals, with a wider distribution in both the S1 and S2 regions• broader distribution of the contralateral axon projection pattern in the corpus callosumEmbryogenesis phenotype:• no obvious midline defects, unlike in Opitz Syndrome patients|Breeder pairs often only litter down after 3 months together, if they litter down at all. Around 1 in 3 produce litters.|C57BL/6NCrlAnu|Yes|Yes|Yes|Unknown|Unknown|Yes|No|Unknown||||No|22-Jun-2016|Cryopreserved sperm|55.0|0.0|Yes|Opitz GBBB syndrome|X-linked, craniofacial, cleft lip|Yes| 8056.0|Properdin KO|B6.1292-Cfp/CmstAdel||Recessive|complement factor properdin|Cfp|Nil|Pfc|MGI:97545|complement factor properdin; targeted mutation 1, Cordula M Stover|Cfp|MGI:3774548|X|||||||||||||||||||||||||||||Increased sensitivity to induced morbidity/mortality: • only 6 of 16 mice survived 7 days after cecal ligation and puncture compared to 14 of 16 wild-type mice as a result of septic peritonitis||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|>10|||No|07-Jun-2016||0.0|0.0|Unknown||Complement, Mast cell, infection, polymicrobial sepsis|Yes| 8064.0|ENU32:002|ENU32:002||Recessive|||Unknown||||||Unknown|||||||||||||||||||||||||||||decreased %CD4 T cells, increased %CD8 T cells and high CD44 MFI on CD4 and CD8 T cells in peripheral blood.||C57BL/6NCrlAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||5||No|05-Jul-2016|Cryopreserved sperm|55.0|0.0|Unknown||T cell, lymphocyte|Yes| 8063.0|ENU32:020:Ebf1|C57BL/6NCrlAnu-Ebf1/AnuApb||Dominant|early B cell factor 1|Ebf1|Unknown|O/E-1, Olf1, Olf-1|MGI:95275|Ebf1; mutation 2, Australian National University|Ebf1||11|ENSMUSG00000057098|ENSMUST00000081265|Ebf1-001||||||||44924576|10|||AAGGGACACCAGGCAGATTCATCTACACAGGTAAGCGTGCCTGCAGATGGGAACCACAGA||||||||||||||Homozygous lethal, unknown at what stage.|Abnormal and reduced numbers of B cells|C57BL/6NCrlAnu|No|No|Yes|No|No|Yes|No|Unknown||5||No|05-Jul-2016|Cryopreserved sperm|33.0|0.0|Unknown||B cell, lymphocyte|Yes| 8062.0|ENU32:083:Bcl11b|C57BL/6NCrlAnu-Bcl11b/AnuApb||Dominant|B cell leukemia/lymphoma 11B|Bcl11b|Unknown|9130430L19Rik, B630002E05Rik, COUP-TF interacting protein 2, CTIP2, Rit1|MGI:1929913|Bcl11b; mutation 1, Australian National University|Bcl11b||12|ENSMUSG00000048251|ENSMUST00000066060|Bcl11b-001|||T to C||||Unknown to Unknown|||||||||||||||||||Homozygous lethal, unknown at what stage.|increased %CD4 T cells, decreased %CD8 T cells and high CD44 MFI on CD4 and CD8 T cells in peripheral blood.|C57BL/6NCrlAnu|No|No|Yes|No|No|Yes|No|Unknown||5||No|05-Jul-2016|Cryopreserved sperm|44.0|0.0|Unknown||T cell, lymphocyte|Yes| 7715.0|BatInbred|C57BL/6J-Frem1/MarpApb||Dominant|Fras1 related extracellular matrix protein 1|Frem1|Unknown|crf11, eye, eyes2, heb, QBRICK|MGI:2670972|Fras1 related extracellular matrix protein 1; bat|Frem1|MGI:3526691|4|||||||||||||||||||||||||||||Cryptophthalmos, absent eyelids, abnormal eye development, syndactyly, abnormal craniofacial morphology.Abnormal conjunctiva morphology:• coloboma defects are associated with defects in formation of the conjunctivaAbnormal cornea morphology:• coloboma defects are associated with cornea fibrosisdecreased cornea thickness• coloboma defects are associated with absence of corneal epithelium leading to thinning of the cornea.Abnormal corneal epithelium morphology:• coloboma defects are associated with absence of corneal epitheliumAbnormal eye development:• defects in the adhesion of the surface ectoderm and corneal stroma.Coloboma:• several mutants exhibit eyelid coloboma similar to that seen in Manitoba-oculo-tricho-anal syndrome, affecting only one part of the eyelid• coloboma defects are associated with failure of eyelid formation, defects in formation of the conjunctiva, and absence of corneal epithelium leading to thinning of the cornea and fibrosis on the external face.Ocular hypertelorism:• greater intercanthal distanceAbsent eyelids:• have no true eyelids and the closed-eye appearance results from the presence of a pseudoblepharon that can be either unilateral or bilateral.Cryptophthalmos:• majority of mutants exhibit cryptophthalmos.Syndactyly:• seen occasionallyAbnormal kidney morphology:• exhibit renal abnormalitiesSingle kidney:• about 20% of adults show unilateral renal agenesis.Bleb:• epidermis separates from the dermis below the level of the lamina densa creating blebs/blisters during embryonic development• Background Sensitivity: blebbing phenotype is 100% penetrant on a C57BL/6J background but is only about 70% penetrant on a mixed C57BL/6J and C3H/NeJ background• from E13.5, develop blebs located predominantly around the eyes and the sides of the head.Abnormal craniofacial morphology:• upper midface is raised along the proximal aspect of the metopic suture and is wider at the level of the coronal suture• abnormalities include medial depression along the internasal suture and/or marked curvature of the nasal bones• slightly shorter philtrum-columella height.Abnormal cranial suture morphology:• most mutants exhibit abnormal maxillary-premaxillary suture morphology.Abnormal metopic suture morphology:• mutants exhibit advanced fusion of the posterior frontal suture compared to wild-type miceAsymmetric snout:• 7 of 16 mutants exhibit varying degrees of midfacial asymmetry and/or midface hypoplasia (J:177282)Short snout:• 7 of 16 mutants exhibit varying degrees of midfacial asymmetry and/or mid face hypoplasia.• reduction in snout length is inversely correlated with both cranial width and intercanthal distance.Abnormal cranial suture morphology:• most mutants exhibit abnormal maxillary-premaxillary suture morphology.Abnormal metopic suture morphology:• mutants exhibit advanced fusion of the posterior frontal suture compared to wild-type miceBroad nasal bone.Premature suture closure:• mutants exhibit anterofrontal cranial deformation similar to Metopic craniosynostosis and trigonocephaly:• mutants exhibit advanced fusion of the posterior frontal suture compared to wild-type mice, with fusion seen at postnatal day 28 compared to day 45 in controls.Rectal prolapse:• 4 of 138 mutants exhibit anal prolapse, showing protrusion of the rectal epithelia and an immune infiltrate in exposed tissue• the musculature of the anal sphincter is present in mutants with anal prolapse but is misplaced• however, anorectal musculature appears normal.Asymmetric snout:• 7 of 16 mutants exhibit varying degrees of midfacial asymmetry and/or midface hypoplasiaShort snout:• 7 of 16 mutants exhibit varying degrees of midfacial asymmetry and/or midface hypoplasia• reduction in snout length is inversely correlated with both cranial width and intercanthal distance.|Abnormal cranial suture morphology:• 42% of heterozygotes exhibit variable sutural abnormalities, including complete fusion, sutural asymmetry and advanced endocranial suture fusionAsymmetric snout:• 2 of 21 mutants exhibit varying degrees of midfacial asymmetry and/or midface hypoplasiaShort snout:• 2 of 21 mutants exhibit varying degrees of midfacial asymmetry and/or midface hypoplasiaPremature suture closure:• mutants exhibit anterofrontal cranial deformation similar to metopic craniosynostosis and trigonocephaly, although less severe than seen in homozygotes.|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|3|10||No|02-Jul-2014|Cryopreserved sperm|50.0|0.0|Yes|Fraser Syndrome- autosomal recessive congenital disorder characterising developmental defects|Fraser Syndrome|Possibly| 8059.0|BTBR|BTBR T<+> Itpr3/J||Recessive|disrupted in schizophrenia 1|Disc1|Nil|C1orf136; SCZD9|MGI:2447658|disrupted in schizophrenia 1; deletion|Disc1|MGI:3623217|8|||||||||||||||||||||||||||||Abnormal allogrooming behaviour:number of bouts of social grooming, in which one member of the pair grooms the other, is less in 21 day old miceAbnormal locomotor activation:locomotion and exploratory activity in a novel open field is initially higher, but mice show normal activity levels after habituation.Abnormal social investigation:mice show reduced social approach, low reciprocal social interactions and impaired juvenile play.Abnormal vocalisation:pups show an usual pattern of calls, emitting high levels of harmonics, two-syllable, and composite calls, but minimal numbers of chevron-shaped syllables, upward, downward, and short calls.Decreased anxiety-related response:percentage of time spent on the open segments of the elevated zero maze is higher, indicating very low anxiety-like traits.Excessive vocalization:pups call more loudly and more frequently when separated from their mothers and siblings.Impaired social transmission of food preference:mice eat less of the food familiarized by interacting with their demonstrator cage mate than of a completely unfamiliar foodmice sniff the whiskers and mouth of their demonstrator cage mate less frequently and for shorter periods of time.Increased grooming behaviour:both juvenile and adult mice exhibit high levels of repetitive self-grooming.Abnormal brain commissure morphology:Probst bundles are present on both sides of the midline in 100% of miceneocortices are not connected by the corpus callosum, through other forebrain commissures, nor via ectopic forebrain connections.no streamline connections between homologous interhemispheric areas via the anterior or hippocampal commissure are seen.Abnormal cerebral cortex morphology:changes in cortical thickness is not due to an increase in cell number of a specific cortical laminar population or due to increased apoptosisthickness of V1 cortical area is increased at P7 but not in adults.Abnormal neocortex morphology:V1 area of the neocortex is reducedlength of the cortex is reduced at P10, the width is reduced at P22the relative position of V1 and the posterior medial barrel subfield of the neocortex are shifted towards the midlinethe relative size of the posterior medial barrel subfield of the neocortex is reduced at P10 and the relative size of the visual area is reduced at P10 and P22the third barrel in row C (C3) of the posterior medial barrel subfield of the neocortex is located in a more medial relative position than in controlsAbsent corpus callosum:agenesis of the corpus callosumDecreased anterior commissure size:anterior commissure is reduced in size and volumeDecreased hippocampal commissure size:hippocampal commissure is greatly reduced in size and volume. Increased body weight:mice are heavier than C57BL/6 controls on P4, 6, 8, and 12Increased growth rate:mice show faster growth and development, having a fully developed righting reflex response by P2 compared to P6 in C57BL/6 controls, full negative geotaxis response acquired by P4 versus P8, earlier detachment of pinnae, opening of the eyes and incisor eruption, shorter latencies on the homing test suggesting more rapid development social olfactory and cognitive abilities, accelerated acquisition of various reflexes, and greater response to an acoustic stimulus on P12|Unknown|C57BL/6J|Yes|Yes|Unknown|Yes|Yes|Unknown|No|Excellent|||brother X sister|Yes|24-Jun-2016|Cryopreserved sperm|50.0|0.0|Yes|Austism Spectrum Disorders|BTBR, austism spectrum disorders|No| 8059.0|BTBR|BTBR T<+> Itpr3/J||Recessive|inositol 1,4,5-triphosphate receptor 3|Itpr3|Unknown|Ip3r3, Itpr-3, tf|MGI:96624|inositol 1,4,5-triphosphate receptor 3; tufted|Itpr3|MGI:1857070|17|||||||||||||||||||||||||||||Abnormal allogrooming behaviour:number of bouts of social grooming, in which one member of the pair grooms the other, is less in 21 day old miceAbnormal locomotor activation:locomotion and exploratory activity in a novel open field is initially higher, but mice show normal activity levels after habituation.Abnormal social investigation:mice show reduced social approach, low reciprocal social interactions and impaired juvenile play.Abnormal vocalisation:pups show an usual pattern of calls, emitting high levels of harmonics, two-syllable, and composite calls, but minimal numbers of chevron-shaped syllables, upward, downward, and short calls.Decreased anxiety-related response:percentage of time spent on the open segments of the elevated zero maze is higher, indicating very low anxiety-like traits.Excessive vocalization:pups call more loudly and more frequently when separated from their mothers and siblings.Impaired social transmission of food preference:mice eat less of the food familiarized by interacting with their demonstrator cage mate than of a completely unfamiliar foodmice sniff the whiskers and mouth of their demonstrator cage mate less frequently and for shorter periods of time.Increased grooming behaviour:both juvenile and adult mice exhibit high levels of repetitive self-grooming.Abnormal brain commissure morphology:Probst bundles are present on both sides of the midline in 100% of miceneocortices are not connected by the corpus callosum, through other forebrain commissures, nor via ectopic forebrain connections.no streamline connections between homologous interhemispheric areas via the anterior or hippocampal commissure are seen.Abnormal cerebral cortex morphology:changes in cortical thickness is not due to an increase in cell number of a specific cortical laminar population or due to increased apoptosisthickness of V1 cortical area is increased at P7 but not in adults.Abnormal neocortex morphology:V1 area of the neocortex is reducedlength of the cortex is reduced at P10, the width is reduced at P22the relative position of V1 and the posterior medial barrel subfield of the neocortex are shifted towards the midlinethe relative size of the posterior medial barrel subfield of the neocortex is reduced at P10 and the relative size of the visual area is reduced at P10 and P22the third barrel in row C (C3) of the posterior medial barrel subfield of the neocortex is located in a more medial relative position than in controlsAbsent corpus callosum:agenesis of the corpus callosumDecreased anterior commissure size:anterior commissure is reduced in size and volumeDecreased hippocampal commissure size:hippocampal commissure is greatly reduced in size and volume. Increased body weight:mice are heavier than C57BL/6 controls on P4, 6, 8, and 12Increased growth rate:mice show faster growth and development, having a fully developed righting reflex response by P2 compared to P6 in C57BL/6 controls, full negative geotaxis response acquired by P4 versus P8, earlier detachment of pinnae, opening of the eyes and incisor eruption, shorter latencies on the homing test suggesting more rapid development social olfactory and cognitive abilities, accelerated acquisition of various reflexes, and greater response to an acoustic stimulus on P12|Unknown|C57BL/6J|Yes|Yes|Unknown|Yes|Yes|Unknown|No|Excellent|||brother X sister|Yes|24-Jun-2016|Cryopreserved sperm|||Yes|Austism Spectrum Disorders|BTBR, austism spectrum disorders|No| 8059.0|BTBR|BTBR T<+> Itpr3/J||Recessive|brachyury|T|Normal|Bra, T1|MGI:98472||||17|||||||||||||||||||||||||||||Abnormal allogrooming behaviour:number of bouts of social grooming, in which one member of the pair grooms the other, is less in 21 day old miceAbnormal locomotor activation:locomotion and exploratory activity in a novel open field is initially higher, but mice show normal activity levels after habituation.Abnormal social investigation:mice show reduced social approach, low reciprocal social interactions and impaired juvenile play.Abnormal vocalisation:pups show an usual pattern of calls, emitting high levels of harmonics, two-syllable, and composite calls, but minimal numbers of chevron-shaped syllables, upward, downward, and short calls.Decreased anxiety-related response:percentage of time spent on the open segments of the elevated zero maze is higher, indicating very low anxiety-like traits.Excessive vocalization:pups call more loudly and more frequently when separated from their mothers and siblings.Impaired social transmission of food preference:mice eat less of the food familiarized by interacting with their demonstrator cage mate than of a completely unfamiliar foodmice sniff the whiskers and mouth of their demonstrator cage mate less frequently and for shorter periods of time.Increased grooming behaviour:both juvenile and adult mice exhibit high levels of repetitive self-grooming.Abnormal brain commissure morphology:Probst bundles are present on both sides of the midline in 100% of miceneocortices are not connected by the corpus callosum, through other forebrain commissures, nor via ectopic forebrain connections.no streamline connections between homologous interhemispheric areas via the anterior or hippocampal commissure are seen.Abnormal cerebral cortex morphology:changes in cortical thickness is not due to an increase in cell number of a specific cortical laminar population or due to increased apoptosisthickness of V1 cortical area is increased at P7 but not in adults.Abnormal neocortex morphology:V1 area of the neocortex is reducedlength of the cortex is reduced at P10, the width is reduced at P22the relative position of V1 and the posterior medial barrel subfield of the neocortex are shifted towards the midlinethe relative size of the posterior medial barrel subfield of the neocortex is reduced at P10 and the relative size of the visual area is reduced at P10 and P22the third barrel in row C (C3) of the posterior medial barrel subfield of the neocortex is located in a more medial relative position than in controlsAbsent corpus callosum:agenesis of the corpus callosumDecreased anterior commissure size:anterior commissure is reduced in size and volumeDecreased hippocampal commissure size:hippocampal commissure is greatly reduced in size and volume. Increased body weight:mice are heavier than C57BL/6 controls on P4, 6, 8, and 12Increased growth rate:mice show faster growth and development, having a fully developed righting reflex response by P2 compared to P6 in C57BL/6 controls, full negative geotaxis response acquired by P4 versus P8, earlier detachment of pinnae, opening of the eyes and incisor eruption, shorter latencies on the homing test suggesting more rapid development social olfactory and cognitive abilities, accelerated acquisition of various reflexes, and greater response to an acoustic stimulus on P12|Unknown|C57BL/6J|Yes|Yes|Unknown|Yes|Yes|Unknown|No|Excellent|||brother X sister|Yes|24-Jun-2016|Cryopreserved sperm|||Yes|Austism Spectrum Disorders|BTBR, austism spectrum disorders|No| 8066.0|ENU36:034:Itpkb|C7BL/6NCrlAnu-Itpkb/AnuApb||Recessive|inositol 1,4,5-trisphosphate 3-kinase B|Itpkb|Unknown|1110033J02Rik, E130307H12Rik|MGI:109235|Itpkb; mutation 1, Australian National University|Itpkb||1||||||||||Unknown to Unknown|||||||||||||||||||Mice lack T cells and have abnormal B cells in blood.||C57BL/6NCrlAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||3||No|05-Jul-2016|Cryopreserved sperm|33.0|0.0|Unknown||T cell, B cell, lymphocyte|Yes| 8067.0|Slc6a19 KO|C57BL/6-Slc6a19/AnuApb||Recessive|solute carrier family 6 (neurotransmitter transporter), member 19|Slc6a19|Nil|4632401C08Rik, B<0>AT1|MGI:1921588|Slc6a19: targeted mutation 2, Australian National University|Slc6a19||13||||||||||Unknown to Unknown|||||||||||||||||||Unknown||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|05-Jul-2016|Cryopreserved sperm|21.0|0.0|Unknown|||Yes| 8068.0|Cx3cr1-cre|B6.129P2(Cg)-Cx3cr1/WganJAnuApb||Dominant|chemokine (C-X3-C motif) receptor 1|Cx3cr1|Unknown||MGI:1333815|chemokine (C-X3-C motif) receptor 1; targeted mutation 2.1, Dan R Littman|Cx3cr1|MGI:5450813|9||||||||||Unknown to Unknown|||||||||||||||||||Normal|Normal|C57BL/6J|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|05-Jul-2016|Cryopreserved sperm|60.0|0.0|Unknown||Cre recombinase|No| 8070.0|Pdgfra-cre|C57BL/6-Tg(Pdgfra-cre)1Clc/JAnuApb||Dominant||||||||||||||||||||||||||transgene insertion 1, Constance L Cepko|mouse platelet derived growth factor receptor alpha|||||||||||Normal|Normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|05-Jul-2016|Cryopreserved sperm|49.0|0.0|Unknown||Cre recombinase|No| 8069.0|Ai14D|B6.Cg-Gt(ROSA)26Sor/JAnuApb||Dominant|gene trap ROSA 26, Philippe Soriano|Gt(ROSA)26Sor|Normal|beta geo, Gtrgeo26, Gtrosa26, R26, ROSA26, Thumpd3as1|MGI:104735|gene trap ROSA 26, Philippe Soriano; targeted mutation 14, Hongkui Zeng|Gt(ROSA)26Sor|MGI:3809524|6||||||||||||||||||||||||||||||No abnormal phenotype detected:• mice are viable and fertile; used for cre reporter expression analysis|C57BL/6J|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|05-Jul-2016|Cryopreserved sperm|83.0|0.0|Unknown||Cre recombinase|No| 8072.0|Mir124a-3 fl|STOCK Mir124a-3/Mmjax||Recessive|microRNA 124a-3|Mir124a-3|Normal|mir-124a-3, Mirn124a-3, mmu-mir-124-3, mmu-mir-124a-3|MGI:3618704|microRNA 124a-3; targeted mutation 1, Michael McManus|Mir124a-3|MGI:5314768|2||||||||||||||||||||||||||||||Normal|C57L/6J|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|06-Jul-2016|Cryopreserved sperm|55.0|0.0|Unknown||micro RNA|No| 8071.0|Ggt1-cre|STOCK Tg(Ggt1-cre)M3Egn/JAnuApb||Dominant||||||||||||||||||||||||||transgene insertion M3, Eric G Neilson|rat proximal||||||||||||Cre expression was limited to cortical tubular epithelium of the kidney, and was first detected around 7 days of age.||Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|06-Jul-2016|Cryopreserved sperm|60.0|0.0|Unknown||Cre recombinase|No| 8076.0|TZF KO|B6(Cg)-Zfp318/RbrcAnuApb||Recessive|zinc finger protein 318|Zfp318|Nil|2610034E08Rik, D530032D06Rik, TZF|MGI:1889348|zinc finger protein 318; targeted mutation 1, Hiromi Hagiwara|Zfp318|MGI:5578603|17|||||||||||||||||||||||||||||Hematopoietic system phenotype:N • normal level of circulating B cells and matured to the CD93-negative stageDecreased IgD level:• expression abolished in immature and mature B cellsIncreased IgM level:• threefold increase in mature B cells||C57BL/6NCrlAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|8||B6NCrl x Het|No|17-Jul-2016|Cryopreserved sperm|30.0|0.0|Unknown||B cell|Yes| 8080.0||ENU17:017||Recessive|dvs||||||||Unknown|||||||||||||||||||||||||||||Unknwon||C57BL/6JAnu|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|25-Jul-2016|Cryopreserved sperm|30.0|0.0|Unknown||ENU|Yes| 8078.0|SJL Jax|B6(Cg).SJL-Ptprc/JAnuApb||Recessive||||||||||||||||||||||||||||||||||||||T cells express the Ptprc allele instead of Ptprc allele usually carried by Lymphocytes isolated from C57BL/6 mice.||C57BL/6JAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|8|1|a x a|No|25-Jul-2016|Cryopreserved sperm|55.0|0.0|Unknown||Ly5a|Yes| 8074.0|Adar1 -/- Ifih1-/-|B6.129-Adar1 Ifih1/Apb||Recessive|adenosine deaminase, RNA-specific|Adar|Nil|ADAR1, Adar1p110, Adar1p150, mZaADAR|MGI:1889575|adenosine deaminase, RNA-specific; targeted mutation 1, Peter H Seeburg|Adar|MGI:3029789|3|||||||||||||||||||||||||||||Double homozygous are lethal at or near birth|Adar1+/- Ifih1-/- are viable and normal (likely susceptible to viral infection due to Ifih1-/-)Ifih1+/- = normalAdar1+/- = normal|C57BL6|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|14-Jul-2016|Cryopreserved sperm|30.0|0.0|Unknown||RNA editing, double stranded|Yes| 8074.0|Adar1 -/- Ifih1-/-|B6.129-Adar1 Ifih1/Apb||Recessive|interferon induced with helicase C domain 1|Ifih1|Nil|9130009C22Rik, Helicard, MDA5, MDA-5|MGI:1918836|interferon induced with helicase C domain 1; targeted mutation 1.1, Marco Colonna|Ifih1|MGI:3663677|2|||||||||||||||||||||||||||||Double homozygous are lethal at or near birth|Adar1+/- Ifih1-/- are viable and normal (likely susceptible to viral infection due to Ifih1-/-)Ifih1+/- = normalAdar1+/- = normal|C57BL6|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|14-Jul-2016|Cryopreserved sperm|||Unknown||RNA editing, double stranded|Yes| 8075.0|Adar1E861A/E861A Ifih1-/-|B6.129-Adar1 Ifih1/Apb||Recessive|adenosine deaminase, RNA-specific|Adar||ADAR1, Adar1p110, Adar1p150, mZaADAR|MGI:1889575|Adar1E861A/E861A Ifih1-/-|||3|||||||||||||||||||||||||||||Adar1E861A/E861A Ifih1-/- and viable, fertile, and largely normal. They are smaller at birth and weaning but recover by 12 weeks.|Heterozygous animals are normal and fertile for both alleles individually and as compound mutants.|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|14-Jul-2016|Cryopreserved sperm|50.0|0.0|Unknown||RNA editing, erythropoiesis|Yes| 8075.0|Adar1E861A/E861A Ifih1-/-|B6.129-Adar1 Ifih1/Apb||Recessive|interferon induced with helicase C domain 1|Ifih1|Nil|9130009C22Rik, Helicard, MDA5, MDA-5|MGI:1918836|interferon induced with helicase C domain 1; targeted mutation 1.1, Marco Colonna|Ifih1|MGI:3663677|2|||||||||||||||||||||||||||||Adar1E861A/E861A Ifih1-/- and viable, fertile, and largely normal. They are smaller at birth and weaning but recover by 12 weeks.|Heterozygous animals are normal and fertile for both alleles individually and as compound mutants.|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|14-Jul-2016|Cryopreserved sperm|||Unknown||RNA editing, erythropoiesis|Yes| 8079.0|SJL NCrl|B6(Cg).SJL-Ptprc/NCrlAnuApb||Recessive|||||||||||||||||||||||||||||protein tyrosine phosphatase, receptor type, C|Ptprc||B220, CD45, Ly-5, Lyt-4, T200|MGI:97810|protein tyrosine phosphatase, receptor type, C; a variant|Ptprc|MGI:4819849|1|T cells express the Ptprc allele instead of Ptprc allele usually carried by Lymphocytes isolated from C57BL/6 mice.||C57BL/6NCrlAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|9|2|a x a|No|25-Jul-2016|Cryopreserved sperm|87.0|0.0|Unknown||Ly5a|Yes| 10427.0|Cst-II|C57BL/6N-Tg(TcrCst-II)5Anu||Dominant|protein tyrosine phosphatase receptor type C|Ptprc a variant ; b variant||CD45, Ly-5|MGI:97810||||1|ENSMUSG00000026395||||||||||||||||transgene insertion, Circumsporozoite protein specific TCR, MHC classII restricted|||||||||||| MHC classII pressenting cells have a circumsporozoite protein specific TCR||ASD1142:Tcr:Alpha:Beta|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Good||||No|28-May-2024|Cryopreserved sperm|54.0|0.0|Unknown|||Possibly| 8081.0|Dicer1flox/flox x EsrCRE|B6.129-Dicer Gt(ROSA)26Sor/MarpApb||Recessive|dicer 1, ribonuclease type III|Dicer1|Normal|1110006F08Rik, D12Ertd7e, Dicer1, mKIAA0928|MGI:2177178|dicer 1, ribonuclease type III; targeted mutation 1, Brian D Harfe|Dicer1|MGI:3589208|12|||||||||||||||||CreERT |Rosa26|||||||||||Normal|Normal|C57BL/6×129 |Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|01-Aug-2016|Cryopreserved sperm|50.0|45.0|Unknown|||Yes| 8081.0|Dicer1flox/flox x EsrCRE|B6.129-Dicer Gt(ROSA)26Sor/MarpApb||Recessive|gene trap ROSA 26, Philippe Soriano|Gt(ROSA)26Sor||beta geo, Gtrgeo26, Gtrosa26, R26, ROSA26, Thumpd3as1|MGI:104735|gene trap ROSA 26, Philippe Soriano; targeted mutation 1, Jeremy Nathans|Gt(ROSA)26Sor|MGI:2669525|6|||||||||||||||||||||||||||||Normal|Normal|C57BL/6×129 |Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|01-Aug-2016|Cryopreserved sperm|||Unknown|||Yes| 8093.0|ENU35:029:ppp3cb|C57BL/6NCrlAnu-Ppp3cb/AnuApb||Recessive|protein phosphatase 3, catalytic subunit, beta isoform|Ppp3cb|Unknown|1110063J16Rik, Calnb, Cnab, CnAbeta, PP2BA beta|MGI:107163|Ppp3cb; mutation 1, Australian National University|Ppp3cb||14|ENSMUSG00000021816|ENSMUST00000159027.7|Ppp3cb-001||||||||20520552|6|||ATGGTCTTTACCATTTGTTGGAGAAAAAGGTGCGATTTTTGTTTTTTTGGGGGGGTATTT||||||||||||||Reduced numbers of peripheral blood T cells.T cells are activated.||C57BL/6NCrlAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||4||No|01-Sep-2016|Cryopreserved sperm|55.0|0.0|Unknown||ENU, T cell|Yes| 8082.0|ASD661:Pique:7|C57BL/6NCrlAnu-Zfr2/AnuApb||Recessive|zinc finger RNA binding protein 2|Zfr2|Unknown|2010013I23Rik, 9130206N08Rik|MGI:2143792||||10|||||||||||||||||||||||||||||Unknown at this stage||C57BL/6NCrlAnu|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|Yes|Poor||||No|11-Aug-2016|Cryopreserved sperm|11.0|0.0|Unknown||CRISPR|Possibly| 8084.0|RHBDF1_PKD_1|C57BL/6-Rhbdf1/MarpApb||Recessive|rhomboid 5 homolog 1|Rhbdf1|Unknown|Dist, Dist1, Egfr-rs|MGI:104328||||11|ENSMUSG00000020282|ENSMUST00000020524.14|Rhbdf1-006|584|740|C to T|ENSMUSE00001312827|5|195|Serine to Phenylalanine|||||TGCAGCCTCCCTCTGCTCTTTCTCCAGCTCCCGCTCAGGTTTCAACCGACTCCCTCGGCGT||||||||||||||Unknown|Unknown|C57BL/6|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|24-Aug-2016|Cryopreserved sperm|50.0|0.0|Unknown|||Yes| 8095.0|CD11c-DTR|B6.Cg-Tg(Itgax-DTR/EGFP)57Lan/MelbApb||Semi-dominant||||||||||||||||||||||||||transgene insertion 57, Richard A Lang|mouse Itgax promoter (CD11c)||||||||||||CD11c positive dendritic cells will be deleted upon treatment of mice with diphtheria toxin.|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|06-Sep-2016|Cryopreserved sperm|20.0|0.0|Unknown||Cytotoxic T lymphocytes (CTL) , Dentritic cells|Yes| 8088.0|RHBDF1 KO|C57BL/6-Rhbdf1/MarpApb||Recessive|rhomboid 5 homolog 1|Rhbdf1|Unknown|Dist, Dist1, Egfr-rs|MGI:104328||||11|||||||||||||||||||||||||||||Unknown|Unknown|C57BL/6|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|24-Aug-2016||0.0|0.0|Unknown|||Yes| 8821.0|Npffr2 flox|B6.Cg-Npffr2/Apb||Recessive|neuropeptide FF receptor 2|Npffr2||Gpr74, NPFF2|1860130|neuropeptide FF receptor 2; targeted mutation 1, H Herzog|Npffr2|MGI:6313710|5|||||||||||||||||||||||||||||Normal||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|29-Oct-2019|Cryopreserved sperm|4.0|0.0|Unknown||Adipose, thernogenesis|Yes| 8090.0|LAT3_SRNS_1|C57BL/6-Slc43a1/MarpApb||Recessive|solute carrier family 43, member 1|Slc43a1|Unknown|2610016F07Rik, Lat3, PB39, Pov1|MGI:1931352||||2|ENSMUSG00000027075|ENSMUST00000121114.7|Slc43a1-001|597|1442|G to C|ENSMUSE00001223444|7|199|Methionine to Isoleucine|||||GATGCCGGAGTCCCCTTCACTGTCATCATGTTCACATGGTCTGGCCTGGCCTGTCTCATCT||||||||||||||Unknown|Unknown|C57BL/6|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|25-Aug-2016|Cryopreserved sperm|40.0|0.0|Unknown|||Yes| 8091.0|ENU36:080|C57BL/6NCrlAnu-Car2/AnuApb||Recessive|carbonic anhydrase 2|Car2|Unknown|CAII, CA II, Car-2, Ltw-5, Lvtw-5|MGI:88269||||3|ENSMUSG00000027562|ENSMUST00000029078.8|Car2-001|143|465|T to A| ENSMUSE00000371047 |2|47|Leucine to Glutamine|||||||||||||||||||RBC resistant to lysis||C57BL/6NCrlAnu|Unknown|Yes|Yes|Unknown|Yes|Yes|No|Unknown||3||No|29-Aug-2016|Cryopreserved sperm|22.0|0.0|Unknown||ENU|Yes| 8094.0|ENU28:008:Slc1a5|C57BL/6NCrlAnu-Slc1a5/AnuApb||Recessive|solute carrier family 1 (neutral amino acid transporter), member 5|Slc1a5|Unknown|ASCT2|MGI:105305|solute carrier family 1 (neutral amino acid transporter), member 5; mutation 1, Australian National University|Slc1a5|MGI:6446934|7||||||||||Unknown to Unknown|||||||||||||||||||||C57BL/6NCrlAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||10||No|05-Sep-2016|Cryopreserved sperm|31.0|0.0|Unknown||ENU|Yes| 8096.0|Cliff79B-A3|C57BL/6NCrlAnu-Cd79b/AnuApb||Recessive|CD79B antigen|Cd79b|Unknown|B29, Igb, Igbeta, Ig-beta|MGI:96431||||11|||||||||||||||||||||||||||||||C57BL/6NCrlAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|07-Sep-2016|Cryopreserved sperm|44.0|0.0|Unknown|||Yes| 8097.0|Cliff79B-A4|C57BL/6NCrlAnu-Cd79b/AnuApb||Recessive|CD79B antigen|Cd79b|Unknown|B29, Igb, Igbeta, Ig-beta|MGI:96431||||11|||||||||||||||||||||||||||||||C57BL/6NCrlAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|07-Sep-2016|Cryopreserved sperm|22.0|0.0|Unknown|||Yes| 8098.0|Cliff79B-A5|C57BL/6NCrlAnu-Cd79b/AnuApb||Recessive|CD79B antigen|Cd79b|Unknown|B29, Igb, Igbeta, Ig-beta|MGI:96431||||11|||||||||||||||||||||||||||||||C57BL/6NCrlAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|07-Sep-2016|Cryopreserved sperm|11.0|0.0|Unknown|||Yes| 8099.0|ENU34:047:Olfr603|C57BL/6NCrlAnu-Olfr603/AnuApb||Recessive|olfactory receptor 603|Olfr603|Unknown|GA_x6K02T2PBJ9-6092550-6092362, GA_x6K02T2PBJ9-6096387-6095449, MOR32-14_i, MOR32-2, Olfr604|MGI:3030437||||7|ENSMUSG00000059874|ENSMUST00000071844.1|Olfr603-001|386|386|C to T|ENSMUSE00001043266|1|129|Cysteine to Tyrosine|||||CATGGCAATTGACCGTTTTGTTGCCATCTGTTACCCACTTAGGTATACCTCTGTTCTCACC||||||||||||||Unknown||C57BL/6NCrlAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|08-Sep-2016|Cryopreserved sperm|44.0|0.0|Unknown|||Yes| 8115.0||Swiss||Dominant||||||||||||||||||||||||||||||||||||||Background, outbred strain|||Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|26-Oct-2016|Cryopreserved sperm|22.0|44.0|Unknown|||No| 7749.0|DBC1 / DBC2 / DBC3 knockout|C57BL/6-Brinp1 Brinp2 Brinp3/MarpApb||Recessive|bone morphogenic protein/retinoic acid inducible neural specific 1|Brinp1|Nil|Dbc1, Dbccr1, Fam5a|MGI:1928478||||4|||||||||||||||||||||||||||||Reduced body size|Unknown|C57BL/6|Yes|Yes|Yes|Yes|Unknown|Yes|No|Poor|14||From hetrozygous breeding|No|02-Oct-2014||0.0|0.0|Unknown|||Yes| 7749.0|DBC1 / DBC2 / DBC3 knockout|C57BL/6-Brinp1 Brinp2 Brinp3/MarpApb||Recessive|bone morphogenic protein/retinoic acid inducible neural-specific 2|Brinp2||6430517E21Rik, Fam5b, mKIAA1747|MGI:2443333||||1|||||||||||||||||||||||||||||Reduced body size|Unknown|C57BL/6|Yes|Yes|Yes|Yes|Unknown|Yes|No|Poor|14||From hetrozygous breeding|No|02-Oct-2014||||Unknown|||Yes| 7749.0|DBC1 / DBC2 / DBC3 knockout|C57BL/6-Brinp1 Brinp2 Brinp3/MarpApb||Recessive|bone morphogenetic protein/retinoic acid inducible neural specific 3|Brinp3|||MGI:2443035||||1|||||||||||||||||||||||||||||Reduced body size|Unknown|C57BL/6|Yes|Yes|Yes|Yes|Unknown|Yes|No|Poor|14||From hetrozygous breeding|No|02-Oct-2014||||Unknown|||Yes| 1961.0|available from Animal Resources Centre - www.arc.wa.gov.au|C57BL/10ScSnArc||Dominant|Inbred black: a, H-2||Unknown||||||Unknown||||||||||||||||No|||||||||||||Good breeding performance 0.85 young/female/month, average litter 6. Active, long lived mouse (males 2 years, females 22 months). Very low mammary tumour incidence. Behaviour traits differ from C57BL/10J. High incidence of spontaneous deviants (possible mutants). Primarily a genetic "tool" strain. The most commonly used strain for development of congenic resistant lines differing from the parenteral strain by single histocompatibility loci. High degree of genetic distinctiveness.|||Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|04-Sep-2007||0.0|0.0|No|||Yes| 8104.0|Cliff79B-A2|C57BL/6NCrlAnu-Cd79b/AnuApb||Recessive|CD79B antigen|Cd79b|Unknown|B29, Igb, Igbeta, Ig-beta|MGI:96431|Cd79b; endonuclease mutation 5, Australian National University|Cd79b||11||||||||||Unknown to Unknown|||||||||||||||||||||C57BL/6NCrlAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|21-Sep-2016|Cryopreserved sperm|11.0|0.0|Unknown|||Yes| 8105.0|Cliff79B-A1|C57BL/6NCrlAnu-Cd79b/AnuApb||Recessive|CD79B antigen|Cd79b|Unknown|B29, Igb, Igbeta, Ig-beta|MGI:96431||||11|||||||||||||||||||||||||||||||C57BL/6NCrlAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|21-Sep-2016|Cryopreserved sperm|20.0|0.0|Unknown|||Yes| 8106.0|T1germTg|Germline SIRT1 transgenics||Dominant||||||||||||||||||||||||||||||||||||||Improved glucose tolerance,resistance to ageing, expected prolonged lifespan.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|21-Sep-2016|Cryopreserved sperm|50.0|0.0|Unknown||Glucose, body weight|Possibly| 8101.0|ASD543:Weidenfeller|C57BL/6NCrlAnu-Vps51/AnuApb||Recessive|VPS51 GARP complex subunit|Vps51|Unknown|1110014N23Rik, 3110057M17Rik|MGI:1915755||||19|||||||||||||||||||||||||||||Embryonic lethal||C57BL/6NCrlAnu|No|No|Yes|No|No|Yes|No|Unknown||||No|09-Sep-2016|Cryopreserved sperm|22.0|0.0|Unknown|||Yes| 8114.0||ASD565:Hummels:F1#12:Mertk:Timd4||Recessive|c-mer proto-oncogene tyrosine kinase|Mertk|Unknown|Eyk, Mer, nmf12, Nyk, Tyro 12|MGI:96965||||2|||||||||||||||||||||||||||||Unknown|Normal|C57BL/6NCrlAnu|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|21-Oct-2016|Cryopreserved sperm|24.0|0.0|Unknown|||No| 8114.0||ASD565:Hummels:F1#12:Mertk:Timd4||Recessive|T cell immunoglobulin and mucin domain containing 4|Timd4||B430010N18Rik, Tim4, TIM-4|MGI:2445125||||11|||||||||||||||||||||||||||||Unknown|Normal|C57BL/6NCrlAnu|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|21-Oct-2016|Cryopreserved sperm|||Unknown|||No| 8112.0|Ets1Flp|C57BL/6-Ets1/Pjh||Recessive|E26 avian leukemia oncogene 1, 5' domain|Ets1|Normal|Ets-1, MGC:18571, p42Ets-1, p51Ets-1, Tpl1, vs|MGI:95455|E26 avian leukemia oncogene 1, 5' domain #198Flp#20|Ets1||9||||||||||Unknown to Unknown|||||||||||||||||||Normal|Normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|10-Oct-2016|Cryopreserved sperm|50.0|0.0|Unknown||Transcription factor|Possibly| 8113.0|B6S|C57BL/6JSfdAnu||Dominant|||||||||||||||||||||||||||||||||||||||||Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|12-Oct-2016|Cryopreserved sperm, Embryo|180.0|656.0|Unknown|||No| 8119.0||ASD565:Hummels:F1#12:Timd4||Recessive|T cell immunoglobulin and mucin domain containing 4|Timd4||B430010N18Rik, Tim4, TIM-4|MGI:2445125||||11|||||||||||||||||||||||||||||Unknown|Normal|C57BL/6NCrlAnu|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|26-Oct-2016|Cryopreserved sperm|12.0|0.0|Unknown|||No| 8118.0||ASD565:Hummels:F1#12:Mertk:Timd4 #2||Recessive|c-mer proto-oncogene tyrosine kinase|Mertk|Unknown|Eyk, Mer, nmf12, Nyk, Tyro 12|MGI:96965||||2|||||||||||||||||||||||||||||Unknown|Normal|C57BL/6NCrlAnu|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|26-Oct-2016|Cryopreserved sperm|12.0|0.0|Unknown|||No| 8118.0||ASD565:Hummels:F1#12:Mertk:Timd4 #2||Recessive|T cell immunoglobulin and mucin domain containing 4|Timd4||B430010N18Rik, Tim4, TIM-4|MGI:2445125||||11|||||||||||||||||||||||||||||Unknown|Normal|C57BL/6NCrlAnu|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|26-Oct-2016|Cryopreserved sperm|||Unknown|||No| 8120.0||ASD565:Hummels:F1#12:Timd4 #2||Recessive|T cell immunoglobulin and mucin domain containing 4|Timd4||B430010N18Rik, Tim4, TIM-4|MGI:2445125||||11|||||||||||||||||||||||||||||Unknown|Normal|C57BL/6NCrlAnu|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|26-Oct-2016|Cryopreserved sperm|12.0|0.0|Unknown|||No| 7800.0|Krt76 tm1d|B6(Cg)-Krt76/MarpApb||Recessive|keratin 76|Krt76|Nil|2310001L23Rik|MGI:1924305||||15|||||||||||||||||||||||||||||Unkempt, dull coats and smaller body size, scaling of skin of the tail, abnormal paw pad hyperpigmentation |Abnormal sebaceous gland morphology, abnormal hair cycle, abnormal epidermis stratum basale morphology, hyperkerotosis, parakerotosis|C57BL/6J|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|2|4||No|26-Nov-2014|Cryopreserved sperm|50.0|0.0|No||Keratin 76, tight junctions, CLDN1, inflammation, skin|Possibly| 8107.0|Vps51 tm1a|C57BL/6N-Vps51/WtsiHAnu||Recessive|VPS51 GARP complex subunit|Vps51|Normal|1110014N23Rik, 3110057M17Rik|MGI:1915755|VPS51 GARP complex subunit; targeted mutation 1a, Wellcome Trust Sanger Institute|Vps51|MGI:4458528|19|||||||||||||||||||||||||||||Normal||C57BL/6NCrlAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|28-Sep-2016|Cryopreserved sperm|42.0|0.0|Unknown|||Yes| 8108.0|gp130Y757F x Nlrp3 KO|B6.129- Il6st Nlrp3/MarpApb||Recessive|interleukin 6 signal transducer|Il6st|Unknown|CD130, D13Ertd699e, gp130|MGI:96560|interleukin 6 signal transducer; targeted mutation 1, Matthias Ernst|Il6st|MGI:2388478|13||||||||||||||||Yes|||||||||||||Mice develop gastric tumours and emphysema||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|10||heterozogous x homozygous|No|06-Oct-2016|Cryopreserved sperm|50.0|0.0|Yes||gp130|Yes| 8108.0|gp130Y757F x Nlrp3 KO|B6.129- Il6st Nlrp3/MarpApb||Recessive|NLR family, pyrin domain containing 3|Nlrp3|Nil|Cias1, cryopyrin, Mmig1, NALP3, Pypaf1|MGI:2653833|NLR family, pyrin domain containing 3; targeted mutation 1, Richard A Flavell|Nlrp3|MGI:3686871|11||||||||||||||||No|||||||||||||Mice develop gastric tumours and emphysema||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|10||heterozogous x homozygous|No|06-Oct-2016|Cryopreserved sperm|||Yes||gp130|Yes| 8122.0|ENU31:065|C57BL/6NCrlAnu-Eif2ak4/AnuApb||Recessive|eukaryotic translation initiation factor 2 alpha kinase 4|Eif2ak4|Unknown|GCN2|MGI:1353427|Eif2ak4: mutation 1, Australian National University|Eif2ak4||2|||||||||||||||||||||||||||||Unknown||C57BL/6NCrlAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|27-Oct-2016|Cryopreserved sperm|48.0|0.0|Unknown|||Yes| 8124.0|Er81 fl:Lhx6-Cre|B6.129-Etv1 Tg(Lhx6-icre)1Kess/Anu||Recessive|ets variant 1|Etv1|Unknown|ER81, Etsrp81|MGI:99254|ets variant 1; targeted mutation 1, William D Snider|Etv1|MGI:2663693|12|||||||||||||||||transgene insertion 1, Nicoletta Kessaris|LIM homeobox protein 6||||||||||||||Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|28-Oct-2016||0.0|0.0|Unknown|||Yes| 8126.0|Er81 fl:RCE:LoxP|B6.129-Etv1 Gt(ROSA)26Sor/Anu||Recessive|ets variant 1|Etv1|Unknown|ER81, Etsrp81|MGI:99254|ets variant 1; targeted mutation 1, William D Snider|Etv1|MGI:2663693|12|||||||||||||||||||||||||||||Unknown||C57BL/6J|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|28-Oct-2016||0.0|0.0|Unknown|||Yes| 8126.0|Er81 fl:RCE:LoxP|B6.129-Etv1 Gt(ROSA)26Sor/Anu||Recessive|gene trap ROSA 26, Philippe Soriano|Gt(ROSA)26Sor||beta geo, Gtrgeo26, Gtrosa26, R26, ROSA26, Thumpd3as1|MGI:104735|gene trap ROSA 26, Philippe Soriano; targeted mutation 1.1, Gordon Fishell|Gt(ROSA)26Sor|MGI:4412373|6|||||||||||||||||||||||||||||Unknown||C57BL/6J|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|28-Oct-2016||||Unknown|||Yes| 8127.0|Nkx2.1-CreER|B6.129-Nkx2-1/JAnu||Dominant|NK2 homeobox 1|Nkx2-1||T/EBP, thyroid-specific enhancer-binding protein, thyroid transcription factor-1, tinman, Titf1, Ttf-1|MGI:108067|NK2 homeobox 1; targeted mutation 1.1, Z Josh Huang|Nkx2-1|MGI:5302534|12|||||||||||||||||||||||||||||Unknown||C57BL/6J|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|28-Oct-2016||0.0|0.0|Unknown||Cre recombinase|Yes| 8117.0||ASD565:Hummels:F1#12: MerTK||Recessive|c-mer proto-oncogene tyrosine kinase|Mertk|Unknown|Eyk, Mer, nmf12, Nyk, Tyro 12|MGI:96965||||2|||||||||||||||||||||||||||||Unknown|Normal|C57BL/6NCrlAnu|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|26-Oct-2016|Cryopreserved sperm|12.0|0.0|Unknown|||Yes| 8123.0|PV-cre:RCE:LoxP|B6.129P2-Gt(ROSA)26Sor Pvalb/Anu||Recessive|parvalbumin|Pvalb||Parv, PV, Pva|MGI:97821|parvalbumin; targeted mutation 1, Silvia Arber|Pvalb|MGI:3590684|15|||||||||||||||||||||||||||||Unknown||C57BL/6J|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|28-Oct-2016|Cryopreserved sperm|11.0|0.0|Unknown||dorsal root ganglion|Yes| 8123.0|PV-cre:RCE:LoxP|B6.129P2-Gt(ROSA)26Sor Pvalb/Anu||Recessive|gene trap ROSA 26, Philippe Soriano|Gt(ROSA)26Sor|Unknown|beta geo, Gtrgeo26, Gtrosa26, R26, ROSA26, Thumpd3as1 |MGI:104735|gene trap ROSA 26, Philippe Soriano; targeted mutation 1.1, Gordon Fishell|Gt(ROSA)26Sor|MGI:4412373|6|||||||||||||||||||||||||||||Unknown||C57BL/6J|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|28-Oct-2016|Cryopreserved sperm|||Unknown||dorsal root ganglion|Yes| 8128.0|ENU18:021:Baff|B6(Cg)-Tnfsf13b/AnuApb||Recessive|tumor necrosis factor (ligand) superfamily, member 13b|Tnfsf13b||BAFF, BLyS, D8Ertd387e, TALL-1, zTNF4|MGI:1344376|Tnfsf13b: mutation 2, Australian National University|Tnfsf13b||8|||||||||||||||||||||||||||||Block in B cell development||C57BL/6NCrlAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|10|||No|31-Oct-2016|Cryopreserved sperm|45.0|0.0|Unknown||B cell|Yes| 8129.0|Sst-cre|STOCK Sst/JAnu||Recessive|somatostatin|Sst||preprosomatostatin, Smst, SOM, SRIF|MGI:98326|somatostatin; targeted mutation 2.1, Z Josh Huang|Sst|MGI:4838416|16|||||||||||||||||||||||||||||No abnormal phenotype detected: • homozygous mice are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities||Mixed|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|01-Nov-2016|Cryopreserved sperm|67.0|5.0|Unknown||Cre recombinase|Yes| 8132.0|WEHIG1:Fcho1:C57Crl|B6.Cg-Fcho1/Anuapb||Recessive|FCH domain only 1|Fcho1|Unknown|3322402E17Rik|MGI:1921265||||8|||||||||||||||||||||||||||||Unknown||C57BL/6NCrlAnu|Yes|Unknown|Yes|Yes|Unknown|Yes|No|Unknown||||No|04-Nov-2016|Cryopreserved sperm|33.0|0.0|Unknown||ENU|Yes| 8116.0|ENU18:Olfr603:B6|C57BL/6NCrlAnu-Olfr603/AnuApb||Recessive|olfactory receptor 603|Olfr603|Unknown|GA_x6K02T2PBJ9-6092550-6092362, GA_x6K02T2PBJ9-6096387-6095449, MOR32-14_i, MOR32-2, Olfr604|MGI:3030437||||7|ENSMUSG00000059874|ENSMUST00000071844.1|Olfr603-001||||||||||||||||||||||||||Unknown||C57BL/6NCrlAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|26-Oct-2016|Cryopreserved sperm|42.0|0.0|Unknown|||Yes| 8133.0|Blimp1 fl|B6.Cg-Prdm1/WehiMarpAnu||Recessive|PR domain containing 1, with ZNF domain|Prdm1||b2b1765Clo, Blimp1, Blimp-1, PRDI-BF1|MGI:99655|PR domain containing 1, with ZNF domain; targeted mutation 2.1, Stephen L Nutt|Prdm1|MGI:4355900|10|||||||||||||||||||||||||||||Normal||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|10|||No|14-Nov-2016|Cryopreserved sperm|66.0|0.0|Unknown||T cell|Yes| 8135.0|Sm22-rtTA|FVB/N-Tg(Tagln-rtTA)E1Jwst||Dominant||||||||||||||||||||||||||transgene insertion E1, James West|murine smooth muscle-specific SM22-alpha|||||||||||Same as wildtype|Same as wildtype|FVB/N|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|15-Nov-2016|Cryopreserved sperm|50.0|0.0|Unknown||SM22, Tetracycline|Yes| 8137.0|Rosa26-FlagCep55 Tg|BALB/c-Gt(ROSA)26Sor||Dominant|gene trap ROSA 26, Philippe Soriano|Gt(ROSA)26Sor|Increased|beta geo, Gtrgeo26, Gtrosa26, R26, ROSA26, Thumpd3as1|MGI:104735|Flag-Cep55 Floxed|||6|||||||||||||||||||||||||||||Normal|Normal|BALB/c|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|5|||No|16-Nov-2016|Cryopreserved sperm|50.0|0.0|Unknown|||Possibly| 8139.0|Cd11c-cre-GFP|C57BL/6J-Tg(Itgax-cre,-EGFP)4097Ach/J||Dominant||||||||||||||||||||||||||transgene insertion 4097, Alexander V Chervonsky|Itgax|||||||||||Normal||C57BL/6J|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|24-Nov-2016|Cryopreserved sperm|45.0|0.0|Unknown||GFP|No| 8140.0|Pvr KO|B6N.129S2-Pvr/JAnu||Recessive|poliovirus receptor|Pvr|Nil|3830421F03Rik, CD155, D7Ertd458e, mE4, necl-5, Taa1, Tage4|MGI:107741|poliovirus receptor; targeted mutation 1, Gunter Bernhardt|Pvr|MGI:3719436|7|||||||||||||||||||||||||||||Decreased IgA level: • following oral immunization with cholera toxin, IgA levels are decreased relative to wild-type miceDecreased IgG level: • following oral immunization with cholera toxin, IgG1, IgG2a and IgG2b levels are decreased relative to wild-type miceDecreased IgG1 level.Decreased IgG2a level. Decreased IgG2b level.Abnormal response to infection: • following oral immunization with cholera toxin, IgA, IgG1, IgG2a and IgG2b levels are decreased relative to wild-type mice||C57BL/6N|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|10|||No|24-Nov-2016|Cryopreserved sperm|44.0|0.0|Unknown||receptor, CD155|No| 8141.0|Lck-icre|B6.Cg-Tg(Lck-icre)3779Nik/JAnu||Dominant||||||||||||||||||||||||||transgene insertion 3779, Nigel Killeen|distal Lck|T cells||||||||||Cre recombinase is expressed in T cells||C57BL/6J|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|12|||No|24-Nov-2016|Cryopreserved sperm|54.0|0.0|Unknown||Cre recombinase|No| 8822.0||NOD.129S7B6-Rag1 H2d1Ab1Ea2 Ins1 Tg(hCD4) Tg(HLA-DR4,HLA-DQ8) Tg(TCR A1.2)||Recessive|recombination activating 1|Rag1|||MGI:97848|recombination activating 1; targeted mutation 1, Peter Mombaerts|Rag1|MGI:1857241|2|ENSMUSG00000061311|ENSMUST00000078494|||||||||||||||transgene insertion 2362, Dan R Littman|murine Cd4 and human CD4|equivalent to human CD4+ cells||||||||||Unknown|Unknown|NOD|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|01-Nov-2019|Cryopreserved sperm|50.0|0.0|Unknown|||Yes| 8822.0||NOD.129S7B6-Rag1 H2d1Ab1Ea2 Ins1 Tg(hCD4) Tg(HLA-DR4,HLA-DQ8) Tg(TCR A1.2)||Recessive|histocompatibility 2, D region locus 1|H2-D1||H-2D|MGI:95896|H2-D1Ab1Ea2|||17|ENSMUSG00000073411 ||||||||||||||||Tg(TCR A1.2)||||||||||||Unknown|Unknown|NOD|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|01-Nov-2019|Cryopreserved sperm|||Unknown|||Yes| 8822.0||NOD.129S7B6-Rag1 H2d1Ab1Ea2 Ins1 Tg(hCD4) Tg(HLA-DR4,HLA-DQ8) Tg(TCR A1.2)||Recessive|insulin I|Ins1|||MGI:96572||Ins1||19|ENSMUSG00000035804 ||||||||||||||||Tg(HLA-DR4,HLA-DQ8)||||||||||||Unknown|Unknown|NOD|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|01-Nov-2019|Cryopreserved sperm|||Unknown|||Yes| 8131.0|TetO7-BMPR2 R899X|FVB/N-Tg(tetO-Bmpr2*R899X)#Jwst||Dominant||||||||||||||||||||||||||transgene insertion, James West|A septad of tetracycline respons element with a minimal CMV promoter|||||||||||Same as wildtype|Same as wildtype|FVB/N|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|02-Nov-2016|Cryopreserved sperm|50.0|0.0|Unknown||Familial pulmonary arterial hypertension (PAH), muscle, BMPR2|Yes| 8138.0|Vps51:35bp deletion|B6(Cg)-Vps51/AnuApb||Recessive|VPS51 GARP complex subunit|Vps51|Unknown|1110014N23Rik, 3110057M17Rik|MGI:1915755||||19|||||||||||||||||||||||||||||Embryonic lethal||C57BL/6NCrlAnu|No|No|Yes|No|No|Yes|No|Unknown|4|||No|18-Nov-2016|Cryopreserved sperm|36.0|0.0|Unknown|||Yes| 8159.0|NODlga|NOD-Ifnlr1 Ifngr1 Ifnar1||Recessive|Interferon lambda receptor 1|Ifnlr1|Unknown|CRF2-12, IFNLR1, Il28ra|MGI:2429859||em13Tcb||4|||||||||||||||||||||||||||||Unknown|Unknown|NOD/LtJ|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|17-Dec-2016|Cryopreserved sperm|40.0|0.0|Yes|Type 1 diabetes||Possibly| 8159.0|NODlga|NOD-Ifnlr1 Ifngr1 Ifnar1||Recessive|Interferon gamma receptor 1|Ifngr1|Unknown|CD119, Ifgr, IFN-gammaR, IFN-gamma R, Ifngr, Nktar|MGI:107655||em15Tcb||10|||||||||||||||||||||||||||||Unknown|Unknown|NOD/LtJ|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|17-Dec-2016|Cryopreserved sperm|||Yes|Type 1 diabetes||Possibly| 8159.0|NODlga|NOD-Ifnlr1 Ifngr1 Ifnar1||Recessive|Interferon alpha receptor 1|Ifnar1|Unknown|Ifar, IFN-alpha/betaR, Ifrc|MGI:107658||em16Tcb||16|||||||||||||||||||||||||||||Unknown|Unknown|NOD/LtJ|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|17-Dec-2016|Cryopreserved sperm|||Yes|Type 1 diabetes||Possibly| 8147.0|ASD726:Taco|ASD726:Taco||Recessive||||||||||||||||||||||||||||||||||||||||C57BL/6|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|30-Nov-2016|Cryopreserved sperm|10.0|0.0|Unknown||CRISPR|No| 8142.0|St3gal1 fl|B6.129-St3gal1/JAnu||Recessive|ST3 beta-galactoside alpha-2,3-sialyltransferase 1|St3gal1|Normal|CMP-N-acetylneuraminate: [beta-galactosidase alpha-2,3] sialytransferase, Siat4, Siat4a, ST3GalI|MGI:98304|ST3 beta-galactoside alpha-2,3-sialyltransferase 1; targeted mutation 2, Jamey Marth MGI ID: |St3gal1|MGI:3699717|15|||||||||||||||||||||||||||||Normal||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|10|||No|24-Nov-2016||0.0|0.0|Unknown||T cell, O-glycans|No| 8148.0|Arpc1b KO, Arpc1b fl|C57BL/6N-Arpc1b/WtsiAnu||Recessive|actin related protein 2/3 complex, subunit 1B|Arpc1b|Normal|L72, p41-ARC, SOP2Hs|MGI:1343142|actin related protein 2/3 complex, subunit 1B; targeted mutation 1a, Wellcome Trust Sanger Institute|Arpc1b|MGI:4431851|5|||||||||||||||||||||||||||||Normal||C57BL/6NCrlAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|07-Dec-2016|Cryopreserved sperm|58.0|0.0|Unknown|||Yes| 8149.0|NODCrisprGzmA|NOD-Gzma||Recessive|granzyme A|Gzma|Unknown|BLT esterase, Ctla3, Ctla-3, Hanukah factor, Hf, H factor, SE1, serine esterase 1, TSP1, TSP-1 |MGI:109266||||13|||||||||||||||||||||||||||||Unknown|Unknown|NOD/LtJ|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|11-Dec-2016|Cryopreserved sperm|50.0|0.0|Yes|Type 1 diabetes||Possibly| 8151.0|NODCrisprGzmA|NOD-Gzma||Recessive|granzyme A|Gzma|Unknown|BLT esterase, Ctla3, Ctla-3, Hanukah factor, Hf, H factor, SE1, serine esterase 1, TSP1, TSP-1|MGI:109266||em3Tcb||13|||||||||||||||||||||||||||||Unknown|Unknown|NOD/LtJ|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|15-Dec-2016|Cryopreserved sperm|50.0|0.0|Yes|Type 1 diabetes||Possibly| 8152.0|NODSTING|NOD-Tmem173||Recessive|Transmembrane protein 173|Sting1|Unknown|2610307O08Rik, ERIS, MPYS, Sting, Tmem173|MGI:1919762|stimulator of interferon response cGAMP interactor 1; endonuclease-mediated mutation 1, Thomas Brodnicki|Sting1|MGI:7341356|18||||||||||Unknown to Unknown|||||||||||||||||||Unknown|Unknown|NOD/LtJ|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|15-Dec-2016|Cryopreserved sperm|50.0|0.0|Yes|Type 1 diabetes||Possibly| 8154.0|NODlga|NOD-Ifnlr1||Recessive|Interferon lambda receptor 1|Ifnlr1|Unknown|CRF2-12, IFNLR1, Il28ra|MGI:2429859||em13Tcb||4|||||||||||||||||||||||||||||Unknown|Unknown|NOD/LtJ|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|16-Dec-2016|Cryopreserved sperm|70.0|0.0|Yes|Type 1 diabetes||Possibly| 8156.0|NODlga|NOD-Ifngr1||Recessive|Interferon gamma receptor 1|Ifngr1|Unknown|CD119, Ifgr, IFN-gammaR, IFN-gamma R, Ifngr, Nktar|MGI:107655||em15Tcb||10|||||||||||||||||||||||||||||Unknown|Unknown|NOD/LtJ|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|16-Dec-2016|Cryopreserved sperm|50.0|0.0|Yes|Type 1 diabetes||Possibly| 8157.0|NODlga|NOD-Ifnar1||Recessive|Interferon alpha receptor 1|Ifnar1|Unknown|Ifar, IFN-alpha/betaR, Ifrc|MGI:107658||em16Tcb||16|||||||||||||||||||||||||||||Unknown|Unknown|NOD/LtJ|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|16-Dec-2016|Cryopreserved sperm|50.0|0.0|Yes|Type 1 diabetes||Possibly| 8162.0|Casp11 KO|B6.129S4(D2)-Casp4/JAnu||Recessive|caspase 4, apoptosis-related cysteine peptidase|Casp4|Nil|Casp11, Caspase-11, ich-3|MGI:107700|caspase 4, apoptosis-related cysteine peptidase; targeted mutation 1, Junying Yuan|Casp4|MGI:2159366|9|||||||||||||||||||||||||||||Decreased circulating interleukin-1 alpha level: • decreased levels of serum IL-1alpha after lipopolysaccharide stimulationDecreased circulating interleukin-1 beta level: • decreased levels of serum IL-1beta after lipopolysaccharide stimulationDecreased susceptibility to endotoxin shock: • resistance to septic shock following LPS injection||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|23-Jan-2017||0.0|0.0|Unknown||ICE, Caspase, apoptosis|Yes| 8165.0|Prox1enhCRISPR-Shenzi|C57BL/6-Prox1||Recessive|prospero homeobox 1|Prox1|Unknown|A230003G05Rik|MGI:97772||||1|||||||||||||||||||||||||||||Unknown|Unknown|C57BL/6|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|23-Jan-2017|Cryopreserved sperm|50.0|0.0|Unknown|||Yes| 8169.0|Prox1enhCRISPR-Zazu|C57BL/6-Prox1||Recessive|prospero homeobox 1|Prox1|Unknown|A230003G05Rik|MGI:97772||||1|||||||||||||||||||||||||||||Unknown|Unknown|C57BL/6|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|23-Jan-2017|Cryopreserved sperm|50.0|0.0|Unknown|||Yes| 8153.0|NODSTING|NOD-Tmem173||Recessive|Transmembrane protein 173|Sting1|Unknown|2610307O08Rik, ERIS, MPYS, Sting, Tmem173|MGI:1919762|stimulator of interferon response cGAMP interactor 1; endonuclease-mediated mutation 2, Thomas Brodnicki|Sting1|MGI:7341357|18||||||||||Unknown to Unknown|||||||||||||||||||Unknown|Unknown|NOD/LtJ|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|16-Dec-2016|Cryopreserved sperm|50.0|0.0|Yes|Type 1 diabetes||Possibly| 8160.0||ENU36:080:Car2||Recessive|carbonic anhydrase 2|Car2|Unknown|CAII, CA II, Car-2, Ltw-5, Lvtw-5|MGI:88269||||3|ENSMUSG00000027562|ENSMUST00000029078.8|Car2-001|140|465|T to A|ENSMUSE00000371047|2|47|Leucine to Glutamine|||||TGCCCAGCATGACCCTGCCCTACAGCCTCTGCTCATATCTTATGATAAAGCTGCGTCCAAG||||||||||||||Red blood cells are resistent to lysis||C57BL/6NCrlAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|22-Dec-2016|Cryopreserved sperm|36.0|0.0|Unknown||Red blood cell|Possibly| 8170.0|Prox1enhCRISPR-Ed|C57BL/6-Prox1||Recessive|prospero homeobox 1|Prox1|Unknown|A230003G05Rik|MGI:97772||||1|||||||||||||||||||||||||||||unknown|unknown|C57BL/6|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|23-Jan-2017|Cryopreserved sperm|50.0|0.0|Unknown|||Yes| 8161.0|Casp1 KO|B6.129S2-Casp1/JAnu||Recessive|caspase 1|Casp1|Nil|Caspase-1, ICE, Il1bc, interleukin 1 beta-converting enzyme|MGI:96544|caspase 1; targeted mutation 1, Richard Flavell|Casp1|MGI:2158744|9|||||||||||||||||||||||||||||Mice lack expression of interleukin-1 converting enzyme (or caspase-1) and therefore cannot proteolytically cleave interleukin 1β and interleukin 18 into active mature peptides. |unknown|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Excellent|13|||Yes|23-Jan-2017||0.0|0.0|Unknown||caspase-1, IL-1b, IL-18|Yes| 8158.0|NODlga|NOD-Ifnlr1 Ifngr1 Ifnar1||Recessive|interferon lambda receptor 1|Ifnlr1|Unknown|CRF2-12, IFNLR1, Il28ra|MGI:2429859||em4Tcb||4|||||||||||||||||||||||||||||Unknown|Unknown|NOD/LtJ|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|17-Dec-2016||0.0|0.0|Unknown||CRISPR|Yes| 8158.0|NODlga|NOD-Ifnlr1 Ifngr1 Ifnar1||Recessive|interferon gamma receptor 1|Ifngr1|Unknown|CD119, Ifgr, IFN-gammaR, IFN-gamma R, Ifngr, Nktar|MGI:107655||em15Tcb||10|||||||||||||||||||||||||||||Unknown|Unknown|NOD/LtJ|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|17-Dec-2016||||Unknown||CRISPR|Yes| 8158.0|NODlga|NOD-Ifnlr1 Ifngr1 Ifnar1||Recessive|interferon (alpha and beta) receptor 1|Ifnar1|Unknown|Ifar, IFN-alpha/betaR, Ifrc|MGI:107658||em16Tcb||16|||||||||||||||||||||||||||||Unknown|Unknown|NOD/LtJ|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|17-Dec-2016||||Unknown||CRISPR|Yes| 7681.0|ENU7PMH:130:B6 ; Krusty|B6(Cg)-Ndfip1/AnuApb|B6(Cg)-Ndfip1/AnuApb|Recessive|Nedd4 family interacting protein 1|Ndfip1||0610010M22Rik|MGI:1929601|Nedd4 family interacting protein 1; krusty|Ndfip1|MGI:5442611|18|ENSMUSG00000024425|ENSMUST00000025293|Ndfip1-201||||||||38612084|5|||TCTCTAATTAAGTGGATCCTTATTGTCAGGGTAAGTTGCATAGCAGAGAACAGATTGTGA||||||||||||||Autoimmune disease.Spontaneous mast cell-rich dermatitis with median onset age 90 d, followed by weight loss and premature mortality at a median age of 160 d||C57BL/6NCrlAnu|Yes|Unknown|Yes|Yes|Yes|Yes|No|Unknown||G4N5|Het x Het ; Het x Hom|No|13-May-2014|Cryopreserved sperm|26.0|0.0|Unknown||T cell, autoimmunity, CD4, ENU|Yes| 8175.0|Ccnf|Ccnf||Recessive|cyclin F|Ccnf|Unknown|CycF, Fbxo1|MGI:102551||||17|||||||||||||||||||||||||||||Normal|Normal|C57BL/6|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|30-Jan-2017||0.0|0.0|Unknown|||Yes| 7679.0|ENU7PMH:130:B10:B6-ATkk:G9 ; Krusty:3A9:H2|B6.Cg-H2 Ndfip1 Tg(TcrHEL3A9)1Mmd/AnuApb||Recessive|Nedd4 family interacting protein 1|Ndfip1|Unknown|0610010M22Rik|MGI:1929601|krusty|kru||18|ENSMUSG00000024425|ENSMUST00000025293|Ndfip1-201||||||||38612084|5|||TCTCTAATTAAGTGGATCCTTATTGTCAGGGTAAGTTGCATAGCAGAGAACAGATTGTGA||transgene insertion 1, Mark M Davis|TCR||histocompatibility-2, MHC|H2||H-2, MHC-II|MGI:95894|histocompatibility-2, MHC; k variant|H2|MGI:3579322|17|Spontaneous mast cell-rich dermatitis with median onset age 90 d, followed by weight loss and premature mortality at a median age of 160 d. This was accompanied by lymph- adenopathy, splenomegaly, increased CD86 and CD23 activation markers on B cells, expansion of the activated/memory subset of CD4<+> and CD8<+> T cells, greatly elevated serum IgE, and for- mation of a prominent population of IL-4<+> and IFN-γ<+> CD4<+>.Autonomous accumulation of CD4<+> effector cells not corrected by normal Foxp3<+> cells.Absence of Ndfip1 did not result in spontaneous activation of naïve CD4+ T cells. Naive Ndfip1 Tg(TcrHel3A9) CD4<+> transferred to congenic B10.BR CD45 mice injected with hen egg lysozyme. After 6 days continued to increase in frequency, a further 4 fold over d3 levels, whereas WT cells decreased 5 fold from d3 levels.||C57BL/6JSfdAnu x B10.BR-H2|Yes|Unknown|Yes|Yes|Unknown|Yes|No|Unknown||||No|13-May-2014|Cryopreserved sperm|50.0|0.0|Unknown||T cell, autoimmune, CD4, FoxP3, tolerance|Yes| 8177.0|ENU36:195:Map3k8|C57BL/6NCrlAnu-Map3k8/AnuApb||Recessive|mitogen-activated protein kinase kinase kinase 8|Map3k8|Unknown|c-COT, Cot, Cot/Tpl2, Tpl2, Tpl-2|MGI:1346878||||18|||||||||||||||||||||||||||||Unknown|Unknown|C57BL/6NCrlAnu|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|03-Feb-2017|Cryopreserved sperm|36.0|0.0|Unknown||ENU|Yes| 8178.0|ENU37:055:Casp4|C57BL/6NCrlAnu-Casp4/AnuApb||Recessive|caspase 4, apoptosis-related cysteine peptidase|Casp4|Unknown|Casp11, Caspase-11, ich-3|MGI:107700||||9|||||||||||||||||||||||||||||Unknown|Unknown|C57BL/6NCrlAnu|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|03-Feb-2017|Cryopreserved sperm|36.0|0.0|Unknown||ENU|Yes| 8176.0|ENU35:180:Nlrp3|C57BL/6NCrlAnu-Nlrp3/Anu||Recessive|NLR family, pyrin domain containing 3|Nlrp3|Unknown|Cias1, cryopyrin, Mmig1, NALP3, Pypaf1|MGI:2653833||||11|||||||||||||||||||||||||||||Unknown|Unknown|C57BL/6NCrlAnu|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|03-Feb-2017|Cryopreserved sperm|22.0|0.0|Unknown||ENU|Yes| 8179.0|ENU26:003:Nlrp3|C57BL/6NCrlAnu-Nlrp3/Anu||Recessive|NLR family, pyrin domain containing 3|Nlrp3|Unknown|Cias1, cryopyrin, Mmig1, NALP3, Pypaf1|MGI:2653833||||11|||||||||||||||||||||||||||||Unknown|Unknown|C57BL/6NCrlAnu|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|03-Feb-2017|Cryopreserved sperm|24.0|0.0|Unknown||ENU|Yes| 7873.0|ACTFLPtg|B6.Cg-Tg(ACTFLPe)9205Dym/JAusbAnuApb||Dominant||||||||||||||||||||||||||transgene insertion 9205, Susan Dymecki|ACTB, actin, beta, human|The FLPe recombinase variant exhibits enhanced thermostability with recombination activity being 4X and 10X that of wildtype FLP at 37°C and 40°C, respectively||||||||||The FLPe recombinase variant exhibits enhanced thermostability with recombination activity being 4X and 10X that of wildtype FLP at 37°C and 40°C, respectively. |Hemizygous transgenic mice are viable, fertile, normal in size, and do not display any gross physical or behavioral abnormalities.|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|16-Apr-2015|Cryopreserved sperm|43.0|1228.0|Unknown||recombinase, deleter, Cre, actin|Yes| 8190.0|BigMac|BigMac||Recessive|Unknown||||||||Unknown|||||||||||||||||||||||||||||Unknown|||Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|16-Feb-2017|Cryopreserved sperm|60.0|0.0|Unknown||CRISPR|Yes| 8187.0|WEHIG1:Srgap1:C57Crl|B6.Cg-Srgap1/WehiAnuApb||Recessive|SLIT-ROBO Rho GTPase activating protein 1|Srgap1|Unknown|4930572H05Rik, Arhgap13|MGI:2152936||||10|ENSMUSG00000020121|ENSMUST00000081688.12|Srgap1-201|1994|2116|G to A|ENSMUSE00001215240|17|665|Proline to Leucine|||||||||||||||||||Unknown||C57BL/6NCrlAnu|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|10-Feb-2017|Cryopreserved sperm|48.0|0.0|Unknown||ENU|Yes| 8181.0|Tap1/Tap2 KO ET26|C57BL/6J-Tap1/Tap2/26MarpAnu||Recessive|transporter 1, ATP-binding cassette, sub-family B (MDR/TAP)|Tap1|Nil|Abcb2, Ham1, Ham-1, MTP1, PSF-1, RING4, TAP, Tap-1|MGI:98483||||17|||||||||||||||||||||||||||||Unknown|Unknown|C57BL/6|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|07-Feb-2017|Cryopreserved sperm|24.0|0.0|Unknown|||Yes| 8181.0|Tap1/Tap2 KO ET26|C57BL/6J-Tap1/Tap2/26MarpAnu||Recessive|transporter 2, ATP-binding cassette, sub-family B (MDR/TAP)|Tap2|Nil|Abcb3, Ham2, Ham-2, HAM2, MTP2, PSF2, Tap-2|MGI:98484||||17|||||||||||||||||||||||||||||Unknown|Unknown|C57BL/6|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|07-Feb-2017|Cryopreserved sperm|||Unknown|||Yes| 8180.0|hTAP1/hTAP2 BAC Tg ET18|C57BL/6J-Tg(hTAP1/hTAP2)/18MarpAnu||Recessive||||||||||||||||||||||||||human transporter 1, ATP-binding cassette, sub-family B (MDR/TAP) / human transporter 2, ATP-binding cassette, sub-family B (MDR/TAP)||||||||||||Unknown|Unknown|C57BL/6J|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|07-Feb-2017|Cryopreserved sperm|72.0|0.0|Unknown|||Yes| 8185.0|Tcf3 6bp KO|C57BL/6NCrlAnu-Tcf3/Anu||Recessive|transcription factor 3|Tcf3|Unknown|A1, ALF2, bHLHb21, E12, E2A, E47, Pan1, Pan2, Tcfe2a|MGI:98510||||10|||||||||||||||||||||||||||||Unknown|Unknown|C57BL/6NCrlAnu|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown|1|||No|09-Feb-2017|Cryopreserved sperm|24.0|0.0|Unknown||CRISPR, transcription factor|Yes| 8186.0|Tcf3 1bp KI|C57BL/6NCrlAnu-Tcf3/Anu||Recessive|transcription factor 3|Tcf3|Unknown|A1, ALF2, bHLHb21, E12, E2A, E47, Pan1, Pan2, Tcfe2a|MGI:98510||||10|||||||||||||||||||||||||||||Unknown|Unknown|C57BL/6NCrlAnu|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown|1|||No|09-Feb-2017|Cryopreserved sperm|48.0|0.0|Unknown||CRISPR, transcription factor|Yes| 8189.0|ENU36:091:Rag2|C57BL/6NCrlAnu-Rag2/AnuApb||Recessive|recombination activating gene 2|Rag2|Unknown|Rag-2|MGI:97849||||2|ENSMUSG00000032864|ENSMUST00000044031.3|Rag2-001|173|414|A to G|ENSMUSE00000230533|3|58|Lysine to Glutamic acid|||||TGATATAAAACAAAATCATCTCAAACTGAAGCCTGCAATCTTCTCTAAAGATTCCTGCTAC||||||||||||||FACS phenotype: Low B cells numbers in peripheral blood|Normal|C57BL/6NCrlAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|16-Feb-2017|Cryopreserved sperm|35.0|0.0|Unknown||ENU, B cell|Yes| 8183.0|Par1 KO|B6.129-F2r||Recessive|coagulation factor II (thrombin) receptor|F2r|Nil|Cf2r, Par1, thrombin receptor, ThrR|MGI:101802|coagulation factor II (thrombin) receptor; targeted mutation 1, Andrew J Connolly|F2r|MGI:1857306|13|||||||||||||||||||||||||||||Embryonic lethality during organogenesis, incomplete penetrance:• by E12.5, 52% of mutant embryos are dead with extensive bleeding; the remaining embryos survive to adulthood and appear grossly normalSkeleton phenotype:N • osteoblast number and surface are not significantly different between controls and mutant mice• no changes in osteoclast number and surfaceLong femur:• small, albeit significant, increase in femur lengthIncreased bone mineral density.Abnormal bone volume.Increased compact bone volume:• diaphyseal endocortical volume is increased• endocortical and cortical volumes are significantly increasedIncreased trabecular bone volume:• trabecular bone volume fraction in the distal metaphyseal bone compartment is elevated• significantly increased trabecular bone volume in the femoral metaphysis and diaphysisDecreased compact bone thickness:• diaphyseal thickness was reducedIncreased bone trabecula number.Decreased bone trabecular spacing.Abnormal vitelline vasculature morphology:• at E8.75 to E10.5, embryos with gross bleeding are pale and display a disorganized yolk sac vasculature or delayed remodelingAbsent vitelline blood vessels:• at E12.5, mutant yolk sacs lack blood-filled vesselsAbnormal sinus venosus morphology:• at E9.5, 2 out of 3 mutant embryos exhibit a defect in the wall of the sinus venosus that is large enough to allow blood cells into the pericardial cavityDistended pericardium:• at E9.5, hemorrhagic embryos often display a dilated pericardial sac, indicating cardiovascular failure• at this stage, 4 out of 19 mutant embryos with microscopic bleeding display normal pericardial sacsHaemorrhage:• by E9.5, ~66% of mutant embryos display microscopic bleeding in the pericardial and/or peritoneal, amniotic, and/or exocoelomic cavity• live E9.5 to E10.5 embryos with both gross bleeding and vigorous heart beats are occasionally observedHaemopericardium:• at E9.5, 22% of mutant embryos exhibit hemorrhage in the exocoelomic and/or pericardial cavities.Embryonic growth retardation:• at E9.5, mutant embryos show a variable developmental delay but no gross vascular anomaliesIncreased body weightAbnormal cell physiology:• relative to wild-type, mutant endothelial cells display a 20-30% reduction in F10 (coagulation protease factor Xa)-triggered phosphoinositide hydrolysis• a similar reduction is observed when ERK1/2 phosphorylation is used to assess F10 signaling• in contrast, mutant lung fibroblasts exhibit a complete absence of F10-induced phosphoinositide hydrolysisAbnormal neuron apoptosis:• cortical neurons from mutant fetuses exhibit a complete loss of activated protein C (APC)-mediated neuronal protection against NMDA-induced apoptosisHomeostasis/metabolism phenotype:N • urinary Ca2+ excretion is not affected• serum Ca2+ concentration is not affected• serum Na+ and K+ values appear similar to controlsAbnormal circulating protein level:• serum RANKL level is significantly decreased, and the OPG level is increased, resulting in a significantly reduced RANKL/OPG ratioIncreased urine sodium level:• urinary Na+ excretion was enhancedIncreased urine pH.Abnormal urine protein level:• urinary DPD (degradation products of collagen I) concentration in homozygous mutant mice is reduced.|Normal|C57BL/6J|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|9|||No|08-Feb-2017|Cryopreserved sperm|50.0|0.0|Unknown||Thrombin receptor|Yes| 8174.0|NODSOCS1/hCD4|NOD.B6-Socs1JWehi|Tkay|Semi-dominant|suppressor of cytokine signaling 1|Socs1|Nil|Cish1, Cish7, JAB, JAK2-binding protein, JAK-binding protein, SOCS-1, SSI-1, STAT-induced STAT inhibitor 1|MGI:1354910|suppressor of cytokine signaling 1; targeted mutation 3.1, Walter and Eliza Hall Institute of Medical Research|Socs1|MGI:2656956|16|||||||||||||||||||||||||||||These mice die at weaning and are runted.|Normal|NOD/Lt|No|No|Yes|No|No|Yes|No|Good|10+|NA|NOD/Lt x SOCS1/hCD4 Heterozygous|No|24-Jan-2017|Cryopreserved sperm|50.0|0.0|No||Suppressor of cytokine signalling, NOD/Lt, hCD4|Possibly| 8184.0|Par2 KO|B6.129-F2rl1||Recessive|coagulation factor II (thrombin) receptor-like 1|F2rl1|Nil|Gpcr11, Par2, PAR-2, Protease-activated receptor-2, proteinase-activated receptor-2|MGI:101910|coagulation factor II (thrombin) receptor-like 1; targeted mutation 1, Shaun R Coughlin|F2rl1|MGI:2179844|13|||||||||||||||||||||||||||||Decreased dendritic cell number:• mice fail to develop bone marrow-derived dendritic cells with to without soy bean trypsin inhibitor treatment unlike wild-type mice• however, stimulation with TNG-alpha or by crosslinking CD40 results in mature dendritic cell development|Normal|C57BL/6J|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|08-Feb-2017|Cryopreserved sperm|50.0|0.0|Unknown||Thrombin|Yes| 8191.0|B6.Cg-Tg(Thy1-YFP)HJrs/J x B6.Cg-Sgshmps3a/Ldru|B6.Cg-Sgsh Tg(Thy1-YFP)HJrs/J||Recessive|N-sulfoglucosamine sulfohydrolase (sulfamidase)|Sgsh||4632406A19Rik, sulphamidase|MGI:1350341|N-sulfoglucosamine sulfohydrolase (sulfamidase); mucopolysaccharidosis IIIA|Sgsh|MGI:2151181|11|||||||||||||||||transgene insertion H, Joshua R Sanes|Thy1, thymus cell antigen 1, theta, mouse, laboratory|||||||||||These thy1-YFP-H transgenic mice express yellow fluorescent protein at high levels in motor and sensory neurons, as well as subsets of central neurons. Axons are brightly fluorescent all the way to the terminals. This line provides a strong and specific "Golgi-like" vital marker for several widely studied neuronal subsets, with minimal labeling of nearby axons. These mice carry a spontaneous mutation at the Sgsh locus characterized by scruffy coat, hunched posture, and reduced activity, and corneal opacity as a result of extensive lysosomal accumulation of heparin sulfate most prominently in neuronal tissue and liver and, to a lesser degree, in the spleen. |These thy1-YFP-H transgenic mice express yellow fluorescent protein at high levels in motor and sensory neurons, as well as subsets of central neurons. Axons are brightly fluorescent all the way to the terminals. This line provides a strong and specific "Golgi-like" vital marker for several widely studied neuronal subsets, with minimal labeling of nearby axons. They do not have a Sanfilippo phenotype.|C57BL/6|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|17-Feb-2017|Cryopreserved sperm|50.0|0.0|Unknown|||No| 8192.0|Tg(Thy1-EGFP)MJrs/J x B6.Cg-Sgshmps3a/Ldru|B6.Cg-Sgsh Tg(Thy1-EGFP)MJrs/J||Recessive|N-sulfoglucosamine sulfohydrolase (sulfamidase)|Sgsh||4632406A19Rik, sulphamidase|MGI:1350341|Mucopolysaccharidosis IIIA|N-sulfoglucosamine sulfohydrolase (sulfamidase); mucopolysaccharidosis IIIA|Sgsh|11|||||||||||||||||transgene insertion M, Joshua R Sanes|Thy1, thymus cell antigen 1, theta, mouse, laboratory|||||||||||These Thy1-GFP-M transgenic mice may be useful in neurobiological studies for fluorescent labeling of neural tissues, especially for mossy fibers in the cerebellum and intense, yet sparse, labeling of a variety of neuronal subsets. These mice carry a spontaneous mutation at the Sgsh locus characterized by scruffy coat, hunched posture, and reduced activity, and corneal opacity as a result of extensive lysosomal accumulation of heparin sulfate most prominently in neuronal tissue and liver and, to a lesser degree, in the spleen. |These Thy1-GFP-M transgenic mice may be useful in neurobiological studies for fluorescent labeling of neural tissues, especially for mossy fibers in the cerebellum and intense, yet sparse, labeling of a variety of neuronal subsets. Mice that are heterozygous for the Sgsh gene appear normal but express 50% SGSH activity. |C57BL/6|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|17-Feb-2017|Cryopreserved sperm|48.0|0.0|Unknown|||No| 8193.0|hPAR1-KI|C57BL/6J-F2rl2||Recessive|coagulation factor II (thrombin) receptor-like 2|F2rl2|Nil|PAR3|MGI:1298208||||13|||||||||||||||||||||||||||||Platelets fail to express human PAR1 protein and do not respond to PAR1 specific antagonists.|Normal|C57BL/6J|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|20-Feb-2017|Cryopreserved sperm|50.0|0.0|Unknown||platelet, thrombin|Yes| 8197.0|ENU36:028:Gfi1|C57BL/6NCrlAnu-Gfi1/AnuApb||Recessive|growth factor independent 1|Gfi1|Unknown|Gfi-1, Pal1, Pal-1|MGI:103170||||5|||||||||||||||||||||||||||||Reduced CD44 mean fluorescence intensity (MFI) on CD4<+> T cells and increased number of CD44 CD4<+> and CD8<+> T cells in peripheral blood as measured by flow cytometry.|Normal|C57BL/6NCrlAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|21-Feb-2017|Cryopreserved sperm|36.0|0.0|Unknown||T cell, CD4, CD8, CD44|Yes| 8195.0|ASD552:Cahill:62bpdel|C57BL/6NCrlAnu-Ikbkb/1AnuApb||Recessive|inhibitor of kappaB kinase beta|Ikbkb|Unknown|IKK2, IKK-2, IKK[b], IKKbeta, IKK-beta|MGI:1338071||||8|||||||||||||||||||||||||||||Unknown||C57BL/6NCrlAnu|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|20-Feb-2017|Cryopreserved sperm|72.0|0.0|Unknown||CRISPR|Yes| 4865.0|C3H-Kumba|C3H/HeH.Cg-Zic2/AnuApb|C3H/HeH.Cg-Zic2/AnuApb|Recessive|zinc finger protein of the cerebellum 2|Zic2|Unknown|GENA 29, Ku, odd-paired homolog|MGI:106679|kumba|Zic2|MGI:1862004|14||||||||||||||||Yes|||||||||||||Lethal during embryogenesis|Incomplete penetrance and variable expressivity of the following: ventral spot, curled tail, distal tail kink, spina bifida (rare).|C3H/HeH|No|No|Yes|No|No|Yes|No|Good||||No|24-Sep-2009|Cryopreserved sperm|75.0|0.0|Yes|Holoprosencephaly and spina bifida|Gastrulation, Neuralation, holoprosencephaly|Yes| 8198.0|pKZ1|B6.Cg-Tg(CAG<*>-LacZ)||Dominant||||||||||||||||||||||||||E.coli lac Z|Chicken beta actin enhancer complex|||||||||||Normal physiology. In cells where a somatic intrachromosomal recombination event occurs, beta galactosidase protein is expressed which can be detected using the chromogenic substrate 5-bromo-4-chloro-3-indolyl-b-D-galactoside (X-gal) which appears as a small blue punctate dot.|Normal physiology. In cells where a somatic intrachromosomal recombination event occurs, beta galactosidase protein is expressed which can be detected using the chromogenic substrate 5-bromo-4-chloro-3-indolyl-b-D-galactoside (X-gal) which appears as a small blue punctate dot.|C57BL/6J|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|23-Feb-2017|Cryopreserved sperm|40.0|0.0|Unknown||Radiation, DNA damage, LacZ|Yes| 8194.0|ASD552:Cahill:V203I|C57BL/6NCrlAnu-Ikbkb/3AnuApb||Recessive|inhibitor of kappaB kinase beta|Ikbkb|Unknown|IKK2, IKK-2, IKK[b], IKKbeta, IKK-beta|MGI:1338071|Ikbkb:endonuclease-mediated mutation 1, Australian National University|Ikbkb||8|||||||||||||||||||||||||||||Unknown||C57BL/6NCrlAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|20-Feb-2017|Cryopreserved sperm|24.0|0.0|Unknown||CRISPR|Yes| 8196.0|ASD544:Leckie:P450S|C57BL/6NCrlAnu-Stat4/AnuApb||Recessive|signal transducer and activator of transcription 4|Stat4|Unknown||MGI:103062|Stat4:endonuclease-mediated mutation 1, Australian National University|Stat4||1|||||||||||||||||||||||||||||Unknown|Normal|C57BL/6NCrlAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|20-Feb-2017|Cryopreserved sperm|24.0|0.0|Unknown||signal transduction, CRISPR|Yes| 8825.0||ASD892:Rye:F0||Recessive|GBP chrom5 C2 KO||||||||Unknown|||||||||||||||||||||||||||||Unknown|Unknown|C57BL/6NCrlAnu|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|12-Nov-2019|Cryopreserved sperm|12.0|0.0|Unknown|||Yes| 8200.0|ENU23:Etaa1|C57BL/6NCrlAnu-Etaa1/AnuApb||Recessive|Ewing tumor-associated antigen 1|Etaa1|Unknown|5730466H23Rik|MGI:1915395||||11|ENSMUSG00000016984|ENSMUST00000076661.6|Etaa1-001|498|579|A to T|ENSMUSE00000471991|4|166|Cysteine to STOP|||||GTATGGATTGGTGAAACTGCTATTCCTTGTACTCCTGGCGTAGCAAAAGAGAAGTCAAGAG||||||||||||||Absence of antigen specific T cells following immunisation.|Normal|C57BL/6NCrlAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|24-Feb-2017|Cryopreserved sperm|82.0|0.0|Unknown||T cell, immunisation|Yes| 8201.0|Thy1-EGFP|B6.CBA-Tg(Thy1-EGFP)MJrs/J||Dominant||||||||||||||||||||||||||transgene insertion M, Joshua R Sanes|Thy1, thymus cell antigen 1, theta, mouse, laboratory|||||||||||Unknown|Mice harboring the Thy1-GFP transgene are viable and fertile with enhanced green fluorescent protein (EGFP) expression under the control of a modified Thy1 promoter region (containing the sequences required for neuronal expression but lacking the sequences required for expression in non-neural cells). Homozygous or hemizygous Thy1-GFP mice derived from founder line M (Thy1-GFP-M or Thy1-GFPM) express EGFP in sparse subsets of neurons within specific populations; providing a bright, vital Golgi-like stain. Less than 10% of all motor axons, retinal ganglion cells, lumbar dorsal root ganglion, and cortex express EGFP. These Thy1-GFPM transgenic mice may be useful in neurobiological studies for fluorescent labeling of neural tissues, especially for mossy fibers in the cerebellum and intense, yet sparse, labeling of a variety of neuronal subsets. |C57BL/6J|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|27-Feb-2017|Cryopreserved sperm|56.0|0.0|Unknown||GFP|Yes| 5286.0|B6.CD73.KO|C57BL/6-Nt5e||Recessive|5' nucleotidase, ecto|Nt5e|Nil|CD73, ecto-5'-nucleotidase, Nt5|MGI:99782|5' nucleotidase, ecto; targeted mutation 1, Linda F Thompson|Nt5e|MGI:3522017|9||||||||||||||||No|||||||||||||Increased aggression toward humans: under hypoxic conditions mutants are less compliant compared to wild-type littermates.Lethargy: under hypoxic conditions mutants are more lethargic compared to wild-type littermates.Increased vascular permeability: * under hypoxic conditions increased vascular leakage is seen. * under normoxic conditions increased vascular permeability is seen in the lung and colon.Altered response to myocardial infarction: * ischemic preconditioning fails to attenuate infarct size as in wild-type mice. * however, treatment of mice with adenosine or 5' nucleotidase infusion partially-restores cardioprotection offered by ischemic preconditioning.Increased infarction size: mice exhibit increased infarct size after 60 minutes of ischemia compared to in similarly-treated wild-type mice.Edema: under hypoxic conditions increased edema is seen in all organs except the brain.Abnormal response/metabolism to endogenous compounds: mice exhibit an attenuated bradycardia response to AMP.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||21||No|28-Oct-2010|Cryopreserved sperm|50.0|0.0|Yes||ischemia, infarction, myocardium, hypoxia|Yes| 8206.0|Tap1/Tap2 KO ET33|C57BL/6J-Tap1/Tap2/33MarpAnu||Recessive|transporter 1, ATP-binding cassette, sub-family B (MDR/TAP)|Tap1|Nil|Abcb2, Ham1, Ham-1, MTP1, PSF-1, RING4, TAP, Tap-1|MGI:98483||||17|||||||||||||||||||||||||||||Unknown|Unknown|C57BL/6|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|02-Mar-2017|Cryopreserved sperm|24.0|0.0|Unknown|||Yes| 8206.0|Tap1/Tap2 KO ET33|C57BL/6J-Tap1/Tap2/33MarpAnu||Recessive|transporter 2, ATP-binding cassette, sub-family B (MDR/TAP)|Tap2|Nil|Abcb3, Ham2, Ham-2, HAM2, MTP2, PSF2, Tap-2|MGI:98484||||17|||||||||||||||||||||||||||||Unknown|Unknown|C57BL/6|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|02-Mar-2017|Cryopreserved sperm|||Unknown|||Yes| 8207.0|Tap1/Tap2 KO x Tg(hTAP1/hTAP2) BAC #2|C57BL/6J-Tap1/Tap2 Tg(hTAP1/hTAP2)20/2MarpAnu||Recessive|transporter 1, ATP-binding cassette, sub-family B (MDR/TAP)|Tap1|Nil|Abcb2, Ham1, Ham-1, MTP1, PSF-1, RING4, TAP, Tap-1|MGI:98483||||17|||||||||||||||||human transporter 1, ATP-binding cassette, sub-family B (MDR/TAP) / human transporter 2, ATP-binding cassette, sub-family B (MDR/TAP)||||||||||||Unknown|Unknown|C57BL/6J|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|02-Mar-2017|Cryopreserved sperm|12.0|0.0|Unknown|||Yes| 8207.0|Tap1/Tap2 KO x Tg(hTAP1/hTAP2) BAC #2|C57BL/6J-Tap1/Tap2 Tg(hTAP1/hTAP2)20/2MarpAnu||Recessive|transporter 2, ATP-binding cassette, sub-family B (MDR/TAP)|Tap2|Nil|Abcb3, Ham2, Ham-2, HAM2, MTP2, PSF2, Tap-2|MGI:98484||||17|||||||||||||||||||||||||||||Unknown|Unknown|C57BL/6J|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|02-Mar-2017|Cryopreserved sperm|||Unknown|||Yes| 8205.0|hTAP1/hTAP2 BAC Tg ET20|C57BL/6J-Tg(hTAP1/hTAP2)/20MarpAnu||Recessive||||||||||||||||||||||||||human transporter 1, ATP-binding cassette, sub-family B (MDR/TAP) / human transporter 2, ATP-binding cassette, sub-family B (MDR/TAP)||||||||||||Unknown|Unknown|C57BL/6J|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|02-Mar-2017|Cryopreserved sperm|36.0|0.0|Unknown|||Yes| 8204.0|NSG.VNTR.HuINS|NOD.Cg-Prkdc H2-Ab1 Il2rg Tg(HLA-DQA1,HLA-DQB1)1Dv Tg(INS*VNTR)/J||Recessive|protein kinase, DNA activated, catalytic polypeptide|Prkdc|Unknown|DNAPDcs, DNA-PK, DNA-PKcs, DOXNPH, dxnph, slip, XRCC7|MGI:104779|protein kinase, DNA activated, catalytic polypeptide; severe combined immunodeficiency|Prkdc|MGI:1857113|16|||||||||||||||||transgene insertion 1, Chella David||||||||||||Immunocompromised.Expresses HLA-DQ8 and human insulin.|Immunocompromised.Expresses HLA-DQ8 and human insulin.|NOD (NSG)|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|01-Mar-2017|Cryopreserved sperm|50.0|0.0|Unknown||H2, Insulin|No| 8204.0|NSG.VNTR.HuINS|NOD.Cg-Prkdc H2-Ab1 Il2rg Tg(HLA-DQA1,HLA-DQB1)1Dv Tg(INS*VNTR)/J||Recessive|histocompatibility 2, class II antigen A, beta 1|H2-Ab1|Nil|Abeta, A beta, H-2Ab, H2-Ab, Ia2, Ia-2, IAb, I-Ab, I-Abeta, Rmcs1|MGI:103070|histocompatibility 2, class II antigen A, beta 1; targeted mutation 1, Michael J Grusby|H2-Ab1|MGI:2158420|17|||||||||||||||||human insulin with microsatellite variable number tandem repeat (VNTR) region|human insulin|||||||||||Immunocompromised.Expresses HLA-DQ8 and human insulin.|Immunocompromised.Expresses HLA-DQ8 and human insulin.|NOD (NSG)|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|01-Mar-2017|Cryopreserved sperm|||Unknown||H2, Insulin|No| 8204.0|NSG.VNTR.HuINS|NOD.Cg-Prkdc H2-Ab1 Il2rg Tg(HLA-DQA1,HLA-DQB1)1Dv Tg(INS*VNTR)/J||Recessive|interleukin 2 receptor, gamma chain|Il2rg|Nil|CD132, common cytokine receptor gamma chain, common gamma chain, gamma(c), gammaC, gamma C receptor, gc, [g]c|MGI:96551|interleukin 2 receptor, gamma chain; targeted mutation 1, Warren J Leonard|Il2rg|MGI:1857455|X|||||||||||||||||||||||||||||Immunocompromised.Expresses HLA-DQ8 and human insulin.|Immunocompromised.Expresses HLA-DQ8 and human insulin.|NOD (NSG)|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|01-Mar-2017|Cryopreserved sperm|||Unknown||H2, Insulin|No| 8216.0|PV-Cre|B6.129-Pvalb|MGI:3590684|15|||||||||||||||||||||||||||||Unknown||C57BL/6J|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|15-Mar-2017||0.0|0.0|Unknown|||Yes| 8214.0|DEREG|C57BL/6-Tg(Foxp3-DTR/EGFP)23.2Spar/Mmjax||Dominant||||||||||||||||||||||||||transgene insertion 23.2, Tim Sparwasser|Foxp3 (forkhead box P3)|||||||||||Normal|Normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|08-Mar-2017|Cryopreserved sperm|110.0|0.0|Unknown||T cell, scurfy|Yes| 8215.0|R1584P KI ; Cav3.2 R1584P Knock-in|C57BL/6-Cacna1h||Dominant|calcium channel, voltage-dependent, T type, alpha 1H subunit|Cacna1h|Unknown|alpha13.2, Cav3.2, mKIAA1120, T-type Cav3.2|MGI:1928842||||17|||||||||||||||||||||||||||||Unknown|Unknown|C57BL/6|Yes|Unknown|Yes|Yes|Unknown|Yes|No|Good|||Brother x Sister|No|09-Mar-2017|Cryopreserved sperm|50.0|0.0|Unknown|||Possibly| 8212.0|B6 – HSPA5tm1Dtau|C57BL/6N-Hspa5/MarpDtau||Recessive|heat shock protein 5|Hspa5|Unknown|78kDa, baffled, Bip, D2Wsu141e, D2Wsu17e, Grp78, Hsce70, mBiP, Sez7, XAP-1 antigen|MGI:95835|heat shock protein 5; targeted mutation 1, Velocigene|Hspa5|MGI:4399453|2|||||||||||||||||||||||||||||Lethal|Heterozygous mice expressed 50% level ofwild type HSPA5 expression. However, there was no difference in biochemical induction of the ER stress response in vivo.|C57BL/6N|No|No|Yes|No|No|Yes|No|Unknown||||No|07-Mar-2017|Cryopreserved sperm|47.0|0.0|Unknown|||Yes| 8217.0|RCE:LoxP|B6.129P2-Gt(ROSA)26Sor/Anu||Recessive|gene trap ROSA 26, Philippe Soriano|Gt(ROSA)26Sor|Unknown|beta geo, Gtrgeo26, Gtrosa26, R26, ROSA26, Thumpd3as1 |MGI:104735|gene trap ROSA 26, Philippe Soriano; targeted mutation 1.1, Gordon Fishell|Gt(ROSA)26Sor|MGI:4412373|6|||||||||||||||||||||||||||||Unknown||C57BL/6J|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|15-Mar-2017||0.0|0.0|Unknown||dorsal root ganglion|Yes| 8209.0|Ngn3-GFP/RIP-DsRed|B6.Cg-Tg(Neurog3-GFP) Tg(Ins2-DsRed)#/Arc||Dominant||||||||||||||||||||||||||Green Fluorescent Protein|Neurog3|||||||||||Normal|Normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|10|||No|05-Mar-2017|Cryopreserved sperm|50.0|0.0|Unknown|||Yes| 8209.0|Ngn3-GFP/RIP-DsRed|B6.Cg-Tg(Neurog3-GFP) Tg(Ins2-DsRed)#/Arc||Dominant||||||||||||||||||||||||||DsRed|Rat insulin promoter (RIP)|||||||||||Normal|Normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|10|||No|05-Mar-2017|Cryopreserved sperm|||Unknown|||Yes| 8243.0|gp130Y757F x Asc KO|B6.129- Il6st Pycard/MarpApb||Recessive|interleukin 6 signal transducer|Il6st|Unknown|CD130, D13Ertd699e, gp130|MGI:96560|interleukin 6 signal transducer; targeted mutation 1, Matthias Ernst|Il6st|MGI:2388478|13||||||||||||||||Yes|||||||||||||Mice develop gastric tumours, emphysema and splenomegaly.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|10||heterozogous x homozygous|No|05-Apr-2017|Cryopreserved sperm|50.0|0.0|Yes||gp130|Yes| 8243.0|gp130Y757F x Asc KO|B6.129- Il6st Pycard/MarpApb||Recessive|PYD and CARD domain containing|Pycard|Nil|9130417A21Rik, Asc, TMS-1|MGI:1931465|PYD and CARD domain containing; targeted mutation 1, Gabriel Nunez|Pycard|MGI:3771030|7||||||||||||||||No|||||||||||||Mice develop gastric tumours, emphysema and splenomegaly.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|10||heterozogous x homozygous|No|05-Apr-2017|Cryopreserved sperm|||Yes||gp130|Yes| 8218.0|Roquin fl:Lck-cre|B6.Cg-Rc3h1 Tg(Lck-cre)157Jxm/AnuApb||Recessive|RING CCCH (C3H) domains 1|Rc3h1|Unknown|5730557L09Rik, roquin|MGI:2685397|RING CCCH (C3H) domains 1; targeted mutation 1.1, Carola Vinuesa|Rc3h1|MGI:5508920|1|||||||||||||||||targeted mutation I57, Jamey Marth; transgene insertion I57, Jamey Marth|mouse proximal Lck promoter|active in thymocytes and splenocytes|||||||||||No phenotypic analysis|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||15||No|19-Mar-2017|Cryopreserved sperm|84.0|0.0|Unknown||T cell, arthritis, autoimmunity, mRNA, stress granules|Yes| 8226.0|CD4cre:AhRflox|B6.129-Ahr Tg(Cd4-cre)1Cwi/MarpAnu||Recessive|aryl-hydrocarbon receptor|Ahr|Normal|Ah, Ahh, Ahre, bHLHe76, dioxin receptor, In|MGI:105043|aryl-hydrocarbon receptor; targeted mutation 3.1, Christopher A Bradfield|Ahr|MGI:3612477|12|||||||||||||||||transgene insertion 1, Christopher B Wilson||||||||||||||C57BL/6J|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|28-Mar-2017|Cryopreserved sperm|21.0|0.0|Unknown||Cd4, T cell|Yes| 8221.0|ASDxxx:TCF-Lef_H2B-GFP|STOCK Tg(TCF/Lef1-HIST1H2BB/EGFP)61Hadj/J||Dominant||||||||||||||||||||||||||transgene insertion 61, Anna-Katerina Hadjantonakis|T cell specific transcription factor/lymphoid enhancer-binding factor 1 (TCF/Lef1) DNA binding site and a heat shock protein 1B (Hspa1b) minimal promoter|||||||||||Mice homozygous for the transgene are viable, fertile, and normal in size.GFP expression is evident in cells of the extraembryonic visceral endoderm, the primitive streak, the mature node, presomitic mesoderm and newly formed somites, posterior neural plate, cranial neural crest, face, and branchial arches. By E12.5 fluorescence is also seen in the kidney, gonads, and some neuronal subsets in the brain.||Unknown|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|20-Mar-2017||0.0|0.0|Unknown||GFP, Wnt, transcription factor|Yes| 8225.0|ASD543:Weidenfeller:R78P-CC-Ins|C57BL/6NCrlAnu-Vps51/AnuApb||Recessive|VPS51 GARP complex subunit|Vps51|Unknown|1110014N23Rik, 3110057M17Rik|MGI:1915755||||19|ENSMUSG00000024797|ENSMUST00000159832.7|ps51-001||||||||||||||||||||||||||Unknown||C57BL/6NCrlAnu|Yes|Unknown|Yes|Yes|Unknown|Yes|No|Unknown||||No|27-Mar-2017|Cryopreserved sperm|48.0|0.0|Unknown|||Yes| 8249.0|ENU37:044|ENU37:044||Recessive|Unknown||||||||Unknown|||||||||||||||||||||||||||||Unknown|Normal|C57BL/6NCrlAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|28-Apr-2017|Cryopreserved sperm|46.0|0.0|Unknown||ENU|Yes| 8222.0|ENU35:014:Fam129c|C57BL/6NCrlAnu-Fam129c/AnuApb||Recessive|family with sequence similarity 129, member C|Fam129c|Unknown|Bcnp1|MGI:3686743||||8|ENSMUSG00000043243|ENSMUST00000143662.7|Fam129c-001|184|305|A to T|ENSMUSE00001283995|2|62|Lysine to STOP|||||ACCCAGCCGGATGCCAGCTGTCCCACACCAAAAAGCTGCCTCGAGTCAGGGAGCACCAAGG||||||||||||||Increased IgM expression on mature B cells in mice homozygous for the mutation, as measured by peripheral blood flow cytometry.|Normal|C57BL/6NCrlAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|21-Mar-2017|Cryopreserved sperm|24.0|0.0|Unknown||Immunoglobulin, B cell|Yes| 8220.0|ASD662:Casillas|C57BL/6NCrlAnu-Tirap/AnuApb||Recessive|toll-interleukin 1 receptor (TIR) domain-containing adaptor protein|Tirap|Unknown|C130027E04Rik, Mal, Mal, MyD88-adapter-like, wyatt|MGI:2152213||||9|||||||||||||||||||||||||||||Unknown|Normal|C57BL/6NCrlAnu|Yes|Unknown|Yes|Yes|Unknown|Yes|No|Unknown||||No|19-Mar-2017|Cryopreserved sperm|33.0|0.0|Unknown||CRISPR|Yes| 8826.0|CaMKK2 SD KI|CaMKK2 (S129D/S133D/S137D) KI||Recessive|CaMKK2|CaMKK2|||||||5|||||||||||||||||||||||||||||Normal|Normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|18-Nov-2019|Cryopreserved sperm|47.0|30.0|Unknown|||Yes| 8827.0|ASD534:C57BL/6-Ins2Akita/JArc:::G12|C57BL/6JArc-Ins2/AnuApb||Dominant|insulin II|Ins2||Ins-2, InsII, Mody, Mody4|MGI:96573|insulin II; Akita|Ins2|MGI:1857572|7|||||||||||||||||||||||||||||Postnatal lethality.Hyperglycemia:• blood glucose levels are slightly higher at 1 day of age and much higher at 14 days of age with no gender differences seen.Abnormal pancreatic alpha cell morphology: • alpha cell density is markedly increasedAbnormal pancreatic beta cell morphology: • density of beta cells is decreased within 24 hours of birth and at 2 weeks of age• beta cell granules are fewer in number and smaller and mitochondrial swelling and an increase in endoplasmic reticulum are seen at 2 weeks of ageSmall pancreatic islets:• islet area is reducedDecreased insulin secretion:• the pancreatic ratio of insulin to glucagon is decreased to 0.21 and 0.01 at birth and 14 days of age, respectively, compared to 1.17 and 1.11 in wild-type mice.Premature death:• untreated homozygous mice rarely survive past 12 weeks of age, with death resulting from extreme hyperglycemia;|unknown|C57BL/6J|No|No|Yes|No|No|Yes|No|Unknown||||No|20-Nov-2019|Cryopreserved sperm|58.0|0.0|Unknown||Hypoglycaemia|Yes| 8233.0|Smarta_Ly5a|B6.Cg-Ptprc Tg(TcrLCMV)Aox)/MarpAnu||Semi-dominant||||||||||||||||||||||||||transgene insertion, Annette Oxenius||||||||||||Expresses TCR specific for LCMV GP-derived epitpoe P13||C57BL/6J|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|28-Mar-2017||0.0|0.0|Unknown||LCMV, TCR|Yes| 8232.0|PD1 KO|B6.129S2-Pdcd1/HonRbrcMarpAnu||Recessive|programmed cell death 1|Pdcd1|Nil|PD-1, Pdc1|MGI:104879|programmed cell death 1; targeted mutation 1, Tasuku Honjo|Pcdc1|MGI:2386184|1|||||||||||||||||||||||||||||Arthritis:• increased layers of synovial tissues in foot joints at 6 months of age• arthritic lesions more pronounced at 14 months of ageGlomerulonephritis:• mild proliferative glomerulonephritis at 6 months age• less than 50% of glomeruli affected• by 14 months, 50% of mice with a lupus-like glomerulonephritisAbnormal response to transplant:• only about 80% of mice show long term MHC class II mismatch allograft survival (Bm12 into B6) compared to about 100% survival in wild-type mice• however, survival time of MHC class I mismatch allografts is the same as wild-type controls||C57BL/6J|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|28-Mar-2017|Cryopreserved sperm|79.0|0.0|Yes|systemic lupus erythematosus|Lupus, autoimmunity, T cell|Yes| 8230.0|hIL21R:OT1|B6-Il21r Tg(TcraTcrb)1100Mjb/MarpAnu||Recessive|interleukin 21 receptor|Il21r||NILR|MGI:1890475||||7|||||||||||||||||transgene insertion 1100, Michael J Bevan|H-2K promoter|||||||||||Carry OVA-specific, H-2K-restricted T cell receptor||C57BL/6J|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|28-Mar-2017|Cryopreserved sperm|84.0|0.0|No||T cell, receptor, ovalbumin, CD8|Yes| 8231.0|hIL21Tg_hIL21RKI_mIL21KO |B6-Il21 Tg(IL21R)/MarpAnu||Recessive|interleukin 21|Il21|||MGI:1890474||||3|||||||||||||||||human interleukin 21 receptor||||||||||||Unknown||C57BL/6J|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|28-Mar-2017||0.0|0.0|Unknown||IL21|Yes| 8235.0|Jalpha 33 knock out|C57BL/6-Traj33||Recessive|T cell receptor alpha joining 33|Traj33||Gm16666|MGI:4439590||||14|||||||||||||||||||||||||||||Normal|Normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|30-Mar-2017|Cryopreserved sperm|40.0|0.0|Unknown||T cell receptor|No| 8237.0||NOD-Gzma Tmem173||Recessive|Transmembrane protein 173|Tmem173|Unknown|2610307O08Rik, ERIS, MPYS, Sting|MGI:1919762||||18|||||||||||||||||||||||||||||Unknown|Unknown|NOD/LtJ|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|31-Mar-2017|Cryopreserved sperm|50.0|0.0|Yes|Type 1 diabetes||No| 8237.0||NOD-Gzma Tmem173||Recessive|granzyme A|Gzma|Unknown|BLT esterase, Ctla3, Ctla-3, Hanukah factor, Hf, H factor, SE1, serine esterase 1, TSP1, TSP-1|MGI:109266||em3Tcb||13|||||||||||||||||||||||||||||Unknown|Unknown|NOD/LtJ|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|31-Mar-2017|Cryopreserved sperm|||Yes|Type 1 diabetes||No| 8242.0|Cntnap2 KO|B6.129(Cg)-Cntnap2/JAnu||Recessive|contactin associated protein-like 2|Cntnap2|Nil|5430425M22Rik, Caspr2, mKIAA0868|MGI:1914047|contactin associated protein-like 2; targeted mutation 1, Elior Peles|Cntnap2|MGI:2677631|6|||||||||||||||||||||||||||||Seizures:• mutants older than 6 months of age commonly exhibit spontaneous seizuresEnvironmentally induced seizures:• seizures are induced by mild stressors during routine handlingAbnormal brain interneuron morphology:• mutants exhibit a reduction in parvalbumin+ interneurons in the hippocampus• mutants exhibit a decrease in the number of GABAergic interneurons in all laminae and in the striatumAbnormal corpus callosum morphology:• ectopic neurons are seen in the corpus callosum of mutants at P14; ectopic neurons are seen through adulthoodAstrocytosis:• reactive astrocytosis is seen throughout the hippocampus after onset of seizures, especially in the hilus• however, neuronal loss is not seen in the hippocampusAbnormal brain wave pattern:• at 8 months of age, freely moving mutants exhibit generalized interictal spike discharges during slow-wave sleepAbnormal neuron physiology:• mutants exhibit reduced cortical neuronal synchrony as indicated by two-photon calcium imaging of layer II/III neurons from somatosensory cortex showing that neuronal firing pattern is highly asynchronous compared to wild-type mice• however, neither the average firing amplitude nor the average firing rate are changed, suggesting that the defect is due to a network dysfunction rather than abnormalities in neuronal activity or conduction per seAbnormal neuronal migration:• ectopic neurons are seen in the corpus callosum of mutants at P14• mutants exhibit abnormal migration of cortical projection neurons as evidenced by the higher numbers of CUX1+ cells in deep cortical layersAbnormal olfaction:• mutants perform better than wild-type mice in the buried food test, indicating better olfactionBehavior/neurological phenotype:N • no differences are seen in the light-dark exploration test between mutants and wild-type mice• mutants treated with the drug Risperidone exhibit rescue of the hyperactivity, repetitive behavior/perseveration and nesting deficitsAbnormal inhibitory learning:• mutants perform similarly to wild-type mice in the Morris water maze probe trials, however in a classic reversal task using the Morris water maze, mutants show impaired learning of the new location of the platform and perform poorly in the probe testIncreased grooming behavior:• mutants spend almost 3 times more time grooming than wild-type miceAbnormal motor coordination/ balance:• mutants perform better than wild-type mice on the rotorodHyperactivity:• mutants show greater locomotor activity than wild-type mice in the open field test• mutants treated with the drug Risperidone exhibit rescue of the hyperactivityIncreased stereotypic behaviour:• in the spontaneous alternation T maze test, mutants show higher number of no alternations in a standard 10 trial test, indicating preservation• mutants treated with the drug Risperidone exhibit rescue of the repetitive behavior/perseverationDecreased thermal nociceptive threshold:• mutants exhibit hyperreactivity to thermal sensory stimuli• however, no differences seen in the acoustic startle response or prepulse inhibitionAbnormal nest building behaviour:• mutants are impaired in nest-building behavior, scoring less than half of the wild-type criterion• mutants treated with the drug Risperidone exhibit rescue of the nesting deficitsSocial withdrawal:• in a juvenile play test, mutants at P21 spend less time interacting with each other and instead show increased repetitive behaviors such as grooming and digging• in a three-chamber social interaction test in adults, mutants do not show a preference for the cup with a mouse as seen in wild-type miceDecreased vocalization:• mutants emit a lower number of ultrasonic calls than wild-type mice at all ages||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|31-Mar-2017||0.0|50.0|Unknown||K+ channel, myelin, axon|Yes| 8829.0|ASD091:NOD/Scid:::EXP|NOD.CB17-Prkdc/AnuApb||Dominant|protein kinase, DNA activated, catalytic polypeptide|Prkdc|Unknown|DNAPDcs, DNA-PK, DNA-PKcs, DOXNPH, dxnph, slip, XRCC7|MGI:104779|protein kinase, DNA activated, catalytic polypeptide; severe combined immunodeficiency|Prkdc|MGI:1857113|16|||||||||||||||||||||||||||||premature death:• average lifespan in SPF housing is 257 days for females and 269 days for males• the major cause of death is thymic lymphoma• median life span is 37 weeks; death is a result of thymic lymphomasAbnormal thymus lobule morphology: • thymic lobes are small and may contain cystsAbnormal thymus corticomedullary boundary morphology: • the cortico-medullary junction is not demarcated in tissues from a 10 week old female.Thymus cysts:• may be presentIncreased granulocyte number:• Gr1+ splenic and bone marrow granulocytes are increased in comparison to controlDecreased lymphocyte cell number:• percentages of circulating lymphocytes are significantly decreased in comparison to control, however, percentages of monocytes, neutrophils and eosinophils are increased and total peripheral leukocyte counts are similar• thymus, spleen and lymph nodes are depleted of lymphoid cells.Decreased B cell number:• B220+ splenic B cells are decreased (36.0% vs. 10.4%) in comparison to NOD control as measured by flow cytometryDecreased mature B cell number:• spleens are deficient in B220+ IgK+ B cellsDecreased pre-B cell number:• there is a significant absence of splenic B cells bearing the Ig kappa light chain (30.7% vs. 2.8%)• B220+ bone marrow pre-B cells are decreased in number (19.0% vs. 10.2%)Decreased NK cell number:• no NK1.1+ splenic NK cells were detected by flow cytometry, however some NK cell activity is detected.Decreased T cell number:• significant numbers of CD3+ splenic T cells are absent in comparison to control (44.9% vs. 0.2%)Decreased CD4-positive, alpha beta T cell number:• spleens are deficient in mature T cellsDecreased CD8-positive, alpha-beta T cell number: • spleens are deficient in mature T cellsIncreased macrophage cell number:• F4/80+ splenic macrophages are increased in comparison to controlSpleen hypoplasia:• spleen cellularity is decreased four fold in comparison to NOD control• splenic follicles are hypoplasticAbnormal spleen white pulp morphology:• splenic follicles exhibit a marked loss of lymphoid cells, however, red pulp is normal• splenic follicles are hypoplasticDecreased immunoglobulin level:• only 1/11 homozygotes can produce greater than 1 ug/ml serum Ig at up to 100 days of age• only 2/30 homozygotes can produce greater than 1 ug/ml serum Ig between 100-200 days of ageImpaired natural killer cell mediated cytotoxicity :• Background Sensitivity: NK cell activity in homozygous spleen cell suspensions is markedly decreased in comparison to homozygotes on the CB17 backgroundAbnormal lymph node morphology:• lymph nodes lack follicles and consist mostly of stromal cells• lymph nodes are hypocellularDecreased level of surface class I molecules.Impaired complement classical pathway:• complement activity is not detected in either homozygous or control sera using a 51Cr-release assayAbnormal response to transplant:• following injection of human T lymphoblastoid cells, 80% of nucleated spleen cells are of human origin by 4 weeks post injection• peripheral blood has a five fold increase of human cells by 4 weeks post injection• mice support CD34+ human stem cell engraftment, although not as well as mice homozygous for Il2rg and Prkdc• human CD45+ cells comprise 5.2% of cells in the spleen, 6.2% in bone marrow, 0.4% in thymus at 10 weeks post-engraftment.Increased length of allograft survival:• homozygotes (5-6 weeks of age) do not reject orthotopic tail skin allografts throughout a 3 month observation period||NOD|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|25-Nov-2019|Cryopreserved sperm|60.0|0.0|Unknown||scid, T cell, B cell|Yes| 8241.0|TgDNPKR|C57BL/6-Tg(Vav1-EIF2AK2*K296R)1Wsmay/JAnu||Dominant||||||||||||||||||||||||||transgene insertion 1, W May|mouse vav 1 oncogene|||||||||||Mice express a catalytically-null/dominant-negative (K296R) mutant variant of human PKR (DNPKR) exclusively in hematopoietic cells/tissues under control of the mouse HS21/45-vav regulatory elements.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|31-Mar-2017|Cryopreserved sperm|55.0|0.0|Unknown||interferon, infection|Yes| 8238.0|Goldenticket|C57BL/6J-Tmem173/JAnu||Recessive|transmembrane protein 173|Tmem173|Nil|2610307O08Rik, ERIS, MPYS, Sting|MGI:1919762|transmembrane protein 173; goldenticket|Tmem173|MGI:4939597|18|||||||||||||||||||||||||||||Transmembrane protein 173; goldenticket (Tmem173gt) mice do not produce IFN-β in response to cyclic dinucleotides or Listeria monocytogenes infection, and may be useful in studies of cytosolic detection of pathogen DNA and innate immune response. ||C57BL/6J|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|31-Mar-2017||0.0|0.0|Unknown||infection, interferon, c-di-GMP|Yes| 8239.0|Mb21d1-KO |B6(C)-Mb21d1/JAnu||Recessive|Mab-21 domain containing 1|Mb21d1||cGas, E330016A19Rik|MGI:2442261|Mab-21 domain containing 1; targeted mutation 1d, Helmholtz Zentrum Muenchen GmbH|Mb21d1|MGI:5578170|9|||||||||||||||||||||||||||||Mb21d1 (cGAS) knockout mice exhibit increased susceptibility to DNA viruses (murine gamma-herpesvirus 68 and vaccinia virus), and to West Nile virus. ||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|31-Mar-2017||0.0|0.0|Unknown||Infection, interferon|Yes| 8240.0|TgPKR|C57BL/6-Tg(Vav1-EIF2AK2)#Wsmay/JAnu||Dominant||||||||||||||||||||||||||transgene insertion, W May|mouse vav 1 oncogene|||||||||||TgPKR mice express wildtype (catalytically-active) human PKR exclusively in hematopoietic cells/tissues under control of the mouse HS21/45-vav regulatory elements. This PKR overexpression results in significantly defective hematopoiesis, bone marrow failure and increased sensitivity to apoptosis-inducing cell stress. These TgPKR mice may be useful in studying increased PKR activity in diseases such as myelodysplastic syndrome (MDS). ||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|31-Mar-2017||0.0|0.0|Unknown||infection, interferon|Yes| 8236.0|IFNAR-/- IFNGR-/- ADAR1 E861A/+|B6-Ifnar1 Ifngr1 Adar||Recessive|interferon (alpha and beta) receptor 1|Ifnar1|Nil|Ifar, IFN-alpha/betaR, Ifrc |MGI:107658|interferon (alpha and beta) receptor 1; targeted mutation 1, Michel Aguet|Ifnar1|MGI:1930950|16|||||||||||||||||||||||||||||Homozygous triple nulls are not viable (embryonic lethal - time point not determined yet).|Viable, fertile and apparently normal|C57BL/6|No|No|Yes|No|No|Yes|No|Unknown||||No|31-Mar-2017|Cryopreserved sperm|50.0|0.0|Unknown|||Possibly| 8236.0|IFNAR-/- IFNGR-/- ADAR1 E861A/+|B6-Ifnar1 Ifngr1 Adar||Recessive|interferon gamma receptor 1|Ifngr1 |Nil|CD119, Ifgr, IFN-gammaR, IFN-gamma R, Ifngr, Nktar|MGI:107655|interferon gamma receptor 1; targeted mutation 1, Michel Aguet|Ifngr1|MGI:1857286|10|||||||||||||||||||||||||||||Homozygous triple nulls are not viable (embryonic lethal - time point not determined yet).|Viable, fertile and apparently normal|C57BL/6|No|No|Yes|No|No|Yes|No|Unknown||||No|31-Mar-2017|Cryopreserved sperm|||Unknown|||Possibly| 8236.0|IFNAR-/- IFNGR-/- ADAR1 E861A/+|B6-Ifnar1 Ifngr1 Adar||Recessive|adenosine deaminase, RNA-specific|Adar |Nil|ADAR1, Adar1p110, Adar1p150, mZaADAR Feature Type |MGI:1889575|adenosine deaminase, RNA-specific; targeted mutation 1.1, Taconic Biosciences|Adar|MGI:5805648|3|||||||||||||||||||||||||||||Homozygous triple nulls are not viable (embryonic lethal - time point not determined yet).|Viable, fertile and apparently normal|C57BL/6|No|No|Yes|No|No|Yes|No|Unknown||||No|31-Mar-2017|Cryopreserved sperm|||Unknown|||Possibly| 4864.0|Kumba: 129SvEv|129/SvEv.Cg-Zic2/AnuApb|129/SvEv.Cg-Zic2/AnuApb|Recessive|zinc finger protein of the cerebellum 2|Zic2|Unknown|GENA 29, Ku, odd-paired homolog|MGI:106679|kumba|Zic2|MGI:1862004|14||||||||||||||||Yes|||||||||||||Lethal during embryogenesis|Incomplete penetrance and variable expressivity of the following: ventral spot, curled tail, distal tail kink, spina bifida (rare).|129SvEv|No|No|Yes|No|No|Yes|No|Good|30||Heterozygote male paired with wild-type 129/SvEv female|No|24-Sep-2009|Cryopreserved sperm|80.0|0.0|Yes|Holoprosencephaly and spina bifida|Gastrulation, Neuralation, holoprosencephaly|Yes| 8253.0|Warpy B6|B6(Cg)-Dzip1l/AnuUqApb||Recessive|DAZ interacting protein 1-like|Dzip1l|||MGI:1919757|DAZ interacting protein 1-like; Warpy|Dzip1l|MGI:5563494|9|ENSMUSG00000037784|ENSMUST00000078367|Dzip-1l-001|1123|1326|C to T|ENSMUSE00000325142|8|375|Glutamine to STOP|||||TGTCTCAGGACCAGAAGAAAGCAGCTGCCCAGTCTCAGCGCCATATCAATGCCCTCCGTGC|Yes|||||||||||||Polydactlyly and craniofacial dismorphology in embryos at e14.5.Extra digits on each limb some have 6 some have 7) and there is a craniofacial dismorphology (the front of the head protrudes, the eye position is changed and there is a mandible malformation.|Normal|C57BL/6JUq|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Excellent|10|||No|08-May-2017|Cryopreserved sperm|40.0|0.0|Unknown||polydactyly, ENU|No| 8255.0|Vil1-cre|B6.Cg-Tg(Vil1-cre)1000Gum/J||Dominant||||||||||||||||||||||||||transgene insertion 1000, Deborah L Gumucio|Vilin1|||||||||||Normal||C57BL/6J|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|12-May-2017|Cryopreserved sperm|59.0|0.0|Unknown||Cre recombinase|Yes| 8252.0|Warpy CD1|CD1-Dzip1l/AnuUqApb||Recessive|DAZ interacting protein 1-like|Dzip1l|||MGI:1919757|DAZ interacting protein 1-like; Warpy|Dzip1l|MGI:5563494|9|ENSMUSG00000037784|ENSMUST00000078367|Dzip-1l-001|1123|1326|C to T|ENSMUSE00000325142|8|375|Glutamine to STOP|||||TGTCTCAGGACCAGAAGAAAGCAGCTGCCCAGTCTCAGCGCCATATCAATGCCCTCCGTGC|Yes|||||||||||||Polydactlyly and craniofacial dismorphology in embryos at e14.5.Extra digits on each limb some have 6 some have 7) and there is a craniofacial dismorphology (the front of the head protrudes, the eye position is changed and there is a mandible malformation.|Normal|CD1|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Excellent|10|||No|08-May-2017|Cryopreserved sperm|50.0|0.0|Unknown||polydactyly, ENU|No| 8250.0|Ywhaz-EUCE0076e02|129(Cg)-Ywhaz||Recessive|tyrosine 3-monooxygenase/tryptophan 5-monooxygenase activation protein, zeta polypeptide|Ywhaz|Unknown|1110013I11Rik, 14-3-3 zeta|MGI:109484|tyrosine 3-monooxygenase/tryptophan 5-monooxygenase activation protein, zeta polypeptide; gene trap EUCE0076e02, Helmholtz Zentrum Muenchen GmbH|Ywhaz|MGI:4393774|15|||||||||||||||||||||||||||||Unknown, we have not been able to generate homozygous mutants for this line.|In Heterozygous state the mice are smaller than WT, some have hind limb paralysis, and do not socialise with littermates.|129Sv|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|04-May-2017|Cryopreserved sperm|60.0|0.0|Unknown||signal transduction|Yes| 8254.0||ASD733:Forge:::F0||Recessive|RING CCCH (C3H) domains 1|Rc3h1||5730557L09Rik, roquin|MGI:2685397||||1|||||||||||||||||||||||||||||Unknown|TBA|C57BL/6NCrlAnu|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|12-May-2017|Cryopreserved sperm|11.0|0.0|Unknown|||No| 8245.0|ENU32:096:Pank4|C57BL/6NCrlAnu-Pank4/AnuApb||Recessive|pantothenate kinase 4|Pank4|Unknown|D030031I12Rik|MGI:2387466||||4|ENSMUSG00000029056|ENSMUST00000030931.10|Pank4-001|625|648|T to C|ENSMUSE00000231970|5|209|Phenylalanine to Leucine|||||CCATCGTGAAGGTGGAGACAGAGGACCGGTTTGAGTGGATTGGTGGAAGCTCCATTGGAGG||||||||||||||Normal|Normal|C57BL/6NCrIAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|19-Apr-2017|Cryopreserved sperm|36.0|0.0|Unknown|||Yes| 8831.0|ASD902:Durian:SO54|C57BL/6NCrlAnu-Socs1/AnuApb||Recessive|suppressor of cytokine signaling 1|Socs1|Unknown|Cish1, Cish7, JAB, JAK2-binding protein, JAK-binding protein, SOCS-1, SSI-1, STAT-induced STAT inhibitor 1|MGI:1354910|Socs1; endonuclease-mediated mutation 1, Australian National University|Socs1||16||||||||||Unknown to Unknown|||||||||||||||||||Unknown|Unknown|C57BL/6NCrlAnu|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|28-Nov-2019|Cryopreserved sperm|58.0|70.0|Unknown|||Yes| 8832.0|Csf2rb fl/fl|C57BL/6N-Csf2rb||Recessive|colony stimulating factor 2 receptor, beta, low-affinity (granulocyte-macrophage)|Csf2rb||AIC2B, Bc, beta c, CDw131, common beta chain, Csf2rb1, Il3r, Il3rb1, Il5rb|MGI:1339759|colony stimulating factor 2 receptor, beta, low-affinity (granulocyte-macrophage); targeted mutation 1c, Helmholtz Zentrum Muenchen GmbH|Csf2rb|MGI:5792881|15|||||||||||||||||||||||||||||Normal|Normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|04-Dec-2019|Cryopreserved sperm|50.0|0.0|Unknown||GM-CSF|Yes| 8259.0|PbT-II|C57BL/6-Tg(Tcra,TcrbPbA)1Cbn||Dominant||||||||||||||||||||||||||T cell receptor alpha, T cell receptor beta||||||||||||Expression of a TCR specific for the malaria parasite Plasmodium||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|24-May-2017|Cryopreserved sperm|14.0|0.0|Unknown|||Yes| 8262.0|Nlrc4 KO|B6(Cg)-Nlrc4/VmdUqAnu||Recessive|NLR family, CARD domain containing 4|Nlrc4|Nil|9530011P19Rik, Card12, Ipaf|MGI:3036243|NLR family, CARD domain containing 4; targeted mutation 1, Vishva M Dixit|Nlrc4|MGI:3046934|17|||||||||||||||||||||||||||||Abnormal cell death:• caspase dependent cell death resulting from infection with Salmonella typhimurium reduced to minor levelsDecreased interleukin-1 beta secretion:• negligible amounts of Il-1beta produced when infected with Salmonella typhimurium||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|31-May-2017|Cryopreserved sperm|23.0|0.0|Unknown||Apaf-1, Caspase, Toll|Yes| 8263.0|Asc KO|B6.129-Pycard/VmdUqAnu||Recessive|PYD and CARD domain containing|Pycard|Nil|9130417A21Rik, Asc, TMS-1|MGI:1931465|PYD and CARD domain containing; targeted mutation 1, Vishva M Dixit|Pycard|MGI:3046932|7|||||||||||||||||||||||||||||Abnormal macrophage physiology:• improved bone marrow derived macrophage viability following infection with F. tularensisDecreased circulating interleukin-1 beta level:• in response to LPS challenge in a model of acute septic shockDecreased circulating interleukin-18 level:• in response to LPS challenge in a model of acute septic shockIncreased interferon-beta secretion:• in bone marrow derived macrophages stimulated by poly(dA:dT) or pcDNA3Decreased interleukin-1 beta secretion:• in LPS-primed bone marrow derived macrophages stimulated by S. typhimurium or dsDNA• bone marrow derived macrophages do not secrete IL1B in response to F. tularensis• from LPS-primed bone marrow-derived macrophages stimulated with E. coli, C. rodentium, C. cholera and CTBIncreased tumor necrosis factor secretion:• in bone marrow derived macrophages stimulated by poly(dA:dT) or pcDNA3Decreased susceptibility to endotoxin shock:• mice treated with LPS challenge in a model of acute septic shock exhibit reduced serum levels of IL1b and IL18 compared with controls• however, mice do not survive beyond 20 hours and serum levels of IL1a are increased||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|31-May-2017|Cryopreserved sperm|10.0|0.0|Unknown||Toll, caspase, interleukin, inflammasome|Yes| 5150.0|McBride|C;B6-Myd88/AnuApb||Recessive|myeloid differentiation primary response gene 88|Myd88|Nil||MGI:108005|myeloid differentiation primary response gene 88; targeted mutation 1, Shizuo Akira|Myd88|MGI:2385681|9||||||||||||||||Yes|||||||||||||Increased apoptosis:* 5 days after lung injury, mutants show significantly increased numbers of apoptotic lung epithelial and inflammatory cells.Increased physiological sensitivity to xenobiotics:* knockout mice are more susceptible to bleomycin-induced lung injury.Abnormal dendritic cell differentiation:* dendritic cell maturation fails to occur in vivo upon exposure to TLR9 agonists.Increased dendritic cell number:* increased numbers of dendritic cells in brains of mice infected with Plasmodium.Abnormal immune system physiology:* response to LPS and CpG is completely abrogatedAbnormal dendritic cell physiology:* cytokine secretion elicited by zymosan or LPS is impaired.* following infection with attenuated yellow fever vaccine 17D (YF-17D), dendritic cells produce less IL-12p40, IL-6 and interferon-gamma relative to wild-type mice.Abnormal macrophage physiology:* TNF production is impaired in thioglycollate-elicited macrophages treated with intact zymosan.* cytokine production by macrophages cultured with P. carinii cysts is reduced compared to wild-type.Abnormal NK cell physiology:* NK cells fail to make IFN-gamma in response to injections of TLR9 agonists.Abnormal T cell physiology:* induction of the antigen-specific CD8+ T-cell response by immunizing with soluble ovalbumin and TLR9 agonists, but not TLR2 and TLR6 agonists, was severely impaired.Abnormal cytokine secretion:* LPS-induced cytokine production by BMDCs is almost abolished compared to controls and Myd88-sufficient mutantsAbnormal chemokine secretion:* hyaluronan fragment-induced expression of chemokines by peritoneal macrophages is completely abolished in double knockout mice.Decreased interferon-alpha secretion:* CpG-A or RNA polyuridylic acid induced production of interferon-alpha was abolished in plasmacytoid dendritic cells.Decreased interferon-gamma secretion:* less up regulation of INF-gamma in Plasmodium infection.* following infection with attenuated yellow fever vaccine 17D (YF-17D), dendritic cells produce less interferon-gamma.Decreased interleukin-12 secretion:* after stimulation with zymosan, TNF production is significantly reduced in Myd88-deficient animals.Decreased interleukin-12b secretion:* less upregulation of IL-12b in Plasmodium infection>* following infection with attenuated yellow fever vaccine 17D (YF-17D), dendritic cells produce less IL-12p40 relative to wild-type mice.Decreased interleukin-6 secretion:* following treatment with PbA(Plasmodium bergbei ANKA)-parasitized erythrocytes or LPS-stimulation, IL-6 secretion is reduced.* following infection with attenuated yellow fever vaccine 17D (YF-17D), dendritic cells produce less IL-6 relative to wild-type mice.Decreased tumor necrosis factor secretion:* less upregulation of TNF-alpha in Plasmodium infection.* following treatment with PbA(Plasmodium bergbei ANKA)-parasitized erythrocytes or LPS-stimulation, TNF secretion is reduced.* after stimulation with zymosan, TNF production is significantly reduced in Myd88-deficient animals.Decreased inflammatory response:* in a model of induced pneumococcal meningitis-associated labyrinthitis, homozygotes exhibit a significantly lower granulocytic infiltration of the labyrinth and increased bacterial density in the cochlea at 24 hrs post-infection relative to wild-type control mice.Abnormal response to infection:* following treatment with PbA (Plasmodium bergbei ANKA)-parasitized erythrocytes, mice have a decreased immune response in terms of TNF and IL-6 secretion and response to CpG.Decreased susceptibility to parasitic infection:* resistant to cerebral malaria but eventually die of extremely high parasitemia.Increased susceptibility to viral infection:* increased susceptibility to encephalomyocarditis virus (EMCV) infection compared to wildtype.||BALB/c x C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|09-Jun-2010|Cryopreserved sperm|40.0|0.0|Unknown||T cell, Natural Killer, IL-18, IL-1 receptor, interferon, eosinophil, dendritic cell, cytokine, infection|Yes| 8261.0||NOD-Ins1/Tkay||Recessive|insulin I|Ins1|||MGI:96572|INS knockin|||19|||||||||||||||||||||||||||||Normal|Normal|NOD/Lt|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|25-May-2017|Cryopreserved sperm|50.0|0.0|Unknown||insulin|Yes| 8257.0|ENU35:042:Ifih1|C57BL/6NCrlAnu-Ifih1/AnuApb||Recessive|interferon induced with helicase C domain 1|Ifih1|Unknown|9130009C22Rik, Helicard, MDA5, MDA-5|MGI:1918836||||2|||||||||||||||||||||||||||||Mice exhibit activated lymphocytes in peripheral blood and require ethical culling around 6 months of age due to poor health||C57BL/6NCrlAnu|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|19-May-2017|Cryopreserved sperm|95.0|0.0|Unknown||Lymphocyte|Yes| 8258.0||ASD696:Thunderbird:1del::F2||Recessive||||||||||||||||||||||||||||||||||||||Unknown||C57BL/6NCrlAnu|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|22-May-2017|Cryopreserved sperm|24.0|0.0|Unknown||CRISPR|Yes| 8060.0|Thy1-GFP|STOCK Tg(Thy1-EGFP)MJrs/J||Dominant||||||||||||||||||||||||||transgene insertion M, Joshua R Sanes|Thy1, thymus cell antigen 1, theta, mouse, laboratory|||||||||||Unknown|Mice harboring the Thy1-GFP transgene are viable and fertile with enhanced green fluorescent protein (EGFP) expression under the control of a modified Thy1 promoter region (containing the sequences required for neuronal expression but lacking the sequences required for expression in non-neural cells). Homozygous or hemizygous Thy1-GFP mice derived from founder line M (Thy1-GFP-M or Thy1-GFPM) express EGFP in sparse subsets of neurons within specific populations; providing a bright, vital Golgi-like stain. Less than 10% of all motor axons, retinal ganglion cells, lumbar dorsal root ganglion, and cortex express EGFP. These Thy1-GFPM transgenic mice may be useful in neurobiological studies for fluorescent labeling of neural tissues, especially for mossy fibers in the cerebellum and intense, yet sparse, labeling of a variety of neuronal subsets. |C57BL/6J|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|30-Jun-2016|Cryopreserved sperm|50.0|0.0|Unknown||GFP|No| 8061.0|Thy1-YFP|B6.Cg-Tg(Thy1-YFP)HJrs/JApb||Dominant||||||||||||||||||||||||||transgene insertion H, Joshua R Sanes|Thy1, thymus cell antigen 1, theta, mouse, laboratory|||||||||||Unknown|These thy1-YFP-H transgenic mice express yellow fluorescent protein at high levels in motor and sensory neurons, as well as subsets of central neurons. Axons are brightly fluorescent all the way to the terminals. This line provides a strong and specific "Golgi-like" vital marker for several widely studied neuronal subsets, with minimal labeling of nearby axons. |C57BL/6J|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|30-Jun-2016|Cryopreserved sperm|50.0|0.0|Unknown|||No| 8264.0||Adidas #81||Recessive|nuclear factor of kappa light polypeptide gene enhancer in B cells 2, p49/p100|Nfkb2|Unknown|NF kappaB2, p52|MGI:1099800||||19|||||||||||||||||||||||||||||Unknown||C57BL/6NCrlAnu|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|02-Jun-2017||0.0|0.0|Unknown||CRISPR|Yes| 1523.0|Yaa|BXSB/MpJ||Dominant|accelerated autoimmunity and lymphoproliferation transposition|Yaa|Unknown|Tp(X;Y)1Ekw|MGI:99140|accelerated autoimmunity and lymphoproliferation|Yaa|MGI:1856277|Y||||||||||||||||Yes|||||||||||||Mutant males have accelerated autoimmunity, lymphoproliferation, splenomegaly, hemolytic anemia, hypergammaglobulinemia and glomerulonephritis. The syndrome is strain-dependent, requiring presence of certain autosomal allelic combinations.Males have premature death - half the life span of females.||BXSB/MpJ|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|05-Jul-2007|Cryopreserved sperm|120.0|0.0|Unknown||Monocytes, T cell, lymphoma, glomerulonephritis, autoantibody, splenomegaly|Yes| 4796.0|NODLt|NOD/Lt||Dominant||||||||||||||||||||||||||||||||||||||Predisposed to diabetes||NOD/Lt|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|06-Sep-2009|Cryopreserved sperm|150.0|0.0|Unknown||NOD|No| 8087.0|RHBDF1_PKD_2|C57BL/6-Rhbdf12/MarpApb||Recessive|rhomboid 5 homolog 1|Rhbdf1|Unknown|Dist, Dist1, Egfr-rs|MGI:104328||||11|ENSMUSG00000020282|ENSMUST00000020524.14|Rhbdf1-006|584|740|C to T|ENSMUSE00001312827|5|195|Serine to Phenylalanine|||||TGCAGCCTCCCTCTGCTCTTTCTCCAGCTCCCGCTCAGGTTTCAACCGACTCCCTCGGCGT||||||||||||||Unknown|Unknown|C57BL/6|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|24-Aug-2016|Cryopreserved sperm|50.0|0.0|Unknown|||Yes| 8172.0|Prox1enhCRISPR-Rafiki|C57BL/6-Prox1||Recessive|prospero homeobox 1|Prox1|Unknown|A230003G05Rik|MGI:97772||||1|||||||||||||||||||||||||||||Unknown|Unknown|C57BL/6|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|23-Jan-2017|Cryopreserved sperm|50.0|0.0|Unknown|||Yes| 10429.0|BCL6-flox:FoxP3-cre|B6.129-Bcl6 Foxp3/Anu||Recessive|B cell leukemia/lymphoma 6|Bcl6||Bcl5|MGI:107187|B cell leukemia/lymphoma 6; targeted mutation 1.1, Alexander Dent|Bcl6|MGI:5518542|16|ENSMUSG00000022508|ENSMUST00000023151|||||||||||||||||||||||||||TFR cell development blocked|Normal|C57Bl/6N|Yes|Unknown|Yes|Yes|Unknown|Yes|No|Unknown||||No|14-Jun-2024|Cryopreserved sperm|33.0|0.0|Unknown|||Possibly| 10429.0|BCL6-flox:FoxP3-cre|B6.129-Bcl6 Foxp3/Anu||Recessive|forkhead box P3|Foxp3||JM2, scurfin|MGI:1891436|forkhead box P3; targeted mutation 4, Alexander Y Rudensky|Foxp3|MGI:3790499|X|ENSMUSG00000039521||||||||||||||||||||||||||||TFR cell development blocked|Normal|C57Bl/6N|Yes|Unknown|Yes|Yes|Unknown|Yes|No|Unknown||||No|14-Jun-2024|Cryopreserved sperm|||Unknown|||Possibly| 4466.0|B10.PD1|C57BL/10-Tg(PD1)/AnuApb||Dominant||||||||||||||||||||||||||porcine class I major histocompatibility complex (SLA) gene||||||||||||This transgenic mouse expressed SLA antigen on its cell surfaces and transmitted the gene to offspring, in which the gene is also expressed. Skin grafts of such transgenic mice were rejected by normal C57BL/10 mice, suggesting that the foreign SLA antigen expressed in the transgenic mice is recognized as a functional transplantation antigen.||C57BL/10|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|22-Feb-2009|Cryopreserved sperm|150.0|0.0|Unknown||xenotransplant, transplantation, class I, porcine, major histocompatibility class (MHC)|Yes| 8182.0|Tap1/Tap2 KO x Tg(hTAP1/hTAP2) BAC #1|C57BL/6J-Tap1/Tap2 Tg(hTAP1/hTAP2)18/1MarpAnu||Recessive|transporter 1, ATP-binding cassette, sub-family B (MDR/TAP)|Tap1|Nil|Abcb2, Ham1, Ham-1, MTP1, PSF-1, RING4, TAP, Tap-1|MGI:98483||||17|||||||||||||||||human transporter 1, ATP-binding cassette, sub-family B (MDR/TAP) / human transporter 2, ATP-binding cassette, sub-family B (MDR/TAP)||||||||||||Unknown|Unknown|C57BL/6J|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|07-Feb-2017|Cryopreserved sperm|9.0|0.0|Unknown|||Yes| 8182.0|Tap1/Tap2 KO x Tg(hTAP1/hTAP2) BAC #1|C57BL/6J-Tap1/Tap2 Tg(hTAP1/hTAP2)18/1MarpAnu||Recessive|transporter 2, ATP-binding cassette, sub-family B (MDR/TAP)|Tap2|Nil|Abcb3, Ham2, Ham-2, HAM2, MTP2, PSF2, Tap-2|MGI:98484||||17|||||||||||||||||||||||||||||Unknown|Unknown|C57BL/6J|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|07-Feb-2017|Cryopreserved sperm|||Unknown|||Yes| 8202.0|Ryr2 Y2932H ; ASD589:Mystique|C57BL/6-Ryr2/AnuApb||Recessive|ryanodine receptor 2, cardiac|Ryr2|Unknown|9330127I20Rik|MGI:99685||||13|||||||||||||||||||||||||||||Unkown|Unkown|C57BL/6|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|27-Feb-2017|Cryopreserved sperm|34.0|0.0|Unknown||CRISPR|Yes| 4088.0||KRN:001||Recessive|||||||||Unknown||||||||||||||||Yes|transgene insertion KRN, Diane Mathis|Natural TCR alpha and -beta promoter/enhancer elements.|||||||||||Hypo response post arthritogenic serum transfer. Candidate gene position likely to be Chr 6 or 14.||C57BL/6 x NODk x C57BL/10 x Balb/b|Yes|Yes|Yes|Yes|Yes|Yes|No|Poor||||No|04-Dec-2008|Cryopreserved sperm|30.0|0.0|Yes||Autoimmunity, Arthritis, KRN, ENU, Serum transfer|No| 4083.0||ENU7PMH:118, Metabolic_Lean_1||Recessive|||||||||Unknown||||||||||||||||Yes|||||||||||||Low percentage of body fat when fed on a high fat diet.||C57BL/6 x C57BL/10|Yes|Yes|Yes|Yes|Yes|Yes|No|Poor||3||No|04-Dec-2008|Cryopreserved sperm|20.0|0.0|Yes||ENU, obesity, diet, fat, adipose|No| 4084.0||ENU7PMH:133, Metabolic Lean 2||Recessive|||||||||Unknown||||||||||||||||Yes|||||||||||||Low percentage of body fat when fed on a high fat diet.||C57BL/6 x C57BL/10|Yes|Yes|Yes|Yes|Yes|Yes|No|Poor||||No|04-Dec-2008|Cryopreserved sperm|30.0|0.0|Yes||ENU, Obesity, Diet, Fat, Adipose|No| 6803.0|APN 183|C57BL/6N-Csf3r/Marp||Recessive|colony stimulating factor 3 receptor (granulocyte) |Csf3r |Unknown||MGI:1339755 |colony stimulating factor 3 receptor (granulocyte); targeted mutation 1, Velocigene |Csf3rtm1(KOMP)Vlcg|MGI:4452883|4||||||||||||||||Yes|||||||||||||Unknown - Not bred to homozygocity |Normal |C57BL/6N|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|23-Jan-2012|Cryopreserved sperm|50.0|0.0|Unknown||ES cell|Yes| 6906.0|APN 297|C57BL/6N-Hhex/Marp||Recessive|hematopoietically expressed homeobox|Hhex |Unknown|Hex, Hhex-rs2, Prhx |MGI:96086 |gene trap IST11279G10, Texas A&M Institute for Genomic Medicine |Gt(IST11279G10)Tigm|MGI:3996083|19||||||||||Unknown to Unknown||||||Yes|||||||||||||Unknown - Not bred to homozygocity |Normal |C57BL/6N|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|01-Jun-2012|Cryopreserved sperm|50.0|0.0|Unknown||ES cell, Gene Trap|Possibly| 4089.0||KRN:005||Recessive|||||||||Unknown||||||||||||||||Yes|transgene insertion KRN, Diane Mathis|Natural TCR alpha and -beta promoter/enhancer elements.|||||||||||No arthritis, no GPI autoantibodies in KRN/H2g7 model.||C57BL/6 x NODk x C57BL/10 x Balb/b|Yes|Yes|Yes|Yes|Yes|Yes|No|Poor||3||No|04-Dec-2008|Cryopreserved sperm|165.0|0.0|Yes||Autoimmunity, Arthritis, KRN, ENU|No| 8269.0|Lifr fl:LysMcre|B6.129P2-Lifr Lyz2/JAusbAnu||Recessive|lysozyme 2|Lyz2|Normal|Lys, Lysm, Lyzs, Lzm, Lzm-s1, Lzp|MGI:96897|lysozyme 2; targeted mutation 1, Irmgard Forster|Lyz2|MGI:1934631|10|||||||||||||||||||||||||||||Unknown|Enlarged spleen:*Rare|C57BL/6NCrlAnu|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|16-Jun-2017|Cryopreserved sperm|12.0|0.0|Unknown||Macrophage, Granulocyte, Conditional mutagenesis|Yes| 8269.0|Lifr fl:LysMcre|B6.129P2-Lifr Lyz2/JAusbAnu||Recessive|leukemia inhibitory factor receptor|Lifr||A230075M04Rik, soluble differentiation-stimulating factor receptor|MGI:96788|leukemia inhibitory factor receptor; targeted mutation 1a, Helmholtz Zentrum Muenchen GmbH|Lifr|MGI:4841519|15|||||||||||||||||||||||||||||Unknown|Enlarged spleen:*Rare|C57BL/6NCrlAnu|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|16-Jun-2017|Cryopreserved sperm|||Unknown||Macrophage, Granulocyte, Conditional mutagenesis|Yes| 4090.0||KRN:044||Recessive|||||||||Unknown||||||||||||||||Yes|transgene insertion KRN, Diane Mathis|Natural TCR alpha and -beta promoter/enhancer elements.|||||||||||Hypo response post arthritogenic serum transfer||C57BL/6 x NODk x C57BL/10 x Balb/b|Yes|Yes|Yes|Yes|Yes|Yes|No|Poor||2||No|04-Dec-2008|Cryopreserved sperm|75.0|0.0|Yes||Autoimmunity, Arthritis, KRN, ENU, Serum transfer|No| 4092.0||KRN:048||Recessive|||||||||Unknown||||||||||||||||Yes|transgene insertion KRN, Diane Mathis|Natural TCR alpha and -beta promoter/enhancer elements.|||||||||||No arthritis in KRN/H2g7 model||C57BL/6 x NODk x C57BL/10 x Balb/b|Yes|Yes|Yes|Yes|Yes|Yes|No|Poor||2||No|04-Dec-2008|Cryopreserved sperm|30.0|0.0|Yes||Autoimmunity, Arthritis, KRN, ENU|No| 4093.0||KRN:065||Recessive|||||||||Unknown||||||||||||||||Yes|transgene insertion KRN, Diane Mathis|Natural TCR alpha and -beta promoter/enhancer elements.|||||||||||No arthritis, no GPI autoantibodies in KRN/H2g7 model. Candidate gene position likely to be Chr 1 or 5.||C57BL/6 x NODk x C57BL/10 x Balb/b|Yes|Yes|Yes|Yes|Yes|Yes|No|Poor||3||No|04-Dec-2008|Cryopreserved sperm|15.0|0.0|Yes||Autoimmunity, Arthritis, KRN, ENU|No| 4094.0||KRN:072||Recessive|||||||||Unknown||||||||||||||||Yes|transgene insertion KRN, Diane Mathis|Natural TCR alpha and -beta promoter/enhancer elements.|||||||||||No arthritis in KRN/H2g7 model. Candidate gene position likely to be Chr 4 or 8.||C57BL/6 x NODk x C57BL/10 x Balb/b|Yes|Yes|Yes|Yes|Yes|Yes|No|Poor||1||No|04-Dec-2008|Cryopreserved sperm|75.0|0.0|Yes||Autoimmunity, Arthritis, KRN, ENU|No| 4095.0||KRN:088||Recessive|||||||||Unknown||||||||||||||||Yes|transgene insertion KRN, Diane Mathis|Natural TCR alpha and -beta promoter/enhancer elements.|||||||||||No arthritis in KRN/H2g7 model, and hypo response post arthritogenic serum transfer||C57BL/6 x NODk x C57BL/10 x Balb/b|Yes|Yes|Yes|Yes|Yes|Yes|No|Poor||||No|04-Dec-2008|Cryopreserved sperm|75.0|0.0|Yes||Autoimmunity, Arthritis, KRN, ENU, Serum transfer|No| 4096.0||KRN:123||Recessive|||||||||Unknown||||||||||||||||Yes|transgene insertion KRN, Diane Mathis|Natural TCR alpha and -beta promoter/enhancer elements.|||||||||||Hypo response post arthritogenic serum transfer. Candidate gene position likely to be Chr 5 or 11.||C57BL/6 x NODk x C57BL/10 x Balb/b|Yes|Yes|Yes|Yes|Yes|Yes|No|Poor||2||No|04-Dec-2008|Cryopreserved sperm|45.0|0.0|Yes||Autoimmunity, Arthritis, KRN, ENU, Serum transfer|No| 4097.0||KRN:026||Recessive|||||||||Unknown||||||||||||||||Yes|transgene insertion KRN, Diane Mathis|Natural TCR alpha and -beta promoter/enhancer elements.|||||||||||No arthritis in KRN/H2g7 model. Candidate gene position likely to be Chr 1 or 5.||C57BL/6 x NODk x C57BL/10 x Balb/b|Yes|Yes|Yes|Yes|Yes|Yes|No|Poor||3||No|04-Dec-2008|Cryopreserved sperm|15.0|0.0|Unknown||Autoimmunity, Arthritis, KRN, ENU|No| 4100.0||KRN:196||Recessive|||||||||Unknown||||||||||||||||Yes|transgene insertion KRN, Diane Mathis|Natural TCR alpha and -beta promoter/enhancer elements.|||||||||||Hypo response post arthritogenic serum transfer||C57BL/6 x NODk x C57BL/10 x Balb/b|Yes|Yes|Yes|Yes|Yes|Yes|No|Poor||1||No|04-Dec-2008|Cryopreserved sperm|45.0|0.0|Yes||Autoimmunity, Arthritis, KRN, ENU, Serum transfer|No| 4101.0||KRN:207||Recessive|||||||||Unknown||||||||||||||||Yes|transgene insertion KRN, Diane Mathis|Natural TCR alpha and -beta promoter/enhancer elements.|||||||||||Hypo response post arthritogenic serum transfer.||C57BL/6 x NODk x C57BL/10 x Balb/b|Yes|Yes|Yes|Yes|Yes|Yes|No|Poor||2||No|04-Dec-2008|Cryopreserved sperm|10.0|0.0|Yes||Autoimmunity, Arthritis, KRN, ENU, Serum transfer|No| 4103.0||KRN:234||Recessive|||||||||Unknown||||||||||||||||Yes|transgene insertion KRN, Diane Mathis|Natural TCR alpha and -beta promoter/enhancer elements.|||||||||||No arthritis in KRN/H2g7 model||C57BL/6 x NODk x C57BL/10 x Balb/b|Yes|Yes|Yes|Yes|Yes|Yes|No|Poor||1||No|04-Dec-2008|Cryopreserved sperm|105.0|0.0|Yes||Autoimmunity, Arthritis, KRN, ENU|No| 4105.0||KRN:030||Recessive|||||||||Unknown||||||||||||||||Yes|transgene insertion KRN, Diane Mathis|Natural TCR alpha and -beta promoter/enhancer elements.|||||||||||No arthritis in KRN/H2g7 model||C57BL/6 x NODk x C57BL/10 x Balb/b|Yes|Yes|Yes|Yes|Yes|Yes|No|Poor||||No|05-Dec-2008|Cryopreserved sperm|10.0|0.0|Yes||Autoimmunity, Arthritis, KRN, ENU|No| 4106.0||KRN:037||Recessive|||||||||Unknown||||||||||||||||Yes|transgene insertion KRN, Diane Mathis|Natural TCR alpha and -beta promoter/enhancer elements.|||||||||||No arthritis in KRN/H2g7 model||C57BL/6 x NODk x C57BL/10 x Balb/b|Yes|Yes|Yes|Yes|Yes|Yes|No|Poor||||No|05-Dec-2008|Cryopreserved sperm|10.0|0.0|Yes||Autoimmunity, Arthritis, KRN, ENU|No| 4109.0||KRN:137||Recessive|||||||||Unknown||||||||||||||||Yes|transgene insertion KRN, Diane Mathis|Natural TCR alpha and -beta promoter/enhancer elements.|||||||||||No arthritis in KRN/H2g7 model||C57BL/6 x NODk x C57BL/10 x Balb/b|Yes|Yes|Yes|Yes|Yes|Yes|No|Poor||||No|05-Dec-2008|Cryopreserved sperm|40.0|0.0|Yes||Autoimmunity, Arthritis, KRN, ENU|No| 8130.0|Stat6 -/-|B6.129P2-Stat6/Wehi||Recessive|signal transducer and activator of transcription 6|Stat6|Nil||MGI:103034|signal transducer and activator of transcription 6; targeted mutation 1, Shizuo Akira|Stat6|MGI:2386746|10|||||||||||||||||||||||||||||Unable to transduce IL-4/13 intracellular signalling.Decreased T-helper 2 cell number. Decreased B cell proliferation:• B cell proliferation in response to anti-IgM plus IL-4 is impaired• however, B cell proliferation in response to LPS is normalIncreased IgA level:• IgA levels are slightly increased following infection with N. brasiliensisDecreased IgE level:• IgE levels are lower than in wild-type mice following infection with N. brasiliensisDecreased IgG1 level:• IgG1 levels are 16-fold lower than in wild-type mice and following infection with N. brasiliensis they are 10-fold lower than in infected wild-type miceIncreased IgG level: • IgG2 and IgG3 levels are slightly increased following infection with N. brasiliensisAbnormal T-helper 2 physiology: • mice fail to produce increased levels of Th2 cytokines in response to infection with N. brasiliensisDecreased T cell proliferation: • thymocyte proliferation in response to TPA is impaired• however, thymocyte proliferate in response to other stimuliSkin inflammation: • mice exhibit mild dermal infiltration of inflammatory cells• few CD4+ cells infiltrate the perioral dermis and epidermis|Normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|02-Nov-2016|Cryopreserved sperm|50.0|0.0|Unknown||T cell, signal transduction, phosphorylation|Yes| 8016.0|ENU6WTNIH:033 Th 1 B6|ENU6WTNIH:33 Th1 B6||Recessive|signal transducer and activator of transcription 1 and Th1|Stat1 and Th1|||||||1||||||||||||||||Yes|||||||||||||Defective antibody response to immunization: failure to mount a normal Th1 polarized IgG2c antibody response to heat killed B pertussis bacteria. Spontaneous formation of B cell lymphomas has also been observed in this pedigree, but it is not yet known if the two traits are linked.This strain is linked to a strain with the above phenotype with Th1 included also|unknown|C57BL/6JSfdAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|07-Jan-2016||0.0|0.0|Unknown||B cell, immunization, Th1, ENU, Wellcome Trust, NH|Possibly| 8270.0||C57BL/6J-Serpinb9a||Recessive|serine (or cysteine) peptidase inhibitor, clade B, member 9|Serpinb9|Unknown|ovalbumin, PI-9, Spi6|MGI:106603|serine (or cysteine) peptidase inhibitor, clade B, member 9; targeted mutation 2, Phillip I Bird|Serpinb9a||13||||||||||Unknown to Unknown|||||||||||||||||||Normal|Normal|C57BL/6|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|21-Jun-2017|Cryopreserved sperm|50.0|0.0|Unknown|||Yes| 8266.0||ENU37:009||Recessive|Unknown||||||||Unknown|||||||||||||||||||||||||||||Homozygous mice have increased immature B cells in the blood and absence of marginal zone B cells in the spleen.||C57BL/6NCrlAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|07-Jun-2017|Cryopreserved sperm|24.0|0.0|Unknown||B cell, marginal zone|Yes| 8268.0|CXCR5KO:P14 TCR:Ly5a|B6.Cg-Cxcr5 Ptprc Tg(TcrLCMV)#Sdz/MarpAnu||Recessive|chemokine (C-X-C motif) receptor 5|Cxcr5||Blr1, CXCR-5, Gpcr6|MGI:103567|chemokine (C-X-C motif) receptor 5; targeted mutation 1, Martin Lipp|Cxcr5|MGI:2158677|9|||||||||||||||||transgene insertion, Birgit Ledermann|||protein tyrosine phosphatase, receptor type, C|Ptprc||B220, CD45, Ly-5, Lyt-4, T200|MGI:97810|protein tyrosine phosphatase, receptor type, C; a variant|Ptprc|MGI:4819849|1|Cxcr5 KO mice:Abnormal leukocyte migration:• homozygotes exhibit a severely impaired lymphocyte migration to the Peyer's pathces and the B cell follicles of the spleen, resulting in morphologically abnormal primary lymphoid follicles• activated B cells fail to migrate from the T cell-rich zone into B cell follicles of the spleenIncreased B cell number:• homozygotes display a 2- to 4-fold increase in spleen or peripheral blood cells co-expressing B220 and high amounts fo IgMAbnormal spleen primary B follicle morphology:• at 8 wks of age, homozygotes display defective formation of primary splenic follicles, including: the T cell zone is located centrally but not polarized in the follicle; the T cell zone is completely surrounded by a small rim of B cell-expressing IgD but not IgM (i.e. IgM+IgD+ subset is absent); a prominent marginal zone surrounds the follicle completelyAbnormal spleen secondary B follicle morphology.Absent spleen germinal centre:• despite high numbers of germinal center founder cells, no functional germinal centers develop in mutant spleen after immunization with the T cell-dependent antigen DNP-KHLAbsent follicular dendritic cells:• absence of primary follicular dendritic cellsAbnormal Peyer's patch morphology:• ~30% (26 of 76) of homozygotes exhibit 1-4 small and rudimentary structures resembling Peyer's patches• ~16% (12 of 76) of homozygotes exhibit normally sized Peyer's patches with multiple B and T cell-rich zones instead of the large follicles present in wild-type miceAbsent Peyer's patches:• 55% (42 of 76) of homozygotes show complete absence of Peyer's patchesAbsent axillary lymph nodes Absent brachial lymph nodes Absent cervical lymph nodes Absent inguinal lymph nodes:• homozygotes lack inguinal lymph nodesAbsent lymph nodes:• absence of inguinal, iliac/periaortic, axillary, branchial, deep cervical, sacral/caudal, and parathymic lymph nodesTransgenic mice carry a T-cell receptor (Tcra-V2, Tcra-J TA31 / Tcrb-V8.1, Tcrb-D, Tcrb-J 2.4) specific for LCMV (lymphocytic choriomeningitis virus), H2-Db||C57BL/6J|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|14-Jun-2017|Cryopreserved sperm|34.0|0.0|Unknown||T cell, CMV|Yes| 8277.0|CXCR5tg:P14|B6.Cg-Tg(Lck-Cxcr5)Cys Tg(TcrLCMV)#Sdz/MarpAnu||Dominant||||||||||||||||||||||||||chemokine (C-X-C motif) receptor 5|lymphocyte protein tyrosine kinase|||||||||||||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|02-Aug-2017|Cryopreserved sperm|24.0|0.0|Unknown||receptor (TCR), CD4, CXCR5, thymic selection|Possibly| 8277.0|CXCR5tg:P14|B6.Cg-Tg(Lck-Cxcr5)Cys Tg(TcrLCMV)#Sdz/MarpAnu||Dominant||||||||||||||||||||||||||transgene insertion, Birgit Ledermann||||||||||||||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|02-Aug-2017|Cryopreserved sperm|||Unknown||receptor (TCR), CD4, CXCR5, thymic selection|Possibly| 8278.0|Ebi2 KO:CXCR5tg:P14|B6.Cg-Gpr183 Tg(Lck-Cxcr5)Cys Tg(TcrLCMV)#Sdz/MarpAnu||Recessive|G protein-coupled receptor 183|Gpr183|Reduced|Ebi2|MGI:2442034|G protein-coupled receptor 183; targeted mutation 1.1, Jason G Cyster|Gpr183|MGI:4399081|14|||||||||||||||||chemokine (C-X-C motif) receptor 5|lymphocyte protein tyrosine kinase|||||||||||||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|02-Aug-2017||0.0|62.0|Unknown||receptor (TCR), CD4, CXCR5, thymic selection|Possibly| 8278.0|Ebi2 KO:CXCR5tg:P14|B6.Cg-Gpr183 Tg(Lck-Cxcr5)Cys Tg(TcrLCMV)#Sdz/MarpAnu||Recessive||||||||||||||||||||||||||transgene insertion, Birgit Ledermann||||||||||||||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|02-Aug-2017||||Unknown||receptor (TCR), CD4, CXCR5, thymic selection|Possibly| 8421.0|ENU31:016::MD4 ML5:G3|B6.Cg-ENU mutant Tg(IghelMD4)4Ccg Tg(ML5sHEL)5Ccg/Anu||Recessive|Unknown||||||||Unknown|||||||||||||||||transgene insertion 4, Christopher C Goodnow||High||||||||||Usually double Tg mice delete many of their self reactive B cells and downregulate expression of both IgM and IgD on the cell surface of the remaining B cells. The phenotype in these interesting mice is a variable lack of deletion and IgM/IgD downregulation||C57BL/6NCrlAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|17-Jan-2018||0.0|0.0|Unknown||Autoimmunity, B cell, Immunoglobulin, Hen Egg Lysozyme (HEL)|Yes| 8421.0|ENU31:016::MD4 ML5:G3|B6.Cg-ENU mutant Tg(IghelMD4)4Ccg Tg(ML5sHEL)5Ccg/Anu||Recessive||||||||||||||||||||||||||transgene insertion 5, Christopher C Goodnow|mouse metallothionein I|||||||||||Usually double Tg mice delete many of their self reactive B cells and downregulate expression of both IgM and IgD on the cell surface of the remaining B cells. The phenotype in these interesting mice is a variable lack of deletion and IgM/IgD downregulation||C57BL/6NCrlAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|17-Jan-2018||||Unknown||Autoimmunity, B cell, Immunoglobulin, Hen Egg Lysozyme (HEL)|Yes| 8283.0|hIL21R:P14|B6.Cg-Il21r Tg(TcrLCMV)#Sdz/Marp||Recessive|interleukin 21 receptor|Il21r||NILR|MGI:1890475||||7|||||||||||||||||transgene insertion, Birgit Ledermann|H-2K promoter||||||||||||Carry LCMV-specific, H-2K-restricted T cell receptor. Express human IL21R instead of mouse Il21R.|C57BL/6J|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|15-Aug-2017||0.0|0.0|No||T cell, receptor, LCMV, CD8, IL21 receptor|Yes| 8282.0|Cd23-cre|B6.Cg-Tg(Fcer2a-cre)5Mbu/JMarp||Dominant||||||||||||||||||||||||||transgene insertion 5, Meinrad Busslinger|Fcer2a||||||||||||These Cd23-cre transgenic mice express cre under the control of the Fcer2a promoter. Cre recombinase expression is detected in immature, transitional and late B cells in the bone marrow and spleen. Mice that are hemizygous for the transgene are viable and fertile.|C57BL/6J|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|.20|||No|15-Aug-2017||0.0|0.0|Unknown||B cell, Cre recombinase|Yes| 8276.0|Ccr6 KO: P14|B6.129-Ccr6 Tg(TcrLCMV)#Sdz/MarpAnu||Recessive|chemokine (C-C motif) receptor 6|Ccr6|Nil|Cmkbr6|MGI:1333797|chemokine (C-C motif) receptor 6; targeted mutation 1, Deltagen|Ccr6|MGI:3604541|17|||||||||||||||||transgene insertion, Birgit Ledermann||||||||||||Unknown||C57BL/6J|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|02-Aug-2017|Cryopreserved sperm|24.0|0.0|Unknown||T cell, CD8|Yes| 8281.0|Tg (Tff1-CreERT2; Tff2-rtTA; Tff3-Luc); TRE-Stat3.1348; R26-LSL-YFP; LSL-LacZ13|B6-Tg(Tff1-CreERT2;Tff2-rtTA;Tff3-luc) Gt(ROSA)26Sor Gt(ROSA)26Sor Col1a1||Recessive|collagen, type I, alpha 1|Col1a1||Col1a-1, Cola1, Cola-1, Mov-13|MGI:88467||||11|||||||||||||||||Trefoil|Tff1 driving CreERT2; Tff2 driving rtTA; Tff3 driving luciferase|||||||||||||C57BL/6|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|11-Aug-2017|Cryopreserved sperm|50.0|0.0|Unknown||Gastric, epithelium|Yes| 8281.0|Tg (Tff1-CreERT2; Tff2-rtTA; Tff3-Luc); TRE-Stat3.1348; R26-LSL-YFP; LSL-LacZ13|B6-Tg(Tff1-CreERT2;Tff2-rtTA;Tff3-luc) Gt(ROSA)26Sor Gt(ROSA)26Sor Col1a1||Recessive||||||||||||||||||||||||||gene trap ROSA 26, Philippe Soriano; targeted mutation 1, Frank Costantini||||||||||||||C57BL/6|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|11-Aug-2017|Cryopreserved sperm|||Unknown||Gastric, epithelium|Yes| 8281.0|Tg (Tff1-CreERT2; Tff2-rtTA; Tff3-Luc); TRE-Stat3.1348; R26-LSL-YFP; LSL-LacZ13|B6-Tg(Tff1-CreERT2;Tff2-rtTA;Tff3-luc) Gt(ROSA)26Sor Gt(ROSA)26Sor Col1a1||Recessive||||||||||||||||||||||||||gene trap ROSA 26, Philippe Soriano; targeted mutation 1, Philippe Soriano||||||||||||||C57BL/6|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|11-Aug-2017|Cryopreserved sperm|||Unknown||Gastric, epithelium|Yes| 8290.0||ENU36:003||Recessive|Unknown||||||||Unknown|||||||||||||||||||||||||||||Increased CD44 expression on naive CD4 and CD8 T cells||C57BL/6NCrlAnu|Yes|Unknown|Yes|Yes|Unknown|Yes|No|Unknown||||No|22-Aug-2017|Cryopreserved sperm|44.0|0.0|Unknown||T cell|Yes| 8286.0|ASD749:Tacr3|C57BL/6NCrlAnu-Tacr3/Anu||Recessive|tachykinin receptor 3|Tacr3|Unknown|neuromedin K receptor, Nk3r, Tac3r|MGI:892968||||3|||||||||||||||||||||||||||||Unknown||C57BL/6JAnu|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|21-Aug-2017|Cryopreserved sperm|15.0|0.0|Unknown|||Yes| 1.0|Plastic|C57BL/6JSfdAnu-Ikzf1/AnuApb|C57BL/6JSfdAnu-Ikzf1/AnuApb|Recessive|IKAROS family zinc finger protein 1|Ikzf1|Nil|Ikaros, hlk-1, LyF-1, Zfpn1a1|MGI:1342540|IKAROS family zinc finger 1; plastic|Ikzf1|MGI:2669987|11|ENSMUSG00000018654|ENSMUST00000076700|Ikzf1-201|572|842|A to G|ENSMUSE00000655504|5|191|Histidine to Arginine|||||CTGCCGCCGGAGGGACGCCCTCACCGGCCACCTGAGGACGCACTCCGTTGGTAAGCCTCAC|Yes|||||||||||||Embryonic lethal E15.5-17.5AnemiaFailure of normal erythroblast growth and differentiation in fetal liverExpansion of myeloid cells including: CD34⁺CD45⁺FcγR⁺ and Mac-1hi and Gr-1lo cell populationsNo detectable Gr-1hi cellsEarly lymphocyte development arrestAccumulation of precursor B cells in thymus at expense of T cell developmentPremature down regulation of c-kit expressionCell intrinsic defectFetal liver cells fail to engraft|T cell Lymphoma, arrested at DN (pro-T3) stage orLymphoblastic lymphoma/leukaemia (pre-T-LBL)|C57BL/6JSfdAnu|No|No|Yes|No|No|Yes|Yes|Good||7||No|25-Nov-2005|Cryopreserved sperm|152.0|0.0|Unknown||haemopoiesis, T cell, B cell, transcription factor, ENU|Yes| 8203.0|A2b923flox,A2b923/Germ-line Cre |B6.Cg-Adora2b||Recessive|adenosine A2b receptor|Adora2b|Nil|A2b, A2BAR, A2BR, A2b, Rs, AA2BR|MGI:99403|adenosine A2b receptor; targeted mutation 1.1, Michail Sitkovsky|Adora2b|MGI:4941886|11|||||||||||||||||||||||||||||No overt difference in phenotype is apparent under normal circumstances. No special monitoring or care is required.|No overt difference in phenotype is apparent under normal circumstances. No special monitoring or care is required.|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|28-Feb-2017|Cryopreserved sperm|50.0|0.0|Unknown||receptor, Macrophage|Yes| 8285.0|Mir155 KO:CMV-cre|B6.Cg-Mir155 Tg(CMV-cre)1Cgn/J||Recessive|microRNA 155|Mir155|Unknown|Mirn155, mmu-mir-155|MGI:2676840||||16|||||||||||||||||transgene insertion 1, University of Cologne|CMV|||||||||||Unknown||C57BL/6NCrlnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|18-Aug-2017|Cryopreserved sperm|70.0|0.0|Unknown|||Yes| 8288.0|AMPK a1(S496A) KI|C57BL/6-Prkaa1||Recessive|protein kinase, AMP-activated, alpha 1 catalytic subunit|Prkaa1||AMPKalpha1, C130083N04Rik|MGI:2145955||||15|||||||||||||||||||||||||||||Normal|Normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|22-Aug-2017|Cryopreserved sperm|18.0|0.0|Unknown|||Yes| 8289.0|AMPK a1(T481/S487A) KI|C57BL/6-Prkaa1/Ausb||Recessive|protein kinase, AMP-activated, alpha 1 catalytic subunit|Prkaa1|Unknown|AMPKalpha1, C130083N04Rik|MGI:2145955||||15|||||||||||||||||||||||||||||Normal|Normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|22-Aug-2017|Cryopreserved sperm|70.0|0.0|Unknown|||Yes| 8316.0|GLUT12FloxMCKCre|C57BL/6-Slc2a12 Tg(Ckm-cre)28Arte/Apb||Semi-dominant|solute carrier family 2 (facilitated glucose transporter), member 12|Slc2a12||Glut12, GLUT-12|MGI:3052471||||10|||||||||||||||||transgene insertion 28, TaconicArtemis||||||||||||Normal|Normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|02-Oct-2017|Cryopreserved sperm|50.0|0.0|Unknown|||Yes| 8292.0||ASD820:CBA/CaJAnu:F1||Recessive||||||||||||||||||||||||||||||||||||||This widely used general purpose strain is the only CBA substrain that carries the Pde6brd1 mutation, which causes blindness by wean age. Renal tubulointerstitial lesions have been observed in this strain at a high frequency. Some CBA/J mice spontaneously develop exocrine pancreatic insufficiency syndrome. Research includes immunology and inflammation, metabolism, hearing and cochlear function, infectious disease, and fetal development. |Normal Wildtype|CBA/CaJ|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|23-Aug-2017|Cryopreserved sperm|80.0|0.0|Unknown|||No| 8295.0|HeparanaseKO|B6.129-Hpse/AnuApb||Recessive|heparanase|Hpse|Nil|Hpa|MGI:1343124|heparanase; targeted mutation 1, Jin-Ping Li|Hpse|MGI:3844469|5|||||||||||||||||||||||||||||Heparanase KO mice are fertile with no immunological phenotype observed.|Normal.|C57BL/6JAnu|Yes|Yes|Unknown|Yes|Yes|Yes|No|Unknown||||No|29-Aug-2017|Cryopreserved sperm|58.0|0.0|Unknown||Heparan sulphate, MMP2|Yes| 8298.0|ENU34:60:Trmt1|C57BL/6NCrlAnu-Trmt1/AnuApb||Recessive|tRNA methyltransferase 1|Trmt1|Unknown|6720406L13Rik, D8Ertd812e|MGI:1289155||||8|ENSMUSG00000001909|ENSMUST00000001974.10|Trmt1-201|1001|1532|T to G|ENSMUSE00001239169|8|334|Valine to Glycine|||||TGTACGTGTTTTCACAGGCCAGGCCAAGGTTAAGTCCTCAGCCAGCAAACAGGCCCTGGTG||||||||||||||Homozygous mice show poor response to infection|Normal|C57BL/6NCrlAnu|Unknown|Yes|Yes|Unknown|Yes|Yes|No|Unknown||||No|06-Sep-2017|Cryopreserved sperm|24.0|0.0|Unknown||Infection|Yes| 8302.0|IGFBP-3-null |B6J.129S-Igfbp3||Recessive|insulin-like growth factor binding protein 3|Igfbp3|Nil|IGFBP-3|MGI:96438|insulin-like growth factor binding protein 3; targeted mutation 1, John E Pintar|Igfbp3|MGI:3663361|11|||||||||||||||||||||||||||||Normal|Normal|C57BL/6J|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|12-Sep-2017|Cryopreserved sperm|30.0|0.0|Unknown||Growth, metabolism|Yes| 8299.0|IRF4:T95R|C57BL/6NCrlAnu-Irf4/Anu||Recessive|interferon regulatory factor 4|Irf4|Unknown|IRF-4, Spip|MGI:1096873|Irf4, endonuclease-mediated mutation 2, Australian National University|Irf4||13|ENSMUSG00000021356.11|ENSMUST00000110307.3|Irf4-202|284|386|C to G|ENSMUSE00000117279|3||Threonine to Arginine|||||CGACAAGCCAGATCCTCCTACTTGGAAGACAAGATTACGATGTGCTCTGAACAAGAGCAAT||||||||||||||Unknown||C57BL/6NCrlAnu|Yes|Unknown|Yes|Yes|Unknown|Yes|No|Unknown||||No|07-Sep-2017|Cryopreserved sperm|48.0|0.0|Unknown|||Yes| 8301.0|IRF4:47bp deletion|C57BL/6NCrlAnu-Irf4/Anu||Recessive|interferon regulatory factor 4|Irf4|Unknown|IRF-4, Spip|MGI:1096873|Irf4, endonuclease-mediated mutation 5, Australian National University|Irf4||13||||||||||Unknown to Unknown|||||||||||||||||||Unknown||C57BL/6NCrlAnu|Yes|Unknown|Yes|Yes|Unknown|Yes|No|Unknown||||No|07-Sep-2017|Cryopreserved sperm|36.0|0.0|Unknown|||Yes| 8839.0|ASD956:Seville:T3803 XM|C57BL/6NCrlAnu-Tlr3/AnuApb||Recessive|toll-like receptor 3|Tlr3|Unknown||MGI:2156367||||8|||||||||||||||||||||||||||||Unknown|Unknown|C57BL/6NCrlAnu|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|16-Jan-2020|Cryopreserved sperm|60.0|0.0|Unknown|||Yes| 8297.0|ASD547:Tle2|C57BL/6NCrlANu-Tle2/Anu||Recessive|transducin-like enhancer of split 2|Tle2|Unknown|Grg2|MGI:104635|Tle2, endonuclease-mediated mutation 1, Australian National University|Tle2||10||||||||||Unknown to Unknown|||||||||||||||||||Unknown||C57BL/6NCrlAnu|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|05-Sep-2017|Cryopreserved sperm|36.0|0.0|Unknown||CRISPR|Yes| 8296.0|ASD737:Zic2|C57BL/6NCrlAnu-Zic2/AnuApb||Recessive|zinc finger protein of the cerebellum 2|Zic2|Unknown|GENA 29, Ku, odd-paired homolog|MGI:106679|Zic2, endonuclease-mediated mutation 1, Australian National University|Zic2||14||||||||||Unknown to Unknown|||||||||||||||||||Unknown||C57BL/6NCrlAnu|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|05-Sep-2017|Cryopreserved sperm|12.0|0.0|Unknown||CRISPR, Zic2|Yes| 8293.0|AMPK a1(S487A) KI|C57BL/6-Prkaa1/Ausb||Recessive|protein kinase, AMP-activated, alpha 1 catalytic subunit|Prkaa1||AMPKalpha1, C130083N04Rik|MGI:2145955||||15|||||||||||||||||||||||||||||Normal|Normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|28-Aug-2017|Cryopreserved sperm|50.0|0.0|Unknown|||Possibly| 8304.0|Gpx4 fl|B6.129S6-Gpx4/JAnu||Recessive|glutathione peroxidase 4|Gpx4|Unknown|1700027O09Rik, mtPHGPx, PHGPx, phospholipid hydroperoxide glutathione peroxidase, snGPx, sperm nuclei glutathione peroxidase|MGI:104767|glutathione peroxidase 4; targeted mutation 1.1, Qitao Ran|Gpx4|MGI:5425616|10|||||||||||||||||||||||||||||Normal||C57L/6J|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|14-Sep-2017||0.0|66.0|Unknown||hydroperoxides, lipids|Yes| 8303.0|ObR fl|B6.129P2-Lepr/JAnu||Recessive|leptin receptor|Lepr|Unknown|Leprb, LEPROT, leptin receptor gene-related protein, Modb1, obese-like, obl, Obr, OB-RGRP|MGI:104993|leptin receptor; targeted mutation 1, Jeffrey M Friedman|Lepr|MGI:2176774|4|||||||||||||||||||||||||||||Normal||C57L/6J|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|14-Sep-2017||0.0|0.0|Unknown||Leptin|Yes| 8307.0|Slp2 KO|B6.129P2-Sytl2/RbrcAnuApb||Recessive|synaptotagmin-like 2|Sytl2|Nil|Slp2, Slp2-a, Slp2-b, Slp2-c, Slp2-d|MGI:1933366|synaptotagmin-like 2; targeted mutation 1, Mitsunori Fukuda|Sytl2|MGI:3693881|7|||||||||||||||||||||||||||||Abnormal gastric surface mucous cell morphology:• the number of mucus granules is decreased, 2.8-fold fewer granules are docked with the apical membrane, mucus granule size is increased, and irregular apical membranes are frequently observed• however, no clear abnormalities are seen in the thickness of the epithelia or the numbers of parietal, neck, or chief cellsDecreased digestive secretion:• reduced basal mucin secretion by gastric epithelial cells; however when stimulated with A23187 mucus secretion is similar to wild-type cells||C57BL/6NCrlAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|20-Sep-2017|Cryopreserved sperm|33.0|0.0|Unknown||Rab27, mucus granules|Yes| 8308.0|Helios floxed:Lck-cre|B6.Cg-Ikzf2 Tg(Lck-Cre)/Anu||Recessive|IKAROS family zinc finger 2|Ikzf2||A730095J18Rik, Helios, Zfpn1a2|MGI:1342541|IKAROS family zinc finger 2; targeted mutation 1.1, Ethan M Shevach|Ikzf2|MGI:4456473|1|||||||||||||||||targeted mutation I57, Jamey Marth; transgene insertion I57, Jamey Marth|mouse proximal Lck promoter|active in thymocytes and splenocytes||||||||||||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|22-Sep-2017|Cryopreserved sperm|55.0|0.0|Unknown||CD4, T cell, Treg|Yes| 8309.0|CD19-cre.Egr2f/f.Egr3-/-|B6.129-Egr2 Egr3 Cd19/AnuApb||Recessive|early growth response 2|Egr2||Egr-2, Krox20, Krox-20, NGF1-B, Zfp-25|MGI:95296|early growth response 2; targeted mutation 3, Patrick Charnay|Egr2|MGI:2183227|10|||||||||||||||||||||||||||||Egr2 f/f.Egr3-/-.CD4-cre+ mice develop autoimmune disease at around three months of age or older. Egr2 f/f.CD4-cre+ mice develop milder autoimmune disease and at a slower rate. Egr3-/- exhibit some neurological defects.||C57BL/6|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown|>10|||No|22-Sep-2017|Cryopreserved sperm|44.0|0.0|Unknown||B cell|Yes| 8309.0|CD19-cre.Egr2f/f.Egr3-/-|B6.129-Egr2 Egr3 Cd19/AnuApb||Recessive|early growth response 3|Egr3|Nil|Pilot|MGI:1306780|early growth response 3; targeted mutation 1, Jeffrey Milbrandt|Egr3|MGI:2180063|14|||||||||||||||||||||||||||||Egr2 f/f.Egr3-/-.CD4-cre+ mice develop autoimmune disease at around three months of age or older. Egr2 f/f.CD4-cre+ mice develop milder autoimmune disease and at a slower rate. Egr3-/- exhibit some neurological defects.||C57BL/6|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown|>10|||No|22-Sep-2017|Cryopreserved sperm|||Unknown||B cell|Yes| 8309.0|CD19-cre.Egr2f/f.Egr3-/-|B6.129-Egr2 Egr3 Cd19/AnuApb||Recessive|CD19 antigen|Cd19|||MGI:88319|CD19 antigen; targeted mutation 1, University of Cologne|Cd19|MGI:1931143|7|||||||||||||||||||||||||||||Egr2 f/f.Egr3-/-.CD4-cre+ mice develop autoimmune disease at around three months of age or older. Egr2 f/f.CD4-cre+ mice develop milder autoimmune disease and at a slower rate. Egr3-/- exhibit some neurological defects.||C57BL/6|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown|>10|||No|22-Sep-2017|Cryopreserved sperm|||Unknown||B cell|Yes| 8310.0||Kif1bp KO||Recessive|kinesin family member 1 binding protein|Kif1bp|Nil|0710007C18Rik, 2510003E04Rik, mKIAA1279|MGI:1919570|Kif1bp; KBP |||10|||||||||||||||||||||||||||||Neonatal lethal. Die at birth due to breathing difficulties. Mice display broad peripheral neuropathies, as well as small olfactory bulbs and reduced white mater tracts (anterior commissure). |"Normal"|C57BL/6|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|25-Sep-2017|Cryopreserved sperm|50.0|0.0|Unknown|||Yes| 8314.0|ENU37:037:Casp4|C57BL/6NCrlAnu-Casp4/AnuApb||Recessive|caspase 4, apoptosis-related cysteine peptidase|Casp4|Unknown|Casp11, Caspase-11, ich-3|MGI:107700|Casp4, mutation 2, Australian National University|Casp4||9||||||||||Unknown to Unknown|||||||||||||||||||Unknown|Unknown|C57BL/6NCrlAnu|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|28-Sep-2017|Cryopreserved sperm|44.0|0.0|Unknown||ENU|Yes| 7985.0|Recql4 G522EfsX43|C57BL/6-Recql4||Dominant|RecQ protein-like 4|Recql4|Nil||MGI:1931028|Recql4|Recql4 G522EfsX43||15|||||||||||||||||||||||||||||unknown - we havent recovered any homozygous point mutants at time of submission to APN|Hets appear normal and fertile|C57BL/6|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Excellent|generated on pure C57BL/6 so not backcrossed. Only maintained on C57||PM/+ to either PM/+ or WT|No|27-Oct-2015|Cryopreserved sperm|40.0|0.0|Yes|Rothmund-Thomson Syndrome|Recql4|Possibly| 8319.0|SKAM gene trapped|B6.129P2-Fgfr1op2/MarpApb||Recessive|FGFR1 oncogene partner 2|Fgfr1op2||1500031J01Rik|MGI:1914779|FGFR1 oncogene partner 2; gene trap CA0175, Wellcome Trust Sanger Institute|Fgfr1op2|MGI:3858415|6|||||||||||||||||||||||||||||Embryonic lethal|Normal|C57BL/6|No|No|Yes|No|No|Yes|No|Unknown||||No|03-Oct-2017|Cryopreserved sperm|50.0|0.0|Unknown|||Yes| 9408.0|Lcp12|C57BL/6NCrlAnu-Lcp1/Apb||Semi-dominant|lymphocyte cytosolic protein 1|Lcp1|||MGI:104808|Lcp1: endonuclease-mediated mutation 1, Australian National University|Lcp1||14|||||||||||||||||||||||||||||Unknown|Unknown|C57Bl/6N|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|20-Jul-2022|Cryopreserved sperm|55.0|0.0|Unknown|||Possibly| 8313.0||ASD696:Thunderbird:19del::N1||Recessive|||||||||Unknown|||||||||||||||||||||||||||||Unknown||C57BL/6NCrlAnu|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|28-Sep-2017|Cryopreserved sperm|11.0|0.0|Unknown||CRISPR|Yes| 8315.0|GLUT12 KO|C57BL/6-Slc2a12||Recessive|solute carrier family 2 (facilitated glucose transporter), member 12|Slc2a12||Glut12, GLUT-12|MGI:3052471||Slc2a12||10|ENSMUSG00000037490||||||||||||||||||||||||||||Glucose intolerantInsulin intolerantInsulin Resistance|Normal|C57BL/6|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|02-Oct-2017|Cryopreserved sperm|100.0|0.0|Unknown||Glucose|Yes| 8326.0||C57BL/6NCcb||Dominant|N/A|||||N/A|||Unknown|||||||||||||||||||||||||||||Wild type|Wild type|C57BL/6N|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|05-Oct-2017|Cryopreserved sperm|80.0|0.0|Unknown||Control|Yes| 8325.0|Dsg2floxed-Cdh5-iCreER-T2 |C57BL/6N-Dsg2 Tg(Cdh5-creERT2)1Rha/CcbApb||Recessive|desmoglein 2|Dsg2||D18Ertd293e|MGI:1196466||||18|||||||||||||||||transgene insertion 1, Ralf H Adams|VE-cadherin (Cdh5)|||||||||||Phenotypically healthy under normal conditions. Unknown state when induced with tamoxifen, but predicted to exhibit depleted Dsg2 in vascular endothelial cells only, suggested to cause vascular complications.|Predicted to be the same, but less pronounced, than the homozygous mice.|C57BL/6N|Yes|Unknown|Yes|Yes|Unknown|Yes|No|Unknown||||No|05-Oct-2017|Cryopreserved sperm|50.0|0.0|Unknown||Angiogenesis, endothelium|Yes| 8311.0|Surge|C57BL/6NCrlAnu-Foxb1/AnuApb||Recessive|forkhead box B1|Foxb1|Unknown|C43, Fkh5, Foxb1a, Foxb1b, Hfh-e5.1, Mf3, TWH|MGI:1927549|Foxb1, endonuclease-mediated mutation 1, Australian National University|Foxb1||9||||||||||Unknown to Unknown|||||||||||||||||||Unknown||C57BL/6NCrlAnu|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|28-Sep-2017|Cryopreserved sperm|7.0|0.0|Unknown|||Yes| 8324.0|Dsg2fl/fl|C57BL/6N-Dsg2/CcbApb||Recessive|desmoglein 2|Dsg2||D18Ertd293e|MGI:1196466||||18|||||||||||||||||||||||||||||Normal|Normal|C57BL/6N|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|05-Oct-2017|Cryopreserved sperm|50.0|0.0|Unknown||Angiogenesis|Yes| 8328.0|empire ; hSPHK1-Tie2 Tg|C57BL/6-Tg(Tie2-SPHK1)/CcbApb||Dominant||||||||||||||||||||||||||human Sphingosine Kinase 1 (SPHK1)|Tie-2|||||||||||Homozygous mice are viable, fertile, normal in size and to not display any gross physical or behavioural abnormalities. Enhanced SPHK1 expression and activity in the blood vasculature, particularly highly vascularised organs, due to the tie-2 promoter. Some differences seen in blood vessel development and arthritis development compared to wild type. |Normal |C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|4|||No|05-Oct-2017|Cryopreserved sperm|50.0|0.0|Unknown||angiogenesis|Yes| 8331.0|ASD756:RC3H1:1bpins:4:N3|C57BL/6NCrlAnu-Rc3h14/AnuApb||Recessive|RING CCCH (C3H) domains 1|Rc3h1|Unknown|5730557L09Rik, roquin|MGI:2685397|Rc3h1, endonuclease-mediated mutation 1, Australian National University|Rc3h1||1||||||||||Unknown to Unknown|||||||||||||||||||Unknown|Normal|C57BL/6NCrlAnu|Yes|Unknown|Yes|Yes|Unknown|Yes|No|Unknown||||No|12-Oct-2017|Cryopreserved sperm|33.0|0.0|Unknown|||Yes| 8320.0|SK1 KO|B6.129S6-Sphk1/Apb||Recessive|sphingosine kinase 1|Sphk1|Nil|1110006G24Rik, SK1|MGI:1316649|sphingosine kinase 1; targeted mutation 1, Richard L Proia|Sphk1|MGI:3526071|11|||||||||||||||||||||||||||||Normal|Normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|03-Oct-2017|Cryopreserved sperm|50.0|0.0|Unknown||kinase|Yes| 8321.0|DSG2tma1|C57BL/6N-Dsg2/MarpCcbApb||Recessive|desmoglein 2|Dsg2|Reduced|D18Ertd293e|MGI:1196466|DSG2, ARVC10, ARVD10, CDHF5, CMD1BB, HDGC|||18|||||||||||||||||||||||||||||Homozygous mice are viable, fertile, normal in size and Mendelian ratio. They do not display any gross physical or behavioural abnormalities under homeostatic conditions. Notably, when challenged their significant reduction in Dsg2 gene expression translates into noticeable differences in blood vessel development, morphology and function, diabetes susceptibility and cancer progression. A pathology of cardiac fibrosis, which mimics the human condition, has been observed after humane killing but no observable effects related to this have been observed prior. Gene and protein expression experiments confirm that a low level of DSG2 is maintained in these mice; hence Dsg2 lo/lo.|Normal|C57BL/6N|Yes|Unknown|Yes|Yes|Unknown|Yes|No|Unknown||||No|05-Oct-2017|Cryopreserved sperm|50.0|0.0|Unknown||Angiogenesis, endothelium|Yes| 8336.0|ptpn14flox/flox|B6(Cg)-Ptpn14/MarpCcb||Recessive|protein tyrosine phosphatase, non-receptor type 14|Ptpn14||C130080N23Rik, OTTMUSG00000022087, PTP36|MGI:102467||||1|||||||||||||||||||||||||||||Normal|Normal|C57BL/6J|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|27-Oct-2017|Cryopreserved sperm|46.0|0.0|Unknown|||Yes| 8332.0|RBC16|B6.C-Cpox/WehiMarp||Dominant|coproporphyrinogen oxidase|Cpox|Unknown|cac, clone 560, Cpo, nct|MGI:104841|W373*|||16|||||||||||||||||||||||||||||Lethal (approx. e9.5)|Microcytosis|C57BL/6;BALB/c|No|No|Yes|No|No|Yes|No|Unknown||||No|16-Oct-2017||0.0|0.0|Yes|hereditary coproporphyria|erythropoiesis|Yes| 1781.0|Cathepsin L Knockout|C57BL/6-Cstl/WehiAnuApb||Recessive|cathepsin L|Ctsl|Unknown|1190035F06Rik, Cat L, major excreted protein, MEP|MGI:88564|cathepsin L; targeted mutation 1, Christoph Peters|Ctsl|MGI:2136432|13||||||||||||||||Yes|||||||||||||Homozygotes for mutant alleles may exhibit partial or complete hair-loss, skin defects, impaired T cell maturation, dilated cardiomyopathy, and high postnatal mortality. Mutant males for some alleles show both normal and atrophic seminiferous tubules and reduced sperm production.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|03-Aug-2007|Cryopreserved sperm|60.0|0.0|Unknown||Coat, T cell, CD4, Hair Loss, seminiferous tubules, alopecia|Yes| 8339.0|Egr2f/f|B6.129-Egr2/AnuApb||Recessive|early growth response 2|Egr2||Egr-2, Krox20, Krox-20, NGF1-B, Zfp-25|MGI:95296|early growth response 2; targeted mutation 3, Patrick Charnay|Egr2|MGI:2183227|10|||||||||||||||||||||||||||||Unknown||C57BL/6|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown|>10|||No|27-Oct-2017|Cryopreserved sperm|22.0|0.0|Unknown||B cell|Yes| 8339.0|Egr2f/f|B6.129-Egr2/AnuApb||Recessive|early growth response 3|Egr3|Nil|Pilot|MGI:1306780|early growth response 3; targeted mutation 1, Jeffrey Milbrandt|Egr3|MGI:2180063|14|||||||||||||||||||||||||||||Unknown||C57BL/6|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown|>10|||No|27-Oct-2017|Cryopreserved sperm|||Unknown||B cell|Yes| 8334.0|R26 WT-Hoxa1 ki|B6JArc.Cg-Gt(ROSA)26Sor||Semi-dominant|gene trap ROSA 26, Philippe Soriano|Gt(ROSA)26Sor|Unknown|beta geo, Gtrgeo26, Gtrosa26, R26, ROSA26|MGI:104735|gene trap ROSA 26, Philippe Soriano; targeted mutation 3237, TaconicArtemis|Gt(ROSA)26Sor||6|||||||||||||||||||||||||||||Unknown|Unknown|C57BL/6JArc|Yes|Unknown|Yes|Yes|Unknown|Yes|No|Excellent|10|||No|23-Oct-2017|Cryopreserved sperm|50.0|0.0|Unknown|||Yes| 8337.0|ptpn14flox/flox/CMVCre|B6(Cg)-Ptpn14/MarpCcb||Recessive|protein tyrosine phosphatase, non-receptor type 14|Ptpn14|Unknown|C130080N23Rik, OTTMUSG00000022087, PTP36|MGI:102467||Ptpn14||1|||||||||||||||||||||||||||||Periorbital oedema, lower limb oedema|Normal|C57BL/6J|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|27-Oct-2017|Cryopreserved sperm|46.0|0.0|Unknown|||Yes| 8329.0|ASD613:Pyro:8|C57BL/6NCrlAnu-Ptpn22/AnuApb||Recessive|protein tyrosine phosphatase, non-receptor type 22 (lymphoid)|Ptpn22|Unknown|70zpep, Ptpn8|MGI:107170||||3|||||||||||||||||||||||||||||Unknown||C57BL/6CrlAnu|Yes|Unknown|Yes|Yes|No|Yes|No|Unknown||||No|10-Oct-2017|Cryopreserved sperm|33.0|0.0|Unknown||CRISPR|Yes| 8330.0|Chat-cre|B6;129S6-Chat/JAnu||Dominant|choline acetyltransferase|Chat||B230380D24Rik|MGI:88392|choline acetyltransferase; targeted mutation 2, Bradford B Lowell|Chat|MGI:5475195|14|||||||||||||||||||||||||||||Normal||C57BL/6J|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|11-Oct-2017|Cryopreserved sperm|12.0|0.0|Unknown||Glucose|Yes| 8338.0|Egr2f/f.Egr3-/-|B6.129-Egr2 Egr3/AnuApb||Recessive|early growth response 2|Egr2||Egr-2, Krox20, Krox-20, NGF1-B, Zfp-25|MGI:95296|early growth response 2; targeted mutation 3, Patrick Charnay|Egr2|MGI:2183227|10|||||||||||||||||||||||||||||Unknown||C57BL/6|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown|>10|||No|27-Oct-2017|Cryopreserved sperm|24.0|0.0|Unknown||B cell|Yes| 8338.0|Egr2f/f.Egr3-/-|B6.129-Egr2 Egr3/AnuApb||Recessive|early growth response 3|Egr3|Nil|Pilot|MGI:1306780|early growth response 3; targeted mutation 1, Jeffrey Milbrandt|Egr3|MGI:2180063|14|||||||||||||||||||||||||||||Unknown||C57BL/6|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown|>10|||No|27-Oct-2017|Cryopreserved sperm|||Unknown||B cell|Yes| 8344.0|ASD872|B6.SJL-Ptprc/CrlAnu:Line A||Recessive|protein tyrosine phosphatase, receptor type, C|Ptprc||B220, CD45, Ly-5, Lyt-4, T200|MGI:97810|protein tyrosine phosphatase, receptor type, C; a variant|Ptprc|MGI:4819849|1|||||||||||||||||||||||||||||||C57BL/6NCrl|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|03-Nov-2017||0.0|13.0|Unknown||T cell|No| 8343.0|ASD867|BALB/cNCrlAnu:Pink||Dominant|||||||||||||||||||||||||||||||||||||||||Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|03-Nov-2017||0.0|51.0|Unknown|||No| 8341.0|SKAM1A Trangsgenic|C57BL/6-Tg(CAG-FGFR1OP2)/TasqCcb||Dominant|||||||||Unknown|||||||||||||||||human Fibroblast Growth Factor Receptor1 Oncongne partner 2|Chicken Beta actin|All cells||||||||||Unknown|Normal|C57BL/6|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|31-Oct-2017|Cryopreserved sperm|50.0|0.0|Unknown|||Yes| 8342.0|ASD866|C57BL/6NCrlAnu:Green||Dominant||||||||||||||||||||||||||||||||||||||Normal|||Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|03-Nov-2017||0.0|151.0|Unknown|||Yes| 8345.0||ASD873.Pear||Recessive|||||||||Unknown|||||||||||||||||||||||||||||Unknown|||Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|07-Nov-2017|Cryopreserved sperm|10.0|0.0|Unknown|||Yes| 8346.0|AMPK b1 KO|C57BL/6-Prkab1||Recessive|protein kinase, AMP-activated, beta 1 non-catalytic subunit|Prkab1|Nil|1300015D22Rik|MGI:1336167|protein kinase, AMP-activated, beta 1 non-catalytic subunit; targeted mutation 1, Bruce E Kemp|Prkab1|MGI:4439277|5|||||||||||||||||||||||||||||Homeostasis/metabolism phenotype:N• when fed a high-fat diet, mice exhibit resistance to diet induced hyperinsulinemia and insulin resistance.• mice exhibit normal response to renal ischemia-reperfusion injury.Decreased susceptibility to diet-induced obesity:• when fed a high-fat dietDecreased circulating insulin level:• in fasted mice fed a high-fat dietDecreased circulating leptin level:• whether fed chow or a high-fat dietDecreased circulating interleukin-6 level:• whether fed chow or a high-fat dietIncreased insulin sensitivity:• whether fed chow or a high-fat diet, mice exhibit increased insulin sensitivity compared with similarly treated wild-type mice• when fed a high-fat diet, mice exhibit increased glucose infusion rate suggesting improved skeletal muscle insulin sensitivity compared with similarly treated wild-type mice• whether fed chow or a high-fat diet, mice exhibit reduced hepatic glucose output and greater insulin-induced suppression of hepatic glucose production indicating increased hepatic insulin sensitivity compared with similarly treated wild-type miceAbnormal lipid level:• when fed a high-fat diet, mice exhibit decreased hepatic levels of triglyceride, diglyceride, and ceramide compared with wild-type miceDecreased liver triglyceride level:• when fed a high-fat dietDecreased susceptibility to hepatic steatosis:• when fed a high-fat diet, mice exhibit decreased hepatic levels of triglyceride, diglyceride, and ceramide compared with wild-type miceAbnormal hepatocyte physiology:• hepatocytes exhibit increased fatty acid synthesis and reduced fatty acid oxidation compared with wild-type cells• however, insulin sensitivity of hepatocytes is normal.Decreased epididymal fat pad weight:• whether fed chow or a high-fat diet|Normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|13-Nov-2017|Cryopreserved sperm|49.0|0.0|Unknown||AMP-activated protein kinase (AMPK)|Yes| 8347.0|AMPK Beta 2 KO|C57BL/6-Prkab2||Recessive|protein kinase, AMP-activated, beta 2 non-catalytic subunit|Prkab2||5730553K21Rik|MGI:1336185|protein kinase, AMP-activated, beta 2 non-catalytic subunit; targeted mutation 1, Gregory R Steinberg|Prkab2|MGI:5293372|3|||||||||||||||||||||||||||||Normal|Normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|13-Nov-2017|Cryopreserved sperm|50.0|0.0|Unknown||AMP-activated protein kinase (AMPK) β subunits (β1 and β2)|Yes| 8335.0|ptpn14LacZ/+|B6(Cg)-Ptpn14/MarpCcb||Recessive|protein tyrosine phosphatase, non-receptor type 14|Ptpn14|Unknown|C130080N23Rik, OTTMUSG00000022087, PTP36|MGI:102467|protein tyrosine phosphatase, non-receptor type 14; targeted mutation 1a, Helmholtz Zentrum Muenchen GmbH|Ptpn14|MGI:5318763|1|||||||||||||||||||||||||||||Periorbital oedema, lower limb oedema.|Normal|C57/BL/6J|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|27-Oct-2017|Cryopreserved sperm|46.0|0.0|Unknown|||Yes| 8333.0|ASD670:Nacho:::F2|C57BL/6NCrlAnu-Amigo3/AnuApb||Recessive|adhesion molecule with Ig like domain 3|Amigo3|Unknown|E430002N15Rik|MGI:2444854|Amigo3, endonuclease-mediated mutation 1, Australian National University|Amigo3||9||||||||||Unknown to Unknown|||||||||||||||||||Unknown|Unknown|C57BL/6NCrlAnu|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|19-Oct-2017|Cryopreserved sperm|24.0|0.0|Unknown|||Yes| 8351.0|Scn2a R851X|C57BL/6-Scn2a/SpetApb||Dominant|sodium channel, voltage-gated, type II, alpha|Scn2a|Unknown|A230052E19Rik, Nav1.2, Scn2a1|MGI:98248||||2|||||||||||||||||||||||||||||Embryonic lethal|Normal|C57BL/6|No|No|Yes|No|No|Yes|No|Good||||No|14-Nov-2017||0.0|0.0|No|||Yes| 8359.0|ASD866|C57BL/6NCrlAnu:Pink||Dominant||||||||||||||||||||||||||||||||||||||Normal|||Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|04-Dec-2017||0.0|5.0|Unknown|||Yes| 8352.0|GABRG2 R43Q|DBA-Gabrg2||Semi-dominant|gamma-aminobutyric acid (GABA) A receptor, subunit gamma 2 |Gabrg2||GABAA-R, Gabrg-2, gamma2|MGI:95623||||11|||||||||||||||||||||||||||||Partial perinatal lethality:• mice are rarely bornComplete postnatal lethality:• mice that are born die before P19Tremors:• mice that are born exhibit a severe tremorAbnormal gait:• mice that are born have altered gaitsAbnormal brain wave pattern:• mice lack normal brain rhythms|Mice heterozygous for the mutation demonstrated behavioral arrest associated with 6-to 7-Hz spike-and-wave discharges, which are blocked by ethosuximide, a first-line treatment for absence epilepsy in man. Seizures in the mouse showed an abrupt onset at around age 20 days corresponding to the childhood nature of this disease. Reduced cell surface expression of gamma2(R43Q) was seen in heterozygous mice in the absence of any change in alpha1 subunit surface expression|DBA|No|No|Yes|No|No|Yes|No|Unknown||||No|23-Nov-2017|Cryopreserved sperm|47.0|54.0|Unknown||epilepsy, seizures|Yes| 8357.0|ASD740:Cd79b:Y195H|C57BL/6NCrlAnu-Cd79b/AnuApb||Recessive|CD79B antigen|Cd79b|Unknown|B29, Igb, Igbeta, Ig-beta|MGI:96431||||11|||||||||||||||||||||||||||||Unknown||C57BL/6NCrlAnu|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|27-Nov-2017|Cryopreserved sperm|10.0|0.0|Unknown|||Yes| 8353.0|TetTXNIP/Ve-cdh5-rtTA|C57BL/6-Tg(TetO-TXNIP) Tg(Cdh5-tTA)D5Lbjn/Apb||Recessive||||||||||||||||||||||||||Human thioredoxin interacting protein||||||||||||Human TXNIP expressed in endothelial cells after treatment with tetracycline.||C57BL/6|Yes|Unknown|Yes|Yes|Unknown|Yes|No|Unknown||||No|27-Nov-2017|Cryopreserved sperm|50.0|0.0|Unknown|||Yes| 8353.0|TetTXNIP/Ve-cdh5-rtTA|C57BL/6-Tg(TetO-TXNIP) Tg(Cdh5-tTA)D5Lbjn/Apb||Recessive||||||||||||||||||||||||||transgene insertion D5, Laura E Benjamin|VE-cadherin|Endothelial cells||||||||||Human TXNIP expressed in endothelial cells after treatment with tetracycline.||C57BL/6|Yes|Unknown|Yes|Yes|Unknown|Yes|No|Unknown||||No|27-Nov-2017|Cryopreserved sperm|||Unknown|||Yes| 8354.0|TXNIPf-VECcre|C57BL/6-Txnip Tg(Cdh5-cre)/Apb||Recessive|thioredoxin interacting protein|Txnip|Unknown|Hyplip1, mVDUP1, THIF, VDUP1|MGI:1889549||||3|||||||||||||||||Cre recombinase|cadherin 5|Restricted to endothelial cells||||||||||Unknown|Unknown|C57BL6|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|27-Nov-2017|Cryopreserved sperm|50.0|0.0|Unknown|||Yes| 8350.0|ASD726:Taco:3::N1F1|C57BL/6NCrlAnu-Tax1bp1/AnuApb||Recessive|Tax1 (human T cell leukemia virus type I) binding protein 1|Tax1bp1|Unknown|1200003J11Rik, 1700069J21Rik, D6Ertd404e, D6Ertd772e, T6BP, TXBP151|MGI:1289308|Tax1bp1|Tax1bp1, endonuclease-mediated mutation 2, Australian National University||6||||||||||Unknown to Unknown|||||||||||||||||||Unknown|Unknown|C57BL/6NCrlAnu|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|14-Nov-2017|Cryopreserved sperm|36.0|0.0|Unknown|||Yes| 8348.0|A1(T183A) KI|C57BL/6-Prkaa1||Recessive|protein kinase, AMP-activated, alpha 1 catalytic subunit|Prkaa1|Unknown|AMPKalpha1, C130083N04Rik|MGI:2145955||||15|||||||||||||||||||||||||||||Normal|Normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Poor||||No|14-Nov-2017|Cryopreserved sperm|50.0|0.0|Unknown|||Yes| 8358.0|ASD869:Sumo|C57BL/6NCrlANU-Irak2/AnuApb||Recessive|interleukin-1 receptor-associated kinase 2|Irak2||6330415L08Rik, IRAK-2, Irak2a, Irak2b, Irak2c, Irak2d|MGI:2429603|Irak2, endonuclease-mediated mutation 1, Australian National University|Irak2||6|||||||||||||||||||||||||||||Unknown||C57BL/6NCrlAnu|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|29-Nov-2017|Cryopreserved sperm|11.0|0.0|Unknown|||Yes| 8361.0|ASD866|C57BL/6NCrlAnu:Yellow||Dominant||||||||||||||||||||||||||||||||||||||Normal|||Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|04-Dec-2017||0.0|14.0|Unknown|||Yes| 8365.0|ASD872|B6.SJL-Ptprc/CrlAnu:Line B||Recessive|protein tyrosine phosphatase, receptor type, C|Ptprc||B220, CD45, Ly-5, Lyt-4, T200|MGI:97810|protein tyrosine phosphatase, receptor type, C; a variant|Ptprc|MGI:4819849|1|||||||||||||||||||||||||||||||C57BL/6NCrl|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|04-Dec-2017||0.0|337.0|Unknown||T cell|No| 8362.0|ASD867|BALB/cNCrlAnu:Orange||Dominant|||||||||||||||||||||||||||||||||||||||||Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|04-Dec-2017||0.0|615.0|Unknown|||No| 8364.0|ASD867|BALB/cNCrlAnu:Green||Dominant|||||||||||||||||||||||||||||||||||||||||Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|04-Dec-2017||0.0|164.0|Unknown|||No| 8366.0|ASD726:Taco2:11bp del|C57BL/6NCrlANu-Tax1bp1/AnuApb||Recessive|Tax1 (human T cell leukemia virus type I) binding protein 1|Tax1bp1|Unknown|1200003J11Rik, 1700069J21Rik, D6Ertd404e, D6Ertd772e, T6BP, TXBP151|MGI:1289308|Tax1bp1, endonuclease-mediated mutation 1, Australian National University|Tax1bp1||6||||||||||Unknown to Unknown|||||||||||||||||||Unknown||C57BL/6NCrlAnu|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown|2018|||No|08-Dec-2017|Cryopreserved sperm|33.0|0.0|Unknown||CRISPR|Yes| 8368.0|Aire:Cbl-b:Rag1 KO|C57BL/6JSfdAnu-Aire Cblb Rag1/AnuApb||Recessive|Casitas B-lineage lymphoma b|Cblb||Cbl-b|MGI:2146430|Casitas B-lineage lymphoma b; targeted mutation 1, Josef M Penninger|Cblb|MGI:2180570|16|||||||||||||||||||||||||||||||C57BL/6JSfdAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|||sib x sib|No|08-Dec-2017|Cryopreserved sperm|22.0|0.0|No||Hen egg Lysozyme, tolerance, immunity, T cell, B cell, selection|Yes| 8368.0|Aire:Cbl-b:Rag1 KO|C57BL/6JSfdAnu-Aire Cblb Rag1/AnuApb||Recessive|recombination activating gene 1|Rag1||Rag-1|MGI:97848|recombination activating gene 1; targeted mutation 1, Peter Mombaerts|Rag1|MGI:1857241|2|||||||||||||||||||||||||||||||C57BL/6JSfdAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|||sib x sib|No|08-Dec-2017|Cryopreserved sperm|||No||Hen egg Lysozyme, tolerance, immunity, T cell, B cell, selection|Yes| 8368.0|Aire:Cbl-b:Rag1 KO|C57BL/6JSfdAnu-Aire Cblb Rag1/AnuApb||Recessive|autoimmune regulator (autoimmune polyendocrinopathy candidiasis ectodermal dystrophy)|Aire|Nil||MGI:1338803|autoimmune regulator (autoimmune polyendocrinopathy candidiasis ectodermal dystrophy); targeted mutation 1, Leena Peltonen|Aire|MGI:2182940|10|||||||||||||||||||||||||||||||C57BL/6JSfdAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|||sib x sib|No|08-Dec-2017|Cryopreserved sperm|||No||Hen egg Lysozyme, tolerance, immunity, T cell, B cell, selection|Yes| 8367.0|Cblb KO|B6(Cg)-Cblb/AnuApb|B6(Cg)-Cblb/AnuApb|Recessive|Casitas B-lineage lymphoma b|Cblb|Nil|Cbl-b|MGI:2146430|targeted mutation 1, Josef M Penninger|Cblb|MGI:2180570|16||||||||||||||||Yes|||||||||||||Homozygotes for targeted null mutations exhibit elevated IL2 production by T cells, develop spontaneous autoimmunity, and are highly susceptible to experimental autoimmune encephalomyelitis.||C57BL/NCrlAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|2|||No|08-Dec-2017|Cryopreserved sperm|33.0|0.0|No||IL-2, T cell, encephalomyelitis, autoimmune, signal transduction|Yes| 8374.0|NOD.Nkrp1b.CD3z|NOD-Cd247 Klrb1b Nkt1/Bax||Recessive|||||||||||||||||||||||||||||CD247 antigen|Cd247||4930549J05Rik, CD3-eta, Cd3h, Cd3z, CD3zeta, CD3 zeta, CD3-zeta, CD3-zeta/eta, T3z, TCRk, Tcrz|MGI:88334||||1|Mice that are homozygous for this allele are viable, fertile and normal in size. Can be difficult breeders.Congenic Nk Cell Marker. Congenic Marker for NKT1 region. Congenic Marker for CD3z region. Increased Nkt cell numbers.||NOD/Lt|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|10|||No|11-Dec-2017|Cryopreserved sperm|50.0|0.0|Unknown||Nk1.1, TCR, NK cell, autoimmunity|Yes| 8374.0|NOD.Nkrp1b.CD3z|NOD-Cd247 Klrb1b Nkt1/Bax||Recessive|||||||||||||||||||||||||||||killer cell lectin-like receptor subfamily B member 1B|Klrb1b||Klrb1d, Ly55b, Ly55d, Nkrp1-b, NKR-P1B, Nkrp1d, NKR-P1D|MGI:107539||||6|Mice that are homozygous for this allele are viable, fertile and normal in size. Can be difficult breeders.Congenic Nk Cell Marker. Congenic Marker for NKT1 region. Congenic Marker for CD3z region. Increased Nkt cell numbers.||NOD/Lt|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|10|||No|11-Dec-2017|Cryopreserved sperm|||Unknown||Nk1.1, TCR, NK cell, autoimmunity|Yes| 8374.0|NOD.Nkrp1b.CD3z|NOD-Cd247 Klrb1b Nkt1/Bax||Recessive|||||||||||||||||||||||||||||natural killer T cell numbers 1|Nktcn1||Nkt1|MGI:2681136|natural killer T cell numbers 1; C57BL/6J|Nktcn1|MGI:2681149|1|Mice that are homozygous for this allele are viable, fertile and normal in size. Can be difficult breeders.Congenic Nk Cell Marker. Congenic Marker for NKT1 region. Congenic Marker for CD3z region. Increased Nkt cell numbers.||NOD/Lt|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|10|||No|11-Dec-2017|Cryopreserved sperm|||Unknown||Nk1.1, TCR, NK cell, autoimmunity|Yes| 8372.0|NOD.H2b.SCID-/-|NOD.Cg-H2 Prkdc/BaxApb||Recessive|protein kinase, DNA activated, catalytic polypeptide|Prkdc|Nil|DNA-PK, DNA-PKcs, DNAPDcs, slip, XRCC7|MGI:104779|severe combined immunodeficiency|Prkdc|MGI:1857113|16||||||||||||||||Yes||||histocompatibility-2, MHC|H2||H-2, MHC-II|MGI:95894|histocompatibility-2, MHC; b variant|H2|MGI:3579319|17|SCID mutation prevents TCR and BCR rearrangements. This prevents maturation of B and T cells at very early stages of development. These mice, therefore lack, T and B cells in periphery. Please refer to MGI allele page for further information using the link above.Mice that are homozygous for the SCID mutation are viable, fertile, normal in size. This strain is immunocomprimised. Mice homozygous for the severe combined immune deficiency spontaneous mutation (Prkdcscid, commonly referred to as scid) are characterized by an absence of functional T cells and B cells, lymphopenia, hypogammaglobulinemia, and a normal hematopoietic microenvironment. Normal antigen-presenting cell, myeloid, and NK cell functions are strain dependent. scid mice carry a DNA repair defect and a defect in the rearrangement of genes that code for antigen-specific receptors on lymphocytes. Most homozygotes have no detectable IgM, IgG1, IgG2a, IgG2b, IgG3, or IgA. Thymus, lymph nodes, and splenic follicles are virtually devoid of lymphocytes. scid mice accept allogeneic and xenogeneic grafts making them an ideal model for cell transfer experiments. Some scid mice will spontaneously develop partial immune reactivity. scid mice that have serum Ig levels greater than 1 ug/ml are considered "leaky." scid leakiness is highly strain dependent, increases with age, and is higher in mice housed under non-SPF conditions. In general, scid leakiness is high on the C57BL/6J and BALB/cBy genetic backgrounds, low on the C3H/HeJ background, and even lower on the NOD/ShiLtSz background. NOD/ShiLtSz-Prkdcscid mice are both insulitis- and diabetes-free throughout life and serve as a diabetes-free control for comparison to NOD/ShiLtJ mice. Thymic lymphomas occur with high frequency, however, and life span typically is limited to only 8.5 months under specific pathogen-free conditions.Also contains congenic markers MHC haplotype H2ᵇThe NOD.H2ᵇstrain does not develop insulitis, cyclophosphamide-induced diabetes, or spontaneous diabetes, but does develop extensive lymphocytic infiltrates in the pancreas and the submandibular glands.||NOD/Lt|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||19||No|11-Dec-2017|Cryopreserved sperm|50.0|0.0|Yes||SCID, severe combined immunodeficiency, transplant, T cell, B cell|Yes| 8373.0|NOD.Nkrp1b.Nkt1|NOD-Klrb1b Nkt1/Bax||Recessive|||||||||||||||||||||||||||||killer cell lectin-like receptor subfamily B member 1B|Klrb1b||Klrb1d, Ly55b, Ly55d, Nkrp1-b, NKR-P1B, Nkrp1d, NKR-P1D|MGI:107539||||6|Mice that are homozygous for this allele are viable, fertile, normal in size.Congenic Nk Cell Marker. Congenic Marker for NKT1 region. Increased Nkt cell numbers.||NOD/Lt|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|10|||No|11-Dec-2017|Cryopreserved sperm|50.0|0.0|Unknown||Nk1.1, TCR, NK cell, autoimmunity|Yes| 8373.0|NOD.Nkrp1b.Nkt1|NOD-Klrb1b Nkt1/Bax||Recessive|||||||||||||||||||||||||||||natural killer T cell numbers 1|Nktcn1||Nkt1|MGI:2681136|natural killer T cell numbers 1; C57BL/6J|Nktcn1|MGI:2681149|1|Mice that are homozygous for this allele are viable, fertile, normal in size.Congenic Nk Cell Marker. Congenic Marker for NKT1 region. Increased Nkt cell numbers.||NOD/Lt|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|10|||No|11-Dec-2017|Cryopreserved sperm|||Unknown||Nk1.1, TCR, NK cell, autoimmunity|Yes| 8909.0|ASD901:Plantain:IK512|C57BL/6NCrlAnu-Ikzf2/AnuApb||Recessive|IKAROS family zinc finger 2|Ikzf2||A730095J18Rik, Helios, Zfpn1a2|MGI:1342541||||1|||||||||||||||||||||||||||||Unknown|Unknown|C57BL/6NCrlAnu|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|20-Mar-2020|Cryopreserved sperm|40.0|0.0|Unknown|||Yes| 8376.0|NOD.Nkrp1b.Slam1c|NOD-Klrb1b Nkt1 Slam1c/Bax||Recessive||||||||||||||||||||||||||||||||||||||Mice that are homozygous for this allele are viable, fertile and normal in size.Congenic Nk Cell Marker. Congenic Marker for NKT1 region. Congenic Marker for Slam1c region. Increased Nkt cell numbers.||NOD/Lt|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|10|||No|11-Dec-2017|Cryopreserved sperm|50.0|0.0|Unknown||Nk1.1, TCR, NK cell, autoimmunity|Yes| 8380.0|NOD.Nkrp1b.Nkt2e|NOD-Klrb1b Nktcn2e/Bax||Recessive|||||||||||||||||||||||||||||killer cell lectin-like receptor subfamily B member 1B|Klrb1b||Klrb1d, Ly55b, Ly55d, Nkrp1-b, NKR-P1B, Nkrp1d, NKR-P1D|MGI:107539||||6|Mice that are homozygous for this allele are viable, fertile and normal in size.Congenic Nk Cell Marker. Congenic Marker for NKT2 region. Increased Nkt cell numbers.|Differences in susceptibility to autoimmunity.|NOD/Lt|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|11-Dec-2017||0.0|0.0|Unknown||Nk1.1, TCR, NK cell, autoimmunity|Yes| 8380.0|NOD.Nkrp1b.Nkt2e|NOD-Klrb1b Nktcn2e/Bax||Recessive|||||||||||||||||||||||||||||natural killer T cell numbers 2|Nktcn2||Nkt2|MGI:2681137|natural killer T cell numbers 2; C57BL/6J|Nktcn2|MGI:2681151|2|Mice that are homozygous for this allele are viable, fertile and normal in size.Congenic Nk Cell Marker. Congenic Marker for NKT2 region. Increased Nkt cell numbers.|Differences in susceptibility to autoimmunity.|NOD/Lt|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|11-Dec-2017||||Unknown||Nk1.1, TCR, NK cell, autoimmunity|Yes| 8385.0|Prox1enhCRISPR-Banzai|C57BL/6-Prox1||Recessive|prospero homeobox 1|Prox1||A230003G05Rik|MGI:97772||||1|||||||||||||||||||||||||||||Unknown|Normal|C57BL/6|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|18-Dec-2017|Cryopreserved sperm|50.0|0.0|Unknown|||Yes| 8851.0|mHEL3x|B6.Cg-Gt(ROSA)26Sor/Anu||Dominant|gene trap ROSA 26, Philippe Soriano|Gt(ROSA)26Sor|Unknown|beta geo, Gtrgeo26, Gtrosa26, R26, ROSA26, Thumpd3as1|MGI:104735|gene trap ROSA 26, Philippe Soriano; targeted mutation 1.1, Robert Brink|Gt(ROSA)26Sor||6||||||||||||||||||||||||||||||Ubiquitous expression of HEL3x|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|11-Feb-2020|Cryopreserved sperm|52.0|39.0|Unknown||HEL, selection|Yes| 8381.0|TCR7|C57BL/6-Tg(TcraBO4H9.1,TcrbBO4H9.1)7Aog||Dominant||||||||||||||||||||||||||transgene insertion 7 Anne O'Garra||||||||||||T cells express anti-hen egg lysozyme (HEL) TCR Valpha11 and Vbeta3 chains||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|12-Dec-2017|Cryopreserved sperm|1.0|127.0|Unknown||T cell, TCR, HEL, CD4|Yes| 8383.0|Integrin beta3 Knockout|C.129S2-Itgb3||Recessive|integrin beta 3|Itgb3|Nil|CD61, platelet glycoprotein IIIa (GP3A)|MGI:96612|integrin beta 3; targeted mutation 1, Richard Hynes|Itgb3|MGI:2175913|11|||||||||||||||||||||||||||||Mice look normal, are fertile and breed normally. They have a mild bone phenotype due to dysfunctional osteoclasts. Mice a prone to excesasive bleeding after injury due to defective platelets lacking alphaIIbBeta3 integrin. Females may have placental defects that can lead to fetal mortality. For this reason, only heterozygote females are used for breeding.|Normal, as WT mice|BALB/c|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|13-Dec-2017|Cryopreserved sperm|30.0|0.0|Unknown||Glanzmann thrombasthenia, thrombosis|Yes| 8386.0|Prox1enhCRISPR-Timon|C57BL/6-Prox1||Recessive|prospero homeobox 1|Prox1||A230003G05Rik|MGI:97772||||1|||||||||||||||||||||||||||||Unknown|Normal|C57BL/6|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|18-Dec-2017|Cryopreserved sperm|50.0|0.0|Unknown|||Yes| 8388.0|Prox1enhCRISPR-Pumbaa|C57BL/6-Proz1||Recessive|prospero homeobox 1|Prox1||A230003G05Rik|MGI:97772||||1|||||||||||||||||||||||||||||Unknown|Normal|C57BL/6|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|18-Dec-2017|Cryopreserved sperm|40.0|0.0|Unknown|||Yes| 8371.0|NOD.H2b.Nkrp1b|NOD-H2 Klrb1b/Bax||Recessive|||||||||||||||||||||||||||||histocompatibility-2, MHC|H2||H-2, MHC-II|MGI:95894|histocompatibility-2, MHC; b variant|H2|MGI:3579319|17|Mice that are homozygous for this allele are viable, fertile, normal in size.||NOD/Lt|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|10|||No|11-Dec-2017|Cryopreserved sperm|50.0|0.0|Unknown||Nk1.1, TCR, NK cell, autoimmunity|Yes| 8371.0|NOD.H2b.Nkrp1b|NOD-H2 Klrb1b/Bax||Recessive|||||||||||||||||||||||||||||killer cell lectin-like receptor subfamily B member 1B|Klrb1b||Klrb1d, Ly55b, Ly55d, Nkrp1-b, NKR-P1B, Nkrp1d, NKR-P1D|MGI:107539||||6|Mice that are homozygous for this allele are viable, fertile, normal in size.||NOD/Lt|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|10|||No|11-Dec-2017|Cryopreserved sperm|||Unknown||Nk1.1, TCR, NK cell, autoimmunity|Yes| 8379.0|NOD.Nkrp1b.Nkt2a|NOD-Klrb1b Nktcn2a/Bax||Recessive|||||||||||||||||||||||||||||killer cell lectin-like receptor subfamily B member 1B|Klrb1b||Klrb1d, Ly55b, Ly55d, Nkrp1-b, NKR-P1B, Nkrp1d, NKR-P1D|MGI:107539||||6|Mice that are homozygous for this allele are viable, fertile and normal in size.Congenic Nk Cell Marker. Congenic Marker for NKT2 region. Increased Nkt cell numbers.|Differences in susceptibility to autoimmunity.|NOD/Lt|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|11-Dec-2017|Cryopreserved sperm|50.0|0.0|Unknown||Nk1.1, TCR, NK cell, autoimmunity|Yes| 8379.0|NOD.Nkrp1b.Nkt2a|NOD-Klrb1b Nktcn2a/Bax||Recessive|||||||||||||||||||||||||||||natural killer T cell numbers 2|Nktcn2||Nkt2a|MGI:2681137|natural killer T cell numbers 2; C57BL/6J|Nktcn2|MGI:2681151|2|Mice that are homozygous for this allele are viable, fertile and normal in size.Congenic Nk Cell Marker. Congenic Marker for NKT2 region. Increased Nkt cell numbers.|Differences in susceptibility to autoimmunity.|NOD/Lt|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|11-Dec-2017|Cryopreserved sperm|||Unknown||Nk1.1, TCR, NK cell, autoimmunity|Yes| 8392.0|NOD.Idd13|NOD-Idd13/Bax||Recessive|||||||||||||||||||||||||||||insulin dependent diabetes susceptibility 13|Idd13|||MGI:99415|insulin dependent diabetes susceptibility 13; C57BL/6|Idd13|MGI:3044074|2|Mice that are homozygous for this allele are viable, fertile, normal in size.Difference in autoimmunity susceptibility compared to NOD.This strain is congenic for a 32 cM segment of Chr 2 extending from D2Mit274 through D2Mit343 that includes the insulin dependent diabetes susceptibility locus Idd13.||NOD/Lt|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|19-Dec-2017|Cryopreserved sperm|50.0|0.0|Unknown||NK cell, autoimmunity|Yes| 8390.0|Fat4 flox|B6.129-Fat4/HmcApb||Recessive|FAT atypical cadherin 4|Fat4||6030410K14Rik|MGI:3045256|FAT atypical cadherin 4; targeted mutation 1.1, Helen McNeill|Fat4|MGI:3846573|3|||||||||||||||||||||||||||||Normal|Normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|18-Dec-2017|Cryopreserved sperm|50.0|0.0|Unknown||cystic kidney disease|Yes| 8389.0|Conditional SMAD1 f/f|C.129-Smad1||Recessive|SMAD family member 1|Smad1||Madh1, Madr1, Smad 1|MGI:109452|SMAD family member 1; targeted mutation 2, Elizabeth J Robertson|Smad1|MGI:2155484|8|||||||||||||||||||||||||||||Normal|Normal|BALB/c |Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown|10|||No|18-Dec-2017|Cryopreserved sperm|50.0|0.0|Unknown||TGF, BMP|Yes| 8391.0|Gata2 flox|B6.129-Gata2||Recessive|GATA binding protein 2|Gata2||Gata-2|MGI:95662|GATA binding protein 2; targeted mutation 1, Marjo Salminen|Gata2|MGI:4818492|6|||||||||||||||||||||||||||||Normal|Normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|19-Dec-2017|Cryopreserved sperm|50.0|0.0|Unknown||transcription factor|Yes| 8395.0|NOD.Nkrplb.Slam1D.CD-1|NOD-CD1 Klrb1b Slamf1D/Bax||Recessive|CD1 antigen complex|Cd1|Nil||MGI:102561|CD1 antigen complex; targeted mutation 1, Michael Grusby|Cd1|MGI:1857482|3||||||||||||||||||||killer cell lectin-like receptor subfamily B member 1B|Klrb1b||Klrb1d, Ly55b, Ly55d, Nkrp1-b, NKR-P1B, Nkrp1d, NKR-P1D|MGI:107539||||6|Animals homozygous for CD1 KO mutation lack an NK-like cell subset (HSA<-/low>, NK1.1+, TCRint, CD44high, CD122+) of thymocytes. TCR cross-linking and anti-CD3 stimulation fails to induce IL-4 production."Mice can have trouble breeding. Keep a close eye on progress and increase breeders as required to maintain line. If a case of breeding ceasing, may need to cross back onto a parental line. Ideally NOD.Nkrplb.Nktl.SlamlD to reduce genotyping.Nkrplb:Congenic Nk Cell Marker. Nktl:Congenic Marker for NKT1 region. Increased Nkt cell numbers.CD-1:Knockout lacking the CD1 antigen complex gene. Lack an NK-like cell subset.SlamlD:Congenic Marker for Slam1D region. Increased Nkt cell numbers.||NOD/Lt|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|10|||No|19-Dec-2017|Cryopreserved sperm|50.0|0.0|Unknown||Nk1.1, TCR, NK cell, autoimmunity|Yes| 8395.0|NOD.Nkrplb.Slam1D.CD-1|NOD-CD1 Klrb1b Slamf1D/Bax||Recessive|||||||||||||||||||||||||||||signaling lymphocytic activation molecule family member 1|Slamf1||CD150, CDw150, ESTM51, IPO-3, Slam|MGI:1351314||||1|Animals homozygous for CD1 KO mutation lack an NK-like cell subset (HSA<-/low>, NK1.1+, TCRint, CD44high, CD122+) of thymocytes. TCR cross-linking and anti-CD3 stimulation fails to induce IL-4 production."Mice can have trouble breeding. Keep a close eye on progress and increase breeders as required to maintain line. If a case of breeding ceasing, may need to cross back onto a parental line. Ideally NOD.Nkrplb.Nktl.SlamlD to reduce genotyping.Nkrplb:Congenic Nk Cell Marker. Nktl:Congenic Marker for NKT1 region. Increased Nkt cell numbers.CD-1:Knockout lacking the CD1 antigen complex gene. Lack an NK-like cell subset.SlamlD:Congenic Marker for Slam1D region. Increased Nkt cell numbers.||NOD/Lt|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|10|||No|19-Dec-2017|Cryopreserved sperm|||Unknown||Nk1.1, TCR, NK cell, autoimmunity|Yes| 8394.0|NOD.Idd13.Nkrp1b.Cd-1-/-|NOD-CD1 Idd13 Klrb1b/Bax||Recessive|CD1 antigen complex|Cd1|Nil||MGI:102561|CD1 antigen complex; targeted mutation 1, Michael Grusby|Cd1|MGI:1857482|3||||||||||||||||||||killer cell lectin-like receptor subfamily B member 1B|Klrb1b||Klrb1d, Ly55b, Ly55d, Nkrp1-b, NKR-P1B, Nkrp1d, NKR-P1D|MGI:107539||||6|Animals homozygous for CD1 KO mutation lack an NK-like cell subset (HSA<-/low>, NK1.1+, TCRint, CD44high, CD122+) of thymocytes. TCR cross-linking and anti-CD3 stimulation fails to induce IL-4 production.Idd13:Idd13 is congenic for a 32 cM segment of Chr 2 extending from D2Mit274 through D2Mit343 that includes the insulin dependent diabetes susceptibility locus Idd13.H2b:Congenic markers MHC haplotype H2ᵇ. Nkrplb:Congenic Nk Cell Marker. Congenic markers MHC haplotype H2ᵇ"||NOD/Lt|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|10|||No|19-Dec-2017|Cryopreserved sperm|30.0|0.0|Unknown||Nk1.1, TCR, NK cell, autoimmunity|Yes| 8394.0|NOD.Idd13.Nkrp1b.Cd-1-/-|NOD-CD1 Idd13 Klrb1b/Bax||Recessive|||||||||||||||||||||||||||||insulin dependent diabetes susceptibility 13|Idd13|||MGI:99415|insulin dependent diabetes susceptibility 13; C57BL/6|Idd13|MGI:3044074|2|Animals homozygous for CD1 KO mutation lack an NK-like cell subset (HSA<-/low>, NK1.1+, TCRint, CD44high, CD122+) of thymocytes. TCR cross-linking and anti-CD3 stimulation fails to induce IL-4 production.Idd13:Idd13 is congenic for a 32 cM segment of Chr 2 extending from D2Mit274 through D2Mit343 that includes the insulin dependent diabetes susceptibility locus Idd13.H2b:Congenic markers MHC haplotype H2ᵇ. Nkrplb:Congenic Nk Cell Marker. Congenic markers MHC haplotype H2ᵇ"||NOD/Lt|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|10|||No|19-Dec-2017|Cryopreserved sperm|||Unknown||Nk1.1, TCR, NK cell, autoimmunity|Yes| 8396.0|NOD.Nkrp1b.Nkt2b.CD-1|NOD-Cd1 Klrb1b Nktcn2b/Bax||Recessive|CD1 antigen complex|Cd1|Nil||MGI:102561|CD1 antigen complex; targeted mutation 1, Michael Grusby|Cd1|MGI:1857482|3||||||||||||||||||||killer cell lectin-like receptor subfamily B member 1B|Klrb1b||Klrb1d, Ly55b, Ly55d, Nkrp1-b, NKR-P1B, Nkrp1d, NKR-P1D|MGI:107539||||6|Difficult breeders. Have had to restart the breeding, multiple times due to the difficulty in getting them homozygous. Seems homozygous mice do not breed. Congenic Nk Cell Marker. Congenic Marker for NKT2 region. Increased Nkt cell numbers.Knockout lacking the CD1 antigen complex gene||NOD/Lt|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|10|||No|19-Dec-2017|Cryopreserved sperm|50.0|0.0|Unknown||Nk1.1, TCR, NK cell, autoimmunity|Yes| 8396.0|NOD.Nkrp1b.Nkt2b.CD-1|NOD-Cd1 Klrb1b Nktcn2b/Bax||Recessive|||||||||||||||||||||||||||||natural killer T cell numbers 2|Nktcn2||Nkt2b|MGI:2681137||||2|Difficult breeders. Have had to restart the breeding, multiple times due to the difficulty in getting them homozygous. Seems homozygous mice do not breed. Congenic Nk Cell Marker. Congenic Marker for NKT2 region. Increased Nkt cell numbers.Knockout lacking the CD1 antigen complex gene||NOD/Lt|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|10|||No|19-Dec-2017|Cryopreserved sperm|||Unknown||Nk1.1, TCR, NK cell, autoimmunity|Yes| 8397.0|NOD.Faslm1|NOD-Fasl/Bax||Recessive|Fas ligand (TNF superfamily, member 6)|Fasl|Unknown|APT1LG1, CD178, CD95L, Fasl, Fas-L, Tnfsf6|MGI:99255||Fasl||1|||||||||||||||||||||||||||||Mice that are homozygous for these alleles are viable, fertile, normal in size. Mice have affected severity of autoimmunity compared to controls.Spontaneous Mutation of Ligand||NOD/Lt|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|||Hom x Hom|No|19-Dec-2017|Cryopreserved sperm|50.0|0.0|Unknown||autoimmunity|Yes| 8398.0|NOD.Faslm2|NOD-Fasl/Bax||Recessive|Fas ligand (TNF superfamily, member 6)|Fasl|Unknown|APT1LG1, CD178, CD95L, Fasl, Fas-L, Tnfsf6|MGI:99255||Fasl||1|||||||||||||||||||||||||||||Mice that are homozygous for these alleles are viable, fertile, normal in size. Affects severity of autoimmunity compared to controlsSpontaneous Mutation of LigandFaslm2bSpontaneous Mutation of Ligand from C57Bl6 Identical to NOD.Faslm2||NOD/Lt|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|||Hom x Hom|No|19-Dec-2017|Cryopreserved sperm|50.0|0.0|Unknown||autoimmunity|Yes| 8399.0|NOD.Faslm2b|NOD-Fasl/Bax||Recessive|Fas ligand (TNF superfamily, member 6)|Fasl|Unknown|APT1LG1, CD178, CD95L, Fasl, Fas-L, Tnfsf6|MGI:99255||Fasl||1|||||||||||||||||||||||||||||Mice that are homozygous for these alleles are viable, fertile, normal in size. Affects severity of autoimmunity compared to controlsSpontaneous Mutation of LigandFaslm2bSpontaneous Mutation of Ligand from C57Bl6 Identical to NOD.Faslm2||NOD/Lt|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|||Hom x Hom|No|19-Dec-2017|Cryopreserved sperm|149.0|0.0|Unknown||autoimmunity|Yes| 8400.0|NOD.Trail|NOD.129-Tnfsf10/MjsBax||Recessive|tumor necrosis factor (ligand) superfamily, member 10|Tnfsf10|Nil|A330042I21Rik, APO-2L, Trail|MGI:107414|tumor necrosis factor (ligand) superfamily, member 10; targeted mutation 1, Mark J Smyth|Tnfsf10|MGI:2179709|3||||||||||||||||||||||||||||| Thymus hyperplasia, abnormal negative T cell selection, increased susceptibility to autoimmune diseases and to tumor initiation and metastasis, and resistance to induced hepatitis.||NOD/Lt|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|19-Dec-2017|Cryopreserved sperm|50.0|0.0|Unknown||TNF, metastasis|Yes| 8401.0|BALB.4220-3855|BALB/c-Gasa/Bax||Recessive|||||||||||||||||||||||||||||Unknown||||||||Unknown|Altered response to induced neonatal thymectomy induced gastritis compared to BALB/c mcie.||BALB/c|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|||Hom x Hom|No|19-Dec-2017|Cryopreserved sperm|80.0|0.0|Unknown||autoimmunity, gastritis|Yes| 8403.0|BALB.8755-3855|BALB/c-Gasa/Bax||Recessive|||||||||||||||||||||||||||||Unknown||||||||Unknown|Altered response to induced neonatal thymectomy induced gastritis compared to BALB/c mcie.||BALB/c|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|||Hom x Hom|No|19-Dec-2017|Cryopreserved sperm|50.0|0.0|Unknown||autoimmunity, gastritis|Yes| 8404.0|BALB.931-189B|BALB/c-Gasa/Bax||Recessive|||||||||||||||||||||||||||||Unknown||||||||Unknown|Altered response to induced neonatal thymectomy induced gastritis compared to BALB/c mcie.||BALB/c|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|||Hom x Hom|No|19-Dec-2017|Cryopreserved sperm|50.0|0.0|Unknown||autoimmunity, gastritis|Yes| 8405.0|BALB.931-203.344-3855|BALB/c-Gasa/Bax||Recessive|||||||||||||||||||||||||||||Unknown||||||||Unknown|Altered response to induced neonatal thymectomy induced gastritis compared to BALB/c mcie.||BALB/c|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|||Hom x Hom|No|19-Dec-2017|Cryopreserved sperm|50.0|0.0|Unknown||autoimmunity, gastritis|Yes| 8411.0|NOD.H2k.Nkrp1b|NOD-H2 Klrb1b/Bax||Recessive|||||||||||||||||||||||||||||histocompatibility-2, MHC|H2||H-2, MHC-II|MGI:95894|histocompatibility-2, MHC; k variant|H2|MGI:3579322|17|Mice that are homozygous for this allele are viable, fertile, normal in size.Nkrplb:Congenic Nk Cell Marker.H2k:Congenic Nk Cell Marker. Congenic markers MHC haplotype H2k. ||NOD/Lt|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|10||Hom x Hom|No|19-Dec-2017||0.0|0.0|Unknown||Nk1.1, TCR, NK cell, autoimmunity|Yes| 8411.0|NOD.H2k.Nkrp1b|NOD-H2 Klrb1b/Bax||Recessive|||||||||||||||||||||||||||||killer cell lectin-like receptor subfamily B member 1B|Klrb1b||Klrb1d, Ly55b, Ly55d, Nkrp1-b, NKR-P1B, Nkrp1d, NKR-P1D|MGI:107539||||6|Mice that are homozygous for this allele are viable, fertile, normal in size.Nkrplb:Congenic Nk Cell Marker.H2k:Congenic Nk Cell Marker. Congenic markers MHC haplotype H2k. ||NOD/Lt|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|10||Hom x Hom|No|19-Dec-2017||||Unknown||Nk1.1, TCR, NK cell, autoimmunity|Yes| 8406.0|BALB.931-203.64-3855|BALB/c-Gasa/Bax||Recessive|||||||||||||||||||||||||||||Unknown||||||||Unknown|Altered response to induced neonatal thymectomy induced gastritis compared to BALB/c mcie.||BALB/c|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|||Hom x Hom|No|19-Dec-2017|Cryopreserved sperm|50.0|0.0|Unknown||autoimmunity, gastritis|Yes| 8409.0|NOD.Idd5r|NOD-Idd5r/Bax||Recessive|||||||||||||||||||||||||||||insulin dependent diabetes susceptibility 5r|Idd5r|||||||2|Mice that are homozygous for this allele are viable, fertile, normal in size.This strain is congenic for a 32 cM segment of Chr 2 extending from D2Mit274 through D2Mit343 that includes the insulin dependent diabetes susceptibility locus Idd5r||NOD/Lt|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|19-Dec-2017|Cryopreserved sperm|50.0|0.0|Unknown||insulin|Yes| 8410.0|NOD.H2d.Nkrp1b|NOD-H2 Klrb1b/Bax||Recessive|||||||||||||||||||||||||||||histocompatibility-2, MHC|H2||H-2, MHC-II|MGI:95894|histocompatibility-2, MHC; d variant|H2|MGI:3579320|17|Mice that are homozygous for this allele are viable, fertile, normal in size.Nkrplb:Congenic Nk Cell Marker.H2d:Congenic Nk Cell Marker. Congenic markers MHC haplotype H2d. ||NOD/Lt|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|10||Hom x Hom|No|19-Dec-2017|Cryopreserved sperm|50.0|0.0|Unknown||Nk1.1, TCR, NK cell, autoimmunity|Yes| 8410.0|NOD.H2d.Nkrp1b|NOD-H2 Klrb1b/Bax||Recessive|||||||||||||||||||||||||||||killer cell lectin-like receptor subfamily B member 1B|Klrb1b||Klrb1d, Ly55b, Ly55d, Nkrp1-b, NKR-P1B, Nkrp1d, NKR-P1D|MGI:107539||||6|Mice that are homozygous for this allele are viable, fertile, normal in size.Nkrplb:Congenic Nk Cell Marker.H2d:Congenic Nk Cell Marker. Congenic markers MHC haplotype H2d. ||NOD/Lt|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|10||Hom x Hom|No|19-Dec-2017|Cryopreserved sperm|||Unknown||Nk1.1, TCR, NK cell, autoimmunity|Yes| 8414.0|Cd25 KO;OT-I|B6.Cg-Il2ra Tg(TcraTcrb)1100Mjb/WehiAnu||Recessive|interleukin 2 receptor, alpha chain|Il2ra||CD25, Il2r, IL-2R alpha chain, Ly-43|MGI:96549|interleukin 2 receptor, alpha chain; targeted mutation 1, Dennis M Willerford|Il2ra|MGI:1857192|2|||||||||||||||||transgene insertion 1100, Michael J Bevan|MGI:3054907|||||||||||Mice homozygous for the CD25 (IL2Ra) targeted mutation are characterized by a lymphoproliferative disorder, hemolytic anemia and an inflammatory bowel disease beginning at approximately 9 weeks of age. Homozygous females may not be healthy enough to breed. ||C57BL/6J|Yes|Unknown|No|Yes|Unknown|No|No|Unknown||||No|10-Jan-2018|Cryopreserved sperm|21.0|0.0|Unknown||T cell|Yes| 8418.0|ENU39:064:Casp1:G3|C57BL/6NCrlAnu-Casp1/AnuApb||Recessive|caspase 1|Casp1|Unknown|Caspase-1, ICE, Il1bc, interleukin 1 beta-converting enzyme|MGI:96544||||9|||||||||||||||||||||||||||||Unknown||C57BL/6NCrlAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|17-Jan-2018|Cryopreserved sperm|44.0|0.0|Unknown||Caspase|Yes| 8413.0||ASD827:Fry||Recessive|Unknown||||||||Unknown|||||||||||||||||||||||||||||Unknown|||Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|21-Dec-2017|Cryopreserved sperm|12.0|0.0|Unknown|||Yes| 8419.0|Tcf7 fl|B6(Cg)-Tcf7/WehiAnuApb||Recessive|transcription factor 7, T cell specific|Tcf7||T cell factor-1, T-cell factor 1, Tcf1, TCF-1|MGI:98507|transcription factor 7, T cell specific; targeted mutation 1c, Wellcome Trust Sanger Institute|Tcf7|MGI:5816259|11||||||||||Unknown to Unknown|||||||||||||||||||Normal||C57BL/6|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|17-Jan-2018|Cryopreserved sperm|21.0|0.0|Unknown|||Yes| 8407.0|NOD.H2d|NOD-H2/Bax||Recessive|||||||||||||||||||||||||||||histocompatibility-2, MHC|H2||H-2, MHC-II|MGI:95894|histocompatibility-2, MHC; d variant|H2|MGI:3579320|17|Mice that are homozygous for this allele are viable, fertile, normal in size.Congenic markers MHC haplotype H2||NOD/Lt|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|19-Dec-2017|Cryopreserved sperm|49.0|0.0|Unknown||MHC|Yes| 8408.0|NOD.Idd27|NOD-Idd27/Bax||Recessive|||||||||||||||||||||||||||||insulin dependent diabetes susceptibility 27|Idd27|||MGI:3608893||||7|Mice that are homozygous for this allele are viable, fertile, normal in size.This strain is congenic for a 32 cM segment of Chr 2 extending from D2Mit274 through D2Mit343 that includes the insulin dependent diabetes susceptibility locus Idd27||NOD/Lt|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|19-Dec-2017|Cryopreserved sperm|50.0|0.0|Unknown||insulin|Yes| 8416.0|Pad4 fl|B6.Cg-Padi4/KmowAnu||Recessive|peptidyl arginine deiminase, type IV|Padi4|Nil|Pad4, PAD type IV, Pdi4|MGI:1338898|peptidyl arginine deiminase, type IV; targeted mutation 1.2, Kerri A Mowen|Padi4|MGI:5695766|4|||||||||||||||||||||||||||||Normal||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|16-Jan-2018|Cryopreserved sperm|44.0|0.0|Unknown||Infection, neutrophil, extracellular traps|Yes| 8412.0|ELF5-rRTA-TetO-Cre-Neu|FVB/N.Cg-Tg(Elf5-rtTA,tetO-cre)||Dominant||||||||||||||||||||||||||ELF5-rRTA, TetO-Cre, Neu|ELF5, TetO, MMTV|||||||||||Normal|Normal|FVB/N X BL6/129|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|20-Dec-2017|Cryopreserved sperm|30.0|0.0|Unknown|||No| 8426.0|RBC19|SJL-Tpi||Semi-dominant|triosephosphate isomerase 1|Tpi1|Unknown|Tpi-1|MGI:98797|Tpi^F57S/F57S|||6|||||||||||||||||||||||||||||Macrocytosis and haemolytic anaemia, high MCV, low RBC, splenomegaly, viable and fertile.|Macrocytosis, high MCV.|SJL|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|25-Jan-2018|Cryopreserved sperm|50.0|0.0|Unknown|||Yes| 8428.0|Wnt11-myrTagRFP-IRES-CE|B6.Cg-Tg(Wnt11-TagRFP/cre/ERT2)28Amc||Dominant||||||||||||||||||||||||||transgene insertion 28, Andrew McMahon|Wnt11, wingless-type MMTV integration site family, member 11, mouse, laboratory|||||||||||Unknown|Unknown|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|29-Jan-2018|Cryopreserved sperm|49.0|0.0|Unknown||Wnt11, RFP|Yes| 8422.0|uPAR KO|B6.129-Plaur||Recessive|plasminogen activator, urokinase receptor|Plaur||Cd87, uPAR, u-PAR, urokinase-type plasminogen activator receptor|MGI:97612|plasminogen activator, urokinase receptor; targeted mutation 1, Jay L Degen|Plaur|MGI:1857290|7|||||||||||||||||||||||||||||Liver inflammationTrachea inflammation|Normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|10||brother x sister|Yes|18-Jan-2018|Cryopreserved sperm|50.0|0.0|No||Haemostasis|Possibly| 8423.0|Kif1bp KO #2|C57BL/6-Kif1bp/Hmy||Recessive|KIF1 binding protein|Kif1bp||0710007C18Rik, 2510003E04Rik, mKIAA1279|MGI:1919570|kinesin family binding protein; endonuclease-mediated mutation 1, Heather Young|Kif1bp|MGI:6150321|10||||||||||Unknown to Unknown|||||||||||||||||||Neonatal lethal. Die at birth due to breathing difficulties. Mice display broad peripheral neuropathies, as well as small olfactory bulbs and reduced white mater tracts (anterior commissure).|Normal|C57BL/6|No|No|Yes|No|No|Yes|No|Unknown||||No|19-Jan-2018|Cryopreserved sperm|50.0|0.0|Yes|Goldberg-Shprintzen syndrome|Nerve, olfactory, commissures|Yes| 8427.0|tPA-/-|B6.129-Plat/Mlg||Recessive|plasminogen activator, tissue|Plat|Nil|D8Ertd2e, MGC:18508, tPA, t-PA|MGI:97610|plasminogen activator, tissue; targeted mutation 1, Richard C Mulligan|Plat|MGI:1857288|8|||||||||||||||||||||||||||||Normal|Normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Excellent||||No|25-Jan-2018|Cryopreserved sperm|50.0|0.0|Unknown||fibrin, clot|Yes| 8425.0|RBC21|B6.Cg-Tfrc||Semi-dominant|transferrin receptor|Tfrc|Unknown|2610028K12Rik, CD71, E430033M20Rik, Mtvr1, Mtvr-1, p90, TfR1, Trfr|MGI:98822|Tfrc^R654H|||16|||||||||||||||||||||||||||||Homozygous lethal E16.5-18.5 due to profound anaemia.|Mild anaemia, low MCV, high RBC, low Hb.|C57BL/6|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|25-Jan-2018|Cryopreserved sperm|50.0|0.0|Unknown|||Yes| 8430.0|RBC16|BALB/c-Cpox/WehiMarpApb||Dominant|coproporphyrinogen oxidase|Cpox|Nil|cac, clone 560, Cpo, nct|MGI:104841|Cpox|||16|||||||||||||||||||||||||||||Lethal (e9.5) |Microcytosis (low MCV), low Hb|BALB/c|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|02-Feb-2018||0.0|0.0|Unknown||Haem, porphyrins, Hereditary coproporphyria, Anaemia|Yes| 8434.0|14-3-3zeta(Gt(OST062)Lex ; Armada|C.129S5-Ywhaz/Apb||Recessive|tyrosine 3-monooxygenase/tryptophan 5-monooxygenase activation protein, zeta polypeptide|Ywhaz|Nil|1110013I11Rik, 14-3-3 zeta|MGI:109484|tyrosine 3-monooxygenase/tryptophan 5-monooxygenase activation protein, zeta polypeptide; gene trap OST432062, Lexicon Genetics|Ywhaz|MGI:4315078|15|||||||||||||||||||||||||||||Homozygous KO mice are smaller than their littermate and have behavioural abnormalities, including hyperactivity and congnitive defects. 20% of KO mice die prior to weaning.|Normal|BALB/c|No|No|Yes|No|No|Yes|No|Unknown||||No|08-Feb-2018|Cryopreserved sperm|50.0|0.0|Unknown||Dopamine, schizophrenia|Yes| 8432.0|14-3-3zetaGt(OST062)Lex ; Savvy|129(Cg)-Ywhaz/Apb||Recessive|tyrosine 3-monooxygenase/tryptophan 5-monooxygenase activation protein, zeta polypeptide|Ywhaz|Nil|1110013I11Rik, 14-3-3 zeta|MGI:109484|tyrosine 3-monooxygenase/tryptophan 5-monooxygenase activation protein, zeta polypeptide; gene trap OST432062, Lexicon Genetics|Ywhaz|MGI:4315078|15|||||||||||||||||||||||||||||Mice have behavioural abnormalities, including hyperactivity and reduced cognitive abilities. KO mice are smaller than their littermates and around 20% die prior to weaning. |Normal|129/Sv|No|No|Yes|No|No|Yes|No|Unknown||||No|08-Feb-2018|Cryopreserved sperm|50.0|0.0|Unknown||Dopamine, schizophrenia|Yes| 8435.0|14-3-3zeta(Gt(OST062)Lex ; Jaxx|B6.129S5-Ywhaz/Apb||Recessive|tyrosine 3-monooxygenase/tryptophan 5-monooxygenase activation protein, zeta polypeptide|Ywhaz|Nil|1110013I11Rik, 14-3-3 zeta|MGI:109484|tyrosine 3-monooxygenase/tryptophan 5-monooxygenase activation protein, zeta polypeptide; gene trap OST432062, Lexicon Genetics|Ywhaz|MGI:4315078|15|||||||||||||||||||||||||||||Homozygous animals are smaller than their littermate and have mild hyperactivity and cognitive defects. 20% of KO mice die prior to weaning.|Normal|C57BL/6|No|No|Yes|No|No|Yes|No|Unknown||||No|08-Feb-2018|Cryopreserved sperm|40.0|0.0|Unknown||Dopamine, schizophrenia|Yes| 8424.0|ASD735:Cannonball:F0|C57BL/6NCrlAnu-Camk2d/Anu||Recessive|calcium/calmodulin-dependent protein kinase II, delta|Camk2d|Unknown|2810011D23Rik, 8030469K03Rik, CaMK II, MGC:60852|MGI:1341265|Camk2d, endonuclease-mediated mutation 1, Australian National University|Camk2d||3||||||||||Unknown to Unknown|||||||||||||||||||Unknown|Unknown|C57BL/6NCrlAnu|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|24-Jan-2018|Cryopreserved sperm|56.0|0.0|Unknown|||Yes| 8431.0|Dmp1Cre.SOCS3f/f|B6-Socs3 Tg(Dmp1-cre)1Jqfe/StVApb||Recessive|suppressor of cytokine signaling 3|Socs3||CIS3, Cish3, cytokine-inducible SH2 protein 3, E2a-Pbx1 target gene in fibroblasts 10, EF-10, SOCS-3, SSI-3, STAT-induced STAT inhibitor 3|MGI:1201791|suppressor of cytokine signaling 3; targeted mutation 2, Warren S Alexander|Socs3|MGI:2663917|11|||||||||||||||||transgene insertion 1, Jian Q Feng|Dmp1|odontoblast-specific expression||||||||||Sex-specific delay in bone corticalization. |Normal|C75BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|06-Feb-2018|Cryopreserved sperm|50.0|0.0|Unknown||corticalization, IL6, androgen|Yes| 8438.0|TREML4 KO|C57BL/6-Treml4/Apb||Recessive|triggering receptor expressed on myeloid cells-like 4|Treml4||5031403H21Rik|MGI:1923239||||17|||||||||||||||||||||||||||||Normal|Normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|16-Feb-2018||0.0|0.0|Unknown||CRISPR|Yes| 8429.0|mFX knockout|C57Bl/6-F10/Apb||Recessive|coagulation factor X|F10||AI194738, Cf10, fX|MGI:103107||||8|||||||||||||||||||||||||||||Possibly lethal|Normal status|C57BL/6J|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|31-Jan-2018|Cryopreserved sperm|50.0|0.0|Unknown|||Yes| 8436.0||Actc1-TRE||Dominant||||||||||||||||||||||||||||||||||||||Unknown|||Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|09-Feb-2018|Cryopreserved sperm|50.0|0.0|Unknown|||Yes| 8445.0|CTR flox|B6(Cg).129-Calcr/AnuApb||Dominant|calcitonin receptor|Calcr||Clr|MGI:101950|calcitonin receptor; targeted mutation 1, Rachel A Davey|Calcr|MGI:4352932|6|||||||||||||||||||||||||||||Normal.|Normal|C57BL/6NCrlAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|>20|||No|14-Mar-2018|Cryopreserved sperm|60.0|0.0|Unknown||hypercalcemia|Yes| 8439.0|Tlt2|C57BL/6-Treml2/Apb||Recessive|triggering receptor expressed on myeloid cells-like 2|Treml2||LOC328833|MGI:2147038||||17|||||||||||||||||||||||||||||Normal|Normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|16-Feb-2018|Cryopreserved sperm|40.0|0.0|Unknown||CRISPR|Yes| 8440.0|TREML4/TLT2 DKO|C57BL/6-Treml4 Treml2/Apb||Recessive|triggering receptor expressed on myeloid cells-like 2|Treml2|Unknown|LOC328833|MGI:2147038||||17|||||||||||||||||||||||||||||Embryonic lethal|Normal|C57BL/6|No|No|Yes|No|No|Yes|No|Unknown||||No|16-Feb-2018|Cryopreserved sperm|30.0|0.0|Unknown||CRISPR|Yes| 8440.0|TREML4/TLT2 DKO|C57BL/6-Treml4 Treml2/Apb||Recessive|triggering receptor expressed on myeloid cells-like 4|Treml4||5031403H21Rik|MGI:1923239||||17|||||||||||||||||||||||||||||Embryonic lethal|Normal|C57BL/6|No|No|Yes|No|No|Yes|No|Unknown||||No|16-Feb-2018|Cryopreserved sperm|||Unknown||CRISPR|Yes| 8442.0|Mdm2|B6(Cg).129(Cg)-Mdm2/JAnu||Recessive|transformed mouse 3T3 cell double minute 2|Mdm2||1700007J15Rik, Mdm-2|MGI:96952|transformed mouse 3T3 cell double minute 2; targeted mutation 1.1, Yangping Zhang|Mdm2|MGI:4836988|10|||||||||||||||||||||||||||||Unknown||C57BL/6J|Yes|Unknown|Yes|Yes|Unknown|Yes|No|Unknown||||No|05-Mar-2018|Cryopreserved sperm|123.0|0.0|Unknown|||Yes| 8437.0|TREML4 KO ; FUMR|C57BL/6-Treml4/Apb||Recessive|triggering receptor expressed on myeloid cells-like 4|Treml4|Unknown|5031403H21Rik|MGI:1923239||||17|||||||||||||||||||||||||||||Mice are immune to polymicrobial sepsis i.e. peritonitis and subsequent pneumonia.|Normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|16-Feb-2018|Cryopreserved sperm|20.0|0.0|Unknown||CRISPR, Sepsis, peritonitis|Yes| 8441.0|Lx12|B6.129-Abca12/MarpApb|3528440|Dominant|ATP-binding cassette, sub-family A (ABC1), member 12|Abca12||4832428G11Rik, 4833417A11Rik|MGI:2676312|ATP-binding cassette, sub-family A (ABC1), member 12; targeted mutation 1, Lexicon Genetics|Abca12|MGI:3528440|1|||||||||||||||||||||||||||||Neonatal lethality, epidermal hyperkeratosis, fail to develop epidermal permability barrier, disrupted interstitial lamellar lipid structure, |Normal|C57BL/6|No|No|Yes|No|No|Yes|No|Good|11||heterozygote to wildtype|No|05-Mar-2018|Cryopreserved sperm|50.0|0.0|Yes|harlequin ichthyosis||No| 8450.0|BALB.931-343|BALB/c-Gasa/Bax||Recessive|||||||||||||||||||||||||||||Unknown||||||||Unknown|Altered response to induced neonatal thymectomy induced gastritis compared to BALB/c mcie.||BALB/c|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|||Hom x Hom|No|19-Mar-2018|Cryopreserved sperm|50.0|0.0|Unknown||autoimmunity, gastritis|Yes| 699.0|NID5MD4|NOD-IDD5 Tg(IghelMD4)4Ccg||Dominant|QTL - Idd5||Unknown|||insulin dependent diabetes susceptibility 5|Idd5|MGI:2389023|1||||||||||||||||Yes|transgene insertion 4, Christopher C Goodnow ||High||||||||||This allele confers resistance to insulin dependent diabetes compared to NOD. ||NOD|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|01-May-2007||0.0|0.0|Unknown||B cell, diabetes, autoimmunity, immunoglobulin|Yes| 3411.0|Socs3 KO|C57BL/6-Socs3/Wehi||Recessive|suppressor of cytokine signaling 3|Socs3|Nil|CIS3, Cish3, cytokine-inducible SH2 protein 3, E2a-Pbx1 target gene in fibroblasts 10, EF-10, SOCS-3, SSI-3, STAT-induced STAT inhibitor 3|MGI:1201791|targeted mutation 1, Warren S Alexander|Socs3|MGI:2180861|11||||||||||||||||No|||||||||||||Embryonic lethal. SOCS3-/- embryos were slightly smaller than wild type but appeared otherwise normal, and histological analysis failed to detect any anatomical abnormalities responsible for the lethal phenotype. Rather, in all SOCS3-/- embryos examined, defects were evident in placental development that would account for their developmental arrest and death. The placental spongiotrophoblast layer was significantly reduced and accompanied by increased numbers of giant trophoblast cells. Delayed branching of the chorioallantois was evident, and, although embryonic blood vessels were present in the labyrinthine layer of SOCS3-/- placentas, the network of embryonic vessels and maternal sinuses was poorly developed. Yolk sac erythropoiesis was normal, and, although the SOCS3-/- fetal liver was small at day 12.5 of gestation (E12.5), normal frequencies of erythroblasts and hematopoietic progenitor cells, including blast forming unit-erythroid (BFU-E) and, colony forming unit-erythroid (CFU-E) were present at both E11.5 and E12.5. Colony formation for both BFU-E and CFU-E from SOCS3-/- mice displayed wild-type quantitative responsiveness to erythropoietin (EPO), in the presence or absence of IL-3 or stem cell factor (SCF). These data suggest that SOCS3 is required for placental development but dispensable for normal hematopoiesis in the mouse embryo.||C57BL/6|No|No|Yes|No|No|Yes|No|Unknown||||No|14-Jul-2008||0.0|0.0|Unknown||placenta, embryonic lethal, erythropoeisis, spongiotrophoblast layer, trophoblast cells|Yes| 1742.0|C57BL/6 Bak knockout|C57BL/6-Bak/Wehi||Recessive|BCL2-antagonist/killer 1|Bak1|Nil|Bak, N-Bak|MGI:1097161|BCL2-antagonist/killer 1; targeted mutation 1, Craig B Thompson|Bak1|MGI:2159364|17||||||||||||||||Yes|||||||||||||Normal.Increased platelet cell number.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|01-Aug-2007||0.0|0.0|Unknown||BH3, Bax, Bim, proapoptotic, Bcl2|Yes| 1733.0|BALB/c.EµSV-v-abl 40|BALB/c-Tg(Igh-Abl1)2Sco/Wehi||Dominant||||||||||||||||||||||||||transgene insertion 2, Suzanne Cory|mouse Igh enhancer and the SV40 early promoter||||||||||||Start to develop tumours from approx 120 days. Increase incidences of plasmacytoma (symtoms: weight loss, scruffy, respirations rate increases, paralysis of hind legs).Watch for intersusception (intestines fold in on themselves). Comments: At 12 weeks mice will bear one of the following tumours: Splenomegaly, messentery associated, abdominal, dediastinal, caecal, Also problems with small bowel obstruction, intestinal haemorrhage, interssusception, Peyer's Patch.|BALB/c|Yes|No|Yes|Yes|No|Yes|No|Unknown||||No|01-Aug-2007||0.0|0.0|Unknown||Oncogene, Plasmacytoma, B cell, myc|Yes| 8444.0|ASD541:Lifr flox:Flpe:Cre-ERT2|B6(Cg)-Lifr/AnuApb||Recessive|leukemia inhibitory factor receptor|Lifr||A230075M04Rik, soluble differentiation-stimulating factor receptor|MGI:96788|LIF receptor alpha; targeted mutation 1c, Helmholtz Zentrum Muenchen GmbH|Lifr|MGI:5692896|15||||||||||Unknown to Unknown|||||||||||||||||||Unknown|Unknown|C57BL/6NCrlAnu|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|09-Mar-2018|Cryopreserved sperm|36.0|0.0|Unknown|||Yes| 8449.0|35bp del|C57BL/6NCrlAnu-Arpc1b/Anu||Recessive|actin related protein 2/3 complex, subunit 1B|Arpc1b|Normal|L72, p41-ARC, SOP2Hs|MGI:1343142|actin related protein 2/3 complex, subunit 1B; endonuclease-mediated mutation 2, Australian National University|Arpc1b||5||||||||||Unknown to Unknown|||||||||||||||||||Unknown||C57BL/6NCrlAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|19-Mar-2018|Cryopreserved sperm|22.0|0.0|Unknown|||Yes| 6715.0|TRAILKO|B6.129-Tnfsf10/Ausb||Recessive|tumor necrosis factor (ligand) superfamily, member 10 |Tnfsf10|Nil|A330042I21Rik, APO-2L, Trail |MGI:107414|tumor necrosis factor (ligand) superfamily, member 10; targeted mutation 1, Mark J Smyth |Tnfsf10|MGI:2179709|3|||||||||||||||||||||||||||||Immune system phenotype:*Defective negative selection of T cells observed in one study is not observed in this study. Abnormal negative T cell selection: *Anti-CD3 fails to induce apoptosis of CD4+CD8+ thymocytes in vivo, or in fetal thymic organ culture. Thymus hyperplasia: *Mean thymic cellularity is increased about 10% at 6-7 weeks of age. Increased IgG1 level: *There are higher levels of antigen-specific IgG1 in mice immunized with collagen compared to controls. Increased IgG2a level: *There are higher levels of antigen-specific IgG2a in mice immunized with collagen compared to controls. Increased interferon-gamma secretion: *Splenocyte IFN-gamma secretion is enhanced from collagen-immunized mice upon reencounter with antigen compared to controls. Increased interleukin-2 secretion: *Splenocyte IL-2 secretion is enhanced from collagen-immunized mice upon reencounter with antigen compared to controls. Increased susceptibility to autoimmune diabetes: *Streptozotocin induced diabetes has an earlier onset, higher incidence and is more severe than in controls mice. *Onset of disease is first detected 20 days after injection compared to over 30 days for controls. *Incidence reaches 80% versus 40% of controls. *Insulitis and islet destruction is much more severe than in streptozotocin-injected wild-type mice. Increased susceptibility to experimental autoimmune encephalomyelitis: *Mice have increased susceptibility to EAE induced by peptide derived from myelin oligodendrocyte glycoprotein (MOG). *2 of 6 mice die within 40 days of MOG administration compared to none of the wild-type controls. *Mean maximal disease score and cumulative disease scores are significantly higher than controls. Increased susceptibility to induced arthritis: *Mice develop severe arthritis 4 weeks after collagen immunization compared to C57BL/6 controls that do not develop disease. *Arthritis is characterized by footpad swelling, pannus formation, cartilage destruction of paw joints.Hematopoietic system phenotype:*Defective negative selection of T cells observed in one study is not observed in this study. Abnormal negative T cell selection: *Anti-CD3 fails to induce apoptosis of CD4<+>CD8<+> thymocytes in vivo, or in fetal thymic organ culture. Thymus hyperplasia: *Mean thymic cellularity is increased about 10% at 6-7 weeks of age.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|02-Dec-2011||0.0|0.0|Unknown||TNF-related apoptosis-inducing ligand (TRAIL), Tumor initiation, Tumor metastasis|Yes| 1746.0|SOCS-1 KO|C57BL/6-SOCS1/Wehi||Recessive|suppressor of cytokine signaling 1|Socs1|Nil|Cish1, Cish7, JAB, JAK-binding protein, JAK2-binding protein, SOCS-1, SSI-1, STAT-induced STAT inhibitor 1|MGI:1354910|targeted mutation 1, Walter and Eliza Hall Institute of Medical Research|Socs1|MGI:1934607|16||||||||||||||||No|||||||||||||Postnatal lethality:* homozygotes become ill and die before reaching 3 weeks of age.* mice die from inflammatory disease before weaning.Decreased body weight:* homozygotes become smaller within 10 days after birthPostnatal growth retardation.Pancreas inflammation: monocytic infiltration.Decreased hematocrit.Decreased lymphocyte cell number.Decreased B cell number:* progressive loss of maturing B lymphocytes in the marrow, spleen, and peripheral blood.Decreased pre-B cell number:* pre-B cells are depleted significantly in the marrow.Decreased eosinophil cell number:* moderate reduction in eosinophil numbersAbnormal mature B cell morphology:* number of mature B cells expressing surface Ig in the bone marrow is reduced.Abnormal follicular B cell morphology:* lymphoid follicles of the spleen are either completely absent or are composed of immature cells.Increased spleen red pulp amount:* most spleens show expanded areas of red pulp with nucleated erythroid cells as the main cell population.Thymus cortex hypoplasia:* the cortex becomes progressively depleted of lymphoid cellsSmall thymus.Abnormal Peyer's patch morphology:* Peyer's patches are present but contain few lymphocytes.Abnormal lymph node B cell domain:* lymph nodes show absence of lymphoid follicle formation.Increased inflammatory response:* mice die from massive generalized inflammation that affects multiple organs.Heart inflammation: monocytic, and less frequently, granulocytic infiltration.Pancreas inflammation: monocytic infiltration.Liver inflammation: livers exhibit both focal and generalized infiltration, predominantly by immature and mature monocytic and granulocytic cells, and less frequently, megakaryocytes and eosinophils.Hepatic steatosis: parenchymal cells contain an accumulation of lipid-containing vacuoles.Liver degeneration: fatty degeneration either involves local areas not related to portal vessels or is generalized to the entire liver.Abnormal respiratory alveoli morphology: increase in cellularity of alveolar walls in the lung, often associated with macrophage cuffing around major vessels.||C57BL/6|No|No|Yes|No|No|Yes|No|Unknown||||No|02-Aug-2007||0.0|0.0|Unknown||Cytokine signalling, phosphorylation, signal transduction, IL-6 receptor, growth retardation|Yes| 5283.0|B6.A2AR.KO|C57BL/6-Adora2a||Recessive|adenosine A2a receptor|Adora2a|Nil|A2a, Rs, A2AAR, A2aR, AA2AR|MGI:99402|adenosine A2a receptor; targeted mutation 1, Jiang-Fan Chen|Adora2a|MGI:2155985|10||||||||||||||||No|||||||||||||Impaired behavioral response to addictive substance: * no significant increase in wakefulness is seen in homozygotes after injection of 15 mg/kg, 10 mg/kg, or 5 mg/kg caffeine, unlike wild-type mice. * single exposure amphetamine or cocaine stimulated increases in locomotor activity are reduced compared to wild-type mice. * however, baseline circadian sleep-wake profiles are identical to wild-type. * however, amphetamine stimulated increases in fine movement are not significantly different from wild-type.Hypoactivity: reduced spontaneous activity most prominently in the dark cycle; however normal locomotor circadian rhythms are seen.Decreased susceptibility to ischemic brain injury: 24 hours after middle cerebral arterial occlusion neurological deficit scores for homozygotes are reduced by 50-60% compared to wild-type mice.Decreased cerebral infarction size: after middle cerebral arterial occlusion total infarct volume is reduced by 26% using hematoxylin and eosin staining or by 77% using TTC staining (marker of intact cellular metabolism) compared to wild-type mice.Nervous system phenotype: * morphology of cortex and striatum appears normal. * dopaminergic innervation is normal.Cardiovascular system phenotype: basal mean arterial blood pressure, absolute blood flow, and cortical cerebral blood flow before, during. and after middle cerebral arterial occlusion is similar to wild-type mice.Vision/eye phenotype: normal growth in the anterior segment and normal pupil size.Abnormal sclera morphology: sclera contains denser collagen fibrils with reduced diameter.Myopia: mice develop greater myopia than wild-type mice, that is associated with increases in vitreous chamber depth and axial length from P28 to P56.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|28-Oct-2010||0.0|0.0|Yes|Myopia|ischemia, brain, sclera, vitreous chamber|Possibly| 4783.0|WT-286|WT Control for hGM-CSF transgenic mutants||Dominant|||||||||Unknown||||||||||||||||No|human GM-CSF|human GM-CSF promoter and enhancer (10.5kb)|||||||||||Express human GM-CSF. hGM-CSF detected in serum by ELISA. Murine GM-CSF used as internal control.|||Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|06-Sep-2009||0.0|0.0|No||T cell, lymphocyte, transcription, chromatin remodelling, NF-kappaB|Yes| 773.0|NMD4NML5|NOD-Tg(IghelMD4)4Ccg Tg(ML5sHEL)5Ccg||Dominant||||||||||||||||||||||||||transgene insertion 4, Christopher C Goodnow||High|||||||||||Abnormal B cell morphology:* there is no decrease in the number of B cells expressing the transgenic antibody compared to singly transgenic NOD mice that carry just the antibody transgene.* this suggests defect in the NOD strain of deleting B cells that recognize soluble self antigens.Abnormal B cell clonal deletion:* Background Sensitivity: the normal number of B cells found in these mice demonstrate a defect in the NOD strain of deleting B cells that recognize soluble self antigens.Decreased IgM level:* very little IgM is detectable in the sera despite the presence of soluble antigen for the transgenic antibody.Abnormal B cell anergy:* B cells expressing the transgenic antibody are anergic as determined by the lack of HEL specific antibody found in the sera.* anergy occurs both centrally (i.e. in the bone marrow) and in the periphery.* this anergy can be reversed by stimulating B cells in vitro.* when compared to singly transgenic controls, antibody production following BCR and CD40 stimulation is less suppressed in doubly transgenic NOD mice than in doubly transgenic C57BL/6 mice (2.6-fold less vs 4.5 fold less).|NOD|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|18-May-2007||0.0|0.0|Unknown||Autoimmunity, B cell, Immunoglobulin, Hen Egg Lysozyme (HEL)|Yes| 773.0|NMD4NML5|NOD-Tg(IghelMD4)4Ccg Tg(ML5sHEL)5Ccg||Dominant||||||||||||||||||||||||||transgene insertion 5, Christopher C Goodnow|mouse metallothionein I||||||||||||Abnormal B cell morphology:* there is no decrease in the number of B cells expressing the transgenic antibody compared to singly transgenic NOD mice that carry just the antibody transgene.* this suggests defect in the NOD strain of deleting B cells that recognize soluble self antigens.Abnormal B cell clonal deletion:* Background Sensitivity: the normal number of B cells found in these mice demonstrate a defect in the NOD strain of deleting B cells that recognize soluble self antigens.Decreased IgM level:* very little IgM is detectable in the sera despite the presence of soluble antigen for the transgenic antibody.Abnormal B cell anergy:* B cells expressing the transgenic antibody are anergic as determined by the lack of HEL specific antibody found in the sera.* anergy occurs both centrally (i.e. in the bone marrow) and in the periphery.* this anergy can be reversed by stimulating B cells in vitro.* when compared to singly transgenic controls, antibody production following BCR and CD40 stimulation is less suppressed in doubly transgenic NOD mice than in doubly transgenic C57BL/6 mice (2.6-fold less vs 4.5 fold less).|NOD|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|18-May-2007||||Unknown||Autoimmunity, B cell, Immunoglobulin, Hen Egg Lysozyme (HEL)|Yes| 6201.0|IL-12b|B6.129S1-Il12b/J||Recessive|interleukin 12b|Il12b|Nil|IL-12 p40, Il-12b, Il-12p40, IL-23 subunit p40|MGI:96540|interleukin 12b; targeted mutation 1, Jeanne Magram|Il12b|MGI:1857201|11|||||||||||||||||||||||||||||Increased sensitivity to xenobiotic induced morbidity/mortality:*Increase in mortality following a single dose of N-methyl-N-nitrosourea (MNU) compared to similarly treated wild-type controls.Decreased circulating interferon-gamma level:*Serum levels of IFNG in LPS-injected mice are only 17 +/- 5% of LPS-induced controls.Abnormal macrophage physiology:*Fewer than expected macrophages in the dermis of carcinogen treated skin.Abnormal granulocyte physiology:*Fewer than expected granulocytes in the dermis of carcinogen treated skin.Abnormal lymphocyte physiology:*Lymph node cells from keyhole limpet hemocyanin (KLH) immunized mice are severely impaired in their ability to produce IFNG when cultured with KLH; however, their production of IL4 is increased. Abnormal NK cell physiology: *Mean NK lytic activity is about 66% of controls; however when cultured with IL2 lytic activity is similar to controls. Abnormal CD8-positive T cell physiology: *Dramatic increase in the number of cytotoxic CD8+ cells in the dermis and epidermis of carcinogen treated skin.Decreased susceptibility to type IV hypersensitivity reaction:*Specific foot pad swelling 48 hours after challenge with methylated bovine serum albumin is inhibited by 47 +/- 3% compared to wild-type mice; however, cytotoxic T lymphocyte responses are similar to wild-type.Decreased interleukin-17 secretion:*Barely detectable levels of IL17 in the skin after carcinogen treatment unlike wild-type mice which express high levels of IL17.Increased susceptibility to bacterial infection:*Vaccination does not produce a protective response to M. tuberculosis.Decreased incidence of chemically-induced tumors:*Resistant to induction of papillomas compared to wild-type mice after treatment with DMBA and TPA in a 2 step skin carcinogenesis protocol.*However, there is an increase in the incidence of tumors following intradermal challenge with PDV squamous carcinoma cells.Abnormal alveolar process:*3 fold increase in alveolar bone loss at 30 weeks relative to mice at 6 and 16 weeks.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown||IL-12, IFN gamma|Yes| 6675.0|FLATLEY|BALB/c-Tg(DO11.10)10Dlo/Ausb||Semi-dominant||||||||||||||||||||||||||transgene insertion 10, Dennis Y Loh||||||||||||Decreased CD4-positive T cell number:*CD4+ CD8- TCR thymocytes are reduced in absolute numbers after administration of OVA 323-339 peptide.Decreased double-positive T cell number:*CD4+CD8+TCR cells in thymic cortex are reduced by 55% after administration of OVA 323-339 peptide.Abnormal thymus physiology:*20 hours after administration of OVA323-339 peptide, apoptosis, DNA degradation, chromatin condensation, and cell shrinkage occur in the majority of cortical thymocytes.*Apoptosis occurs throughout the thymus including the subcapsular and deep cortical areas. 3 days after administration of peptide the cortical thymus is acellular; however, normal cellularity exists in the medulla peptide administration does not effect small number of thymocytes that express only the beta chain transgene Vb8||BALB/c|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|02-Dec-2011||0.0|0.0|Unknown||CD4, CD8, TCR|Yes| 5293.0|B6-TgN(rtTA2-MUSMRIP7:VEGF-A-TREtight)|C57BL/6-Tg(Ins2-rrTA,tetO-VEGFA)Cpj||Dominant||||||||||||||||||||||||||reverse tetracycline transactivator (rtTA) ; human vascular endothelial growth factor a|rat insulin 2 gene (RIP7) ; TRE (tetO)|||||||||||The mice were not expected to show any overt phenotype. But the transgenic mice are spontaneously diabetic. The onset of diabetes is as early as 3 wks of age and severe in male mice. The transgenic mice are healthy, breed normally and can survive without insulin administration.The genetically modified mice was to be used as islet donors which express angiogenic factor VEGF-A , but the expression will be restricted to islet beta cell and only after doxycycline treatment. The mice constitutively expressing these factors in the pancreas have been reported and do not suffer any detrimental side effects. ||C57BL/6|Yes|Unknown|Yes|Yes|Unknown|Yes|No|Unknown||||No|29-Oct-2010||0.0|0.0|Unknown|||Possibly| 700.0||NOD.Cg-Igh-6 Tg(IghelMD4)4Ccg/Dvs||Dominant||||||||||||||||||||||||||transgene insertion 4, Christopher C Goodnow||High||||||||||Do not express endogenous IgM, viable, fertile, normal in size, and do not display any gross physical or behavioral abnormalities.All B lymphocytes in NOD.Igh-6 deficient transgenic mice express Ig molecules specific for HEL.||NOD|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|01-May-2007||0.0|0.0|Unknown||autoimmunity, B cell, immunoglobulin, Hen egg lysozyme|Yes| 8464.0|Heparanase KO:OT-I|B6.129-Hpse Tg(TcraTcrb)1100Mjb/AnuApb||Recessive|heparanase|Hpse|Nil|Hpa|MGI:1343124|heparanase; targeted mutation 1, Jin-Ping Li|Hpse|MGI:3844469|5|||||||||||||||||transgene insertion 1100, Michael J Bevan||||||||||||Heparanase KO mice are fertile with no immunological phenotype observed.|Normal.|C57BL/6JAnu|Yes|Yes|Unknown|Yes|Yes|Yes|No|Unknown||||No|09-Apr-2018|Cryopreserved sperm|55.0|0.0|Unknown||Heparan sulphate, MMP2, T cell|Yes| 3596.0||C57BL/6-Tg(UBC-GFP)30Scha/J Tg(TcraTcrb)1100Mjb||Recessive||||||||||||||||||||||||||transgene insertion 30, Brian Schaefer|human ubiquitin C promoter||||||||||||Mice with mono-specific T cells repertoire have an impaired immune response but no phenotype expected in a clean housing environment. Transgenic mice on a C57BL/6 background are somewhat immunodeficient, and may be used to study the role of peptides in positive selection and the response of CD8+ T cells to antigen. Carry OVA-specific, H-2Kb-restricted T cell receptorOT-I mice have an increased thymoma incidence from 4 months of age. These mice express GFP in all tissues examined. Expression levels vary between certain hematapoetic cell types. GFP expression is uniform within a cell type lineage and remains constant throughout development. T cells have a 2-fold higher GFP expression than CD19+B220+ B cells or peripheral blood cells. Leukocytes and red blood cells from homozygous transgenic mice fluoresce at approximately twice the level of cells from hemizygous mice.|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|06-Aug-2008||0.0|0.0|Unknown||T cell receptor (TCR), ovalbumin, GFP|Yes| 3596.0||C57BL/6-Tg(UBC-GFP)30Scha/J Tg(TcraTcrb)1100Mjb||Recessive||||||||||||||||||||||||||transgene insertion 1100, Michael J Bevan|||||||||||||Mice with mono-specific T cells repertoire have an impaired immune response but no phenotype expected in a clean housing environment. Transgenic mice on a C57BL/6 background are somewhat immunodeficient, and may be used to study the role of peptides in positive selection and the response of CD8+ T cells to antigen. Carry OVA-specific, H-2Kb-restricted T cell receptorOT-I mice have an increased thymoma incidence from 4 months of age. These mice express GFP in all tissues examined. Expression levels vary between certain hematapoetic cell types. GFP expression is uniform within a cell type lineage and remains constant throughout development. T cells have a 2-fold higher GFP expression than CD19+B220+ B cells or peripheral blood cells. Leukocytes and red blood cells from homozygous transgenic mice fluoresce at approximately twice the level of cells from hemizygous mice.|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|06-Aug-2008||||Unknown||T cell receptor (TCR), ovalbumin, GFP|Yes| 4931.0|VavP-BCL2-69|CBA-Tg(Vav-BCL2)1Jad/Wehi||Dominant||||||||||||||||||||||||||transgene insertion 1, Jerry M Adams|mouse Vav promoter|High, haemopoietic cells|||||||||||Abnormal lymphocyte cell number:* the ratio of CD4 cells per B cell is 25% to 50% lower than in wild-type mice.Increased B cell number: 5-fold higher in the spleen at 18 weeksIncreased T cell number:* mice exhibit higher splenic T cell numbers than in wild-type and Tg(BCL2)22Wehi or Tg(BCL2)36Wehi mice.Increased CD4-positive T cell number:* the increase in CD4+ T cells is greater than the increase in CD8+ T cells.Increased CD8-positive T cell number:* the increase in CD4+ T cells is greater than the increase in CD8+ T cells.Abnormal class switch recombination:* the total number of B cells that undergo class switching is 50-fold higher than in wild-type mice.Abnormal somatic hypermutation frequency:* 22 of 23 clones isolated from class-switching cells harbor on average about 6 somatic mutations compared to in wild-type cells where no mutations are found.Enlarged spleen:Abnormal spleen germinal center morphology:* mice exhibit a larger pool of cycling B cells with a germinal center phenotype than in wild-type mice.* at 18 weeks, mice exhibit an increased in germinal center size and number compared to in wild-type mice.* however, expansion of germinal centers is dependent on CD4 T cell help.Increased spleen germinal center number: at 18 weeks.Increased spleen germinal center size: at 18 weeks.Enlarged lymph nodes.Glomerulonephritis:* at 40 weeks, 15% to 25% of mice develop autoimmune glomerulonephritis.Increased tumor incidence:* 12% of mice develop plasma cell tumorsLymphoma: less than 10% of mice develop lymphoblastic lymphomas.B cell derived lymphoma:* less than 10% of mice develop large cell B lymphomasFollicular lymphoma:* at 18 months, 37% to 50% of mice develop monoclonal follicular lymphoma.Thymic lymphoma: in less than 10% of miceHistiocytic sarcoma: in less than 10% of mice.|CBA|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|19-Nov-2009||0.0|0.0|Unknown||B cell, bcl-2, vav, Progenitor, lymphoma, germinal centre|Yes| 789.0|Y4 KO|B6.129-Ppyr1||Recessive|pancreatic polypeptide receptor 1|Ppyr1|Nil|Npy4r, NYYR-D, Y4|MGI:105374|targeted mutation 1.1, Herbert Herzog|Ppyr1|MGI:2183929|14||||||||||||||||Yes|||||||||||||Decreased body weight:* 4-week old females weigh significantly less than controlsWeight gain:* males and females gain significantly less weight between 4 and 16 weeks of age.Homeostasis/metabolism phenotype:* levels of leptin, insulin, and glucose do not differ from wild type.* testosterone tends to be lower in mutants but this does not become significant.Abnormal circulating pancreatic peptide level:males exhibit 2- to 3-fold higher plasma levels of pancreatic polypeptide (PP).Abnormal drinking behavior:* mutants drink more water during the dark phase, but this is only significant on the second and third days of the 3 day observation period.* this behavior is maintained following injection of physiological saline (vehicle). beta-adrenoreceptor antagonist propanolol, or angiotensin AT1 receptor antagonist telmisartan.Abnormal water consumption:* daily water intake is elevated only on second and third day compared to controls.* this behavior is maintained following injection of physiological saline (vehicle). beta-adrenoreceptor antagonist propanolol, or angiotensin AT1 receptor antagonist telmisartan.Abnormal food intake:* males have lower food intake/24 hours than wild type controlsIncreased aggression to other mice:* male mutants show very aggressive behavior, with instances of fighting between littermates causing injuries.* female mutants become aggressive toward littermates after 20-24 weeks of age.Decreased white adipose tissue amount:* male mice have a significantly lower mass of white adipose tissue (WAT) compared to controls.Abnormal fat pad:* mesenteric WAT is major contributor to reduced WAT mass (0.65 % of body weight in male mutant vs 0.84% in male wild type and 0.53% in female mutant vs 0.76% in female wild type).Abnormal mammary gland growth during pregnancy:* lobuloalveolar development is accelerated compared to wild type (lobuloalveolar content on day 16 is 18.74% area of 4th gland compared to 15.79% in wild type).||C57BL/6 x 129|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|19-May-2007||0.0|0.0|Unknown||receptor, neuropeptide, obesity, mammary|Yes| 809.0|Y2 KO x Y4 KO|B6.129-Npy2r Ppyr1||Recessive|neuropeptide Y receptor Y2|Npy2r|Nil|NPY-Y2 receptor|MGI:108418|targeted mutation 1.1, Herbert Herzog|Npy2r|MGI:2447398|3||||||||||||||||Yes|||||||||||||Abnormal bone structure:* periosteal diameter of the cortical shaft is reduced compared to in wild-type mice.Abnormal cancellous bone morphology:* mice exhibit an increase in cancellous bone volume, trabeculae number, and trabecular thickness compared with wild-type mice and single homozygotes.Increased cancellous bone thickness.Decreased cortical bone thickness:* cortical bone area and thickness are decreased compared to in wild-type mice.Abnormal osteogenesis:* mice exhibit increased bone turnover with osteoblast, osteoclast, and osteoid surfaces increased compared with wild-type mice and single homozygotes.* however, osteoblast and osteoclast numbers are normal.Abnormal bone mineralization:* mineral apposition rate is increased compared to in wild-type mice.Abnormal osteoblast physiology:* osteoblast bone formation is increased compared to in wild-type mice.Decreased circulating insulin level:* in male mice compared with wild-type mice.Decreased circulating leptin level:* in male mice compared with wild-type mice and Ppyr1 homozygotes.Abnormal circulating pancreatic peptide level:* plasma pancreatic peptide levels are increased compared to in wild-type mice.Decreased brown adipose tissue amount.Decreased white adipose tissue amount:* male mice exhibit a decreased in white adipose tissue compared to in wild-type mice or single homozygotes.Decreased body weight:* male mice exhibit decreased body weight compared with wild-type mice that is not as severe as in single homozygotes.Increased eating behavior:* in male mice compared to in wild-type mice and single homozygotes.||C57BL/6 x 129|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|21-May-2007||0.0|0.0|Unknown||neuropeptide, obesity, adipose, neuronal, mammary, osteoblast, bone mass|Yes| 809.0|Y2 KO x Y4 KO|B6.129-Npy2r Ppyr1||Recessive|pancreatic polypeptide receptor 1|Ppyr1|Unknown|Npy4r, NYYR-D, Y4|MGI:105374|targeted mutation 1.1, Herbert Herzog|Ppyr1|MGI:2183929|14|||||||||||||||||||||||||||||Abnormal bone structure:* periosteal diameter of the cortical shaft is reduced compared to in wild-type mice.Abnormal cancellous bone morphology:* mice exhibit an increase in cancellous bone volume, trabeculae number, and trabecular thickness compared with wild-type mice and single homozygotes.Increased cancellous bone thickness.Decreased cortical bone thickness:* cortical bone area and thickness are decreased compared to in wild-type mice.Abnormal osteogenesis:* mice exhibit increased bone turnover with osteoblast, osteoclast, and osteoid surfaces increased compared with wild-type mice and single homozygotes.* however, osteoblast and osteoclast numbers are normal.Abnormal bone mineralization:* mineral apposition rate is increased compared to in wild-type mice.Abnormal osteoblast physiology:* osteoblast bone formation is increased compared to in wild-type mice.Decreased circulating insulin level:* in male mice compared with wild-type mice.Decreased circulating leptin level:* in male mice compared with wild-type mice and Ppyr1 homozygotes.Abnormal circulating pancreatic peptide level:* plasma pancreatic peptide levels are increased compared to in wild-type mice.Decreased brown adipose tissue amount.Decreased white adipose tissue amount:* male mice exhibit a decreased in white adipose tissue compared to in wild-type mice or single homozygotes.Decreased body weight:* male mice exhibit decreased body weight compared with wild-type mice that is not as severe as in single homozygotes.Increased eating behavior:* in male mice compared to in wild-type mice and single homozygotes.||C57BL/6 x 129|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|21-May-2007||||Unknown||neuropeptide, obesity, adipose, neuronal, mammary, osteoblast, bone mass|Yes| 3524.0||NOD.B6 Idd9D||Recessive|||Unknown|||insulin dependent diabetes susceptibility 9|Idd9|MGI:96411|4||||||||||||||||Yes|||||||||||||Non obese diabetic (NOD) mice exhibit a susceptibility to Spontaneous development of type 1 diabetes.||NOD|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|28-Jul-2008||0.0|0.0|Unknown||diabetic, T cell, autoimmunity, insulin|Yes| 1734.0|B6.EµSV-v-abl 40|C57BL/6-Tg(Igh-Abl1)2Sco/Wehi||Dominant||||||||||||||||||||||||||transgene insertion 2, Suzanne Cory |mouse Igh enhancer and the SV40 early promoter||||||||||||Low incidences of plasmacytoma. Look out for dragging hind legs, enlarged spleen, enlarged menteric lymph nodes - tumours. Visually check daily.1-2% will die at 20 weeks of age, 19-20% will die at 1 year. Mice die as a result of plasmcytoma. Mice will bear one of the following tumours: lymphoma, splenomegaly, messentary associated, abdominal, caecal, Peyer's Patches. They may also suffer from small bowel obstruction, intestinal haemorrhage, hind leg paralysis, intussusception.|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|01-Aug-2007||0.0|0.0|Unknown||plasmacytoma, B cell, Oncogene, Lymphoma, Abelson virus|Yes| 1970.0|available from Animal Resources Centre - www.arc.wa.gov.au|C.B10-H2b/LilMcdJArc (BALB/b)||Dominant|Congenic albino: A, Tyr, Tyrp1, Congenic partner BALB/c.||Unknown||||||Unknown||||||||||||||||No||||||||||||||||Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||Yes|04-Sep-2007||0.0|0.0|No|||Yes| 1765.0|Eµ-myc-Caspase-9 knockout|C57BL/6-Tg(IghMyc)22Bri Casp9/Wehi||Dominant|caspase 9|Casp9|Nil|Caspase-9, ICE-LAP6, Mch6|MGI:1277950|targeted mutation 1, Richard A Flavell|Casp9|MGI:2158755|4||||||||||||||||Yes|transgene insertion 22, Ralph L Brinster|Lymphoid-specific immunoglobulin heavy chain enhancer (Eμ)|B cell lineage||||||||||Due to perinatal lethality, Emu-myc transgenic Apaf-1(-/-) or caspase-9(-/-) fetal liver cells were used to reconstitute lethally irradiated recipient mice. Surprisingly, no differences were seen in rate, incidence, or severity of lymphoma with loss of Apaf-1 or caspase-9, and Apaf-1 was not a critical determinant of anticancer drug sensitivity of c-myc-induced lymphomas. Moreover, loss of Apaf-1 did not promote oncogene-induced transformation of mouse embryo fibroblasts. Thus, Apaf-1 and caspase-9 do not suppress c-myc-induced lymphomagenesis and embryo fibroblast transformation.||C57BL/6|No|No|Yes|No|No|Yes|No|Unknown||||No|03-Aug-2007||0.0|0.0|Unknown||Caspase, Bcl-2, Lymphoma, B cell, myc, apoptosome, cell death|Yes| 1835.0|X linked GFP|Un-Tg(CAG-EGFP)D4Nagy/Wehi||X-linked||||||||||||||||||||||||||transgene insertion D4, Andras Nagy|chicken beta-actin promoter and CMV intermediate early enhancer|Ubiquitous||||||||||Hemizygous males/Homozygous females will be fluorescent under dertain conditions due to the expression of GFP. Transgene expression is seen as early as ~E2.75, as morula stage embryos begin to compact. Expression of GFP is spatiotemporally ubiquitous, though levels differ between different lineages (e.g., expression is slightly higher in the heart).|||Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|08-Aug-2007||0.0|0.0|Unknown||GFP, ubiquitous, X-linked|Yes| 1808.0|Oncostatin M Receptor Knockout|C57BL/6-Osmr/Wehi||Recessive|oncostatin M receptor|Osmr|Unknown|OSMRB|MGI:1330819|targeted mutation 1, Minoru Tanaka|Osmr|MGI:2680723|15||||||||||||||||Yes|||||||||||||Reduced numbers of progenitors of the erythroid and megakaryocyte lineages in bone marrow.Reduced number of peripheral erythrocytes relative to wild type. Reduced number of platelets relative to wild type.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|06-Aug-2007||0.0|0.0|Unknown||IL-6, LIF, receptor, T cell, haemopoiesis|Yes| 1979.0|Smad1f x MesP1Cre|B6;Swiss-Smad1 Mesp1||Recessive|MAD homolog 1 (Drosophila)|Smad1|Normal|Madh1, Madr1, Smad 1|MGI:109452|MAD homolog 1 (Drosophila); targeted mutation 2, Elizabeth J Robertson|Smad1|MGI:2155484|8||||||||||||||||No|||||||||||||Smad 1 deleted in cells expressing MesP1.Conditional deletion of Smad1 in the left lateral plate mesoderm (LPM) led to precocious and bilateral pathway activation.|||No|No|Yes|No|No|Yes|No|Unknown||||No|04-Sep-2007||0.0|0.0|Unknown||heart, mesoderm, primitive streak, TGF, bone morphogenic protein, left-right|Yes| 1979.0|Smad1f x MesP1Cre|B6;Swiss-Smad1 Mesp1||Recessive|mesoderm posterior 1|Mesp1|Normal|bHLHc5|MGI:107785|mesoderm posterior 1; targeted mutation 2, Yumiko Saga|Mesp1|MGI:2176467|7|||||||||||||||||||||||||||||Smad 1 deleted in cells expressing MesP1.Conditional deletion of Smad1 in the left lateral plate mesoderm (LPM) led to precocious and bilateral pathway activation.|||No|No|Yes|No|No|Yes|No|Unknown||||No|04-Sep-2007||||Unknown||heart, mesoderm, primitive streak, TGF, bone morphogenic protein, left-right|Yes| 8465.0|Heparanase KO:OT-II|B6.129-Hpse Tg(TcraTcrb)425Cbn/AnuApb||Recessive|heparanase|Hpse|Nil|Hpa|MGI:1343124|heparanase; targeted mutation 1, Jin-Ping Li|Hpse|MGI:3844469|5|||||||||||||||||transgene insertion 425, Frank Carbone||||||||||||Heparanase KO mice are fertile with no immunological phenotype observed.|Normal.|C57BL/6JAnu|Yes|Yes|Unknown|Yes|Yes|Yes|No|Unknown||||No|09-Apr-2018|Cryopreserved sperm|55.0|0.0|Unknown||Heparan sulphate, MMP2, T cell|Yes| 6233.0|BXK|B6.129-Bak1 Bax||Recessive|BCL2-antagonist/killer 1|Bak1|Nil|Bak, N-Bak|MGI:1097161|BCL2-antagonist/killer 1; targeted mutation 1, Craig B Thompson|Bak1|MGI:2159364|17|||||||||||||||||||||||||||||Partial neonatal lethality:*Majority die within 48 hours of birth, although some survive to adulthood.Interdigital webbing:*Mutants retain interdigital webs on both fore and rear paws.Vagina atresia:*Seen in all adult females.Circling:*Display circling behavior when exposed to external stress.Seizures:*Stress-induced seizure activity.Abnormal hearing physiology:*Unresponsive to auditory stimuli.Abnormal hematopoiesis:*Hematopoietic colony assays show an increase in the number of myeloid colony forming units and a mild increase in erythroid and megakaryocyte colony forming units. Anemia: *Mild anemia. Increased leukocyte cell number: Increased lymphocyte cell number: *Increases within the circulation and the peripheral lymphoid organs. *Lymphocytic infiltration is seen in parenchymal organs, liver, and kidney. Decreased platelet cell number Abnormal B cell morphology: *B220+ B cells present in the lymph node and spleen are skewed toward a B220IgD- phenotype, indicating an increase in the number of class-switched or memory B cells. Abnormal T cell morphology: *T cells that accumulate in mutants are skewed toward a memory cell phenotype.Increased spleen red pulp amount:*Expanded red pulp contains a large increase in the number of plasma cells and histiocytes.Enlarged spleenIncreased spleen white pulp amount:*Pronounced hyperplasiaAbnormal splenocyte physiology:*Isolated splenocytes cultured in suspension show enhanced survival.Enlarged lymph nodesAbnormal brain morphology:*Increase in the number of neurons in multiple regions of the brain.*Large accumulation of small neuronal cells (neural stem cells) with dense chromatin staining in the periventricular region. Increased brain sizeIncreased neuron number:*In multiple regions of the brain.Decreased cellular sensitivity to gamma-irradiation:*Thymocytes show enhanced survival compared to wild-type when exposed to gamma irradiation.Decreased physiological sensitivity to xenobiotic:*Thymocytes are resistant to treatment with etoposide, a chemotherapeutic agent that normally induces cell death.||C57BL/6|No|No|Yes|No|Unknown|Yes|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown||Bak, Bax|Yes| 6233.0|BXK|B6.129-Bak1 Bax||Recessive|BCL2-associated X protein|Bax|Nil||MGI:99702|BCL2-associated X protein; targeted mutation 1, Stanley J Korsmeyer|Bax|MGI:1857429|7|||||||||||||||||||||||||||||Partial neonatal lethality:*Majority die within 48 hours of birth, although some survive to adulthood.Interdigital webbing:*Mutants retain interdigital webs on both fore and rear paws.Vagina atresia:*Seen in all adult females.Circling:*Display circling behavior when exposed to external stress.Seizures:*Stress-induced seizure activity.Abnormal hearing physiology:*Unresponsive to auditory stimuli.Abnormal hematopoiesis:*Hematopoietic colony assays show an increase in the number of myeloid colony forming units and a mild increase in erythroid and megakaryocyte colony forming units. Anemia: *Mild anemia. Increased leukocyte cell number: Increased lymphocyte cell number: *Increases within the circulation and the peripheral lymphoid organs. *Lymphocytic infiltration is seen in parenchymal organs, liver, and kidney. Decreased platelet cell number Abnormal B cell morphology: *B220+ B cells present in the lymph node and spleen are skewed toward a B220IgD- phenotype, indicating an increase in the number of class-switched or memory B cells. Abnormal T cell morphology: *T cells that accumulate in mutants are skewed toward a memory cell phenotype.Increased spleen red pulp amount:*Expanded red pulp contains a large increase in the number of plasma cells and histiocytes.Enlarged spleenIncreased spleen white pulp amount:*Pronounced hyperplasiaAbnormal splenocyte physiology:*Isolated splenocytes cultured in suspension show enhanced survival.Enlarged lymph nodesAbnormal brain morphology:*Increase in the number of neurons in multiple regions of the brain.*Large accumulation of small neuronal cells (neural stem cells) with dense chromatin staining in the periventricular region. Increased brain sizeIncreased neuron number:*In multiple regions of the brain.Decreased cellular sensitivity to gamma-irradiation:*Thymocytes show enhanced survival compared to wild-type when exposed to gamma irradiation.Decreased physiological sensitivity to xenobiotic:*Thymocytes are resistant to treatment with etoposide, a chemotherapeutic agent that normally induces cell death.||C57BL/6|No|No|Yes|No|Unknown|Yes|No|Unknown||||No|13-Sep-2011||||Unknown||Bak, Bax|Yes| 2802.0|CS-GMCSF MT lme|B6;SJL-Tg(MoMLV-Csf2)/Wehi||Dominant||||||||||||||||||||||||||colony stimulating factor 2 (granulocyte-macrophage)|Molony murine leukemia virus (MoMLV) long terminal repeat|Haemopoietic specific expression||||||||||Eyes are opaque. Physical check when cleaning. Pick mouse up by tail. If it is sick the hind legs will not be splayed in a relaxed manner. The sick mouse will be shaking and trying to bring the hind feet together. They will lose weight: coat will get scruff and dull, may shake. Sick mice should be culled. Will show signs of sickness from 8wks of age. Exhibit elevated levels of GM-CSF in the serum, urine, peritoneal cavity, and eye. The eyes of transgenic mice are opaque, contain accumulations of macrophages, and develop retinal damage. Similarly, lesions containing macrophages develop in striated muscle. The mice also display an accumulation of large, often multinucleate, activated macrophages in the peritoneal and pleural cavities. The transgene is transcribed in peritoneal cells, as well as in eyes and infiltrated striated muscle. A high proportion of transgenic mice die with muscle wasting when aged 2-4 months, possibly because of macrophage activation resulting from the high levels of GM-CSF.||C57BL/6 x SJL|Yes|No|Yes|Yes|No|Yes|No|Unknown||||No|22-Feb-2008||0.0|0.0|Unknown||Leukemia, thymoma, tumorigenic, growth factor, receptor, muscle, eye, peritoneal, macrophage|Yes| 7096.0|Nude|B6-Foxn1||Recessive|forkhead box N1|Foxn1|Unknown|D11Bhm185e, Hfh11, whn|MGI:102949|nude|Foxn1|MGI:1856108|11||||||||||||||||Yes|||||||||||||Postnatal lethality:some mice die within 1 week of birth55% mortality within 2 weeksPremature death:100% mortality by 25 weeksDecreased body size and weight.Postnatal growth retardation.Abnormal T cell differentiation.Athymia.Abnormal cell-mediated immunity.Abnormal liver morphology:liver lobes were atrophied and covered with red scarsvariable degrees of severity, typically increasing with age at time of death.Small ovaryCoiled sperm flagellum: many sperm had coiled tailsAbnormal estrous cycle: many females exhibited continuous dioestrus and metaoestrus phasesFemale infertility: severely reduced fertilityReduced male fertility.Asthenozoospermia.Nude: sparse hair growth around 5 weeks of agein some mice, cephalo-caudal migration of an irregular band of short sparse hairThin skin:reduction in skin thickness at 3 weeks of age, corresponding to the catagen stage of normal skinAbsent vibrissae: absent at birthShort and wavy vibrissae: older mice show repeated growth and loss of short and wavy vibrissae.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|28-Sep-2012||0.0|0.0|Unknown||hair loss, T cell, thymus, body size / mass, growth retardation, alopecia, keratin|Yes| 6680.0|BURKE|BALB/c-Il4ra/J/Ausb||Recessive|interleukin 4 receptor, alpha |Il4ra|Nil|CD124, IL-4 receptor alpha chain, Il4r |MGI:105367|interleukin 4 receptor, alpha; targeted mutation 1, Leonard Shultz |Il4ra|MGI:1861951|7|||||||||||||||||||||||||||||Abnormal microglial cell morphology:*Microglial cells fail to express the cell marker Ym1 (Chi3l3).Decreased IgE level:*Lower circulating levels of IgE in normal and bacterial infected mice.Decreased IgG1 level:*Lower circulating levels in normal and bacterial infected mice.Increased IgG2a levelAbnormal T-helper 2 physiology:*Mice are unable to mount an effective Th2 response to N. brasiliensis bacteria as determined by Th2 cyotkine production by T cells.Decreased interleukin-10 secretion:*Decrease production by T cells from mice infected with N. brasiliensis bacteria.Decreased interleukin-4 secretion:*Decrease production of IL-4 by T cells from mice infected with N. brasiliensis bacteria.Decreased interleukin-5 secretion:*Decrease production of IL-5 by T cells from mice infected with N. brasiliensis bacteria.||BALB/c|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|02-Dec-2011||0.0|0.0|Unknown||IL-4, NKT cells, CD4, CD62L|Yes| 8466.0|Heparanase KO:RIP-OVA|B6.129-Hpse Tg(Ins2-OVA)59Wehi/AnuApb||Recessive|heparanase|Hpse|Nil|Hpa|MGI:1343124|heparanase; targeted mutation 1, Jin-Ping Li|Hpse|MGI:3844469|5|||||||||||||||||transgene insertion 59, Walter and Eliza Hall Institute of Medical Research|rat insulin 2|High - 49 Copies||||||||||Heparanase KO mice are fertile with no immunological phenotype observed.Mice bearing RIP-OVA transgene express a secreted form of ovalbumin from the full-length chicken ovalbumin cDNA under control of the rat insulin 2 promoter.|Normal.|C57BL/6JAnu|Yes|Yes|Unknown|Yes|Yes|Yes|No|Unknown||||No|09-Apr-2018|Cryopreserved sperm|55.0|0.0|Unknown||Heparan sulphate, MMP2, T cell, ovalbumin|Yes| 3434.0|common beta chain + IL3 beta chain double KO|B6.129-Csf2rb Csf2rb2/Wehi||Recessive|colony stimulating factor 2 receptor, beta, low-affinity (granulocyte-macrophage)|Csf2rb|Nil|AIC2B, Bc, beta c, CDw131, common beta chain, Csf2rb1, Il3r, Il3rb1, Il5rb|MGI:1339759|targeted mutation 1, Clare L Scott|Csf2rb|MGI:3653883|15||||||||||||||||Yes|||||||||||||Cells from mice generated with the doublytargeted embryonic stem cells wereunresponsive to GM-CSF, IL3 and IL5 cytokines. Alveolar proteinosis, normal lifespan.||C57BL/6 x 129|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|16-Jul-2008||0.0|0.0|Unknown||growth factor, cytokine, receptor, tyrosine kinase, signal transduction|Yes| 3434.0|common beta chain + IL3 beta chain double KO|B6.129-Csf2rb Csf2rb2/Wehi||Recessive|colony stimulating factor 2 receptor, beta 2, low-affinity (granulocyte-macrophage)|Csf2rb2|Unknown|AIC2A, BetaIl3, Bil3, Il3r, Il3rb2|MGI:1339760|colony stimulating factor 2 receptor, beta 2, low-affinity (granulocyte-macrophage); targeted mutation 1, C Glenn Begley|Csf2rb2|MGI:3652583|15|||||||||||||||||||||||||||||Cells from mice generated with the doublytargeted embryonic stem cells wereunresponsive to GM-CSF, IL3 and IL5 cytokines. Alveolar proteinosis, normal lifespan.||C57BL/6 x 129|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|16-Jul-2008||||Unknown||growth factor, cytokine, receptor, tyrosine kinase, signal transduction|Yes| 3438.0|OPGL KO (RANKL KO)|C57BL/6-Tnfsf11||Recessive|tumor necrosis factor (ligand) superfamily, member 11|Tnfsf11|Unknown|Ly109l, ODF, OPG, OPGL, osteoclast differentiation factor, RANKL, Trance|MGI:1100089||||14||||||||||Unknown to Unknown||||||Yes|||||||||||||Oesteoporosis, impaired tooth eruption OPGL mice retarded at 4 weeks of age due to poor nutrition as a result of impaired tooth eruption and oesteoporosis. Maximal severity of phenotype according to age (juvenile): runted ||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|16-Jul-2008||0.0|0.0|Unknown||tooth eruption, dental, osteoporosis, growth retardation|Yes| 6239.0|B6del/448|B6.C-Bid||Recessive|BH3 interacting domain death agonist|Bid|Nil|2700049M22Rik|MGI:108093|BH3 interacting domain death agonist; targeted mutation 1.1, Andreas Strasser|Bid|MGI:4440571|6|||||||||||||||||||||||||||||Decreased sensitivity to induced morbidity/mortality:*Unlike wild-type mice that die from fatal hepatitis within 3?4 hr of anti-Fas antibody treatment, all mutants survive.*Homozygous mice develop and age normally and have no increased incidence of tumor development.*Cell subset composition and total cellularity of thymus, spleen, and lymph nodes were normal.Decreased susceptibility to injury:*Animals survive with little or no liver damage and normal serum levels of ALT and AST and normal liver architecture after injection with anti-Fas antibodies.Cellular phenotype:*Unlike other reports, hematopoietic cell and fibroblasts from homozygous mice are normally sensitive to apoptotic stimuli including DNA damage and gamma-irradiation or treatment with etoposide.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown||Bid, Cell-cycle arrest, Apoptosis|Yes| 3451.0|Socs7 KO|C57BL/6-Socs7/Wehi||Recessive|suppressor of cytokine signaling 7|Socs7|Nil|2310063P06Rik, Nap4|MGI:2651588|suppressor of cytokine signaling 7; targeted mutation, Warren S Alexander|Socs7|MGI:3487375|11||||||||||||||||No|||||||||||||Homozygous null mice display partial penetrance of hydroencephaly, premature death (around 50% of homozygotes die between 3-15 weeks of age), mutants fail to eat, intracranial hemorrhage, abnormally large islets of Langerhans and fully penetrant disorganization of the subcommissural organ and reduced body weight.Premature death: around 50% of homozygotes die between 3-15 weeks of age.Aphagia: mutants fail to eat.Hypoactivity: mutants exhibit reduced activity.Lethargy: lethargy is seen with hydroencephaly.Enlarged pancreatic islets: the islets are larger than normal and show more intense insulin staining.Abnormal subcommissural organ morphology: the subcommissural organ is disorganized in the presence or absence of hydroencephaly.Decreased body weight: homozygotes weigh 7-10% less than wild-type littermates from 4 to 14 weeks of age.Intracranial hemorrhage: bleeding on the surface of the brain is seen in some mutants with hydroencephaly.Hydroencephaly: enlargement of the fluid-filled lateral ventricles and in severely affected mutants the fourth ventricle is seenmany areas of the brain are compressed and displaced caudally.Abnormal hippocampus morphology: transition from the retrosplenial cortex to the hippocampus is disrupted in mutants with hydroencephaly.Abnormal cerebral cortex morphology: the cerebral cortex is thinner than normal with less discrete layers in mutants with hydroencephaly.Abnormal cranial suture morphology: mutants with overt hydrocephalus ehxibit a failure of calvarial bone suture closure.Megacephaly.||C57BL/6|Yes|No|Yes|Yes|No|Yes|No|Unknown||||No|18-Jul-2008||0.0|0.0|Unknown||hydroencephaly, growth, intracranial hemorrhage, food intake, islets of Langerhans|Yes| 5556.0|T14; IL1RA T14OX|B6;CBA-Tg(Il1rn)1Dih/Anu||Dominant||||||||||||||||||||||||||transgene insertion 1, David Hirsh|IL1RA promoter|||||||||||Increased circulating interleukin-1 level: serum IL-1 levels are higher following lipopolysaccharide (LPS) endotoxin challenge.Decreased susceptibility to endotoxin shock: less susceptible to lipopolysaccharide (LPS) endotoxin challenge.Increased susceptibility to bacterial infection: more susceptible to experimental Listeria monocytogenes infection.|Abnormal angiogenesis: reduced angiogenesis observed in stromal keratitis caused by herpes simplex virus (HSV) ocular infection, reduced vascular endothelial growth factor (VEGF) and vascular endothelial growth factor receptor 2 (VEGFR-2) levels.Decreased circulating interleukin-6 level: reduced IL-6 levels in response to stromal keratitis caused by herpes simplex virus (HSV) ocular infection.Abnormal circulating serum amyloid protein level: 30% decrease in serum amyloid P levels after subcutaneous turpentine administration.Decreased susceptibility to endotoxin shock: less susceptible to lipopolysaccharide (LPS) endotoxin challenge, hemizygotes exhibit an intermediate phenotype when compared to wild-type and homozygous.Decreased inflammatory response: reduced polymorphonuclear leukocyte infiltration in response to stromal keratitis caused by herpes simplex virus (HSV) ocular infection.Decreased susceptibility to viral infection: severity of stromal keratitis caused by herpes simplex virus (HSV) ocular infection is diminished.Increased susceptibility to bacterial infection: more susceptible to experimental Listeria monocytogenes infection, hemizygotes exhibit an intermediate phenotype when compared to wild-type and homozygous.|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|Unknown|2 since arrival at ANU||No|12-Aug-2011||0.0|0.0|Unknown||IL1, infection, interleukin, LPS, endotoxin, infection, cytokine|Possibly| 8452.0|Hrg KO|B6.129-Hrg/WjaAnuApb||Recessive|histidine-rich glycoprotein|Hrg|Nil|D16JH2, D18020|MGI:2146636|histidine-rich glycoprotein; targeted mutation 1, Willi Jahnen-Dechent|Hrg|MGI:3789962|16|||||||||||||||||||||||||||||Homeostasis/metabolism phenotype:Normal • despite abnormalities in coagulation and fibrinolysis no significant differences are detected in skin wound healingAbnormal circulating fibrinogen level:• 35% increase in plasma fibrinogen levels in females compared to wild-type controlsAbnormal blood coagulation:• significant reduction in prothrombin time compared to wild-type controlsAbnormal thrombolysis:• faster spontaneous clot lysisDecreased bleeding time:• in a tail bleed assayIncreased monocyte cell number:• mild||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|27-Mar-2018|Cryopreserved sperm|55.0|0.0|Unknown||cystatin, haemostasis , innate, thrombin|Yes| 8457.0|ASD867:F2|BALB/cNCrlAnu:Pink:F2||Dominant|||||||||||||||||||||||||||||||||||||||||Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||2||No|06-Apr-2018||0.0|403.0|Unknown|||No| 8458.0|ASD867:F2|BALB/cNCrlAnu:Orange:F2||Dominant|||||||||||||||||||||||||||||||||||||||||Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||2||No|06-Apr-2018||0.0|70.0|Unknown|||No| 8459.0|ASD867:F2|BALB/cNCrlAnu:Yellow:F2||Dominant|||||||||||||||||||||||||||||||||||||||||Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||2||No|06-Apr-2018||0.0|288.0|Unknown|||No| 8460.0|ASD867:F2|BALB/cNCrlAnu:Green:F2||Dominant|||||||||||||||||||||||||||||||||||||||||Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||2||No|06-Apr-2018||0.0|557.0|Unknown|||No| 8461.0|ASD872:F2|B6.SJL-Ptprc/CrlAnu:Line A:F2||Recessive|protein tyrosine phosphatase, receptor type, C|Ptprc||B220, CD45, Ly-5, Lyt-4, T200|MGI:97810|protein tyrosine phosphatase, receptor type, C; a variant|Ptprc|MGI:4819849|1|||||||||||||||||||||||||||||||C57BL/6NCrl|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||2||No|06-Apr-2018||0.0|255.0|Unknown||T cell|No| 8462.0|ASD872:F2|B6.SJL-Ptprc/CrlAnu:Line B:F2||Recessive|protein tyrosine phosphatase, receptor type, C|Ptprc||B220, CD45, Ly-5, Lyt-4, T200|MGI:97810|protein tyrosine phosphatase, receptor type, C; a variant|Ptprc|MGI:4819849|1|||||||||||||||||||||||||||||||C57BL/6NCrl|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||2||No|06-Apr-2018||0.0|481.0|Unknown||T cell|No| 8455.0|ASD866:F2|C57BL/6NCrlAnu:Orange:F2||Dominant||||||||||||||||||||||||||||||||||||||Normal|||Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|||2|No|06-Apr-2018||0.0|0.0|Unknown|||Yes| 8454.0|ASD866:F2|C57BL/6NCrlAnu:Pink:F2||Dominant||||||||||||||||||||||||||||||||||||||Normal|||Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||2||No|06-Apr-2018||0.0|108.0|Unknown|||Yes| 8456.0|ASD866:F2|C57BL/6NCrlAnu:Yellow:F2||Dominant||||||||||||||||||||||||||||||||||||||Normal|||Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||2||No|06-Apr-2018||0.0|239.0|Unknown|||Yes| 8473.0|Gpx1 KO|B6.129-Gpx1/KolaAnu||Recessive|glutathione peroxidase 1|Gpx1|Nil|cellular GPx, CGPx, Gpx, GPx-1, GSHPx-1|MGI:104887|glutathione peroxidase 1; targeted mutation 1, Ismail Kola|Gpx1|MGI:2388705|9|||||||||||||||||||||||||||||Immune system phenotype:Normal: • upon infection with P. berghei ANKA or P. berghei K173, homozygotes show no significant differences in malaria parasite burdens relative to wild-type mice, suggesting normal intraerythrocytic parasite progression and malarial immunityIncreased inflammatory response:• at 24 hrs after cold-induced brain injury, homozygotes exhibit an accelerated neuroinflammatory response, with a significant increase in Mac-1+ cells which rapidly declines by 96 hrs and reappears at 10 days post-injury, suggesting changes in response/activation/recruitment of macrophages and microglia to this type of injuryIncreased neuron apoptosis:• at 24 hrs after ischemia/reperfusion damage in the mid cerebral artery (MCA), homozygotes exhibit increased neuronal apoptosis, as shown by accelerated caspase-3 activation and increased TUNEL staining in post-ischemic mutant brains • at 24 and 96 hrs after cold-induced brain injury, homozygotes display significantly increased neuronal cell death in regions immediately proximal to the infarct core (penumbra)Increased susceptibility to ischemic brain injury :• upon MCA stroke surgery, homozygotes display increased susceptibility to ischemia/reperfusion injury relative to wild-type miceincreased cerebral infarction size ( J:71798 )• in response to ischemia/reperfusion damage in the MCA, homozygotes exhibit a a significantly increased infarct size (area in mm2) relative to wild-type miceCNS ischemia:• in response to ischemia/reperfusion damage in the MCA, homozygotes show an increased neurological deficit score (1.97 vs 0.9) and higher mortality rates (19% vs 7%) relative to wild-type mice, with most mutants dying from severe stroke rather than surgical complications||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|16-Apr-2018||0.0|0.0|Unknown||H2O2, oxidative stressors, neurodegenerative disorders|Yes| 8471.0|Pad4 KO|B6.Cg-Padi4/JAnu||Recessive|peptidyl arginine deiminase, type IV|Padi4|Nil|Pad4, PAD type IV, Pdi4|MGI:1338898|peptidyl arginine deiminase, type IV; targeted mutation 1.1, Kerri A Mowen|Padi4|MGI:5285854|4|||||||||||||||||||||||||||||Abnormal neutrophil physiology:• neutrophils lack histone deimination unlike wild-type cellsDecreased susceptibility to viral infection:• influenza-infected mice exhibit decreased weight loss compared with similarly treated wild-type mice• however, influenza-infected mice exhibit normal survival, neutrophil recruitment into the lung, lung viral titers, and pro-inflammatory cytokine levelsDecreased susceptibility to weight loss:• influenza-infected mice exhibit decreased weight loss compared with similarly treated wild-type mice||C57BL/6J|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|13-Apr-2018|Cryopreserved sperm|5.0|63.0|Unknown||Infection, Inflammation, neutrophil extracellular traps (NETs)|Yes| 8470.0|Clec7a KO|B6.129-Clec7a/JAnuApb||Recessive|C-type lectin domain family 7, member a|Clec7a|Nil|beta-glucan receptor, beta-GR, BGR, Clecsf12, dectin-1|MGI:1861431|C-type lectin domain family 7, member a; targeted mutation 1, Gordon D Brown|Clec7a|MGI:3695710|6|||||||||||||||||||||||||||||Abnormal circulating interleukin level:• IL-22 production in response to Aspergillus fumigatus challenge is severely reducedDecreased circulating interleukin-17 level:• lower levels of IL-17A after lung infection with Aspergillus fumigatusLung inflammation:• impaired inflammatory reactivity of alveolar macrophage• impaired recruitment of macrophage to lungs• highly susceptible to lung infection with Aspergillus fumigatus• little antifungal activity in lung lavage fluidIncreased susceptibility to fungal infection:• highly susceptible to lung infection with Aspergillus fumigatusIncreased sensitivity to induced morbidity/mortality:• mice infected with sublethal dose of C. albicans have much lower survival rate compared to controlsAbnormal neutrophil physiology:• cells do not have beta-glucan dependent recognition of unopsonized zymosan; respiratory burst is attenuated when cultured with unopsonized yeast, and response is not fully restored when opsonized zymosan particles are usedAbnormal macrophage physiology:• thioglycollate-elicited macrophages show impaired recognition of zymosan (fungal beta-glucan particle); prior opsonization with mouse serum restores binding by macrophages• elicited mutant macrophages show impairment of cytokine production when cultured with zymosan• recognition of unopsonized yeast by macrophages is impaired compared to controlsAbnormal cytokine secretion:• mutant macrophages show impaired production of Il10 and Il12 when cultured with zymosanAbnormal inflammatory response:• inflammatory response to zymosan fails to occur; defect is specific for fungal particles as other microbial stimuli elicit a response• inflammatory response to yeast is not restored after opsonization of yeast with mouse serum, although fungal recognition is restored to macrophagesIncreased susceptibility to fungal infection:• mice infected with sublethal dose of C. albicans have much lower survival rate compared to controls• at day 9 after infection, mutant mice have higher fungal burdens than controls in the gastrointestinal tract; enhanced systemic dissemination of C. albicans is evident within 24 hours of infection• at time of death, mutant kidneys show enhanced fungal colonization by C. albicans, particularly in pelvic region with extension up renal tubules compared to controls which lack such colonization• fungal hyphae extend through tubular epithelium into interstitium and are surrounded by acute neutrophilic inflammation (invasive candidiasis)Enlarged stomach:• mice which succumb to infection show macroscopic enlargement of stomachAbnormal digestive system physiology:• mice which succumb to infection have stomachs full of food, suggesting blockage of gastrointestinal tract||C57BL/6J|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|13-Apr-2018|Cryopreserved sperm|31.0|0.0|Unknown||Infection, Beta-glucan, Toll|Yes| 8472.0|MxCreS1P1floxed|B6.Cg-S1pr1 Tg(Mx1-cre)1Cgn/UsaApb||Recessive|sphingosine-1-phosphate receptor 1|S1pr1||Edg1, S1P, S1P1|MGI:1096355|sphingosine-1-phosphate receptor 1; targeted mutation 2, Richard L Proia|S1pr1|MGI:2681911|3|||||||||||||||||transgene insertion 1, University of Cologne|inducible Mx1|||||||||||No phenotype unless the Cre is activated.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|15-Apr-2018|Cryopreserved sperm|40.0|0.0|Unknown||Stem cell, bone marrow egress, Cxcr4|Yes| 8476.0|Tg(Dmp1-cre)1Jqfe. Pthlhtm1Ack|B6.129-Pthlh Tg(Dmp1-cre)1Jqfe/SviApb||Recessive|parathyroid hormone-like peptide|Pthlh|Normal|parathyroid hormone-like hormone, parathyroid hormone-related peptide, parathyroid hormone-related protein, PTH-like, PTH-related peptide, Pthrp|MGI:97800|parathyroid hormone-like peptide; targeted mutation 1, Andrew C Karaplis|Pthlh|MGI:2387462|6|||||||||||||||||transgene insertion 1, Jian Q Feng||||||||||||Adult mice had lower trabecular bone mass and lower bone formation. There was no difference in body weight or bone length compared to controls.|Unknown|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|23-Apr-2018|Cryopreserved sperm|50.0|0.0|Unknown||Osteocyte, Osteoblast, cortical|Yes| 3525.0|NOD.B6 Idd11C|NOD.B6-Idd11||Recessive|||Unknown|||insulin dependent diabetes susceptibility 11; C57BL/6 |Idd11|MGI:3036811|4||||||||||||||||Yes|||||||||||||Non obese diabetic (NOD) mice exhibit a susceptibility to Spontaneous development of type 1 diabetes.||NOD|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|28-Jul-2008||0.0|0.0|Unknown||Diabetic, insulin, T cell, autoimmunity|Yes| 7486.0|Slc11a1|NOD.B10-Idd5.1 Tg(CMV-RNAi:Slc11a1)915Dil/ArcApb||Dominant||||||||||||||||||||||||||transgene insertion 915, Linda Wicker|cytomegalovirus||insulin dependent diabetes susceptibility 5.1|Idd5.1||Idd5.1, Idd5a|MGI:2158421|insulin dependent diabetes susceptibility 5.1; C57BL/10SnJ|Idd5.1|MGI:3036875|1|The Idd5.1 allele confers resistance to insulin dependent diabetes compared to NOD/MrkTac.When challenged with S. enteric, animals expressing RNAi do not survive (7/7). By comparison challenged WT mice were resistant to S. enteric infection (7/8) survived.Diabetes susceptibility is greatly reduced in females expressing Slc11a1 RNAi compared to Idd5.1 female mice not carrying the RNAi transgene.||NOD|Yes|Yes|Yes|Yes|Yes|Yes|No|Excellent|||GFP positive male to NOD female|No|18-Nov-2013|Embryo|0.0|0.0|Unknown||Idd5.1, insulin, RNAi, infection|Yes| 3523.0|NOD.B6 Idd1B|NOD.B6-Idd11||Recessive|||Unknown|||insulin dependent diabetes susceptibility 11|Idd11|MGI:3036811|4||||||||||||||||Yes|||||||||||||Non obese diabetic (NOD) mice exhibit a susceptibility to Spontaneous development of type 1 diabetes.||NOD|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|28-Jul-2008||0.0|0.0|Unknown||diabetic, T cell, autoimmunity, insulin, non obese|Yes| 8860.0|ASD954:Pomelo:DH16pbdel|C57BL/6NCrlAnu-Dhx8/AnuApb||Recessive|DEAH (Asp-Glu-Ala-His) box polypeptide 8|Dhx8|Unknown|Ddx8, mDEAH6, MGC:31290, RNA helicase|MGI:1306823||||11|||||||||||||||||||||||||||||Unknown|Unknown|C57BL/6NCrlAnu|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|18-Feb-2020|Cryopreserved sperm|39.0|0.0|Unknown|||Yes| 7521.0|TgC100.V717F|B6.DBA-Tg(ACTB-APP*V717F)1Colm/ArcApb|B6.DBA-Tg(ACTB-APP*V717F)1Colm/Arc|Dominant||||||||||||||||||||||||||transgene insertion 1, Colin L Masters|human beta actin|High||||||||||Enhanced behavioral response to addictive substance:• amphetamine-treated mice exhibit increased hyperactivity compared with similarly treated wild-type mice.Behavioural despair:• young, but not old, mice exhibit increased immobility during a forced swim test compared with wild-type mice.Abnormal learning/memory/conditioning:• mice exhibit reduced alternation in a Y-maze compared with wild-type mice.Impaired passive avoidance behaviour:• mice exhibit reduced retention in a passive avoidance test compared with wild-type mice.Increased startle reflex:• old, but not young, mice exhibit an increase in startle amplitude compared with wild-type mice.Hyperactivity:• in young, but not old, mice exhibit increased activity in an open field test and entries in an elevated plus maze or Y-maze compared with wild-type mice• at 9 months, mice exhibit slight hyperactivity compared with wild-type mice• however, mice exhibit normal activity levels at 22 monthsInduced hyperactivity:• amphetamine-treated mice exhibit increased hyperactivity compared with similarly treated wild-type mice.Abnormal axon morphology.Increased apoptosis:• in CA1 of the hippocampus||C57BL/6 x DBA|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||26|sib x sib|No|29-Nov-2013|Embryo|0.0|0.0|Yes|Alzheimer's disease|amyloid beta-protein (A beta), APP, Alzheimer's disease , metal, γ-secretase|Yes| 327.0|spasmodic oscillator|C57BL/6-Glra1||Recessive|glycine receptor, alpha 1 subunit|Glra1|Nil|B230397M16Rik, oscillator, ot|MGI:95747|spasmodic oscillator|Glra1|MGI:1856177|11||||||||||||||||No|||||||||||||Postnatal lethality:homozygotes die by the end of the third week after birthNervous system phenotype:mice exhibit normal spontaenous glycinergic inhibitory postsynaptic currents in amacrine cellsDecreased neuron number:in mutants there is a reduction or absence of post-inspiratory neurons compared to wild-typeAbnormal nervous system electrophysiology:phrenic nerve discharge patterns of mutant mice vary with respect to burst frequency and duration of expiration and inspiration compared to wild-type mice; mutants displayed more frequent phrenic nerve discharges with shorter, less regular expiratory intervalsMuscle spasm:after rapid breathing episodes, single or multiple whole-body spasms occur with intervals between spasms of 6 seconds to more than 1 minuteAbnormal breathing frequency:conscious mutants (P16-23) display disturbed respiratory patterns characterized by periods of slow breathing and intermittent episodes of rapid breathing; episodes are of variable (2-10 sec).||C57BL/6|Yes|No|Yes|Yes|No|Yes|Yes|Unknown||||No|05-May-2006||0.0|0.0|Yes||ataxia, tremors, Hyperekplexia, glycine receptor, synapse|Yes| 8853.0|IL13 KO|Balb/C:B6129-IL13/AnuApb||Recessive|interleukin 13|Il13|Unknown|Il13|MGI:96541|targeted mutation 2, Andrew NJ McKenzie|Il13|MGI:1931804|11||||||||||||||||No|||||||||||||abnormal T helper 2 physiology: homozygotes display impaired pulmonary granuloma formation in response to schistosome egg immunizationeosinophil infiltration is impaired in response to schistosome egg immunizationincreased susceptibility to parasitic infection:the expulsion of parasitic worms from the gut is delayedA neomycin cassette was inserted into exon 3.||BALB/c|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|12-Feb-2020|Cryopreserved sperm|60.0|0.0|Unknown||IL4, IL5, T cell, infection|Yes| 8855.0|Naip1-6 KO|B6.Cg-Del(13Naip1-Naip5)1Vnce Naip2/JAnu||Recessive||||||deletion, Chr 13, Russell Vance 1|Del(13Naip1-Naip5)1Vnce|MGI:6246513|13|||||||||||||||||||||||||||||Homozygous Naip1-6Δ mice fail to respond to cytosolic flagellin, consistent with previous biochemical data implicating Naip6 in flagellin detection. They also fail to respond to type III secretion system needle or inner rod protein.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|12-Feb-2020||0.0|30.0|Unknown||flagellin|Yes| 8855.0|Naip1-6 KO|B6.Cg-Del(13Naip1-Naip5)1Vnce Naip2/JAnu||Recessive|NLR family, apoptosis inhibitory protein 2|Naip2||Birc1b, Naip2, Naip-rs6|MGI:1298226|NLR family, apoptosis inhibitory protein 2; endonuclease-mediated mutation 2, Russell Vance|Naip2|MGI:6246533|13|||||||||||||||||||||||||||||Homozygous Naip1-6Δ mice fail to respond to cytosolic flagellin, consistent with previous biochemical data implicating Naip6 in flagellin detection. They also fail to respond to type III secretion system needle or inner rod protein.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|12-Feb-2020||||Unknown||flagellin|Yes| 8854.0|TgECD-CACG Cre|C57BL/6-Tg(Cd8-Cre/Ecd)/Apb||Dominant||||||||||||||||||||||||||Cre recombinase|Cd8 / CAGG|||||||||||This is CD8 Cre mice with Ecdysone-deducible promoter|Heterozygous|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|12-Feb-2020||0.0|0.0|Unknown|||Yes| 8862.0|foz|BALB/c-Alms1/AnuTchApb||Recessive|Alstrom syndrome 1 homolog (human)|Alms1|Unknown||MGI:1934606|Alstrom syndrome 1 homolog (human); fat aussie|Alms1|MGI:3621984|6||||||||||||||||Yes|||||||||||||Mice are hyperphagic leading to obesity . Males are sterile. High fat feeding accelerates obesity development. Compared to foz/foz mice on NOD.B10 background, BALB/c foz/foz mice do not develop diabetes and liver disease is less severe.|normal|BALB/c|Yes|Unknown|Yes|Yes|No|Yes|Yes|Good|>10||heterozygote mating|No|20-Feb-2020||0.0|149.0|Yes|Alstrom syndrome is a disorder of childhood obesity, diabetes development and infertility.|obesity, diabetes, nonalcoholic fatty liver disease, alstrom syndrome, cilia|Yes| 8881.0|Nampt knockout|C57BL/6J-Nampt/DunwApb||Recessive|nicotinamide phosphoribosyltransferase|Nampt|Unknown|1110035O14Rik, Pbef1, Visfatin|MGI:1929865|Nampt; endonuclease-mediated mutation 1, Sally L Dunwoodie|Nampt||12||||||||||Unknown to Unknown|||||||||||||||||||Homozygous loss of Nampt is embryonic lethal|Nampt heterozygous mice reported to have hydroencephaly, abnormal skin morphology and enlarged heart. No reported lethality|C57BL/6J|No|No|Yes|No|No|Yes|No|Unknown||||No|11-Mar-2020|Cryopreserved sperm|40.0|0.0|Unknown|||Yes| 8873.0|Prss57 KO|B6;129S5-Prss57/MmucdMarpApb||Recessive|protease, serine 57|Prss57|Nil|2900092M14Rik, GLGL782, Prssl1, UNQ782|MGI:1920356|protease, serine 57; targeted mutation 1, Lexicon Pharmaceuticals|Prss57|MGI:5007300|10|||||||||||||||||||||||||||||||B6|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|07-Mar-2020||0.0|0.0|Unknown|||Yes| 8893.0|ENU32:002|C57BL/6NCrlAnu-Pcgf5/AnuApb||Recessive|polycomb group ring finger 5|Pcgf5|Unknown||MGI:1923505|Pcgf5;mutation 1, Australian National University|Pcgf5||19||||||||||Unknown to Unknown|||||||||||||||||||||C57BL/6NCrlAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|8|||No|17-Mar-2020|Cryopreserved sperm|22.0|0.0|Unknown|||Yes| 8451.0|Todr1KO|C57BL/6N-2610318N02Rik/Wtsi||Recessive|RIKEN cDNA 2610318N02 gene|2610318N02Rik|||MGI:1917708|RIKEN cDNA 2610318N02 gene; targeted mutation 1a, Wellcome Trust Sanger Institute|2610318N02Rik|MGI:4451963|16|||||||||||||||||||||||||||||Unknown|Normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|22-Mar-2018|Cryopreserved sperm|20.0|0.0|Unknown||Dendritic cell, RNA, myelopoiesis|Yes| 8872.0|Jinx|C57BL/6-Unc13d/MmucdMarpApb||Recessive|unc-13 homolog D|Unc13d|Nil|2610108D09Rik, Jinx, Munc13-4|MGI:1917700|unc-13 homolog D; Jinx|Unc13d|MGI:3628822|11|||||||||||||||||||||||||||||Increased neutrophil cell number:• after receiving 2 x 104 PFU MCMV, a 4-fold increase in neutrophil number is observed on day 7 compared to wild-type; this resolves by day 14• 12 days after infection with LCMV, mice show neutrophilia, rather than neutropenia.Increased CD8-positive, alpha-beta T cell number:spleen, after LCMV infection.Increased monocyte cell number:• after receiving 2 x 104 PFU MCMV, a 3-fold increase in monocyte number is observed on day 7 compared to wild-type; this does not resolve.Enlarged spleen:• 12 days after infection with LCMV, mice have splenomegaly.Abnormal NK cell physiology:• NK cell-mediated cytotoxicity against beta2microglobulin-null cells in vivo and against YAC-1 cells in vitro is abolished.Decreased cytotoxic T cell cytolysis:• polyclonal stimulation of CTLs show defect in ability to degranulateAbnormal macrophage physiology:• the susceptibility of activated mutant macrophages to ex vivo vesicular stomatitis virus (VSV) infection was reversed by the addition of type I interferon.Absent lymph node germinal center:• germinal center depletion and replacement by macrophages is observed in peripheral lymph nodes after LCMV infectionAbnormal cytokine secretion:• homozygotes show exaggerated production of Il12, IFNgamma, and type I INF (alpha/beta) 36 hours after inoculation with the virus• 12 days after infection with LCMV, serum IFNgamma levels show sustained elevation; increased production of IFNgamma by splenic CD8+ T cells is evidentIncreased susceptibility to viral infection:• mice are susceptible to infection by mouse cytomegalovirus (MCMV)• mice are severely ill and have high viral loads in the spleen five days following infection with MCMV• activated macrophages from these mice are susceptible to ex vivo VSV infection• when infected with 105 PFU of Smith strain MCMV (mouse cytomegalovirus), mice show severe illness with 4-5 orders of magnitude higher viral titers after 5 days, whereas wild-type C57BL/6 mice survive infection with no signs of illness and very few PFU in the spleen after 5 days (J:119974)• dose of 2.5 x 105 PFU MCMV is lethal to mutants and BALB/c controls within 6 days while C57BL/6 controls mice do not exhibit any lethality.• hemophagocytic lymphohistiocytosis (HLH) is observed in mice infected with LCMV (lymphocytic choriomeningitis virus - Armstrong strain)• infection by LCMV can not be controlled, such that titers are >1000 fold higher in mutants vs controls 12 days after inoculation, except in the liver.Anemia:• 12 days after infection with LCMV, mice are anemic||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|07-Mar-2020||0.0|0.0|Yes|familial hemophagocytic lymphohistiocytosis 3|NK cell, CTL|Yes| 8880.0|Mal fl LysM-cre|C57BL/6-Mal Lyz2/PjhApb||Recessive|myelin and lymphocyte protein, T cell differentiation protein|Mal|Normal|VIP17|MGI:892970||||2|||||||||||||||||||||||||||||Normal||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|11-Mar-2020|Cryopreserved sperm|50.0|0.0|Unknown|||Yes| 8880.0|Mal fl LysM-cre|C57BL/6-Mal Lyz2/PjhApb||Recessive|lysozyme 2|Lyz2||Lys, Lysm, Lyzs, Lzm, Lzm-s1, Lzp|MGI:96897|lysozyme 2; targeted mutation 1, Irmgard Forster|Lyz2|MGI:1934631|10|||||||||||||||||||||||||||||Normal||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|11-Mar-2020|Cryopreserved sperm|||Unknown|||Yes| 8863.0|Foz:NOD|NOD.B10-Alms1/AnuTchApb||Recessive|Alstrom syndrome 1 homolog (human)|Alms1|Unknown||MGI:1934606|Alstrom syndrome 1 homolog (human); fat aussie|Alms1|MGI:3621984|6||||||||||||||||Yes|||||||||||||Mice are hyperphagic leading to obesity and diabetes. Males are sterile. High fat feeding accelerates obesity and diabetes development, and leads to nonalcoholic steatohepatitis which progresses to liver fibrosis.Insulin resistance: female mice develop insulin resistance by 200 days of age.Increased eating behavior: mutants eat more than wild-type.Abnormal hepatocyte morphology: mutant livers show many hepatocytes with ballooning degeneration and extensive lobular inflammation with polymorphs and mononuclear cells.Enlarged liver: mice fed high-fat diet show hepatomegaly compared to wild-type (8.9g vs. 2g).Increased liver weight: liver weights in mutant are twice that of wild-type (3.4g vs. 1.6g).Liver fibrosis: mutant livers show pericellular and pericentral fibrosis.Hepatic steatosis: chow-fed mutants develop steatosis; mutants fed the high-fat diet develop severe steatohepatitis.|Normal|NOD.B10|Yes|Yes|Yes|Yes|No|Yes|Yes|Excellent|>10||heterozygote mating|No|20-Feb-2020|Cryopreserved sperm|44.0|0.0|Yes|Alstrom syndrome is a disorder of childhood obesity, diabetes development and infertility.|obesity, diabetes, nonalcoholic fatty liver disease, alstrom syndrome, cilia|Yes| 8864.0|ENU19:Ninj1|C57BL/6JAnu-Ninj1/AnuApb||Recessive|ninjurin 1|Ninj1|Unknown||MGI:1196617||||13|||||||||||||||||||||||||||||||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|20-Feb-2020|Cryopreserved sperm|44.0|0.0|Unknown|||Yes| 10426.0|Tet-IGRP#11|NOD-Tg(TetO-IGRP) Tg(IEa-tTA)/Apb||Dominant|glucose-6-phosphatase, catalytic, 2|G6pc2|Increased|IGRP, islet specific glucose-6-phosphatase|MGI:1277193||||2|ENSMUSG00000005232|ENSMUST00000005364|||||||||||||||IGRP|CMV-tetracycline response element|||||||||||Normal|Normal|NOD/LtJ|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|16-May-2024|Cryopreserved sperm|50.0|0.0|Unknown|||Possibly| 10426.0|Tet-IGRP#11|NOD-Tg(TetO-IGRP) Tg(IEa-tTA)/Apb||Dominant||||||||||||||||||||||||||tet-transactivator|MHC class II IEa|||||||||||Normal|Normal|NOD/LtJ|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|16-May-2024|Cryopreserved sperm|||Unknown|||Possibly| 8867.0|Rab30 CRISPR KO #15|C57BL/6-Rab30/Apb||Recessive|RAB30, member RAS oncogene family|Rab30|Unknown|5033421K01Rik|MGI:1923235||||7|||||||||||||||||||||||||||||Normal|Normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|28-Feb-2020|Cryopreserved sperm|50.0|0.0|Unknown|||Yes| 8874.0|Ets2 fl|C57BL/6-Ets2/PjhApb||Recessive|E26 avian leukemia oncogene 2, 3' domain|Ets2|Normal|Ets-2|MGI:95456||||16|||||||||||||||||||||||||||||Normal||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|07-Mar-2020|Cryopreserved sperm|46.0|0.0|Unknown|||Yes| 8870.0|Cldn10 PM|C57BL/6-Cldn10/MarpApb||Recessive|claudin 10|Cldn10||6720456I16Rik, Cldn10a, Cldn10b, D14Ertd728e|MGI:1913101||||14|||||||||||||||||||||||||||||Normal|Normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|04-Mar-2020|Cryopreserved sperm|50.0|0.0|Unknown|||Yes| 8868.0|Snx5 KO-3064| B6(Cg)-Snx5/Apb||Recessive|sorting nexin 5|Snx5||0910001N05Rik, 1810032P22Rik, D2Ertd52e|MGI:1916428|sorting nexin 5; targeted mutation 1a, Wellcome Trust Sanger Institute|Snx5|MGI:4362512|2|||||||||||||||||||||||||||||Normal|Normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|28-Feb-2020|Cryopreserved sperm|50.0|0.0|Unknown||Macrophage, ruffling, macropinocytosis|Yes| 8871.0|Tip2#78|NOD-Tg(TetO-Ins2) Tg(IEa-tTA)/Apb||Dominant||||||||||||||||||||||||||Insulin II|TetO|||||||||||Normal|Normal|NOD/LtJ|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|06-Mar-2020|Cryopreserved sperm|50.0|0.0|Unknown|||Yes| 8871.0|Tip2#78|NOD-Tg(TetO-Ins2) Tg(IEa-tTA)/Apb||Dominant||||||||||||||||||||||||||tetracycline transactivator|IEa|||||||||||Normal|Normal|NOD/LtJ|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|06-Mar-2020|Cryopreserved sperm|||Unknown|||Yes| 8876.0|NOD.B6Idd11F|NOD-Idd11F/Apb||Recessive|||||||||||||||||||||||||||||insulin dependent diabetes susceptibility 11|Idd11|||MGI:96402|nsulin dependent diabetes susceptibility 11; C57BL/6|Idd11|MGI:3036811|4|Mice exhibit decreased diabetes incidence compared to NOD/Lt wildtype mice|Unknown|NOD/Lt|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|08-Mar-2020|Cryopreserved sperm|30.0|0.0|Yes|Type 1 Diabetes|T1D|Yes| 8819.0|ENU43:266:Lgals3|C57BL/6NCrlAnu-Lgals3/AnuApb||Recessive|lectin, galactose binding, soluble 3|Lgals3|Unknown|gal3, galectin-3, L-34, Mac-2|MGI:96778||||14|||||||||||||||||||||||||||||Unknown||C57BL/6NCrlAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|24-Oct-2019|Cryopreserved sperm|132.0|0.0|Unknown||ENU|Yes| 8474.0|ASD598:Albiol:Aire:HIVEP2Indel|B6.129-Aire Hivep2/Anuapb||Recessive|autoimmune regulator (autoimmune polyendocrinopathy candidiasis ectodermal dystrophy)|Aire|Nil||MGI:1338803|Aire, endonuclease-mediated mutation 1, Australian National University|Aire||10||||||||||Unknown to Unknown|||||||||||||||||||Unknown|Unknown|B10.BR|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|16-Apr-2018|Cryopreserved sperm|11.0|0.0|Unknown|||Yes| 8474.0|ASD598:Albiol:Aire:HIVEP2Indel|B6.129-Aire Hivep2/Anuapb||Recessive|human immunodeficiency virus type I enhancer binding protein 2|Hivep2||Gm20114, MIBP1, Schnurri-2, Shn-2|MGI:1338076|Hivep2, endonuclease-mediated mutation 1, Australian National University|Hivep2||10||||||||||Unknown to Unknown|||||||||||||||||||Unknown|Unknown|B10.BR|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|16-Apr-2018|Cryopreserved sperm|||Unknown|||Yes| 8884.0|ASD893:Amaranth:41|C57BL/6NCrlAnu-Nlrp9b/AnuApb||Recessive|NLR family, pyrin domain containing 9B|Nlrp9b|Unknown|Nalp9b, Nalp-delta|MGI:2675377||||7|||||||||||||||||||||||||||||Unknown|Normal|C57BL/6NCrlAnu|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|13-Mar-2020|Cryopreserved sperm|11.0|0.0|Unknown|||Yes| 8885.0|ASD749:Spot:42|C57BL/6NCrlAnu-Tacr3/AnuApb||Recessive|tachykinin receptor 3|Tacr3|Unknown|neuromedin K receptor, Nk3r, Tac3r|MGI:892968||||3|||||||||||||||||||||||||||||Unknown|Normal|C57BL/6NCrlAnu|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|13-Mar-2020|Cryopreserved sperm|22.0|0.0|Unknown|||Yes| 8887.0|ASD755:Tcf7 fl|B6(Cg)-Tcf7/WehiAnuApb||Recessive|transcription factor 7, T cell specific|Tcf7||T cell factor-1, T-cell factor 1, Tcf1, TCF-1|MGI:98507|transcription factor 7, T cell specific; targeted mutation 1c, Wellcome Trust Sanger Institute|Tcf7|MGI:5816259|11|||||||||||||||||||||||||||||Normal|Normal|C57BL/6NCrlAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|13-Mar-2020|Cryopreserved sperm|33.0|0.0|Unknown|||Yes| 8888.0|ASD723:Beast:DH314|C57BL/6NCrlAnu-Dhx58/AnuApb||Recessive|DEXH (Asp-Glu-X-His) box polypeptide 58|Dhx58|Unknown|B430001I08Rik, D11Lgp2e, LPG2|MGI:1931560||||11|||||||||||||||||||||||||||||Unknown |Unknown|C57BL/6NCrlAnu|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|17-Mar-2020|Cryopreserved sperm|33.0|0.0|Unknown|||Yes| 8891.0|ASD973:Guzman:90|C57BL/6NCrlAnu-Cyld/AnuApb||Recessive|CYLD lysine 63 deubiquitinase|Cyld|Unknown|2010013M14Rik, 2900009M21Rik, C130039D01Rik, CYLD1, mKIAA0849|MGI:1921506||||8|||||||||||||||||||||||||||||Unknown|Unknown|C57BL/6NCrlAnu|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|17-Mar-2020|Cryopreserved sperm|11.0|0.0|Unknown|||Yes| 8883.0|ASD1014:Cabbage|C57BL/6NCrlAnu-Dock11/AnuApb||Recessive|dedicator of cytokinesis 11|Dock11|Unknown|5033414A21Rik, Zizimin2|MGI:1923224||||X|||||||||||||||||||||||||||||Unknown|Unknown|C57BL/6NCrlAnu|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|13-Mar-2020|Cryopreserved sperm|11.0|0.0|Unknown|||Yes| 8468.0|Tcf7-GFP|C57BL/6-Tcf7/HhxAnu||Recessive|transcription factor 7, T cell specific|Tcf7||T cell factor-1, T-cell factor 1, Tcf1, TCF-1|MGI:98507|transcription factor 7, T cell specific; targeted mutation 1, Hai-Hui Xue|Tcf7|MGI:5805838|11|||||||||||||||||||||||||||||Using newly-generated Tcf7GFP reporter mice, we identified novel early innate lymphoid progenitors that express high levels of TCF-1 but lack surface markers of adaptive and innate lymphocyte lineages. These early innate lymphoid progenitors closely resemble bone marrow lymphoid progenitors at the transcriptome level, but lack efficient T and B lymphocyte potential. Instead, they efficiently gave rise to various ILC lineages, including conventional NK cells as well as cytokine-producing helper ILC at the clonal level, indicating that they are the earliest identifiable ILC progenitors. ||C57BL/6NCrlAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|12-Apr-2018|Cryopreserved sperm|19.0|0.0|Unknown||T cell, ILC, Tcf-1|Yes| 8889.0|ASD742:ZFRKO:ZF1bpins|C57BL/6NCrlAnu-Zfr/AnuApb||Recessive|zinc finger RNA binding protein|Zfr|Unknown|C920030H05Rik|MGI:1341890||||15|||||||||||||||||||||||||||||Unknown|Unknown|C57BL/6NCrlAnu|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|17-Mar-2020|Cryopreserved sperm|60.0|0.0|Unknown|||Yes| 8890.0|ASD896:Eureka:56|C57BL/6NCrlAnu-Setd5/AnuApb||Recessive|SET domain containing 5|Setd5|Unknown|2900045N06Rik, mKIAA1757|MGI:1920145||||6|||||||||||||||||||||||||||||Unknown|Unknown|C57BL/6NCrlAnu|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|17-Mar-2020|Cryopreserved sperm|12.0|0.0|Unknown|||Yes| 8892.0|Vps51:35bp deletion:Vav1-Cre:Vps51 tm1c|C57BL/6NCrlAnu-Vps51 Vps51 Tg(Vav1-Cre)1Awr/AnuApb||Recessive|VPS51 GARP complex subunit|Vps51|Unknown|1110014N23Rik, 3110057M17Rik|MGI:1915755||||19|||||||||||||||||transgene insertion 1, Andrew W Roberts|Vav1|||||||||||||C57BL/6NCrlAnu|No|No|Yes|No|No|Yes|No|Unknown||||No|17-Mar-2020|Cryopreserved sperm|11.0|0.0|Unknown|||Yes| 8892.0|Vps51:35bp deletion:Vav1-Cre:Vps51 tm1c|C57BL/6NCrlAnu-Vps51 Vps51 Tg(Vav1-Cre)1Awr/AnuApb||Recessive|VPS51 GARP complex subunit|Vps51|Nil|1110014N23Rik, 3110057M17Rik|MGI:1915755|VPS51 GARP complex subunit; targeted mutation 1c, Wellcome Trust Sanger Institute|Vps51||19|||||||||||||||||||||||||||||||C57BL/6NCrlAnu|No|No|Yes|No|No|Yes|No|Unknown||||No|17-Mar-2020|Cryopreserved sperm|||Unknown|||Yes| 8836.0||NOL3-KO||Recessive|Nol3-Ko||||||||Unknown|||||||||||||||||||||||||||||Homozygous|Homozygous|C57Bl6|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|09-Jan-2020|Cryopreserved sperm|50.0|0.0|Unknown|||Yes| 8846.0||SJL/JAnu||Dominant||||||||||||||||||||||||||||||||||||||Normal|Normal|SJL/J|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|31-Jan-2020|Cryopreserved sperm|55.0|0.0|Unknown|||No| 8840.0|ASD956:Seville:T31bpdel XM|C57BL/6NCrlAnu-Tlr3/AnuApb||Recessive|toll-like receptor 3|Tlr3|Unknown||MGI:2156367||||8|||||||||||||||||||||||||||||Unknown|Unknown|C57BL/6NCrlAnu|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|16-Jan-2020|Cryopreserved sperm|72.0|0.0|Unknown|||Yes| 8841.0|ASD947:Packham:AG368 XM|C57BL/6NCrlAnu-Ager/AnuApb||Recessive|advanced glycosylation end product-specific receptor|Ager||RAGE|MGI:893592||||17|||||||||||||||||||||||||||||Unknown|Unknown|C57BL/6NCrlAnu|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|16-Jan-2020|Cryopreserved sperm|48.0|0.0|Unknown|||Yes| 8842.0|Scn2a R1882Q conditional |C57BL/6-Scn2a/Apb||Recessive|sodium channel, voltage-gated, type II, alpha|Scn2a|Unknown|A230052E19Rik, Nav1.2, Scn2a1|MGI:98248||||2|||||||||||||||||||||||||||||Unknown |Normal|C57BL/6|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|22-Jan-2020|Cryopreserved sperm|50.0|0.0|Unknown|||Yes| 8844.0|Scn2a E1211K|C57BL/6-Scn2a/Apb||Recessive||||||||||||||||||||||||||||||||||||||Unknown |Normal|C57BL/6|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|23-Jan-2020|Cryopreserved sperm|50.0|0.0|Unknown|||Yes| 8845.0|Scn2a K905N conditional |C57BL/6-Scn2a/Apb||Recessive|sodium channel, voltage-gated, type II, alpha|Scn2a|Unknown||MGI:98248||||2|||||||||||||||||||||||||||||Unknown |Normal|C57BL/6|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|23-Jan-2020|Cryopreserved sperm|50.0|0.0|Unknown|||Yes| 8849.0|ASD1035:Melon:AC424|C57BL/6NCrlANu-Actr5/AnuApb||Recessive|ARP5 actin-related protein 5|Actr5|Unknown|B430109J19Rik|MGI:1924748||||2|||||||||||||||||||||||||||||Unknown|Unknown|C57BL/6NCrlAnu|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|10-Feb-2020|Cryopreserved sperm|72.0|0.0|Unknown|||Yes| 8850.0|ASD1003:Fuji:TN1bpdel|C57BL/6NCrlAnu-Tnfrsf25/AnuApb||Recessive|tumor necrosis factor receptor superfamily, member 25|Tnfrsf25|Unknown|APO-3, DDR3, DR3, LARD, Tnfrsf12, TR3, TRAMP, Wsl, WSL-1, WSL-LR|MGI:1934667||||4|||||||||||||||||||||||||||||Unknown|Unknown|C57BL/6NCrlAnu|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|10-Feb-2020|Cryopreserved sperm|33.0|0.0|Unknown|||Yes| 8894.0|ASD1014:Cabbage|C57BL/6NCrlAnu-Dock11/AnuApb||Recessive|dedicator of cytokinesis 11|Dock11|Unknown|5033414A21Rik, Zizimin2|MGI:1923224||||X|||||||||||||||||||||||||||||||C57BL/6NCrlAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|4|||No|17-Mar-2020|Cryopreserved sperm|33.0|0.0|Unknown|||Yes| 8895.0|ASD1014:Cabbage:2bp|C57BL/6NCrlAnu-Dock11/AnuApb||Recessive|dedicator of cytokinesis 11|Dock11|Unknown|5033414A21Rik, Zizimin2|MGI:1923224||||X|||||||||||||||||||||||||||||||C57BL/6NCrlAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|4|||No|17-Mar-2020|Cryopreserved sperm|32.0|0.0|Unknown|||Yes| 8857.0|ASD886:Cavendish:SH372|C57BL/6NCrlAnu-Sh2b3/AnuApb||Recessive|SH2B adaptor protein 3|Sh2b3|Unknown|Lnk|MGI:893598||||5|||||||||||||||||||||||||||||Unknown|Unknown|C57BL/6NCrlAnu|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|17-Feb-2020|Cryopreserved sperm|23.0|0.0|Unknown|||Yes| 8856.0|Gp130Y757F;Dclk1(tm1a)|B6-Dclk1 Il6st/Apb||Recessive|doublecortin-like kinase 1|Dclk1|Unknown|1700113D08Rik, 2810480F11Rik, Click-I, CPG16, Dcamkl1, Dcl, DCLK, mKIAA0369|MGI:1330861|doublecortin-like kinase 1; targeted mutation 1a, Wellcome Trust Sanger Institute|Dclk1|MGI:5543459|3|||||||||||||||||||||||||||||Gp130Y757F: spontaneous development of gastric adenomasDclk1(tm1a): targeted Dclk1 allele - hypomorph Dclk1 allele|Gp130Y757F: normalDclk1(tm1a): normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|14-Feb-2020|Cryopreserved sperm|50.0|0.0|Unknown|||Yes| 8856.0|Gp130Y757F;Dclk1(tm1a)|B6-Dclk1 Il6st/Apb||Recessive|interleukin 6 signal transduce|Il6st||5133400A03Rik, CD130, D13Ertd699e, gp130|MGI:96560|interleukin 6 signal transducer; targeted mutation 1, Matthias Ernst|Il6st|MGI:2388478|13|||||||||||||||||||||||||||||Gp130Y757F: spontaneous development of gastric adenomasDclk1(tm1a): targeted Dclk1 allele - hypomorph Dclk1 allele|Gp130Y757F: normalDclk1(tm1a): normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|14-Feb-2020|Cryopreserved sperm|||Unknown|||Yes| 8869.0|Furinflox/flox |B6.129-Furin/Apb||Recessive|furin (paired basic amino acid cleaving enzyme)|Furin|Normal|9130404I01Rik, Fur, PACE, Pcsk3, SPC1|MGI:97513|Furin, Paired Basic Amino Acid Cleaving Enzyme|furin (paired basic amino acid cleaving enzyme); targeted mutation 1, John W M Creemers|Furin|7|||||||||||||||||||||||||||||Normal|Normal|C57BL/6J|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|03-Mar-2020|Cryopreserved sperm|20.0|0.0|Unknown||Liver|Yes| 10440.0|Dnase1L3/Dnase1 (6)|C57BL6NCrl-Dnase1L3Dnase1/ANU||Recessive|deoxyribonuclease 1-like 3|Dnase1l3||DNasegamma|MGI:1314633|Dnase1L3:endonuclease-mediated mutation 5, Australian National University|Dnase1L3||14|ENSMUSG00000025279||||||||||||||||||||||||||||The DNase double knockout mice do not express two deoxyribonucleases (DNases), DNase1and DNase1-like 3, which are responsible for the degradation of neutrophil extracellular traps (NETs) in circulation during sterile neutrophilia and septicemia. Inthe absence of both DNases, intravascular NETs formed clots that obstructed blood vesselsand caused organ damage. These mice do not express two DNase enzyme|Unknown|C57BL6/NCrl/Anu|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|09-Jul-2024|Cryopreserved sperm|55.0|0.0|Unknown|||Possibly| 10440.0|Dnase1L3/Dnase1 (6)|C57BL6NCrl-Dnase1L3Dnase1/ANU||Recessive|deoxyribonuclease I|Dnase1|||MGI:103157|Dnase1:endonuclease-mediated mutation 5, Australian National University|Dnase1||16|ENSMUSG00000005980 ||||||||||||||||||||||||||||The DNase double knockout mice do not express two deoxyribonucleases (DNases), DNase1and DNase1-like 3, which are responsible for the degradation of neutrophil extracellular traps (NETs) in circulation during sterile neutrophilia and septicemia. Inthe absence of both DNases, intravascular NETs formed clots that obstructed blood vesselsand caused organ damage. These mice do not express two DNase enzyme|Unknown|C57BL6/NCrl/Anu|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|09-Jul-2024|Cryopreserved sperm|||Unknown|||Possibly| 8705.0|gBT-I.1|C57BL/6-Tg(TcraHsv2.3,TcrbHsv2.3)L118-1Cbn/CbnAnuapb||Dominant||||||||||||||||||||||||||transgene insertion L118-1, Francis R Carbone |a 2 kb fragment of the H-2Kb and a 700 bp fragment including the Igh enhancer.|||||||||||TCR transgenics are immunocompromised by having a mono-specific T cell receptor however, in a clean envirnoment, mice show no difference in phenotype from wild-type B6 mice.T cells express Va2<+>Vb8<+> TCR derived from the K,B> restricted HSV-1 glycoprotein B (gB498-505)-specific CTL clone HSV2.3.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|02-May-2019|Cryopreserved sperm|42.0|0.0|Unknown||T cell, CD4 , CD8, T cell receptor (TCR), herpes Simplex Virus (HSV), selection, thymus|Yes| 8865.0|Amigo2 KO:::A1A2A3|B6.Cg-Amigo1 Amigo2 Amigo3/AnuApb||Dominant|adhesion molecule with Ig like domain 1|Amigo1|||MGI:2653612|adhesion molecule with Ig like domain 1; targeted mutation 1, Velocigene|Amigo1|MGI:3847467|3|||||||||||||||||||||||||||||Unknown|Unknown|C57BL/6|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|21-Feb-2020|Cryopreserved sperm|36.0|0.0|Unknown|||Yes| 8865.0|Amigo2 KO:::A1A2A3|B6.Cg-Amigo1 Amigo2 Amigo3/AnuApb||Dominant|adhesion molecule with Ig like domain 2|Amigo2|Unknown||MGI:2145995||Amigo2||15|||||||||||||||||||||||||||||Unknown|Unknown|C57BL/6|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|21-Feb-2020|Cryopreserved sperm|||Unknown|||Yes| 8865.0|Amigo2 KO:::A1A2A3|B6.Cg-Amigo1 Amigo2 Amigo3/AnuApb||Dominant|adhesion molecule with Ig like domain 3|Amigo3|Unknown|E430002N15Rik|MGI:2444854||||9|||||||||||||||||||||||||||||Unknown|Unknown|C57BL/6|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|21-Feb-2020|Cryopreserved sperm|||Unknown|||Yes| 8858.0|ASD958:LadyFinger:SH530|C57BL/6NCrlAnu-Sh2b3/AnuApb||Recessive|SH2B adaptor protein 3|Sh2b3|Unknown|Lnk|MGI:893598||||5|||||||||||||||||||||||||||||Unknown|Unknown|C57BL/6NCrlAnu|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|17-Feb-2020|Cryopreserved sperm|36.0|0.0|Unknown|||Yes| 8859.0|ASD954:Pomelo:DH903|C57BL/6NCrlAnu-Dhx8/AnuApb||Recessive|DEAH (Asp-Glu-Ala-His) box polypeptide 8|Dhx8|Unknown|Ddx8, mDEAH6, MGC:31290, RNA helicase|MGI:1306823||||10|||||||||||||||||||||||||||||Unknown|Unknown|C57BL/6NCrlAnu|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|18-Feb-2020|Cryopreserved sperm|62.0|0.0|Unknown|||Yes| 8861.0|ASD661:Pique:ZF704|C57BL/6NCrlAnu-Zfr2/AnuApb||Recessive|zinc finger RNA binding protein 2|Zfr2|Unknown|2010013I23Rik, 9130206N08Rik|MGI:2143792||||10|||||||||||||||||||||||||||||Unknown|Unknown|C57BL/6NCrlAnu|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|19-Feb-2020|Cryopreserved sperm|24.0|0.0|Unknown|||Yes| 7992.0|2D2tg|C57BL/6-Tg(Tcra2D2,Tcra2D2)1Kuch/AusbAnuApb||Semi-dominant||||||||||||||||||||||||||transgene insertion 1, Vijay Kuchroo ||||||||||||Homozygous lethal|Expanded T cells population.Spontaneus cases of paralysis might occur.Altered inmunoregulation in brain.Spontaneus optic neuritis.|C57BL/6|No|No|Yes|No|No|Yes|No|Unknown|||+/+ sibling x Hemizygote (Female x Male) |No|11-Nov-2015|Cryopreserved sperm|32.0|0.0|Unknown||T cells, Experimental autoimmune encephalomyelitis, CNS, Optic Nerve, multiple sclerosis |Yes| 8011.0|Rag2 / IL2rg KO / hGM/IL3|C;129SV4-Rag2 Csf2/Il3 Il2rg/JAnuApb||Recessive|recombination activating gene 2|Rag2|||MGI:97849 ||||2||||||||||Unknown to Unknown|||||||||||||||||||||BALB/c|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|16-Dec-2015|Cryopreserved sperm|24.0|0.0|Unknown|||Yes| 8011.0|Rag2 / IL2rg KO / hGM/IL3|C;129SV4-Rag2 Csf2/Il3 Il2rg/JAnuApb||Recessive|colony stimulating factor 2 (granulocyte-macrophage)|Csf2||Csfgm, Gm-CSf, GMCSF, MGI-IGM |MGI:1339752||||11|ENSMUSG00000018916|||||||||Unknown to Unknown|||||||||||||||||||||BALB/c|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|16-Dec-2015|Cryopreserved sperm|||Unknown|||Yes| 8011.0|Rag2 / IL2rg KO / hGM/IL3|C;129SV4-Rag2 Csf2/Il3 Il2rg/JAnuApb||Recessive|interleukin 2 receptor, gamma chain|Il2rg||CD132, common cytokine receptor gamma chain, common gamma chain, gamma(c), gammaC, gamma C receptor|||||X|ENSMUSG00000031304 |||||||||Unknown to Unknown|||||||||||||||||||||BALB/c|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|16-Dec-2015|Cryopreserved sperm|||Unknown|||Yes| 10416.0|Kimba|B6-Tg(mRho- tr029VEGF)/Kimba. ||Recessive|human vascular endothelial growth factor|hVEGF|||||||Unknown|||||||||||||||||transgene insertion 029, Elizabeth Piroska Rakoczy|Rodopsin|||||||||||a transgenic mouse model expressing low VEGF levels which would lead to a slow progression of retinal neovascularisation akin to vascular changes observed in Diabetic retinopathy|a transgenic mouse model expressing low VEGF levels which would lead to a slow progression of retinal neovascularisation akin to vascular changes observed in Diabetic retinopathy,||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|12-Apr-2024|Cryopreserved sperm|50.0|0.0|Unknown|||Possibly| 10416.0|Kimba|B6-Tg(mRho- tr029VEGF)/Kimba. ||Recessive|rhodopsin|Rho||LWS opsin|MGI:97914||||6|ENSMUSG00000030324 |ENSMUST00000032471|||||||||||||||||||||||||||a transgenic mouse model expressing low VEGF levels which would lead to a slow progression of retinal neovascularisation akin to vascular changes observed in Diabetic retinopathy|a transgenic mouse model expressing low VEGF levels which would lead to a slow progression of retinal neovascularisation akin to vascular changes observed in Diabetic retinopathy,||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|12-Apr-2024|Cryopreserved sperm|||Unknown|||Possibly| 8902.0||DBA/2J-Tg(fos-tau/LacZ)/Apb||Dominant||||||||||||||||||||||||||Fos-tau/LacZ||||||||||||NORMAL|NORMAL|DBA/2J|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|19-Mar-2020||0.0|0.0|Unknown||Fear, memory|Yes| 8904.0||B6.D2-CHR12-STR1-Tg(fos-tau/LacZ)/Apb||Dominant||||||||||||||||||||||||||FOS-TAU-LACZ|||Stress response QTL||||||||12|Decreased activity in open field activity test. Increased stress responsiveness.Decreased fear memory.|Decreased activity in open field activity test. Increased stress responsiveness.|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|19-Mar-2020|Cryopreserved sperm|50.0|0.0|Unknown||Fear, memory|Yes| 8905.0||B6.D2-CHR12-STR2-Tg(fos-tau/LacZ)/Apb||Dominant||||||||||||||||||||||||||Fos-tau/LacZ|||Stress response QTL||||||||12|Decreased activity in open field activity test. Increased stress responsiveness.Increased fear memory|Decreased activity in open field activity test. Increased stress responsiveness.|C57BL6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|19-Mar-2020|Cryopreserved sperm|50.0|0.0|Unknown||Fear, Memory, Stress|Yes| 8908.0|ASD947:Packham:AG4bpdel|C57BL/6NCrlAnu-Ager/AnuApb||Recessive|advanced glycosylation end product-specific receptor|Ager||RAGE|MGI:893592||||17|||||||||||||||||||||||||||||Unknown|Unknown|C57BL/6NCrlAnu|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|20-Mar-2020|Cryopreserved sperm|55.0|0.0|Unknown|||Yes| 8919.0|Dicer fl:CMV-cre|B6.129-Dicer1 Tg(CMV-cre)/WehiAnuApb||Recessive|dicer 1, ribonuclease type III|Dicer1|||MGI:2177178|dicer 1, ribonuclease type III; targeted mutation 1, Brian D Harfe|||12|||||||||||||||||Cre recombinase|CMV|||||||||||Unknown||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|24-Mar-2020|Cryopreserved sperm|57.0|0.0|Unknown||microRNA, Cre|Yes| 8911.0|ASD765:Tnip1:TN346|C57BL/6NCrlAnu-Tnip1/AnuApb||Recessive|TNFAIP3 interacting protein 1|Tnip1|Unknown|A20-binding inhibitor of NF-kappa B activation, ABIN1, Nef, VAN|MGI:1926194||||11|||||||||||||||||||||||||||||autoimmune phenotype|autoimmune phenotype|C57BL/6NCrlAnu|Yes|Unknown|Yes|Yes|Unknown|Yes|No|Unknown||||No|23-Mar-2020|Cryopreserved sperm|30.0|0.0|Unknown||autoimmunity|Yes| 8917.0|ASD823:Choko|C57BL/6NCrlAnu-Slc6a17/AnuApb||Recessive|solute carrier family 6 (neurotransmitter transporter), member 17|Slc6a17||D130012J15Rik, NTT4|MGI:2442535||||3|||||||||||||||||||||||||||||Normal|Normal|C57BL/6NCrlAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|24-Mar-2020|Cryopreserved sperm|57.0|0.0|Unknown|||Yes| 8918.0|ASD085:C57BL/6:MyD88-/-|B6.Cg-Myd88/AnuApb||Recessive|myeloid differentiation primary response gene 88|Myd88|Nil||MGI:108005|targeted mutation 1, Shizuo Akira|Myd88|MGI:2385681|9|||||||||||||||||||||||||||||Increased apoptosis:* 5 days after lung injury, mutants show significantly increased numbers of apoptotic lung epithelial and inflammatory cells.Increased physiological sensitivity to xenobiotics:* knockout mice are more susceptible to bleomycin-induced lung injury.Abnormal dendritic cell differentiation:* dendritic cell maturation fails to occur in vivo upon exposure to TLR9 agonists.Increased dendritic cell number:* increased numbers of dendritic cells in brains of mice infected with Plasmodium.Abnormal immune system physiology:* response to LPS and CpG is completely abrogatedAbnormal dendritic cell physiology:* cytokine secretion elicited by zymosan or LPS is impaired.* following infection with attenuated yellow fever vaccine 17D (YF-17D), dendritic cells produce less IL-12p40, IL-6 and interferon-gamma relative to wild-type mice.Abnormal macrophage physiology:* TNF production is impaired in thioglycollate-elicited macrophages treated with intact zymosan.* cytokine production by macrophages cultured with P. carinii cysts is reduced compared to wild-type.Abnormal NK cell physiology:* NK cells fail to make IFN-gamma in response to injections of TLR9 agonists.Abnormal T cell physiology:* induction of the antigen-specific CD8+ T-cell response by immunizing with soluble ovalbumin and TLR9 agonists, but not TLR2 and TLR6 agonists, was severely impaired.Abnormal cytokine secretion:* LPS-induced cytokine production by BMDCs is almost abolished compared to controls and Myd88-sufficient mutantsAbnormal chemokine secretion:* hyaluronan fragment-induced expression of chemokines by peritoneal macrophages is completely abolished in double knockout mice.Decreased interferon-alpha secretion:* CpG-A or RNA polyuridylic acid induced production of interferon-alpha was abolished in plasmacytoid dendritic cells.Decreased interferon-gamma secretion:* less up regulation of INF-gamma in Plasmodium infection.* following infection with attenuated yellow fever vaccine 17D (YF-17D), dendritic cells produce less interferon-gamma.Decreased interleukin-12 secretion:* after stimulation with zymosan, TNF production is significantly reduced in Myd88-deficient animals.Decreased interleukin-12b secretion:* less upregulation of IL-12b in Plasmodium infection * following infection with attenuated yellow fever vaccine 17D (YF-17D), dendritic cells produce less IL-12p40 relative to wild-type mice. Decreased interleukin-6 secretion: * following treatment with PbA(Plasmodium bergbei ANKA)-parasitized erythrocytes or LPS-stimulation, IL-6 secretion is reduced. * following infection with attenuated yellow fever vaccine 17D (YF-17D), dendritic cells produce less IL-6 relative to wild-type mice. Decreased tumor necrosis factor secretion: * less upregulation of TNF-alpha in Plasmodium infection. * following treatment with PbA(Plasmodium bergbei ANKA)-parasitized erythrocytes or LPS-stimulation, TNF secretion is reduced. * after stimulation with zymosan, TNF production is significantly reduced in Myd88-deficient animals. Decreased inflammatory response: * in a model of induced pneumococcal meningitis-associated labyrinthitis, homozygotes exhibit a significantly lower granulocytic infiltration of the labyrinth and increased bacterial density in the cochlea at 24 hrs post-infection relative to wild-type control mice. Abnormal response to infection: * following treatment with PbA (Plasmodium bergbei ANKA)-parasitized erythrocytes, mice have a decreased immune response in terms of TNF and IL-6 secretion and response to CpG. Decreased susceptibility to parasitic infection:* resistant to cerebral malaria but eventually die of extremely high parasitemia. Increased susceptibility to viral infection: * increased susceptibility to encephalomyocarditis virus (EMCV) infection compared to wildtype. ||C57BL/6NCrlAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|24-Mar-2020|Cryopreserved sperm|6.0|0.0|Unknown||IL1 receptor, T cell, IL18 receptor|Yes| 8913.0|Arjuna:B10.BR:Rag1(tm1Mom)|B6.B10-H2 Rag1 Tg(ILK3mHEL)3Ccg/AnuApb||Recessive|recombination activating 1|Rag1||Rag-1|MGI:97848|recombination activating 1; targeted mutation 1, Peter Mombaerts|Rag1|MGI:1857241|2|||||||||||||||||transgene insertion 3, Christopher C Goodnow|Rat insulin promoter||histocompatibility-2, MHC|H2|||MGI:95894|histocompatibility-2, MHC; k variant|H2|MGI:3579322|17|Rag1 KO mice lack mature T and B cells. Hen egg lysozyme expressed on the pancreatic islet beta cells.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|23-Mar-2020|Cryopreserved sperm|24.0|0.0|Unknown||Hen Egg Lysozyme (HEL), T cell, B cell, autoimmune|Yes| 8914.0|Arjuna:Rag1(tm1Mom)::B6|B6(Cg)-Rag1 Tg(ILK3mHEL)3Ccg/AnuApb||Recessive|recombination activating 1|Rag1||Rag-1|MGI:97848|recombination activating 1; targeted mutation 1, Peter Mombaerts|Rag1|MGI:1857241|2|||||||||||||||||transgene insertion 3, Christopher C Goodnow|Rat insulin promoter|||||||||||Rag1 KO mnice are deficient of mature T and B cells. Hen egg lysozyme expressed on surface og pancreatic islet beta cells.H2b background||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|23-Mar-2020|Cryopreserved sperm|36.0|0.0|Unknown||T cell, B cell, autoimmunity, Hen Egg Lysozyme (HEL)|Yes| 8920.0|Spi6 KO:Spi6 fl|C57BL/6-Serpinb9 Serpinb9/AnuApb||Recessive|serine (or cysteine) peptidase inhibitor, clade B, member 9|Serpinb9|Unknown|ovalbumin, PI-9, Spi6|MGI:106603||||13|||||||||||||||||||||||||||||Unknown||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|24-Mar-2020|Cryopreserved sperm|22.0|0.0|Unknown|||Yes| 8920.0|Spi6 KO:Spi6 fl|C57BL/6-Serpinb9 Serpinb9/AnuApb||Recessive|serine (or cysteine) peptidase inhibitor, clade B, member 9|Serpinb9||ovalbumin, PI-9, Spi6|MGI:106603||||13|||||||||||||||||||||||||||||Unknown||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|24-Mar-2020|Cryopreserved sperm|||Unknown|||Yes| 8916.0|| ASD937:Pomegranate:132bp:Hom||Recessive|Blicr||||||||Unknown|||||||||||||||||||||||||||||normal|normal|C57BL/6NCrlAnu|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|24-Mar-2020|Cryopreserved sperm|33.0|0.0|Unknown|||Yes| 8910.0|ASD901:Plantain:IK1bpins|C57BL/6NCrlAnu-Ikzf2/AnuApb||Recessive|IKAROS family zinc finger 2|Ikzf2|Unknown|A730095J18Rik, Helios, Zfpn1a2|MGI:1342541||||1||||||||||Unknown to Unknown|||||||||||||||||||Unknown|Unknown|C57BL/6NCrlAnu|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|20-Mar-2020|Cryopreserved sperm|40.0|0.0|Unknown|||Yes| 8933.0|Aicda fl:mT/mG:mb1CreERT2|C57BL/6N(Cg)-Aicda Gt(ROSA)26Sor Cd79a/AnuApb||Recessive|activation-induced cytidine deaminase|Aicda|Normal|Aid|MGI:1342279|activation-induced cytidine deaminase; targeted mutation 1a, Helmholtz Zentrum Muenchen GmbH|Aicda|MGI:4460367|6|||||||||||||||||||||||||||||Unknown||C57BL/6N|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||4||No|27-Mar-2020|Cryopreserved sperm|31.0|0.0|Unknown||EuCOMM|Yes| 8933.0|Aicda fl:mT/mG:mb1CreERT2|C57BL/6N(Cg)-Aicda Gt(ROSA)26Sor Cd79a/AnuApb||Recessive|CD79A antigen (immunoglobulin-associated alpha)|Cd79a||Cd79a, Iga, Igalpha, Ig alpha, Ig-alpha, Ly54, Ly-54, mb-1|MGI:101774|CD79A antigen (immunoglobulin-associated alpha); targeted mutation 3, Michael Reth|Cd79a|MGI:5568505|7|||||||||||||||||||||||||||||Unknown||C57BL/6N|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||4||No|27-Mar-2020|Cryopreserved sperm|||Unknown||EuCOMM|Yes| 8933.0|Aicda fl:mT/mG:mb1CreERT2|C57BL/6N(Cg)-Aicda Gt(ROSA)26Sor Cd79a/AnuApb||Recessive|gene trap ROSA 26, Philippe Soriano|Gt(ROSA)26Sor||beta geo, Gtrgeo26, Gtrosa26, R26, ROSA26|MGI:104735|gene trap ROSA 26, Philippe Soriano; targeted mutation 4, Liqun Luo|Gt(ROSA)26Sor|MGI:3716464|6|||||||||||||||||||||||||||||Unknown||C57BL/6N|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||4||No|27-Mar-2020|Cryopreserved sperm|||Unknown||EuCOMM|Yes| 8924.0|F10epi|C57BL/6-F10/Csl||Recessive|coagulation factor X|F10||AI194738, Cf10, fX|MGI:103107||||8|||||||||||||||||||||||||||||Normal|Normal|C57BL/6J|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|27-Mar-2020|Cryopreserved sperm|50.0|0.0|Unknown|||Yes| 8925.0|PRINCE|BALB/c-Csf2rb/Apb||Recessive|colony stimulating factor 2 receptor, beta, low-affinity (granulocyte-macrophage)|Csf2rb||AIC2B, Bc, beta c, CDw131, common beta chain, Csf2rb1, Il3r, Il3rb1, Il5rb|MGI:1339759||||15|||||||||||||||||||||||||||||Normal|Normal||Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|27-Mar-2020|Cryopreserved sperm|50.0|0.0|Unknown|||Yes| 8927.0|Aicdafl Mb1Cre ERT2:TCF7-GFP|B6(Cg)-Aicda Cd79a Tcf7/MarpAnuApb ||Recessive|activation-induced cytidine deaminase|Aicda||Aid|MGI:1342279|activation-induced cytidine deaminase; targeted mutation 1c, Helmholtz Zentrum Muenchen GmbH|Aicda|MGI:4460367|6|||||||||||||||||||||||||||||unknown|unknown|C57BL/6|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|27-Mar-2020|Cryopreserved sperm|82.0|0.0|Unknown|||Yes| 8927.0|Aicdafl Mb1Cre ERT2:TCF7-GFP|B6(Cg)-Aicda Cd79a Tcf7/MarpAnuApb ||Recessive|CD79A antigen (immunoglobulin-associated alpha)|Cd79a||Cd79a, Iga, Igalpha, Ig alpha, Ig-alpha, Ly54, Ly-54, mb-1|MGI:101774|CD79A antigen (immunoglobulin-associated alpha); targeted mutation 3, Michael Reth|Cd79a|MGI:5568505|7|||||||||||||||||||||||||||||unknown|unknown|C57BL/6|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|27-Mar-2020|Cryopreserved sperm|||Unknown|||Yes| 8927.0|Aicdafl Mb1Cre ERT2:TCF7-GFP|B6(Cg)-Aicda Cd79a Tcf7/MarpAnuApb ||Recessive|transcription factor 7, T cell specific|Tcf7||T cell factor-1, T-cell factor 1, Tcf1, TCF-1|MGI:98507|transcription factor 7, T cell specific; targeted mutation 1, Hai-Hui Xue|Tcf7|MGI:5805838|11|||||||||||||||||||||||||||||unknown|unknown|C57BL/6|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|27-Mar-2020|Cryopreserved sperm|||Unknown|||Yes| 8928.0||ASD937:Pomegranate:Bl87bp||Recessive|Blicr||||||||Unknown|||||||||||||||||||||||||||||unknown|unknown|C57BL/6NCrlAnu|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|27-Mar-2020|Cryopreserved sperm|35.0|0.0|Unknown|||Yes| 8922.0|ASD882:Mango:Ik283|C57BL/6NCrlAnu-Ikzf4/AnuApb||Recessive|IKAROS family zinc finger 4|Ikzf4||A630026H08Rik, Eos, Zfpn1a4|MGI:1343139||||10|||||||||||||||||||||||||||||Unknown|Unknown|C57BL/6NCrlAnu|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|24-Mar-2020|Cryopreserved sperm|55.0|0.0|Unknown|||Yes| 8930.0|ASD938:Corella:PH1bpins|C57BL/6NCrlAnu-Phlpp2/AnuApb||Recessive|PH domain and leucine rich repeat protein phosphatase 2|Phlpp2||C130044A18Rik, Phlppl|MGI:2444928||||8|||||||||||||||||||||||||||||unknown|unknown|C57BL/6NCrlAnu|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|27-Mar-2020|Cryopreserved sperm|35.0|0.0|Unknown|||Yes| 8931.0|ASD938:Corella:PH1056|C57BL/6NCrlAnu-Phlpp2/AnuApb||Recessive|PH domain and leucine rich repeat protein phosphatase 2|Phlpp2||C130044A18Rik, Phlppl|MGI:2444928||||8|||||||||||||||||||||||||||||unknown|unknown|C57BL/6NCrlAnu|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|27-Mar-2020|Cryopreserved sperm|35.0|0.0|Unknown|||Yes| 8935.0|ASD1059:WizzFizz|C57BL/6NCrlAnu-Fads2/AnuApb||Recessive|fatty acid desaturase 2|Fads2||2900042M13Rik, Fads2a|MGI:1930079||||19|||||||||||||||||||||||||||||Unknown.Mice homozygous for a null allele display absence of long-chain polyunsaturated fatty acids, infertility, arrest of spermiogenesis and folliculogenesis, and impaired platelet function. ||C57BL/6NCrlAnu|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|27-Mar-2020|Cryopreserved sperm|23.0|0.0|Unknown|||Yes| 8340.0|Spi6 fl; SerpinB9 conditional|C57BL/6J-SerpinB9/PibMarpAnuApb||Dominant|serine (or cysteine) peptidase inhibitor, clade B, member 9|Serpinb9||ovalbumin, PI-9, Spi6|MGI:106603||||13|||||||||||||||||||||||||||||Normal|Normal|C57BL/6J|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|30-Oct-2017|Cryopreserved sperm|12.0|0.0|Unknown|||Yes| 8944.0|Ai14D:Pdgfr-cre|B6.Cg-Gt(ROSA)26Sor Tg(Pdgfra-cre)1Clc/JAnuApb||Recessive|gene trap ROSA 26, Philippe Soriano|Gt(ROSA)26Sor|Normal|beta geo, Gtrgeo26, Gtrosa26, R26, ROSA26, Thumpd3as1|MGI:104735|gene trap ROSA 26, Philippe Soriano; targeted mutation 14, Hongkui Zeng|Gt(ROSA)26Sor|MGI:3809524|6|||||||||||||||||transgene insertion 1, Constance L Cepko|mouse platelet derived growth factor receptor alpha|||||||||||||C57BL/6J|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|29-Mar-2020|Cryopreserved sperm|57.0|0.0|Unknown||Cre recombinase|No| 8956.0|ASD661:Pique:ZFKO|C57BL/6NCrlAnu-Zfr2/AnuApb||Recessive|zinc finger RNA binding protein 2|Zfr2||2010013I23Rik, 9130206N08Rik|MGI:2143792||||10|||||||||||||||||||||||||||||Unknown|Unknown |C57BL/6NCrlAnu|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|03-Apr-2020|Cryopreserved sperm|47.0|0.0|Unknown|||Yes| 8946.0|ENU47:G2|ANU:ENU47:G2||Recessive||||||||||||||||||||||||||||||||||||||Unknown|Unknown|C57BL/6NCrlAnu|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||1||No|29-Mar-2020|Cryopreserved sperm|289.0|0.0|Unknown||ENU, random, mutagenesis, screen|Yes| 8940.0|ENU33::Prkcd|C57BL/6NCrlAnu-Prkcd/AnuApb||Recessive|protein kinase C, delta|Prkcd||D14Ertd420e, Pkcd, PKC[d], PKCdelta|MGI:97598||||14|||||||||||||||||||||||||||||unknown|unknown|C57BL/6NCrlAnu|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|28-Mar-2020|Cryopreserved sperm|50.0|0.0|Unknown|||Yes| 8941.0|ENU35:042::Ifnar-/-|B6.Cg-Ifih1 Ifnar1/AnuApb||Recessive|interferon induced with helicase C domain 1|Ifih1|||MGI:1918836||||2|||||||||||||||||||||||||||||unknown|unknown|C57BL/6NCrlAnu|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|28-Mar-2020|Cryopreserved sperm|36.0|0.0|Unknown|||Yes| 8941.0|ENU35:042::Ifnar-/-|B6.Cg-Ifih1 Ifnar1/AnuApb||Recessive|interferon (alpha and beta) receptor 1|Ifnar1||CD118, Ifar, Ifrc, INF-a receptor, Infar|MGI:107658|targeted mutation 1, Michel Aguet|Ifnar1|MGI:1930950|16|||||||||||||||||||||||||||||unknown|unknown|C57BL/6NCrlAnu|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|28-Mar-2020|Cryopreserved sperm|||Unknown|||Yes| 8943.0|Ai14D:Cx3cr1-cre|B6.Cg-Cx3cr1 Gt(ROSA)26Sor/JAnuApb||Recessive|gene trap ROSA 26, Philippe Soriano|Gt(ROSA)26Sor|Normal|beta geo, Gtrgeo26, Gtrosa26, R26, ROSA26, Thumpd3as1|MGI:104735|gene trap ROSA 26, Philippe Soriano; targeted mutation 14, Hongkui Zeng|Gt(ROSA)26Sor|MGI:3809524|6|||||||||||||||||||||||||||||||C57BL/6J|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|29-Mar-2020|Cryopreserved sperm|56.0|0.0|Unknown||Cre recombinase|No| 8943.0|Ai14D:Cx3cr1-cre|B6.Cg-Cx3cr1 Gt(ROSA)26Sor/JAnuApb||Recessive|chemokine (C-X3-C motif) receptor 1|Cx3cr1|||MGI:1333815|chemokine (C-X3-C motif) receptor 1; targeted mutation 2.1, Dan R Littman|Cx3cr1|MGI:5450813|9|||||||||||||||||||||||||||||||C57BL/6J|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|29-Mar-2020|Cryopreserved sperm|||Unknown||Cre recombinase|No| 8955.0|Scn2a R853Q conditional |C57BL/6-Scn2a/SpetApb||Recessive|sodium channel, voltage-gated, type II, alpha|Scn2a||A230052E19Rik, Nav1.2, Scn2a1|MGI:98248||||2||||||||||Unknown to Unknown|||||||||||||||||||Unknown |Normal|C57BL/6|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|02-Apr-2020|Cryopreserved sperm|50.0|0.0|Unknown|||Yes| 8939.0|ENU33:003:Ramos:1bp del|C57BL/6NCrlAnu-Tlr7 Trex1/AnuApb||Recessive|toll-like receptor 7|Tlr7|||MGI:2176882||||X|||||||||||||||||||||||||||||unknown|unknown|C57BL/6NCrlAnu|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|28-Mar-2020|Cryopreserved sperm|35.0|0.0|Unknown|||Yes| 8939.0|ENU33:003:Ramos:1bp del|C57BL/6NCrlAnu-Tlr7 Trex1/AnuApb||Recessive|three prime repair exonuclease 1|Trex1|||MGI:1328317||||9|||||||||||||||||||||||||||||unknown|unknown|C57BL/6NCrlAnu|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|28-Mar-2020|Cryopreserved sperm|||Unknown|||Yes| 8937.0|Heatr3:Flpe|C57BL/6NTac-Heatr3 Tg(ACTFLPe)9205Dym/AnuApb||Recessive|HEAT repeat containing 3|Heatr3|Normal|C030036P15Rik|MGI:2444491|HEAT repeat containing 3; targeted mutation 1a, Helmholtz Zentrum Muenchen GmbH|Heatr3||8||||||||||Unknown to Unknown|||||||transgene insertion 9205, Susan Dymecki|ACTB, actin, beta, human|The FLPe recombinase variant exhibits enhanced thermostability with recombination activity being 4X and 10X that of wildtype FLP at 37°C and 40°C, respectively||||||||||Unknown|Normal|C57BL/6NCrlAnu|Unknown|Yes|Yes|Unknown|Yes|Yes|No|Unknown||||No|27-Mar-2020|Cryopreserved sperm|112.0|0.0|Unknown||EUCOMM|Yes| 8947.0|ENU48:G2|ANU:ENU48:G2||Recessive||||||||||||||||||||||||||||||||||||||Unknown|Unknown|C57BL/6NCrlAnu|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||1||No|29-Mar-2020|Cryopreserved sperm|170.0|0.0|Unknown||ENU, random, mutagenesis, screen|Yes| 8951.0|ASD928:Goldfinger:TL79|C57BL/6NCrlAnu-Tlr8/AnuApb||Recessive|toll-like receptor 8|Tlr8|||MGI:2176887||||X|||||||||||||||||||||||||||||Unknown|Unknown|C57BL/6NCrlAnu|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|30-Mar-2020|Cryopreserved sperm|12.0|0.0|Unknown|||Yes| 8921.0|Edamame|C57BL/6NCrlAnu-Ryr2/AnuApb||Recessive|ryanodine receptor 2, cardiac|Ryr2|Unknown|9330127I20Rik|MGI:99685||||13|||||||||||||||||||||||||||||||C57BL/6NCrlAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|24-Mar-2020|Cryopreserved sperm|44.0|0.0|Unknown|||Yes| 8954.0|ASD1035:Melon:AC18bpdel|C57BL/6NCrlAnu-Actr5/AnuApb||Recessive|ARP5 actin-related protein 5|Actr5|Unknown|B430109J19Rik|MGI:1924748||||2|||||||||||||||||||||||||||||Unknown|Unknown|C57BL/6NCrlAnu|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|30-Mar-2020|Cryopreserved sperm|48.0|0.0|Unknown|||Yes| 8934.0|Ighg1-cre Igk KO:Ly5a|B6.129P2(Cg)-Ighg1 Igk Ptprc/AnuApb||Recessive|immunoglobulin kappa chain complex|Igk|Nil|kappa|MGI:96494|immunoglobulin kappa chain complex; targeted mutation 1, Dennis Huszar|Igk|MGI:2429510|6|||||||||||||||||||||||||||||Homozygous mice are viable, fertile, normal in size, and do not display any gross physical or behavioural abnormalities. They do exhibit a reduction in IgG1+ memory B cells and in IgG1 serum antibody titers.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|27-Mar-2020|Cryopreserved sperm|24.0|0.0|Unknown||B cell, Germinal Centre, Immunoglobulin|Yes| 8934.0|Ighg1-cre Igk KO:Ly5a|B6.129P2(Cg)-Ighg1 Igk Ptprc/AnuApb||Recessive|immunoglobulin heavy constant gamma 1 (G1m marker)|Ighg1||IgG1, Igh-4|MGI:96446|immunoglobulin heavy constant gamma 1 (G1m marker); targeted mutation 1, University of Cologne|Ighg1|MGI:3652526|12|||||||||||||||||||||||||||||Homozygous mice are viable, fertile, normal in size, and do not display any gross physical or behavioural abnormalities. They do exhibit a reduction in IgG1+ memory B cells and in IgG1 serum antibody titers.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|27-Mar-2020|Cryopreserved sperm|||Unknown||B cell, Germinal Centre, Immunoglobulin|Yes| 8934.0|Ighg1-cre Igk KO:Ly5a|B6.129P2(Cg)-Ighg1 Igk Ptprc/AnuApb||Recessive|protein tyrosine phosphatase, receptor type, C|Ptprc||B220, CD45, Ly-5, Lyt-4, T200|MGI:97810|protein tyrosine phosphatase, receptor type, C; a variant|Ptprc|MGI:4819849|1|||||||||||||||||||||||||||||Homozygous mice are viable, fertile, normal in size, and do not display any gross physical or behavioural abnormalities. They do exhibit a reduction in IgG1+ memory B cells and in IgG1 serum antibody titers.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|27-Mar-2020|Cryopreserved sperm|||Unknown||B cell, Germinal Centre, Immunoglobulin|Yes| 8945.0|ENU46:G2|ANU:ENU46:G2||Recessive|Unknown||||||||Unknown||||||||||||||||Unknown|||||||||||||Unknown|Unknown|C57BL/6NCrlAnu|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||1||No|29-Mar-2020|Cryopreserved sperm|11.0|0.0|Unknown||ENU, random, mutagenesis, screen|Yes| 8950.0|ASD1049:Zinger|C57BL/6NCrlAnu-Calm2/AnuApb||Recessive|calmodulin 2|Calm2||1500001E21Rik|MGI:103250||||17|||||||||||||||||||||||||||||unknown|unknown|C57BL/6NCrlAnu|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|30-Mar-2020|Cryopreserved sperm|44.0|0.0|Unknown|||Yes| 10445.0|ASD1138:Tlr4 D298G:19|C57BL/6NcrlAnu-Tlr4/19Anu||Dominant|toll-like receptor 4|Tlr4||Lps, Rasl2-8|MGI:96824|Tlr4; endonuclease-mediated mutation 1, Australian National University|Tlr4||4|ENSMUSG00000039005 ||||||||||||||||||||||||||||Normal|Normal|C57Bl/6N|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Aug-2024|Cryopreserved sperm|40.0|0.0|Unknown|||Possibly| 8953.0|Blimp1 fl:CD23-cre|B6.Cg-Prdm1 Tg(Fcer2a-cre)5Mbu/WehiMarpAnuApb||Recessive|PR domain containing 1, with ZNF domain|Prdm1||b2b1765Clo, Blimp1, Blimp-1, PRDI-BF1|MGI:99655|PR domain containing 1, with ZNF domain; targeted mutation 2.1, Stephen L Nutt|Prdm1|MGI:4355900|10|||||||||||||||||transgene insertion 5, Meinrad Busslinger|Fcer2a|||||||||||||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|10|||No|30-Mar-2020|Cryopreserved sperm|44.0|0.0|Unknown||T cell, Cre|Yes| 8208.0|Tap1/Tap2 KO x Tg(hTAP1/hTAP2) BAC #3|C57BL/6J-Tap1/Tap2 Tg(hTAP1/hTAP2)18/3MarpAnu||Recessive|transporter 1, ATP-binding cassette, sub-family B (MDR/TAP)|Tap1|Nil|Abcb2, Ham1, Ham-1, MTP1, PSF-1, RING4, TAP, Tap-1|MGI:98483||||17|||||||||||||||||human transporter 1, ATP-binding cassette, sub-family B (MDR/TAP) / human transporter 2, ATP-binding cassette, sub-family B (MDR/TAP)||||||||||||Unknown|Unknown|C57BL/6J|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|02-Mar-2017|Cryopreserved sperm|12.0|0.0|Unknown|||Yes| 8208.0|Tap1/Tap2 KO x Tg(hTAP1/hTAP2) BAC #3|C57BL/6J-Tap1/Tap2 Tg(hTAP1/hTAP2)18/3MarpAnu||Recessive|transporter 2, ATP-binding cassette, sub-family B (MDR/TAP)|Tap2|Nil|Abcb3, Ham2, Ham-2, HAM2, MTP2, PSF2, Tap-2|MGI:98484||||17|||||||||||||||||||||||||||||Unknown|Unknown|C57BL/6J|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|02-Mar-2017|Cryopreserved sperm|||Unknown|||Yes| 4514.0|Thebes ; ENU7B6:039 (CD4)|B6JAnu;CBA-Cd4/AnuApb|B6JAnu;CBA-Cd4/AnuApb|Recessive|CD4 antigen|Cd4|Unknown|L3T4, Ly-4|MGI:88335|CD4 antigen; thebes|Cd4|MGI:5007797|6|ENSMUSG00000023274|ENSMUST00000024044|Cd4-001|339|508|G to T|ENSMUSE00000246632|4|112|Glutamic acid to Aspartic acid|||||ATGGAAGACTCTCAGACTTATATCTGTGAGCTGGAGAACAGGAAAGAGGAGGTGGAGTTGT|Yes|||||||||||||Reduced CD4 expression||B6 x CBA|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|26-Feb-2009|Cryopreserved sperm|142.0|0.0|Unknown||autoimmunity, antinuclear antibodies (ANA), ENU, Wellcome Trust, CD4|Yes| 8964.0|ASD1041:Lettuce ; Irf4|C57BL/6NCrlAnu-Irf4/AnuApb||Recessive|interferon regulatory factor 4|Irf4|Unknown|IRF-4, Spip|MGI:1096873||||13|||||||||||||||||||||||||||||||C57BL/6NCrlAnu|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|05-Apr-2020|Cryopreserved sperm|36.0|0.0|Unknown|||Yes| 8966.0|Vps51 tm1c|C57BL/6NCrlAnu-Vps51/AnuApb||Recessive|VPS51 GARP complex subunit|Vps51|Nil|1110014N23Rik, 3110057M17Rik|MGI:1915755|VPS51 GARP complex subunit; targeted mutation 1c, Wellcome Trust Sanger Institute|Vps51||19|||||||||||||||||||||||||||||||C57BL/6NCrlAnu|No|No|Yes|No|No|Yes|No|Unknown||||No|05-Apr-2020|Cryopreserved sperm|34.0|0.0|Unknown|||Yes| 8958.0|ASD765:Tnip1:TN1bpins|C57BL/6NCrlAnu-Tnip1/AnuApb||Recessive|TNFAIP3 interacting protein 1|Tnip1||A20-binding inhibitor of NF-kappa B activation, ABIN1, Nef, VAN|MGI:1926194||||11|||||||||||||||||||||||||||||Unknown|Unknown |C57BL/6NCrlAnu|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|03-Apr-2020|Cryopreserved sperm|40.0|0.0|Unknown|||Yes| 8965.0|ASD1041:Lettuce ; Irf4|C57BL/6NCrlAnu-Irf4/AnuApb||Recessive|interferon regulatory factor 4|Irf4|Unknown|IRF-4, Spip|MGI:1096873||||13|||||||||||||||||||||||||||||FACS Phenotype||C57BL/6NCrlAnu|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|05-Apr-2020|Cryopreserved sperm|54.0|0.0|Unknown|||Yes| 8903.0||B6.D2-Cfq# Tg(Fos-tau/LacZ)/Apb||Dominant||||||||||||||||||||||||||Fos-tau/LacZ|||conditioned fear QTL|Cfq|||||||1|Decreased activity in open field activity test. Increased stress responsiveness.Increased fear memory.|Decreased activity in open field activity test. Increased stress responsiveness.|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|19-Mar-2020||0.0|0.0|Unknown||c-fos, fear, memory|Yes| 8961.0|ASD765:Tnip1:TN346:MyD88-/-|B6(Cg)-Myd88 Tnip1/AnuApb||Recessive|myeloid differentiation primary response gene 88|Myd88|Nil||MGI:108005|myeloid differentiation primary response gene 88; targeted mutation 1, Shizuo Akira|Myd88|MGI:2385681|9|||||||||||||||||||||||||||||Unknown|Unknown|C57BL/6NCrlAnu|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|03-Apr-2020||0.0|0.0|Unknown|||Yes| 8961.0|ASD765:Tnip1:TN346:MyD88-/-|B6(Cg)-Myd88 Tnip1/AnuApb||Recessive|TNFAIP3 interacting protein 1|Tnip1||A20-binding inhibitor of NF-kappa B activation, ABIN1, Nef, VAN|MGI:1926194||||11|||||||||||||||||||||||||||||Unknown|Unknown|C57BL/6NCrlAnu|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|03-Apr-2020||||Unknown|||Yes| 8962.0|ASD766:H2B:RH2B_1bpdel|C57BL/6NCrlAnu-Rnaseh2b/AnuApb ||Recessive|ribonuclease H2, subunit B|Rnaseh2b|||MGI:1914403||||14|||||||||||||||||||||||||||||Unknown|Unknown|C57BL/6NCrlAnu|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|03-Apr-2020|Cryopreserved sperm|24.0|0.0|Unknown|||Yes| 8963.0|Fcho2Del2Ins|C57BL/6NCrlAnu-Fcho2/AnuApb||Recessive|FCH domain only 2|Fcho2|Unknown|5832424M12Rik|MGI:3505790||||13|||||||||||||||||||||||||||||Unknown||C57BL/6NCrlAnu|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|05-Apr-2020|Cryopreserved sperm|58.0|0.0|Unknown|||Yes| 8970.0|Vav-cre|B6.Cg-Tg(Vav1-Cre)1Awr/WehiAnuApb||Dominant||||||||||||||||||||||||||transgene insertion 1, Andrew W Roberts|Vav1|Haemopoietic||||||||||Normal|Normal|C57BL/6NCrlAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|2|||No|09-Apr-2020|Cryopreserved sperm|60.0|0.0|Unknown||Cre recombinase|Yes| 8972.0|Ubtf|B6(Cg)-Ubtf/AnuApb||Recessive|upstream binding transcription factor, RNA polymerase I|Ubtf||A930005G04Rik, Tcfubf, UBF, UBF1|MGI:98512|pstream binding transcription factor, RNA polymerase I; targeted mutation 1, Mark LeDoux|Ubtf|MGI:6695077|11|||||||||||||||||||||||||||||Unknown||C57BL/6NCrlAnu|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown|1|||No|09-Apr-2020|Cryopreserved sperm|59.0|0.0|Unknown|||Yes| 8971.0|Ubf fl|B6(Cg)-Ubtf/AnuApb||Recessive|upstream binding transcription factor, RNA polymerase I|Ubtf||A930005G04Rik, Tcfubf, UBF, UBF1|MGI:98512||||11|||||||||||||||||||||||||||||Normal||C57BL/6NCrlAnu|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown|1|||No|09-Apr-2020||0.0|0.0|Unknown||RNA polymerase, rRNA|Yes| 8967.0|ENU7B6:039 (CD8)|B6(Cg)-Senp2/AnuApb|B6(Cg)-Senp2/AnuApb|Recessive|SUMO/sentrin specific peptidase 2|Senp2|Unknown||MGI:1923076|SUMO/sentrin specific peptidase 2; mutation 1, The Australian National University|Senp2|MGI:5563407|16|ENSMUSG00000022855|ENSMUST00000023561| Senp2-201|939|1097|A to G|ENSMUSE00000131327|11|313|Glycine to Glycine|||||CTCCGATTTGAAAAGGAAGGTACAAGAGGACACCAAATGGAGCCTGATCTGTCAGAAGAAG|Yes|||||||||||||Subclinical autoimmune susceptibility. Antinuclear autoantibodies: homogeneous nuclear.Low CD8 protein expression and reduced T cell numbers.||C57BL/6NCrlAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|8 onto B6JAnu and then 3 onto C57BL/6NCrlAnu|||No|05-Apr-2020|Cryopreserved sperm|44.0|0.0|Unknown||autoimmunity, antinuclear antibodies (ANA), ENU, Wellcome Trust, T cell, CD8|Yes| 8879.0|Nadsyn1 null|C57BL/6-Nadsyn1/DunwApb||Recessive|NAD synthetase 1|Nadsyn1|Nil|9130012B15Rik|MGI:1926164|Nadsyn1; endonuclease-mediated mutation 1, Sally L Dunwoodie|Nadsyn1||7||||||||||Unknown to Unknown|||||||||||||||||||No overt phenotypes|Normal|C57BL/6J|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|11-Mar-2020|Cryopreserved sperm|50.0|0.0|Unknown|||Yes| 8977.0||C57BL/6-ENSMUSG00000085389.7/TcbApb||Recessive|ENSMUSG00000085389.7 |||1700003M07Rik|MGI:1919475||tm1.1Tcb||4|||||||||||||||||||||||||||||This mouse strain exhibits increased susceptibility to different models of autoimmune disease: autoimmune diabetes induced by multiple low dose streptozotocin , experimental autoimmune encephalomyelitis and experimental anti-neutrophil cytoplasmic antibody-associated vasculitis. Dendritic cells derived from this mouse strain exhibit enhance cytokine production in response to toll-like receptor activation. |Unknown|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|12-Apr-2020|Cryopreserved sperm|40.0|0.0|Unknown|||Yes| 8969.0|ENU15NIH:036a|C57BL/6JAnu-Itgal/AnuApb||Recessive|integrin alpha L|Itgal|Unknown|Cd11a, LFA-1, Ly-15, Ly-21|MGI:96606||||7|||||||||||||||||||||||||||||||C57BL/6JAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|09-Apr-2020|Cryopreserved sperm|71.0|0.0|Unknown||CD8, LFA-1, hepatic|Yes| 8968.0||B6.Cg-Tg(TcraBO4H9.1,TcrbBO4H9.1)7Aog/AnuApb||Dominant||||||||||||||||||||||||||transgene insertion 7 Anne O'Garra|||||||||||||Mice carry a TCR transgene specific for Hen egg lysozyme peptide|C57BL/6NCrlAnu|Unknown|Yes|Yes|Yes|Yes|Yes|No|Unknown|4|||No|08-Apr-2020|Cryopreserved sperm|33.0|0.0|Unknown||T cell, CD4, CTLA-4|Yes| 8976.0|ASD666:Ramos:1bp del|C57BL/6NCrlAnu-Tlr7/AnuApb||X-linked|toll-like receptor 7|Tlr7|Unknown||MGI:2176882||||X|||||||||||||||||||||||||||||Unknown||C57BL/6NCrlAnu|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|11-Apr-2020|Cryopreserved sperm|36.0|0.0|Unknown|||Yes| 8975.0|ASD666:Ramos:TtoC|C57BL/6NCrlAnu-Tlr7/AnuApb||X-linked|toll-like receptor 7|Tlr7|Unknown||MGI:2176882||||X||||||||||Unknown to Unknown|||||||||||||||||||Unknown||C57BL/6NCrlAnu|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|11-Apr-2020|Cryopreserved sperm|20.0|0.0|Unknown|||Yes| 8284.0|Spi6 KO ; Spi6|C57BL/6-Serpinb9/Marp||Recessive|serine (or cysteine) peptidase inhibitor, clade B, member 9|Serpinb9|Unknown|ovalbumin, PI-9, Spi6|MGI:106603|serine (or cysteine) peptidase inhibitor, clade B, member 9; targeted mutation 1.1, Phillip I Bird|Serpinb9|MGI:5140012|13|||||||||||||||||||||||||||||immune system phenotype ( J:252016 )N • mice exhibit normal thymus and spleen cellularity and numbers of dendritic cells, splenic CD4 T cells, CD8 T cells, NK cells and CD103+CD8+ dendritic cellsabnormal immune system morphology ( J:252016 ) • authors state that the base phenotype resembles that of Serpinb9tm1Arpabnormal immune system physiology ( J:252016 ) • authors state that the base phenotype resembles that of Serpinb9tm1Arpdecreased cytotoxic T cell apoptosis ( J:252016 ) • in mice immunized with apoptotic cells displaying ovalbumin due to a dendritic cell dependent priming deficitabnormal dendritic cell antigen presentation ( J:252016 ) • impaired cross-presentation• however, dendritic cells exhibit normal antigen uptake, survival after antigenic challenge and antigen degradation machinery||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|16-Aug-2017|Cryopreserved sperm|12.0|0.0|Unknown|||Yes| 8877.0|NOD.B6Idd14R6|NOD/Lt-Idd31/Apb||Recessive|||||||||||||||||||||||||||||insulin dependent diabetes susceptibility 31|Idd31|||MGI:5509150||||13|Mice exhibit decreased diabetes incidence compared to NOD/Lt wildtype mice|Unknown|NOD/Lt|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|10-Mar-2020|Cryopreserved sperm|50.0|0.0|Yes|Type 1 Diabetes|Pulmonary mycoplasmosis, Mycoplasma pulmonis|Yes| 8878.0|NOD.B6Idd14R8|NOD/Lt-Idd14/Apb||Recessive|||||||||||||||||||||||||||||insulin dependent diabetes susceptibility 14|Idd14/Listr2|||MGI:99416||||13|Mice exhibit increased diabetes incidence compared to NOD/Lt wildtype mice|Unknown|NOD/Lt|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|10-Mar-2020|Cryopreserved sperm|40.0|0.0|Yes|Type 1 Diabetes|Mycoplasma pulmonis, Pulmonary mycoplasmosis|Yes| 8896.0|DmdS3059A|C57BL/6-Dmd/Apb||Recessive|Dystrophin, muscular dystrophy|Dmd||Dp427, Dp71, Duchenne muscular dystrophy, dys, mdx, pke, X-linked muscular dystrophy|MGI:94909||||X|||||||||||||||||||||||||||||Unknown|Unknown|C57BL/6|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|18-Mar-2020|Cryopreserved sperm|60.0|0.0|Yes|Muscular dystrophy||Yes| 8974.0|ASD940:Lef1 fl Tcf7 fl|B6(Cg)-Lef1 Tcf7 Gt(ROSA)26Sor/HhxAnuApb||Recessive|lymphoid enhancer binding factor 1|Lef1||Lef-1, lymphoid enhancer factor 1|MGI:96770|lymphoid enhancer binding factor 1; targeted mutation 1, Hai-Hui Xue|Lef1|MGI:5447957|3|||||||||||||||||||||||||||||normal|normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|11-Apr-2020|Cryopreserved sperm|22.0|0.0|Unknown||T cell, autoimmunity, CD8|Yes| 8974.0|ASD940:Lef1 fl Tcf7 fl|B6(Cg)-Lef1 Tcf7 Gt(ROSA)26Sor/HhxAnuApb||Recessive|transcription factor 7, T cell specific|Tcf7||T cell factor-1, T-cell factor 1, Tcf1, TCF-1|MGI:98507|transcription factor 7, T cell specific; targeted mutation 1c, Wellcome Trust Sanger Institute|Tcf7|MGI:5816259|11|||||||||||||||||||||||||||||normal|normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|11-Apr-2020|Cryopreserved sperm|||Unknown||T cell, autoimmunity, CD8|Yes| 8974.0|ASD940:Lef1 fl Tcf7 fl|B6(Cg)-Lef1 Tcf7 Gt(ROSA)26Sor/HhxAnuApb||Recessive|gene trap ROSA 26, Philippe Soriano|Gt(ROSA)26Sor||beta geo, Gtrgeo26, Gtrosa26, R26, ROSA26, Thumpd3as1|MGI:104735|gene trap ROSA 26, Philippe Soriano; targeted mutation 2, Stuart Orkin|Gt(ROSA)26Sor|MGI:2136519|6|||||||||||||||||||||||||||||normal|normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|11-Apr-2020|Cryopreserved sperm|||Unknown||T cell, autoimmunity, CD8|Yes| 8420.0|Lef1 fl|B6(Cg)-Lef1 Tcf7 Gt(ROSA)26Sor Tg(CD2-cre)1Lov/HhxAnuApb||Recessive|lymphoid enhancer binding factor 1|Lef1||Lef-1, lymphoid enhancer factor 1|MGI:96770|lymphoid enhancer binding factor 1; targeted mutation 1, Hai-Hui Xue|Lef1|MGI:5447957|3|||||||||||||||||transgene insertion 1, Paul Love|human CD2|||||||||||Mice do not have T cell–development defects or aberrant activation of mature T cells.On day 8 after infection with vaccinia virus the frequency and number of SLAMCxcr5<+> TFH cells were diminished.Mice exhibited a significantly lower frequency and number of GL7+Fas+ GC B cells than that of control mice|normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|17-Jan-2018|Cryopreserved sperm|29.0|0.0|Unknown||T cell, autoimmunity, CD8|Yes| 8420.0|Lef1 fl|B6(Cg)-Lef1 Tcf7 Gt(ROSA)26Sor Tg(CD2-cre)1Lov/HhxAnuApb||Recessive|transcription factor 7, T cell specific|Tcf7||T cell factor-1, T-cell factor 1, Tcf1, TCF-1|MGI:98507|transcription factor 7, T cell specific; targeted mutation 1c, Wellcome Trust Sanger Institute|Tcf7|MGI:5816259|11|||||||||||||||||||||||||||||Mice do not have T cell–development defects or aberrant activation of mature T cells.On day 8 after infection with vaccinia virus the frequency and number of SLAMCxcr5<+> TFH cells were diminished.Mice exhibited a significantly lower frequency and number of GL7+Fas+ GC B cells than that of control mice|normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|17-Jan-2018|Cryopreserved sperm|||Unknown||T cell, autoimmunity, CD8|Yes| 8420.0|Lef1 fl|B6(Cg)-Lef1 Tcf7 Gt(ROSA)26Sor Tg(CD2-cre)1Lov/HhxAnuApb||Recessive|gene trap ROSA 26, Philippe Soriano|Gt(ROSA)26Sor||beta geo, Gtrgeo26, Gtrosa26, R26, ROSA26, Thumpd3as1|MGI:104735|gene trap ROSA 26, Philippe Soriano; targeted mutation 2, Stuart Orkin|Gt(ROSA)26Sor|MGI:2136519|6|||||||||||||||||||||||||||||Mice do not have T cell–development defects or aberrant activation of mature T cells.On day 8 after infection with vaccinia virus the frequency and number of SLAMCxcr5<+> TFH cells were diminished.Mice exhibited a significantly lower frequency and number of GL7+Fas+ GC B cells than that of control mice|normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|17-Jan-2018|Cryopreserved sperm|||Unknown||T cell, autoimmunity, CD8|Yes| 8882.0|Pbx1 R184P|C57BL/6J-Pbx1R184P/DunwApb||Recessive|pre B cell leukemia homeobox 1|Pbx1|Unknown|2310056B04Rik, D230003C07Rik, Pbx-1, Pbx1a, Pbx1b|MGI:97495|Pbx1R184P;endonuclease-mediated mutation 1, Sally L Dunwoodie|Pbx1R184P||1||||||||||Unknown to Unknown|||||||||||||||||||Multiple embryonic defects- congenital heart defects (persistent truncus arteriosus, ventricular septal defect), hypoplastic lungs, aplastic adrenal glands, hypoplastic/ectopic kidneys, palate defects, aplastic spleen, hypoplastic/ectopic thymi, defects in sex determination/ gonad development, subcutaneous edema, umbilical hernia, embryonic death.|A proportion of heterozygotes display heart defects (ventricular septal defect, cardiac edema), lung defects (hypoplastic), kidney defects (hypoplastic, pelvic), and subcutaneous edema. |C57BL/6J|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|12-Mar-2020|Cryopreserved sperm|30.0|0.0|Yes|CAKUTHED syndrome|transcription faactor, pulmonary valve, congenital|Yes| 8979.0|NOD.B6 Idd11D|NOD/Lt-C57BL/6<(D4Mit72-D4Mit339)>/TcbApb||Recessive|Insulin dependent diabetes locus 11|Idd11|Unknown|||Idd11|Idd11|96402|4||||||||||||||||||||Insulin dependent diabetes locus 11|Idd11|||96402|insulin dependent diabetes susceptibility 11; C57BL/6|Idd11||4|These homozygous congenic mice exhibit a decreased diabetes incidence compared to NOD/Lt wildtype mice.|Unknown|NOD/Lt|Yes|Yes|Yes|Yes|Yes|Unknown|No|Good|10|||No|12-Apr-2020|Cryopreserved sperm|50.0|0.0|Yes|type 1 diabetes||Possibly| 8749.0|Arjuna:TCR:B10:kk|B6.B10-H2 Tg(ILK3mHEL)3Ccg Tg(TcrHEL3A9)1Mmd/AnuApb||Recessive||||||||||||||||||||||||||transgene insertion 3, Christopher C Goodnow|Rat insulin promoter||histocompatibility-2, MHC|H2|||MGI:95894|histocompatibility-2, MHC; k variant|H2|MGI:3579322|17||||Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|09-Jul-2019|Cryopreserved sperm|40.0|0.0|Unknown|||Yes| 8749.0|Arjuna:TCR:B10:kk|B6.B10-H2 Tg(ILK3mHEL)3Ccg Tg(TcrHEL3A9)1Mmd/AnuApb||Recessive||||||||||||||||||||||||||transgene insertion 1, Mark M Davis|||||||||||||||Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|09-Jul-2019|Cryopreserved sperm|||Unknown|||Yes| 8915.0|SwHel:RAG1KO:Hc.Lc:Ly5a|B6(Cg)-Ptprc Rag1 Igh Tg(IgkHyHEL10)1Rbr/AnuApb||Recessive|recombination activating 1|Rag1||Rag-1|MGI:97848|recombination activating 1; targeted mutation 1, Peter Mombaerts|Rag1|MGI:1857241|2|||||||||||||||||transgene insertion 1, Robert Brink|||protein tyrosine phosphatase, receptor type, C|Ptprc||B220, CD45, Ly-5, Lyt-4, T200|MGI:97810|protein tyrosine phosphatase, receptor type, C; a variant|Ptprc|MGI:4819849|1|Rag1 KO mice lack mature T and B cells. Homozygous for SwHEL Heavy chain (Hc/Hc) Heterozygous for SwHEL Light chain (Lc/WT), B cell specific for Hen egg lysozyme.|All B cells are specific for Hen egg lysozyme|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|23-Mar-2020|Cryopreserved sperm|24.0|0.0|Unknown||B cell, Hen Egg Lysozyme (HEL)|Yes| 8915.0|SwHel:RAG1KO:Hc.Lc:Ly5a|B6(Cg)-Ptprc Rag1 Igh Tg(IgkHyHEL10)1Rbr/AnuApb||Recessive|immunoglobulin heavy chain complex|Igh|||MGI:96442|immunoglobulin heavy chain complex; targeted mutation 1, Robert Brink|Igh|MGI:3800383|12|||||||||||||||||||||||||||||Rag1 KO mice lack mature T and B cells. Homozygous for SwHEL Heavy chain (Hc/Hc) Heterozygous for SwHEL Light chain (Lc/WT), B cell specific for Hen egg lysozyme.|All B cells are specific for Hen egg lysozyme|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|23-Mar-2020|Cryopreserved sperm|||Unknown||B cell, Hen Egg Lysozyme (HEL)|Yes| 8247.0|Srsf3-flox|B6;129-Srsf3/MarpApb||Recessive|serine/arginine-rich splicing factor 3|Srsf3|Unknown|Sfrs3, X16|MGI:98285||||17|||||||||||||||||||||||||||||No phenotype|No phenotype|C57BL/6 x 129|Yes|Yes|Yes|Yes|Yes|Yes|No|Excellent||||No|20-Apr-2017|Cryopreserved sperm|20.0|0.0|No||LoxP|Possibly| 8948.0|ASD886:Cavendish:SH2bpdel|C57BL/6NCrlAnu-Sh2b3/AnuApb||Recessive|SH2B adaptor protein 3|Sh2b3||Lnk|MGI:893598||||5|||||||||||||||||||||||||||||unknown|unknown|C57BL/6NCrlAnu|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|29-Mar-2020|Cryopreserved sperm|35.0|0.0|Unknown|||Yes| 8973.0|BPAT4|C57BL/6-Slc36a4/SviApb||Recessive|solute carrier family 36 (proton/amino acid symporter), member 4|Slc16a4|Unknown||MGI:2442595 ||Slc36a4||9|||||||||||||||||||||||||||||Unknown|Unknown|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|10-Apr-2020|Cryopreserved sperm|50.0|0.0|Unknown|||Possibly| 8960.0||C;129SV4-Csf2/Il3 Il2rg Rag2/J AnuApb||Recessive|colony stimulating factor 2 (granulocyte-macrophage)|Csf2||Csfgm, Gm-CSf, GMCSF, MGI-IGM|MGI:1339752|colony stimulating factor 2 (granulocyte-macrophage); targeted mutation 1.1, Richard A Flavell|Csf2/Il3|MGI:4887879|11|||||||||||||||||||||||||||||Abnormal response to transplant:• mice exhibit improved engraftment with CD34+ hematopoietic cells with improved human myeloid cell reconstitution in the lung compared with wild-type mice||BALB/c|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|03-Apr-2020|Cryopreserved sperm|48.0|0.0|Unknown|||Yes| 8960.0||C;129SV4-Csf2/Il3 Il2rg Rag2/J AnuApb||Recessive|interleukin 2 receptor, gamma chain|Il2rg||CD132, common cytokine receptor gamma chain, common gamma chain, gamma(c), gammaC, gamma C receptor, gc, [g]c|MGI:96551|interleukin 2 receptor, gamma chain; targeted mutation 1.1, Richard A Flavell|Il2rg|MGI:4887837|X|||||||||||||||||||||||||||||Abnormal response to transplant:• mice exhibit improved engraftment with CD34+ hematopoietic cells with improved human myeloid cell reconstitution in the lung compared with wild-type mice||BALB/c|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|03-Apr-2020|Cryopreserved sperm|||Unknown|||Yes| 8960.0||C;129SV4-Csf2/Il3 Il2rg Rag2/J AnuApb||Recessive|recombination activating gene 2|Rag2|||MGI:97849|recombination activating gene 2; targeted mutation 1.1, Richard A Flavell|Rag2|MGI:4887836|2|||||||||||||||||||||||||||||Abnormal response to transplant:• mice exhibit improved engraftment with CD34+ hematopoietic cells with improved human myeloid cell reconstitution in the lung compared with wild-type mice||BALB/c|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|03-Apr-2020|Cryopreserved sperm|||Unknown|||Yes| 8978.0|NOD.B6Idd11G|NOD/Lt-C57BL/6<(D4Mit72 -rs27507071)>/TcbApb||Recessive|insulin dependent diabetes susceptibility 11|Idd11|Unknown||MGI:96402|insulin dependent diabetes susceptibility 11; C57BL/6 |Idd11||4||||||||||||||||||||insulin dependent diabetes susceptibility 11; C57BL/6 |Idd11|||96402|Idd11|||4|These homozygous congenic mice exhibit a decreased diabetes incidence compared to NOD/Lt wildtype mice.|Unknown|NOD/Lt|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|10|||No|12-Apr-2020|Cryopreserved sperm|50.0|0.0|Yes|type 1 diabetes|autoimmune disease|No| 8900.0|Tip2#65|NOD/Lt-Tg(TetO-Ins2) Tg(H2-IEa-tTA)/Apb||Dominant||||||||||||||||||||||||||transgene insertion||||||||||||Normal|Normal|NOD/LtJ|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|18-Mar-2020|Cryopreserved sperm|50.0|0.0|Unknown||proinsulin|Yes| 8900.0|Tip2#65|NOD/Lt-Tg(TetO-Ins2) Tg(H2-IEa-tTA)/Apb||Dominant||||||||||||||||||||||||||transgene insertion||||||||||||Normal|Normal|NOD/LtJ|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|18-Mar-2020|Cryopreserved sperm|||Unknown||proinsulin|Yes| 8942.0|ASD1003:Fuji:TN326|C57BL/6NCrlAnu-Tnfrsf25/AnuApb||Recessive|tumor necrosis factor receptor superfamily, member 25|Tnfrsf25|||MGI:1934667||||4|||||||||||||||||||||||||||||unknown|unknown|C57BL/6NCrlAnu|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|28-Mar-2020|Cryopreserved sperm|22.0|0.0|Unknown|||Yes| 8957.0|ASD942:Hamlin:34|C57BL/6NCrlAnu-Tmem39b/AnuApb||Recessive|transmembrane protein 39b|Tmem39b||6330509E05Rik, MGC:59407|MGI:2682939||||4|||||||||||||||||||||||||||||Unknown|Unknown|C57BL/6NCrlAnu|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|03-Apr-2020|Cryopreserved sperm|56.0|0.0|Unknown|||Yes| 8949.0|ASD1047:Pumpkin|C57BL/6NCrlAnu-Dmpk/AnuApb||Recessive|dystrophia myotonica-protein kinase|Dmpk|||MGI:94906||||7|||||||||||||||||||||||||||||Unknown|Unknown|C57BL/6NCrlAnu|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|30-Mar-2020|Cryopreserved sperm|57.0|0.0|Unknown|||Yes| 8778.0|NODk|NOD.Cg-H2/AnuApb||Recessive|histocompatibility-2, MHC|H2||H-2, MHC-II|MGI:95894|histocompatibility-2, MHC; k variant|H2|MGI:3579322|17|||||||||||||||||||||||||||||NODk mice are resistant to diabetes.||NOD|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|15-Aug-2019|Cryopreserved sperm|44.0|517.0|Unknown||Haplotype|Yes| 8248.0|Srsf3-flox UBC-cre/ert tetO-OSKM|B6;129-Srsf3 Tg(tetO-Pou5f1,-Sox2,-Klf4,-Myc)1Srn Tg((UBC-cre/ERT2)1Ejb/MarpApb||Recessive|serine/arginine-rich splicing factor 3|Srsf3|Unknown|Sfrs3, X16|MGI:98285||||17|||||||||||||||||transgene insertion 1, Eric J Brow|human ubiquitin C (UBC) promoter|||||||||||Unknown|Normal|C57BL/6 x 129|Yes|Yes|Yes|Yes|Yes|Yes|No|Excellent||||No|28-Apr-2017|Cryopreserved sperm|40.0|0.0|No||LoxP|Possibly| 8248.0|Srsf3-flox UBC-cre/ert tetO-OSKM|B6;129-Srsf3 Tg(tetO-Pou5f1,-Sox2,-Klf4,-Myc)1Srn Tg((UBC-cre/ERT2)1Ejb/MarpApb||Recessive||||||||||||||||||||||||||transgene insertion 1, Manuel Serrano||||||||||||Unknown|Normal|C57BL/6 x 129|Yes|Yes|Yes|Yes|Yes|Yes|No|Excellent||||No|28-Apr-2017|Cryopreserved sperm|||No||LoxP|Possibly| 8490.0|C57BL/6.Scmh1-196|C57BL/6N-Scmh1196/BaxApb||Recessive|sex comb on midleg homolog 1|Scmh1||Scml3|MGI:1352762|sex comb on midleg homolog 1; targeted mutation 1a, Wellcome Trust Sanger Institute|Scmh1|MGI:4441791|4|||||||||||||||||||||||||||||Mice homozygous for a knock-out allele exhibit abnormal hematopoiesis but normal fertility and skeleton.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|31-May-2018|Cryopreserved sperm|50.0|0.0|Unknown|||Yes| 8486.0|C57BL/6.Igμ -/-|B6.129S2-Ighm/JApb||Recessive|immunoglobulin heavy constant m|Ighm|Nil|BCR, Igh6, Igh-M, IgM, Ig mu, muH, muMT|MGI:96448|immunoglobulin heavy constant mu; targeted mutation 1, University of Cologne|Ighm|MGI:1857187|12|||||||||||||||||||||||||||||immune system phenotype ( J:73100 , J:118565 )N • T cell numbers in lymph nodes are normal (J:73100)• dendritic cells show normal function in mutants (J:118565)arrested B cell differentiation ( J:119584 ) • a transitional block in early B cell development in evident in bone marrow; pre-B cells are decreased in numberdecreased dendritic cell number ( J:73100 ) • numbers of CD11c+ dendritic cells (DCs) are reduced in mutantsdecreased CD4-positive, alpha beta T cell number ( J:73100 , J:118565 ) • numbers are reduced 3-fold in spleen vs wild-type (J:73100)• there are 5- to 40-fold fewer antigen specific CD4 cells producing Il-2 in mutants compared to controls 6 months after keyhole limpet hemocyanin immunization (J:118565)decreased CD8-positive, alpha-beta T cell number ( J:73100 ) • numbers are reduced 3-fold in spleen vs wild-typeabnormal spleen morphology ( J:73100 ) • in mutants, area of T zone stromal cell network in the spleen is decreased four- to five-fold compared to wild-type• T zone cross sectional area is decreased 2- to 3-folddecreased spleen weight ( J:73100 ) • spleens are ~50% the weight of wild-type spleensabnormal humoral immune response ( J:119584 ) • mice fail to respond to T cell-dependent (OVA) or T cell-independent (dextra) antigenic stimulation and do not produce serum specific antibodies to these antigensdecreased immunoglobulin level ( J:119584 ) • null mice have almost undetectable serum levels of IgG1, IgG2a, IgG2b, IgG3, IgM and IgA compared to wild-type controls or Faslpr micedecreased IgE level ( J:125656 ) • IgE is not detectable in serum of OVA-treated mutants, but high levels are produced in treated wild-typedecreased IgG level ( J:119584 , J:125656 ) • IgG levels drop rapidly after birth due to loss of maternal Ig (J:119584)• IgG is not detectable in OVA-treated mutants, but high levels are produced in treated wild-type (J:125656)decreased IgG1 level ( J:125656 ) • IgG1 is not detected in serum after OVA challengeabnormal cytokine secretion ( J:118565 ) • in mutants, Il-2 secretion is diminished from T cells primed in absence of B cells compared to controls 6 months after keyhole limpet hemocyanin immunizationincreased susceptibility to parasitic infection ( J:74568 ) • mice fail to clear a Giardia muris infection• two weeks after Giardia infection, there are 10-fold more Giardia cysts present in the feces of mice• mice have 10-fold more Giardia trophozoites in the small intestine three weeks after infection and a thousand-fold more 7 weeks after infection compared to controls• mutant mice still have an active Giardia population in the gut one year after infection while wild-type mice clear Giardia after about 7 weeks• mice are not protected from Giardia upon a secondary challenge as wild-type mice are abnormal respiratory system physiology ( J:125656 ) • ovalbumin-sensitized/challenged mice (OVA) are unable to generate an early phase reaction (EPR- initial phase of brochoconstriction) following OVA provocationdecreased bone mineral density ( J:145330 ) • significantly decreased at 10 weeks of ageabnormal compact bone morphology ( J:145330 ) decreased compact bone volume ( J:145330 ) decreased compact bone thickness ( J:145330 ) abnormal trabecular bone morphology ( J:145330 ) • reduced trabecular bone structure in femora• reduced number of trabeculaedecreased trabecular bone thickness ( J:145330 ) ||C57BL/6J|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|31-May-2018|Cryopreserved sperm|49.0|0.0|Unknown||B cell, immunoglobulin|Yes| 8498.0|NOD.Nkrplb.SlamB.CD-1|NOD-Cd1 Klrb1b Tg(Slamf1)1/BaxApb||Recessive|CD1 antigen complex|Cd1|Nil||MGI:102561|CD1 antigen complex; targeted mutation 1, Michael Grusby|Cd1|MGI:1857482|3|||||||||||||||||signaling lymphocytic activation molecule family member 1|||killer cell lectin-like receptor subfamily B member 1B|Klrb1b||Klrb1d, Ly55b, Ly55d, Nkrp1-b, NKR-P1B, Nkrp1d, NKR-P1D|MGI:107539||||6|Mice that are homozygous for this allele are viable, fertile and normal in size. Can be difficult breedersNk Cell Marker Transgenic over expression of Slam. Knockout lacking the CD1 antigen complex gene. Increased Nkt cell numbers. Lack an NK-like cell subset.||NOD/Lt|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|10|||No|31-May-2018|Cryopreserved sperm|49.0|0.0|Unknown||Nk1.1, TCR, NK cell, autoimmunity|Yes| 8495.0|NOD.Hc|NOD-Hc/BaxApb||Recessive|||||||||||||||||||||||||||||hemolytic complement|Hc||C5, C5a, He, Hfib2|MGI:96031||||2|Mice that are homozygous for this allele are viable, fertile, normal in size.Congenic markers C5 Locus|||Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|31-May-2018|Cryopreserved sperm|50.0|0.0|Unknown|||Yes| 8984.0|BecLAFA/GFPLC3Tg|C57BL/6-Becn1 Tg(CAG/CMV-GFP/LC3)/Apb||Recessive|beclin 1, autophagy related|Becn1||Atg6, MGC:6843|MGI:1891828||||11|||||||||||||||||LC3-GFP||||||||||||Normal|Normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|28-Apr-2020|Cryopreserved sperm|50.0|0.0|Unknown|||Yes| 8985.0|BecSGTI/GFPLC3Tg|C57BL/6-Becn1 Tg(CAG/CMV-GFP/LC3)/Apb||Recessive|beclin 1, autophagy related|Becn1||Atg6, MGC:6843|MGI:1891828||||11|||||||||||||||||LC3-GFP||||||||||||Normal|Normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|28-Apr-2020|Cryopreserved sperm|50.0|0.0|Unknown|||Yes| 8497.0|NOD.Il4-/-|NOD.Cg-IL4/BaxApb||Recessive|interleukin 4|Il4|Nil|Il-4|MGI:96556|interleukin 4; targeted mutation 1, University of Cologne|Il4|MGI:1857194|11|||||||||||||||||||||||||||||Insulitis: • at 12 weeks, insulitis incidence is similar in homozygous mutants and heterozygous controls on the NOD background (N4)||NOD|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|31-May-2018|Cryopreserved sperm|49.0|0.0|Yes|type 1 diabetes mellitus||Yes| 8019.0|ePet-cre|B6.Cg-Tg(Fev-cre)1Esd/JAnu||Dominant||||||||||||||||||||||||||transgene insertion 1, Evan S Deneris|ETS oncogene family|serotonergic-specific||||||||||NormalCre recombinase is expressed in serotonergic cells||C57BL/6J|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|26-Jan-2016|Cryopreserved sperm|59.0|0.0|Unknown||Cre recombinase|Yes| 8989.0|ENU15NIH:036a:uGFP|C57BL/6JAnu-Itgal Tg(UBC-GFP)30Scha/AnuApb||Recessive|integrin alpha L|Itgal|Unknown|Cd11a, LFA-1, Ly-15, Ly-21|MGI:96606||||7|||||||||||||||||transgene insertion 30, Brian Schaefer|human ubiquitin C promoter|||||||||||||C57BL/6JAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|06-May-2020|Cryopreserved sperm|33.0|0.0|Unknown||CD8, LFA-1, hepatic|Yes| 8990.0|Scn2a S1758R|C57BL/6-Scn2a/Apb||Recessive|sodium channel, voltage-gated, type II, alpha|Scn2a|Unknown|A230052E19Rik, Nav1.2, Scn2a1|MGI:98248||||2|||||||||||||||||||||||||||||Embryonic lethal|Normal|C57BL/6|No|No|Yes|No|No|Yes|No|Unknown||||No|07-May-2020|Cryopreserved sperm|50.0|0.0|Unknown|||Yes| 8988.0|ASD879:KensingtonPride:PO1206|C57BL/6NCrlAnu-Pola1/AnuApb||Recessive|polymerase (DNA directed), alpha 1|Pola1||Pola|MGI:99660||||X|||||||||||||||||||||||||||||Unknown|Unknown|C57BL/6NCrlAnu|Yes|Unknown|Yes|Yes|Unknown|Yes|No|Unknown||||No|04-May-2020|Cryopreserved sperm|42.0|0.0|Unknown|||Yes| 8500.0|ASD797:Persimmon:10|C57BL/6NCrlAnu-Ifit3b/AnuApb||Recessive|interferon-induced protein with tetratricopeptide repeats 3B|Ifit3b|Unknown|I830012O16Rik|MGI:3698419|Ifit3b, endonuclease-mediated mutation 1, Australian National University|Ifit3b||19||||||||||Unknown to Unknown|||||||||||||||||||Unknown||C57BL/6NCrlAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|05-Jun-2018|Cryopreserved sperm|68.0|0.0|Unknown|||Yes| 8502.0|ASD798:Sapote:4|C57BL/6NCrlAnu-Ifit3 Ifit3b/AnuApb||Recessive|interferon-induced protein with tetratricopeptide repeats 3B|Ifit3b|Unknown|I830012O16Rik|MGI:3698419|Ifit3b, endonuclease-mediated mutation 3, Australian National University |Ifit3b||19||||||||||Unknown to Unknown|||||||||||||||||||Unknown||C57BL/6NCrlAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|05-Jun-2018|Cryopreserved sperm|95.0|0.0|Unknown|||Yes| 8502.0|ASD798:Sapote:4|C57BL/6NCrlAnu-Ifit3 Ifit3b/AnuApb||Recessive|interferon-induced protein with tetratricopeptide repeats 3|Ifit3|Unknown|Ifi49|MGI:1101055|Ifit3, endonuclease-mediated mutation, Australian National University|Ifit3||19||||||||||Unknown to Unknown|||||||||||||||||||Unknown||C57BL/6NCrlAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|05-Jun-2018|Cryopreserved sperm|||Unknown|||Yes| 8503.0|ASD798:Sapote:8|C57BL/6NCrlAnu-Ifit3/AnuApb||Recessive|interferon-induced protein with tetratricopeptide repeats 3|Ifit3|Unknown|Ifi49|MGI:1101055|Ifit3, endonuclease-mediated mutation 2, Australian National University |Ifit3||19||||||||||Unknown to Unknown|||||||||||||||||||Unknown||C57BL/6NCrlAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|05-Jun-2018|Cryopreserved sperm|59.0|0.0|Unknown|||Yes| 8504.0|ASD888:Banana|C57BL/6NCrlAnu-Prdm1/AnuApb||Recessive|PR domain containing 1, with ZNF domain|Prdm1|Unknown||MGI:99655|Prdm1, endonuclease-mediated mutation 2, Australian National University|Prdm1||10||||||||||Unknown to Unknown|||||||||||||||||||Unknown|Normal|C57BL/6NCrlAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|06-Jun-2018|Cryopreserved sperm|12.0|0.0|Unknown|||Yes| 8524.0||C57BL/6N-Abca12/MarpApb||Recessive|ATP-binding cassette, sub-family A (ABC1), member 12|Abca12|Unknown|4832428G11Rik, 4833417A11Rik|MGI:2676312|ATP-binding cassette, sub-family A (ABC1), member 12; targeted mutation 1a, Helmholtz Zentrum Muenchen GmbH|Abca12|MGI:4941545|1|||||||||||||||||||||||||||||Normal|Normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|18-Jun-2018|Cryopreserved sperm|48.0|0.0|Unknown|||Yes| 10446.0|APPV717I|C57BL/6JSah-App/Pqt||Recessive|amyloid beta precursor protein|App||betaAPP, Cvap,|MGI:88059|amyloid beta precursor protein; endonuclease-mediated mutation 1, Paul Thomas|App||16|||||||||||||||||||||||||||||Alzheimer's Disease|Normal|C57Bl/6J|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|16-Aug-2024||0.0|0.0|Unknown|||No| 8986.0|Ets2 fl x lysM-cre|C57BL/6-Ets2 Lyz2 /PjhApb||Recessive|E26 avian leukemia oncogene 2, 3' domain|Ets2|Normal|Ets-2|MGI:95456||||16|||||||||||||||||||||||||||||Unknown||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|01-May-2020|Cryopreserved sperm|50.0|0.0|Unknown|||Yes| 8986.0|Ets2 fl x lysM-cre|C57BL/6-Ets2 Lyz2 /PjhApb||Recessive|lysozyme 2|Lyz2||Lys, Lysm, Lyzs, Lzm, Lzm-s1, Lzp|MGI:96897|lysozyme 2; targeted mutation 1, Irmgard Forster|Lyz2|MGI:1934631|10|||||||||||||||||||||||||||||Unknown||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|01-May-2020|Cryopreserved sperm|||Unknown|||Yes| 8980.0|Progesterone receptor null mouse (PRKO) |C.129S7(B6)-Pgr/OmcJ||Recessive|progesterone receptor|Pgr|Nil|9930019P03Rik, ENSMUSG00000074510, NR3C3, PR, PR-A, PR-B|MGI:97567|progesterone receptor; targeted mutation 1, Bert W O'Malley|Pgr|MGI:1857933|9|||||||||||||||||||||||||||||Abnormal decidualization:• following estrogen and progesterone treatment and mechanical stimulation of the left uterine horn, female homozygotes fail to elicit a typical decidual response, whereas similarly-treated age-matched wild-type females show a greater than 20-fold increase in weight and extensive vascularization of the stimulated horn.Absent corpus luteum:• unlike wild-type mice, PMSG- and hCG-treated female homozygotes show absence of functional corpora lutea at 24 hrs after hCG administration.Increased mature ovarian follicle number:• unlike wild-type mice, PMSG- and hCG -treated female homozygotes display an unexpectedly large number of intact mature preovulatory follicles (unruptured follicles) even at 24 hrs after hCG administration• notably, these follicles are able to undergo strong cumulus cell expansion and dispersion.Uterus inflammation:• following estrogen and progesterone treatment, ovariectomized virgin female homozygotes display abnormal thickening of the uterine wall by extracellular edema, acute inflammatory cells, and proliferation of mucosal and glandular epithelia.• inflammatory changes are restricted to the mucosa, submucosa, and stromal components of the endometrium• a moderate PMN leukocyte infiltration is noted in both endometrial stroma and the overlying luminal epithelium, which appears hyperplastic and disorganized.Abnormal uterus morphology:• following estrogen and progesterone treatment, ovariectomized virgin female homozygotes display an abnormal uterine structure, including hyperplastic luminal and hypertrophic grandular epithelia, loosely arranged stromal layer, and presence of PMN leukocytes.• in contrast, uteri isolated from intact untreated female homozygotes show a normal myometrial and endometrial compartment relative to wild-type females.Enlarged endometrial glands:• following estrogen and progesterone treatment, ovariectomized female homozygotes display greatly enlarged endometrial glands lined by hypertrophied epithelia.Uterus hyperplasia:• following estrogen and progesterone treatment, 6-wk-old ovariectomized virgin female homozygotes display hyperplastic luminal and hypertrophic glandular epithelia.Dilated uterus:• following estrogen and progesterone treatment, 6-wk-old ovariectomized virgin female homozygotes display an abnormally distended fluid-filled uterus relative to age-matched, similarly-treated wild-type females.Anovulation:• unlike wild-type mice, female homozygotes fail to undergo superovulation and produce no oocytes following treatment with exogenous gonadotropins (PMSG and hCG).Female infertility:• adult female homozygotes are infertile when mated with wild-type male mice• in contrast, male homozygotes are fully fertile.Impaired luteinization:• granulosa cells located near the oocyte or positioned near the intact basal lamina of unruptured follicles from PMSG- and hCG -treated female homozygotes display no signs of luteinizationAbnormal mammary gland development:• following treatment with pregnancy levels of estrogen and progesterone, ovariectomized female homozygotes show a severely reduced mammary gland development relative to similarly-treated wild-type females.Abnormal branching of the mammary ductal tree:• following estrogen and progesterone treatment, inguinal mammary glands of ovariectomized female homozygotes exhibit a striking absence of lobuloalveolar development in terminal end buds and a less complex ductal structure with fewer dichotomous and lateral side branches than wild-type mammary glands.Abnormal osteoclast morphology:• at 26 weeks, mice exhibit a tendency towards reduced osteoclast perimeter/bone perimeter and osteoclast perimeter/tissue area compared with wild-type mice.Abnormal humerus morphology:• at 12 weeks, total humoral volume is increased compared to in wild-type mice• the humorus exhibit a tendency for increased cross-sectional volume compared to in wild-type mice• mice exhibit an increase in total, cancellous, and cortical bone mass compared with wild-type mice.Abnormal tibia morphology:• between 6 weeks and 26 weeks, mice exhibit an increase in tibia cross-section area unlike in wild-type mice.Increased compact bone thickness:• at the midshaft of the humorus.Abnormal trabecular bone morphology:• at 6 weeks, mice exhibit less trabecular separation than in wild-type mice• mice fail to exhibit a difference in trabecular separation between week 6 and week 12 unlike wild-type mice• at 26 weeks, mice exhibit an increase in trabecular number and a decrease in trabecular separation unlike in wild-type mice• cancellous bone volume at the epiphysis of the humerus is increased due to increased trabecular thickness compared to in wild-type mice.Increased trabecular bone thickness:• in the humorus.Increased bone mass:• mice exhibit an increase in total, cancellous, and cortical bone mass compared with wild-type mice• however, cortical and cancellous bone mass in the tibia is normal at 12 weeks.Abnormal bone ossification:• at 26, mice exhibit increased mineralizing perimeter/bone perimeter and bone formation rate/tissue area compared with wild-type mice|Normal|BALB/cx129xB6|Yes|No|Yes|Yes|Yes|Yes|No|Unknown||||No|23-Apr-2020|Cryopreserved sperm|50.0|0.0|Unknown|||Yes| 8987.0|Ubf fl Vav-cre|STOCK Ubtf Tg(Vav1-Cre)1Awr/AnuApb||Recessive|upstream binding transcription factor, RNA polymerase I|Ubtf||A930005G04Rik, Tcfubf, UBF, UBF1|MGI:98512||||11|||||||||||||||||transgene insertion 1, Andrew W Roberts|Vav1|Haemopoietic||||||||||Normal||C57BL/6NCrlAnu|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|04-May-2020|Cryopreserved sperm|60.0|0.0|Unknown||RNA polymerase, rRNA|Yes| 1601.0|GAD67-GFP|C57BL/6-Gad1/AnuApb||Dominant|glutamic acid decarboxylase 1|Gad1|Normal|EP10, Gad-1, GAD67, Z49976|MGI:95632|glutamate decarboxylase 1; targeted mutation 1.1, Nobuaki Tamamaki|Gad1|MGI:3590301|2||||||||||||||||Yes|||||||||||||Abnormal involuntary movement:*at E14, the frequency of mouth opening and tongue withdrawal are reduced compared to wild type littermates.Abnormal nervous system electrophysiology:* at E14 the frequency of neural discharges from the hypoglossal nerve and C4 ventral root that stimulate muscle activity in the neck and tongue is reduced however the amplitude of these discharges is similar to wild type.||C57BL/6|No|No|Yes|No|No|Yes|No|Unknown||||No|11-Jul-2007|Cryopreserved sperm|80.0|0.0|Unknown||cerebral cortex, green fluorescence protein, GFP, cleft palate, apnea|Yes| 8993.0|48L|B6(Cg)-Et(tTA/TRE-mCit/Wre)48L/AnuApb||Recessive||||||||||||||||||||||||||Et(tTA/TRE/mCit/Wre)48L||||||||||||Unknown|A subset of neurons in the brain express a construct containing a minimal heat shock promoter, tetracycline response transactivator (tTA), tet response element (TRE), mCitrine (mCit), and the woodchuck hepatitis post-transcriptional regulatory element flanked by long terminal repeats.|C57BL/6NCrlAnu|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|20-May-2020|Cryopreserved sperm|55.0|0.0|Unknown||semilunar (SL) cells, anterior piriform cortex (aPC)|Yes| 8527.0|ASD778:Lrrfip1|C57BL/6NCrlAnu-Lrrfip1/AnuApb||Recessive|leucine rich repeat (in FLII) interacting protein 1|Lrrfip1|Unknown|FLAP (FLI LRR associated protein), Fliiap1|MGI:1342770|Lrrfip1, endonuclease-mediated mutation 1, Australian National University |Lrrfip1||1||||||||||Unknown to Unknown|||||||||||||||||||Unknown||C57BL/6NCrlAnu|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|27-Jun-2018|Cryopreserved sperm|10.0|0.0|Unknown|||Yes| 8994.0|CaMK4(M306V) KI|C57BL/6-Camk4/StVApb||Recessive|calcium/calmodulin-dependent protein kinase IV|Camk4||A430110E23Rik, Ca2+/calmodulin-dependent protein kinase type IV/Gr, CaMKIV, CaMKIV/Gr, D18Bwg0362e |MGI:88258||||18|||||||||||||||||||||||||||||Unknown|Normal|C57BL/6|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown|once|||No|26-May-2020|Cryopreserved sperm|50.0|0.0|Unknown|||Possibly| 8531.0|Srsf2 P95H/+|C57BL/6NTac-Srsf2/Apb||Recessive|serine/arginine-rich splicing factor 2|Srsf2||D11Wsu175e, MRF-1, SC35, Sfrs10, Sfrs2|MGI:98284|serine and arginine-rich splicing factor 2; targeted mutation 2874.1, TaconicArtemis|rsf2|MGI:7408195|11||||||||||Unknown to Unknown|||||||||||||||||||Lethal|Develops myelodysplastic/myeloproliferative syndrome|C57BL/6|No|No|Yes|No|No|Yes|No|Unknown||||No|03-Jul-2018|Cryopreserved sperm|40.0|0.0|Unknown||myelodysplastic (MDS) and myelodysplastic/myeloproliferative (MDS/MPN) syndromes, myeloid bias, monocytosis, dysplasia|Yes| 8530.0|SwHEL x TACI-/-|B6.Cg-Tnfrsf13b Tg(IghelMD4)4Ccg/CmacApb||Recessive|tumor necrosis factor receptor superfamily, member 13b|Tnfrsf13b|Nil|1200009E08Rik, Taci|MGI:1889411|tumor necrosis factor receptor superfamily, member 13b; targeted mutation 1, Charles R Mackay|Tnfrsf13b|MGI:3052983|11|||||||||||||||||transgene insertion 4, Christopher C Goodnow||||||||||||Normal|Normal |C57/BL6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|03-Jul-2018||0.0|0.0|Unknown||TNF, BAFF|Yes| 8251.0|Warpy mix|B6;C3H-Dzip1l/AnuUqApb||Recessive|DAZ interacting protein 1-like|Dzip1l|||MGI:1919757|DAZ interacting protein 1-like; Warpy|Dzip1l|MGI:5563494|9|ENSMUSG00000037784|ENSMUST00000078367|Dzip-1l-001|1123|1326|C to T|ENSMUSE00000325142|8|375|Glutamine to STOP|||||TGTCTCAGGACCAGAAGAAAGCAGCTGCCCAGTCTCAGCGCCATATCAATGCCCTCCGTGC|Yes|||||||||||||Polydactlyly and craniofacial dismorphology in embryos at e14.5.Extra digits on each limb some have 6 some have 7) and there is a craniofacial dismorphology (the front of the head protrudes, the eye position is changed and there is a mandible malformation.|Normal|B6 x C3H|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Excellent||1||No|08-May-2017|Cryopreserved sperm|40.0|0.0|Unknown||polydactyly, ENU|No| 8535.0|TLR9-/-|B6.129-Tlr9/AkiApb||Recessive|toll-like receptor 9|Tlr9|||MGI:1932389|toll-like receptor 9; targeted mutation 1, Shizuo Akira|Tlr9|MGI:2660562|9|||||||||||||||||||||||||||||Abnormal immune system physiology:• response to LPS and CpG is completely abrogatedImpaired natural killer cell mediated cytotoxicity :• no NK cell activation is observed following infection with L. infantum.Decreased interferon-alpha secretion:• following infection with Leishmania baziliensis• however, secretion could be restored by treatment with GU-rich ssRNA, a TLR7 ligand.Decreased interferon-beta secretion:• following infection with Leishmania baziliensis• however, secretion could be restored by treatment with GU-rich ssRNA, a TLR7 ligand.Decreased interleukin-12b secretion: • following infection with attenuated yellow fever vaccine 17D (YF-17D), dendritic cells produce less IL-12p40 relative to wild-type mice (J:118954)• unlike in wild-type mice, IL-12p40 production from dendritic cells following infection with Leishmania infantum is indetectable.Decreased tumor necrosis factor secretion: • following treatment with PbA(Plasmodium bergbei ANKA)-parasitized erythrocytes or LPS-stimulation, TNF secretion is reduced.Decreased susceptibility to experimental autoimmune encephalomyelitis: • myelin oligodendrocyte glycoprotein injection results in delayed onset of disease, 17.9 days after injection rather than 15.9 days as in controls• fewer infiltrating foci in the spinal cord.Abnormal response to infection:• following treatment with PbA (Plasmodium bergbei ANKA)-parasitized erythrocytes, mice have a partially decreased immune response in terms of TNF secretion and response to CpG.Decreased susceptibility to parasitic infection:• resistant to cerebral malaria• reduced accumulation of hemozoin• less upregulation of TNF-alpha in Plasmodium infection|Normal.|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|10-Jul-2018||0.0|0.0|Unknown||receptor, infection, bacteria|Yes| 8996.0|HobitBlimpLck|B6.Cg-Prdm1 Zfp683 Tg(Lck-cre)1Cwi/Apb||Recessive|PR domain containing 1, with ZNF domain|Prdm1||b2b1765Clo, Blimp1, Blimp-1, PRDI-BF1|MGI:99655|PR domain containing 1, with ZNF domain; targeted mutation 2.1, Stephen L Nutt|Prdm1|MGI:4355900|10|||||||||||||||||transgene insertion 1, Christopher B Wilson||||||||||||Mice have defects in tissue resident memory T cells, but are otherwise relatively normal|Normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|27-May-2020|Cryopreserved sperm|40.0|0.0|Unknown||Trm, tissue resident lymphocyte|Yes| 8996.0|HobitBlimpLck|B6.Cg-Prdm1 Zfp683 Tg(Lck-cre)1Cwi/Apb||Recessive|zinc finger protein 683|Zfp683||Hobit|MGI:3650254|zinc finger protein 683; gene trap OST314703, Lexicon Genetics|Zfp683|MGI:4276801|4|||||||||||||||||||||||||||||Mice have defects in tissue resident memory T cells, but are otherwise relatively normal|Normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|27-May-2020|Cryopreserved sperm|||Unknown||Trm, tissue resident lymphocyte|Yes| 8999.0||B6.129-Rarg Tg(Cdh5(PAC)Cre/ERT2)1Rha Gt(ROSA)26Sor/StVApb||Recessive|Retinoic acid receptor, gamma|Rarg|Nil|MGC:11555, MGC:18523, RARgamma2, RAR gamma 2|MGI:97858|retinoic acid receptor, gamma; targeted mutation 3, Pierre Chambon|Rarg|MGI:2386111|15|||||||||||||||||transgene insertion 1, Ralf H Adams|VE-cadherin|||||||||||Unknown|Unknown|C57BL/6|Yes|Yes|Unknown|Yes|Yes|Yes|No|Unknown||||No|05-Jun-2020|Cryopreserved sperm|50.0|0.0|Unknown|||Yes| 8999.0||B6.129-Rarg Tg(Cdh5(PAC)Cre/ERT2)1Rha Gt(ROSA)26Sor/StVApb||Recessive|gene trap ROSA 26, Philippe Soriano|Gt(ROSA)26Sor||beta geo, Gtrgeo26, Gtrosa26, R26, ROSA26, Thumpd3as1|MGI:104735|gene trap ROSA 26, Philippe Soriano; targeted mutation 4, Liqun Luo|Gt(ROSA)26Sor|MGI:3716464|6|||||||||||||||||||||||||||||Unknown|Unknown|C57BL/6|Yes|Yes|Unknown|Yes|Yes|Yes|No|Unknown||||No|05-Jun-2020|Cryopreserved sperm|||Unknown|||Yes| 8529.0|ASD669:Alba|C57BL/6NCrlAnu-Prdm1/AnuApb||Recessive|PR domain containing 1, with ZNF domain|Prdm1||b2b1765Clo, Blimp1, Blimp-1, PRDI-BF1|MGI:99655|Prdm1, endonuclease-mediated mutation 1, Australian National University|Prdm1||10||||||||||Unknown to Unknown|||||||||||||||||||Normal|Normal|C57BL/6NCrlAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|03-Jul-2018|Cryopreserved sperm|46.0|0.0|Unknown|||Yes| 8997.0|Irf4TomatoGfp|C57BL/6-Irf4/Apb||Dominant|interferon regulatory factor 4|Irf4||IRF-4, Spip|MGI:1096873||||13|||||||||||||||||||||||||||||Normal in homeostasis, but immune response is altered.|Normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|27-May-2020|Cryopreserved sperm|50.0|0.0|Unknown|||Yes| 9004.0|Hs6st1 fl x FoxN1 cre|B6.129-Hs6st1 Foxn1/AnuApb||Recessive|heparan sulfate 6-O-sulfotransferase 1|Hs6st1|Normal|6)ST1|MGI:1354958|heparan sulfate 6-O-sulfotransferase 1; targeted mutation 1, Wellington V Cardoso|Hs6st1|MGI:3793786|1||||||||||||||||||||||||||||||Normal|C57BL/6J|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|>10|||No|12-Jun-2020|Cryopreserved sperm|11.0|0.0|Unknown||Heparan sulphate|Yes| 9004.0|Hs6st1 fl x FoxN1 cre|B6.129-Hs6st1 Foxn1/AnuApb||Recessive|forkhead box N1|Foxn1||D11Bhm185e, Hfh11, whn|MGI:102949|forkhead box N1; targeted mutation 3, Nancy R Manley|Foxn1|MGI:3760775|11||||||||||||||||||||||||||||||Normal|C57BL/6J|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|>10|||No|12-Jun-2020|Cryopreserved sperm|||Unknown||Heparan sulphate|Yes| 9005.0|Ndst1 fl x FoxN1 cre|B6.129-Ndst1 Foxn1/AnuApb||Recessive|N-deacetylase/N-sulfotransferase (heparan glucosaminyl) 1|Ndst1|Normal|1200015G06Rik, b2b2230Clo, glucosaminyl N-deacetylase/N-sulfotransferase 1, Hsst, Ndst-1|MGI:104719|N-deacetylase/N-sulfotransferase (heparan glucosaminyl) 1; targeted mutation 1, Jeffrey D Esko|Ndst1|MGI:3589211|18||||||||||||||||||||||||||||||Normal|C57BL/6J|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|>10|||No|12-Jun-2020|Cryopreserved sperm|11.0|0.0|Unknown||heparan sulphate, endothelial, chemokine, neutrophil|Yes| 9005.0|Ndst1 fl x FoxN1 cre|B6.129-Ndst1 Foxn1/AnuApb||Recessive|forkhead box N1|Foxn1||D11Bhm185e, Hfh11, whn|MGI:102949|forkhead box N1; targeted mutation 3, Nancy R Manley|Foxn1|MGI:3760775|11||||||||||||||||||||||||||||||Normal|C57BL/6J|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|>10|||No|12-Jun-2020|Cryopreserved sperm|||Unknown||heparan sulphate, endothelial, chemokine, neutrophil|Yes| 9001.0|Cd11c-cre-GFP:Hs2st1 fl|B6.129-Hs2st1 Tg(Itgax-cre,-EGFP)4097Ach/AnuApb||Recessive|heparan sulfate 2-O-sulfotransferase 1|Hs2st1|Normal|Hs2st, mKIAA0448|MGI:1346049|heparan sulfate 2-O-sulfotransferase 1; targeted mutation 1.1, Jeffrey D Esko|Hs2st1|MGI:4439161|3|||||||||||||||||transgene insertion 4097, Alexander V Chervonsky|Itgax||||||||||||Normal|C57BL/6J|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|>10|||No|12-Jun-2020|Cryopreserved sperm|55.0|0.0|Unknown||Heparan sulphate, sulfation, triglyceride|Yes| 9002.0|Cd11c-cre-GFP:Hs6st1 fl|B6.129-Hs6st1 Tg(Itgax-cre,-EGFP)4097Ach/AnuApb||Recessive|heparan sulfate 6-O-sulfotransferase 1|Hs6st1|Normal|6)ST1|MGI:1354958|heparan sulfate 6-O-sulfotransferase 1; targeted mutation 1, Wellington V Cardoso|Hs6st1|MGI:3793786|1|||||||||||||||||transgene insertion 4097, Alexander V Chervonsky|Itgax||||||||||||Normal|C57BL/6J|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|>10|||No|12-Jun-2020|Cryopreserved sperm|33.0|0.0|Unknown||Heparan sulphate|Yes| 9003.0|Cd11c-cre-GFP:Ndst1 fl|B6.129-Ndst1 Tg(Itgax-cre,-EGFP)4097Ach/AnuApb||Recessive|N-deacetylase/N-sulfotransferase (heparan glucosaminyl) 1|Ndst1|Normal|1200015G06Rik, b2b2230Clo, glucosaminyl N-deacetylase/N-sulfotransferase 1, Hsst, Ndst-1|MGI:104719|N-deacetylase/N-sulfotransferase (heparan glucosaminyl) 1; targeted mutation 1, Jeffrey D Esko|Ndst1|MGI:3589211|18|||||||||||||||||transgene insertion 4097, Alexander V Chervonsky|Itgax||||||||||||Normal|C57BL/6J|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|>10|||No|12-Jun-2020|Cryopreserved sperm|42.0|0.0|Unknown||heparan sulphate, endothelial, chemokine, neutrophil|Yes| 9006.0|Ndst1 fl x FoxN1 cre:TCRb-transgenic|B6.129-Ndst1 Foxn1 Tg(CD2-Tcrb)/AnuApb||Recessive|N-deacetylase/N-sulfotransferase (heparan glucosaminyl) 1|Ndst1|Normal|1200015G06Rik, b2b2230Clo, glucosaminyl N-deacetylase/N-sulfotransferase 1, Hsst, Ndst-1|MGI:104719|N-deacetylase/N-sulfotransferase (heparan glucosaminyl) 1; targeted mutation 1, Jeffrey D Esko|Ndst1|MGI:3589211|18|||||||||||||||||CD2-mTcrb|||||||||||||Normal|C57BL/6J|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|>10|||No|12-Jun-2020|Cryopreserved sperm|33.0|0.0|Unknown||heparan sulphate, endothelial, chemokine, neutrophil|Yes| 9006.0|Ndst1 fl x FoxN1 cre:TCRb-transgenic|B6.129-Ndst1 Foxn1 Tg(CD2-Tcrb)/AnuApb||Recessive|forkhead box N1|Foxn1||D11Bhm185e, Hfh11, whn|MGI:102949|forkhead box N1; targeted mutation 3, Nancy R Manley|Foxn1|MGI:3760775|11||||||||||||||||||||||||||||||Normal|C57BL/6J|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|>10|||No|12-Jun-2020|Cryopreserved sperm|||Unknown||heparan sulphate, endothelial, chemokine, neutrophil|Yes| 9007.0|Hs6st1 fl x FoxN1 cre:TCRb-transgenic|B6.129-Hs6st1 Foxn1 Tg(CD2-mTcrb)/AnuApb||Recessive|heparan sulfate 6-O-sulfotransferase 1|Hs6st1|Normal|6)ST1|MGI:1354958|heparan sulfate 6-O-sulfotransferase 1; targeted mutation 1, Wellington V Cardoso|Hs6st1|MGI:3793786|1|||||||||||||||||CD2-mTcrb|||||||||||||Normal|C57BL/6J|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|>10|||No|12-Jun-2020||0.0|0.0|Unknown||Heparan sulphate|Yes| 9007.0|Hs6st1 fl x FoxN1 cre:TCRb-transgenic|B6.129-Hs6st1 Foxn1 Tg(CD2-mTcrb)/AnuApb||Recessive|forkhead box N1|Foxn1||D11Bhm185e, Hfh11, whn|MGI:102949|forkhead box N1; targeted mutation 3, Nancy R Manley|Foxn1|MGI:3760775|11||||||||||||||||||||||||||||||Normal|C57BL/6J|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|>10|||No|12-Jun-2020||||Unknown||Heparan sulphate|Yes| 8275.0|Ccr6 KO: OT-I|B6.129-Ccr6 Tg(TcraTcrb)1100Mjb/MarpAnu||Recessive|chemokine (C-C motif) receptor 6|Ccr6|Nil|Cmkbr6|MGI:1333797|chemokine (C-C motif) receptor 6; targeted mutation 1, Deltagen|Ccr6|MGI:3604541|17|||||||||||||||||transgene insertion 1100, Michael J Bevan||||||||||||Unknown||C57BL/6J|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|02-Aug-2017|Cryopreserved sperm|42.0|0.0|Unknown||T cell, Ccl20|Yes| 8536.0|C66 ; Hobit|C57BL/6JMarp-Zfp683/MgmpApb||Recessive|zinc finger protein 683|Zfp683|Unknown|Hobit|3650254 ||||4|||||||||||||||||||||||||||||Normal|Normal|C57BL/6J|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|13-Jul-2018|Cryopreserved sperm|30.0|0.0|Unknown||CRISPR|No| 9008.0|Rag2 KO|BALB/c-Rag2/AnuApb||Recessive|ecombination activating gene 2|Rag2||Rag-2|MGI:97849||||2|||||||||||||||||||||||||||||||BALB/c|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|12-Jun-2020|Cryopreserved sperm|55.0|0.0|Unknown|||Yes| 9044.0|Foxe1 Ko|B6.Foxe1||Recessive|Forkhead box E1|Foxe1 |Reduced|thyroid transcription factor 2|MGI:1353500 |Titf2|||4|ENSMUSG00000070990|ENSMUST00000095097.2|Foxe1-201||||||||||||||||||||||||||Homozygous|Foxe1 null mutant mice exhibit cleft palate and either a sublingual or completely absent thyroid gland. Thus, knockout of Foxe1 results in neonatal hypothyroidism that shows similarity to thyroid dysgenesis in humans.|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|16-Jul-2020|Cryopreserved sperm|50.0|0.0|Unknown||Thyroid, Cleft palate, Titf2|No| 9009.0|Mpl(hlb219)|C.B6-Mpl/JAnuApb||Recessive|myeloproliferative leukemia virus oncogene|Mpl||CD110, c-mpl, c-mpl-I, c-mpl-II, hlb219, thrombopoietin receptor, TPO-R|MGI:97076|myeloproliferative leukemia virus oncogene; heart, lung and blood, 219|Mpl|MGI:2680465|4|||||||||||||||||||||||||||||abnormal definitive hematopoiesis ( J:146577 ) • mutant bone marrow cells gave rise to significantly smaller CFU-granulocyte-macrophage (CFU-GM) and CFU-granulocyte (CFU-G) than controlsdecreased common myeloid progenitor cell number ( J:146577 ) • mutant bone marrow cells gave rise to significantly smaller CFU-granulocyte-erythrocyte-monocytemacrophage (CFU-GEMM) than controlsanemia ( J:146577 ) decreased megakaryocyte cell number ( J:146577 ) • mutant mice exhibit a decreased number of megakaryocytes in the bone marrowabnormal megakaryocyte progenitor cell morphology ( J:146577 ) • mutant bone marrow cells gave rise to significantly smaller CFU-Mk populations than controlsdecreased erythrocyte cell number ( J:146577 ) • significantly fewer red blood cells compared to controlsdecreased hematocrit ( J:146577 ) decreased hemoglobin content ( J:146577 ) thrombocytopenia ( J:82961 , J:146577 ) • mice had a platelet count of 106 X 103 cells/ul at 6 weeks of age (J:82961)• the platelet level is reduced by approximately 80% in comparison to controls (J:146577)• platelet morphology is normal and there is no sign of platelet aggregation in blood smears stained with Wright-Giemsa (J:146577)decreased leukocyte cell number ( J:146577 ) • lower white blood cells counts than controlsenlarged spleen ( J:146577 ) • two of three mice showed minor splenomegaly upon necroscopy||BALB/c|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|12-Jun-2020|Cryopreserved sperm|55.0|0.0|Unknown||Platelet, Megakaryocyte|Yes| 9017.0|Kingsleys #7|C57BL/6NCrlAnu-Rab13/AnuApb||Recessive|RAB13, member RAS oncogene family|Rab13|Unknown|610007N03Rik, B230212B15Rik|MGI:1927232|Rab13; endonuclease-mediated mutation 2, The Australian National University|Rab13||3||||||||||Unknown to Unknown|||||||||||||||||||Unknown||C57BL/6NCrlAnu|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|18-Jun-2020|Cryopreserved sperm|59.0|0.0|Unknown|||Yes| 9015.0|Crust|C57BL/6NCrlAnu-Nae1/AnuApb||Recessive|NEDD8 activating enzyme E1 subunit 1|Nae1||Appbp1, MGC:29435, MGC:36437, MGC:36630|MGI:2384561||||8|||||||||||||||||||||||||||||Unknown||C57BL/6NCrlAnu|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|18-Jun-2020|Cryopreserved sperm|66.0|0.0|Unknown|||Yes| 9014.0|MadMex|C57BL/6NCrlAnu-Fam171a/AnuApb||Recessive|family with sequence similarity 171, member A1|Fam171a1||9630050M13Rik|MGI:2442917||||2|||||||||||||||||||||||||||||Unknown||C57BL/6NCrlAnu|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|18-Jun-2020|Cryopreserved sperm|66.0|0.0|Unknown|||Yes| 9013.0|Agxt|C57BL/6NCrlAnu-Agxt/AnuApb||Recessive|alanine-glyoxylate aminotransferase|Agxt|Unknown|Agt1, Agxt1|MGI:1329033||||1|||||||||||||||||||||||||||||Unknown||C57BL/6NCrlAnu|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|18-Jun-2020|Cryopreserved sperm|55.0|0.0|Unknown|||Yes| 9010.0|Acrv1-hCre|C57BL/6-Acrv1/MarpApb||Recessive|acrosomal vesicle protein 1|Acrv1||Msa63, SP-10|MGI:104590||||9|||||||||||||||||||||||||||||Normal|Normal|C57BL6/J|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|16-Jun-2020|Cryopreserved sperm|50.0|0.0|Unknown|||Yes| 9036.0|Lifr fl:LysMcre|B6.129P2-Lifr Lyz2/JAusbAnuApb||Recessive|lysozyme 2|Lyz2|Normal|Lys, Lysm, Lyzs, Lzm, Lzm-s1, Lzp|MGI:96897|lysozyme 2; targeted mutation 1, Irmgard Forster|Lyz2|MGI:1934631|10|||||||||||||||||||||||||||||Unknown|Enlarged spleen:*Rare|C57BL/6NCrlAnu|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|26-Jun-2020|Cryopreserved sperm|33.0|0.0|Unknown||Macrophage, Granulocyte, Conditional mutagenesis|Yes| 9036.0|Lifr fl:LysMcre|B6.129P2-Lifr Lyz2/JAusbAnuApb||Recessive|leukemia inhibitory factor receptor|Lifr||A230075M04Rik, soluble differentiation-stimulating factor receptor|MGI:96788|leukemia inhibitory factor receptor; targeted mutation 1c, Helmholtz Zentrum Muenchen GmbH|Lifr||15|||||||||||||||||||||||||||||Unknown|Enlarged spleen:*Rare|C57BL/6NCrlAnu|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|26-Jun-2020|Cryopreserved sperm|||Unknown||Macrophage, Granulocyte, Conditional mutagenesis|Yes| 8229.0|hAHRKI|B6.129P2-Ahr/MarpAnu||Recessive|aryl-hydrocarbon receptor|Ahr||Ah, Ahh, Ahre, bHLHe76, dioxin receptor, In|MGI:105043|aryl-hydrocarbon receptor; targeted mutation 1, Masayuki Yamamoto|Ahr|MGI:3776466|12|||||||||||||||||||||||||||||Unknown||C57BL/6J|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|28-Mar-2017|Cryopreserved sperm|73.0|0.0|Unknown||dioxin, toxin|Yes| 9016.0|Kingsleys #6|C57BL/6NCrlAnu-Rab13/AnuApb||Recessive|RAB13, member RAS oncogene family|Rab13|Unknown|610007N03Rik, B230212B15Rik|MGI:1927232||||3|||||||||||||||||||||||||||||Unknown||C57BL/6NCrlAnu|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|18-Jun-2020|Cryopreserved sperm|44.0|0.0|Unknown|||Yes| 9018.0|San Roque|B6N(Cg)-Rc3h1/AnuApb |B6N(Cg)-Rc3h1/AnuApb|Recessive|RING CCCH (C3H) domains 1|Rc3h1|Unknown|Roquin|MGI:2685397|sanroque|Rc3h1|MGI:3581675|1|ENSMUSG00000040423|ENSMUST00000035911|Rc3h1-201|596|981|T to G|ENSMUSE00000536751|5|199|Methionine to Arginine|||||TAGGGGCTGCCAGTTCCTTGGACCAGCGATGCAGGAGGAAGCTCTGAAGCTGGTCTTGCTG|Yes|||||||||||||Spontaneous autoimmune disease. Systemic lupus erythematosus. Anti-nuclear autoantibodies (ANA), hypergammaglobulinemia, autoimmune nephritis, lymphadenopathy, increased numbers of CD44high activated memory T cells, increased numbers of T follicular helper cells, spontaneous germinal centres, CD28-independent activation of T cells. Increased ICOS mRNA and protein expression on T cells, defect in micro-RNA (mir) inhibition of mRNA stability.|Low penetrance in hets|C57BL/6NCrlAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|7|||No|22-Jun-2020|Cryopreserved sperm|55.0|0.0|Yes||Systemic lupus erythematosus (SLE), autoimmunity, T cell, ubiquitin ligase, Wellcome Trust, ENU, lymphadenopathy|Yes| 8228.0|CXCR5KO:OT1:Ly5a|B6.Cg-Cxcr5 Ptprc Tg(TcraTcrb)1100Mjb/MarpAnu||Recessive|chemokine (C-X-C motif) receptor 5|Cxcr5||Blr1, CXCR-5, Gpcr6|MGI:103567|chemokine (C-X-C motif) receptor 5; targeted mutation 1, Martin Lipp|Cxcr5|MGI:2158677|9|||||||||||||||||transgene insertion 1100, Michael J Bevan||||||||||||Cxcr5 KO mice:Abnormal leukocyte migration:• homozygotes exhibit a severely impaired lymphocyte migration to the Peyer's pathces and the B cell follicles of the spleen, resulting in morphologically abnormal primary lymphoid follicles• activated B cells fail to migrate from the T cell-rich zone into B cell follicles of the spleenIncreased B cell number:• homozygotes display a 2- to 4-fold increase in spleen or peripheral blood cells co-expressing B220 and high amounts fo IgMAbnormal spleen primary B follicle morphology:• at 8 wks of age, homozygotes display defective formation of primary splenic follicles, including: the T cell zone is located centrally but not polarized in the follicle; the T cell zone is completely surrounded by a small rim of B cell-expressing IgD but not IgM (i.e. IgM+IgD+ subset is absent); a prominent marginal zone surrounds the follicle completelyAbnormal spleen secondary B follicle morphology.Absent spleen germinal centre:• despite high numbers of germinal center founder cells, no functional germinal centers develop in mutant spleen after immunization with the T cell-dependent antigen DNP-KHLAbsent follicular dendritic cells:• absence of primary follicular dendritic cellsAbnormal Peyer's patch morphology:• ~30% (26 of 76) of homozygotes exhibit 1-4 small and rudimentary structures resembling Peyer's patches• ~16% (12 of 76) of homozygotes exhibit normally sized Peyer's patches with multiple B and T cell-rich zones instead of the large follicles present in wild-type miceAbsent Peyer's patches:• 55% (42 of 76) of homozygotes show complete absence of Peyer's patchesAbsent axillary lymph nodes Absent brachial lymph nodes Absent cervical lymph nodes Absent inguinal lymph nodes:• homozygotes lack inguinal lymph nodesAbsent lymph nodes:• absence of inguinal, iliac/periaortic, axillary, branchial, deep cervical, sacral/caudal, and parathymic lymph nodes||C57BL/6J|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|28-Mar-2017|Cryopreserved sperm|64.0|0.0|Unknown||T cell|Yes| 8109.0||B10.BR-H2/JAnuApb||Dominant|||||||||||||||||||||||||||||histocompatibility-2, MHC|H2||Congenic black: Congenic partner C57BL/10ScSn.|MGI:95894|histocompatibility-2, MHC; k variant|H2|MGI:3579322|17|General Information: See C57BL/10ScSn. Moderate breeders, 0.8 young/female/wk., average litter 6. Fecundity lower than C57BL/10ScSn but can have large litters.|||Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|06-Oct-2016|Cryopreserved sperm|164.0|292.0|No|||Yes| 9045.0|Irf7-|B6;129P2-Irf7/TtgRbrc||Recessive|interferon regulatory factor 7|Irf7|||MGI:3577089||||7|ENSMUSG00000025498|ENSMUST00000106023.7|||||||||||||||||||||||||||Homozygous mutant mice are vulnerable to viral infection with a decreased serum interferon level.|Unknown|C57BL/6J|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|Unknown||Homozygote x Homozygote, Homozygous x B6, Het x het|Yes|21-Jul-2020||0.0|50.0|Unknown||Irf7, Knockout|Possibly| 9046.0|IRF3|B6.Cg-Irf3||Recessive|interferon regulatory factor 3|Irf3|Unknown||MGI:6353293||||7|ENSMUSG00000003184|ENSMUST00000003284.15|Irf3-201|||||||||||||||||Irf3||||||||7|Homozygous mutant mice are vulnerable to viral infection with a decreased serum interferon level.|Unknown|C57BL/6J|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|Unknown||Homozygote x Homozygote, Homozygous x B6, Het x het|Yes|21-Jul-2020||0.0|42.0|Unknown||Irf3, Knockout, Infection, Viral|Possibly| 9042.0|Dynll1 Cd23 Bim|Dynll1Tg(Fcer2a-cre)<5Mbu>Bcl2l11||Recessive|Dynein light chain LC8-type 1|Dynll1|Reduced|8kDa LC, DLC8, Dnclc1, Pin|MGI:1861457|Dynein light chain LC8-type 1|Dynll1|MGI:5755433|5|||||||||||||||||Tg(Fcer2a-cre)5Mbu|Cd23|Unknown||||||||||Moderately reduced Ig class-switchingreduced T cell-indendent (TI-1) immune response in vivo and reduced activation by LPS and IL1 in vitro|Normal|C57BL/6|Yes|Yes|Unknown|Yes|Yes|Unknown|No|Good||||No|14-Jul-2020|Cryopreserved sperm|50.0|0.0|Unknown||Proapoptotic, B Cells, BIM, CRE|No| 9042.0|Dynll1 Cd23 Bim|Dynll1Tg(Fcer2a-cre)<5Mbu>Bcl2l11||Recessive|||||||||Unknown|||||||||||||||||||||||||||||Moderately reduced Ig class-switchingreduced T cell-indendent (TI-1) immune response in vivo and reduced activation by LPS and IL1 in vitro|Normal|C57BL/6|Yes|Yes|Unknown|Yes|Yes|Unknown|No|Good||||No|14-Jul-2020|Cryopreserved sperm|||Unknown||Proapoptotic, B Cells, BIM, CRE|No| 9042.0|Dynll1 Cd23 Bim|Dynll1Tg(Fcer2a-cre)<5Mbu>Bcl2l11||Recessive|BCL2-like 11 (apoptosis facilitator)|Bcl2l11 |Reduced|1500006F24Rik, Bim, Bod|MGI:1197519 |BCL2-like 11 (apoptosis facilitator); targeted mutation 6.1, Philippe Bouillet|Bcl2l11|MGI:5562690|2|||||||||||||||||||||||||||||Moderately reduced Ig class-switchingreduced T cell-indendent (TI-1) immune response in vivo and reduced activation by LPS and IL1 in vitro|Normal|C57BL/6|Yes|Yes|Unknown|Yes|Yes|Unknown|No|Good||||No|14-Jul-2020|Cryopreserved sperm|||Unknown||Proapoptotic, B Cells, BIM, CRE|No| 8550.0|ASD935:Navel:9|C57BL/6NCrlAnu-Tlr3/AnuApb||Recessive|toll-like receptor 3|Tlr3|Unknown||MGI:2156367|Tlr3, endonuclease-mediated mutation 1, Australian National University|Tlr3||8||||||||||Unknown to Unknown|||||||||||||||||||Unknown||C57BL/6NCrlAnu|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|07-Aug-2018|Cryopreserved sperm|11.0|0.0|Unknown||CRISPR|Yes| 9066.0|ENU48:125:St3gal5|C57BL/6NCrl/ApbAnu||Recessive|ST3 beta-galactoside alpha-2,3-sialyltransferase 5|St3gal5||GM3-specific sialytransferase, GM3 synthase, mST3Gal V, Siat9, ST3Gal V|MGI:1339963||||6|ENSMUSG00000056091|ENSMUST00000069994|||||||||||||||||||||||||||Unknown|Unknown|C57Bl/6N|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|28-Aug-2020|Cryopreserved sperm|40.0|0.0|Unknown||ENU, Random, Mutagenesis, Screen|Yes| 8549.0|MIC60|C57BL/6-Immt/Apb||Semi-dominant|inner membrane protein, mitochondrial|Immt||1700082C19Rik, D830041H16Rik, HMP, mitofilin, P87, P87/89, P89|MGI:1923864||||6|||||||||||||||||||||||||||||Normal|Normal|C57BL6J |Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|07-Aug-2018||0.0|0.0|Unknown||FLAG, Immt|Yes| 9043.0|IL3-/-|B6.129S2(B10)-Il3/J ||Recessive|Interleukin 3|Il3|||||||11||||||||||||||||||||Interleukin 3|Il3||BPA, Csfmu, HCGF, Il-3, MCGF, PSF|MGI:96552|Il3 targeted mutation |B10.129S2(B6)-Il3/J |MGI:5516114|11|Homozygous mice are viable and fertile. Bone marrow derived mast cells (BMMC) from IL-3 deficient mice exhibit decreased survival when induced with IgE. Expression of anti-apoptotic proteins, Bcl-xL and Bcl-2 are decreased after IgE-induction.|Normal|C57BL/6J|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|15-Jul-2020|Cryopreserved sperm|40.0|0.0|Unknown||Il3, Haematopoiesis, Blood cells|Possibly| 9060.0|MDM2 C305F|B6(Cg).129(Cg)-Mdm2 /AnuNCrl||Recessive|Transformed mouse 3T3 cell double minute 2|MDM2|Normal|1700007J15Rik, Mdm-2 |MGI:96952|Transformed mouse 3T3 cell double minute 2; targeted mutation 1.1, Yangping Zhang|Mdm2|MGI:4836988|10|||||||||||||||||||||||||||||Homozygote animals smaller in size but otherwise normal|Heterozygote animals smaller in size (less pronounced than homozygotes) but otherwise normal.|C57.BL6 AnuNCrl|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|14-Aug-2020|Cryopreserved sperm|55.0|0.0|Unknown||Mdm2, Ribosomal biogenesis, Cancer, p53|Possibly| 7902.0|K14-Cre|B6.FVB-Tg(KRT14-cre)8Brn/MarpApb||Dominant||||||||||||||||||||||||||transgene insertion 8, Anton Bern|Keratin 14|||||||||||Normal|Normal|C57BL/6J|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|unknown|unknown||No|10-Jun-2015|Cryopreserved sperm|47.0|0.0|No||Skin, dermis, Cre recombinase|Yes| 8539.0|ASD550:Juanfran:::F6|C57BL/6NCrlAnu-Samsn1/AnuApb||Recessive|SAM domain, SH3 domain and nuclear localization signals, 1|Samsn1|Unknown|4930571B16Rik, Hacs1|MGI:1914992|Samsn1, endonuclease-mediated mutation 1, Australian National University|Samsn1||16||||||||||Unknown to Unknown|||||||||||||||||||Normal|Normal|C57BL/6NCrlAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|27-Jul-2018|Cryopreserved sperm|60.0|0.0|Unknown|||Yes| 8538.0|ERT-Cre-SB-Neu|STOCK Tg(Elf5-rtTA/TetO-cre) Tg(MMTVneu) TgTn(sb-T2/Onc2)Njen/OnjcriApb||Recessive||||||||||||||||||||||||||Elf5-rtTA/TetO-cre|E74-like factor 5|||||||||||Normal|Normal|C57BL/6:Balb/c:FVB/N|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|26-Jul-2018|Cryopreserved sperm|50.0|0.0|Unknown|||Yes| 8538.0|ERT-Cre-SB-Neu|STOCK Tg(Elf5-rtTA/TetO-cre) Tg(MMTVneu) TgTn(sb-T2/Onc2)Njen/OnjcriApb||Recessive||||||||||||||||||||||||||Tg(MMTVneu)|MMTV|Mammary gland||||||||||Normal|Normal|C57BL/6:Balb/c:FVB/N|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|26-Jul-2018|Cryopreserved sperm|||Unknown|||Yes| 8538.0|ERT-Cre-SB-Neu|STOCK Tg(Elf5-rtTA/TetO-cre) Tg(MMTVneu) TgTn(sb-T2/Onc2)Njen/OnjcriApb||Recessive||||||||||||||||||||||||||transgenic transposon concatemer, Nancy A Jenkins||||||||||||Normal|Normal|C57BL/6:Balb/c:FVB/N|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|26-Jul-2018|Cryopreserved sperm|||Unknown|||Yes| 9034.0|CD4-cre|B6.Cg-Tg(Cd4-Cre)1Cwi/AnuApb||Dominant||||||||||||||||||||||||||transgene insertion 1, Christopher B Wilson|Cd4|||||||||||Normal||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|26-Jun-2020|Cryopreserved sperm|55.0|0.0|Unknown||Cre recombinase|Yes| 9031.0|TRAIL-R.flox|B6.129-Tnfrs10b/Apb||Recessive|tumor necrosis factor receptor superfamily, member 10b|Tnfrsf10b||DR5, KILLER, Killer/Dr5, Ly98, TRAILR2, TRAIL-R2, Trail Receptor, TRICK2A, TRICK2B, TRICKB|MGI:1341090|Trail-r.flox|tumor necrosis factor receptor superfamily, member 10b; targeted mutation 1, Christopher J Kemp|Tnfrsf10b|14|||||||||||||||||||||||||||||Normal - requires crossing to relevant cre strain to delete TRAIL-R|Normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|25-Jun-2020|Cryopreserved sperm|50.0|0.0|Unknown||Metastasis|Yes| 9030.0||B6.Cg-Rag1 Ptprc Tg(H2-Kb-Tcra,-Tcrb)P25Ktk/JApb||Recessive|recombination activating 1|Rag1||Rag-1|MGI:97848||||2|||||||||||||||||transgene insertion P25, Kiyoshi Takatsu|H-2Kb promoter|||||||||||These P25 TCR-Tg transgenic mice contain CD4 + T cells expressing a T-cell antigen receptor that recognizes Mycobacterium tuberculosis antigen. They are bred onto the RAg-1-/- and express the congenial marker Ly5.1. These mice may be useful for studying the process of the adaptive immune response to M. tuberculosis infection in the lungs.|same as homozygous|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|24-Jun-2020||0.0|0.0|Unknown|||Yes| 9030.0||B6.Cg-Rag1 Ptprc Tg(H2-Kb-Tcra,-Tcrb)P25Ktk/JApb||Recessive|protein tyrosine phosphatase, receptor type, C|Ptprc||B220, CD45, Ly-5, Lyt-4, T200|MGI:97810|protein tyrosine phosphatase, receptor type, C; a variant|Ptprc|MGI:4819849|1|||||||||||||||||||||||||||||These P25 TCR-Tg transgenic mice contain CD4 + T cells expressing a T-cell antigen receptor that recognizes Mycobacterium tuberculosis antigen. They are bred onto the RAg-1-/- and express the congenial marker Ly5.1. These mice may be useful for studying the process of the adaptive immune response to M. tuberculosis infection in the lungs.|same as homozygous|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|24-Jun-2020||||Unknown|||Yes| 9033.0|Hardy|C57BL/6NCrlAnu-Igf1r/AnuApb||Recessive|insulin-like growth factor I receptor|Igf1r|Unknown|A330103N21Rik, CD221, hyft, IGF-1R, line 186|MGI:96433||||7|||||||||||||||||||||||||||||Unknown||C57BL/6NCrlAnu|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|26-Jun-2020|Cryopreserved sperm|55.0|0.0|Unknown|||Yes| 8795.0|DMP1Cre/RosaEYFP/Il6sttm1a(KOMP)Ucd|B6(Cg)-Il6st Gt(ROSA)26Sor Tg(Dmp1-cre)1Jqfe/Apb||Recessive|interleukin 6 signal transducer|Il6st||5133400A03Rik, CD130, D13Ertd699e, gp130|MGI:96560||||13|||||||||||||||||transgene insertion 1, Jian Q Feng|Dmp1|||||||||||Mice exhibited low trabecular bone mass, increased periosteal circumference, and reduced bone formation with no reduction in bone resorption.|Normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|19-Sep-2019|Cryopreserved sperm|40.0|0.0|Unknown|||Yes| 8795.0|DMP1Cre/RosaEYFP/Il6sttm1a(KOMP)Ucd|B6(Cg)-Il6st Gt(ROSA)26Sor Tg(Dmp1-cre)1Jqfe/Apb||Recessive|gene trap ROSA 26, Philippe Soriano|Gt(ROSA)26Sor||beta geo, Gtrgeo26, Gtrosa26, R26, ROSA26, Thumpd3as|MGI:104735|gene trap ROSA 26, Philippe Soriano; targeted mutation 1, Frank Costantini|Gt(ROSA)26Sor|MGI:2449038|6|||||||||||||||||||||||||||||Mice exhibited low trabecular bone mass, increased periosteal circumference, and reduced bone formation with no reduction in bone resorption.|Normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|19-Sep-2019|Cryopreserved sperm|||Unknown|||Yes| 8227.0|CD28KO:H2G7|B6.NOD-Cd28 H2/MarpAnu||Recessive|CD28 antigen|Cd28|||MGI:88327|CD28 antigen; targeted mutation 1, Tak Mak|Cd28|MGI:1857150|1||||||||||||||||||||histocompatibility-2, MHC|H2||H-2, MHC-II|MGI:95894|histocompatibility-2, MHC; g7 variant|H2|MGI:3579321|17|CD28 KO mice:Increased T cell apoptosis:• after 96 hours in culture, only 68% of T cells are alive compared to 83% of controls• more mutant T cells are apoptotic after radiation dosage than in controlsAbnormal NK cell physiology:• alpha-galactosylceramide-induced cytotoxic activity of splenic and hepatic mononuclear cells was reduced compared to wild-type• alpha-galactosylceramide-induced anti-metastatic effect was substantially reduced compared to wild-type, indicating that natural killer cells are not able to fight off cancer cellsDecreased T cell proliferation:• T cells have markedly impaired proliferation in response to T cell co-stimulation (anti-CD3 + anti-CD28)Decreased circulating interferon-gamma level:• alpha-galactosylceramide-induced serum IFN-gamma levels were reduced compared to wild-typeDecreased circulating interleukin-4 level:• alpha-galactosylceramide-induced (an antigen that activates invariant natural killer T cells) serum IL-4 levels were reduced compared to wild-typeIncreased susceptibility to type I hypersensitivity reaction:• mice have reduced airway hyperresponsiveness after sensitization and challenge with OVADecreased interleukin-2 secretion:• T cells secrete less IL-2 when activated compared to controlsDecreased susceptibility to experimental autoimmune encephalomyelitis:• mice fail to develop EAE after immunization with MOG and even lack inflammatory infiltrates into the spinal cord|H2G7 mice are resistant to type 1 diabetes|C57BL/6J|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|28-Mar-2017|Cryopreserved sperm|34.0|0.0|Unknown||T cell|Yes| 8998.0|C57BL/6N RIP3 Knockout|B6.129-Ripk3/VmdApb||Recessive|receptor-interacting serine-threonine kinase 3|Ripk3|Nil|2610528K09Rik, Rip3|MGI:2154952|receptor-interacting serine-threonine kinase 3; targeted mutation 1, Vishva M Dixit|Ripk3|MGI:3028853|14|||||||||||||||||||||||||||||Decreased inflammatory response:• do not develop severe hypothermia or die after treatment with TNF unlike wild-type mice• however, intestinal damage 3 and 6 hours after TNF treatment is similar to wild-type mice• onset of mortality following cecal ligation and puncture is delayed and fewer mice die compared to wild-type mice||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|05-Jun-2020|Cryopreserved sperm|50.0|0.0|Unknown||NF-kappa B|Yes| 7366.0|BCL6-flox |B6.129-Bcl6/AnuApb||Recessive|B cell leukemia/lymphoma 6|Bcl6|Normal|Bcl5|MGI:107187|B cell leukemia/lymphoma 6; targeted mutation 1.1, Alexander Dent|Bcl6|MGI:5518542|16|||||||||||||||||||||||||||||Normal||C57BL/6NCrlAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|03-Jul-2013|Cryopreserved sperm|77.0|0.0|Unknown||T cell, transcription, follicular|Yes| 8570.0|K 14 cre ERT 2 B6 tg|B6-Tg(K14-cre/ERT2)/Vccc||Dominant||||||||||||||||||||||||||K14-cre|K14||||||||||||||Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|27-Sep-2018||0.0|70.0|Unknown|||Yes| 8995.0|Blimp1-Tomato-DT|C57BL/6-Prdm1/Apb||Recessive|PR domain containing 1, with ZNF domain|Prdm1|Normal|b2b1765Clo, Blimp1, Blimp-1, PRDI-BF1|MGI:99655||||10|||||||||||||||||||||||||||||Homozygous lethal, homozygotes die during embryogenesis.|In heterozygous state, this mouse functions as a reporter for Blimp1, expressing tdTomato downstream of Blimp1 expression. It should be phenotypically normal. If crossed to a tissue specific Cre recombinase, diphtheria toxin will be expressed only in Blimp1+Cre+ cells, causing their deletion. |C57BL/6|No|No|Yes|No|No|Yes|No|Unknown||||No|27-May-2020|Cryopreserved sperm|50.0|0.0|Unknown||Blimp1|Yes| 8992.0|GAD67|B6.Cg-Gad1/AnuApb||Dominant|glutamate decarboxylase 1|Gad1||EP10, Gad-1, GAD25, GAD44, GAD67, Z49976|MGI:95632|glutamate decarboxylase 1; targeted mutation 1.1, Nobuaki Tamamaki|Gad1|MGI:3590301|2|||||||||||||||||||||||||||||Homozygous animals die at birth.|Expresses enhanced GFP (green fluorescent protein) in GABA-expressing inhibitory neurons in the brain.|C57BL/6NCrlAnu|No|No|Yes|No|No|Yes|No|Unknown||||No|20-May-2020|Cryopreserved sperm|55.0|0.0|Unknown||(GABA)ergic neurons|Yes| 7481.0|cpg15 fl|C57BL/6-Nrn1/AnuApb||Dominant|neuritin 1|Nrn1|Normal|0710008J23Rik, cpg15|MGI:1915654|neuritin 1; targeted mutation 1.1, Elly Nedivi|Nrn1|MGI:5307917|13|||||||||||||||||||||||||||||Normal|Normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|14-Nov-2013|Cryopreserved sperm|61.0|0.0|Unknown||synapse|Yes| 9029.0||B10.BR.(Cg)-Rag1 Tg(CAG-DsRed*MST)1Nagy Tg(TcraKB5.C20,TcrbKB5.C20)10395Arnd/Apb||Recessive|recombination activating |Rag1||Rag-1|MGI:97848||||2|||||||||||||||||transgene insertion 1, Andras Nagy|chicken beta actin promoter coupled with the cytomegalovirus (CMV) immediate early enhancer|||||||||||Tg mice in which all CD8 T cells express a transgenic TCR recognizing H-2Kb + self peptide and a ubiquitous strong red fluorescence in all cells . Mice have been bred onto a RAG-1 -/- background and have no B cells, no CD4 T cells and no NKT cells). Endogenous alpha and beta TCR chain recombination is also excluded so that all CD8 T cells are naive and express the Tg TCR. DsRed mice (Actb-DsRed.T3 transgenic mice express the red fluorescent protein variant DsRed.MST under the control of the chicken beta actin promoter coupled with the cytomegalovirus (CMV) immediate early enhancer and may be useful for widespread fluorescent protein expression) were originally on a B6 background and have been backrossed with Des-RAG-/- for more than 10 generations. Mice homozygous for this Actb-DsRed.T3 transgene are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. These transgenic mice express the red fluorescent protein variant DsRed.MST under the control of the chicken beta actin promoter coupled with the cytomegalovirus (CMV) immediate early enhancer. All tissues of homozygotes fluoresce red. Mice hemizygous for the transgene express red fluorescent protein less intensely than homozygotes. Expression is observed throughout all embryonic and adult stages and very high expression is found in pancreas, skeletal muscle, heart and seminal vesicle. |Same phenotype as homozygous mice|B10.BR|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|24-Jun-2020|Cryopreserved sperm|40.0|0.0|Unknown|||Yes| 9029.0||B10.BR.(Cg)-Rag1 Tg(CAG-DsRed*MST)1Nagy Tg(TcraKB5.C20,TcrbKB5.C20)10395Arnd/Apb||Recessive||||||||||||||||||||||||||transgene insertion 10395, Bernd Arnold||||||||||||Tg mice in which all CD8 T cells express a transgenic TCR recognizing H-2Kb + self peptide and a ubiquitous strong red fluorescence in all cells . Mice have been bred onto a RAG-1 -/- background and have no B cells, no CD4 T cells and no NKT cells). Endogenous alpha and beta TCR chain recombination is also excluded so that all CD8 T cells are naive and express the Tg TCR. DsRed mice (Actb-DsRed.T3 transgenic mice express the red fluorescent protein variant DsRed.MST under the control of the chicken beta actin promoter coupled with the cytomegalovirus (CMV) immediate early enhancer and may be useful for widespread fluorescent protein expression) were originally on a B6 background and have been backrossed with Des-RAG-/- for more than 10 generations. Mice homozygous for this Actb-DsRed.T3 transgene are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. These transgenic mice express the red fluorescent protein variant DsRed.MST under the control of the chicken beta actin promoter coupled with the cytomegalovirus (CMV) immediate early enhancer. All tissues of homozygotes fluoresce red. Mice hemizygous for the transgene express red fluorescent protein less intensely than homozygotes. Expression is observed throughout all embryonic and adult stages and very high expression is found in pancreas, skeletal muscle, heart and seminal vesicle. |Same phenotype as homozygous mice|B10.BR|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|24-Jun-2020|Cryopreserved sperm|||Unknown|||Yes| 9019.0|Lang-GFP|B6.129S2-Cd207/JApb||Dominant|CD207 antigen|Cd207||Langerin|MGI:2180021|CD207|CD207 antigen; targeted mutation 1, Bernard Malissen|Cd207|6|||||||||||||||||||||||||||||Lang-EGFP mutant mice contain an internal ribosome entry site (IRES) and an enhanced green fluorescent protein (EGFP) downstream of the internal stop codon of the CD207 antigen (Cd207 or Langerin) gene. Homozygotes are viable, fertile, and normal in size. Langerin is a transmembrane receptor produced by specialized antigen-presenting cells located in the skin called Langerhans cells (LCs), and other dendritic cells including dermal DCs and splenic CD8+ DCs. Langerin is specifically localized in the Birbeck granules, where it is necessary for their formation. In these mice, EGFP expression is evident in the cytosol of immature Langerin-derived DCs and CD8+ DCs and is decreased upon LC maturation. These mice may be useful for visualizing Langerhans cells and monitoring their movement during inflammation.|same phenotype as homozygous|C57BL/6J|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|23-Jun-2020|Cryopreserved sperm|50.0|0.0|Unknown||Langerhans cells|Yes| 9113.0|B1B2(G2A) DKI|B1B2(G2A) DKI||Semi-dominant|AMPK beta 1 and AMPK beta 2||||||||Unknown|||||||||||||||||||||||||||||Normal|Normal|C57BL/6|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|16-Dec-2020|Cryopreserved sperm|40.0|0.0|Unknown|||Possibly| 9038.0||c-mpl(tm1Wsa) KO||Recessive|Thrombopoietin receptor |c-mpl|Nil||2660811||||4|ENSMUSG00000022847||||||||||||||||||||||||||||Platelet deficient mice|Unknown|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|07-Jul-2020|Cryopreserved sperm|55.0|0.0|Unknown||c-Mpl, Thrombopoietin, TPO, Hematopoiesis, Hematopoietic stem cells|No| 8256.0||ASD565:Hummels:F1#14||Recessive|c-mer proto-oncogene tyrosine kinase|Mertk|Unknown|Eyk, Mer, nmf12, Nyk, Tyro 12|MGI:96965||||2|||||||||||||||||||||||||||||Unknown|Normal|C57BL/6NCrlAnu|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|18-May-2017|Cryopreserved sperm|36.0|0.0|Unknown||ENU, CRISPR|Yes| 9037.0|Winnie|B6N;B6JAnu-Muc2/AnuApb||Recessive|mucin 2|Muc2|Nil||MGI:1339364|Winnie|Muc2|MGI:3614806|7|ENSMUSG00000025515|ENSMUST00000026590|Muc2-202|2963|2968|G to A|ENSMUSE00000467940|25|988|Cysteine to Tyrosine|||||GCTGGACCCCTCTTACAAGGGCACTGTATGTGGTCTGTGTGGGAACTTTGATGACCAGACC|Yes|||||||||||||Diarrhoea, soft feces at weaning, some develop rectal prolapse. GIT does not appear inflamed, goblet cell hyperplasia and developmental or functional deficiency - malabsorption syndrome||C57BL/6JSfdAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Poor|1|1||No|02-Jul-2020|Cryopreserved sperm|101.0|0.0|Unknown||diarrhoea, malabsorption, goblet cell, ENU|Yes| 8553.0|bhlhe40, C65|C57BL/6-Bhlhe40/MarpApb||Recessive|basic helix-loop-helix family, member e40|Bhlhe40|Unknown|Bhlhb2, C130042M06Rik, Clast5, CR8, cytokine response gene 8, DEC1, eip1 (E47 interaction protein 1), Sharp2, Stra13, Stra14|MGI:1097714|Conditional KO|||6|||||||||||||||||||||||||||||unknown|normal|C57BL/6|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|30-Aug-2018|Cryopreserved sperm|50.0|0.0|Unknown|||Yes| 9049.0|ENU33::Prkcd:Ifnar-/-|C57BL/6NCrlAnu-PrkcdIfnar1/AnuApb ||Recessive|protein kinase C, delta|Prkcd |Unknown|D14Ertd420e, Pkcd, PKC[d], PKCdelta |MGI:97598||||14|||||||||||||||||||||||||||||Homozygotes for targeted null mutations exhibit increased susceptibility to viral infection, elevated levels of myeloid lineage cells in the peripheral blood and bone marrow, and reduced immune response to immunostimulatory DNA.|Unknown|C57BL/6NCrlAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|31-Jul-2020|Cryopreserved sperm|22.0|0.0|Unknown||T-cells, Inflammatory response, Immune response|Possibly| 9049.0|ENU33::Prkcd:Ifnar-/-|C57BL/6NCrlAnu-PrkcdIfnar1/AnuApb ||Recessive|interferon (alpha and beta) receptor 1 |Ifnar1|Reduced|Ifar, IFN-alpha/betaR, Ifrc |MGI:107658 |interferon (alpha and beta) receptor 1; targeted mutation 1, Michel Aguet|Ifnar1tm1Agt|MGI:1930950|16|||||||||||||||||||||||||||||Homozygotes for targeted null mutations exhibit increased susceptibility to viral infection, elevated levels of myeloid lineage cells in the peripheral blood and bone marrow, and reduced immune response to immunostimulatory DNA.|Unknown|C57BL/6NCrlAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|31-Jul-2020|Cryopreserved sperm|||Unknown||T-cells, Inflammatory response, Immune response|Possibly| 9047.0|ASD528:B1-8 High Affinity +/-:(Rosa)td Tomato -/- KI|C57BL/6NCrl-Igh:Gt(ROSA)26Sor/APB||Recessive|Immunoglobulin heavy chain complex| Igh |Normal||MGI:96442|Immunoglobulin heavy chain complex; targeted mutation 1, Michel C Nussenzweig|Igh|MGI:3712224|12|||||||||||||||||tdTomato|Gt(ROSA)26Sor|Normal||||||||||These mice carry a tdTomato red fluorescent protein reporter in the Rosa26 locus and thus, ubiquitously express tdTomato throughout their bodies and are visibly red compared to WT littermates. These mice were then crossed to B1-8hi mice, that carry a Trp to Leu point mutation at codon 33 of the heavy chain variable region. When combined to a lambda light chain, the resulting B cell receptor has a 40-fold increase in antigen binding affinity to the hapten NP (4-hydroxy-3-nitrophenylacetyl). Homozygous mice for B1-8hi have around 12% of NP-binding B cells from total splenic B cells.|Heterozygous and homozygous mice have a similar phenotype, although tdTomato cells are less bright in the heterozygous mice.|ASD866:C57BL/6NCrl|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|27-Jul-2020|Cryopreserved sperm|33.0|0.0|Unknown||B Cells, TI-2 responses, (4-hydroxy-3-nitrophenyl)-acetyl , Heavy chain|No| 9143.0||ENU49:188:Tmem173||Semi-dominant|stimulator of interferon response cGAMP interactor 1|Sting1|| 2610307O08Rik, ERIS, MPYS, Sting, Tmem173|MGI:1919762||||18||||||||||||||||||||||||||||| | |C57BL/6NcrlAnu|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|14-Feb-2021|Cryopreserved sperm|36.0|0.0|Unknown|||Possibly| 6208.0|B6.MRL-lpr|B6.MRL-Fas/J||Recessive|Fas (TNF receptor superfamily member 6)|Fas |Nil|APO-1, CD95, TNFR6, Tnfrsf6|MGI:95484|Fas (TNF receptor superfamily member 6); lymphoproliferation|Fas|MGI:1856334|19|||||||||||||||||||||||||||||Premature death:*Median survival is 284 days, compared to 795 days for controls.*50% mortality is observed at 13.5 months with 90% mortality at 16 months, significantly reduced from wild-type.*64% survival at 24 weeks.Increased double-negative T cell numberEnlarged spleenAbnormal lymph node morphology:*Larger lymph nodes often show extensive hemorrhage and necrosis. Enlarged lymph nodes: *By 4 months of age, lymph nodes are increased 10- to 20-fold. *Nodes are 13 times normal size. *Generalized lymphadenopathy.Increased immunoglobulin level:*IgG and IgM levels are increased in serum at 6 months.Decreased interleukin-2 secretion:*Defect in Il2 activity begins during early life and worsens with age; spleen cells show no stimulated Il2 production upon stimulation with concanavalin A.Increased autoantibody level:*Increase in thymocytotoxic autoantibodies at 6 months is seen.*Mice have elevated levels of anti-chromatin antibodies compared to double mutants. Increased anti-nuclear antigen antibody level: *Anti-nuclear antibodies are present at 6 months of age. *Mice have significantly increased levels of anti-ssDNA antibodies. *Mice have elevated levels of anti-chromatin (anti-nucleosome) antibodies compared to double mutants. Increased anti-double stranded DNA antibody level: *Antibodies are increased relative to controls.Glomerulonephritis:*Background Sensitivity: immune complex glomerulonephritis develops by 1 year of age but is much milder than in MRL homozygotes.*Interstitial lymphoid infiltration is observed at 6 months; glomerular IgG deposits that are exclusively mesangial are observed.Abnormal renal glomerulus morphology:*Nephritic changes consist of focal increase in mesangial substance and mild mesangial proliferation.||C57BL/6|Yes|No|Yes|Yes|No|Yes|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown||Systemic lupus erythematosus (SLE)-like disease|Yes| 301.0|MRL-Fas|B6.MRL-Fas/AnuApb||Recessive|Fas (TNF receptor superfamily member)|Fas|Unknown|APO-1, APT1, CD95, Fas, TNFR6, Tnfrsf6|MGI:95484|lymphoproliferation|Fas|MGI:1856334|19||||||||||||||||No|||||||||||||Premature death:median survival is 284 days, compared to 795 days for controls.50% mortality is observed at 13.5 months with 90% mortality at 16 months, significantly reduced from wild-type.64% survival at 24 weeks.Increased double-negative T cell number.Enlarged spleen.Abnormal lymph node morphology:larger lymph nodes often show extensive hemorrhage and necrosis.Enlarged lymph nodes:by 4 months of age, lymph nodes are increased 10- to 20-fold.nodes are 13 times normal size.generalized lymphadenopathy.Increased immunoglobulin level:IgG and IgM levels are increased in serum at 6 monthsDecreased interleukin-2 secretion:defect in Il2 activity begins during early life and worsens with age; spleen cells show no stimulated Il2 production upon stimulation with concanavalin A.Increased autoantibody level:increase in thymocytotoxic autoantibodies at 6 months is seen.mice have elevated levels of anti-chromatin antibodies compared to double mutants.Increased anti-nuclear antigen antibody level:anti-nuclear antibodies are present at 6 months of age.mice have significantly increased levels of anti-ssDNA antibodies.mice have elevated levels of anti-chromatin (anti-nucleosome) antibodies compared to double mutants.Increased anti-double stranded DNA antibody level:antibodies are increased relative to controlsIncreased immature B cell number:plasmablast numbers in spleen are increased relative to wild-type.Increased transitional stage B cell number:higher numbers of T2 B cells in spleen relative to wild-typeIncreased follicular B cell number:higher in spleen relative to wild-type.Increased marginal zone B cell number:higher in spleen relative to wild-type, Fas homozygotes, and Bcl2l11-deficient mice.Abnormal splenic cell ratio:T1:follicular B cell ratio is higher than wild-type or Bcl2l11-deficient mice.Increased splenocyte number:total number of CD19+ splenocytes is higher than wild-typetotal number of splenocytes is increased relative to wild-type.Glomerulonephritis:Immune complex glomerulonephritis develops by 1 year of age but is much milder than in MRL homozygotes.interstitial lymphoid infiltration is observed at 6 months; glomerular IgG deposits that are exclusively mesangial are observed.Abnormal renal glomerulus morphology:nephritic changes consist of focal increase in mesangial substance and mild mesangial proliferation||C57BL/6 x MRL|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|03-May-2006|Cryopreserved sperm|102.0|0.0|Unknown||B cell, Immunoglobulin, lymphadenopathy, T cell, autoimmunity, glomerulonephritis|Yes| 8665.0||ASD1000:Corn||Recessive|Corn||||||||Unknown||||||||||||||||||||||||||||||||Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|26-Feb-2019|Cryopreserved sperm|11.0|0.0|Unknown|||Yes| 9144.0||ENU50:113:P2rx7||Semi-dominant|purinergic receptor P2X, ligand-gated ion channel, 7|P2rx7|||MGI:1339957||||5||||||||||||||||||||||||||||| | |C57BL/6NcrlAnu|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|14-Feb-2021|Cryopreserved sperm|12.0|0.0|Unknown|||Possibly| 9158.0|Mb1cre ERT2:Rosa26:lef1:tcf7|C57Bl/6-Mb1(cre ERT2):Rosa26:lef1:tcf7/Apb||Semi-dominant|activation-induced cytidine deaminase|Aicda|||MGI:1342279||||6|||||||||||||||||||||||||||||Normal|Normal|B6|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|11-Mar-2021|Cryopreserved sperm|36.0|0.0|Unknown|||Yes| 9158.0|Mb1cre ERT2:Rosa26:lef1:tcf7|C57Bl/6-Mb1(cre ERT2):Rosa26:lef1:tcf7/Apb||Semi-dominant|transcription factor 7, T cell specific|Tcf7|||MGI:98507||||11|||||||||||||||||||||||||||||Normal|Normal|B6|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|11-Mar-2021|Cryopreserved sperm|||Unknown|||Yes| 9158.0|Mb1cre ERT2:Rosa26:lef1:tcf7|C57Bl/6-Mb1(cre ERT2):Rosa26:lef1:tcf7/Apb||Semi-dominant|lymphoid enhancer binding factor 1|Lef1|||MGI:96770||||3|||||||||||||||||||||||||||||Normal|Normal|B6|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|11-Mar-2021|Cryopreserved sperm|||Unknown|||Yes| 8300.0|IRF4:1 bp deletion|C57BL/6NCrlAnu-Irf4/Anu||Recessive|interferon regulatory factor 4|Irf4|Unknown|IRF-4, Spip|MGI:1096873|Irf4, endonuclease-mediated mutation 2.1, Australian National University|Irf4||13||||||||||Unknown to Unknown|||||||||||||||||||Unknown||C57BL/6NCrlAnu|Yes|Unknown|Yes|Yes|Unknown|Yes|No|Unknown||||No|07-Sep-2017|Cryopreserved sperm|45.0|0.0|Unknown|||Yes| 8559.0|ENU41:157:Pycard:G3|C57BL/6NCrlAnu-Pycard/AnuApb||Recessive|PYD and CARD domain containing|Pycard|Unknown|9130417A21Rik, Asc, TMS-1|MGI:1931465||||7|||||||||||||||||||||||||||||||C57BL/6NCrlAnu|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|13-Sep-2018|Cryopreserved sperm|48.0|0.0|Unknown||ENU|Yes| 8317.0|CIB1 Transgenic |C57BL/6-Tg(CAG-CIB1)/CcbApb||Dominant||||||||||||||||||||||||||human Calcium and Integrin Binding Protein 1|Chicken Beta actin|||||||||||Unknown|Normal|C57BL/6|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|03-Oct-2017|Cryopreserved sperm|50.0|0.0|Unknown|||Yes| 9048.0|BCMA-/-|B6;129S-Tnfrsf17/Apb||Recessive|Tumor necrosis factor receptor superfamily, member 17|TNFrsf17|Nil|CM, BCMA, Tnfrsf13, Tnfrsf13a |MGI:1343050|Tumor necrosis factor receptor superfamily, member 17; targeted mutation 1, Martin L Scott|Tnfrsf17|MGI:2387427|16|||||||||||||||||||||||||||||BCMA-/- mice have a deficiency in long lived plasma cells due to ablated expression of the receptor B cell maturation antigen (BCMA). |BCMA+/- mice are normal|C57BL/6 |Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|28-Jul-2020||0.0|0.0|Unknown||B cell development, B cell survival, lymphoid organs|Possibly| 8291.0|NSG.DQ8.HuPI|NOD.Cg-Prkdc H2-Ab1 Il2rg Ins1 Tg(HLA-DQA1,HLA-DQB1)1Dv ||Recessive|protein kinase, DNA activated, catalytic polypeptide|Prkdc|Unknown|DNAPDcs, DNA-PK, DNA-PKcs, DOXNPH, dxnph, slip, XRCC7|MGI:104779|protein kinase, DNA activated, catalytic polypeptide; severe combined immunodeficiency|Prkdc|MGI:1857113|16|||||||||||||||||transgene insertion 1, Chella David||||||||||||Immunocompromised.Expresses HLA-DQ8 and human insulin.|Immunocompromised.Expresses HLA-DQ8 and human insulin.|NOD (NSG)|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|22-Aug-2017|Cryopreserved sperm|50.0|0.0|Unknown||H2, Insulin|No| 8291.0|NSG.DQ8.HuPI|NOD.Cg-Prkdc H2-Ab1 Il2rg Ins1 Tg(HLA-DQA1,HLA-DQB1)1Dv ||Recessive|histocompatibility 2, class II antigen A, beta 1|H2-Ab1|Nil|Abeta, A beta, H-2Ab, H2-Ab, Ia2, Ia-2, IAb, I-Ab, I-Abeta, Rmcs1|MGI:103070|histocompatibility 2, class II antigen A, beta 1; targeted mutation 1, Michael J Grusby|H2-Ab1|MGI:2158420|17|||||||||||||||||||||||||||||Immunocompromised.Expresses HLA-DQ8 and human insulin.|Immunocompromised.Expresses HLA-DQ8 and human insulin.|NOD (NSG)|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|22-Aug-2017|Cryopreserved sperm|||Unknown||H2, Insulin|No| 8291.0|NSG.DQ8.HuPI|NOD.Cg-Prkdc H2-Ab1 Il2rg Ins1 Tg(HLA-DQA1,HLA-DQB1)1Dv ||Recessive|interleukin 2 receptor, gamma chain|Il2rg|Nil|CD132, common cytokine receptor gamma chain, common gamma chain, gamma(c), gammaC, gamma C receptor, gc, [g]c|MGI:96551|interleukin 2 receptor, gamma chain; targeted mutation 1, Warren J Leonard|Il2rg|MGI:1857455|X|||||||||||||||||||||||||||||Immunocompromised.Expresses HLA-DQ8 and human insulin.|Immunocompromised.Expresses HLA-DQ8 and human insulin.|NOD (NSG)|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|22-Aug-2017|Cryopreserved sperm|||Unknown||H2, Insulin|No| 8291.0|NSG.DQ8.HuPI|NOD.Cg-Prkdc H2-Ab1 Il2rg Ins1 Tg(HLA-DQA1,HLA-DQB1)1Dv ||Recessive|insulin I|Ins1|Nil||MGI:96572||||19|||||||||||||||||||||||||||||Immunocompromised.Expresses HLA-DQ8 and human insulin.|Immunocompromised.Expresses HLA-DQ8 and human insulin.|NOD (NSG)|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|22-Aug-2017|Cryopreserved sperm|||Unknown||H2, Insulin|No| 9039.0|FANCM KO|C57BL/6-FancM/Apb||Recessive|Fanconi anemia, complementation group M|Fancm||C730036B14Rik, D12Ertd364e|MGI:2442306||||12|ENSMUSG00000055884|ENSMUST00000058889.4 |Fancm-201||||||||||||||||||||||||||Normal|Normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|10-Jul-2020|Cryopreserved sperm|50.0|0.0|Unknown|||No| 9061.0|GBPchrom3|B6.Gbp||Recessive|Guanylate binding protein 2|Gbp2 |Reduced||MGI:102772||||3|||||||||||||||||||||||||||||Mice lacking Gbpchr3 were highly susceptible to T. gondii infection, resulting in increased parasite burden in immune organs. Furthermore,Gbpchr3-deleted macrophages were defective in IFN-g-mediated suppression of T. gondii intracellular growth and recruitment of IFN-g-inducible p47GTPase Irgb6 to the parasitophorous vacuole. Gbpchr3 play a pivotal role in anti-T.gondii host defense by controlling IFN-g-mediated Irgb6-dependent cellular innate immunity.|Unknown|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|||Homozygote x Homozygote|No|18-Aug-2020|Cryopreserved sperm|72.0|0.0|Unknown||Gbp2, Gbp5, IFN-γ, guanylate binding protein , Gbp|No| 9061.0|GBPchrom3|B6.Gbp||Recessive|Guanylate binding protein 2b |Gbp2b|Reduced||||||3|ENSMUSG00000040264|ENSMUST00000029936.4|||||||||||||||||||||||||||Mice lacking Gbpchr3 were highly susceptible to T. gondii infection, resulting in increased parasite burden in immune organs. Furthermore,Gbpchr3-deleted macrophages were defective in IFN-g-mediated suppression of T. gondii intracellular growth and recruitment of IFN-g-inducible p47GTPase Irgb6 to the parasitophorous vacuole. Gbpchr3 play a pivotal role in anti-T.gondii host defense by controlling IFN-g-mediated Irgb6-dependent cellular innate immunity.|Unknown|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|||Homozygote x Homozygote|No|18-Aug-2020|Cryopreserved sperm|||Unknown||Gbp2, Gbp5, IFN-γ, guanylate binding protein , Gbp|No| 9061.0|GBPchrom3|B6.Gbp||Recessive|Guanylate binding protein 3|Gbp3|Reduced||MGI:1926263||||3|ENSMUSG00000028268|ENSMUST00000106221.7|Gbp3-202||||||||||||||||||||||||||Mice lacking Gbpchr3 were highly susceptible to T. gondii infection, resulting in increased parasite burden in immune organs. Furthermore,Gbpchr3-deleted macrophages were defective in IFN-g-mediated suppression of T. gondii intracellular growth and recruitment of IFN-g-inducible p47GTPase Irgb6 to the parasitophorous vacuole. Gbpchr3 play a pivotal role in anti-T.gondii host defense by controlling IFN-g-mediated Irgb6-dependent cellular innate immunity.|Unknown|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|||Homozygote x Homozygote|No|18-Aug-2020|Cryopreserved sperm|||Unknown||Gbp2, Gbp5, IFN-γ, guanylate binding protein , Gbp|No| 9061.0|GBPchrom3|B6.Gbp||Recessive|Guanylate binding protein 7|Gbp7|Reduced||MGI:2444421||||3|ENSMUSG00000040253|ENSMUST00000045097.10|Gbp7-201||||||||||||||||||||||||||Mice lacking Gbpchr3 were highly susceptible to T. gondii infection, resulting in increased parasite burden in immune organs. Furthermore,Gbpchr3-deleted macrophages were defective in IFN-g-mediated suppression of T. gondii intracellular growth and recruitment of IFN-g-inducible p47GTPase Irgb6 to the parasitophorous vacuole. Gbpchr3 play a pivotal role in anti-T.gondii host defense by controlling IFN-g-mediated Irgb6-dependent cellular innate immunity.|Unknown|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|||Homozygote x Homozygote|No|18-Aug-2020|Cryopreserved sperm|||Unknown||Gbp2, Gbp5, IFN-γ, guanylate binding protein , Gbp|No| 9061.0|GBPchrom3|B6.Gbp||Recessive|Guanylate binding protein 5|Gbp5|Reduced||MGI:2429943||||3|ENSMUSG00000105504|ENSMUST00000090127.6|Gbp5-201||||||||||||||||||||||||||Mice lacking Gbpchr3 were highly susceptible to T. gondii infection, resulting in increased parasite burden in immune organs. Furthermore,Gbpchr3-deleted macrophages were defective in IFN-g-mediated suppression of T. gondii intracellular growth and recruitment of IFN-g-inducible p47GTPase Irgb6 to the parasitophorous vacuole. Gbpchr3 play a pivotal role in anti-T.gondii host defense by controlling IFN-g-mediated Irgb6-dependent cellular innate immunity.|Unknown|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|||Homozygote x Homozygote|No|18-Aug-2020|Cryopreserved sperm|||Unknown||Gbp2, Gbp5, IFN-γ, guanylate binding protein , Gbp|No| 8556.0||hRhD L3 het ||Recessive|human RhD||||||||Unknown||||||||||Unknown to Unknown|||||||||||||||||||human RhD expressed on murine RBC|human RhD expressed on murine RBC||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2018|Cryopreserved sperm|70.0|0.0|Unknown|||Yes| 8557.0||hRhD L5 het ||Dominant|murine RhD||||||||Unknown|||||||||||||||||human RhD||||||||||||human RhD expressed on murine RBC|human RhD expressed on murine RBC|C57BL/6|Yes|Unknown|Yes|Unknown|Unknown|Yes|No|Good|3|||No|13-Sep-2018|Cryopreserved sperm|80.0|0.0|No|||Yes| 8571.0|Pb-1 cre fvb/n|FVB/N-Tg(Pb1-cre)VcccApb||Dominant||||||||||||||||||||||||||Pb1-cre||||||||||||||FVB/N|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|27-Sep-2018||0.0|84.0|Unknown|||Yes| 8572.0|Brca2|FVB/N-Brca2/VcccApb||Recessive|Brca2||||||||Unknown|||||||||||||||||||||||||||||||FVB/N|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|27-Sep-2018||0.0|55.0|Unknown|||Yes| 4452.0|BALB/c.B6 TLR-4tm1 ; Billy Whiz|BALB/c-Tlr4/AnuApb||Recessive|toll-like receptor 4|Tlr4|Nil|lipopolysaccharide response, Lps, Rasl2-8|MGI:96824|toll-like receptor 4; targeted mutation 1, Shizuo Akira|Tlr4|MGI:1860885|4||||||||||||||||Yes|||||||||||||Homozygotes for spontaneous or targeted mutations are hyporesponsive to bacterial lipopolysaccharide and more susceptible to infection by gram negative bacteria.||BALB/c|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|10|||No|20-Feb-2009|Cryopreserved sperm|115.0|0.0|Unknown||infection, lipopolysaccharide (LPS), bacterial infection, hyoresponse, macrophage|Yes| 9041.0|Asciz Mb-1 Dynll1|Atmin Cd79 Dynll1||Recessive|ATM interactor|Atmin |Reduced|Asciz, gpg6, MGC:79206, mKIAA0431 |MGI:2682328|ATM interactor; targeted mutation 1.2, Jorg Heierhorst|Atmin|MGI:5463937|8|||||||||||||||||CD79A antigen (immunoglobulin-associated alpha); targeted mutation 1, Michael Reth|Cd79a|Unknown||||||||||Severe reduction of B cell numbers (in Asciz f/f Mb1-Cre Ki/+ Dynll1 f/f conditional cKO mice)|Normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|14-Jul-2020|Cryopreserved sperm|50.0|0.0|Unknown||B cell development, Adaptive and innate B cells, Lymphoid cells|Possibly| 9041.0|Asciz Mb-1 Dynll1|Atmin Cd79 Dynll1||Recessive|Dynein light chain LC8-type 1|Dynll1 ||8kDa LC, DLC8, Dnclc1, Pin|MGI:1861457|Dynein light chain LC8-type 1; targeted mutation 1.1, Jorg Heierhorst|Dynll1|MGI:5755433|5|||||||||||||||||||||||||||||Severe reduction of B cell numbers (in Asciz f/f Mb1-Cre Ki/+ Dynll1 f/f conditional cKO mice)|Normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|14-Jul-2020|Cryopreserved sperm|||Unknown||B cell development, Adaptive and innate B cells, Lymphoid cells|Possibly| 9064.0|Galanin receptor-3 knockout|C57BL/6J-Galr3/Apb||Recessive|Galanin receptor 3|Galnr3|Reduced||MGI:1329003 |galanin receptor 3; targeted mutation 1, Lexicon Genetics|Galr3|MGI:3528737|15|||||||||||||||||||||||||||||Increased anxiety-like behaviour and preference for alcohol over water.|Normal.|C57BL/6J|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|28-Aug-2020|Cryopreserved sperm|50.0|0.0|Unknown||Depression , Anxiety disorders, Neuropeptides, Stress-related diseases, Mood disorders|No| 8564.0|CD4MLL1EED|B6.129-Kmt2a/Apb||Recessive|lysine (K)-specific methyltransferase 2A|Kmt2a|Nil|All1, ALL-1, Cxxc7, HTRX1, Mll, Mll1, trithorax Drosophila|MGI:96995|lysine (K)-specific methyltransferase 2A; targeted mutation 1.2, Patricia Ernst|Kmt2a|MGI:3839795|9|||||||||||||||||||||||||||||normal|normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|18-Sep-2018||0.0|0.0|Unknown|||Yes| 10325.0|Irf4c.127AG (1)|C57BL/6NCrlAnu-Irf4em12Anu/ANU||Recessive|interferon regulatory factor 4|IRF4|||MGI:1096873 ||||13|||||||||||||||||||||||||||||Unknown|Unknown|C57Bl/6N|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|18-Apr-2023|Cryopreserved sperm|54.0|0.0|Unknown|||Possibly| 9065.0|ENU49:B3galt4|ANU:ENU49:084:B3galt4||Recessive|Unknown||||||||Unknown|||||||||||||||||||||||||||||Unknown|Unknown|C57BL/6NCrlAnu|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|28-Aug-2020|Cryopreserved sperm|55.0|0.0|Unknown||ENU, Random, Mutagenesis, Screen|Yes| 7015.0|ENU21:035:a:B6:G3|ANU:ENU21:035:a:G3||Recessive|Unknown||||||||Unknown||||||||||||||||Unknown|||||||||||||Unknown|Unknown|C57BL/6NCrlAnu|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||1||No|06-Jul-2012|Cryopreserved sperm|60.0|0.0|Unknown||ENU, random, mutagenesis, screen|Yes| 7940.0|ENU30:045:B6|C57BL/6NCrlAnu-Rasgrp1/AnuApb||Recessive|RAS guanyl releasing protein 1|rasgrp1|Unknown||MGI:1314635|Rasgrp1; mutation 2, Australian National University|Rasgrp1||2|ENSMUSG00000027347|ENSMUST00000102534|Rasgrp1-001|1473|1785|T to C|ENSMUSE00000295156|12|498|Isoleucine to Valine|||||||||||||||||||Increased CD44 expression on CD4 T cells|Normal|C57BL/6NCrlAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|26-Jun-2015|Cryopreserved sperm|39.0|0.0|Unknown||T cell, ENU|Yes| 8583.0|ASD546:Cazorla|C57BL/6NCrlAnu-Blk/AnuApb||Recessive|B lymphoid kinase|Blk|Unknown||MGI:88169|Blk, endonuclease-mediated mutation 1, Australian National University |Blk||14||||||||||Unknown to Unknown|||||||||||||||||||Unknown|Unknown|C57BL/6NCrlAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|04-Oct-2018|Cryopreserved sperm|48.0|0.0|Unknown|||Yes| 9070.0|Myostatin KO|BALB/c-Mstn/APB||Recessive|Myostatin|Mstn|Reduced|Gdf8|MGI:95691|myostatin; targeted mutation 1, Se-Jin Lee|Mstntm1Sjl|MGI:2148177|1|NCBI Gene: 17700||||||||||||||||||||||||||||Increased muscle mass|Increased muscle mass|BALB/c|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|03-Sep-2020|Cryopreserved sperm|50.0|0.0|Unknown|||No| 9071.0|FXYD1 KO|B6;129S-Fxyd1/APB||Recessive|FXYD domain-containing ion transport regulator 1|Fxyd1 |Reduced|0610012C17Rik, 1110006M24Rik, phospholemman, PLM, PML |MGI:1889273 |FXYD domain-containing ion transport regulator 1; targeted mutation 1, Amy L Tucker|Fxyd1|MGI:3576231|7||||||||||||||||||||FXYD domain-containing ion transport regulator 1|Fxyd1 ||0610012C17Rik, 1110006M24Rik, phospholemman, PLM, PML |MGI:1889273|FXYD domain-containing ion transport regulator 1; targeted mutation 1, Amy L Tucker|Fxyd1|MGI:3576231|7|Hypertrophy, increased ejection fraction, and reduced Na-K-ATPase activity|unknown|C57BL/6N|Yes|Yes|Yes|Yes|Unknown|Yes|No|Unknown||||No|04-Sep-2020|Cryopreserved sperm|50.0|0.0|Unknown||Hypertrophy, Ejection fraction, Phospholemman, Ion channel, Na-K-ATPase|Possibly| 8582.0|ASD874:Whopper:F0|C57BL/6NCrlAnu-Irf7/AnuApb||Recessive|interferon regulatory factor 7|Irf7|Unknown||MGI:1859212|Irf7, endonuclease-mediated mutation 1, Australian National University |Irf7||7||||||||||Unknown to Unknown|||||||||||||||||||Normal |Normal|C57BL/6NCrlAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|03-Oct-2018|Cryopreserved sperm|55.0|0.0|Unknown|||Yes| 8558.0|ASD891:Sorghum|C57BL/6NCrlAnu-Nlrp9a/AnuApb||Recessive|NLR family, pyrin domain containing 9A|Nlrp9a|Unknown|D7Ertd565e, Nalp9a, Nalp-theta|MGI:2675292|Nlrp9a, endonuclease-mediated mutation 1, Australian National University |Nlrp9a||7||||||||||Unknown to Unknown|||||||||||||||||||Normal|Normal|C57BL/6NCrlAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|13-Sep-2018|Cryopreserved sperm|11.0|0.0|Unknown|||Yes| 9072.0||ENU49:115:Nlrp3||Semi-dominant|Unknown||||||||Unknown|||||||||||||||||||||||||||||Normal|Normal|C57BL/6NCrlAnu|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|04-Sep-2020|Cryopreserved sperm|12.0|0.0|Unknown|||Possibly| 4508.0|ENU7B6:071|C57BL/6JAnu-Ltb/AnuApb||Recessive|lymphotoxin B|Ltb||LTbeta, lymphotoxin beta, p33, Tnfc, Tnfsf3|MGI:104796||Ltb||17|ENSMUSG00000024399|ENSMUST00000025262|Ltb-001|623|706|G to A|ENSMUSE00000930622|3|208|Arginine to Lysine|||||CTATTACCTCTACTGCCACGTCGGGTACAGGGGCAGGACGCCCCCTGCCGGCCGAAGCCGT|Yes|||||||||||||Defective antibody response to immunization: failure to mount a normal Th1 polarized IgG2c antibody response to heat killed B pertussis bacteria. |||Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|26-Feb-2009|Cryopreserved sperm|83.0|0.0|Unknown||B cell, antibody, immunization, ENU, Wellcome Trust|Yes| 8223.0|Enu32:025:Tmem2|C57BL/6NCrlAnu-Cemip2/AnuApb||Recessive|cell migration inducing hyaluronidase 2|Cemip2|Unknown|3110012M15Rik, mKIAA1412, Tmem2|MGI:1890373|mutation 1, Australian National University|Cemip2||19|ENSMUSG00000024754|ENSMUST00000096194.8|Tmem2-202||||||||21811978|9|||TCACCGTGCACGGGACCAGTGGCTTGCTAGTAAGTAGCCTCACCTTGTGTTGACATGCAG||||||||||||||Embryonic lethal. Embryos die before E14.|Unknown|C57BL/6NCrlAnu|No|No|Yes|No|No|Yes|No|Unknown||||No|21-Mar-2017|Cryopreserved sperm|33.0|0.0|Unknown||embryonic lethal|Yes| 7855.0|ENU31:049|C57BL/6NCrlANu-Blnk/AnuApb||Recessive|B cell linker|Blnk|Unknown|BASH, Bca, BCA, BLNK, Ly57, Ly-57, SLP-65|MGI:96878|mutation 1, Australian National University|Blnk||19|ENSMUSG00000061132|ENSMUST00000054769|Blnk-001|1197|1674|A to G|ENSMUSE00000519585|16|399|Valine to Alanine|||||||||||||||||||High IgM expression on mature B cells||C57BL/6NCrlAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|05-Mar-2015|Cryopreserved sperm|55.0|0.0|Unknown||B cell, IgM|Yes| 7371.0|ENU26:044:G6pc:B6:G2|C57BL/6NCrlAnu-G6pc/AnuApb||Recessive|glucose-6-phosphatase, catalytic|G6pc|Unknown|G6Pase, G6pt, Glc-6-Pase, Glc-6-Pase-alpha|MGI:95607|mutation 1, The Australian National University|G6pc||11|ENSMUSG00000078650|ENSMUST00000019469|G6pc-001|248|484|G to T|ENSMUSE00000113003|2|83|Arginine to Leucine|||||CGTCTTCAAGTGGATTCTGTTTGGACAACGCCCGTATTGGTGGGTCCTGGACACCGACTAC||||||||||||||Unknown||C57BL/6NCrlAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|05-Jul-2013|Cryopreserved sperm|55.0|0.0|Unknown||ENU|Yes| 7734.0|ENU24:043 - CD4|C57BL/6NCrlAnu-Cd4/AnuApb||Recessive|CD4 antigen|Cd4||L3T4, Ly-4|MGI:88335|mutation 1, Australian National University|Cd4||6|||||||||||||||||||||||||||||defective upregulation of CD4 expression during T cell development||C57BL/6NCrlAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|05-Sep-2014|Cryopreserved sperm|52.0|0.0|Unknown|||Yes| 7854.0|ENU27:041:Card11|C57BL/6NCrlAnu-Card11/AnuApb||Recessive|caspase recruitment domain family, member 1|Card11|Unknown|0610008L17Rik, 2410011D02Rik, BIMP3, CARMA1|MGI:1916978|mutation 1, Australian National University|Card11||5|ENSMUSG00000036526|ENSMUST00000085786|Card11-201|1093|1414|A to T|ENSMUSE00000431469|8|365|Methionine to Lysine|||||GGAAGGACTGTGAAATGTACAAGCACCGCATGAACACAGTTATGCTGCAGCTGGAGGAGGT||||||||||||||Unknown||C57BL/6NCrlAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|05-Mar-2015|Cryopreserved sperm|33.0|0.0|Unknown||ENU|Possibly| 10448.0|Ubf1 KO bp1|C57BL/6NCrlAnu-Ubtf/ANU||Recessive|upstream binding transcription factor, RNA polymerase I|Ubtf ||Tcfubf, UBF, UBF1|MGI:98512|Ubtf|Ubf1 Ko||11|ENSMUSG00000020923||||||||||||||||||||||||||||Embryonic lethal|Normal|C57Bl/6N|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|06-Sep-2024|Cryopreserved sperm|48.0|0.0|Unknown|||No| 8681.0|Dicer del|B6.129-Dicer1/WehiAnuApb||Recessive|dicer 1, ribonuclease type III|Dicer1|||MGI:2177178|dicer 1, ribonuclease type III; targeted mutation 1.1, Brian D Harfe|Dicer1|MGI:3589209|12|||||||||||||||||||||||||||||Embryonic growth arrest:• homozygous embryos arrest at E7.5||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|29-Mar-2019|Cryopreserved sperm|53.0|0.0|Unknown||microRNA|Yes| 8717.0|Pfn1 KO|BALB/c-Pfr1/SdzApb||Recessive|perforin 1 (pore forming protein)|Prf1|Nil|perforin, Pfn, Pfp, Prf-1|MGI:97551|perforin 1 (pore forming protein); targeted mutation 1, Sandoz Pharmaceuticals|Prf1|MGI:1857235|10|||||||||||||||||||||||||||||These mice breed and develop normally. Loss of this gene has no significant effect on the immune function of these mice.There is a high susceptibility to ectromelia virus. Aged mice are susceptible to tumour growth.|Normal|BALB/c (H-2Kd)|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|21-May-2019|Cryopreserved sperm|50.0|0.0|Unknown||T cell, CD8|Yes| 318.0||BALB/c-Prf1||Recessive|perforin 1 (pore forming protein)|Prf1|Nil|perforin, Pfn, Pfp, Prf-1|MGI:97551|targeted mutation 1, Sandoz Pharmaceutical|Prf1|MGI:1857235|10||||||||||||||||No|||||||||||||Homozygous null mice exhibit increased susceptibility to viral infection and defective cytotoxic T cell cytolysis and NK cell cytolysis.||BALB/c|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|04-May-2006||0.0|0.0|Unknown||cytotoxic T cell, CD8, Natural Killer cell, cytolysis, infection|Yes| 142.0|Plexin B2|STOCK Plxnb2/AnuApb||Recessive|plexin B2|Plxnb2|Unknown|Debt|MGI:2154239|plexin B2; targeted mutation 1, Marc Tessier-Lavigne|Plxnb2|MGI:3620317|15||||||||||||||||Yes|||||||||||||Homozygotes for a targeted mutation of this gene die perinatally of exencephaly or survive and seem normal despite severe abnormalities in cerebellar layering and foliation; the external granule cell layer is disorganized due to continued proliferation and migration of differentiated granule cells. Survivors among mutant mice of a mixed, partly (outbred) CD-1 background behave normally and even breed, although their cerebellar architecture is severly disrupted.||CD1|Yes|No|Yes|Yes|No|Yes|No|Good||||No|06-Feb-2006|Cryopreserved sperm|105.0|0.0|No||Cerebellar granule cells, Pukinje, transmembrane receptor, differentiation, progenitor|Yes| 8706.0|Pedro:PR36 SJ|C57BL/6-Prdm1/AnuApb||Recessive|PR domain containing 1, with ZNF domain|Prdm1|Unknown|b2b1765Clo, Blimp1, Blimp-1, PRDI-BF1|MGI:99655|Prdm1, endonuclease-mediated mutation 3, Australian National University|Prdm1||10||||||||||Unknown to Unknown|||||||||||||||||||Normal|Normal|C57BL/6NCrlAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|03-May-2019|Cryopreserved sperm|36.0|0.0|Unknown|||Yes| 8566.0|ASD949:PKR big del:EIF2AK2|C57BL/6NCrlAnu-Eif2ak2/AnuApb||Recessive|eukaryotic translation initiation factor 2-alpha kinase 2|Eif2ak2|Unknown|2310047A08Rik, 4732414G15Rik, dsRNA-activated kinase, eIF-2 alpha, eIF-2 alpha, IFN-induced and double-stranded RNA-activated kinase, IFN- type I-induced and dsRNA-activated kinase, Pkr, Prkr, Tik|MGI:1353449|Eif2ak2, endonuclease-mediated mutation 2, Australian National University |Eif2ak2||17||||||||||Unknown to Unknown|||||||||||||||||||Normal|Normal|C57BL/6NCrlAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|21-Sep-2018|Cryopreserved sperm|53.0|0.0|Unknown|||Yes| 8579.0|Tweak KO/C57BL/6 |C57BL/6-Tnfsf12/Apb||Recessive|tumor necrosis factor (ligand) superfamily, member 12|Tnfsf12||APO3L, DR3L, Tweak|MGI:1196259||||11|||||||||||||||||||||||||||||Normal|Normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|02-Oct-2018|Cryopreserved sperm|50.0|0.0|Unknown|||Yes| 9174.0|ASD1112:Gsto2:F0 KO|C57Bl/6N-Gsto2/A[b||Semi-dominant|glutathione S-transferase omega 2|Gsto2|||MGI:1915464||||19|||||||||||||||||||||||||||||male #4|unknown|C57Bl/6NCrl|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|08-Apr-2021|Cryopreserved sperm|12.0|0.0|Unknown|||Possibly| 7733.0|Prox1-GFP|STOCK Tg(Prox1-EGFP)KY221Gsat/AnuApb||Dominant||||||||||||||||||||||||||transgene insertion KY221, GENSAT Project at Rockefeller University|Prox1|||||||||||Unknown|||Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|05-Sep-2014|Cryopreserved sperm|54.0|0.0|Unknown|||Yes| 10449.0|TANZ|C57BL/6-Tspan2||Semi-dominant|tetraspanin 2|Tspan2|||MGI:1917997|tetraspanin 2; targeted mutation 1, Hauke B Werner|Tspan2|MGI:5556057|3|ENSMUSG00000027858 ||||||||||||||||||||||||||||Normal|Normal|C57Bl/6J|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|09-Sep-2024||0.0|0.0|Unknown|||No| 8134.0|ROSA-Cas9|B6J.129(B6N)-Gt(ROSA)26Sor/J||Dominant|gene trap ROSA 26, Philippe Soriano|Gt(ROSA)26Sor|Normal|beta geo, Gtrgeo26, Gtrosa26, R26, ROSA26, Thumpd3as1|MGI:104735|gene trap ROSA 26, Philippe Soriano; targeted mutation 1.1, Feng Zhang|Gt(ROSA)26Sor|MGI:5583838|6|||||||||||||||||||||||||||||Normal||C57BL/6J|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|15-Nov-2016|Cryopreserved sperm|59.0|0.0|Unknown||CRISPR, Cas9|Yes| 9052.0|cCblA/+|C57BL/6 x 129SvJ-Cbl/APB||Recessive|Casitas B-lineage lymphoma|Cbl |Normal|4732447J05Rik, Cbl-2, c-Cbl|MGI:88279|Casitas B-lineage lymphoma; targeted mutation 2, Wallace Y Langdon|Cbl|MGI:3610727|9|||||||||||||||||||||||||||||A point mutation resulted in a cysteine to alanine substitution at position 379 (C379A). Western blot showed that protein levels in thymocytes were not affected by the mutation.Homozygous rarely viable|Heterozygous animals develop myeloproliferative disease (exacerbated by cross to null allele)|C57Bl/6 x 129SvJ|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|06-Aug-2020|Cryopreserved sperm|40.0|0.0|Unknown||T-cell receptor, c-Cbl, Thymus, p85, PI 3-kinase|No| 8526.0|Cas9_Cre|B6.Cg-Gt(ROSA)26Sor Tg(CMV-cre)1Cgn/Anu||Dominant|gene trap ROSA 26, Philippe Soriano|Gt(ROSA)26Sor|Normal|beta geo, Gtrgeo26, Gtrosa26, R26, ROSA26, Thumpd3as1|MGI:104735|gene trap ROSA 26, Philippe Soriano; targeted mutation 1.1, Feng Zhang|Gt(ROSA)26Sor|MGI:5583838|6|||||||||||||||||transgene insertion 1, University of Cologne|human cytomegalovirus (CMV) promoter|||||||||||Express Cas9 protein and CMV-cre||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|26-Jun-2018||0.0|0.0|Unknown||CRISPR, Cas9, CMV-cre|Yes| 9077.0|Rag1 KO:Charles|RAG:CharlesHom:B6||Dominant|.|.|||||||Unknown|||||||||||||||||||||||||||||unknown|unknown|.|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|10-Sep-2020||0.0|0.0|Unknown|||Possibly| 8735.0|ASD976:Gomez:2:N1|C57BL/6NCrlAnu-Ryr2/AnuApb||Recessive|ryanodine receptor 2, cardiac|Ryr2|Unknown|9330127I20Rik|MGI:99685|Ryr2, endonuclease-mediated mutation 3, Australian National University|Ryr2||13||||||||||Unknown to Unknown|||||||||||||||||||Normal|Normal|C57BL/6NCrlAnu|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|19-Jun-2019|Cryopreserved sperm|11.0|0.0|Unknown|||Yes| 9090.0||ASD538:Xander:B6||Dominant|only for L2 reder|only for L2 reder|||||||Unknown|||||||||||||||||||||||||||||.|.|B6|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|30-Oct-2020||0.0|0.0|Unknown|||Possibly| 9087.0|GABRB3.D120N|C57BL/6J-Gabrb3/Nathan Absalom||Semi-dominant|gamma-aminobutyric acid (GABA) A receptor, subunit beta 3|GABRB3|Unknown|A230092K12Rik, beta3, Gabrb-3|MGI:95621|endonuclease mediated targeting 1; Nathan Absalom|Gabrb3||7||||||||||Unknown to Unknown|||||||||||||||||||Unknown, likely lethal.|Febrile seizures, behavioural abnormalities expected|C57Bl/6J|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|23-Sep-2020||0.0|0.0|Unknown|||Possibly| 9040.0|FANCM-LoxP|C57BL/6-FancM/Apb||Recessive|Fanconi anemia complementation group M|FancM||C730036B14Rik, D12Ertd364e |MGI:2442306||||Unknown|||||||||||||||||||||||||||||Normal|Normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|10-Jul-2020|Cryopreserved sperm|50.0|0.0|Unknown||Fanconi anemia, chromosome fragility, breast cancer, ATPase|No| 9091.0||C57Bl/6N-ENU48:196:Tlr4||Semi-dominant|Tlr4||||||||Unknown|||||||||||||||||||||||||||||||C57BL/6NCrlAnu|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|03-Nov-2020|Cryopreserved sperm|55.0|0.0|Unknown|||Possibly| 9088.0|C1ra null|C57Bl/6J-C1ra/Apb||Recessive|Complement 1 receptor a|Cr1a|||MGI:1355313| C57BL/6J (C1ra)|||6|||||||||||||||||||||||||||||Normal|Normal|C57Bl/6J|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|08-Oct-2020|Cryopreserved sperm|40.0|0.0|Unknown|||Possibly| 8605.0|Cldn10 KO|C57BL/6-Cldn10/MarpApb||Recessive|claudin 10|Cldn10||6720456I16Rik, Cldn10a, Cldn10b, D14Ertd728e|MGI:1913101||||14|||||||||||||||||||||||||||||Embryonic lethal|Normal|C57BL/6|No|No|Yes|No|No|Yes|No|Unknown||||No|14-Nov-2018|Cryopreserved sperm|50.0|0.0|Unknown|||Yes| 8594.0|Katnal2 Y86C|C57BL/6-Katnal2/MarpApb||Recessive|katanin p60 subunit A-like 2|Katnal2||3110023G01Rik, 4933439B08Rik|MGI:1924234||Katnal2||18||||||||||Unknown to Unknown|||||||||||||||||||Male infertility |Normal|C57BL/6J|Yes|Yes|Yes|Yes|No|Yes|No|Unknown||||No|30-Oct-2018|Cryopreserved sperm|50.0|0.0|Unknown||infertility, sperm|Yes| 8613.0|ASD661:Pique:10|C57BL/6NCrlAnu-Zfr2/AnuApb||Recessive|zinc finger RNA binding protein 2|Zfr2|Unknown|2010013I23Rik, 9130206N08Rik|MGI:2143792|Zfr2, endonuclease-mediated mutation 1, Australian National University|Zfr2||10||||||||||Unknown to Unknown|||||||||||||||||||Unknown at this stage||C57BL/6NCrlAnu|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|Yes|Poor||||No|21-Nov-2018|Cryopreserved sperm|12.0|0.0|Unknown||CRISPR|Yes| 9092.0|Met-K|B10.BR-Met-H2-K/APB||Dominant|Major histocompatibility-2, MHC; b variant|H-2Kb|||MGI:3579319|histocompatibility 2, K region; b haplotype mutation 1|H2-K|MGI:3618114|17||||||||||Unknown to Unknown|||||||Major histocompatibility-2, MHC; b variant|sheep metallothionein promoter|||||||||||These transgenic mice have a normal phenotype but express a transgenic H-2Kb MHC I molecule in hepatocytes under the control of the sheep metallothionein promoter. These transgenic mice were originally bred onto a B10.BR background and have been bred for more than 10 generations onto an H-2Kbm1 background. |Same as homozygous mice |H-2Kbm1|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|03-Nov-2020|Cryopreserved sperm|50.0|0.0|Unknown|||Possibly| 9093.0|BALB/c-MstnD76A|BALB/c-Mstn/Apb||Semi-dominant|Mstn|||||myostatin; targeted mutation 2, Se-Jin Lee|Mstn|MGI:3778375|Unknown|||||||||||||||||||||||||||||Hyperplasia and hypertrophy of skeletal muscle.|Indistinguisable from Mstn wildtype mice of the same genetic background.|BALB/c|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|06-Nov-2020||0.0|0.0|Unknown|||Possibly| 9097.0|Mstn D76A|C57Bl/6-Mstn/Apb||Semi-dominant|Mstn|||||myostatin; targeted mutation 2, Se-Jin Lee|Mstn|MGI:3778375|1|||||||||||||||||||||||||||||Hyperplasia and hypertrophy of skeletal muscle.|Indistinguishable from Mstn wildtype mice of the same genetic background|C57Bl/6|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|06-Nov-2020|Cryopreserved sperm|50.0|0.0|Unknown|||Possibly| 9054.0|R26-LSL-Adar1p150|C57BL/6-Gt(ROSA)26Sor/CwaApb ||Recessive|gene trap ROSA 26, Philippe Soriano|Gt(ROSA)26Sor|Increased|beta geo, Gtrgeo26, Gtrosa26, R26, ROSA26, Thumpd3as1|MGI:104735||Gt(ROSA)26Sor||6|||||||||||||||||Adar1p150-ires-GFP|R26 endogenous|Moderate to low||||||||||normal - lox-stop-lox Adar1p150 only expressed after Cre|normal - lox-stop-lox Adar1p150 only expressed after Cre|C57Bl/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|Unknown||Unknown|No|06-Aug-2020|Cryopreserved sperm|40.0|0.0|Unknown||Adenosine Deaminase RNA specific, RNA , Dyschromatosis symmetrica hereditaria|No| 9094.0|BALB/c-MstnD76A|BALB/c-Mstn/AnuApb||Semi-dominant|myostatin|Mstn||Gdf8 |MGI:95691|myostatin; targeted mutation 2, Se-Jin Lee|Mstn|MGI:3778375|1|||||||||||||||||||||||||||||Hyperplasia and hypertrophy of skeletal muscle.|Indistinguisable from Mstn wildtype mice of the same genetic background.|Balb/cJ|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|06-Nov-2020||0.0|0.0|Unknown|||Possibly| 9096.0|Mstn D76A|BALB/c-MstnANUApb||Semi-dominant|myostatin|Mstn||Gdf8 |MGI:95691|myostatin; targeted mutation 2, Se-Jin Lee|Mstn||1|||||||||||||||||||||||||||||Hyperplasia and hypertrophy of skeletal muscle.|Indistinguisable from Mstn wildtype mice of the same genetic background.|BALB/c|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|06-Nov-2020|Cryopreserved sperm|50.0|0.0|Unknown||Muscle, Metabolism, Adipose tissue|Possibly| 9095.0|Mstn KO|C57Bl/6-MstnANUApb||Semi-dominant|myostatin|Mstn|Nil|Gdf8|MGI:95691|myostatin; targeted mutation 1, Se-Jin Lee|Mstn|http://www.informatics.jax.org/allele/MGI:2148177|1|||||||||||||||||||||||||||||Hypertrophy and hyperplasia of skeletal muscle.|Indistinguishable from Mstn wildtype mice on the same genetic background.|B6N.129|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|06-Nov-2020||0.0|0.0|Unknown||Adipose tissue, Metabolism, Muscle, Liver|Possibly| 8618.0|ASD696:Thunderbird:19del|C57BL/6NCrlAnu-Ifne/AnuApb||Recessive|interferon epsilon|Ifne|Unknown|Ifne1, Ifnt1|MGI:2667156|Ifne, endonuclease-mediated mutation 1, Australian National University|Ifne||4||||||||||Unknown to Unknown|||||||||||||||||||Unknown|Unknown|C57BL/6NCrlAnu|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|07-Dec-2018|Cryopreserved sperm|22.0|0.0|Unknown|||Yes| 8617.0|ASD869:IRAK2:S47Y|C57BL/6NCrlAnu-Irak2/AnuApb||Recessive|interleukin-1 receptor-associated kinase 2|Irak2|Unknown|6330415L08Rik, IRAK-2, Irak2a, Irak2b, Irak2c, Irak2d|MGI:2429603|Irak2, endonuclease-mediated mutation 1, Australian National University|Irak2||6||||||C to A||||Unknown to Unknown|||||||||||||||||||Unknown|Unknown|C57BL/6NCrlAnu|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|05-Dec-2018|Cryopreserved sperm|55.0|0.0|Unknown|||Yes| 9099.0|B10.BR|B10.BR-H2 H2-T18/SgSnJ||Semi-dominant|||||||||||||||||||||||||||||histocompatibility-2, MHC|H2||H2|MGI:95894|Histocompatibility-2, MHC; k2 variant|H2|MGI:4936842|17||||Yes|Yes|Unknown|Yes|Unknown|Yes|No|Unknown||||No|25-Nov-2020||0.0|216.0|Unknown||T cells, leukocyte cellularity, CD4, CD8|Possibly| 9099.0|B10.BR|B10.BR-H2 H2-T18/SgSnJ||Semi-dominant|||||||||||||||||||||||||||||histocompatibility 2, T region locus 18|H2-T18|||MGI:95950|Histocompatibility 2, T region locus 18; a variant|H2-T18|MGI:4820507|17||||Yes|Yes|Unknown|Yes|Unknown|Yes|No|Unknown||||No|25-Nov-2020||||Unknown||T cells, leukocyte cellularity, CD4, CD8|Possibly| 8623.0|Lats1 fl Lats2 fl K5-creERT2|STOCK Lats1 Lats2 Tg(KRT5-cre/ERT2)2Ipc||Recessive|large tumor suppressor|Lats1|||MGI:1333883|large tumor suppressor; targeted mutation 1.1, James F Martin|Lats1|MGI:5568586|10|||||||||||||||||transgene insertion 2, I Pierre Chambon|bovine KRT5|epidermal tissue||||||||||||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|18-Dec-2018||0.0|0.0|Unknown||Hippo, Yap|Yes| 8623.0|Lats1 fl Lats2 fl K5-creERT2|STOCK Lats1 Lats2 Tg(KRT5-cre/ERT2)2Ipc||Recessive|large tumor suppressor 2|Lats2|||MGI:1354386|large tumor suppressor 2; targeted mutation 1.1, James F Martin|Lats2|MGI:5568589|14|||||||||||||||||||||||||||||||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|18-Dec-2018||||Unknown||Hippo, Yap|Yes| 8624.0|Oleoyl-ACP H KO Line1|C57BL/6-Olah/1||Recessive|oleoyl-ACP hydrolase|Olah|Unknown|E230009B14Rik, Thedc1|MGI:2139018||||2|||||||||||||||||||||||||||||Normal|Normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|18-Dec-2018|Cryopreserved sperm|30.0|0.0|Unknown|||Yes| 8625.0|Oleoyl-ACP H KO Line4|C57BL/6-Olah/4||Recessive|oleoyl-ACP hydrolase|Olah|Unknown|E230009B14Rik, Thedc1|MGI:2139018||||2|||||||||||||||||||||||||||||Normal|Normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|18-Dec-2018|Cryopreserved sperm|30.0|0.0|Unknown|||Yes| 8626.0|Oleoyl-ACP H KO Line5|C57BL/6-Olah/5||Recessive|oleoyl-ACP hydrolase|Olah|Unknown|E230009B14Rik, Thedc1|MGI:2139018||||2|||||||||||||||||||||||||||||Normal|Normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|18-Dec-2018|Cryopreserved sperm|40.0|0.0|Unknown|||Yes| 8627.0|Oleoyl-ACP H KO Line6|C57BL/6-Olah/6||Recessive|oleoyl-ACP hydrolase|Olah|Unknown|E230009B14Rik, Thedc1|MGI:2139018||||2|||||||||||||||||||||||||||||Normal|Normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|18-Dec-2018|Cryopreserved sperm|50.0|0.0|Unknown|||Yes| 8628.0|Oleoyl-ACP H KO Line7|C57BL/6-Olah/7||Recessive|oleoyl-ACP hydrolase|Olah|Unknown|E230009B14Rik, Thedc1|MGI:2139018||||2|||||||||||||||||||||||||||||Normal|Normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|18-Dec-2018|Cryopreserved sperm|50.0|0.0|Unknown|||Yes| 8629.0|Oleoyl-ACP H KO Line10|C57BL/6-Olah/10||Recessive|oleoyl-ACP hydrolase|Olah|Unknown|E230009B14Rik, Thedc1|MGI:2139018||||2|||||||||||||||||||||||||||||Normal|Normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|18-Dec-2018|Cryopreserved sperm|50.0|0.0|Unknown|||Yes| 8630.0|LIMK2|C57BL/6-Link2||Recessive|LIM motif-containing protein kinase 2|Limk2|Reduced|A930024P04Rik, Limk2a, Limk2b, LIM kinase 2, whe|MGI:1197517||||11|||||||||||||||||||||||||||||Normal|Unknown|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|19-Dec-2018|Cryopreserved sperm|50.0|0.0|Unknown|||Yes| 9051.0|Stock No: 000664|C57BL/6J|MGI:3028467|Recessive||||||||||||||||||||||||||||||||||||||This strain is homozygous for Cdh23ahl, the age related hearing loss 1 mutation, which on this background results in progressive hearing loss with onset after 10 months of age.|C57BL/6J is the most widely used inbred strain. It is commonly used as a general purpose strain and background strain for the generation of congenics carrying both spontaneous and induced mutations. Although this strain is refractory to many tumors, it is a permissive background for maximal expression of most mutations. C57BL/6J mice are used in a wide variety of research areas including cardiovascular biology, developmental biology, diabetes and obesity, genetics, immunology, neurobiology, and sensorineural research. C57BL/6J mice are also commonly used in the production of transgenic mice. Overall, C57BL/6J mice breed well, are long-lived, and have a low susceptibility to tumors. Primitive hematopoietic stem cells from C57BL/6J mice show greatly delayed senescence relative to BALB/c and DBA/2J. This is a dominant trait. Other characteristics include: 1) a high susceptibility to diet-induced obesity, type 2 diabetes, and atherosclerosis; 2) a high incidence of microphthalmia and other associated eye abnormalities; 3) resistance to audiogenic seizures; 4) low bone density; 5) hereditary hydrocephalus (early reports indicate 1 - 4 %); 6) portosystemic shunts (~5%); 7) hairloss associated with overgrooming; 8) a preference for alcohol and morphine; 9) late-onset hearing loss; and 10) increased incidence of hydrocephalus and malocclusion.C57BL/6J mice fed a high-fat diet develop obesity, mild to moderate hyperglycemia, and hyperinsulinemia (see JAX® Diet-induced Obesity (DIO) Models). C57BL/6J mice fed an atherogenic diet (1.25% cholesterol, 0.5% cholic acid and 15% fat) for 14 weeks develop lesions in the range of 4500 to 8000 um2 atherosclerotic aortic lesions/aortic cross-section. The variation in aortic lesions found among various inbred strains has led to the identification of the existence of eight genes affecting atherosclerosis, Ath1 to Ath8. C57BL/6J mice also develop severe and progressive hearing loss later in life, with the disruption of both outer and inner hair cells, due to the Cdh23Ahl allele. Cheers and McKenzie found C57BL/6J resistant to listeriosis. A naturally occurring deletion in nicotinamide nucleotide transhydrogenase (Nnt) exons 7-11 occurred in C57BL/6J sometime prior to 1984. This deletion results in the absence of the NNT protein, and is associated with impaired glucose homeostasis control and reduced insulin secretion. This mutation is not found in C57BL/6JEi, C57BL/6N, C57BL/6NJ, C57BL/6ByJ, C57BL/10J, C57L/J, or C58/J (Toye AA, et al, Diabetologia, 2005). Since C57BL/6JEi separated from C57BL/6J in 1976, the Nnt deletion arose sometime between 1976 and 1984. Because of the n-Tr20m1J point mutation, which is also present in C57BL/6JEiJ but not C57BL/6NJ or C57BL/6ByJ, extracts from the cerebellum of C57BL/6J mice have increased ribosomal pausing at AGA codons compared with that of other inbred strains (Ishimura et al., 2014). Additionally, an intronic point deletion in Gabra2, which arose sometime between the early 1970's and 1990's, results in decreased transcript and protein expression of this chloride channel component in the brain.C57BL/6J was the DNA source for the international collaboration that generated the first high quality draft sequence of the mouse genome. 5 SNP differences have been identified that distinguish C57BL/6J from C57BL/6ByJ and C57BL/6NJ. Both C57BL/6ByJ and C57BL/6NJ type as follows: 08-015199792-M (rs3709624) is C; 11-004367508-M (rs3659787) is A; 13-041017317-M (rs3722313) is C; 15-057561875-M (rs3702158) is G; 19-049914266-M (rs3724876) is T. C57BL/6J types as follows: 08-015199792-M (rs3709624) is T; 11-004367508-M (rs3659787) is G; 13-041017317-M (rs3722313) is T; 15-057561875-M (rs3702158) is A; 19-049914266-M (rs3724876) is G (Petkov and Wiles, 2004.) Others have subsequently identified further SNP differences between sublines of C57BL/6 (Mekada et al., 2009, Zurita et al., 2010). |C57BL/6J |Yes|Yes|Yes|Yes|Yes|Yes|No|Excellent|35|||No|05-Aug-2020|Embryo|0.0|1601.0|No||C57BL/6J, 000664, Wild type|Yes| 9107.0|Adidas:indel11|C57Bl/6N-Nfkb2/Apf||Semi-dominant|nuclear factor of kappa light polypeptide gene enhancer in B cells 2, p49/p100|Nfkb2|||MGI:1099800||||19|||||||||||||||||||||||||||||Mice develop organ-specific autoimmune disease due to poor T cell selection in the thymus. Mice lose body weight and become unwell between 150 and 200 days old due to major pancreatitis. Homozygous females struggle to feed their pups and so do not maintain litters well.|Heterozygous mice have a mild autoimmune disease phenotype.|C57BL/6|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|04-Dec-2020|Cryopreserved sperm|55.0|0.0|Unknown|||Possibly| 8612.0|ENU41:076:Gsdmd|C57BL/6NCrlAnu-Gsdmd/AnuApb||Recessive|gasdermin D|Gsdmd|Unknown|1810036L03Rik, DF5L, Dfna5l, Gsdmdc1, M2-4|MGI:1916396|Gsdmd; mutation 2, Australian National University|Gsdmd||15||||||||||Unknown to Unknown||||||Unknown|||||||||||||Unknown|Unknown|C57BL/6NCrlAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||1||No|21-Nov-2018|Cryopreserved sperm|60.0|0.0|Unknown||ENU, random, mutagenesis, screen|Yes| 9103.0|ENU29:Areg|C57BL/6NCrlAnu-Areg/AnuApb||Recessive|Amphiregulin|Areg|Unknown|AR, Mcub, Sdgf |MGI:88068|Areg; mutation 2, Australian National University|Areg||5||||||||||Unknown to Unknown|||||||||||||||||||Unknown|Unknown|C57BL/6NCrlAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||1||No|03-Dec-2020||0.0|0.0|Unknown||ENU, Mutagenesis, Mammary Glad|Yes| 9105.0|Adidas|C57BL/6NcrlAnu-Nfkb2/Apb||Semi-dominant|nuclear factor of kappa light polypeptide gene enhancer in B cells 2, p49/p100|Nfkb2|||MGI:1099800|D865G|||19|||||||||||||||||||||||||||||Mice develop organ-specific autoimmune disease due to poor T cell selection in the thymus. Inflammation is present in the pancreas, lung and liver. Mice lose body weight and become unwell between 150 and 200 days old due to major pancreatitis. Homozygous females struggle to feed their pups and so do not maintain litters well.|Heterozygous mice have a mild autoimmune disease phenotype.|C57BL/6|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|04-Dec-2020||0.0|0.0|Unknown|||Possibly| 9106.0|Adidas:indel07|C57BL/6NCrlAnu-Nfkb2/Apb||Semi-dominant|nuclear factor of kappa light polypeptide gene enhancer in B cells 2, p49/p100|Nfkb2|||MGI:1099800|S866fs|||19|||||||||||||||||||||||||||||Homozygous mice are healthy.|Heterozygous mice are healthy.|C57Bl/6N|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|04-Dec-2020|Cryopreserved sperm|33.0|0.0|Unknown|||Possibly| 9110.0|Adidas:PM:Foca|Adidas:PM:Foca||Semi-dominant|Nfkb2 and TCRa|||||Nfkb2 - D865G, and TCRa - knockout|||Unknown|||||||||||||||||||||||||||||Normal|Normal|C57BL/6|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|04-Dec-2020|Cryopreserved sperm|33.0|0.0|Unknown|||Yes| 9108.0|Adidas:PM:Xander|B6(Cg)-Nfkb2 Nfkb2/AnuApb||Recessive|nuclear factor of kappa light polypeptide gene enhancer in B cells 2, p49/p100|Nfkb2|||MGI:1099800|D865G/Xdr|||Unknown|||||||||||||||||||||||||||||This strain produces compound heterozygotes who carry one copy of Nfkb2-D865G and one copy of Nfkb2-Xander. Mice develop organ-specific autoimmune disease due to poor T cell selection in the thymus. Mice lose body weight and become unwell after 250 days old due to major pancreatitis. |Xander heterozgyotes are normal.D865G heterozygotes have mild autoimmune disease.|C57BL/6|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|04-Dec-2020||0.0|0.0|Unknown|||Possibly| 9109.0|Adidas:indel56|C57BL/6NCrlAnu-Nfkb2/AnuApb||Semi-dominant|nuclear factor of kappa light polypeptide gene enhancer in B cells 2, p49/p100|Nfkb2|||MGI:1099800|V862fs|||Unknown|||||||||||||||||||||||||||||Normal|Normal|C57BL/6NAnu|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|04-Dec-2020|Cryopreserved sperm|33.0|0.0|Unknown|||Possibly| 9112.0|Leptin Receptor fl/fl LysMCre|B6.129P2-LeprLyz2/JAusbAnuApb ||Semi-dominant|Leptin receptor; targeted mutation 1.1 Streamson C Chua, Jr|Lepr|Reduced|Leprb, LEPROT, leptin receptor gene-related protein, Modb1, obese-like, obl, Obr, OB-RGRP |MGI:104993 |Leptin receptor; targeted mutation 1.1 Streamson C Chua, Jr|Lepr|MGI:3511284|4|||||||||||||||||||||||||||||Normal|Normal|C57BL/6J|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|11-Dec-2020|Cryopreserved sperm|50.0|0.0|Unknown||Immune response, leptin receptor, Signalling|Possibly| 9112.0|Leptin Receptor fl/fl LysMCre|B6.129P2-LeprLyz2/JAusbAnuApb ||Semi-dominant|Lysozyme 2|Lyz2 ||Lys, Lysm, Lyzs, Lzm, Lzm-s1, Lzp |MGI:96897|Lysozyme 2; targeted mutation 1, Irmgard Forster|Lyz2|MGI:1934631|10|||||||||||||||||||||||||||||Normal|Normal|C57BL/6J|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|11-Dec-2020|Cryopreserved sperm|||Unknown||Immune response, leptin receptor, Signalling|Possibly| 8635.0||Fut 7 KO line 2||Semi-dominant|Fut 7 |Fut 7|||||||Unknown|||||||||||||||||||||||||||||Normal|Normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|15-Jan-2019||0.0|0.0|Unknown|||Yes| 8647.0||ENU43:345:Casp1||Recessive|Casp1||||||||Unknown|||||||||||||||||||||||||||||||C57BL/6NCrlAnu|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|25-Jan-2019|Cryopreserved sperm|44.0|0.0|Unknown|||Yes| 8650.0|Casp1 C284A|C57BL/6-Casp1/Anu||Recessive|caspase 1|Casp1|Unknown|Caspase-1, ICE, Il1bc, interleukin 1 beta-converting enzyme|MGI:96544||||9|||||||||||||||||||||||||||||Unknown||C57BL/6|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|01-Feb-2019||0.0|0.0|Unknown|||Yes| 9102.0|C57Bl/6-Mstn-/-|B6N.129-Mstn||Recessive|Myostatin|Mstn|Reduced|Gdf8|MGI:95691|Mstn||MGI:3790519|1||||||||||||||||||||Myostatin|Mstn ||Gdf8 |95691||||1|Hyperplasia and hypertrophy of muscle tissues.|Mild hyperplasia and hypertrophy of muscle tissues.|C57Bl/6|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|26-Nov-2020|Cryopreserved sperm|50.0|0.0|Unknown|||Possibly| 9098.0|CD8 Cre|Tg(ECD-CACG-Cre)||Semi-dominant|CD8 Cre||||||||Unknown|||||||||||||||||CD8 Cre|CAGG|Unknown||||||||||Normal|Normal|C57Bl/6|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|12-Nov-2020|Cryopreserved sperm|50.0|0.0|Unknown|||Possibly| 8642.0|WHIP.Ly5.1|C57BL/6-Tg(TcraHsv,TcrabHsv)/Cbn||Dominant||||||||||||||||||||||||||transgene insertion||||||||||||Normal; Majority of CD4 T cells are specific for gD peptide 290-302 from HSV-1.|Normal |C57BL/6 |Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|23-Jan-2019|Cryopreserved sperm|50.0|0.0|Unknown||T cell, HSV|Yes| 8645.0|p60 KO|C57BL/6N-Katna1/MarpApb||Recessive|katanin p60 (ATPase-containing) subunit A1|Katna1|Nil|http://www.informatics.jax.org/marker/MGI:1344353|MGI:1344353|katanin p60 subunit A-like 2; targeted mutation 1a, Wellcome Trust Sanger Institute|Katna1|MGI:4458514|10|||||||||||||||||||||||||||||Embryonic lethal|Normal|C57BL/6N|No|No|Yes|No|No|Yes|No|Unknown||||No|24-Jan-2019|Cryopreserved sperm|50.0|0.0|Unknown|||Yes| 9111.0|ASD538:Nfkb2:Kenobi|C57BL/6JSfdAnu-Nfkb2/AnuApb ||Semi-dominant|Nuclear factor of kappa light polypeptide gene enhancer in B cells 2, p49/p100|Nfkb2||NF kappaB2, p52 |MGI:1099800 |Nuclear factor of kappa light polypeptide gene enhancer in B cells 2, p49/p100|Nfkb2||19|||||||||||||||||||||||||||||Immune deficiency. Hypogammaglobulinemia. Absolutely no B cells or pre-B cells due to kenobi mutation.D865G mutation confers autoimmune disease.Mice develop organ-specific autoimmune disease due to poor T cell selection in the thymus. Mice lose body weight and become unwell between 150 and 200 days old due to major pancreatitis. Homozygous females struggle to feed their pups and so do not maintain litters well.|Heterozygous mice have a mild autoimmune disease phenotype.|C57BL/6|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|04-Dec-2020|Cryopreserved sperm|33.0|0.0|Unknown||B Cells, Plasma cells|Possibly| 9111.0|ASD538:Nfkb2:Kenobi|C57BL/6JSfdAnu-Nfkb2/AnuApb ||Semi-dominant|CD79A antigen (immunoglobulin-associated alpha)|Cd79a ||Cd79a, Ig alpha, Ig-alpha, Iga, Ly54, mb-1 |MGI:101774 |CD79A antigen (immunoglobulin-associated alpha); mutation 1, The Australian National University |Cd79|MGI:5006856 |7|||||||||||||||||||||||||||||Immune deficiency. Hypogammaglobulinemia. Absolutely no B cells or pre-B cells due to kenobi mutation.D865G mutation confers autoimmune disease.Mice develop organ-specific autoimmune disease due to poor T cell selection in the thymus. Mice lose body weight and become unwell between 150 and 200 days old due to major pancreatitis. Homozygous females struggle to feed their pups and so do not maintain litters well.|Heterozygous mice have a mild autoimmune disease phenotype.|C57BL/6|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|04-Dec-2020|Cryopreserved sperm|||Unknown||B Cells, Plasma cells|Possibly| 8644.0|p60 flox|C57BL/6N-Katna1/MarpApb||Recessive|katanin p60 (ATPase-containing) subunit A1|Katna1|Nil||MGI:1344353|katanin p60 (ATPase-containing) subunit A1; targeted mutation 1c, Wellcome Trust Sanger Institute|Katna1||10||||||||||Unknown to Unknown|||||||||||||||||||Normal|Normal|C57BL/6N|No|No|Yes|No|No|Yes|No|Unknown||||No|24-Jan-2019|Cryopreserved sperm|50.0|0.0|Unknown||Spermatogenesis|Yes| 8652.0|PKHD1 KO|C57BL/6-Pkhd1/SmyMarp||Recessive|polycystic kidney and hepatic disease 1|Pkhd1||FPC, tigmin|MGI:2155808||||1|||||||||||||||||||||||||||||unknown|Normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|05-Feb-2019|Cryopreserved sperm|50.0|0.0|Unknown|||Yes| 9114.0|BTAT1|C57BL/6J-Slc16a10/AnuApb||Recessive|solute carrier family 16 (monocarboxylic acid transporters), member 10|Slc16a10|Unknown|2610103N14Rik, Mct10, PRO0813, TAT1|MGI:1919722|Slc16a10|Slc16a10||10|||||||||||||||||||||||||||||Unknown|Unknown|C57Bl/6J|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|||homozygous x homozygous or heterozygous x heterozygous|No|06-Jan-2021|Cryopreserved sperm|50.0|0.0|Unknown||amino acid transport|Possibly| 8656.0|LMR|B6.Cg-Msh2 Rag1 Tg(IgkHyHEL10)1Rbr/Cjo||Recessive|mutS homolog 2|Msh2|||MGI:101816||||17|||||||||||||||||transgene insertion 1, Robert Brink||||||||||||||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|15-Feb-2019|Cryopreserved sperm|50.0|0.0|Unknown|||Yes| 8656.0|LMR|B6.Cg-Msh2 Rag1 Tg(IgkHyHEL10)1Rbr/Cjo||Recessive|recombination activating gene 1|Rag1||Rag-1|MGI:97848|recombination activating gene 1; targeted mutation 1, David Baltimore|Rag1|MGI:2448994|2|||||||||||||||||||||||||||||||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|15-Feb-2019|Cryopreserved sperm|||Unknown|||Yes| 8658.0|S25HR|B6(Cg)-Igh Rag1 Samhd1/Cjo||Recessive|immunoglobulin heavy chain complex|Igh|||MGI:96442|immunoglobulin heavy chain complex; targeted mutation 1, Robert Brink|Igh|MGI:3800383|12|||||||||||||||||||||||||||||Unknown||C57BL/6JAusb|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|15-Feb-2019|Cryopreserved sperm|50.0|0.0|Unknown|||Yes| 8658.0|S25HR|B6(Cg)-Igh Rag1 Samhd1/Cjo||Recessive|recombination activating gene 1|Rag1||Rag-1|MGI:97848|recombination activating gene 1; targeted mutation 1, Peter Mombaerts|Rag1|MGI:1857241|2|||||||||||||||||||||||||||||Unknown||C57BL/6JAusb|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|15-Feb-2019|Cryopreserved sperm|||Unknown|||Yes| 8658.0|S25HR|B6(Cg)-Igh Rag1 Samhd1/Cjo||Recessive|SAM domain and HD domain, 1|Samhd1||E330031J07Rik|MGI:1927468||||2|||||||||||||||||||||||||||||Unknown||C57BL/6JAusb|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|15-Feb-2019|Cryopreserved sperm|||Unknown|||Yes| 8659.0|S41LR|B6(Cg)-Rag1 Samhd1 Tg(IgkHyHEL10)1Rbr/Cjo||Recessive|recombination activating gene 1|Rag1||Rag-1|MGI:97848|recombination activating gene 1; targeted mutation 1, Peter Mombaerts|Rag1|MGI:1857241|2|||||||||||||||||transgene insertion 1, Robert Brink||||||||||||Unknown||C57BL/6JAusb|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|15-Feb-2019|Cryopreserved sperm|50.0|0.0|Unknown|||Yes| 8659.0|S41LR|B6(Cg)-Rag1 Samhd1 Tg(IgkHyHEL10)1Rbr/Cjo||Recessive|SAM domain and HD domain, 1|Samhd1||E330031J07Rik|MGI:1927468||||2|||||||||||||||||||||||||||||Unknown||C57BL/6JAusb|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|15-Feb-2019|Cryopreserved sperm|||Unknown|||Yes| 9116.0|Myl9 fl/fl|C57Bl/6-Myl9/AnuApb||Semi-dominant|myosin, light polypeptide 9, regulatory|Myl9|||MGI:2138915|myosin, light polypeptide 9, regulatory; targeted mutation 1c, Wellcome Trust Sanger Institute|Myl9||2||||||||||Unknown to Unknown|||||||||||||||||||Wildtype|Wildtype|C57BL/6|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|11-Jan-2021|Cryopreserved sperm|50.0|0.0|Unknown|||Possibly| 9121.0|Adh5-54|C57BL/6J-Adh5/Apb||Semi-dominant|alcohol dehydrogenase 5 (class III), chi polypeptide|Adh5|||MGI:87929||||3|||||||||||||||||||||||||||||Susceptible to endotoxic shock and low blood pressure under anaesthesia.|Normal|C57Bl/6J|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|19-Jan-2021||0.0|0.0|Unknown|||Possibly| 9117.0|Coro2a|C57BL/6-Coro2a||Semi-dominant|coronin, actin binding protein 2A|Coro2a||9030208C03Rik, coronin 4, IR10 |MGI:1345966|coronin, actin binding protein 2A; targeted mutation 1, Wellcome Trust Sanger Institute|Coro2a|MGI:4364905|4||||||||||Unknown to Unknown|||||||||||||||||||Minor alterations in T cell development, but essentially wildtype|Wildtype|C57BL/6|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|11-Jan-2021|Cryopreserved sperm|50.0|0.0|Unknown|||Possibly| 9120.0|Adh5-54|C57Bl/6-Adh5/Apb||Semi-dominant|alcohol dehydrogenase 5 (class III), chi polypeptide|Adh5|||MGI:87929||||3|||||||||||||||||||||||||||||Susceptible to endotoxic shock and low blood pressure under anaesthesia.|Normal|C57Bl/6J|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|19-Jan-2021|Cryopreserved sperm|50.0|0.0|Unknown|||Possibly| 8633.0|Katnal2 Flox|C57BL/6N-Katnal2/MarpApb||Recessive|katanin p60 subunit A-like 2|Katnal2||3110023G01Rik, 4933439B08Rik|MGI:1924234|katanin p60 subunit A-like 2; targeted mutation 1c, Wellcome Trust Sanger Institute|Katnal2|MGI:6164199|18|||||||||||||||||||||||||||||Normal|Normal|C57/BL6N|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|10-Jan-2019|Cryopreserved sperm|50.0|0.0|Unknown||spermatogenesis|Yes| 8657.0|P18.B6|C57BL/6JAusb-Ipo4/Cjo||Recessive|importin 4|Ipo4||8430408O15Rik|MGI:1923001||||14|||||||||||||||||||||||||||||Unknown||C57BL/6JAusb|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|15-Feb-2019|Cryopreserved sperm|50.0|0.0|Unknown|||Yes| 8653.0|HRGKO|C57BL/6-Hrg||Recessive|histidine-rich glycoprotein|Hrg|Nil|D16JH2, D18020|MGI:2146636|HRG|||16|||||||||||||||||||||||||||||Normal|Normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|08-Feb-2019|Cryopreserved sperm|50.0|0.0|Unknown|||Yes| 9119.0|ASD1069:Rudolph:AD94|C57BL/6NCrlAnu-Adal/AnuApb||Semi-dominant|adenosine deaminase-like|Adal|||MGI:1923144|Adal; endonuclease-mediated mutation 1, Australian National University|AdalAnu||2|ENSMUSG00000027259 |||||||||Unknown to Unknown|||||||||||||||||||Undetermined|Undetermined|C57Bl/6N|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|19-Jan-2021|Cryopreserved sperm|33.0|0.0|Unknown|||Yes| 9128.0||C57BL/6-ATG7LGR5/Apb||Semi-dominant|autophagy related 7|Atg7||1810013K23Rik, Apg7l|MGI:1921494||||Unknown|||||||||||||||||CreERT2|LGR5|||||||||||Normal|Normal|C57BL/6|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|20-Jan-2021|Cryopreserved sperm|50.0|0.0|Unknown||autophagy|Possibly| 9132.0|Pomegranate:87|C57Bl/6-Blicr/Apb||Semi-dominant|Blicr||||||||Unknown|||||||||||||||||||||||||||||Normal|Normal|B6|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|21-Jan-2021||0.0|0.0|Unknown|||Possibly| 9127.0|ATG7Conditional|ATG7Conditional||Recessive|autophagy related 7|Atg7|||MGI:1921494||||6|||||||||||||||||||||||||||||Normal|Normal|C57BL/6|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|20-Jan-2021|Cryopreserved sperm|50.0|0.0|Unknown|||Possibly| 9131.0|Kcnt1 KO|C57BL/6 - Kcnt1||Semi-dominant|potassium channel, subfamily T, member 1|Kcnt1|Unknown|C030030G16Rik, Slack, slo2|MGI:1924627||||2|||||||||||||||||||||||||||||Normal|Normal|C57Bl6|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|20-Jan-2021|Cryopreserved sperm|50.0|0.0|Unknown|||Possibly| 9129.0|BecConRosaCreERT2|BecConRosaCreERT2||Recessive|beclin 1, autophagy related|Becn1|||MGI:1891828||||11|||||||||||||||||CreERT2|Rosa|||||||||||Normal|Normal|C57BL/6|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|20-Jan-2021|Cryopreserved sperm|50.0|0.0|Unknown|||Possibly| 9136.0|ASD990:BlackForest|C57BL/6NCrlAnu-Irf7Anu/Apb||Semi-dominant|interferon regulatory factor 7|Irf7|||MGI:1859212||||7|||||||||||||||||||||||||||||Unknown|Unknown|C57Bl/6 NCrl|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|27-Jan-2021||0.0|0.0|Unknown|||Possibly| 9135.0|ENU47:092:Ikbkb|C57BL/6Ncrl/ApbAnu||Semi-dominant|inhibitor of kappaB kinase beta|Ikbkb ||IKK2, IKK-2, IKK[b], IKKbeta, IKK-beta |MGI:1338071||||8||||||||||||||||||||||||||||| | |C57Bl/6N|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|23-Jan-2021|Cryopreserved sperm|55.0|0.0|Unknown|||Possibly| 9134.0|ENU49:219:Mefv|C57BL/6NcrlAnu-ENU49:219:Mefv/Apb||Semi-dominant|Mediterranean fever|Mefv|||MGI:1859396||||16||||||||||||||||||||||||||||| | |C57BL/6NcrlAnu|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|23-Jan-2021|Cryopreserved sperm|33.0|0.0|Unknown|||Possibly| 9126.0|BecCon/LGR5CreERT2|C57Bl/6-Becn1LGR5(CreERT2)/Apb||Semi-dominant|beclin 1, autophagy related|Becn1|||MGI:1891828||||11|||||||||||||||||CreERT2|LGR5|||||||||||Normal|Normal|C57BL/6|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|20-Jan-2021|Cryopreserved sperm|50.0|0.0|Unknown|||Yes| 9130.0|Kcnt1 P905L|C57BL/6-Kcnt1 ||Semi-dominant|potassium channel, subfamily T, member 1|Kcnt1 ||C030030G16Rik, Slack, slo2|MGI:1924627 |potassium channel, subfamily T, member 1 P905L|Kcnt1 ||2|||||||||||||||||||||||||||||Mice have spontaneous seizure and early mortality|Normal|C57Bl6|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|20-Jan-2021|Cryopreserved sperm|50.0|0.0|Unknown||epilepsy, pottassium channel, brain|No| 9142.0|Tubd1 Flox|C57BL/6J-Tubd1/Apb||Semi-dominant|tubulin, delta 1|Tubd1|||MGI:1891826|Tubd1 Flox|||11|||||||||||||||||||||||||||||Normal|Normal|C57BL6/J|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|12-Feb-2021|Cryopreserved sperm|50.0|0.0|Unknown|||Possibly| 8674.0||ASD981:Pecan:15::N1 ||Recessive|Ku70cKO||||||||Unknown|||||||||||||||||||||||||||||Unknown|Unknown|Charles River B6|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|07-Mar-2019|Cryopreserved sperm|6.0|0.0|Unknown|||Yes| 8667.0|Haao knockout|C57BL/6J-Haao/Dunw||Recessive|3-hydroxyanthranilate 3,4-dioxygenase|Haao||0610007K21Rik, 0610012J07Rik, 3HAO, 3-HAO, 3-HAOxase|MGI:1349444||||17|||||||||||||||||||||||||||||Mice homozygous for a knock-out allele exhibit reduced LPS-induced depressive behaviors and altered kynurenine metabolism.|Normal|C57BL/6J|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|28-Feb-2019|Cryopreserved sperm|50.0|0.0|Unknown|||Yes| 9137.0|MG37_Satb2_chr1_TWAR_5|C57BL/6-MG37-Satb2(chr1-TWAR-5)/Apb||Recessive|special AT-rich sequence binding protein 2|Satb2|||MGI:2679336||||1||||||||||Unknown to Unknown|||||||transgenic lacZ|minimal promoter hsp68, chr1_TWAR_6 (thylacine)|||||||||||Normal|Normal|C57BL6|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|28-Jan-2021|Cryopreserved sperm|50.0|0.0|Unknown|||Possibly| 9138.0|G10flox|C57BL/6J-G10flox/Apb||Semi-dominant|Grb10||||||||Unknown|||||||||||||||||||||||||||||normal|normal|C57BL/6J|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|02-Feb-2021||0.0|0.0|Unknown|||Possibly| 9140.0|Plin5 LKO|C57Bl/6-Plin5 LKO/Apb||Semi-dominant|perilipin 5|Plin5|||MGI:1914218||||17|||||||||||||||||||||||||||||Plin5 is deleted specifically from the liver|Unknown|C57Bl/6|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|05-Feb-2021|Cryopreserved sperm|49.0|0.0|Unknown|||Possibly| 8661.0|Nmnat2 knockout|C57BL/6J-Nmnat2/Dunw||Recessive|nicotinamide nucleotide adenylyltransferase 2|Nmnat2||D030041I09Rik, mKIAA0479, PNAT1|MGI:2444155||||1|||||||||||||||||||||||||||||Perinatal lethality, neuromuscular malformations,lack of functional organ and muscle innervation, distended bladder|Normal|C57BL/6J|No|No|Yes|No|No|Yes|No|Unknown||||No|25-Feb-2019|Cryopreserved sperm|40.0|0.0|Unknown|||Yes| 8662.0|CCDC112KO|C57BL/6J-Ccdc112/MkobMarp||Recessive|coiled-coil domain containing 112|Ccdc112||8430438M01Rik|MGI:1918800||||18|||||||||||||||||||||||||||||Males are infertile, females are normal|Normal|C57BL/6|Yes|Yes|Yes|Yes|No|Yes|No|Unknown||||No|26-Feb-2019|Cryopreserved sperm|50.0|0.0|Unknown||spermatogenesis|Yes| 8675.0|Fcho2|C57BL/6NCrlAnu-Fcho2/AnuApb||Recessive|FCH domain only 2|Fcho2|Unknown|5832424M12Rik|MGI:3505790|Fcho2, endonuclease-mediated mutation 1, Australian National University|Fcho2||13||||||||||Unknown to Unknown|||||||||||||||||||Unknown||C57BL/6NCrlAnu|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|12-Mar-2019|Cryopreserved sperm|33.0|0.0|Unknown|||Yes| 9141.0||ENU15NIH:085:a:MHC II KO||Semi-dominant|histocompatibility-2, MHC|H2|||MGI:95894||||17|||||||||||||||||||||||||||||Lack of expression of MHCII and also failure to degrade CD74 due to lack of SPPL2A|Reduced expression of MHCII|C57BL/6|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|10-Feb-2021||0.0|0.0|Unknown|||Possibly| 9141.0||ENU15NIH:085:a:MHC II KO||Semi-dominant|signal peptide peptidase like 2A|Sppl2a|||MGI:1913802||||2|||||||||||||||||||||||||||||Lack of expression of MHCII and also failure to degrade CD74 due to lack of SPPL2A|Reduced expression of MHCII|C57BL/6|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|10-Feb-2021||||Unknown|||Possibly| 9149.0||C57Bl/6N-ENU30:P2rx7/Apb||Semi-dominant|P2rx7||||||||Unknown||||||||||||||||||||||||||||| | |C57BL/6NcrlAnu|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|19-Feb-2021|Cryopreserved sperm|24.0|0.0|Unknown|||Possibly| 6417.0|GRB7Δ|B6.CBA-Grb7/Ausb||Recessive|growth factor receptor bound protein 7|Grb7|Unknown||MGI:102683||||11|||||||||||||||||||||||||||||Cell metastasis||C57BL/6 x CBA|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Sep-2011|Embryo|0.0|0.0|Unknown|||Possibly| 6416.0|G14Δ|B6.129SV-Grb14/Ausb||Dominant|growth factor receptor bound protein 14|Grb14|Normal||MGI:1355324|growth factor receptor bound protein 14; targeted mutation 1, Roger J Daly|Grb14|MGI:3029164|2|||||||||||||||||||||||||||||Improved glucose tolerance:*Males exhibit increased glucose tolerance between 16 and 24 weeks of age.*Circulating level of insulin is lower in males in response to the same glucose load.*Males exhibit an increase in glucose incorporation into tissue glycogen.Increased insulin sensitivity:*Decrease in blood glucose than wild-type males.*Fasting plasma insulin levels in males are lower at 28-30 and 54-56 weeks of age.*Male skeletal muscle and liver exhibits enhanced insulin-induced glucose uptake.Increased heart weight:*28 week old males exhibit an 18% increase in heart weight.Decreased body weight:*Small but significant decrease in body weight for both males (5-10%) and females (5%).Decreased spleen weight:*28 week old males exhibit a disproportionate decrease (29%) in spleen weight.Decreased liver weight:*28 week old males exhibit a disproportionate decrease (16%) in liver weight.||B6/129SV|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown||Growth factor receptor-bound (Grb)14, Insulin receptor (IR), Tyrosine phosphorylation|Yes| 7697.0|IFNe 202 flp<#65>(FF)|C57BL/6-Ifne/MarpApb||Recessive|Interferon epsilon|Ifne|Normal|Ifne1, Ifnt1 |MGI:2667156|interferon epsilon; targeted mutation 1.1, Paul J Hertzog|Ifne|MGI:5503221|4|||||||||||||||||||||||||||||Normal wild-type|Normal wild-type|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|12-Jun-2014|Cryopreserved sperm|48.0|0.0|Unknown||interferon, receptor, infection|No| 8689.0|Cish wt/wt|BALB/c-Cish/||Dominant|cytokine inducible SH2-containing protein|Cish||Cis, CIS1, cytokine-inducible SH2 protein, F23|MGI:103159||||9|||||||||||||||||||||||||||||Normal|Normal|BALB/c|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|11-Apr-2019||0.0|0.0|Unknown|||Yes| 9150.0|Dmd null|BALB/c.mdx62||Semi-dominant|dystrophin, muscular dystrophy|Dmd||Duchenne muscular dystrophy, dys, mdx, pke, X-linked muscular dystrophy|MGI:94909|dystrophin, muscular dystrophy; endonuclease-mediated mutation 1, Walter and Eliza Hall Institute of Medical Research|Dmd|MGI:7865766|X|ENSMUSG00000045103|ENSMUST00000114000||||||||Unknown to Unknown|||||||||||||||||||Progressive skeletal muscle wasting characterised by degeneration/regeneration of skeletal musculature. Lifespan not characterised but at least 12 months.|Unknown.||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|24-Feb-2021|Cryopreserved sperm|50.0|0.0|Unknown|||Possibly| 9145.0||ENU35:042:Ramos:1bp del||Semi-dominant|interferon induced with helicase C domain 1|Ifih1|||MGI:1918836||||2|||||||||||||||||||||||||||||Have not bred homozygous mice, see below. |Heterozygous GOF allele. Mice develop interferon-mediated autoimmunity. |C57BL/6 Charles River|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|15-Feb-2021||0.0|0.0|Unknown|||Possibly| 9146.0|ENU35:042:Ramos:1bp del|C57Bl/6-ENU35:042:Ramos:1bp del/Apb||Semi-dominant|Ifih1||||||||Unknown|||||||||||||||||||||||||||||Have not bred homozygous mice, see below. |Heterozygous GOF allele. Mice develop interferon-mediated autoimmunity. |C57BL/6 Charles River|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|15-Feb-2021|Cryopreserved sperm|11.0|0.0|Unknown|||Possibly| 6414.0|G10Δ|B6.CBA-Grb10/Ausb||Recessive|growth factor receptor bound protein 10|Grb10|Nil|5730571D09Rik, maternally expressed gene 1, Meg1, mKIAA0207|MGI:103232|growth factor receptor bound protein 10; gene trap 1, Andrew Ward|Grb10|MGI:2668436|11|||||||||||||||||||||||||||||Enlarged placenta:*The size of the placenta was also increased ~30% relative to wild-type.Increased birth body size:*Neonates are ~30% larger than wild-type.Increased fetal size:*Embryonic overgrowth resulting in neonates that are ~30% larger than wild-type.Enlarged liver:*Disproportionate overgrowth of the liver.|Partial perinatal lethality:*Approximately 12% of mice with a maternally inherited allele die shortly after birth.Paternal imprinting:*Only heterozygotes inheriting the allele from the mother display a phenotype.Enlarged placenta:*The size of the placenta is increased ~30% relative to wild-type.Increased birth body size:*Neonates are ~30% larger than wild-type.Increased fetal size:*Embryonic overgrowth resulting in neonates that are ~30% larger than wild-type.Enlarged liver:Disproportionate overgrowth of the liver.Increased glycogen level:*Hepatocytes have a very high glycogen content.Abnormal pulmonary alveolus morphology:*Mice that die shortly after birth exhibit blood-filled alveoli.Abnormal trachea morphology:*Mice that die shortly after birth exhibit a blood-filled trachea.|CBA/B6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown||Grb10 adapter protein, Gene trap|Yes| 819.0|Grb10 KO x Grb14 KO|C57BL/6-Grb10 Grb14||Recessive|growth factor receptor bound protein 10|Grb10|Nil|5730571D09Rik, maternally expressed gene 1, Meg1, mKIAA0207|MGI:103232|gene trap 1, Andrew Ward|Grb10|MGI:2668436|11||||||||||||||||Yes|||||||||||||Double KOs do not show increased insulin signalling over single KOs.Compound KOs exhibit an increase in lean mass.Compound KOs are protected from impaired glucose tolerance that results from high-fat diet whereas sible KOs are not protected.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|21-May-2007||0.0|0.0|Unknown||insulin, receptor, phosphorylation, kinase|Yes| 819.0|Grb10 KO x Grb14 KO|C57BL/6-Grb10 Grb14||Recessive|growth factor receptor bound protein 14|Grb14|Nil||MGI:1355324|targeted mutation 1, Roger J Daly|Grb14|MGI:3029164|2|||||||||||||||||||||||||||||Double KOs do not show increased insulin signalling over single KOs.Compound KOs exhibit an increase in lean mass.Compound KOs are protected from impaired glucose tolerance that results from high-fat diet whereas sible KOs are not protected.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|21-May-2007||||Unknown||insulin, receptor, phosphorylation, kinase|Yes| 9154.0|ASD1056:Teff:9|C57Bl/6-Nlrp1a/Apb||Semi-dominant|nlrp1a||||||||Unknown|||||||||||||||||||||||||||||Normal|Normal|B6|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|05-Mar-2021|Cryopreserved sperm|55.0|0.0|Unknown|||Possibly| 9156.0|Irf4 K59R; Kale|C57BL/6NCrlAnu-Irf4/Anu||Dominant|interferon regulatory factor 4|Irf4||IRF-4, Spip |MGI:1096873|endonuclease mediated targeting 7; Anselm Enders|Irf4|Kale|13|||||||||||||||||||||||||||||unknown|reduced B1a cells|C57Bl/6N|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|09-Mar-2021|Cryopreserved sperm|58.0|0.0|Unknown|||Possibly| 9152.0|ENU47:120|ANU:ENU47:120||Recessive|signal transducer and activator of transcription 2|Stat2|||MGI:103039||||10|ENSMUSG00000040033 |ENSMUST00000085708||||||||||||||||||||||||||| | |C57Bl/6N|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|02-Mar-2021|Cryopreserved sperm|60.0|0.0|Unknown|||Possibly| 9157.0|Jax WT Stock|ASD517:C57BL.6J.JAX/Anu:::G33||Dominant|N/A|N/A|||||||Unknown|||||||||||||||||N/A||||||||||||normal-wildtype|normal-wildtype|C57Bl/6J|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Good|||inbred|No|10-Mar-2021|Cryopreserved sperm|56.0|0.0|Unknown|||No| 9155.0|ASD1073:Wombok|C57BL/6NCrlAnu-Zc3h12b/AnuApb||Semi-dominant|P377L|Zc3h12b|Unknown|A130028J20Rik, LOC245523|MGI:2442133 |P377L|C57BL/6NCrlAnu-Zc3h12b/AnuApb||X|||||||||||||||||||||||||||||Unknown|Unknown|C57Bl/6N|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|09-Mar-2021|Cryopreserved sperm|69.0|0.0|Unknown|||Possibly| 9151.0|ASD656:F4|C57BL/6NcrlAnu-Aicda-flox:CD23cre:Ly5a||Semi-dominant|activation-induced cytidine deaminase|Aicda |||MGI:1342279||||6|||||||||||||||||||||||||||||Lack of Aid expression in mature B cells|Normal|B6/Ncrl ptprca back crossed 4 times|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|26-Feb-2021|Cryopreserved sperm|12.0|0.0|Unknown|||Possibly| 9151.0|ASD656:F4|C57BL/6NcrlAnu-Aicda-flox:CD23cre:Ly5a||Semi-dominant|Fc receptor, IgE, low affinity II, alpha polypeptide|Fcer2a ||CD23, Fce2,|MGI:95497||||8|||||||||||||||||||||||||||||Lack of Aid expression in mature B cells|Normal|B6/Ncrl ptprca back crossed 4 times|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|26-Feb-2021|Cryopreserved sperm|||Unknown|||Possibly| 9151.0|ASD656:F4|C57BL/6NcrlAnu-Aicda-flox:CD23cre:Ly5a||Semi-dominant|protein tyrosine phosphatase receptor type C|Ptprc|||MGI:97810|protein tyrosine phosphatase receptor type C; a variant|Ptprc|MGI:4819849|1|||||||||||||||||||||||||||||Lack of Aid expression in mature B cells|Normal|B6/Ncrl ptprca back crossed 4 times|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|26-Feb-2021|Cryopreserved sperm|||Unknown|||Possibly| 9153.0|Vangl1(KO)|C57BL/6N-Vangl1/MmucdAnu||Semi-dominant|VANGL planar cell polarity 1|Vangl1||Lpp2, mStbm, stbm|MGI:2159344|VANGL planar cell polarity 1; targeted mutation 1e, Wellcome Trust Sanger Institute|Vangl1|MGI:4365105|3|ENSMUSG00000027860 |ENSMUST00000029453|||||||||||||||||||||||||||unknown|unknown|B6Ncrl |Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|03-Mar-2021|Cryopreserved sperm|31.0|9.0|Unknown|||Possibly| 8692.0|C57/Bl6 Cish-lacZ/lacZ|C57BL/6-Cish/||Recessive|cytokine inducible SH2-containing protein|Cish||Cis, CIS1, cytokine-inducible SH2 protein, F23|MGI:103159|lacZ|||9|||||||||||||||||||||||||||||Disrupted haematopoiesis and metabolism|Normal|C57BL/6|Yes|Unknown|Yes|Yes|Unknown|Yes|No|Unknown||||No|11-Apr-2019||0.0|0.0|Unknown|||Yes| 8693.0|C57/Bl6 Gmcsf-/- Cish-wt-wt|C57BL/6-Csf2 Cish/||Recessive|colony stimulating factor 2 (granulocyte-macrophage)|Csf2||Csfgm, Gm-CSf, GMCSF, MGI-IGM|MGI:1339752|colony stimulating factor 2 (granulocyte-macrophage); targeted mutation 1, Ashley R Dunn|Csf2|MGI:1930997|11|||||||||||||||||||||||||||||Altered macrophage biology|Normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|11-Apr-2019||0.0|0.0|Unknown|||Yes| 8690.0|Balb/c Cish-lacZ/lacZ|BALB/c-Cish/||Recessive|cytokine inducible SH2-containing protein|Cish||Cis, CIS1, cytokine-inducible SH2 protein, F23|MGI:103159|lacZ|||9|||||||||||||||||||||||||||||Disrupted haematopoiesis and metabolism|Normal|BALB/c|Yes|Unknown|Yes|Yes|Unknown|Yes|No|Unknown||||No|11-Apr-2019||0.0|0.0|Unknown|||Yes| 8691.0|C57/Bl6 Cish-wt/wt|C57BL/6-Cish/||Dominant|cytokine inducible SH2-containing protein|Cish||Cis, CIS1, cytokine-inducible SH2 protein, F23|MGI:103159|wt (wild-type)|||9|||||||||||||||||||||||||||||Normal|Normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|11-Apr-2019||0.0|0.0|Unknown|||Yes| 8679.0|C2KO-8B|C57BL/6-C2/8b||Recessive|omplement component 2 (within H-2S)|C2|Nil|classical-complement pathway C3/C5 convertase|MGI:88226||||17|||||||||||||||||||||||||||||Normal|Normal |C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|26-Mar-2019|Cryopreserved sperm|50.0|0.0|Unknown|||Yes| 8685.0|IL2Rg del|C57BL/6-Il2rg/Csl||Recessive|interleukin 2 receptor, gamma chain|Il2rg||CD132, common cytokine receptor gamma chain, common gamma chain, gamma(c), gammaC, gamma C receptor, gc, [g]c|MGI:96551||||X|||||||||||||||||||||||||||||Impaired response to polyclonal T cell activators, deficits in their helper function, and a reduction in natural killer cell activity|Unknown||Yes|Unknown|Yes|Yes|Unknown|Yes|No|Unknown||||No|04-Apr-2019|Cryopreserved sperm|50.0|0.0|Unknown|||Yes| 8686.0|Rag2 del 15A|C57BL/6-Rag2/15ACsl||Recessive|recombination activating gene 2|Rag2||Rag-2|MGI:97849||||2|||||||||||||||||||||||||||||Fail to generate mature T or B lymphocytes.|||Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|04-Apr-2019|Cryopreserved sperm|40.0|0.0|Unknown|||Yes| 8701.0|Cep76KO|C57BL/6J-Cep76/MkobMarp||Recessive|centrosomal protein 76|Cep76||6230425F05Rik|MGI:1923401||||18|||||||||||||||||||||||||||||Sub-fertile male|Normal|C57BL/6J|Yes|Unknown|Yes|Yes|Unknown|Yes|No|Unknown||||No|15-Apr-2019|Cryopreserved sperm|50.0|0.0|Unknown|||Yes| 8669.0|CBE1-5|C57BL/6-Cbe1/MarpMob||Recessive|collagen and calcium binding EGF domains 1|Ccbe1|Unknown|Cbe1, Smrp1|MGI:2445053||||13||||||||||Unknown to Unknown|||||||||||||||||||Normal|Normal|C57BL/6J|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|01-Mar-2019|Cryopreserved sperm|50.0|0.0|Unknown|||Yes| 8699.0|INHBB|C57BL/6-Inhbb/Marp||Recessive|inhibin beta-B|Inhbb||activin beta-B|MGI:96571||||1|||||||||||||||||||||||||||||Sub-fertile|Normal|C57BL/6J|Yes|Unknown|Yes|Yes|Unknown|Yes|No|Unknown||||No|15-Apr-2019|Cryopreserved sperm|50.0|0.0|Unknown|||Yes| 8683.0||C57BL/6NCrlAnu-Ikbkb/1AnuApb||Recessive|inhibitor of kappaB kinase beta|Ikbkb||IKK2, IKK-2, IKK[b], IKKbeta, IKK-beta|MGI:1338071|Ikbkb, endonuclease-mediated mutation 2, Australian National University|Ikbkb||8||||||||||Unknown to Unknown|||||||||||||||||||Unknown|Normal|C57BL/6NCrlAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|03-Apr-2019|Cryopreserved sperm|58.0|0.0|Unknown|||Yes| 9160.0|ASD1013:Cacao:5|C57BL/6NCrlAnu-Gbp5/AnuApb||Semi-dominant|guanylate binding protein 5|Gbp5|||MGI:2429943||||3|||||||||||||||||||||||||||||Normal|Normal|C57Bl/6N|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|12-Mar-2021|Cryopreserved sperm|60.0|0.0|Unknown|||Possibly| 9164.0|ASD1110:Lcp1:F0 - founder 5|C57Bl/6N-Lcp1Anu/Apb||Semi-dominant|lymphocyte cytosolic protein 1|Lcp|||MGI:104808||||14|||||||||||||||||||||||||||||unknown|unknown|C57B5NCrl|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|26-Mar-2021|Cryopreserved sperm|12.0|0.0|Unknown|||Possibly| 8710.0|Fut7 KO (line 2) |C57BL/6-Fut7/Apb||Recessive|fucosyltransferase 7|Fut7|Unknown|FTVII, Fuc-TVII, FucT-VII|MGI:107692||||2|||||||||||||||||||||||||||||Unknown. These mice have a defect in immune cell migration, which may make them more susceptible to infections. Regular monitoring is important to establish phenotype of these CRISPR mice. |Unknown. These mice have a defect in immune cell migration, which may make them more susceptible to infections. Regular monitoring is important to establish phenotype of these CRISPR mice. |C57BL/6|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|06-May-2019|Cryopreserved sperm|40.0|0.0|Unknown|||Yes| 9168.0|ASD1105:Bsn KO|C57BL/6NCrlAnu-Bsn12/AnuApb||Semi-dominant|bassoon|Bsn|||MGI:1277955||||9|||||||||||||||||||||||||||||unknown|unknown|C57Bl/6|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|01-Apr-2021|Cryopreserved sperm|12.0|0.0|Unknown|||Yes| 9165.0|ASD1107:Alox5ap:17|C57BL/6NCrlAnu-Alox5ap/AnuApb||Semi-dominant|arachidonate 5-lipoxygenase activating protein|Alox5ap|||MGI:107505||||5|||||||||||||||||||||||||||||unknown|unknown|C57Bl/6N|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|29-Mar-2021|Cryopreserved sperm|12.0|0.0|Unknown|||Possibly| 9166.0|ASD1113:Irf4 K123R|C57Bl/6N-Irf4 KO/Apb||Semi-dominant|Irf4||||||||Unknown|||||||||||||||||||||||||||||unknown|unknown|C57Bl/6N|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|29-Mar-2021|Cryopreserved sperm|12.0|0.0|Unknown|||Possibly| 8700.0|SCRN1KO|C57BL/6J-Scrn1/MkobMarp||Recessive|secernin 1|Scrn1||2810019K23Rik, 6330535A03Rik, mKIAA0193, SES1|MGI:1917188||||6|||||||||||||||||||||||||||||Normal|Normal|C57BL/6J|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|15-Apr-2019|Cryopreserved sperm|50.0|0.0|Unknown|||Yes| 9170.0|ASD985:Starfruit:AP777|C57BL/6NCrlAnu-Apaf1/AnuApb||Semi-dominant|apoptotic peptidase activating factor 1|Apaf1|||MGI:1306796||||10|||||||||||||||||||||||||||||unknown|unknown|C57BL/6NAnu|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|01-Apr-2021|Cryopreserved sperm|60.0|0.0|Unknown|||Possibly| 9167.0|ASD1105:Bsn|C57BL/6NCrlAnu-Bsn8/AnuApb||Semi-dominant|bassoon|Bsn|||MGI:1277955||||9|||||||||||||||||||||||||||||unknown|unknown|C57Bl/6N|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|30-Mar-2021|Cryopreserved sperm|12.0|0.0|Unknown|||Yes| 9169.0|ASD985:Starfruit:AP6bpdel|C57BL/6NCrlAnu-Apaf1/AnuApb||Semi-dominant|apoptotic peptidase activating factor 1|Apaf1|||MGI:1306796||||10|||||||||||||||||||||||||||||unknown|unknown|C57Bl/6N|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|01-Apr-2021|Cryopreserved sperm|48.0|0.0|Unknown|||Possibly| 8698.0|Katbn1 flox|C57BL/6N-Katnb1/Marp||Recessive|katanin p80 (WD40-containing) subunit B 1|Katnb1||2410003J24Rik, KAT|MGI:1921437|katanin p80 (WD40-containing) subunit B 1; targeted mutation 1c, Helmholtz Zentrum Muenchen GmbH|Katnb1||8|||||||||||||||||||||||||||||Normal|Normal|C57BL/6N|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|15-Apr-2019|Cryopreserved sperm|50.0|0.0|Unknown|||Yes| 8697.0|Katnb1KO|C57BL/6N-Katnb1/Marp||Recessive|katanin p80 (WD40-containing) subunit B 1|Katnb1||2410003J24Rik, KAT|MGI:1921437|katanin p80 (WD40-containing) subunit B 1; targeted mutation 1a, Helmholtz Zentrum Muenchen GmbH|Katnb1|MGI:4436305|8|||||||||||||||||||||||||||||Embryonic lethal|Normal|C57BL/6N|No|No|Yes|No|No|Yes|No|Unknown||||No|15-Apr-2019|Cryopreserved sperm|50.0|0.0|Unknown|||Yes| 8696.0|C2 (line 8B) ko|C57BL/6-C2/Apb||Recessive|complement component 2 (within H-2S)|C2|Nil|classical-complement pathway C3/C5 convertase|MGI:88226||||17|||||||||||||||||||||||||||||Normal|Normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|12-Apr-2019||0.0|0.0|Unknown|||Yes| 8707.0|Katnal2 KO|C57BL/6N-Katnal2/MarpApb||Recessive|katanin p60 subunit A-like 2|Katnal2|Nil|3110023G01Rik, 4933439B08Rik|MGI:1924234|katanin p60 subunit A-like 2; targeted mutation 1a, Wellcome Trust Sanger Institute|Katnal2|MGI:4842422|18|||||||||||||||||||||||||||||Male homozygous mice are infertile|Normal|C57BL/6N|Yes|Yes|Yes|Yes|No|Yes|No|Unknown||||No|06-May-2019|Cryopreserved sperm|50.0|0.0|Unknown||Spermatogenesis|Yes| 8798.0|dKO Il2Rg RAg2|BALB/c-Il2rg Rag2/CslApb||Recessive|interleukin 2 receptor, gamma chain|Il2rg||D132, common cytokine receptor gamma chain, common gamma chain, gamma(c), gammaC, gamma C receptor, gc, [g]c|MGI:96551||||X|||||||||||||||||||||||||||||Normal|Normal|BALB/c|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|04-Oct-2019|Cryopreserved sperm|40.0|340.0|Unknown|||Yes| 8798.0|dKO Il2Rg RAg2|BALB/c-Il2rg Rag2/CslApb||Recessive|recombination activating gene 2|Rag2||Rag-2|MGI:97849||||2|||||||||||||||||||||||||||||Normal|Normal|BALB/c|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|04-Oct-2019|Cryopreserved sperm|||Unknown|||Yes| 4951.0|Ifne|C57BL/6-Ifne||Recessive|interferon epsilon|Ifne||Ifne1, Ifnt1|MGI:2667156||||4|||||||||||||||||||||||||||||Normal|Normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|10-Dec-2009||0.0|0.0|No||interferon, reproductive tract|Yes| 9175.0|Vcp fl/fl|C57BL/6J-Vcp/APF||Semi-dominant|valosin containing protein|Vcp ||AAA ATPase p97, CDC48, p97, p97/VCP |MGI:99919|valosin containing protein|Vcp ||4|||||||||||||||||||||||||||||Knockout muscle demonstrated a necrotic myopathy with increased macroautophagic/autophagic proteins and damaged lysosomes|Unknown|C57BL/6N APB|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|23-Apr-2021||0.0|0.0|Unknown||Autophagy, Lysosome, Myopathy, Skeletal muscle, TFEB, VCP|Possibly| 8716.0|Wbp11|C57BL/6-Wbp11/DunwApb||Recessive|WW domain binding protein 11|Wbp11||2510026P17Rik, D6Wsu113e, Npwbp, SIPP1|MGI:1891823|Wbp11; endonuclease-mediated mutation 1, Sally L Dunwoodi|Wbp11||6||||||||||Unknown to Unknown|||||||||||||||||||Embryonic lethal|Multiple congenital defectsPartial lethality|FVB x C57BL/6|No|No|Yes|No|No|Yes|No|Unknown||||No|14-May-2019|Cryopreserved sperm|50.0|0.0|Unknown|||Yes| 8724.0|Adar1E861A/E861A Ifih1-/- Adar2-/- Gria2R/R|B6.129-Adar Adarb1 Gria2 Ifih1/StVApb||Recessive|adenosine deaminase, RNA-specific|Adar||ADAR1, Adar1p110, Adar1p150, mZaADAR|MGI:1889575|adenosine deaminase, RNA-specific; targeted mutation 1.1, Taconic Biosciences|Adar|MGI:5805648|3|||||||||||||||||||||||||||||Compound homozygous animals are normal|Compound heterozygous animals are normal. Note all Adar2-/-Gria2R/+ and Adar2-/-Gria2+/+ die shortly after birth independent of the Adar1/Ifih1 genotypes|C57BL/6|Yes|Unknown|Yes|Yes|Unknown|Yes|No|Unknown||||No|04-Jun-2019|Cryopreserved sperm|40.0|0.0|Unknown|||Yes| 8724.0|Adar1E861A/E861A Ifih1-/- Adar2-/- Gria2R/R|B6.129-Adar Adarb1 Gria2 Ifih1/StVApb||Recessive|adenosine deaminase, RNA-specific, B1|Adarb1||1700057H01Rik, ADAR2, D10Bwg0447e, RED1|MGI:891999|adenosine deaminase, RNA-specific, B1; targeted mutation 1, Peter H Seeburg|Adarb1|MGI:2178079|10|||||||||||||||||||||||||||||Compound homozygous animals are normal|Compound heterozygous animals are normal. Note all Adar2-/-Gria2R/+ and Adar2-/-Gria2+/+ die shortly after birth independent of the Adar1/Ifih1 genotypes|C57BL/6|Yes|Unknown|Yes|Yes|Unknown|Yes|No|Unknown||||No|04-Jun-2019|Cryopreserved sperm|||Unknown|||Yes| 8724.0|Adar1E861A/E861A Ifih1-/- Adar2-/- Gria2R/R|B6.129-Adar Adarb1 Gria2 Ifih1/StVApb||Recessive|glutamate receptor, ionotropic, AMPA2 (alpha 2)|Gria2|Reduced|GluA2, Glur2, Glur-2, GluR2, GluR-B|MGI:95809|glutamate receptor, ionotropic, AMPA2 (alpha 2); targeted mutation 1, Peter H Seeburg|Gria2|MGI:2178124|3|||||||||||||||||||||||||||||Compound homozygous animals are normal|Compound heterozygous animals are normal. Note all Adar2-/-Gria2R/+ and Adar2-/-Gria2+/+ die shortly after birth independent of the Adar1/Ifih1 genotypes|C57BL/6|Yes|Unknown|Yes|Yes|Unknown|Yes|No|Unknown||||No|04-Jun-2019|Cryopreserved sperm|||Unknown|||Yes| 8724.0|Adar1E861A/E861A Ifih1-/- Adar2-/- Gria2R/R|B6.129-Adar Adarb1 Gria2 Ifih1/StVApb||Recessive|interferon induced with helicase C domain 1|Ifih1||9130009C22Rik, Helicard, MDA5, MDA-5|MGI:1918836|interferon induced with helicase C domain 1; targeted mutation 1.1, Marco Colonna|Ifih1|MGI:3663677|2|||||||||||||||||||||||||||||Compound homozygous animals are normal|Compound heterozygous animals are normal. Note all Adar2-/-Gria2R/+ and Adar2-/-Gria2+/+ die shortly after birth independent of the Adar1/Ifih1 genotypes|C57BL/6|Yes|Unknown|Yes|Yes|Unknown|Yes|No|Unknown||||No|04-Jun-2019|Cryopreserved sperm|||Unknown|||Yes| 8726.0||NOD.129S7B6-Rag1 H2d1Ab1Ea2 Ins1 Tg(hCD4) Tg(HLA-DR4,HLA-DQ8) Tg(TCR A1.2)||Recessive|recombination activating 1|Rag1|||MGI:97848|recombination activating 1; targeted mutation 1, Peter Mombaerts|Rag1 |MGI:1857241|2|ENSMUSG00000061311|ENSMUST00000078494||||||||Unknown to Unknown|||||||transgene insertion 2362, Dan R Littman|murine Cd4 and human CD4|equivalent to human CD4+ cells||||||||||Unknown|Unknown|NOD|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|06-Jun-2019|Cryopreserved sperm|50.0|0.0|Unknown|||Yes| 8726.0||NOD.129S7B6-Rag1 H2d1Ab1Ea2 Ins1 Tg(hCD4) Tg(HLA-DR4,HLA-DQ8) Tg(TCR A1.2)||Recessive|histocompatibility 2, D region locus 1|H2-D1||H-2D|MGI:95896||H2-D1Ab1Ea2||17|ENSMUSG00000073411 |||||||||Unknown to Unknown|||||||Tg(TCR A1.2)||||||||||||Unknown|Unknown|NOD|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|06-Jun-2019|Cryopreserved sperm|||Unknown|||Yes| 8726.0||NOD.129S7B6-Rag1 H2d1Ab1Ea2 Ins1 Tg(hCD4) Tg(HLA-DR4,HLA-DQ8) Tg(TCR A1.2)||Recessive|insulin I|Ins1|||MGI:96572||Ins1||19||||||||||Unknown to Unknown|||||||Tg(HLA-DR4,HLA-DQ8)||||||||||||Unknown|Unknown|NOD|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|06-Jun-2019|Cryopreserved sperm|||Unknown|||Yes| 8712.0|Tube1 Flox|C57BL/6J-Tube1/MarpApb||Recessive|epsilon-tubulin 1|Tube1|Unknown|2310061K05Rik|MGI:1919174||Tube1||10||||||||||Unknown to Unknown|||||||||||||||||||Normal|Normal|C57BL/6J|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|06-May-2019|Cryopreserved sperm|50.0|0.0|Unknown|||Yes| 7890.0|Ets1f/fxLysMCre|B6.Cg-Ets1 Lyz2/Marp||Dominant|E26 avian leukemia oncogene 1|Ets1||Ets-1, MGC:18571, p42Ets-1, p51Ets-1, Tpl1|MGI:95455|Ets 1 floxed|Ets1||9|||||||||||||||||||||||||||||Normal but conditionally gives a macrophage specific knockout.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|11-May-2015|Cryopreserved sperm|50.0|0.0|Unknown||Macrophage, Cre recombinase|Possibly| 7890.0|Ets1f/fxLysMCre|B6.Cg-Ets1 Lyz2/Marp||Dominant|lysozyme 2|Lyz2 ||Lys, Lysm, Lyzs, Lzm, Lzm-s1, Lzp|MGI:96897|Lysozyme 2; targeted mutation 1, Irmgard Forster|Lyz2|MGI:1934631|10|||||||||||||||||||||||||||||Normal but conditionally gives a macrophage specific knockout.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|11-May-2015|Cryopreserved sperm|||Unknown||Macrophage, Cre recombinase|Possibly| 8722.0|ASD783:Man2a1:1bp ins|C57BL/6NCrlAnu-Man2a1/AnuApb||Recessive|mannosidase 2, alpha 1|Man2a1||Mana2, Mana-2, Map-2|MGI:104669|Man2a1, endonuclease-mediated mutation 1, Australian National University|Man2a1||17||||||||||Unknown to Unknown|||||||||||||||||||Unknown|Unknown|C57BL/6NCrlAnu|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|31-May-2019|Cryopreserved sperm|48.0|0.0|Unknown|||Yes| 9187.0||B6(Cg).129-Rps6 Tg<(Mx1-Cre)1Cgn/NCrl>/Apb||Semi-dominant|ribosomal protein S6|Rps6||S6R|98159|ribosomal protein S6; targeted mutation 1, George Thomas|Rps6|MGI:2387471|4|||||||||||||||||transgene insertion 1, University of Cologne|Mx1|||||||||||Normal until Cre induction with interferon gamma|Normal until Cre induction with interferon gamma|C57BLN6/NCrl|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-May-2021|Cryopreserved sperm|59.0|0.0|Unknown|||Possibly| 8730.0||ASD852:Tempeh||Recessive|||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|12-Jun-2019|Cryopreserved sperm|11.0|0.0|Unknown|||Yes| 9185.0|ENU52:G2|ANU:ENU52:G2||Recessive|Not known yet||||||||Unknown||||||||||||||||||||||||||||| | |C57BL/6NcrlAnu|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-May-2021|Cryopreserved sperm|1321.0|0.0|Unknown|||Possibly| 5455.0|ENU13NIH:069b|C57BL/6JAnu-Pax5/AnuApb|C57BL/6JAnu-Pax5/AnuApb|Recessive|paired box gene 5|Pax5|Reduced|EBB-1, Pax-5|MGI:97489|paired box gene 5; mutation 1, The Australian National University|Pax5|MGI:5563444|4|ENSMUSG00000014030|ENSMUST00000014174|Pax5-001|1053|1307|T to A|ENSMUSE00000660796|9|351|Tyrosine to STOP|||||TCTGGAAGTCCCTACAGCCACCCTCAGTATTCTTCCTACAATGATTCTTGGAGGTTCCCCA|Yes|||||||||||||No B cells.Small and sick looking.||C57BL/6JAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|07-Mar-2011|Cryopreserved sperm|79.0|0.0|Unknown||B cell, lymphocyte, ENU|Possibly| 9184.0|Rdh5 KO|C57Bl/6N-Rdh5<15:F0>/Apb||Semi-dominant|Rdh5||||||||Unknown|||||||||||||||||||||||||||||unknown|unknown|C57Bl/6NCrl|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|12-May-2021|Cryopreserved sperm|11.0|0.0|Unknown|||Possibly| 9181.0||C57Bl/6N-Itk /Apb||Semi-dominant|Itk||||||||Unknown|||||||||||||||||||||||||||||unknown|unknown|C57Bl/6NCrl|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|07-May-2021|Cryopreserved sperm|12.0|0.0|Unknown|||Possibly| 9179.0|ASD:1127:Irf2bp2 :#6::F0|C57BL/6NCrlAnu-Irf2bp2/AnuApb||Recessive|interferon regulatory factor 2 binding protein 2|Irf2bp2|||MGI:2443921||||8|||||||||||||||||||||||||||||unknown|unknown|C57Bl/6N|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|07-May-2021|Cryopreserved sperm|12.0|0.0|Unknown|||Yes| 9177.0|ASD541:CD4cre/AhRflox:Flpe:CD4-Cre |C57Bl/6N-CD4cre/AhRflox:Flpe:CD4-Cre/Apb||Recessive|||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|06-May-2021||0.0|0.0|Unknown|||Possibly| 9178.0|Arap2 F0:19|C57BL/6NCrlAnu-Arap2/AnuApb||Semi-dominant|ArfGAP with RhoGAP domain, ankyrin repeat and PH domain 2|Arap2||Centd1, mKIAA0580|MGI:2684416 |endonuclease mediated targeting 3;|Arap2 F0:19||Unknown|||||||||||||||||||||||||||||unknown|unknown|C57Bl/6N|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|07-May-2021|Cryopreserved sperm|11.0|0.0|Unknown|||Possibly| 9180.0||C57Bl/6N- Irf2bp2 /Apb||Semi-dominant|Irf2||||||||Unknown|||||||||||||||||||||||||||||Unknown|Unknown|C57Bl/6NCrl|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|07-May-2021|Cryopreserved sperm|12.0|0.0|Unknown|||Possibly| 8727.0|ENU43:270:Nr4a3|C57BL/6NCrlAnu-Nr4a3/AnuApb||Recessive|nuclear receptor subfamily 4, group A, member 3|Nr4a3||MINOR, Nor1, NOR-1, TEC|MGI:1352457||||4|||||||||||||||||||||||||||||Unknown|Unknown|C57BL/6NCrlAnu|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|09-Jun-2019|Cryopreserved sperm|24.0|0.0|Unknown||ENU|Yes| 8728.0|ENU43:375:Nr4a3|C57BL/6NCrlAnu-Nr4a3/AnuApb||Recessive|nuclear receptor subfamily 4, group A, member 3|Nr4a3||MINOR, Nor1, NOR-1, TEC|MGI:1352457||||4|||||||||||||||||||||||||||||Unknown|Unknown|C57BL/6NCrlAnu|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|09-Jun-2019|Cryopreserved sperm|66.0|0.0|Unknown||ENU|Yes| 8729.0|ENU43:395:Nr4a3|C57BL/6NCrlAnu-Nr4a3/AnuApb||Recessive|nuclear receptor subfamily 4, group A, member 3|Nr4a3||MINOR, Nor1, NOR-1, TEC|MGI:1352457||||4|||||||||||||||||||||||||||||Unknown|Unknown|C57BL/6NCrlAnu|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|09-Jun-2019|Cryopreserved sperm|12.0|0.0|Unknown||ENU|Yes| 8733.0|ENU31:075:Irf2|C57BL/6NCrlAnu-Irf2/AnuApb||Recessive|interferon regulatory factor 2|Irf2||9830146E22Rik, Irf-2|MGI:96591||||8|||||||||||||||||||||||||||||||C57BL/6NCrlAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|17-Jun-2019|Cryopreserved sperm|72.0|0.0|Unknown|||Yes| 8734.0|Swiss:TOP UP ONLY|Swiss Webster Outbred:TOP UP ONLY||Dominant||||||||||||||||||||||||||||||||||||||Normal.High fecundity, excellent mothers, ideal for recipients.||Swiss Webster|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|19-Jun-2019||0.0|289.0|Unknown||Swiss|No| 8736.0||ASD1005:Polenta||Recessive|||||||||||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|19-Jun-2019|Cryopreserved sperm|11.0|0.0|Unknown|||Yes| 8745.0|ASD873:Pear:XB151|C57BL/6NCrlAnu-Xbp1/AnuApb||Recessive|X-box binding protein 1|Xbp1||D11Ertd39e, TREB5, TREB-5, XBP-1|MGI:98970|Xbp1, endonuclease-mediated mutation 1, Australian National University|Xbp1||11||||||||||Unknown to Unknown|||||||||||||||||||Unknown|Unknown|C57BL/6NCrlAnu|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|02-Jul-2019|Cryopreserved sperm|44.0|0.0|Unknown|||Yes| 8747.0|ASD960:Orange:XB131|C57BL/6NCrlAnu-Xbp1/AnuApb||Recessive|X-box binding protein 1|Xbp1|Unknown|D11Ertd39e, TREB5, TREB-5, XBP-1|MGI:98970|Xbp1, endonuclease-mediated mutation 3, Australian National University|Xbp1||11||||||||||Unknown to Unknown|||||||||||||||||||Unknown|Unknown|C57BL/6NCrlAnu|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|02-Jul-2019|Cryopreserved sperm|66.0|0.0|Unknown|||Yes| 8708.0|Katnal2 KO x Katna1 Flox|C57BL/6N-Katna1 Katnal2/MarpApb||Recessive|katanin p60 (ATPase-containing) subunit A1|Katna1|||MGI:1344353|katanin p60 (ATPase-containing) subunit A1; targeted mutation 1c, Wellcome Trust Sanger Institute|Katna1||10||||||||||Unknown to Unknown|||||||||||||||||||Male infertile|Normal|C57BL/6N|Yes|Yes|Yes|Yes|No|Yes|No|Unknown||||No|06-May-2019|Cryopreserved sperm|50.0|0.0|Unknown|||Yes| 8708.0|Katnal2 KO x Katna1 Flox|C57BL/6N-Katna1 Katnal2/MarpApb||Recessive|katanin p60 subunit A-like 2|Katnal2||3110023G01Rik, 4933439B08Rik|MGI:1924234|katanin p60 subunit A-like 2; targeted mutation 1a, Wellcome Trust Sanger Institute|Katnal2|MGI:4842422|18|||||||||||||||||||||||||||||Male infertile|Normal|C57BL/6N|Yes|Yes|Yes|Yes|No|Yes|No|Unknown||||No|06-May-2019|Cryopreserved sperm|||Unknown|||Yes| 8739.0|LAMA5 HS PM|C57BL/6-Lama5/MarpApb||Recessive|Laminin, alpha 5|Lama5|Unknown|mKIAA0533|MGI:105382||||2|||||||||||||||||||||||||||||Lethal|unknown|C57BL/6|No|No|Yes|No|No|Yes|No|Unknown||||No|26-Jun-2019|Cryopreserved sperm|50.0|0.0|Unknown||Embryonic lethal|Yes| 9076.0|R26-YAP5SA|C57BL/6-Gt(ROSA)26Sor<(CAGGS-Yap5SA,LacZ)Mao>/Apb||Recessive|gene trap ROSA 26, Philippe Soriano|Gt(ROSA)26Sor||beta geo, Gtrgeo26, Gtrosa26, R26, ROSA26, Thumpd3as1|MGI:104735||||6|||||||||||||||||||||||||||||Overexpression of activated YAP (NLS-YAP-5SA) with Keratin-5 (K5-CreERt) is sufficient to induce rapid formation of both SCC and spSCC in mice. spSCC tumours arise at sites of epithelial scratch wounding, where tumour-initiating epithelial cells undergo EMT to generate spSCC. Expression of the EMT transcription factor ZEB1 arises upon wounding and is a defining characteristic of spSCC in mice and humans. Thus, the wound healing response synergises with YAP to drive metaplastic transformation of SCC to spSCC.||C57BL/6J|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|09-Sep-2020|Cryopreserved sperm|50.0|0.0|Unknown||Hippo, epithelium, Squamous cell carcinoma (SCC) |Yes| 8740.0|ASD977:Zambrero:6|C57BL/6NCrlAnu-Ryr2/AnuApb||Recessive|ryanodine receptor 2, cardiac|Ryr2|Unknown|9330127I20Rik|MGI:99685|Ryr2, endonuclease-mediated mutation 2, Australian National University|Ryr2||13||||||||||Unknown to Unknown|||||||||||||||||||Unknown|Normal|C57BL/6NCrlAnu|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|28-Jun-2019|Cryopreserved sperm|33.0|0.0|Unknown|||Yes| 6641.0|NOD.HinsATriple427|NOD.Cg-H2 Tg(Cd4-CD4)2362Litt Tg(HLA DR4-DQ8)427 Tg(Ins2-INS1)/Apb||Dominant|histocompatibility-2, MHC|H2|Nil|H-2, MHC-II|MGI:95894|histocompatibility-2, MHC; targeted deletion, H2 complex|H2|MGI:2658725|17||||||||||||||||No|human leukocyte antigen class II||||||||||||||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|03-Nov-2011|Cryopreserved sperm|45.0|83.0|Unknown||MHC, B cell, selection, autoimmunity, celiac disease|Yes| 6641.0|NOD.HinsATriple427|NOD.Cg-H2 Tg(Cd4-CD4)2362Litt Tg(HLA DR4-DQ8)427 Tg(Ins2-INS1)/Apb||Dominant||||||||||||||||||||||||||transgene insertion 2362, Dan R Littman|murine Cd4 and human CD4|equivalent to human CD4+ cells||||||||||||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|03-Nov-2011|Cryopreserved sperm|||Unknown||MHC, B cell, selection, autoimmunity, celiac disease|Yes| 6641.0|NOD.HinsATriple427|NOD.Cg-H2 Tg(Cd4-CD4)2362Litt Tg(HLA DR4-DQ8)427 Tg(Ins2-INS1)/Apb||Dominant||||||||||||||||||||||||||human insulin|rat insulin promoter (RIP) (Ins2)|||||||||||||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|03-Nov-2011|Cryopreserved sperm|||Unknown||MHC, B cell, selection, autoimmunity, celiac disease|Yes| 9193.0|DmdS3059E|Balb/c-Dmd/AnuApb||Semi-dominant|Dystrophin|Dmd||Dp427, Dp71, Duchenne muscular dystrophy, dys, mdx, pke, X-linked muscular dystrophy |MGI:94909|Dmd|Dmd||X|||||||||||||||||||||||||||||Unknown|Unknown|Balb/cJ|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|02-Jun-2021|Cryopreserved sperm|50.0|0.0|Unknown|||Possibly| 7957.0|Castella|C.Cg-Rag2 Tg(CD2-IL5)5C2Ldt/AnuApb||Recessive|recombination activating gene 2|Rag2||Rag-2|MGI:97849|recombination activating gene 2; targeted mutation 1, Frederick W Alt|Rag2|MGI:1858556|2|||||||||||||||||transgene insertion 5C2, Lindsay A Dent|the dominant control region (DCR) of the gene encoding human CD2|High - 49 Copies||||||||||Constitutive expression of the IL5 gene is sufficient to induce lifelong high-level eosinophilia. |Appear normal with peripheral blood eosinophilia and increased numbers of eosinophils in the spleen (with splenomegaly), bone marrow. Heterozygous BALB/c and C57BL/6 IL-5 Tg2 mice are resistant to methylcholanthrene-induced carcinogenesis - see Simson, L, et al., 2007, Regulation of carcinogenesis by IL-5 and CCL11: a potential role for eosinophils in tumor immune surveillance. J. Immunol., 178:4222-4229.|BALB/c|No|No|Yes|No|No|Yes|No|Excellent|20||Transgenic male with wild type female|No|28-Jul-2015|Cryopreserved sperm|22.0|0.0|Yes||eosinophil, immune surveillance, resistance to helminthic parasites, asthma, allergy|Yes| 9032.0|Youngs|C.Cg-Tg(CD2-IL5)5C2Ldt/AnuApb||Recessive||||||||||||||||||||||||||transgene insertion 5C2, Lindsay A Dent|the dominant control region (DCR) of the gene encoding human CD2|High - 49 Copies||||||||||||BALB/c|No|No|Yes|No|No|Yes|No|Excellent|20||Transgenic male with wild type female|No|26-Jun-2020|Cryopreserved sperm|55.0|0.0|Yes||eosinophil, immune surveillance, resistance to helminthic parasites, asthma, allergy|Yes| 9195.0|MPO KO CRISP27B|C57BL/6-Mpo/Apb||Semi-dominant|myeloperoxidase|Mpo|||MGI:97137||||11|||||||||||||||||||||||||||||Knockout -/-|N/A|C57Bl/6|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|02-Jun-2021||0.0|0.0|Unknown|||Possibly| 8125.0|Er81 fl:PV-Cre|B6.129-Etv1 Pvalb/Anu||Recessive|ets variant 1|Etv1|Unknown|ER81, Etsrp81|MGI:99254|ets variant 1; targeted mutation 1, William D Snider|Etv1|MGI:2663693|12|||||||||||||||||||||||||||||Unknown||C57BL/6J|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|28-Oct-2016|Cryopreserved sperm|24.0|0.0|Unknown|||Yes| 8125.0|Er81 fl:PV-Cre|B6.129-Etv1 Pvalb/Anu||Recessive|parvalbumin|Pvalb||Parv, PV, Pva|MGI:97821|parvalbumin; targeted mutation 1, Silvia Arber|Pvalb|MGI:3590684|15|||||||||||||||||||||||||||||Unknown||C57BL/6J|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|28-Oct-2016|Cryopreserved sperm|||Unknown|||Yes| 9194.0|Dmd S3059A|BALB/c-Dmd/Anu Apb||Semi-dominant|Dystrophin |Dmd||Dp427, Dp71, Duchenne muscular dystrophy, dys, mdx, pke, X-linked muscular dystrophy|MGI:94909|Dmd|Dmd||X|||||||||||||||||||||||||||||Unknown|Unknown|Balb/cJ|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|02-Jun-2021|Cryopreserved sperm|50.0|0.0|Unknown|||Possibly| 9203.0||C57BL/6NcrlAnu-ENU49:458:Ticam2||Semi-dominant|Ticam2||||||||Unknown||||||||||||||||||||||||||||| | |C57BL/6NcrlAnu|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|14-Jun-2021|Cryopreserved sperm|23.0|0.0|Unknown|||Possibly| 8614.0|Ubtf|C57BL/6J-Ubtf/AnuApb||Recessive|upstream binding transcription factor, RNA polymerase I|Ubtf||A930005G04Rik, Tcfubf, UBF, UBF1|MGI:98512|pstream binding transcription factor, RNA polymerase I; targeted mutation 1, Mark LeDoux|Ubtf|MGI:6695077|11|||||||||||||||||||||||||||||Unknown||C57BL/6J|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|27-Nov-2018|Cryopreserved sperm|10.0|0.0|Unknown|||Yes| 9199.0|ASD1117:Sbds C.258:22:F0|C57BL/6NCrlAnu-Sbds/AnuApb||Semi-dominant|Sbds|SBDS ribosome maturation factor|||MGI:1913961||||5|||||||||||||||||||||||||||||unknown|unknown|C57BL/6NAnu|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|03-Jun-2021|Cryopreserved sperm|12.0|0.0|Unknown|||Yes| 8938.0|ENU33:Trex1:cGAS KO|B6.Cg-Cgas Trex1/AnuApb||Recessive|cyclic GMP-AMP synthase|Cgas|Nil|E330016A19Rik, Mb21d1|MGI:2442261|cyclic GMP-AMP synthase; targeted mutation 1d, Helmholtz Zentrum Muenchen GmbH|Cgas|MGI:5578170|9|||||||||||||||||||||||||||||unknown|unknown|C57BL/6NCrlAnu|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|28-Mar-2020|Cryopreserved sperm|20.0|0.0|Unknown|||Yes| 8938.0|ENU33:Trex1:cGAS KO|B6.Cg-Cgas Trex1/AnuApb||Recessive|three prime repair exonuclease 1|Trex1|||MGI:1328317||||9|||||||||||||||||||||||||||||unknown|unknown|C57BL/6NCrlAnu|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|28-Mar-2020|Cryopreserved sperm|||Unknown|||Yes| 9198.0|ASD1109:Ezr:47:F0|C57Bl/6NCrlAnu-EzrAnu/Apb||Semi-dominant|ezrin|Ezr|||MGI:98931||||17|||||||||||||||||||||||||||||unknown|unknown|C57Bl/6NCrl|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|03-Jun-2021|Cryopreserved sperm|12.0|0.0|Unknown|||Possibly| 9200.0|ASD1117:Sbds 258:F0|C57BL/6NCrlAnu-Sbds/AnuApb||Semi-dominant|SBDS ribosome maturation factor|Sbds|||MGI:1913961||||5|||||||||||||||||||||||||||||unknwon|unknown|C57Bl/6NCrl|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|03-Jun-2021|Cryopreserved sperm|12.0|0.0|Unknown|||Yes| 9197.0|ASD1109:Ezr:20:F0|C57BL/6NCrlAnu-Ifr4/AnuApb||Semi-dominant|ezrin|Ezr||cytovillin, ezrin, p81, Vil2|MGI:98931|Ezr|Ezr:20:F0||17|||||||||||||||||||||||||||||unknown|unknown|C57Bl/6N|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|03-Jun-2021|Cryopreserved sperm|12.0|0.0|Unknown|||Possibly| 9196.0|ASD1076:Naip1-6 KO|ASD1076:Naip1-6 KO||Semi-dominant|naip1-6||||||||Unknown|||||||||||||||||||||||||||||Normal|Normal|B6|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|03-Jun-2021|Cryopreserved sperm|60.0|0.0|Unknown|||Possibly| 8753.0|CLDN10 PM|C57BL/6-Cldn10/MarpApb||Recessive|claudin 10|Cldn10|Unknown|6720456I16Rik, Cldn10a, Cldn10b, D14Ertd728e|MGI:1913101||||14|||||||||||||||||||||||||||||Affects ion transport in the kidney|Normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|18-Jul-2019||0.0|0.0|Unknown|||Yes| 9205.0||C57Bl/6-C-Tg(CMV-cre)1Cgn/J/Apb||Semi-dominant|||||||||Unknown|||||||||||||||||transgene insertion 1, University of Cologne|CMV, cytomegalovirus, human|||||||||||Normal|Normal|C57Bl/6|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|17-Jun-2021|Cryopreserved sperm|40.0|0.0|Unknown|||Possibly| 9204.0|Tek-cre|B6.Cg-Tg<(Tek-cre)1Ywa>/J||Dominant|||||||||Unknown|||||||||||||||||transgene insertion 1, Masashi Yanagisawa|mouse Tek promoter and enhancer|Unknown|sortilin-related VPS10 domain containing receptor 2|Sorcs2 ||mKIAA1329, VPS10 domain receptor protein|MGI:1932289||||5|Normal|Normal|C57Bl/6|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|17-Jun-2021|Cryopreserved sperm|50.0|0.0|Unknown|||Possibly| 8758.0|ASD783:Man2a1:GtoC|C57BL/6NCrlAnu-Man2a1/AnuApb||Recessive|mannosidase 2, alpha 1|Man2a1||Mana2, Mana-2, Map-2|MGI:104669|Man2a1, endonuclease-mediated mutation 2, Australian National University|Man2a1||17|||||||||||||||||||||||||||||Unknown|Unknown|C57BL/6NCrlAnu|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|31-Jul-2019|Cryopreserved sperm|22.0|0.0|Unknown|||Yes| 9207.0|ASD521:cpg15 fl:FoxP3-Cre|C57BL/6-Nrn1Fox3(cre)/Apb||Dominant|neuritin 1|Nrn1|||MGI:1915654||||13|||||||||||||||||||||||||||||||C57BL/6|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|18-Jun-2021||0.0|0.0|Unknown|||Possibly| 8757.0|R26-LSL-Adar1 E861A|C57BL/6-Gt(ROSA)26Sor/CwaApb||Recessive|gene trap ROSA 26, Philippe Soriano|Gt(ROSA)26Sor||beta geo, Gtrgeo26, Gtrosa26, R26, ROSA26, Thumpd3as1|MGI:104735||Gt(ROSA)26Sor||6|||||||||||||||||||||||||||||Normal (requires Cre to induce expression of editing deficient Adar1 - both p110 and p150 isoforms)|Normal (requires Cre to induce expression of editing deficient Adar1 - both p110 and p150 isoforms)|C57BL/6|Yes|Yes|Unknown|Yes|Yes|Yes|No|Unknown||||No|31-Jul-2019|Cryopreserved sperm|70.0|0.0|Unknown|||Yes| 9209.0|ENU49:238|ANU:ENU49:238||Recessive|Unknown||||||||Unknown||||||||||||||||||||||||||||| | |C57BL/6NcrlAnu|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|25-Jun-2021|Cryopreserved sperm|22.0|0.0|Unknown|||Possibly| 8752.0|LAMA5 HS|C57BL/6-Lama5/MarpApb||Recessive|Laminin, alpha 5|Lama5|Unknown|mKIAA0533|MGI:105382||Lama5||2||||||||||Unknown to Unknown|||||||||||||||||||Normal|Normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|18-Jul-2019|Cryopreserved sperm|50.0|0.0|Unknown|||Yes| 8738.0|CRISP4 KO|C57BL/6J-Crisp4/MarpApb||Recessive|cysteine-rich secretory protein 4|Crisp4|Nil|9230112K08Rik|MGI:1925331|cysteine-rich secretory protein 4; targeted mutation 1a, Wellcome Trust Sanger Institute|Crisp4|MGI:4363007|1|||||||||||||||||||||||||||||Sub-fertile|Nomrmal|C57Bl/6J|Yes|Yes|Yes|Yes|No|Yes|No|Unknown||||No|24-Jun-2019|Cryopreserved sperm|50.0|0.0|Unknown||Sperm, epididymis, Capacitation|Yes| 9219.0||C57BL/6NcrlAnu-ASD1114:TbcdA:35||Recessive|Tbcd||||||||Unknown|||||||||||||||||||||||||||||unknown|unknown|C57BL/6NCrl|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|07-Jul-2021|Cryopreserved sperm|12.0|0.0|Unknown|||Possibly| 8762.0|ENU25:041:Casd1:comp|C57BL/6NCrlAnu-Casd1/AnuApb||Recessive|CAS1 domain containing 1|Casd1|Unknown|Cast1, MGC:6840|MGI:2384865||||6|ENSMUSG00000015189|ENSMUST00000015333|Casd1-001|||||||||1|||||||||||||||||TER119 negative RBCs|Normal|C57BL/6NCrlAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|08-Aug-2019|Cryopreserved sperm|57.0|0.0|Unknown|||Yes| 9220.0|ASD1117:Sbds C.258+1G>C:25|C57Bl/6N-Sbds /Apb||Semi-dominant|SBDS ribosome maturation factor|Sbds|||MGI:1913961||||5|||||||||||||||||||||||||||||unknown|unknown|C57BL/6NCrl|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|07-Jul-2021|Cryopreserved sperm|11.0|0.0|Unknown|||Possibly| 9215.0|ASD1125:Itk E42K:8|C57Bl/6N-Itk /Apb||Semi-dominant|IL2 inducible T cell kinase|Itk|||MGI:96621||||11|||||||||||||||||||||||||||||unknwon|unknown|C57Bl/6NCrl|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|07-Jul-2021|Cryopreserved sperm|12.0|0.0|Unknown|||Possibly| 9211.0||TCF7-GFP:B1-8 High Affinity:G4||Recessive|TCF7, B1-8||||||||Unknown|||||||||||||||||||||||||||||Normal|Normal|ASD866 C57BL/6NCrlAnu|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|02-Jul-2021|Cryopreserved sperm|60.0|0.0|Unknown|||Possibly| 9218.0||C57Bl6/N-Sntb1 /Apb||Semi-dominant|syntrophin, basic 1|Sntb1||59-1 DAP, beta1-Syntrophin|MGI:101781||||15|ENSMUSG00000060429|ENSMUST00000039769||||||||Unknown to Unknown|||||||||||||||||||unknown|unknown|C57Bl/6NCrl|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|07-Jul-2021|Cryopreserved sperm|11.0|0.0|Unknown|||Possibly| 9210.0|TCF7-GFP:B1-8 High Affinity|C57Bl/6N-TCF7(GFP:B1-8) High Affinity/Apb||Semi-dominant|transcription factor 7, T cell specific|TCF7, B1-8|||MGI:98507||||11|||||||||||||||||||||||||||||Norma|Normal|ASD872 B6NCrl-Ptprc(a)/Anu|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|02-Jul-2021|Cryopreserved sperm|45.0|0.0|Unknown|||Possibly| 9214.0|Lcp1 KO (founder 17)|C57Bl/6N-Lcp1Anu/Apb||Recessive|lymphocyte cytosolic protein 1|Lcp1|||MGI:104808|Lcp; endonuclease-mediated mutation 5, Australian National University|Lcp1Anu||14||||||||||Unknown to Unknown|||||||||||||||||||unknown|unknown|C57Bl/6NCrl|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|07-Jul-2021|Cryopreserved sperm|42.0|0.0|Unknown|||Possibly| 9217.0|ASD1123:Sntb1 F0:#43|C57BL/6NCrlAnu-Sntb1/AnuApb||Semi-dominant|syntrophin, basic 1|Sntb1|||MGI:101781||||15|||||||||||||||||||||||||||||unknown|unknown|C57Bl/6N|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|07-Jul-2021|Cryopreserved sperm|12.0|0.0|Unknown|||Yes| 8756.0|R26-LSL-Adar1 p110|C57BL/6-Gt(ROSA)26Sor/CwaApb||Recessive|gene trap ROSA 26, Philippe Soriano|Gt(ROSA)26Sor||beta geo, Gtrgeo26, Gtrosa26, R26, ROSA26, Thumpd3as1|MGI:104735||Gt(ROSA)26Sor||6|||||||||||||||||||||||||||||Normal (requires Cre to induce expression of Adar1 p110 isoform ectopically)|Normal (requires Cre to induce expression of Adar1 p110 isoform ectopically)|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|31-Jul-2019|Cryopreserved sperm|40.0|0.0|Unknown|||Yes| 8760.0|ASD873:XBP1:indel|C57BL/6NCrlAnu-Xbp1/AnuApb||Recessive|X-box binding protein 1|Xbp1|Unknown|D11Ertd39e, TREB5, TREB-5, XBP-1|MGI:98970|Xbp1, endonuclease-mediated mutation 4, Australian National University|Xbp1||11||||||||||Unknown to Unknown|||||||||||||||||||Unknown|Unknown|C57BL/6NCrlAnu|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|02-Aug-2019|Cryopreserved sperm|11.0|0.0|Unknown|||Yes| 9212.0|Bsn KO - ASD1106:Bsn:70|C57Bl/6N-Bsn70/Apb||Semi-dominant|bassoon|Bsn||presynaptic cytomatrix protein|MGI:1277955|Bsn:endonuclease-mediated mutation 2, Australian National University|Bsn||9|ENSMUSG00000032589 |ENSMUST00000035208|||||||||||||||||||||||||||unknown|unknown|C57BL/6NCrl|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|07-Jul-2021|Cryopreserved sperm|11.0|0.0|Unknown|||Possibly| 9222.0|Mir17hg Foxp3-cre|C57BL/6-Mirc1Foxp3/Apb||Semi-dominant|microRNA cluster 1, including Mir17 through Mir92-1|Mirc1||miR-17~92, miR-17-92, Mir17-92, Mirn17-92|MGI:3790484|microRNA cluster 1, including Mir17 through Mir92-1; targeted mutation 1.1, Tyler Jacks|Mirc1|MGI:3793628|14|||||||||||||||||||||||||||||Minor perturbations in Treg populations, but otherwise normal.|Normal|C57BL/6 (backcrossed >10 generations)|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|08-Jul-2021|Cryopreserved sperm|49.0|0.0|Unknown|||Possibly| 9222.0|Mir17hg Foxp3-cre|C57BL/6-Mirc1Foxp3/Apb||Semi-dominant|forkhead box P3|Foxp3||JM2, scurfin|MGI:1891436|forkhead box P3; targeted mutation 4, Alexander Y Rudensky|Foxp3|MGI:3790499|X|||||||||||||||||||||||||||||Minor perturbations in Treg populations, but otherwise normal.|Normal|C57BL/6 (backcrossed >10 generations)|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|08-Jul-2021|Cryopreserved sperm|||Unknown|||Possibly| 9225.0|ASD917::Zud1 |C57BL/6N-Zic2/Apb||Semi-dominant|zinc finger protein of the cerebellum 2|Zic2||GENA 29, Ku, odd-paired homolog|MGI:106679|Zic2; endonuclease-mediated mutation 1, Ruth Arkel|Zic2Ark||14|ENSMUSG00000061524 |ENSMUST00000075888|||||||||||||||||||||||||||Homozygous animals are viable in to adulthood and display belly spots (with incomplete penetrance). |No observable phenotype in the heterozygous state.|C57BL.6N|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|14-Jul-2021|Cryopreserved sperm|55.0|0.0|Unknown|||Possibly| 9224.0|B10.BR(B6)-Ptprca/J|B10.BR(B6)-Ptprca/J||Semi-dominant|protein tyrosine phosphatase receptor type C|Ptprc||B220, CD45, Ly-5, Lyt-4, T200|MGI:97810|protein tyrosine phosphatase receptor type C; a variant|Ptprc|MGI:4819849|1||||||||||Unknown to Unknown|||||||||||||||||||B10.BR mice express CD45.1 in all leucocytes instead of CD45.2 |same as above except that hets would express both CD45.1 and CD45.2. |B10.BR|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|08-Jul-2021|Cryopreserved sperm|50.0|0.0|Unknown|||Possibly| 9247.0|Ntsr1-cre|FVB/N-Tg(Ntsr1-cre)||Semi-dominant|neurotensin receptor 1|Ntsr1||NT-1R, NTR1, NTR-1, Ntsr1|Ntsr1|ransgene insertion GN209, GENSAT Project at Rockefeller University|Tg(Ntsr1-cre)GN209Gsat|MGI:4367043|Unknown|||||||||||||||||cre recombinase|Ntsr1|||||||||||Undetermined|Undetermined|FVB/N|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||N1F2| hemizygous state|No|09-Aug-2021||0.0|0.0|Unknown|||Possibly| 8415.0|Mdm2 S6|B6(Cg).129(Cg)-WT/JAnu||Recessive||||||||||||||||||||||||||||||||||||||Normal||C57BL/6J|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|15-Jan-2018|Cryopreserved sperm|55.0|0.0|Unknown|||Yes| 8782.0|R26-Adar1|C57BL/6-Gt(ROSA)26Sor/CwaApb||Recessive|gene trap ROSA 26, Philippe Soriano|Gt(ROSA)26Sor|||MGI:104735|Gt(ROSA)26Sor|||6|||||||||||||||||||||||||||||Normal (Rosa26 Lox-Stop-Lox Adar1 cDNA); needs Cre exposure to activate Adar1 expression|Normal (Rosa26 Lox-Stop-Lox Adar1 cDNA); needs Cre exposure to activate Adar1 expression|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|04-Sep-2019|Cryopreserved sperm|60.0|0.0|Unknown|||Yes| 9123.0|Becn1 floxed|C57BL/6NTac-Becn1||Semi-dominant|beclin 1, autophagy related|Becn1 ||Atg6|MGI:1891828|beclin 1, autophagy related; targeted mutation 1c, Wellcome Trust Sanger Institute|Becn1|MGI:6449262|Unknown|||||||||||||||||||||||||||||Normal|Normal|C57BL/6|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|20-Jan-2021|Cryopreserved sperm|40.0|0.0|Unknown||Autophagy, Human breast , Ovarian cancers, Tumor suppressor|Possibly| 8786.0|R26-LSL-Adar1 p150|C57BL/6-Gt(ROSA)26Sor/CwaApb||Recessive|gene trap ROSA 26, Philippe Soriano|Gt(ROSA)26Sor|||MGI:104735||Gt(ROSA)26Sor||6|||||||||||||||||||||||||||||Normal (requires Cre treatment to activate expression of Adar1 p150 isoform)|Normal (requires Cre treatment to activate expression of Adar1 p150 isoform)|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|06-Sep-2019|Cryopreserved sperm|40.0|0.0|Unknown|||Yes| 8776.0|ENU35:042:B6|B6(Cg)-Ifih1/AnuApb||Recessive|interferon induced with helicase C domain 1|Ifih1||9130009C22Rik, Helicard, MDA5, MDA-5|MGI:1918836|Ifih1, mutation 1, Australian National University|Ifih1||Unknown|||||||||||||||||||||||||||||Unknown|Unknown|C57BL/6NCrlAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|12-Aug-2019|Cryopreserved sperm|65.0|0.0|Unknown|||Yes| 9223.0|Alb-Kb B10.BR| Tg(Alb-H2-Kb)/Apb or Alb-Kb||Semi-dominant|H-2Kb (histocompatibility 2, K region; b haplotype)|h2-k1|Normal||||||Unknown|||||||||||||||||H-2Kb (histocompatibility 2, K region; b haplotype)|mouse albumin promoter|||||||||||This transgenic mouse line expresses a mouse MHC Class I molecule H-2Kb under the control of the mouse albumin promoter, allowing restricted expression of H-2Kb in hepatocytes in addition to endogenous H-2K molecules expression in all cells (Including hepatocytes). The original mouse line was originally generated in the DBA2 background (H-2 d haplotype). To generate Alb-Kb on the B10.BR background (k background), the original line was backcrossed for >10 generations with B10BR mice. Mice have a normal phenotype and no liver anomaly.|Same as above.|B10.BR|Yes|Yes|Yes|Yes|Yes|Yes|No|Excellent|more than 10||Homozygous mice are intercrossed|No|08-Jul-2021|Cryopreserved sperm|50.0|0.0|No||tolerance, liver, CD8 T cells, MHC class I, autoimmunity|Possibly| 7870.0|MHC II KO|B6NCrl.Cg-H2-Aa/AnuApb||Recessive|histocompatibility 2, class II antigen A, alpha|H2-Aa||Aalpha, A alpha, H-2Aa, Ia1, Ia-1, I-Aalpha|MGI:95895|histocompatibility 2, class II antigen A, alpha; targeted mutation 1, Horst Bluethmann|H2-Aa|MGI:2157977|17|||||||||||||||||||||||||||||enlarged thymus ( J:16372 )• slightly enlargedthymus hyperplasia ( J:16372 )• slightly increased cell numberabnormal T cell morphology ( J:16372 )decreased CD4-positive, alpha beta T cell number ( J:16372 )• very few or no CD4+ T-cells in thymus• about 4% CD4+ peripheral T-cells as opposed to 60% normallyincreased CD8-positive, alpha-beta T cell number ( J:16372 )• about 90% of lymph node T-cells are CD8+abnormal MHC II cell surface expression on macrophages ( J:67924 )• Class II expression is absent on bone-marrow derived macrophagesabnormal splenocyte physiology ( J:16372 )• no splenocyte response to staphylococcal enterotoxin B• response to T-cell independent antigens is normalenlarged lymph nodes ( J:16372 )• slightly enlarged||C57BL/6NCrlAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|16-Apr-2015|Cryopreserved sperm|43.0|0.0|Unknown||T cell, MHC class II|Yes| 9246.0|MPO KO CRISP (27B)|C57Bl/6J-Mpo/AnuApb||Semi-dominant|myeloperoxidase|Mpo|||MGI:97137||||11|||||||||||||||||||||||||||||Homozygous|N/A|C57Bl/6J|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|06-Aug-2021|Cryopreserved sperm|50.0|0.0|Unknown|||Possibly| 9245.0|Ggnbp2 fl/fl|C57Bl6/J-Ggnbp2<(tm1.1)Crwy>/AnuApb||Recessive|gametogenetin binding protein 2|Ggnbp2||D330017P12Rik, DIF-3, Zfp403 |MGI:2387356|Ggnbp2<(tm1.1)Crwy>|||Unknown|||||||||||||||||||||||||||||conditional allele; no phenotype in homozygous state; currently unknown after somatic deletion|normal|C57Bl/6J|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|04-Aug-2021|Cryopreserved sperm|50.0|0.0|Unknown|||Possibly| 8779.0|Maggott:13|NOD/Lt-Slc6a19/13AnuApb||Recessive|solute carrier family 6 (neurotransmitter transporter), member 19|Slc6a19||4632401C08Rik, B<0>AT1|MGI:1921588|Slc6a19, endonuclease-mediated mutation 1, Australian National University|Slc6a19||13||||||||||Unknown to Unknown|||||||||||||||||||||NOD/Lt|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|15-Aug-2019|Cryopreserved sperm|55.0|0.0|Unknown|||Yes| 8781.0|ENU23:039:Pola1|C57BL/6NCrlAnu-Pola1 Pola1/AnuApb||Recessive|polymerase (DNA directed), alpha 1|Pola1||Pola|MGI:99660|Pola1, mutation 1, Australian National University|Pola1||X|||||||||||||||||||||||||||||Unknown|Unknown|C57BL/6NCrlAnu|Yes|Unknown|Yes|Yes|Unknown|Yes|No|Unknown||||No|30-Aug-2019|Cryopreserved sperm|33.0|0.0|Unknown|||Yes| 8781.0|ENU23:039:Pola1|C57BL/6NCrlAnu-Pola1 Pola1/AnuApb||Recessive|polymerase (DNA directed), alpha 1|Pola1||Pola1|MGI:99660|Pola1, mutation 2, Australian National University|||X|ENSMUSG00000006678|ENSMUST00000006856|||||||||||||||||||||||||||Unknown|Unknown|C57BL/6NCrlAnu|Yes|Unknown|Yes|Yes|Unknown|Yes|No|Unknown||||No|30-Aug-2019|Cryopreserved sperm|||Unknown|||Yes| 5015.0|MHC II KO|B6.129-H2-Aa/AnuApb||Recessive|histocompatibility 2, class II antigen A, alpha|H2-Aa|Nil|Aalpha, A alpha, H-2Aa, Ia1, Ia-1, I-Aalpha|MGI:95895|histocompatibility 2, class II antigen A, alpha; targeted mutation 1, Horst Bluethmann|H2-Aa|MGI:2157977|17|||||||||||||||||||||||||||||enlarged thymus ( J:16372 )• slightly enlargedthymus hyperplasia ( J:16372 )• slightly increased cell numberabnormal T cell morphology ( J:16372 )decreased CD4-positive, alpha beta T cell number ( J:16372 )• very few or no CD4+ T-cells in thymus• about 4% CD4+ peripheral T-cells as opposed to 60% normallyincreased CD8-positive, alpha-beta T cell number ( J:16372 )• about 90% of lymph node T-cells are CD8+abnormal MHC II cell surface expression on macrophages ( J:67924 )• Class II expression is absent on bone-marrow derived macrophagesabnormal splenocyte physiology ( J:16372 )• no splenocyte response to staphylococcal enterotoxin B• response to T-cell independent antigens is normalenlarged lymph nodes ( J:16372 )• slightly enlarged||C57BL/6JAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|22-Feb-2010|Cryopreserved sperm|77.0|65.0|Unknown||T cell, MHC II|No| 9237.0|ENU52:G3|ANU:ENU52:G3||Recessive|Unknown||||||||Unknown||||||||||||||||||||||||||||| | |C57BL/6NcrlAnu|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|26-Jul-2021|Cryopreserved sperm|84.0|0.0|Unknown|||Possibly| 9231.0|ENU49:355|ANU:ENU49:355||Recessive|interleukin-1 receptor-associated kinase 4|Irak4|||MGI:2182474||||15|ENSMUSG00000059883 |||||||||||||||||||||||||||| | |C57BL/6NcrlAnu|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|26-Jul-2021|Cryopreserved sperm|36.0|0.0|Unknown|||Possibly| 9228.0|Ocn-Cre|B6.FVB-Tg1/Clem/J||Semi-dominant||||||||||||||||||||||||||transgene insertion 1, Thomas L Clemens|human bone gamma carboxyglutamate protein (BGLAP)|Unknown||||||||||Transgenic |unknown|C57Bl/6J|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|19-Jul-2021|Cryopreserved sperm|50.0|0.0|Unknown|||Possibly| 9234.0|ENU50:133|ANU:ENU50:133||Recessive|interleukin-1 receptor-associated kinase 4|Irak4|||MGI:2182474||||15|ENSMUSG00000059883 |||||||||||||||||||||||||||| | |C57BL/6NcrlAnu|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|26-Jul-2021|Cryopreserved sperm|53.0|0.0|Unknown|||Possibly| 9233.0|ENU51:019|C57BL/6Ncrl:ENU51<019>/Anu||Dominant|Not known yet||||||||Unknown||||||||||||||||||||||||||||| | |C57Bl/6N|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|26-Jul-2021|Cryopreserved sperm|12.0|0.0|Unknown|||Possibly| 9240.0|ASD1127:Irf2bp2 KO:::F0|C57BL/6NCrlAnu-Irf2bp2/AnuApb||Semi-dominant|interferon regulatory factor 2 binding protein 2|Irf2bp2|||MGI:2443921||||8|||||||||||||||||||||||||||||unknown|unknown|C57Bl/6N|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|27-Jul-2021|Cryopreserved sperm|12.0|0.0|Unknown|||Yes| 9235.0|ENU50:205|ANU:ENU50:205||Recessive|v-rel reticuloendotheliosis viral oncogene homolog A (avian)|Rela||p65 NF kappaB|MGI:103290|Rela:mutation 1, Australian National University|Rela||19|ENSMUSG00000024927 |ENSMUST00000025867||||||||||||||||||||||||||| | |C57BL/6NcrlAnu|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|26-Jul-2021|Cryopreserved sperm|57.0|0.0|Unknown|||Possibly| 9238.0|ASD1117:Sbds C.258+1G>C:::F0|C57BL/6NCrlAnu-Sbds/AnuApb||Recessive|SBDS ribosome maturation factor|Sbds|||MGI:1913961||||5|||||||||||||||||||||||||||||unknown|unknown|C57Bl/6N|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|27-Jul-2021|Cryopreserved sperm|24.0|0.0|Unknown|||Yes| 9262.0|ASD1043:Crust|C57Bl/6N-Nae1 /Apb||Semi-dominant|Nae1|||||Nae1 |||Unknown|||||||||||||||||||||||||||||Unknown|Unknown|C57BL/6NCrlAnu|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|14-Aug-2021|Cryopreserved sperm|57.0|0.0|Unknown|||Possibly| 9250.0|Akirin F0:#23|C57BL/6NCrlAnu-Akirin/AnuApb||Semi-dominant|akirin 1|Akirin1||6330407G11Rik|MGI:1915300|endonuclease mediated targeting 5;|Akirin F0:#23||Unknown|||||||||||||||||||||||||||||unknown|unknown|C57Bl/6N|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|11-Aug-2021|Cryopreserved sperm|11.0|0.0|Unknown|||Possibly| 9252.0|Sntb1 KO|C57Bl/6N-Sntb1/Apb||Semi-dominant|Sntb1||||||||Unknown|||||||||||||||||||||||||||||unknown|unknown|C57BL/6NCrl|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|11-Aug-2021|Cryopreserved sperm|12.0|0.0|Unknown|||Possibly| 9249.0|ASD1128:Irf2bp2|C57Bl/6N-Irf2bp2 KO/Apb||Semi-dominant|Irf2||||||||Unknown|||||||||||||||||||||||||||||unknown|unknown|C57BL/6NCrl|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|11-Aug-2021|Cryopreserved sperm|12.0|0.0|Unknown|||Possibly| 9248.0|Tlr4 KO|C57Bl/6-Tlr4:F0/Apb||Semi-dominant|Tlr4||||||||Unknown|||||||||||||||||||||||||||||unknown|unknown|C57BL/6NCrl|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|11-Aug-2021|Cryopreserved sperm|12.0|0.0|Unknown|||Possibly| 9258.0|Ezr:Q339R|C57BL/6NCrlAnu-Ezr/AnuApb ||Semi-dominant|Ezrin|Ezr||cytovillin, ezrin, p81, Vil2 |MGI:98931|Ezrin|Ezr ||17|||||||||||||||||||||||||||||Unknown|Unknown|C57Bl/6N|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|12-Aug-2021|Cryopreserved sperm|53.0|0.0|Unknown|||Possibly| 9257.0|Irf2bp2:R38C |C57BL/6NCrlAnu-Irf2bp2/AnuApb ||Semi-dominant|interferon regulatory factor 2 binding protein 2|Irf2bp2||E130305N23Rik |MGI:2443921|Interferon regulatory factor 2 binding protein 2|Irf2bp2 ||8|||||||||||||||||||||||||||||Unknown|Unknown|C57Bl/6N|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|12-Aug-2021|Cryopreserved sperm|55.0|0.0|Unknown|||Possibly| 8791.0|ASD739:ELK KO|C57BL/6NCrlAnu-Elk1/AnuApb||Recessive|ELK1, member of ETS oncogene family|Elk1||Elk-1|MGI:101833|Elk1, endonuclease-mediated mutation 1, Australian National University|Elk1||X||||||||||Unknown to Unknown|||||||||||||||||||Unknown|Unknown|C57BL/6NCrlAnu|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|17-Sep-2019|Cryopreserved sperm|58.0|0.0|Unknown|||Yes| 9266.0||B6.129-Rrn3Tg(Vav1-cre/ERT)1Wehi/AnuApb||Recessive|RRN3 RNA polymerase I transcription factor homolog (yeast)|Rrn3|||MGI:1925255|RRN3 RNA polymerase I transcription factor homolog (yeast); targeted mutation 1.1, Ingrid Grummt|Rrn3|MGI:3584035|16||||||||||Unknown to Unknown|||||||CreERT2|Vav1|||||||||||normal|normal|C57BL/6NCrlAnu|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|20-Aug-2021|Cryopreserved sperm|60.0|0.0|Unknown|||Possibly| 8763.0|F9 human KI, mouse KO (165D) |B6-F9/165DCslApb||Recessive|coagulation factor IX|F9||Cf9, Cf-9|MGI:88384||||X|||||||||||||||||||||||||||||Mice may exhibit haemophilia B - it is unknown to what degree the human F9 clotting factor compensates.|Mice may exhibit haemophilia B - it is unknown to what degree the human F9 clotting factor compensates.|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|09-Aug-2019|Cryopreserved sperm|50.0|0.0|Unknown||Clot|Yes| 8764.0|F8 KO (72A)|C57BL/6-F8/72ACslApb||Recessive|coagulation factor VIII|F8|Nil|Cf8, Cf-8, Factor VIII, FVIII|MGI:88383||||X|||||||||||||||||||||||||||||Mice are haemophilic as they are deficient in the clotting factor, FVIII|Mice may show signs of being haemophilic|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|09-Aug-2019|Cryopreserved sperm|40.0|0.0|Unknown||Haemophilia|Yes| 9268.0||C57Bl/6J-B1<(W100A)>B2<(W98A)>DKI/Apb||Semi-dominant|AMPK beta 1 and AMPK beta 2 (double KI)|||||Prkab1 tm2BEK and Prkab2 tm2BEK|||Unknown|||||||||||||||||||||||||||||Normal|Normal|C57Bl/6J|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|30-Aug-2021|Cryopreserved sperm|50.0|0.0|Unknown|||Possibly| 9263.0|ASD1058:Kingsleys:6|C57BL/6NCrlAnu-Rab13/AnuApb||Semi-dominant|RAB13, member RAS oncogene family|Rab13|||MGI:1927232|Rab13 <3ins15Del>|||3|||||||||||||||||||||||||||||Unknown|Unknown|C57Bl/6N|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|14-Aug-2021|Cryopreserved sperm|60.0|0.0|Unknown|||Possibly| 8792.0|ASD739:ELK KO:37bp-Del|C57BL/6NCrlAnu-Elk1/AnuApb||Recessive|ELK1, member of ETS oncogene family|Elk1||Elk-1|MGI:101833|Elk1, endonuclease-mediated mutation 2, Australian National University|Elk1||X||||||||||Unknown to Unknown|||||||||||||||||||Unknown|Unknown|C57BL/6NCrlAnu|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|17-Sep-2019|Cryopreserved sperm|56.0|0.0|Unknown|||Yes| 8755.0||FVB(Cg)-Ccnd1 Tg(CAG-cre/Esr1*)5Amc Tg(MMTV-rtTA) Tg(tetO-HER2)||Recessive|cyclin D1|Ccnd1|Unknown|bcl-1, cD1, CycD1, Cyl-1, PRAD1 |MGI:88313 |cyclin D1; targeted mutation 5.1, Piotr Sicinski|Ccnd1|MGI:5468336|7|||||||||||||||||transgene insertion 5, Andrew P McMahon||||||||||||||>87.5% FVB|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|30-Jul-2019|Cryopreserved sperm|44.0|0.0|Unknown|||Yes| 8755.0||FVB(Cg)-Ccnd1 Tg(CAG-cre/Esr1*)5Amc Tg(MMTV-rtTA) Tg(tetO-HER2)||Recessive||||||||||||||||||||||||||transgene insertion 1, Lewis A Chodosh||||||||||||||>87.5% FVB|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|30-Jul-2019|Cryopreserved sperm|||Unknown|||Yes| 8755.0||FVB(Cg)-Ccnd1 Tg(CAG-cre/Esr1*)5Amc Tg(MMTV-rtTA) Tg(tetO-HER2)||Recessive||||||||||||||||||||||||||transgene insertion, Jean J Zhao||||||||||||||>87.5% FVB|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|30-Jul-2019|Cryopreserved sperm|||Unknown|||Yes| 8793.0|Ubl3|C57BL/6-Ubl3/Apb||Recessive|ubiquitin-like 3|Ubl3|||MGI:1344373||||5|||||||||||||||||||||||||||||Unknown||C57BL/6|Yes|Unknown|Yes|Yes|Unknown|Yes|No|Unknown||||No|17-Sep-2019|Cryopreserved sperm|50.0|0.0|Unknown|||Yes| 8770.0|F9 human KI, mouse KO (165B) |C57BL/6-F9/165BCslApb||Recessive|coagulation factor IX|F9||Cf9, Cf-9|MGI:88384||||X|||||||||||||||||||||||||||||Mice may exhibit haemophilia B - it is unknown to what degree the human F9 clotting factor compensates.|Mice may exhibit haemophilia B - it is unknown to what degree the human F9 clotting factor compensates.|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|09-Aug-2019|Cryopreserved sperm|50.0|0.0|Unknown||Haemophilia|Yes| 8769.0|F9 human KI, mouse KO (165A) |C57BL/6-F9/165ACslApb||Recessive|coagulation factor IX|F9||Cf9, Cf-9|MGI:88384||||X|||||||||||||||||||||||||||||Mice may exhibit haemophilia B - it is unknown to what degree the human F9 clotting factor compensates.|Mice may exhibit haemophilia B - it is unknown to what degree the human F9 clotting factor compensates.|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|09-Aug-2019|Cryopreserved sperm|50.0|0.0|Unknown||Haemophilia|Yes| 8775.0|F9 human KI, mouse KO (202B)|C57BL/6-F9/202BCslApb||Recessive|coagulation factor IX|F9|Nil|Cf9, Cf-9|MGI:88384||||X|||||||||||||||||||||||||||||Mice may exhibit haemophilia B - it is unknown to what degree the human F9 clotting factor compensates.|Mice may exhibit haemophilia B - it is unknown to what degree the human F9 clotting factor compensates.|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|09-Aug-2019|Cryopreserved sperm|50.0|0.0|Unknown||Haemophilia|Yes| 8766.0|F8 KO (80A)|C57BL/6-F8/80ACslApb||Recessive|coagulation factor VIII|F8|Nil|Cf8, Cf-8, Factor VIII, FVIII|MGI:88383||||X|||||||||||||||||||||||||||||Mice are haemophilic as they are deficient in the clotting factor, FVIII.|Mice may be haemophilic.|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|09-Aug-2019|Cryopreserved sperm|30.0|0.0|Unknown||Haemophilia|Yes| 8767.0|F8 KO (80B)|C57BL/6-F8/80BCslApb||Recessive|coagulation factor VIII|F8||Cf8, Cf-8, Factor VIII, FVIII|MGI:88383||||X|||||||||||||||||||||||||||||Mice are haemophilic as they are deficient in the clotting factor, FVIII.|Mice may be haemophilic.|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|09-Aug-2019|Cryopreserved sperm|50.0|0.0|Unknown||Haemophilia|Yes| 9241.0|PANX1nc|C57BL/6N-PANX1nc/APB||Semi-dominant|Pannexin 1|Panx1 |||MGI:1860055 |Pannexin|PANX1nc||9|||||||||||||||||||||||||||||Normal|Normal|C57Bl/6|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|29-Jul-2021|Cryopreserved sperm|70.0|0.0|Unknown||Phagocytosis, PANX1, neutrophil activation, inflammation, transmembrane channels|Possibly| 9271.0||C57BL/6J-Tg<(mAce2-hACE2)49MGMP>/Apb ||Semi-dominant|angiotensin 1 converting enzyme 2||||||||Unknown|||||||||||||||||pAMP-mAce2 promoter-hACE2 cDNA-pA |mouse Ace2 promoter|||||||||||Unknown|Unknown|C57Bl/6J|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|17-Sep-2021|Cryopreserved sperm|50.0|0.0|Unknown|||Possibly| 8802.0|ASD1034:Blackcurrant:1:N1|C57BL/6NCrlAnu-Slc7a9/AnuApb||Recessive|solute carrier family 7 (cationic amino acid transporter, y+ system), member 9|Slc7a9|Unknown|b, + amino acid transporter, b, +AT, CSNU3|MGI:1353656|Slc7a9; endonuclease-mediated mutation 1, Australian National University|Slc7a9||7||||||||||Unknown to Unknown|||||||||||||||||||Mice may develop lupus-like symptoms|Unknown|C57BL/6NCrlAnu|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|10-Oct-2019|Cryopreserved sperm|12.0|0.0|Unknown||Lupus|Yes| 8803.0|ASD899:Lychee:Ct4bpdel|C57BL/6NCrlAnu-Ctbp1/AnuApb||Recessive|C-terminal binding protein 1|Ctbp1|Unknown|BARS, CtBP1-L, CtBP1-S, CtBP3/BARS, D4S115h, D5H4S115|MGI:1201685|Ctbp1; endonuclease-mediated mutation 1, Australian National University|Ctbp1||5||||||||||Unknown to Unknown|||||||||||||||||||Unknown|Unknown|C57BL/6NCrlAnu|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|11-Oct-2019|Cryopreserved sperm|29.0|0.0|Unknown|||Yes| 8805.0|ASD900:Dragonfruit:PH196|C57BL/6NCrlAnu-Phrf1/AnuApb||Recessive|PHD and ring finger domains 1|Phrf1|||MGI:2141847|Phrf1; endonuclease-mediated mutation 1, Australian National University|Phrf1||7||||||||||Unknown to Unknown|||||||||||||||||||Unknown|Unknown|C57BL/6NCrlAnu|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|21-Oct-2019|Cryopreserved sperm|44.0|0.0|Unknown|||Yes| 8808.0|ASD924:Longan:PA56|C57BL/6NCrlAnu-Pacsin1/AnuApb||Recessive|protein kinase C and casein kinase substrate in neurons 1|Pacsin1|Unknown|A830061D09Rik, mKIAA1379, Syndapin I|MGI:1345181||||17|||||||||||||||||||||||||||||Unknown|Unknown|C57BL/6NCrlAnu|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|21-Oct-2019||0.0|0.0|Unknown|||Yes| 9276.0|Dnajb11 35^1bp|C57Bl6/N-Dnajb11Anu/Apb||Recessive|DnaJ heat shock protein family (Hsp40) member B11|Dnajb11|||MGI:1915088||||16|||||||||||||||||||||||||||||unknwon|unknown|C57Bl/6N|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|28-Sep-2021|Cryopreserved sperm|12.0|0.0|Unknown|||Yes| 8817.0|ASD950:Rambutan:::F1|C57BL/6NCrlAnu-Tet2/Anuapb||Recessive|tet methylcytosine dioxygenase 2|Tet2|Unknown|Ayu17-449, E130014J05Rik, mKIAA1546|MGI:2443298|Tet2; endonuclease-mediated mutation 1, Australian National University|Tet2||3||||||||||Unknown to Unknown|||||||||||||||||||Unknown|Unknown|C57BL/6NCrlAnu|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|22-Oct-2019|Cryopreserved sperm|57.0|50.0|Unknown|||Yes| 9280.0|Tg(mAce2-hACE2)|C57BL/6J /AnuApb||Recessive|||||||||Unknown|||||||||||||||||pAMP-mAce2 promoter-hACE2 cDNA-pA |mouse Ace2 promoter|Unknown||||||||||Unknown|Unknown|C57Bl/6J|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|05-Oct-2021|Cryopreserved sperm|60.0|0.0|Unknown||Coronovirus, Covid19|Possibly| 9277.0|LSA|B6;Balb-Gt(ROSA)26Sor/AnuApb||Recessive|gene trap ROSA 26, Philippe Soriano|Gt(ROSA)26Sor||beta geo, Gtrgeo26, Gtrosa26, R26, ROSA26, Thumpd3as1 |MGI:104735 |gene trap ROSA 26, Philippe Soriano|Gt(ROSA)26Sor||6|||||||||||||||||||||||||||||Unknown|Unknown|Balb/c, C57BL/6J|Yes|Yes|Unknown|Yes|Yes|Unknown|No|Unknown||||No|30-Sep-2021||0.0|0.0|Unknown||Gt(ROSA)26Sor , Beta-actin, Large BiT|Yes| 9279.0|Pthrpflox, PTHrPL2|B6;129-Pthlh/AnuApb|MGI:2387462|Recessive|parathyroid hormone-like peptide|Pthlh|Normal|parathyroid hormone-like hormone, parathyroid hormone-related peptide, parathyroid hormone-related protein, PTH-like, PTH-related peptide, Pthrp |MGI:97800 |parathyroid hormone-like peptide; targeted mutation 1, Andrew C Karaplis|Pthlh|MGI:2387462|6|||||||||||||||||||||||||||||Normal|Normal|C57Bl/6;129|Yes|Yes|Unknown|Yes|Yes|Unknown|No|Good||||No|05-Oct-2021|Cryopreserved sperm|50.0|0.0|Unknown|||Yes| 9275.0|Irf4 em11.2^47bp|C57BL/6NCrlAnu-Ifr4/AnuApb||Semi-dominant|interferon regulatory factor 4|Irf4||IRF-4, Spip|MGI:1096873|endonuclease mediated targeting 11.2;|Irf4 em11.2^47bp||13|||||||||||||||||||||||||||||unknown|unknown|C57Bl/6N|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|28-Sep-2021|Cryopreserved sperm|11.0|0.0|Unknown|||Possibly| 9273.0||B6-Gt(ROSA)26SorApb||Semi-dominant|gene trap ROSA 26, Philippe Soriano|Gt(ROSA)26Sor|||MGI:104735||||6|||||||||||||||||||||||||||||Unknown|Unknown|C57BL/6|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|21-Sep-2021||0.0|0.0|Unknown|||Yes| 8820.0|ASD924:Longan:PA1bpdel|C57BL/6NCrlAnu-Pacsin1/AnuApb||Recessive|protein kinase C and casein kinase substrate in neurons 1|Pacsin1|Unknown|A830061D09Rik, mKIAA1379, Syndapin I|MGI:1345181|Pacsin1; endonuclease-mediated mutation 2, Australian National University|Pacsin1||17||||||||||Unknown to Unknown|||||||||||||||||||Unknown|Unknown|C57BL/6NCrlAnu|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|24-Oct-2019|Cryopreserved sperm|65.0|41.0|Unknown|||Yes| 8810.0|ASD951:Mangosteen:RA203|C57BL/6NCrlAnu-Rasal1/AnuApb||Recessive|RAS protein activator like 1 (GAP1 like)|Rasal1|Unknown|MRASAL|MGI:1330842|Rasal1; endonuclease-mediated mutation 1, Australian National University|Rasal1||5||||||||||Unknown to Unknown|||||||||||||||||||Unknown|Unknown|C57BL/6NCrlAnu|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|21-Oct-2019|Cryopreserved sperm|46.0|42.0|Unknown|||Yes| 9272.0| ASD1068:Apricot| C57Bl/6N-Ctla4/Apb||Semi-dominant|cytotoxic T-lymphocyte-associated protein 4|Ctla4||Ctla-4, Ly-56|MGI:88556|Ctla4; endonuclease-mediated mutation 4, Australian National University|Ctla4||1|ENSMUSG00000026011 ||||||||||||||||||||||||||||Develops autoimmunity when homozygous|normal|C57Bl/6N|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|21-Sep-2021|Cryopreserved sperm|55.0|0.0|Unknown|||Possibly| 8824.0|hIl3_GMCSF 20B|BALB/c-Csf2/Il3||Dominant|colony stimulating factor 2 (granulocyte-macrophage)|Csf2||Csfgm, Gm-CSf, GMCSF, MGI-IGM|MGI:1339752|colony stimulating factor 2 (granulocyte-macrophage); targeted mutation 1.1, Richard A Flavell|Csf2/Il3|MGI:4887879|11|||||||||||||||||||||||||||||mouse IL3 and GM-CSF have been KO and human IL3 and GM-CSF have been KI|unknown|balbc|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|08-Nov-2019|Cryopreserved sperm|50.0|0.0|Unknown||Myeloid|Yes| 8824.0|hIl3_GMCSF 20B|BALB/c-Csf2/Il3||Dominant|interleukin 3|Il3||BPA, Csfmu, HCGF, Il-3, MCGF, PSF|MGI:96552|interleukin 3; targeted mutation 1.1, Richard A Flavell|Csf2/Il3|MGI:4887881|11|||||||||||||||||||||||||||||mouse IL3 and GM-CSF have been KO and human IL3 and GM-CSF have been KI|unknown|balbc|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|08-Nov-2019|Cryopreserved sperm|||Unknown||Myeloid|Yes| 9281.0||C57Bl/6N-Tg(DCLK1-CreERT2)Ernst-Dclk1/Apb||Semi-dominant|doublecortin-like kinase 1|Dclk1||1700113D08Rik, 2810480F11Rik, Click-I, CPG16, Dcamkl1, Dcl, DCLK, mKIAA0369|MGI:1330861|doublecortin-like kinase 1; targeted mutation 1a, Wellcome Trust Sanger Institute|Dclk1|MGI:5543459|3|||||||||||||||||Tg(DCLK1-CreERT2)Ernst||||||||||||Normal|Normal|C57Bl/6N|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|05-Oct-2021||0.0|0.0|Unknown|||Possibly| 9282.0|Tg(DCLK1-CreERT2)Ernst;Dclk1tm1(EUCOMM)|C57Bl/6N-Tg<(DCLK1-CreERT2)Ernst>;Dclk1/AnuApb||Recessive|doublecortin-like kinase 1|DCKL1||1700113D08Rik, 2810480F11Rik, Click-I, CPG16, Dcamkl1, Dcl, DCLK, mKIAA0369 |MGI:1330861|doublecortin-like kinase 1; targeted mutation 1a, Wellcome Trust Sanger Institute|Dclk1|MGI:5543459|3|||||||||||||||||cre recombinase fused to the human estrogen receptor ligand binding domain|DCLK1|||||||||||Normal|Normal|C57Bl/6N|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|05-Oct-2021||0.0|0.0|Unknown|||Possibly| 9288.0|ASD929:Gala:623del:Ly5a:N4 |C57BL/6NCrlAnu-Gm14718 Ptprc/Anu||Dominant|predicted gene 14718|Gm14718|Unknown|lncRNA gene|MGI:3705113 |endonuclease mediated targeting 1|lncRNA <623del>||X|||||||||||||||||||||||||||||A slight decrease in CD40L expression in CD4 T cells when activated in vitro||C57Bl/6N|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|21-Oct-2021|Cryopreserved sperm|46.0|0.0|Unknown|||Possibly| 8823.0|ASD951:Mangosteen:RA1bpdel|C57BL/6NCrlAnu-Rasal1/AnuApb||Recessive|RAS protein activator like 1 (GAP1 like)|Rasal1|Unknown|MRASAL|MGI:1330842|Rasal1; endonuclease-mediated mutation 2, Australian National University|Rasal1||5||||||||||Unknown to Unknown|||||||||||||||||||Unknown|Unknown|C57BL/6NCrlAnu|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|07-Nov-2019|Cryopreserved sperm|65.0|35.0|Unknown|||Yes| 9283.0||C57Bl/6J-PANX1/Apb||Semi-dominant|Panx1|pannexin 1|||MGI:1860055||||9|ENSMUSG00000031934 |||||||||Unknown to Unknown|||||||||||||||||||Normal|Normal|C57Bl/6|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|05-Oct-2021|Cryopreserved sperm|50.0|0.0|Unknown|||Possibly| 9285.0|PANX1TCTStop|C57Bl/6-PANX1/Apb||Semi-dominant|pannexin 1|Panx1|||MGI:1860055||||9|||||||||||||||||||||||||||||Normal|Normal|C57Bl/6J|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|07-Oct-2021|Cryopreserved sperm|50.0|0.0|Unknown|||Possibly| 9286.0|ASD1124:Dst 3991:F0|C57Bl/6N-Dst Anu/Apb||Semi-dominant|dystonin|Dst|||MGI:104627||||1|||||||||||||||||||||||||||||unknown|unknown|C57Bl/6N|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|12-Oct-2021|Cryopreserved sperm|12.0|0.0|Unknown|||Possibly| 9290.0||C57Bl/6N-Ramos/Apb||Semi-dominant|TLR7||||||||Unknown|||||||||||||||||||||||||||||Normal|Normal|C57Bl/6N|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|26-Oct-2021|Cryopreserved sperm|58.0|0.0|Unknown|||Possibly| 8828.0|ASD950:Rambutan:TE1806|C57BL/6NCrlAnu-Tet2/Anuapb||Recessive|tet methylcytosine dioxygenase 2|Tet2|Unknown|Ayu17-449, E130014J05Rik, mKIAA1546|MGI:2443298|Tet2; endonuclease-mediated mutation 2, Australian National University|Tet2||3||||||||||Unknown to Unknown|||||||||||||||||||Unknown|Unknown|C57BL/6NCrlAnu|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|22-Nov-2019|Cryopreserved sperm|73.0|25.0|Unknown|||Yes| 9289.0|FoxP3ko:TCR7:Rag1(Tm1Mom)::F4|B6(Cg)-Foxp3 Rag1 Tg(TcraBO4H9.1,TcrbBO4H9.1)7Aog/Anu||Dominant|forkhead box P3|Foxp3|||MGI:1891436|Foxp3:targeted mutation 1.1, Alexander Y Rudensky|Foxp3 |MGI:2654936|X|||||||||||||||||transgene insertion 7, Anne O'Garra||||||||||||Mice are Foxp3 KO and carry the HEL-specific TCR transgene "TCR7". These mice are on a Rag1 ko background, so they do not have the scurfy phenotype.|Normal|B6/121-Rag1(tm1Mom/ANU) x C57Bl/6N |Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|25-Oct-2021|Cryopreserved sperm|60.0|0.0|Unknown|||Yes| 9289.0|FoxP3ko:TCR7:Rag1(Tm1Mom)::F4|B6(Cg)-Foxp3 Rag1 Tg(TcraBO4H9.1,TcrbBO4H9.1)7Aog/Anu||Dominant|recombination activating 1|Rag1|||MGI:97848|Rag1:targeted mutation 1, Peter Mombaerts|Rag1|MGI:1857241|2|||||||||||||||||||||||||||||Mice are Foxp3 KO and carry the HEL-specific TCR transgene "TCR7". These mice are on a Rag1 ko background, so they do not have the scurfy phenotype.|Normal|B6/121-Rag1(tm1Mom/ANU) x C57Bl/6N |Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|25-Oct-2021|Cryopreserved sperm|||Unknown|||Yes| 9148.0|Stra8-iCre|C57BL6/J-Tg(Stra8-iCre)1Reb/LguJ||Semi-dominant|stimulated by retinoic acid gene 8|Stra8|||MGI:107917||||6|ENSMUSG00000029848 |||||||||Unknown to Unknown|||||||transgene insertion 1, Robert E Braun|Stra8|||||||||||Normal|Normal|C57Bl/6J|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|17-Feb-2021|Cryopreserved sperm|50.0|0.0|Unknown||Spermatogonia, Male Germ Cells, Primordial germ cells|Possibly| 9242.0|Wdr26: 1bp insertion|C57BL/6NCrlAnu-Wdr26/AnuApb||Semi-dominant|WD repeat domain 26|Wdr26 ||1600024A01Rik, Gid7|MGI:1923825||||1|||||||||||||||||||||||||||||Unknown|Unknown|C57Bl/6N|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|29-Jul-2021|Cryopreserved sperm|55.0|0.0|Unknown|||Possibly| 9259.0|Alox5AP:G75R|C57BL/6NCrlAnu-Alox5AP/AnuApb||Semi-dominant|Arachidonate 5-lipoxygenase activating protein|Alox5AP ||arachidonate 5 lipoxygenase activating protein, Flap |MGI:107505|Arachidonate 5-lipoxygenase activating protein|Alox5AP ||Unknown|||||||||||||||||||||||||||||Unknown|Unknown|C57Bl/6N|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|12-Aug-2021|Cryopreserved sperm|57.0|0.0|Unknown|||Possibly| 9294.0|Juric:2|C57BL/6N-IL21R/AnuApb||Semi-dominant|interleukin 21 receptor|IL21R||NILR |MGI:1890475|interleukin 21 receptor|IL21R||7|||||||||||||||||||||||||||||Normal|Normal|C57Bl/6N|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|05-Nov-2021|Cryopreserved sperm|45.0|0.0|Unknown||Class switch, T cells, CD8, IL-21|Possibly| 9274.0|Hoxb7-EGFP|C57BL/6J-Tg<(Hoxb7-EGFP)33Cos>/AnuApb||Semi-dominant||||||||||||||||||||||||||transgene insertion 33, Franklin Costantini|homeobox B7 promoter/enhancer sequences|||||||||||not viable|normal|C57Bl/6J|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|23-Sep-2021|Cryopreserved sperm|50.0|0.0|Unknown|||Possibly| 8199.0|B/c.BlGpA; B/c.TgN(HUFUT1-HUGTA-MUSMICAM2)|C.B6-Tg(Icam2-FUT1, GTA)||Dominant||||||||||||||||||||||||||human H-transferase and human A-transferase|ICAM2|||||||||||These mice are transgenic for two human genes encoding enzymes responsible for the synthesis of the blood group A antigen, which mice do not normally express. They express human blood group A on the surface of blood vessels throughout the body, and on erythrocytes and neutrophils. They develop and behave normally, and do not require special monitoring or care.|These mice are transgenic for two human genes encoding enzymes responsible for the synthesis of the blood group A antigen, which mice do not normally express. They express human blood group A on the surface of blood vessels throughout the body, and on erythrocytes and neutrophils. They develop and behave normally, and do not require special monitoring or care.|BALB/c|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|11|||No|24-Feb-2017|Cryopreserved sperm|50.0|0.0|Unknown||transferase|Yes| 9243.0|Kif13a: G318R substitution|C57BL/6NCrlAnu-Kif13a/AnuApb ||Semi-dominant|kinesin family member 13A|Kif13a||1600024A01Rik, Gid7|MGI:1098264|kinesin family member 13A|Kif13a ||13|||||||||||||||||||||||||||||Unknown|Unknown|C57Bl/6N|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|29-Jul-2021|Cryopreserved sperm|58.0|0.0|Unknown|||Possibly| 9293.0||Adidas:Cahill:Ikbkb-V203I:GFP-Fox||Dominant|only for L2 reder|only for L2 reder|||||||Unknown|||||||||||||||||||||||||||||normal|normal|C57Bl/6N|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|03-Nov-2021||0.0|0.0|Unknown|||Possibly| 8830.0|ASD899:Lychee:Ct96|C57BL/6NCrlAnu-Ctbp1/AnuApb||Recessive|C-terminal binding protein 1|Ctbp1|Unknown|BARS, CtBP1-L, CtBP1-S, CtBP3/BARS, D4S115h, D5H4S115|MGI:1201685|Ctbp1; endonuclease-mediated mutation 2, Australian National University|Ctbp1||5||||||||||Unknown to Unknown|||||||||||||||||||Unknown|Unknown|C57BL/6NCrlAnu|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|28-Nov-2019|Cryopreserved sperm|19.0|0.0|Unknown|||Yes| 9267.0|ENU54:G2|ANU:ENU54:G2||Recessive|Unknown||||||||Unknown||||||||||||||||Unknown|||||||||||||Unknown|Unknown|C57BL/6NCrlAnu|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||1||No|23-Aug-2021|Cryopreserved sperm|6702.0|41.0|Unknown||ENU, random, mutagenesis, screen|Yes| 9306.0|Gabrd L260V|C57Bl/6J-Gabrd/Apb ||Semi-dominant|gamma-aminobutyric acid (GABA) A receptor, subunit delta|GABRD|||MGI:95622||||4|||||||||||||||||||||||||||||Unknown|No overt phenotype, seizures possible|C57Bl/6J|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|24-Nov-2021|Cryopreserved sperm|38.0|0.0|Unknown|||Possibly| 9172.0|ENU53:G2|ANU:ENU53:G2||Recessive|Not known yet||||||||Unknown||||||||||||||||||||||||||||| | |C57Bl/6N|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|08-Apr-2021|Cryopreserved sperm|10829.0|37.0|Unknown||ENU, Random, mutagenesis, screen|Possibly| 9278.0|ENU53:G3|ANU:ENU53:G3||Recessive|Unknown||||||||Unknown||||||||||||||||Unknown|||||||||||||Unknown|Unknown|C57BL/6NCrlAnu|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||1||No|03-Oct-2021|Cryopreserved sperm|80.0|0.0|Unknown||ENU, random, mutagenesis, screen|Yes| 9296.0||ASD663:Kennedy:6||Dominant|BTLA|||||L188F|||Unknown|||||||||||||||||||||||||||||Normal|Normal|C57Bl/6N|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|05-Nov-2021|Cryopreserved sperm|58.0|0.0|Unknown|||Possibly| 9239.0|Itk:KO:10|C57BL/6N-Itk/AnuApb||Recessive|IL2 inducible T cell kinase|Itk||Emt, Tcsk, Tsk|MGI:96621 |ItkAnuApb|Itk||11|||||||||||||||||||||||||||||unknown|unknown|C57Bl/6N|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|27-Jul-2021|Cryopreserved sperm|12.0|0.0|Unknown|||Yes| 9069.0|ASD891:Sorghum|C57BL/6N-NLRP9a/Apb||Recessive|NLR family, pyrin domain containing 9A|Nlrp9a ||D7Ertd565e, Nalp9a, Nalp-theta|MGI:2675292|NLR family, pyrin domain containing 9A |Nlrp9a||7|||||||||||||||||||||||||||||Normal|Normal|C57BL/6NCrlAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|01-Sep-2020|Cryopreserved sperm|48.0|0.0|Unknown||Nlrp9a, ATP binding, Inflammatory response, Innate immune response|Possibly| 9300.0|PRαMCM|C57Bl/6J-Pdgfra/Apb||Dominant|platelet derived growth factor receptor, alpha polypeptide|Pdgfra|Unknown||MGI:97530|platelet derived growth factor receptor, alpha polypeptide; targeted mutation 1, Shin-Ichi Nishikawa|Pdgfra|MGI:5475226|5|||||||||||||||||||||||||||||This strain is reported to be lethal in a homozygous state|Normal|C57Bl/6J|No|No|Yes|No|No|Yes|No|Unknown||||No|09-Nov-2021||0.0|0.0|Unknown|||Possibly| 9295.0||ASD663:Kennedy:4||Dominant|BTLA|||||1bpInsertion|||Unknown|||||||||||||||||||||||||||||Normal|Normal|C57Bl/6N|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|05-Nov-2021|Cryopreserved sperm|60.0|0.0|Unknown|||Possibly| 9298.0||C57Bl/6-Mef2C(AHF)-Cre; Nedd4fl/+; Z/EG/Apb||Semi-dominant|Nedd4||||||||Unknown|||||||||||||||||Cre recombinase and LacZ / EGFP (Z/EG)|Cre driven by Mef2C enhancers in the second heart field and LacZ / EGFP floxed stop reporter in a safe harbour locus|||||||||||Unknown|Normal|C57 - unknown|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|09-Nov-2021|Cryopreserved sperm|50.0|0.0|Unknown|||Possibly| 9299.0|Wnt11 KO|129:B6-Wnt11||Semi-dominant|wingless-type MMTV integration site family, member 11|Wnt11|||MGI:101948 |wingless-type MMTV integration site family, targeted mutation 1; Andrew McMahon|Wnt11 |MGI:2665014|7|||||||||||||||||||||||||||||These mice display incomplete embryonic and perinatal lethality in a homozygous state with defects in kidney development|Normal, with slightly smaller kidneys|129S1/B6|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|09-Nov-2021|Cryopreserved sperm|50.0|0.0|Unknown|||Possibly| 8834.0|Nasp fl|C57BL/6N-Nasp/MarpApb||Recessive|nuclear autoantigenic sperm protein (histone-binding)|Nasp|Unknown|5033430J04Rik, D4Ertd767e, Epcs32, Nasp-T|MGI:1355328|nuclear autoantigenic sperm protein (histone-binding); targeted mutation 1c, Wellcome Trust Sanger Institute|Nasp||4||||||||||Unknown to Unknown|||||||||||||||||||Normal||C57BL/6N|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|11-Dec-2019||0.0|0.0|Unknown|||Yes| 9270.0|Tg(mAce2-hACE2)|C57BL/6J/AnuApb||Recessive|||||||||Unknown|||||||||||||||||pAMP-mAce2 promoter-hACE2 cDNA-pA |mouse Ace2 promoter|Unknown||||||||||Unknown|Unknown|C57Bl/6J|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|17-Sep-2021|Cryopreserved sperm|50.0|0.0|Unknown||Coronovirus, Covid19|Possibly| 5257.0|CathepsinK.gp130fl/fl|C57BL/6-Il6st Ctsk||Recessive|interleukin 6 signal transducer|Il6st|Normal|CD130, gp130|MGI:96560|interleukin 6 signal transducer; targeted mutation 1, Werner Mueller|Il6st|MGI:1931239|13||||||||||||||||Yes|||||||||||||Unknown|Unknown|C57BL/6|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|21-Oct-2010|Cryopreserved sperm|169.0|0.0|Unknown||osteoclast, signal transduction|Possibly| 5257.0|CathepsinK.gp130fl/fl|C57BL/6-Il6st Ctsk||Recessive|cathepsin K|Ctsk||catK, Cat K|MGI:107823|cathepsin K; targeted mutation 1, Shigeaki Kato|Ctsk|MGI:3764465|3|||||||||||||||||||||||||||||Unknown|Unknown|C57BL/6|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|21-Oct-2010|Cryopreserved sperm|||Unknown||osteoclast, signal transduction|Possibly| 8835.0|ENU43:101:abcg8|C57BL/6NCrlAnu-Abcg8/AnuApb||Recessive|ATP binding cassette subfamily G member 8|Abcg8|Unknown|1300003C16Rik, Sterolin-2|MGI:1914720||||17|||||||||||||||||||||||||||||Unknown||C57BL/6NCrlAnu|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|12-Dec-2019|Cryopreserved sperm|24.0|0.0|Unknown|||Yes| 9303.0|Ntsr1-cre|C57BL/6J-Tg<(Ntsr1-cre)GN209Gsat>/AnuApb||Semi-dominant|neurotensin receptor 1|Ntsr1||NT-1R, NTR1, NTR-1, Ntsr1|MGI:97386||||2|||||||||||||||||transgene insertion GN209, GENSAT Project at Rockefeller University|neurotensin receptor 1 gene|||||||||||Unknown|Unknown|C57Bl/6J|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|16-Nov-2021|Cryopreserved sperm, Live|55.0|0.0|Unknown||Nervous system, Brain|Possibly| 9115.0|Drosha:CreER|B6:129-Drosha:Gt(ROSA)26Sor/AnuApb||Semi-dominant|drosha, ribonuclease type III|Drosha|Unknown|1110013A17Rik, Etohi2, Rnasen |MGI:1261425|drosha, ribonuclease type III; targeted mutation 1, Dan R Littman|Drosha|http://www.informatics.jax.org/allele/key/61744|15|||||||||||||||||gene trap ROSA 26, Philippe Soriano; targeted mutation 9, TaconicArtemis|Gt(ROSA)26Sor|||||||||||N/A|N/A|C57BL/6NTac:129P2/OlaHsd|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|11-Jan-2021|Cryopreserved sperm|50.0|0.0|Unknown|||Possibly| 8055.0|Sox2-GiDREADD|B6(Cg).129-Sox2 Gt(ROSA)26Sor/JAusb||Recessive|SRY (sex determining region Y)-box 2|Sox2||lcc, Sox-2, ysb|MGI:98364|SRY (sex determining region Y)-box 2; targeted mutation 1, Konrad Hochedlinger|Sox2|MGI:5295990|3|||||||||||||||||||||||||||||Bi-transgenic mice will enable expression of target gene (i.e. DREADD receptor) in sox2-expressing cells upon tamoxifen administration, which will persist as the cells differentiate and mature.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|03-Jun-2016||0.0|0.0|Unknown|||Yes| 8055.0|Sox2-GiDREADD|B6(Cg).129-Sox2 Gt(ROSA)26Sor/JAusb||Recessive|gene trap ROSA 26, Philippe Soriano|Gt(ROSA)26Sor||beta geo, Gtrgeo26, Gtrosa26, R26, ROSA26, Thumpd3as1|MGI:104735|gene trap ROSA 26, Philippe Soriano; targeted mutation 1, Ute Hochgeschwender|Gt(ROSA)26Sor|MGI:5614050|6|||||||||||||||||||||||||||||Bi-transgenic mice will enable expression of target gene (i.e. DREADD receptor) in sox2-expressing cells upon tamoxifen administration, which will persist as the cells differentiate and mature.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|03-Jun-2016||||Unknown|||Yes| 9305.0|ENU55:G2|ANU:ENU55:G2||Recessive|Unknown||||||||Unknown||||||||||||||||||||||||||||| | |C57BL/6JAnu|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|22-Nov-2021|Cryopreserved sperm|7381.0|0.0|Unknown|||Possibly| 9302.0||C57Bl/6-Il6st/Apb||Semi-dominant|interleukin 6 signal transducer|IL6st||5133400A03Rik, CD130, D13Ertd699e, gp130 |MGI:96560 |interleukin 6 signal transducer; targeted mutation 1b, Mouse Biology Program, UC Davis|Il6sttm1b(KOMP)Mbp|MGI:5474976|13|||||||||||||||||||||||||||||Normal|Normal|C57Bl/6J|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|11-Nov-2021|Cryopreserved sperm|50.0|0.0|Unknown|||Possibly| 9310.0|mettl3 flox/flox|C57BL/6J-Mettl3/AnuApb||Semi-dominant|methyltransferase like 3|Mettl3 ||2310024F18Rik, M6A, Spo8|MGI:1927165|methyltransferase like 3; targeted mutation 1, Jacob Hanna|Mettl3|MGI:5911703|14|||||||||||||||||||||||||||||||C57Bl/6J|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|01-Dec-2021||0.0|0.0|Unknown|||Possibly| 9202.0|C57BL/6J|ASD1136:C57BL/6JAusb.ANU:::EXP||Dominant|N/A|N/A|||||||Unknown|||||||||||||||||||||||||||||wildtype - normal|wildtype - normal|C57Bl6/J|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|09-Jun-2021||0.0|87.0|Unknown|||Possibly| 9182.0||SwHel:Hc.Lc:Ly5a:Ptprca/NCrl||Dominant|protein tyrosine phosphatase, receptor type|only for L2 reder|||||||Unknown||||||||||||||||||||||||||||||||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|07-May-2021||0.0|0.0|Unknown|||Possibly| 9316.0||C57Bl/6N-Dst/Apb||Semi-dominant|dystonin|Dst |||MGI:104627|Dst |||1|||||||||||||||||||||||||||||Unknown|Unknown|C57Bl/6N|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|09-Dec-2021|Cryopreserved sperm|55.0|0.0|Unknown|||Possibly| 8837.0|DNAH5/PKHD1|C57BL/6-Dnah5 Pkhd1/Marp||Recessive|dynein, axonemal, heavy chain 5|Dnah5|Unknown|b2b1134Clo, b2b1154Clo, b2b1537Clo, b2b1565Clo, b2b3491Clo, Dnahc5, Mdnah5|MGI:107718||||15|||||||||||||||||||||||||||||Normal|Normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|10-Jan-2020|Cryopreserved sperm|50.0|0.0|Unknown|||Yes| 8837.0|DNAH5/PKHD1|C57BL/6-Dnah5 Pkhd1/Marp||Recessive|polycystic kidney and hepatic disease 1|Pkhd1|Unknown|FPC, tigmin|MGI:2155808||||1|||||||||||||||||||||||||||||Normal|Normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|10-Jan-2020|Cryopreserved sperm|||Unknown|||Yes| 9308.0|Adar1 em2Crwy|C57Bl/6J-Adar1/Apb||Dominant|adenosine deaminase, RNA-specific|Adar||Adar1p110, Adar1p150|MGI:1889575|adenosine deaminase, RNA-specific; endonuclease-mediated mutation 3, Carl R Walkley|Adar||3|ENSMUSG00000027951||||||||||||||||||||||||||||Would be expected to be embryonic lethal (not tested prior to cryopreservation)|Normal, fertile and health. No discernable phenotype|C57Bl/6J|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|26-Nov-2021|Cryopreserved sperm|30.0|0.0|Unknown|||Possibly| 9313.0||C57Bl/6-Tcf3 KO/Apb||Semi-dominant|Tcf3||||||||Unknown|||||||||||||||||||||||||||||unknown|unknown|C57Bl/6N|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|02-Dec-2021|Cryopreserved sperm|11.0|0.0|Unknown|||Possibly| 9314.0|Opg -/-|C57BL/6J-Tnfrsf11b/Apb||Semi-dominant|tumor necrosis factor receptor superfamily, member 11b (osteoprotegerin)|Tnfrsf11b||OCIF, Opg, OPG, osteoclastogenesis inhibitory factor, TR1|MGI:109587||Tnfrsf11b|tumor necrosis factor receptor superfamily, member 11b (osteoprotegerin); targeted mutation 1, Edward A Clark|15|||||||||||||||||||||||||||||Homozygous|Unknown |C57Bl/6J|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|06-Dec-2021|Cryopreserved sperm|50.0|0.0|Unknown|||Possibly| 9312.0||C57Bl/6N-Tcf3 KO/Apb||Semi-dominant|Tcf||||||||Unknown|||||||||||||||||||||||||||||unknown|unknown|C57Bl/6N|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|02-Dec-2021||0.0|0.0|Unknown|||Possibly| 9309.0|CTV VEZT|C57Bl/6J-Wehi/AnuApb||Semi-dominant|vezatin, adherens junctions transmembrane protein|Vetz|||MGI:2143698|Rosa26tm1(VEZT)WEHI|||Unknown|||||||||||||||||||||||||||||Normal|Normal|C57Bl/6J|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|29-Nov-2021|Cryopreserved sperm|50.0|0.0|Unknown|||Possibly| 9323.0||C57Bl/6N-ENU51:015:Irak2/Apb||Semi-dominant|Irak2||||||||Unknown||||||||||||||||||||||||||||| | |C57Bl/6J|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|19-Dec-2021|Cryopreserved sperm|47.0|0.0|Unknown|||Possibly| 7966.0|Heatr3 KO|C57BL/6NTac-Heatr3/IcsOrlAnu|C57BL/6NTac-Heatr3/IcsOrlAnu|Recessive|HEAT repeat containing 3|Heatr3|Normal|C030036P15Rik|MGI:2444491|HEAT repeat containing 3; targeted mutation 1a, Helmholtz Zentrum Muenchen GmbH|Heatr3|MGI:4435825|8|||||||||||||||||||||||||||||Normal|Normal|C57BL/6NTac|Unknown|Yes|Yes|Unknown|Yes|Yes|No|Unknown||||No|04-Sep-2015|Cryopreserved sperm|31.0|0.0|Unknown||EUCOMM|Yes| 9318.0|Irf4:K123R |C57BL/6NCrl-Irf4/Anu||Dominant|interferon regulatory factor 4|Irf4||IRF-4, Spip |MGI:1096873|endonuclease mediated targeting 8; Anselm Enders|Irf4 ||13|||||||||||||||||||||||||||||Unknown|Unknown|C57Bl/6N|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Dec-2021|Cryopreserved sperm|54.0|0.0|Unknown|||Possibly| 8838.0|ENU46:327:Casp1|C57BL/6NCrlAnu-Casp1/AnuApb||Recessive|caspase 1|Casp1|Unknown|Caspase-1, ICE, Il1bc, interleukin 1 beta-converting enzyme|MGI:96544||||9|||||||||||||||||||||||||||||Unknown||C57BL/6NCrlAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|14-Jan-2020|Cryopreserved sperm|72.0|0.0|Unknown||Caspase|Yes| 9354.0|ENU43:055:B6:G2rN1|C57BL/6Ncrl:ENU43/Anu||Dominant|Unknown||||||||Unknown||||||||||||||||||||||||||||| | |C57Bl/6N|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Mar-2022|Cryopreserved sperm|32.0|0.0|Unknown|||Possibly| 8843.0|Rab30 CRISPR KO #4|C57BL/6-Rab30/Apb||Recessive|RAB30, member RAS oncogene family|Rab30|Unknown|5033421K01Rik|MGI:1923235||||7|||||||||||||||||||||||||||||Normal|Normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|23-Jan-2020|Cryopreserved sperm|50.0|0.0|Unknown|||Yes| 9320.0|ASD1117:Sbds C.258+1G>C|Sbds C.258+1G>C||Recessive|Sbds|||||Sbds < C.258+1G>C >|||Unknown|||||||||||||||||||||||||||||Unknown|Unknown|C57Bl/6N|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Dec-2021|Cryopreserved sperm|54.0|0.0|Unknown|||Possibly| 8224.0|R26 MUT-Hoxa1 ki|B6JArc.Cg-Gt(ROSA)26Sor||Semi-dominant|gene trap ROSA 26, Philippe Soriano|Gt(ROSA)26Sor|Unknown|beta geo, Gtrgeo26, Gtrosa26, R26, ROSA26|MGI:104735|gene trap ROSA 26, Philippe Soriano; targeted mutation 3237, TaconicArtemis|Gt(ROSA)26Sor||6|||||||||||||||||||||||||||||Unknown|Unknown|C57BL/6JArc|Yes|Unknown|Yes|Yes|Unknown|Yes|No|Excellent|>6|||No|27-Mar-2017|Cryopreserved sperm|40.0|0.0|Unknown|||Possibly| 9322.0|ENU54:G3|ANU:ENU54:G3||Recessive|Unknown||||||||Unknown||||||||||||||||||||||||||||| | |C57Bl/6N|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|19-Dec-2021|Cryopreserved sperm|151.0|0.0|Unknown|||Possibly| 9325.0|Irf4 KO|C57Bl/6N-Irf4L116R(#36 35bpdel)>||Semi-dominant|Ifr4||||||||Unknown|||||||||||||||||||||||||||||unknown|unknown|C57Bl/6N|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|20-Dec-2021|Cryopreserved sperm|11.0|0.0|Unknown|||Possibly| 9216.0|Irf4:F0:23|C57BL/6NCrlAnu-Ifr4/AnuApb||Semi-dominant|interferon regulatory factor 4|Irf4||IRF-4, Spip|MGI:1096873 |Irf4|Irf4:F0:23||13|||||||||||||||||||||||||||||unknown|unknown|C57Bl/6N|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|07-Jul-2021|Cryopreserved sperm|12.0|0.0|Unknown|||Possibly| 8848.0|ENU47:327:Casp4|C57BL/6NCrlAnu-Casp4/AnuApb||Recessive|caspase 4, apoptosis-related cysteine peptidase|Casp4|Unknown|Casp11, Caspase-11, ich-3|MGI:107700||||9|||||||||||||||||||||||||||||Unknown|Unknown|C57BL/6NCrlAnu|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|06-Feb-2020|Cryopreserved sperm|92.0|0.0|Unknown||ENU, caspase|Yes| 8866.0|129X1/SvJ:B6 ; Casp11<129>|B6NCrlAnu;129X1-Casp4/AnuApb||Recessive|caspase 4, apoptosis-related cysteine peptidase|Casp4|Nil|Casp11, Caspase-11, ich-3|MGI:107700|caspase 4, apoptosis-related cysteine peptidase; deletion|Casp4|MGI:5473345|9|||||||||||||||||||||||||||||Mice exhibited defects in IL-1β production and harboured a mutation in the Casp11 locus that attenuated caspase-11 expression.Caspase-11 rather than caspase-1, however, was required for non-canonical inflammasome-triggered macrophage cell death, indicating that caspase-11 orchestrates both caspase-1-dependent and -independent outputs. Caspase-1 activation by non-canonical stimuli required NLRP3 and ASC, but caspase-11 processing and cell death did not, implying that there is a distinct activator of caspase-11. Lastly, loss of caspase-11 rather than caspase-1 protected mice from a lethal dose of lipopolysaccharide.||C57BL/6NCrlAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|24-Feb-2020||0.0|0.0|Unknown||inflammasome, Caspase 1, Caspase 11, bacteria|Yes| 9328.0|Myl9tm1a(KOMP)Wtsi|C57BL/6J-Myl9/Apb||Semi-dominant|myosin, light polypeptide 9, regulatory|Myl9||MLC20, Mylc2c, RLC-C |MGI:2138915 |myosin, light polypeptide 9, regulatory; targeted mutation 1a, Wellcome Trust Sanger Institute|Myl9|MGI:5299665|2|||||||||||||||||||||||||||||Perinatal lethal around Day 1 after birth due to loss of muscularis propria function in the bladder and small intestine|Normal. Expresses LacZ under control of the Mtl9 promoter.|C57Bl/6J|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|24-Jan-2022|Cryopreserved sperm|50.0|0.0|Unknown|||Possibly| 9330.0||C57BL/6NCrlAnu-Itk25Anu/Apb||Semi-dominant|IL2 inducible T cell kinase|Itk|||MGI:96621|Itk |||Unknown|||||||||||||||||||||||||||||Unknown|Unknown|C57Bl/6N|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|28-Jan-2022|Cryopreserved sperm|53.0|0.0|Unknown|||Possibly| 9333.0|B10.BR:Foxp3 KO:TCR/Apb |B6.B10-H2 Foxp3 Tg(TcrHEL3A9)1Mmd/Anu||Semi-dominant|histocompatibility-2, MHC|H2||H-2, MHC-II|MGI:95894|histocompatibility-2, MHC; k variant|H2|MGI:3579322|17|||||||||||||||||transgene insertion 1, Mark M Davis||||||||||||mice harbour the TCR3A9 transgene, which recognizes HELThey are also knockout for Foxp3 and Rag1||B10BR N6|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|04-Feb-2022|Cryopreserved sperm|18.0|0.0|Unknown|||Possibly| 9333.0|B10.BR:Foxp3 KO:TCR/Apb |B6.B10-H2 Foxp3 Tg(TcrHEL3A9)1Mmd/Anu||Semi-dominant|forkhead box P3|Foxp3|||MGI:1891436|forkhead box P3; targeted mutation 1.1, Alexander Y Rudensky|Foxp3|MGI:2654936|X|ENSMUSG00000039521 ||||||||||||||||||||||||||||mice harbour the TCR3A9 transgene, which recognizes HELThey are also knockout for Foxp3 and Rag1||B10BR N6|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|04-Feb-2022|Cryopreserved sperm|||Unknown|||Possibly| 8886.0|ASD941:TCF7-GFP|C57BL/6-Tcf7/HhxAnuApb||Recessive|transcription factor 7, T cell specific|Tcf7||T cell factor-1, T-cell factor 1, Tcf1, TCF-1|MGI:98507|transcription factor 7, T cell specific; targeted mutation 1, Hai-Hui Xue|Tcf7|MGI:5805838|11|||||||||||||||||||||||||||||Using newly-generated Tcf7GFP reporter mice, we identified novel early innate lymphoid progenitors that express high levels of TCF-1 but lack surface markers of adaptive and innate lymphocyte lineages. These early innate lymphoid progenitors closely resemble bone marrow lymphoid progenitors at the transcriptome level, but lack efficient T and B lymphocyte potential. Instead, they efficiently gave rise to various ILC lineages, including conventional NK cells as well as cytokine-producing helper ILC at the clonal level, indicating that they are the earliest identifiable ILC progenitors. |Normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|13-Mar-2020|Cryopreserved sperm|33.0|0.0|Unknown||innate lymphoid cells (ILCs), T cell, B cell, lineage|Yes| 9335.0||C57Bl/6N-ENU53:366:Irf9||Semi-dominant|Irf9||||||||Unknown||||||||||||||||||||||||||||| | |C57Bl/6N|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|14-Feb-2022|Cryopreserved sperm|11.0|0.0|Unknown|||Possibly| 9339.0|Matk cKO|C57BL/6J-Matk/HaqueWehi||Semi-dominant|megakaryocyte-associated tyrosine kinase|Matk||CHK, Csk homologous kinase, HYL, Ntk |MGI:99259 |Matk|Matk cKO||10|NCBI Gene: 17179|||||||||Unknown to Unknown|||||||||||||||||||Normal|Normal|C57Bl/6J|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|22-Feb-2022|Cryopreserved sperm|50.0|0.0|Unknown||Heamatopoietic system, Megakaryocyte, Kinases|Possibly| 9342.0||C57Bl/6N-Atg16L2 (29)/Apb||Semi-dominant|autophagy related 16-like 2|Atg16L2|||MGI:1920933|Atg16L2 c997-2A>G|||7|||||||||||||||||||||||||||||Unknown|Unknown|C57Bl/6N|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|23-Feb-2022|Cryopreserved sperm|52.0|0.0|Unknown|||Possibly| 8267.0|ENU36:006:Acss1|C57BL/6NCrlAnu-Acss1/AnuApb||Recessive|acyl-CoA synthetase short-chain family member 1|Acss1||1110032O15Rik, Acas2, Acas2l, AceCS2|MGI:1915988||||2|ENSMUSG00000027452|ENSMUST00000028944.3|Acss1-201|908|969|C to T|ENSMUSE00001270508|5|303|Glycine to Aspartic acid|||||ACCCAAGGGACTCGTTCATACACAGGCAGGCTATCTACTGTATGCCGCCATGACGCACAAG||||||||||||||Homozygous mice have increased CD44 MFI on T cells in the blood||C57BL/6NCrlAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|07-Jun-2017|Cryopreserved sperm|48.0|0.0|Unknown||T cell, CD44|Yes| 9341.0||C57BL/6-Myo1f/HaqueWehi||Dominant|myosin IF|Myo1f|||MGI:107711||||17||||||||||Unknown to Unknown|||||||||||||||||||Normal|Normal|C57Bl/6J|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|22-Feb-2022|Cryopreserved sperm|50.0|0.0|Unknown|||Possibly| 9343.0||C57BL/6J-Prr13/HaqueWehi||Semi-dominant|proline rich 13|Prr13|||MGI:1913401||||15|||||||||||||||||||||||||||||Normal|Normal|C57Bl/6J|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|24-Feb-2022|Cryopreserved sperm|50.0|0.0|Unknown|||Possibly| 9340.0|Asap1 fl/fl|C57BL/6-Asap1/Wehi||Semi-dominant|ArfGAP with SH3 domain, ankyrin repeat and PH domain1|Asap1||Ddef1, mKIAA1249 |MGI:1342335 ||Asap1||15||||||||||Unknown to Unknown|||||||||||||||||||Normal|Normal|C57Bl/6J|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|22-Feb-2022|Cryopreserved sperm|50.0|0.0|Unknown|||Yes| 9338.0|Akirin F0:60|C57BL/6NCrlAnu-Akirin/AnuApb||Semi-dominant|akirin 1|Akirin1 |Unknown|6330407G11Rik|MGI:1915300 |endonuclease mediated targeting 4;|Akirin F0:#60||4|||||||||||||||||||||||||||||unknown|unknown|C57Bl/6N|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|21-Feb-2022|Cryopreserved sperm|10.0|0.0|Unknown|||Possibly| 9321.0|ASD953:Bake:1|C57BL/6NCrlAnu-Zfp64em1Anu Zfp64em2Anu/Anu||Semi-dominant|zinc finger protein 64|ZFP64|||MGI:107342 ||||2|||||||||||||||||||||||||||||Unknown|Unknown|C57Bl/6N|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|16-Dec-2021|Cryopreserved sperm|52.0|0.0|Unknown|||Possibly| 9336.0||C57Bl/6-ENU53:180:Tmem173||Semi-dominant|Tmem173||||||||Unknown||||||||||||||||||||||||||||| | |C57Bl/6N|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|14-Feb-2022|Cryopreserved sperm|11.0|0.0|Unknown|||Possibly| 8929.0|CD23cre|B6.Cg-Tg(Fcer2a-cre)5Mbu/JMarpAnuApb||Dominant||||||||||||||||||||||||||transgene insertion 5, Meinrad Busslinger|Fcer2a|||||||||||These Cd23-cre transgenic mice express cre under the control of the Fcer2a promoter. Cre recombinase expression is detected in immature, transitional and late B cells in the bone marrow and spleen. Mice that are hemizygous for the transgene are viable and fertile.|These Cd23-cre transgenic mice express cre under the control of the Fcer2a promoter. Cre recombinase expression is detected in immature, transitional and late B cells in the bone marrow and spleen. Mice that are hemizygous for the transgene are viable and fertile.|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|27-Mar-2020|Cryopreserved sperm|17.0|18.0|Unknown||Cre recombinase, CD23, B cell|Yes| 4078.0|Frink ; ENU6PH:052 |C;B6JAnu-Irf4/AnuApb||Recessive|interferon regulatory factor 4|Irf4||IRF-4, Spip|MGI:1096873|rf4: mutation 1, The Australian National University|Irf4||13|ENSMUSG00000021356|ENSMUST00000021784|Irf4-001|332|434|T to A|ENSMUSE00000117279|3|111|Valine to Aspartic acid|||||GAACAAGAGCAATGACTTTGAGGAATTGGTCGAGAGGAGCCAGCTGGATATCTCTGACCCA|Yes|||||||||||||Hypo IgE response following allergic challenge.Panhypogamma.||C57BL/6 x BALB/b|Yes|Yes|Yes|Yes|Yes|Yes|No|Poor||||No|04-Dec-2008|Cryopreserved sperm|195.0|0.0|Unknown||allergic challenge, ENU, Immunoglobulin, IgE, autoimmune disease, arthritis|No| 9351.0||C57BL/6J-Prr13/HaqueWehi||Semi-dominant|proline rich 13|Prr13||1110020C13Rik, 2010324E22Rik|MGI:1913401||Prr13||15||||||||||Unknown to Unknown|||||||||||||||||||Normal|Normal|C57Bl/6J|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|10-Mar-2022|Cryopreserved sperm|50.0|0.0|Unknown|||Possibly| 9349.0|Mef2C-LacZ; Nedd4fl/fl|C57;129S1/Sv;CD1-Tg(Mef2c-lacZ)-Nedd4/Apb||Semi-dominant|neural precursor cell expressed, developmentally down-regulated 4|Nedd4 ||E430025J12Rik, mKIAA0093, Nedd4, Nedd4-1, Nedd4a |MGI:97297||||9|||||||||||||||||LacZ|Mef2C|||||||||||Mice are fully viable|Mice are fully viable|C57Bl/6; 129S1/Sv; CD1|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|05-Mar-2022|Cryopreserved sperm|50.0|0.0|Unknown|||Possibly| 9287.0|Fancl:del336_337-Adh5:del448bp|C57Bl/6J-Fancl-Adh5/AnuApb||Semi-dominant|Fanconi anemia, complementation group L |Fancl |Unknown|2010322C19Rik, B230118H11Rik, gcd, Phf9, Pog |MGI:1914280|Fanconi anemia, complementation group L |Fanl||11|||||||||||||||||||||||||||||Mice homozygous for Fancl present microphtalmia in one or both eyes, slightly reduced size when young, and infertility.Mice homozygous for Adh5 present increased susceptibility to various toxins, and abnormal blood pressure regulation under anaesthesia.|Normal|C57Bl/6J|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|18-Oct-2021|Cryopreserved sperm|50.0|0.0|Unknown|||Possibly| 9287.0|Fancl:del336_337-Adh5:del448bp|C57Bl/6J-Fancl-Adh5/AnuApb||Semi-dominant|Alcohol dehydrogenase 5 (class III), chi polypeptide|Adh5||Adh3, Adh-5, GSNOR, S-nitrosoglutathione reductase |MGI:87929|Alcohol dehydrogenase 5 (class III), chi polypeptide|Adh5||Unknown|||||||||||||||||||||||||||||Mice homozygous for Fancl present microphtalmia in one or both eyes, slightly reduced size when young, and infertility.Mice homozygous for Adh5 present increased susceptibility to various toxins, and abnormal blood pressure regulation under anaesthesia.|Normal|C57Bl/6J|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|18-Oct-2021|Cryopreserved sperm|||Unknown|||Possibly| 9350.0||C57BL/6J-Prr13/HaqueWehi||Semi-dominant|proline rich 13|Prr13|||MGI:1913401||Prr13||15||||||||||Unknown to Unknown|||||||||||||||||||Normal|Normal|C57Bl/6J|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|10-Mar-2022|Cryopreserved sperm|50.0|0.0|Unknown|||Yes| 8188.0|ENU33:009:Clk1|C57BL/6NCrlAnu-Clk1/AnuApb||Recessive|CDC-like kinase 1|Clk1|Unknown|Clk1, STY|MGI:107403||||1|ENSMUSG00000026034|ENSMUST00000034868.13|Clk1-001|971|1118|T to C|ENSMUSE00001227858|9|324|Aspartic acid to Glycine|||||TATAGTAAATCCAGATATTAAAGTGGTGGACTTTGGAAGTGCAACATATGATGATGAACAC||||||||||||||FACS phenotype: Increase IgM and decreased IgD on mature B cells.|Normal|C57BL/6NCrlAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|16-Feb-2017|Cryopreserved sperm|48.0|0.0|Unknown||ENU, B cell, IgD|Yes| 9347.0|SwHel:RAG1KO:B10BR N3|B6N(Cg)-Igh Tg(IgkHyHEL10)1Rbr H2 Rag<1tm1Mom>/Anu||Dominant|recombination activating 1|Rag1|||MGI:97848|recombination activating 1; targeted mutation 1, Peter Mombaerts|Rag1|MGI:1857241|2|ENSMUSG00000061311||||||||||||||||transgene insertion 1, Robert Brink||||||||||||Mice carry BCR knocked in alleles that recognise HEL protein so that ~10% of B cells recognise HELMice are also deficient for Rag1 (lacking mature B and T cells)||B10BR Rag1KO|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|28-Feb-2022|Cryopreserved sperm|27.0|0.0|Unknown|||No| 9347.0|SwHel:RAG1KO:B10BR N3|B6N(Cg)-Igh Tg(IgkHyHEL10)1Rbr H2 Rag<1tm1Mom>/Anu||Dominant|immunoglobulin heavy chain complex|Igh|||MGI:96442|immunoglobulin heavy chain complex; targeted mutation 1, Robert Brink|Igh|MGI:3800383|12|||||||||||||||||||||||||||||Mice carry BCR knocked in alleles that recognise HEL protein so that ~10% of B cells recognise HELMice are also deficient for Rag1 (lacking mature B and T cells)||B10BR Rag1KO|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|28-Feb-2022|Cryopreserved sperm|||Unknown|||No| 9347.0|SwHel:RAG1KO:B10BR N3|B6N(Cg)-Igh Tg(IgkHyHEL10)1Rbr H2 Rag<1tm1Mom>/Anu||Dominant|histocompatibility-2, MHC|H2|||MGI:95894|histocompatibility 2, K region|H2||17|||||||||||||||||||||||||||||Mice carry BCR knocked in alleles that recognise HEL protein so that ~10% of B cells recognise HELMice are also deficient for Rag1 (lacking mature B and T cells)||B10BR Rag1KO|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|28-Feb-2022|Cryopreserved sperm|||Unknown|||No| 9348.0|cpg15 fl:FoxP3-Cre:TCR.B10BR|B6.B10-Nrn1 Foxp3 Tg(TcrHEL3A9)1Mmd/Apb||Dominant|neuritin 1|Nrn1||cpg15|MGI:1915654|neuritin 1; targeted mutation 1.1, Elly Nedivi|Nrn1 |MGI:5307917|13|ENSMUSG00000039114 ||||||||||||||||transgene insertion 1, Mark M Davis||||||||||||Mice carry the TCR3a9 transgene together with floxed Cpg15 and cre under the Foxp3 promotor|-|B10BR N3|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|28-Feb-2022|Cryopreserved sperm|35.0|0.0|Unknown|||No| 9348.0|cpg15 fl:FoxP3-Cre:TCR.B10BR|B6.B10-Nrn1 Foxp3 Tg(TcrHEL3A9)1Mmd/Apb||Dominant|forkhead box P3|Foxp3||scurfin|MGI:1891436|forkhead box P3; targeted mutation 4, Alexander Y Rudensky|Foxp3|MGI:3790499|X|ENSMUSG00000039521||||||||||||||||||||||||||||Mice carry the TCR3a9 transgene together with floxed Cpg15 and cre under the Foxp3 promotor|-|B10BR N3|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|28-Feb-2022|Cryopreserved sperm|||Unknown|||No| 10453.0|B6.A2G-Mx1 Wildtype|B6.A2G-Mx1/AnuApb||Dominant|myxovirus (influenza virus) resistance 1|Mx1|Normal|Mx, Mx-1, myxovirus (influenza) resistance 1 polypeptide|MGI:97243|myxovirus (influenza virus) resistance 1; myxovirus resistance|Mx1|MGI:3715151|16|||||||||||||||||||||||||||||Normal, i.e. highly influenza resistant.|Normal.|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|23-Sep-2024||0.0|0.0|Unknown||Infection, resistance, Interferon|Yes| 9360.0|Bsn|C57BL/6NCrlAnu-Bsn/Anu||Semi-dominant|bassoon|Bsn||presynaptic cytomatrix protein|MGI:1277955|Bsn, endonuclease-mediated mutation 2, Australian National University|Bsn||9|ENSMUSG00000032589 |ENSMUST00000035208||||||||Unknown to Unknown|||||||||||||||||||May develop epilepsy|May develop epilepsy|C57Bl/6N|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|18-Mar-2022|Cryopreserved sperm|29.0|0.0|Unknown|||Possibly| 9355.0|ENU56:G2|ANU:ENU56:G2||Recessive|Unknown||||||||Unknown||||||||||||||||||||||||||||| | |C57Bl/6N|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Mar-2022|Cryopreserved sperm|8006.0|0.0|Unknown|||Possibly| 9357.0||C57BL/6NcrlAnu-Tlr4/19Anu||Semi-dominant|toll-like receptor 4|Tlr4|||MGI:96824|Tlr4|||4|||||||||||||||||||||||||||||Unknown|Unknown|C57Bl/6N|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|15-Mar-2022|Cryopreserved sperm|54.0|0.0|Unknown|||Possibly| 9356.0|RaraC88R KO|C57BL/6NCrlAnu-Rara KO/Apb||Semi-dominant|retinoic acid receptor, alpha|Rara||RARalpha1, RAR alpha 1 |MGI:97856||||11|||||||||||||||||||||||||||||unknown|unknown|C57Bl/6N|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|15-Mar-2022||0.0|0.0|Unknown|||Possibly| 9373.0|UBC-Cre-ERT2|C57BL/6J-Ndor1/Apb||Dominant|ERT2|||||NADPH dependent diflavin oxidoreductase 1; transgene insertion 1, Eric J Brown|Ndor1|MGI:3707333|Unknown|||||||||||||||||(UBC-cre/ERT2)||||||||||||normal|normal|C57Bl/6J|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|11-Apr-2022|Cryopreserved sperm|50.0|0.0|Unknown|||Possibly| 9297.0|Robo2 KO|C57Bl/6J-Robo2/AnuApb||Semi-dominant|Roundabout guidance receptor 2|Robo2|Unknown|2600013A04Rik, 9430089E08Rik, D230004I22Rik, mKIAA1568|MGI:1890110|Roundabout guidance receptor 2|Robo2||16|||||||||||||||||||||||||||||Homozygous mice have duplex kidneys during development. Adult phenotype unknown for this line.|Normal|C57Bl/6J|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|08-Nov-2021|Cryopreserved sperm|50.0|0.0|Unknown|||Possibly| 9368.0||C57BL/6N-Myb<(em1)41Δ2bp>/Apb||Semi-dominant|myeloblastosis oncogene|Myb||c-myb|MGI:97249||||10|||||||||||||||||||||||||||||unknown|unknown|C57Bl/6N|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|06-Apr-2022|Cryopreserved sperm|10.0|0.0|Unknown|||Possibly| 9375.0|ENU54:182|ANU:ENU54:182||Recessive|eukaryotic translation initiation factor 2 alpha kinase 4|Eif2ak4||Eif2ak4|MGI:1353427|Eif2ak4:mutation 3, Australian National University|||2|ENSMUSG00000005102 |ENSMUST00000005233||||||||||||||||||||||||||| | |C57Bl/6N|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|20-Apr-2022|Cryopreserved sperm|9.0|0.0|Unknown|||Possibly| 9367.0||C57Bl/6NCrlAnu-Fads2Anu/Apb||Semi-dominant|fatty acid desaturase 2|Fads2|||MGI:1930079|Fads2; endonuclease-mediated mutation 1, Australian National University|Fads2Anu||19||||||||||Unknown to Unknown|||||||||||||||||||Defective in fatty acid desaturase. Mice are mostly normal. Male mice are defective in reproduction (e.g. low sperm numbers) unless supplied with a high DHA diet.|Normal|C57Bl/6N|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|02-Apr-2022|Cryopreserved sperm|102.0|0.0|Unknown|||Possibly| 9366.0|Aicda fl:Ly5a|B6(Cg)-Aicda Ptprc/AnuApb||Recessive|activation-induced cytidine deaminase|Aicda|||MGI:1342279|activation-induced cytidine deaminase; targeted mutation 1c, Helmholtz Zentrum Muenchen GmbH|Aicda|MGI:6478196|6|ENSMUSG00000040627||||||||||||||||||||||||||||Normal|Normal|Founder strain C57Bl/6N (Agouti) JM8A3.N1. Current mice: 7 backcrosses (N7) to C57Bl/6N Ly5a|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|29-Mar-2022|Cryopreserved sperm|31.0|0.0|Unknown|||Yes| 9366.0|Aicda fl:Ly5a|B6(Cg)-Aicda Ptprc/AnuApb||Recessive|protein tyrosine phosphatase receptor type C|Ptprc||Ly-5, Lyt-4, T200||protein tyrosine phosphatase receptor type C; a variant|Ptprca|MGI:4819849|1||||||||||Unknown to Unknown|||||||||||||||||||Normal|Normal|Founder strain C57Bl/6N (Agouti) JM8A3.N1. Current mice: 7 backcrosses (N7) to C57Bl/6N Ly5a|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|29-Mar-2022|Cryopreserved sperm|||Unknown|||Yes| 9365.0||B6.129P-Mgea5/NIDDK||Semi-dominant|O-GlcNAcase (OGA / Mgea5)|Oga||Hy5, Mgea5,|MGI:1932139|O-GlcNAcase; targeted mutation 2, John A Hanover|Oga||19||||||||||Unknown to Unknown|||||||||||||||||||Normal|Normal|C57Bl/6J|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|24-Mar-2022|Cryopreserved sperm|50.0|0.0|Unknown|||Possibly| 9370.0||C57BL/6NCrlAnu-Sntb/48Anu||Recessive|syntrophin, basic 1|Sntb1|||MGI:101781|Sntb1|||15|||||||||||||||||||||||||||||Unknown|Unknown|C57Bl/6N|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|07-Apr-2022|Cryopreserved sperm|55.0|0.0|Unknown|||Possibly| 9374.0|ENU53:293|ANU:ENU53:293||Recessive|Unknown||||||||Unknown||||||||||||||||||||||||||||| | |C57Bl/6N|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|20-Apr-2022|Cryopreserved sperm|9.0|0.0|Unknown|||Possibly| 9369.0|Rara:F0:Indel|C57BL/6NCrlAnu-Rara/AnuApb||Semi-dominant|retinoic acid receptor, alpha|Rara|Unknown|RARalpha1, RAR alpha 1 |MGI:97856|Rara|Rara:F0:Indel||11|||||||||||||||||||||||||||||unknown|unknown|C57Bl/6N|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|06-Apr-2022|Cryopreserved sperm|19.0|0.0|Unknown|||Possibly| 9353.0|Asap1 Floxed|C57BL/6-Asap1/Wehi||Semi-dominant|ArfGAP with SH3 domain, ankyrin repeat and PH domain1|Asap1|Unknown|Ddef1, mKIAA124|MGI:1342335 |endonuclease mediated targeting 2; Ashraful Haque|Asap1||15|||||||||||||||||||||||||||||Normal|Normal|C57Bl/6J|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|10-Mar-2022|Cryopreserved sperm|50.0|0.0|Unknown|||Possibly| 9192.0|Wdr1rd/rd|C57BL/6- Wdr1/ApbAnu||Semi-dominant|WD repeat domain 1|Wdr1||Aip1, D5Wsu185e, rede |MGI:1337100|Wdr1|Wdr1 rd/rd||5|||||||||||||||||||||||||||||Homozygous mice begin to develop inflamed ears after ~100 days of age. The inflammation at the ears emerge in ‘pockets’ at the tip of the ears and as the mice age, the ears will have redness and oedema with immune infiltration. The inflammation at the tail would also emerge in pockets throughout the tail, though most prominently at the tip of the tail. As the mice age, the tail will become hardened and inflamed.|unknown|C57BL/6 “The rd mutation was induced on an inbred C57BL/6 background, isolated on a mixed C57BL/6J: 129S6/SvEv:C3HeB/FeJ background,38 and back-crossed 10 generations to C57BL/6.” (Kile et al., 2007, Blood, PMID: 17515402)|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|01-Jun-2021|Cryopreserved sperm|50.0|0.0|Unknown||platelets, neutrophils, Megakaryocyte|Possibly| 9352.0|Myo1f flox|C57BL/6-Myo1f/HaqueWehi||Recessive|myosin IF|Myo1f||C330006B10Rik|MGI:107711|Myo1f|Myo1 flox||17|||||||||||||||||||||||||||||Normal|Normal|C57Bl/6J|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|10-Mar-2022|Cryopreserved sperm|50.0|0.0|Unknown|||Possibly| 9376.0|SwHel:Hc.Lc:Ly5a:Ptprca/NCrl|SwHel:Hc.Lc:Ly5a:Ptprca/NCrl||Dominant|immunoglobulin heavy chain complex ||||||||Unknown|||||||||||||||||The HyHEL10 hybridoma produces an antibody that binds hen egg lysozyme peptide (HEL) with high affinity. The rearranged variable heavy gene segment from the HyHEL10 hybridoma replaced the endogenous J gene segments of the IgH locus. A floxed neomycin cassette was placed upstream for targeting purposes. About 0.4% of B cells produce antibody that bind HEL with high affinity. The strain also express congenic mark Ly5a||||||||||||B cells express Immunoglobulin specific for hen egg lysozyme and are capable of undergoing class switch.|Normal|C57Bl/6N|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|22-Apr-2022|Cryopreserved sperm|22.0|0.0|Unknown|||Yes| 9319.0|Arap2 P1233S:8|C57BL/6NCrlAnu-Arap2/AnuApb||Semi-dominant|ArfGAP with RhoGAP domain, ankyrin repeat and PH domain 2|Arap2||Centd1, mKIAA0580|MGI:2684416|endonuclease mediated targeting 1; Anselm Enders|Arap2 ||5|||||||||||||||||||||||||||||Unknown|Unknown|C57Bl/6N|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Dec-2021|Cryopreserved sperm|54.0|0.0|Unknown|||Possibly| 9344.0|Tbc1d4 Floxed|C57BL/6-Tbc1d4/Wehi||Semi-dominant|TBC1 domain family, member 4|Tbc1d4|Unknown|5930406J04Rik, AS160 |MGI:2429660|endonuclease mediated targeting 1.1; Ashraful Haque|Tbc1d4||14|||||||||||||||||||||||||||||Normal|Normal|C57Bl/6J|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|24-Feb-2022|Cryopreserved sperm|50.0|0.0|Unknown|||Possibly| 9176.0|Zic5R (Kiska; Ki)|C57BL/6J Zic5R /ApbAnu||Recessive|zinc finger protein of the cerebellum 5|Zic5||1700049L20Rik, odd-paired related, Opr |MGI:1929518|Zic5|K363R (Kiska; Ki)||14|||||||||||||||||||||||||||||This hypomorphic allele of Zic5 leads to hypoplasia of the neural crest. This leads to a small proportion of homozygous animals will develop hydrocephaly post birth (5%). Homozygous animals also are more likely to have a ventral spot/colour change on their coat or line of white hair (13%) compared with heterozygous animals (3%). |A small proportion of heterozygous animals have a ventral spot/colour change on their coat or line of white hair (3%). |C57Bl/6J|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|27-Apr-2021|Cryopreserved sperm|57.0|0.0|Unknown|||Possibly| 9208.0|ENU50:073|C57BL/6Ncrl/ApbAnu||Semi-dominant|reticuloendotheliosis oncogene|Rel||c-Rel|MGI:97897||||11||||||||||||||||||||||||||||| | |C57Bl/6N|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|25-Jun-2021|Cryopreserved sperm|22.0|0.0|Unknown|||Possibly| 9208.0|ENU50:073|C57BL/6Ncrl/ApbAnu||Semi-dominant|dynein axonemal assembly factor 10|Dnaaf10 ||Wdr92 |MGI:2144224||||11||||||||||||||||||||||||||||| | |C57Bl/6N|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|25-Jun-2021|Cryopreserved sperm|||Unknown|||Possibly| 9232.0|ENU50:129|C57BL/6Ncrl/AnuApb||Semi-dominant|Not known yet||||||||Unknown||||||||||||||||||||||||||||| | |C57Bl/6N|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|26-Jul-2021|Cryopreserved sperm|12.0|0.0|Unknown|||Possibly| 9147.0|MR1-K43A/MR1-Tom|C57BL/6J Mr1<(em1)UniMel>Mr1<(tm1)UniMel>/ApbAnu||Semi-dominant|major histocompatibility complex, class I-related|Mr1||H2ls, MR1 |MGI:1195463|Mr1; endonuclease mutation 1, Hamish McWilliam|Mr1 mutant||1|||||||||||||||||Tandem dimer Tomato|Mr1 endogenous promoter|Unknown||||||||||Normal|Normal|C57Bl/6|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|16-Feb-2021|Cryopreserved sperm|50.0|0.0|Unknown|||Possibly| 9186.0|Marchf8 KO|C57BL6/J-Marchf8||Semi-dominant|membrane-associated ring finger (C3HC4) 8|Marchf8 ||1300017E09Rik, March8, Mir|MGI:1919029|endonuclease mediated targeting 1; Haiyin Liu|Marchf8 KO||6|||||||||||||||||||||||||||||Marchf8 K.O. mice have enriched surface expression of MHC II in thymic epithelial cells compared to WT mice|The same as homozygous K.O. but to a lesser extent|C57Bl/6J|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-May-2021|Cryopreserved sperm|50.0|0.0|Unknown|||Possibly| 9400.0|Lyn KO|C57BL/6NCrlAnu-LynAnu/Apb||Semi-dominant|LYN proto-oncogene, Src family tyrosine kinase|Lyn|||MGI:96892||||4|||||||||||||||||||||||||||||Unknown|UnknownMale #4 1bp deletion|C57Bl/6N|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|08-Jul-2022|Cryopreserved sperm|10.0|0.0|Unknown|||Possibly| 9382.0|Tlr4 KO|C57Bl6NCrl-Tlr4Anu/Apb||Semi-dominant|toll-like receptor 4|Tlr4|||MGI:96824||||4|||||||||||||||||||||||||||||unknown|unknown|C57Bl/6N|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|17-May-2022|Cryopreserved sperm|11.0|0.0|Unknown|||Possibly| 10454.0|B6.A2G-Mx1 (Cg/Cg)|B6.A2G-Mx1/AnuApb||Dominant|myxovirus (influenza virus) resistance 1|Mx1|Normal|Mx, Mx-1, myxovirus (influenza) resistance 1 polypeptide|MGI:97243|myxovirus (influenza virus) resistance 1; myxovirus resistance|Mx1|MGI:3715151|16|||||||||||||||||||||||||||||Sensitive to influenza infection|Normal, i.e. highly influenza resistant.|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|23-Sep-2024||0.0|0.0|Unknown||Infection, resistance, Interferon|Yes| 9383.0|Tlr4 KO|C57Bl6NCrlTlr4/Apb||Semi-dominant|toll-like receptor 4|Tlr4|||MGI:96824||||4|||||||||||||||||||||||||||||unknown|unknown|C57Bl/6N|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|17-May-2022|Cryopreserved sperm|10.0|0.0|Unknown|||Possibly| 9380.0|ENU53:263|ANU:ENU53:263||Recessive|Unknown||||||||Unknown||||||||||||||||||||||||||||| | |C57Bl/6N|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|11-May-2022|Cryopreserved sperm|22.0|0.0|Unknown|||Possibly| 9361.0|Bsn A353T|C57BL/6NCrl-Bsn/AnuApb||Semi-dominant|bassoon|Bsn||presynaptic cytomatrix protein |MGI:1277955 |endonuclease mediated targeting 1; Carola Vinuesa|Bsn||9|||||||||||||||||||||||||||||May develop epilepsy|May develop epilepsy|C57Bl/6N|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|18-Mar-2022|Cryopreserved sperm|20.0|0.0|Unknown|||Possibly| 9020.0|Scn2a R853Q|C57BL/6-Scn2a /Apb||Recessive|Scn2a|NCBI Gene: 110876||A230052E19Rik, Nav1.2, Scn2a1|MGI:98248||||2|ENSMUSG00000075318|ENSMUST00000028377.13|Scn2a-201||||||||||||||||||||||||||Not born|No obvious behavioural phenotype or health issue|C57Bl6|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|23-Jun-2020|Cryopreserved sperm|50.0|0.0|Unknown|||No| 9035.0|Dazzler|C57BL/6NCrlAnu-Nrn1/AnuApb||Dominant|neuritin 1|Nrn1||0710008J23Rik, cpg15|MGI:1915654||||13|||||||||||||||||||||||||||||Normal||C57BL/6NCrlAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|26-Jun-2020|Cryopreserved sperm|55.0|0.0|Unknown||GFP, Nrn1|Yes| 9384.0|Prox1enh-LacZ(Nala)|C57Bl/6-Tg(Prox1enh-LacZ(Nala))/Apb||Dominant|Prox1||||| -11kb enhancer|||Unknown|||||||||||||||||LacZ|Hsp68|||||||||||Presence of the transgene drives LacZ expression, chiefly in lymphatic vessels and valves.|Presence of the transgene drives LacZ expression, chiefly in lymphatic vessels and valves.|C57Bl/6J|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|19-May-2022||0.0|0.0|Unknown|||Possibly| 9390.0||C57Bl/6J-Mdfic<(em)H133fs* 8 bp>/Apb||Dominant|MyoD family inhibitor domain containing|Mdfic|Normal||MGI:104611||||6|||||||||||||||||||||||||||||Chylothorax develops between 8-45 days after birth resulting in death within 24 hours.|Normal|C57Bl/6J|No|Unknown|Yes|No|Unknown|Yes|No|Excellent|||Het x Het|No|19-May-2022|Cryopreserved sperm|40.0|0.0|No|||No| 9401.0|Lyn KO|C57BL/6NCrlAnu-Lyn/Anu||Semi-dominant|LYN proto-oncogene, Src family tyrosine kinase|Lyn|||MGI:96892||||4|||||||||||||||||||||||||||||unknown|unknown|C57Bl/6N|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|08-Jul-2022|Cryopreserved sperm|11.0|0.0|Unknown|||Possibly| 9388.0|Prox1enh-LacZ(Simba)|C57Bl/6J-Prox1(enh-LacZ)(Simba)/Apb||Dominant|prospero homeobox 1|Prox1|Normal||MGI:97772| -11kb enhancer|||1|||||||||||||||||LacZ|Hsp68|||||||||||Presence of the transgene drives LacZ expression, chiefly in lymphatic vessels and valves.|Presence of the transgene drives LacZ expression, chiefly in lymphatic vessels and valves.|C57Bl/6J|Yes|Yes|Yes|Yes|Yes|Yes|No|Excellent||||No|19-May-2022|Cryopreserved sperm|40.0|0.0|No|||No| 9392.0|BSN stop|C57Bl/6N-BsnAnu/Apb||Semi-dominant| bassoon|Bsn|||MGI:1277955|Bsn, mutation 1, Australian National University|Bsn||9||||||||||Unknown to Unknown|||||||||||||||||||May develop epilepsy|normal|C57Bl/6N|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|20-May-2022|Cryopreserved sperm|17.0|0.0|Unknown|||Possibly| 9389.0|MDFIC-CRISPR(Dory)|C57Bl/6j-Mdfic/AnuApb||Dominant|MyoD family inhibitor domain containing|Mdfic|Normal||MGI:104611||||6|||||||||||||||||||||||||||||Chylothorax develops between 8-45 days after birth resulting in death within 24 hours.|Normal|C57Bl/6J|No|Unknown|Yes|No|Unknown|Yes|No|Excellent|||Het x Het|No|19-May-2022|Cryopreserved sperm|40.0|0.0|No|||No| 9391.0|Hamlin:34:bpins|C57Bl/6-TMEM39B<34 bpins>/Apb||Semi-dominant|TMEM39B||||||||Unknown|||||||||||||||||||||||||||||Unknown|Unknown|C57Bl/6N|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|20-May-2022|Cryopreserved sperm|46.0|0.0|Unknown|||Possibly| 9385.0||C57Bl/6J-Prox1/Apb||Semi-dominant|Prox1||||| -11kb enhancer|||Unknown|||||||||||||||||LacZ|Hsp68|||||||||||Presence of the transgene drives LacZ expression, chiefly in lymphatic vessels and valves.|Presence of the transgene drives LacZ expression, chiefly in lymphatic vessels and valves.|C57Bl/6J|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|19-May-2022||0.0|0.0|Unknown|||Possibly| 8604.0|Abca4 KO:Rdh8 KO|B6;129-Abca4 Rdh8/JAnuApb||Recessive|ATP-binding cassette, sub-family A (ABC1), member 4|Abca4|Nil|Abc10, D430003I15Rik, Rim protein, RmP |MGI:109424|ATP-binding cassette, sub-family A (ABC1), member 4; targeted mutation 1, Gabriel H Travis|Abca4|MGI:1857860|3|||||||||||||||||||||||||||||Retinal neovascularization: • Choroidal Neovascularization (CNV) in 22.2% (2/9) of the eyes• no Choroidal Neovascularization (CNV) in the eyes of sirolimus-treated mice.Abnormal retinal photoreceptor morphology.Decreased retinal photoreceptor cell number: • reduced number of photoreceptor nuclei along the inferior retinal regions and severe retinal degeneration at 5 months and 10 months of age, respectively.Decreased retinal cone cell number:• reduced number of cone photoreceptors• retinylamine treatment largely preserve cone photoreceptors• antioxidant, 9cRAc, and sirolimus treatment preserve cone photoreceptors, but not as well as retinylamine.Abnormal retinal pigment epithelium morphology: • swollen retinal pigment epithelium (RPE) with increased pigmented granules that included lipofuscin in mice kept in room light at 5 months of age• disrupted inner membrane cristae in RPE cells at 5 months of age• dead RPE cells lacking mitochondrial inner membrane cristae at 10 months of age.Abnormal retinal pigmentation:• increased pigmented granules that included lipofuscin in mice kept in room light at 5 months of age• di-retinoidpyridinium-ethanolamine (A2E) accumulation• retinylamine significantly decreased A2E accumulation.Thin retinal outer nuclear layer:• severely reduced outer nuclear layerRetinal degeneration: • early retinal degeneration is detected by 6 to 8 weeks of age in mice kept in dim room light (3-5 lux)• reduced lengths of photoreceptor outer segments (less than 5 micrometers)• antioxidant, 9cRAc, retinylamine and sirolimus treatment have efficacy in preventing retinal degeneration.Retinal deposits:• hyaline-like deposits in the rosette structure in 3- to 5-month-old mutant miceAbnormal Bruch membrane morphology:• complement deposition on Bruch's membrane• reduced complement deposition in antioxidant, 9cRAc, and sirolimus-treated mice• no complement deposition in retinylamine-treated mice.Abnormal eye electrophysiology. Abnormal cone electrophysiology:• reduced a- and b-wave amplitudes• both a- and b-wave amplitudes are maintained significantly better in antioxidant, 9cRAc, retinylamine and sirolimus-treated mice.Abnormal rod electrophysiology:• reduced Flicker ERG responses• responses of some antioxidant- and 9cRAc-treated mice are significantly retained after both 20- and 30-Hz stimuli||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|14-Nov-2018|Cryopreserved sperm|50.0|0.0|Yes|age related macular degeneration 2|retina|Yes| 8604.0|Abca4 KO:Rdh8 KO|B6;129-Abca4 Rdh8/JAnuApb||Recessive|retinol dehydrogenase 8|Rdh8|Nil|LOC235033, prRDH|MGI:2685028|retinol dehydrogenase 8; targeted mutation 1, Krzysztof Palczewski|Rdh8|MGI:3586327|9|||||||||||||||||||||||||||||Retinal neovascularization: • Choroidal Neovascularization (CNV) in 22.2% (2/9) of the eyes• no Choroidal Neovascularization (CNV) in the eyes of sirolimus-treated mice.Abnormal retinal photoreceptor morphology.Decreased retinal photoreceptor cell number: • reduced number of photoreceptor nuclei along the inferior retinal regions and severe retinal degeneration at 5 months and 10 months of age, respectively.Decreased retinal cone cell number:• reduced number of cone photoreceptors• retinylamine treatment largely preserve cone photoreceptors• antioxidant, 9cRAc, and sirolimus treatment preserve cone photoreceptors, but not as well as retinylamine.Abnormal retinal pigment epithelium morphology: • swollen retinal pigment epithelium (RPE) with increased pigmented granules that included lipofuscin in mice kept in room light at 5 months of age• disrupted inner membrane cristae in RPE cells at 5 months of age• dead RPE cells lacking mitochondrial inner membrane cristae at 10 months of age.Abnormal retinal pigmentation:• increased pigmented granules that included lipofuscin in mice kept in room light at 5 months of age• di-retinoidpyridinium-ethanolamine (A2E) accumulation• retinylamine significantly decreased A2E accumulation.Thin retinal outer nuclear layer:• severely reduced outer nuclear layerRetinal degeneration: • early retinal degeneration is detected by 6 to 8 weeks of age in mice kept in dim room light (3-5 lux)• reduced lengths of photoreceptor outer segments (less than 5 micrometers)• antioxidant, 9cRAc, retinylamine and sirolimus treatment have efficacy in preventing retinal degeneration.Retinal deposits:• hyaline-like deposits in the rosette structure in 3- to 5-month-old mutant miceAbnormal Bruch membrane morphology:• complement deposition on Bruch's membrane• reduced complement deposition in antioxidant, 9cRAc, and sirolimus-treated mice• no complement deposition in retinylamine-treated mice.Abnormal eye electrophysiology. Abnormal cone electrophysiology:• reduced a- and b-wave amplitudes• both a- and b-wave amplitudes are maintained significantly better in antioxidant, 9cRAc, retinylamine and sirolimus-treated mice.Abnormal rod electrophysiology:• reduced Flicker ERG responses• responses of some antioxidant- and 9cRAc-treated mice are significantly retained after both 20- and 30-Hz stimuli||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|14-Nov-2018|Cryopreserved sperm|||Yes|age related macular degeneration 2|retina|Yes| 9397.0|ROCK1nc|C57BL/6-Rock1/Apb||Semi-dominant|Rho-associated coiled-coil containing protein kinase 1|Rock1 |||MGI:107927|Rho-associated coiled-coil containing protein kinase 1; targeted mutation 1.1, Cancer Research UK Beatson Institute|Rock1tm1.1Bicrq|MGI:6696418|18|||||||||||||||||||||||||||||Normal|Normal|C57Bl/6|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|15-Jun-2022|Cryopreserved sperm|50.0|0.0|Unknown|||Possibly| 9398.0|Agxt (4)|C57BL/6NCrlAnu-AgxtAnu/Apb||Semi-dominant|alanine-glyoxylate aminotransferase|Agxt|||MGI:1329033||||1|||||||||||||||||||||||||||||unknown|unknown|C57Bl/6N|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|16-Jun-2022|Cryopreserved sperm|52.0|0.0|Unknown|||Possibly| 9402.0|Lyn KO|C57BL/6NCrlAnu-LynAnu/Apb||Recessive|LYN proto-oncogene, Src family tyrosine kinase|Lyn|||MGI:96892||||4|||||||||||||||||||||||||||||unknown|unknown|C57Bl/6N|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|08-Jul-2022|Cryopreserved sperm|10.0|0.0|Unknown|||Possibly| 9399.0|Nod1fl/fl x A33 cre|C57Bl/6J-Nod1 Gpa33/Apb||Dominant|nucleotide-binding oligomerization domain containing 1|Nod1||Nlrc1, Card4|MGI:1341839|Nucleotide-binding oligomerisation domain-containing protein 1, targeted mutation 1|Nod1||6|ENSMUSG00000038058 ||||||||||||||||||||||||||||Normal|Normal|C57Bl/6J|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|21-Jun-2022|Cryopreserved sperm|50.0|0.0|Unknown|||No| 9399.0|Nod1fl/fl x A33 cre|C57Bl/6J-Nod1 Gpa33/Apb||Dominant|glycoprotein A33 transmembrane|Gpa33||A33 antigen|MGI:1891703|glycoprotein A33 transmembrane; targeted mutation 2, Matthias Ernst|Gpa33|MGI:6806128|1|ENSMUSG00000000544 ||||||||||||||||||||||||||||Normal|Normal|C57Bl/6J|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|21-Jun-2022|Cryopreserved sperm|||Unknown|||No| 9394.0||C57Bl/6N-Tyk2 /Apb||Semi-dominant|Tyk2|||||Tyk2 |||Unknown|||||||||||||||||||||||||||||Unknown|Unknown|C57Bl/6N|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|31-May-2022|Cryopreserved sperm|53.0|0.0|Unknown|||Possibly| 8718.0|FANCM KO|FVB-Fancm/StVApb||Recessive|Fanconi anemia, complementation group M|Fancm|Nil|C730036B14Rik, D12Ertd364e|MGI:2442306||||11|||||||||||||||||||||||||||||Reduced fertility: smaller testis and epidydmis. Reduced sperm count and sperm motility.May have decreased lifespan.May have increased cancer susceptibility.|May have increased cancer susceptibility.|FVB/N|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|23-May-2019|Cryopreserved sperm|50.0|0.0|Unknown|||Yes| 9393.0||ENU54:016:Stat2||Semi-dominant|signal transducer and activator of transcription 2|Stat2|||MGI:103039||||10||||||||||||||||||||||||||||| | |C57Bl/6N|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|30-May-2022|Cryopreserved sperm|22.0|0.0|Unknown|||Possibly| 9403.0|Aire KO|C57BL/6NCrlAnu-Aire/Anu||Semi-dominant|Aire||||||||Unknown|||||||||||||||||||||||||||||unknown|unknown|C57Bl/6N|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|08-Jul-2022|Cryopreserved sperm|10.0|0.0|Unknown|||Possibly| 1858.0|Eu-myc/mOVA|C57BL/6-Tg(IghMyc)22Bri Tg(act-mOVA)||Dominant||||||||||||||||||||||||||transgene insertion 22, Ralph L Brinster|Lymphoid-specific immunoglobulin heavy chain enhancer (Eμ)|B cell lineage|||||||||||Phenotype expected to be similar to parental Emu-myc line. These mice will develop high incidence pre-B and B lymphoma. More than 90% of Emu-myc mice die between 6 and 18 weeks of age (median 11 weeeks). Enlargement of all lymph nodes, spleen, infiltration of thymus (thymoma), bone marrow, liver, lung, weight loss. Further more, these mice will express ubiquitously the membrane bound chicken ovalbumin under the chicken beta - actin promoter. MICE WILL BE MONITORED BY PALPATION OF LYMPH NODES AND SPLEEN 3X/WEEK. act-mOVa are on a C57BL/6 background. Homozygous breeding considerably less productive than heterozygous B6 myc: excess pre - B cells in bone marrow.||Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|||Mate - transgenic males with wild type B6 females|No|10-Aug-2007||0.0|0.0|Unknown||Lymphoma, ovalbumin, B cell|Yes| 1858.0|Eu-myc/mOVA|C57BL/6-Tg(IghMyc)22Bri Tg(act-mOVA)||Dominant||||||||||||||||||||||||||membrane bound ovalbumin|actin||||||||||||Phenotype expected to be similar to parental Emu-myc line. These mice will develop high incidence pre-B and B lymphoma. More than 90% of Emu-myc mice die between 6 and 18 weeks of age (median 11 weeeks). Enlargement of all lymph nodes, spleen, infiltration of thymus (thymoma), bone marrow, liver, lung, weight loss. Further more, these mice will express ubiquitously the membrane bound chicken ovalbumin under the chicken beta - actin promoter. MICE WILL BE MONITORED BY PALPATION OF LYMPH NODES AND SPLEEN 3X/WEEK. act-mOVa are on a C57BL/6 background. Homozygous breeding considerably less productive than heterozygous B6 myc: excess pre - B cells in bone marrow.||Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|||Mate - transgenic males with wild type B6 females|No|10-Aug-2007||||Unknown||Lymphoma, ovalbumin, B cell|Yes| 1860.0|Mcl-1flox/Bak/Bax knockout|Un-Mcl1 Bak1 Bax/Wehi||Recessive|myeloid cell leukemia sequence 1|Mcl1|Normal|Mcl-1|MGI:101769|targeted mutation 3, Stanley J Korsmeyer|Mcl1|MGI:2684151|3||||||||||||||||Yes|||||||||||||Mcl-1 - No -/- offsrping as -/- blastocysts die at E4 prior to implanation. Therefore only +/+ and +/- which are completely normal. Mice lacking bax display limited phenotypic abnormalities. Bak(-/-) mice were found to be developmentally normal and reproductively fit and failed to develop any age-related disorders. However, when Bak-deficient mice were mated to Bax-deficient mice to create mice lacking both genes, the majority of bax(-/-)bak(-/-) animals died perinatally with fewer than 10% surviving into adulthood. bax(-/-)bak(-/-) mice displayed multiple developmental defects, including persistence of interdigital webs, an imperforate vaginal canal, and accumulation of excess cells within both the central nervous and hematopoietic systems. Thus, Bax and Bak have overlapping roles in the regulation of apoptosis during mammalian development and tissue homeostasis. Those that survive are runted and grey.|||No|No|Yes|No|No|Yes|No|Unknown||||No|10-Aug-2007||0.0|0.0|No||Bcl2, BH3 only, Lymphocyte, B cell, T cell|Yes| 1860.0|Mcl-1flox/Bak/Bax knockout|Un-Mcl1 Bak1 Bax/Wehi||Recessive|BCL2-antagonist/killer 1|Bak1|Nil|Bak, N-Bak|MGI:1097161|BCL2-antagonist/killer 1; targeted mutation 1, Craig B Thompson|Bak1|MGI:2159364|17|||||||||||||||||||||||||||||Mcl-1 - No -/- offsrping as -/- blastocysts die at E4 prior to implanation. Therefore only +/+ and +/- which are completely normal. Mice lacking bax display limited phenotypic abnormalities. Bak(-/-) mice were found to be developmentally normal and reproductively fit and failed to develop any age-related disorders. However, when Bak-deficient mice were mated to Bax-deficient mice to create mice lacking both genes, the majority of bax(-/-)bak(-/-) animals died perinatally with fewer than 10% surviving into adulthood. bax(-/-)bak(-/-) mice displayed multiple developmental defects, including persistence of interdigital webs, an imperforate vaginal canal, and accumulation of excess cells within both the central nervous and hematopoietic systems. Thus, Bax and Bak have overlapping roles in the regulation of apoptosis during mammalian development and tissue homeostasis. Those that survive are runted and grey.|||No|No|Yes|No|No|Yes|No|Unknown||||No|10-Aug-2007||||No||Bcl2, BH3 only, Lymphocyte, B cell, T cell|Yes| 1860.0|Mcl-1flox/Bak/Bax knockout|Un-Mcl1 Bak1 Bax/Wehi||Recessive|Bcl2-associated X protein|Bax|Nil||MGI:99702|BCL2-associated X protein; targeted mutation 1, Stanley J Korsmeyer|Bax|MGI:1857429|7|||||||||||||||||||||||||||||Mcl-1 - No -/- offsrping as -/- blastocysts die at E4 prior to implanation. Therefore only +/+ and +/- which are completely normal. Mice lacking bax display limited phenotypic abnormalities. Bak(-/-) mice were found to be developmentally normal and reproductively fit and failed to develop any age-related disorders. However, when Bak-deficient mice were mated to Bax-deficient mice to create mice lacking both genes, the majority of bax(-/-)bak(-/-) animals died perinatally with fewer than 10% surviving into adulthood. bax(-/-)bak(-/-) mice displayed multiple developmental defects, including persistence of interdigital webs, an imperforate vaginal canal, and accumulation of excess cells within both the central nervous and hematopoietic systems. Thus, Bax and Bak have overlapping roles in the regulation of apoptosis during mammalian development and tissue homeostasis. Those that survive are runted and grey.|||No|No|Yes|No|No|Yes|No|Unknown||||No|10-Aug-2007||||No||Bcl2, BH3 only, Lymphocyte, B cell, T cell|Yes| 1825.0|PUT/Mxcre|C57BL/6-Sfpi1 Tg(Mx1-cre)1Cgn||Recessive|SFFV proviral integration 1|Sfpi1|Unknown|Dis-1, PU.1, Sfpi-1, Spi-1, Tcfpu1, Tfpu.1|MGI:98282|targeted mutation 1.2, Stephen L Nutt|Sfpi1|MGI:3578011|2||||||||||||||||Yes|transgene insertion 1, University of Cologne|Inducible MX1|||||||||||Prior to PolyIC treatment the phenotype is the same as wild type phenotype of the same genetic background. After polyIC treatment (ie after the deletion of PU.1 gene) mice exhibit transient weight loss, which sometimes can be sever (more than 10%) and splenomegaly. Myeloid leukaemia development in average 6 months after polyIC treatment.Absent erythrocytes: bone marrow lacked the nucleated erythroid cells that represent 17% of the control bone marrow.Decreased B cell number: B lymphocyte numbers were reduced variably in the bone marrow, with most cells having a preB cell phenotype.Increased granulocyte number: expansion of granulocyte precursors in the bone marrow and spleen.Abnormal granulocyte differentiation: granulocytes maintained c-kit expression and displayed some, but not complete, maturation.Extramedullary hematopoiesis: spleen cells generated vastly increased numbers of granulocytic colonies, excessive numbers of megakaryocytic colonies and IL-3 responsive macrophage-containing colonies.Abnormal bone marrow cell morphology/development: the bone marrow contained normal total cellularity but exhibited an increased proportion of blast cells, and immature cells of the granulocyte lineage (promyelocytes and myelocytes).Absent common myeloid progenitor cells:* bone marrow lacked eosinophil colony-forming cells that were responsive to granulocyte-macrophage colony-stimulating factor (GM-CSF), IL-3 or IL-5, but had greatly elevated numbers of granulocytic colonies developed when stimulated by G-CSF, IL-3 or stem cell factor but not with IL-6.* few or no megakaryoctye colonies developed in cultures of bone marrow cells under optimal culture for megakaryoctye formation.* loss of any readily identifiable lymphoid and myeloid progenitor or stem cell populations.Abnormal spleen morphology: in severe cases, spleen showed homogeneous infiltration by immature granulocytic forms and loss of splenic architecture.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|06-Aug-2007||0.0|0.0|Unknown||B cell, lymphocyte, Myeloid Leukaemia, granulocyte, erythrocyte|Yes| 3406.0|act-mOVA / MHCII I-Ab -/-|C57BL/6-H2-Ab1 Tg(CAG-OVA)916Jen/Wehi||Recessive|histocompatibility 2, class II antigen A, beta 1|H2-Ab1|Unknown|A beta, Abeta, H-2Ab, H2-Ab, I-Ab, I-Abeta, Ia-2, Ia2, IAb, Rmcs1|MGI:103070||||17||||||||||||||||Yes|transgene insertion 916, Marc K Jenkins|chicken β-actin|||||||||||Ubiquitously express membrane bound chicken ovalbumin under the control of chicken β-actin promoter. Breed less well than hets. Homozygotes for targeted null mutations exhibit depletion of mature CD4+ T cells, deficiency in cell-mediated immune responses, and increased susceptibility to viral infections.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|13-Jul-2008||0.0|0.0|Unknown||Autoimmunity, ovalbumin, MHC Class II, T cell, CD4|Yes| 4789.0||BALB/c||Dominant||||||||||||||||||||||||||||||||||||||Normal.||Balb/cJ|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|06-Sep-2009||0.0|0.0|Unknown||BALB/c|No| 9417.0|Solox H x AR2 -/-|C57BL/6J-Solox H x AR2 -/-/Apb||Semi-dominant|Ifnar2 -/- x Soluble Ifnar2 ||||||||Unknown|||||||||||||||||||||||||||||normal|normal|C57Bl/6J|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|08-Aug-2022|Cryopreserved sperm|50.0|0.0|Unknown|||Possibly| 9410.0||C57Bl/6-Tnfaip3 /Apb||Semi-dominant|TNFAIP3||||||||Unknown|||||||||||||||||||||||||||||unknown|unknown|C57Bl/6N|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|22-Jul-2022|Cryopreserved sperm|55.0|0.0|Unknown|||Possibly| 9404.0|Stag2|C57BL/6J-Stag2/Apb|MGI:J:278649|X-linked|stromal antigen 2|Stag2||9230105L23Rik, B230112I07Rik, nuclear protein SA2, SA-2, SAP2|MGI:1098583 |stromal antigen 2; targeted mutation 1c, Wellcome Trust Sanger Institute|Stag2|MGI:5909046|X||||||||||||||||||||||||||||| Homozygous females (Stag2flox/flox) are viable and fertile, with no reported gross phenotypic abnormalities or breeding problems. When maintaining a live colony, homozygous females may be bred to hemizygous males.| Hemizygous males (Stag2flox/Y) are viable and fertile, with no reported gross phenotypic abnormalities or breeding problems. When maintaining a live colony, homozygous females may be bred to hemizygous males.|C57Bl/6J|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|13-Jul-2022||0.0|30.0|Unknown|||Possibly| 9407.0||ENU24:004:Usp8:B6||Semi-dominant|Unknown||||||||Unknown||||||||||||||||||||||||||||| | |C57Bl/6N|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|17-Jul-2022|Cryopreserved sperm|22.0|0.0|Unknown|||Possibly| 9412.0|Nlrp3|ENU55:051:Nlrp3:B6||Semi-dominant|NLR family, pyrin domain containing 3|Nlrp3||Cias1, cryopyrin, Mmig1, NALP3, Pypaf1 |MGI:2653833||||11||||||||||||||||||||||||||||| | |C57Bl/6N|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|03-Aug-2022|Cryopreserved sperm|21.0|0.0|Unknown|||Possibly| 9414.0|IFNAR2 KO|C57Bl/6J-Ifnar2/AnuApb||Semi-dominant|interferon (alpha and beta) receptor 2|Ifnar2|||MGI:1098243 ||||16|||||||||||||||||||||||||||||normal|normal|C57Bl/6J|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|08-Aug-2022|Cryopreserved sperm|50.0|0.0|Unknown|||Possibly| 9413.0|IFNAR1 KO|C57Bl/6J-Ifnar1/AnuApb||Semi-dominant|interferon (alpha and beta) receptor 1|Ifnar1|||MGI:107658||||16|||||||||||||||||||||||||||||normal|normal|C57Bl/6J|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|08-Aug-2022|Cryopreserved sperm|50.0|0.0|Unknown|||Possibly| 9416.0|Solox High|C57Bl/6J- Ifnar2/Apb||Recessive|interferon (alpha and beta) receptor 2 |Ifnar2 |||MGI:1098243||||16|ENSMUSG00000022971 |||||||||Unknown to Unknown|||||||||||||||||||normal|normal|C57Bl/6J|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|08-Aug-2022|Cryopreserved sperm|40.0|0.0|Unknown|||Possibly| 9415.0|Ifne KO|C57Bl/6-Ifne KO/AnuApb||Semi-dominant|Interferon epsilon|Ifne|||MGI:2667156||||4|ENSMUSG00000045364 |||||||||Unknown to Unknown|||||||||||||||||||normal|normal|C57Bl/6J|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|08-Aug-2022|Cryopreserved sperm|50.0|0.0|Unknown|||Possibly| 9409.0|Zfp64(8) |C57BL6NCrlAnu-Zfp64em6Anu(8)||Semi-dominant|Zfp64||||||||Unknown|||||||||||||||||||||||||||||Unknown|Unknown|C57Bl/6N|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|20-Jul-2022|Cryopreserved sperm|55.0|0.0|Unknown|||Possibly| 9406.0|ENU57:G2|ANU:ENU57:G2||Recessive|Unknown||||||||Unknown||||||||||||||||||||||||||||| | |C57Bl/6N|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|15-Jul-2022|Cryopreserved sperm|8020.0|0.0|Unknown|||Possibly| 9426.0|AkirinR180W(64)|C57Bl/6N-Akirin/Apb||Semi-dominant|akirin 1|Akirin1|||MGI:1915300||||4|||||||||||||||||||||||||||||Unknown|Unknown|C57Bl/6N|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|31-Aug-2022|Cryopreserved sperm|54.0|0.0|Unknown|||Possibly| 9420.0|Itk|C57BL/6NCrlAnu-ItkAnu/Anu||Recessive|IL2 inducible T cell kinase|Itk|||MGI:96621|236bpDel|||11|||||||||||||||||||||||||||||Unknown|Unknown|C57Bl/6N|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|22-Aug-2022|Cryopreserved sperm|52.0|0.0|Unknown|||Possibly| 9428.0|Lyn KO|C57BL/6NCrlAnu-Lyn/Apb||Recessive|LYN proto-oncogene, Src family tyrosine kinase|Lyn||Hck-2, Yamaguchi sarcoma viral (v-yes-1) oncogene homolog |MGI:96892||||4|||||||||||||||||||||||||||||unknown|unknown|C57Bl/6N|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|19-Sep-2022|Cryopreserved sperm|10.0|0.0|Unknown|||Yes| 9429.0||C57BL/6NCrlAnu-Lyn8/AnuApb||Semi-dominant|LYN proto-oncogene, Src family tyrosine kinase|Lyn|||MGI:96892|Lyn: endonuclease mutation 1, Australian National University|Lyn||4|||||||||||||||||||||||||||||unknown|unknown|C57Bl/6N|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|19-Sep-2022|Cryopreserved sperm|10.0|0.0|Unknown|||Possibly| 9427.0|ENU56:G3|ANU:ENU56:G3||Recessive|Unknown||||||||Unknown||||||||||||||||||||||||||||| | |C57Bl/6N|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|18-Sep-2022|Cryopreserved sperm|65.0|0.0|Unknown|||Possibly| 9421.0|Hcn1 M294L|C57BL/6J-Hcn1/Apb||Recessive|hyperpolarization activated cyclic nucleotide gated potassium channel 1|Hcn1||Bcng1, C630013B14Rik, HAC2, hyperpolarization-activated, cyclic nucleotide-gated K+ 1|MGI:1096392||||Unknown|||||||||||||||||||||||||||||Unknown|Mice have a mild epilepsy phenotype with rare spontaneous seizures. They are smaller and very hyperactive. They are otherwise normal. |C57Bl/6J|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|31-Aug-2022||0.0|0.0|Unknown|||No| 9438.0|Gsdme-|C57BL/6N-Gsdmeem1Fsha/J||Recessive|gasdermin E|L2 reder|||||||Unknown|||||||||||||||||||||||||||||Normal|Normal|C57Bl/6N|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|25-Oct-2022||0.0|0.0|Unknown|||Possibly| 9101.0||B6.Abca12;Tg(KRT14-cre/ERT)||Semi-dominant|ATP-binding cassette, sub-family A (ABC1), member 12|Abca12|Reduced|4832428G11Rik, 4833417A11Rik |MGI:2676312 |ATP-binding cassette, sub-family A (ABC1), member 12; targeted mutation 1c|Abca12||1|||||||||||||||||Transgene insertion 1|KRT14|Unknown||||||||||normal|normal|C57BL/6|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|25-Nov-2020|Cryopreserved sperm|50.0|0.0|Unknown||Skin, Stem Cells, Tamoxifen-inducible, Carcinomas|Possibly| 9433.0||C57Bl/6J-Tg<(Ace2-ACE2)4Pqt>/Apb||Semi-dominant|angiotensin converting enzyme 2|Ace2 |||MGI:1917258|mAce2-hACE2|||X||||||||||Unknown to Unknown|||||||transgene insertion 4, Paul Q Thomas|mAce2|||||||||||Normal|Normal|C57Bl/6J|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|21-Sep-2022|Cryopreserved sperm|40.0|0.0|Unknown|||Possibly| 9431.0||C57Bl/6J-Tg<(Ace2-ACE2)2Pqt>/Apb||Semi-dominant|angiotensin converting enzyme 2|Ace2 |||MGI:1917258|MAce2-hACE2|||X||||||||||Unknown to Unknown|||||||transgene insertion 2, Paul Q Thomas|mAce2|||||||||||Normal|Normal|C57Bl/6J|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|21-Sep-2022|Cryopreserved sperm|50.0|0.0|Unknown|||Possibly| 9443.0|Kenobi:Nfkb2|B6(Cg)-Cd79a Nfkb2/Anu||Recessive|CD79A antigen (immunoglobulin-associated alpha)|Cd79a||Igalpha, Ly-54, Ly54, mb-1|MGI:101774|Cd79a; mutation 1, Australian National University|Cd79a||7|ENSMUSG00000003379 |||||||||Unknown to Unknown|||||||||||||||||||Unknown|Unknown|C57Bl/6N|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|02-Nov-2022|Cryopreserved sperm|43.0|0.0|Unknown|||Possibly| 9443.0|Kenobi:Nfkb2|B6(Cg)-Cd79a Nfkb2/Anu||Recessive|nuclear factor of kappa light polypeptide gene enhancer in B cells 2|Nfkb2 |||MGI:1099800|Nfkb2:endonuclease-mediated mutation 1, Australian National University|Nfkb2||19|||||||||||||||||||||||||||||Unknown|Unknown|C57Bl/6N|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|02-Nov-2022|Cryopreserved sperm|||Unknown|||Possibly| 9432.0||C57BL/6J-Tg<(Ace2-ACE2)3Pqt>/Apb||Semi-dominant|angiotensin converting enzyme 2|Ace2 ||Ace3 |MGI:1917258|mAce2-hACE2|||X||||||||||Unknown to Unknown|||||||transgene insertion 3, Paul Q Thomas|mAce2|||||||||||Normal|Normal|C57Bl/6J|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|21-Sep-2022|Cryopreserved sperm|30.0|0.0|Unknown|||Possibly| 9437.0|GAD67-GFP|C57BL/6J-Tg(Gad1-EGFP)/Apb||Semi-dominant|GAD67-GFP|||||GAD67-GFP|||Unknown|||||||||||||||||||||||||||||Transgenic knock In |Heterozygous|C57Bl/6J|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|29-Sep-2022|Cryopreserved sperm|50.0|0.0|Unknown|||Possibly| 9440.0|ENU58:G2|ANU:ENU58:G2||Recessive|Unknown||||||||Unknown||||||||||||||||||||||||||||| | |C57Bl/6N|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|26-Oct-2022|Cryopreserved sperm|10542.0|0.0|Unknown|||Possibly| 9442.0|Leckie ; Stat4|C57BL/6NCrlAnu-Stat4em1Anu/Anu||Recessive|signal transducer and activator of transcription 4|Stat4|||MGI:103062||||1|||||||||||||||||||||||||||||Unknown|Unknown|C57Bl/6N|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|02-Nov-2022|Cryopreserved sperm|55.0|0.0|Unknown|||Possibly| 9436.0|Brca2 KO|Balb/c-Brca2/Anu||Dominant|breast cancer 2, early onset|BRCA2|||MGI:109337|Brca2: endonuclease mutation 2, Australian National University|Brca2||5||||||||||Unknown to Unknown|||||||||||||||||||embryonic lethal|normal|Balb/cJ|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|28-Sep-2022|Cryopreserved sperm|49.0|0.0|Unknown|||Yes| 9439.0|ENU58:G2|ANU:ENU58:G2||Recessive|Unknown||||||||Unknown||||||||||||||||||||||||||||| | |C57Bl/6N|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|26-Oct-2022||0.0|0.0|Unknown|||Possibly| 9446.0|ENU18NIH17a:Adidas|B6(Cg)-Tnfsf13bm1Anu Nfkb2em1Anu/Anu||Recessive||||||||||||||||||||||||||||||||||||||Unknown|Unknown|C57Bl/6N|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|02-Nov-2022|Cryopreserved sperm|32.0|0.0|Unknown|||Possibly| 9448.0|OsxCherry.Col1a1GFP|C57Bl/6J-Tg(Sp7/mCherry)2Pmay Tg(Col1a1*2.3-GFP)1Rowe/Apb||Dominant| Tg(Sp7/mCherry)2Pmay. Tg(Col1a1*2.3-GFP)1Rowe .||||||||Unknown|||||||||||||||||transgene insertion 2, Peter Maye|Transgene 1: 2.3 kb (from the upstream promoter sequence to 22300 bp) rat procollagen, type 1, alpha 1( Col1a1) promoter. Transgene 2: 39 kb BAC (#RP24-362M3) containing the entire mouse Sp7 gene. |||||||||||Normal|Normal|C57Bl/6J|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|08-Nov-2022|Cryopreserved sperm|50.0|0.0|Unknown|||Yes| 9448.0|OsxCherry.Col1a1GFP|C57Bl/6J-Tg(Sp7/mCherry)2Pmay Tg(Col1a1*2.3-GFP)1Rowe/Apb||Dominant||||||||||||||||||||||||||transgene insertion 1, David Rowe||||||||||||Normal|Normal|C57Bl/6J|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|08-Nov-2022|Cryopreserved sperm|||Unknown|||Yes| 9450.0|Olig2Cre; 14-3-3zeta fl/fl|C57:129-Olig2(Cre)Ywhaz/Apb||Semi-dominant|tyrosine 3-monooxygenase/tryptophan 5-monooxygenase activation protein, zeta polypeptide|Ywhaz||1110013I11Rik, 14-3-3 zeta|MGI:109484|tyrosine 3-monooxygenase/tryptophan 5-monooxygenase activation protein, zeta polypeptide; gene trap EUCE0076e02, Helmholtz Zentrum Muenchen GmbH|Ywhaz|MGI:4393774|15|||||||||||||||||||||||||||||Normal with mild behavioural anomolies|Normal|129S1/Sv, C57Bl/6|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|08-Nov-2022|Cryopreserved sperm|40.0|0.0|Unknown|||Possibly| 9455.0||C57Bl/6-eIF2αk2/Apb||Semi-dominant|eukaryotic translation initiation factor 2-alpha kinase 2|Eif2ak2|||MGI:1353449||||17|ENSMUSG00000024079 |ENSMUST00000024884||||||||Unknown to Unknown|||||||mutagenic casette subsequently removed by CRE-mediated excision||||||||||||normal|normal|C57Bl/6J|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|29-Nov-2022|Cryopreserved sperm|50.0|0.0|Unknown|||Possibly| 9449.0||C57BL/6J-Gt(ROSA)26SorTg(Dmp1-cre/ERT2)0022Pdp/IkalJ/Apb||Semi-dominant||||||gene trap ROSA 26, Philippe Soriano; targeted mutation 9, Hongkui Zeng|B6.Cg-Gt(ROSA)26Sor|MGI:3809523|6||||||||||||||||||Dmp1-cre/ERT2|||||||||||Normal|Normal|C57Bl/6J|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|08-Nov-2022||0.0|0.0|Unknown|||Possibly| 9454.0||C57Bl/6-Eif2αk2Anu/Apb||Recessive|transcription factor 3|Tcf3|||MGI:98510|Tcf3:KO|||10|||||||||||||||||||||||||||||embryonic lethal|mild reduction in B cells. Altered light chain ratio.|C57Bl/6N|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|10-Nov-2022||0.0|0.0|Unknown|||Possibly| 10455.0|B6.A2G-Mx1 (Cg/Cg)|B6.A2G-Mx1/AnuApb||Dominant|myxovirus (influenza virus) resistance 1|Mx1|Normal|Mx, Mx-1, myxovirus (influenza) resistance 1 polypeptide|MGI:97243|myxovirus (influenza virus) resistance 1; myxovirus resistance|Mx1|MGI:3715151|16|||||||||||||||||||||||||||||Sensitive to influenza infection|Normal, i.e. highly influenza resistant.|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|23-Sep-2024||0.0|0.0|Unknown||Infection, resistance, Interferon|Yes| 9457.0|Akirin1<6-11bpDel>|C57BL/6NCrlAnu-Akirin1em1Anu/Anu||Recessive|Akirin1|akirin 1|||MGI:1915300||||4||||||||||Unknown to Unknown|||||||||||||||||||Unknown|Unknown|C57Bl/6N|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|05-Dec-2022|Cryopreserved sperm|33.0|0.0|Unknown|||Possibly| 9460.0|Taco:2 ; Taco<11bp del>|C57BL/6NCrlAnu-Tax1bp1/Anu||Recessive|Tax1 (human T cell leukemia virus type I) binding protein 1|Tax1bp1|||MGI:1289308 ||||6|||||||||||||||||||||||||||||Unknown|Unknown|C57Bl/6N|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown|2022|||No|05-Dec-2022|Cryopreserved sperm|44.0|0.0|Unknown|||Yes| 9461.0|Taco:3 ; Tax1bp1|C57BL/6NCrlAnu-Tax1bp1/Anu||Recessive|Tax1 (human T cell leukemia virus type I) binding protein 1|Tax1bp1|||MGI:1289308||||6|||||||||||||||||||||||||||||Unknown|Unknown|C57Bl/6N|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|05-Dec-2022|Cryopreserved sperm|44.0|0.0|Unknown|||Yes| 9459.0|Adidas:Cahill:GFP-FoxP3|C57BL/6NCrlAnu-Nfkb2 Ikbkb Foxp3/Anu||Semi-dominant|nuclear factor of kappa light polypeptide gene enhancer in B cells 2|Nfkb2 |||MGI:1099800 ||||19|||||||||||||||||||||||||||||||C57Bl/6N|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|05-Dec-2022|Cryopreserved sperm|22.0|0.0|Unknown|||Possibly| 9459.0|Adidas:Cahill:GFP-FoxP3|C57BL/6NCrlAnu-Nfkb2 Ikbkb Foxp3/Anu||Semi-dominant|inhibitor of kappaB kinase beta|Ikbkb|||MGI:1338071 ||||8|||||||||||||||||||||||||||||||C57Bl/6N|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|05-Dec-2022|Cryopreserved sperm|||Unknown|||Possibly| 9459.0|Adidas:Cahill:GFP-FoxP3|C57BL/6NCrlAnu-Nfkb2 Ikbkb Foxp3/Anu||Semi-dominant|forkhead box P3|Foxp3|||MGI:1891436 ||||X|||||||||||||||||||||||||||||||C57Bl/6N|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|05-Dec-2022|Cryopreserved sperm|||Unknown|||Possibly| 337.0|C57BL/6J-Rag1TgN(OT-I)|B6.129-Rag1 Tg(TcraTcrb)1100Mjb||Recessive|recombination activating gene 1|Rag1|Unknown|Rag-1|MGI:97848|recombination activating gene 1; targeted mutation 1, David Baltimore|Rag1|MGI:2448994|2||||||||||||||||Yes|transgene insertion 1100, Michael J Bevan||||||||||||||C57BL/6 x 129|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|05-May-2006||0.0|0.0|Unknown||T cell, Ovalbumin, CD8, H2|Yes| 106.0|4-1BBL -/-|B6.129Apb-Tnfsf9/Apb||Recessive|tumor necrosis factor (ligand) superfamily, member 9|Tnfsf9|Nil|4-1BB ligand, 4-1BB-L, 4-1BBL, Cd137l, Ly63l|MGI:1101058|targeted mutation 1, Tania H Watts|Tnfsf9|MGI:2179297|17||||||||||Unknown to Unknown||||||Yes|||||||||||||Mice homozygous for a null allele exhibit increased susceptibility to viral infection and defective memory T cell activation.||C57BL/6 x 129|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|06-Feb-2006|Cryopreserved sperm|119.0|0.0|Unknown||TNF, T cell, viral infection, CD28, memory|Yes| 294.0|eotaxin Tg(IL5)|C;B6-Ccl11 Tg(CD2-Il5)5C2Ldt||Dominant|small chemokine (C-C motif) ligand 11|Ccl11|Nil|eotaxin, Scya11|MGI:103576|chemokine (C-C motif) ligand 11; targeted mutation 1, Marc E Rothenberg|Ccl11|MGI:2384435|11||||||||||||||||Yes|transgene insertion 5C2, Lindsay A Dent|the dominant control region (DCR) of the gene encoding human CD2|High||||||||||Eosinophil-deficient. Tumor incidence was greatly increased.Eotaxin(-/-) mice with or without the IL-5 transgene, were no more susceptible than WT or IL-5 Tg mice to protracted primary infections with Heligmosomoides bakeri, a parasitic nematode that is restricted to the gut. ||BALB/c x C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||10||No|03-May-2006||0.0|0.0|Unknown||interleukin, eosinophil, tumour, immune surveillance, infection|Yes| 340.0|TgAPP751 (Tg72-3 line)|B6.SJL-Tg(APP751)72-3Aust ||Dominant||||||||||||||||||||||||||amyloid beta (A4) precursor protein|moPrP, hamster prion protein promotor|||||||||||Transgene primarily expressed in brain.No overt phenotype, normal growth and breeding.|No overt phenotype, normal growth and breeding.|C57BL/6 x SJL|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|||Strain is homozygous for transgene. Positive male breeds with female.|Yes|22-Sep-2006|Cryopreserved sperm|90.0|0.0|Yes||Amyloid precursor protein, amyloid Aβ, Alzheimer's disease, early onset Australian FAD mutation|No| 9456.0|Ctla4:1926bpDel; Apricot 8|C57BL/6NCrlAnu-Ctla4em1Anu/Anu||Recessive|cytotoxic T-lymphocyte-associated protein 4|Ctla4|||MGI:88556||||1|||||||||||||||||||||||||||||Unknown|Unknown|C57Bl/6N|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|05-Dec-2022|Cryopreserved sperm|33.0|0.0|Unknown|||Possibly| 9458.0|Ikbkb:Rag1 KO|B6(Cg)-Ikbkbem1Anu Rag1tm1Mom/Anu||Recessive|inhibitor of kappaB kinase beta|Ikbkb |||MGI:1338071||||8|||||||||||||||||||||||||||||Unknown|Unknown|C57Bl/6N+Rag1|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|05-Dec-2022|Cryopreserved sperm|22.0|0.0|Unknown|||Possibly| 9458.0|Ikbkb:Rag1 KO|B6(Cg)-Ikbkbem1Anu Rag1tm1Mom/Anu||Recessive|recombination activating 1|Rag1|||MGI:97848||||2|||||||||||||||||||||||||||||Unknown|Unknown|C57Bl/6N+Rag1|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|05-Dec-2022|Cryopreserved sperm|||Unknown|||Possibly| 649.0|HAP KO|Un.129-Hap1||Recessive|huntingtin-associated protein 1|Hap1|Nil|HAP-1|MGI:1261831|huntingtin-associated protein 1; targeted mutation 1, Xiao-Jiang Li|Hap1|MGI:2670598|11||||||||||||||||Yes|||||||||||||Postnatal lethality:* most homozygotes die at 3 to 4 days after birth.* a few survive beyond 9 days of age, in the absence of skin, bone, or organ abnormalities* no homozygotes survive beyond 15 days of age.Absent gastric milk in neonates: mutant pups contain very little gastric milk, suggesting a feeding defect that may retard postnatal growth.Abnormal hypothalamus morphology:* at P1, TUNEL-positive cells are observed in the paraventricular nuclei (PVN) and the lateral hypothalamus (LH) of mutant but not wild-type mice; very few or no TUNEL-positive cells are noted in the arcuate nucleus (ARC) of mutant mice.* by P3, TUNEL-labeled cells are more widely spread in various regions of the hypothalamus which control eating, food intake, and energy metabolism, including the ventromedial hypothalamic nucleus (VMN).Neurodegeneration:* as early as P1, homozygotes display degeneration in specific regions of the hypothalamus that control feeding behavior, as determined by TUNEL staining.* in contrast, other brain regions (e.g. cortex, striatum, cerebellum, and hippocampus) display significantly fewer TUNEL-positive cells or show no difference relative to wild-type mice.|||No|No|Yes|No|No|Yes|No|Unknown||||No|25-Apr-2007||0.0|0.0|Yes|Huntington's disease|nerve, degeneration, hypothalamus, huntingtin, EGFR|Yes| 650.0|Fat Aussie|NOD-Alms1||Recessive|Alstrom syndrome 1 homolog (human)|Alms1|Nil||MGI:1934606|fat aussie|Alms1|MGI:3621984|6||||||||||||||||No|||||||||||||Hyperglycemia: female mice are diabetic by 200 days of age.Increased circulating insulin level: female mice develop insulinemia (20ng/mL insulin vs. 2-5ng/mL in wild-type).Insulin resistance: female mice develop insulin resistance by 200 days of age.Increased eating behaviour: mutants eat more than wild-type.Abnormal hepatocyte morphology: mutant livers show many hepatocytes with ballooning degeneration and extensive lobular inflammation with polymorphs and mononuclear cells.Enlarged liver: mice fed high-fat diet show hepatomegaly compared to wild-type (8.9g vs. 2g).Increased liver weight: liver weights in mutant are twice that of wild-type (3.4g vs. 1.6g).Hepatic steatosis: chow-fed mutants develop steatosis; mutants fed the high-fat diet develop severe steatohepatitis.Liver fibrosis: mutant livers show pericellular and pericentral fibrosis.||NOD|Yes|No|Yes|Yes|No|Yes|No|Poor||||No|25-Apr-2007||0.0|0.0|Yes||obesity, diabetes, diet|Yes| 8491.0|C57BL/6.Scmh1-197|C57BL/6N-Scmh1197/BaxApb||Recessive|sex comb on midleg homolog 1|Scmh1||Scml3|MGI:1352762|sex comb on midleg homolog 1; targeted mutation 1a, Wellcome Trust Sanger Institute|Scmh1|MGI:4441791|4|||||||||||||||||||||||||||||Mice homozygous for a knock-out allele exhibit abnormal hematopoiesis but normal fertility and skeleton.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|31-May-2018|Cryopreserved sperm|50.0|0.0|Unknown|||Yes| 638.0|HtrA3-KO (MP10 Cre65)|C57BL/6-Htra3||Dominant|HtrA serine peptidase 3|Htra3|Nil|2210021K23Rik, 9530081K03Rik|MGI:1925808||||5||||||||||||||||Yes|||||||||||||Mice are fertile and do not show any clear signs of immunodeficiency.|Normal|C57BL/6J|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|25-Apr-2007|Cryopreserved sperm|55.0|0.0|Unknown||HtrA3, placentation, pregnancy, serine protease, placental insufficiency|No| 37.0|Dwarf|C57BL/6JSfdAnu-Wars/Apb||Recessive|tryptophanyl-tRNA synthetase|Wars|Unknown|dwarf|MGI:104630|tukkuburko|Wars|MGI:4819385|12|ENSMUSG00000021266|ENSMUST00000078788|Wars-201|89|220|T to C|ENSMUSE00000116158|2|30|Leucine to Proline|||||AGCTACTCAAGGGGAGCTCGTGAGGTCCCTCAAAGCTGGAAATGCACCAAAAGATGAGATT|Yes|||||||||||||Dwarfism; small at weaning/adult 60% of wt sib.Small to non-existant pituitary gland.Low IGF levels in serum.Phenotype unique to this chromosome location|||Yes|Unknown|Yes|Yes|Unknown|Yes|Yes|Good||6|het x het|No|06-Feb-2006|Cryopreserved sperm|126.0|0.0|Unknown||Dwarfism, pituitary, Small, ENU, runted|Yes| 8402.0|BALB.5702-3855|BALB/c-Gasa/Bax||Recessive|||||||||||||||||||||||||||||Unknown||||||||Unknown|Altered response to induced neonatal thymectomy induced gastritis compared to BALB/c mcie.||BALB/c|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|||Hom x Hom|No|19-Dec-2017|Cryopreserved sperm|50.0|0.0|Unknown||autoimmunity, gastritis|Yes| 171.0|DbHnlacZ|B6.129-Tg(DBHn-lacZ)8Rpk||Recessive||||||||||||||||||||||||||transgene insertion 8, Raj P Kapur|human dopamine beta hydroxylase (DBH)|||||||||||lacZ is expressed by all DbH-expressing cells in the CNS and periphery, plus some cells that are not thought to contain DbH (eg the enteric nervous system)||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|17-Apr-2006||0.0|0.0|Unknown||lacZ, neuron, sympathetic, ganglion, noradrenergic brain stem nuclei|Yes| 176.0|OVE591|OVE591||Dominant||||||||||||||||||||||||||truncated TGFβ receptor II, kinase deficient|αA-crystallin|||||||||||Nuclear cataract, characterised by rapid apoptosis and death of terminally differentiating lens fibres cells at PND3.||FVB/N|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|17-Apr-2006||0.0|0.0|Unknown||cataract, lens fibres, eye|Yes| 178.0|OMP-tau:LacZ|B6.129-Omp ||Dominant|olfactory marker protein|Omp|Nil||MGI:97436|targeted mutation 1, Peter Mombaerts|Omp|MGI:2179520|7||||||||||||||||Yes|LacZ|tau|||||||||||All olfactory neurons express LacZ||129/Sv x C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|17-Apr-2006||0.0|0.0|Unknown||LacZ, olfactory neurons|Yes| 188.0||VR2-IRES-tau:GFP||Dominant||||||||||||||||||||||||||||||||||||||A subpopulation of vomeronasal neruons innervating the caudall accessory olfactory bulb express GFP|||Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|17-Apr-2006||0.0|0.0|Unknown||GFP, olfactory, neuron|Yes| 189.0|M72-IRES-tau:GFP|Olfr160||Dominant|olfactory receptor 160|Olfr160|Unknown|GA_x6K02T2PVTD-31389446-31388517, M72, MOR171-3, MOR171-3|MGI:1931271|targeted mutation 6, Peter Mombaerts|Olfr160|MGI:3692202|9||||||||||||||||No|||||||||||||M72 odorant receptor neruons express GFP||C57BL/6 x 129|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|17-Apr-2006||0.0|0.0|Unknown||odorant neuron, GFP, olfactory, glomeruli|Yes| 202.0|TGFbRIII floxed|Tgfbr3||Recessive|transforming growth factor, beta receptor III|Tgfbr3|Normal|betaglycan, TBRIII|MGI:104637||||5||||||||||||||||Yes|||||||||||||Phenotypically normal. When crossed to Cre transgenics, will create knockout of TGFbRIII gene||C57BL/6 x 129|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|20-Apr-2006||0.0|0.0|Unknown||Growth factor, signal transduction|Yes| 8393.0|NOD.Idd13.H2b.Nkrp1b|NOD-H2 Idd13 Klrb1b/Bax||Recessive|||||||||||||||||||||||||||||histocompatibility-2, MHC|H2||H-2, MHC-II|MGI:95894|histocompatibility-2, MHC; b variant|H2|MGI:3579319|17|Mice that are homozygous for this allele are viable, fertile, normal in size.Idd13:Idd13 is congenic for a 32 cM segment of Chr 2 extending from D2Mit274 through D2Mit343 that includes the insulin dependent diabetes susceptibility locus Idd13.H2b:Congenic markers MHC haplotype H2ᵇ. Nkrplb:Congenic Nk Cell Marker. Congenic markers MHC haplotype H2ᵇ"||NOD/Lt|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|10|||No|19-Dec-2017|Cryopreserved sperm|49.0|0.0|Unknown||Nk1.1, TCR, NK cell, autoimmunity|Yes| 8393.0|NOD.Idd13.H2b.Nkrp1b|NOD-H2 Idd13 Klrb1b/Bax||Recessive|||||||||||||||||||||||||||||killer cell lectin-like receptor subfamily B member 1B|Klrb1b||Klrb1d, Ly55b, Ly55d, Nkrp1-b, NKR-P1B, Nkrp1d, NKR-P1D|MGI:107539||||6|Mice that are homozygous for this allele are viable, fertile, normal in size.Idd13:Idd13 is congenic for a 32 cM segment of Chr 2 extending from D2Mit274 through D2Mit343 that includes the insulin dependent diabetes susceptibility locus Idd13.H2b:Congenic markers MHC haplotype H2ᵇ. Nkrplb:Congenic Nk Cell Marker. Congenic markers MHC haplotype H2ᵇ"||NOD/Lt|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|10|||No|19-Dec-2017|Cryopreserved sperm|||Unknown||Nk1.1, TCR, NK cell, autoimmunity|Yes| 8393.0|NOD.Idd13.H2b.Nkrp1b|NOD-H2 Idd13 Klrb1b/Bax||Recessive|||||||||||||||||||||||||||||insulin dependent diabetes susceptibility 13|Idd13|||MGI:99415|insulin dependent diabetes susceptibility 13; C57BL/6|Idd13|MGI:3044074|2|Mice that are homozygous for this allele are viable, fertile, normal in size.Idd13:Idd13 is congenic for a 32 cM segment of Chr 2 extending from D2Mit274 through D2Mit343 that includes the insulin dependent diabetes susceptibility locus Idd13.H2b:Congenic markers MHC haplotype H2ᵇ. Nkrplb:Congenic Nk Cell Marker. Congenic markers MHC haplotype H2ᵇ"||NOD/Lt|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|10|||No|19-Dec-2017|Cryopreserved sperm|||Unknown||Nk1.1, TCR, NK cell, autoimmunity|Yes| 207.0|Tbx20 floxed|Tbx20||Recessive|T-box 20|Tbx20|Nil|Tbx12|MGI:1888496|targeted mutation 1, Richard P Harvey|Tbx20|MGI:3579478|9||||||||||||||||No|||||||||||||Normal|Normal|C57BL/6 x 129|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|24-Apr-2006||0.0|0.0|Unknown||transcription factor, heart|Yes| 209.0|Tie2-Cre|C57BL/6-Tg(Tek-cre)12Flv||Dominant|||Normal||||||Unknown||||||||||||||||Yes|transgene insertion 12, Richard A Flavell|mouse endothelial-specific receptor tyrosine kinase promoter/enhancer|Recombinase activity is detected in endothelial cells during embryogenesis and adulthood. Expression was also detected in hematopoietic cells.||||||||||Expression in endothelial cells during embryogenesis and adulthood.Hemizigous mice for transgenic insert are viable and fertile.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|24-Apr-2006||0.0|0.0|Unknown||endothelial, embryogenesis, Cre recombinase|Yes| 210.0|NRG1 TM/TM|NRG1 TM/TM||Recessive|neuregulin 1|Nrg1|Nil|GGF, GGFII, heregulin, HGL, Hgl, HRG, HRGalpha, NDF, SMDF, ARIA|MGI:96083||||8||||||||||||||||Yes|||||||||||||Embryonic NRG1 TM/TM mice die at E10.5 due to severe cardiac defects (lack of cardiac trabeculae). They also have impaired development of Schwann cell precursors, cranial ganglia, and radial glia cells.|Heterozygotes are hyperactive with reduced NMDA receptors.|C57BL/6|No|No|Yes|No|No|Yes|No|Unknown||||No|24-Apr-2006||0.0|0.0|Unknown||transmembrane domain, embryonic lethal, heart, schwann, glial, schizophrenia|Yes| 211.0|NRG1 KO|C57BL/6-Nrg1 ||Recessive|neuregulin 1|Nrg1|Unknown|GGF, GGFII, heregulin, HGL, Hgl, HRG, HRGalpha, NDF, SMDF, ARIA|MGI:96083|targeted mutation 1, Carmen Birchmeier|Nrg1|MGI:1928489|8||||||||||||||||No|||||||||||||Mice die at E10.5 due to severe cardiac defects (lack of cardiac trabeculae). In addition, Schwann cell precursors and cranial ganglia fail to develop normally in NRG1-/- mice.|None reported|C57BL/6J|No|No|Yes|No|No|Yes|No|Unknown||||No|24-Apr-2006||0.0|0.0|Unknown||schwann cell, ganglia embryonic lethal, heart, EGF, erbB, cardiac|Yes| 212.0|Nkx2-5 Cre|B6.129-Nkx2-5||Recessive|NK2 transcription factor related, locus 5 (Drosophila)|Nkx2-5|Normal|Csx, Csx, Nkx-2.5, Nkx2.5, tinman|MGI:97350|targeted mutation 2, Richard P Harvey|Nkx2-5|MGI:2448972|17||||||||||||||||No|Cre Recombinase|Nkx2-5|||||||||||Normal|Normal|C57BL/6 x 129/Sv|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|24-Apr-2006||0.0|0.0|Unknown||Cardiac, heart, Cre recombinase|Yes| 213.0||MLC3F-lacZ||Recessive|||Nil||||||Unknown||||||||||||||||Yes|nLacZ|myosin light chain 3f|||||||||||Mice are viable and fertile. ||C57BL/6 x FVB|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|24-Apr-2006||0.0|0.0|Unknown||LacZ, muscle, myogenesis|Yes| 215.0|Deleter|C57BL/6-Tg(CMV-cre)1Cgn||Dominant||||||||||||||||||||||||||transgene insertion 1, University of Cologne|human cytomegalovirus minimal promoter (PBi-2)CMV|active in most cells and tissues||||||||||Viable and fertile||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|24-Apr-2006||0.0|0.0|Unknown||Cre recombinase, CMV, expression, deletion|Yes| 217.0|MesP1-Cre|C57BL/6-Mesp1||Recessive|mesoderm posterior 1|Mesp1|Nil||MGI:107785|targeted mutation 2, Yumiko Saga|Mesp1|MGI:2176467|7||||||||||||||||No|Cre recombinase|endogenous MesP1|||||||||||Embryonic lethal as is MesP1 knockout.|Viable|C57BL/6 |No|No|Yes|No|No|Yes|No|Unknown||||No|24-Apr-2006||0.0|0.0|Unknown||mesoderm, cardia bifida, heart tube precursor, primitive streak, gastrulation|Yes| 218.0|Pitx2-lacZ|Pitx2-lacZ||Dominant|paired-like homeodomain transcription factor 2|Pitx2|Unknown|Brx1, Brx1a, Brx1b, Munc30, Otlx2, Pitx2a, Pitx2b, Pitx2c, Ptx2, Rieg, solurshin|MGI:109340||||3||||||||||||||||Yes|LacZ|Pitx2|||||||||||Viable and fertile||C57BL/6 x FVB|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|24-Apr-2006||0.0|0.0|Unknown||left / right axis, mesoderm, transcription factor, homeodomain|Yes| 222.0|D4X|Tg(CAG-EGFP)D4Nagy||X-linked||||||||||||||||||||||||||transgene insertion D4, Andras Nagy|chicken beta-actin promoter and CMV intermediate early enhancer|Widespread expression of the eGFP transgene throughout development, subject to X-inactivation mosaicism||||||||||Mice that are homozygous for the transgenic insert are viable, fertile, normal in size and do not display any gross physical or behavioural abnormalities.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|25-Apr-2006||0.0|0.0|No||X inactivation mosaicism, GFP, placenta, imprint, embryo|Yes| 8377.0|NOD.Nkrp1b.Slam1D|NOD-Klrb1b Nkt1 Slam1D/Bax||Recessive|||||||||||||||||||||||||||||killer cell lectin-like receptor subfamily B member 1B|Klrb1b||Klrb1d, Ly55b, Ly55d, Nkrp1-b, NKR-P1B, Nkrp1d, NKR-P1D|MGI:107539||||6|Mice that are homozygous for this allele are viable, fertile and normal in size.Congenic Nk Cell Marker. Congenic Marker for NKT1 region. Congenic Marker for Slam1d region. Increased Nkt cell numbers.||NOD/Lt|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|10|||No|11-Dec-2017|Cryopreserved sperm|50.0|0.0|Unknown||Nk1.1, TCR, NK cell, autoimmunity|Yes| 8377.0|NOD.Nkrp1b.Slam1D|NOD-Klrb1b Nkt1 Slam1D/Bax||Recessive|||||||||||||||||||||||||||||natural killer T cell numbers 1|Nktcn1||Nkt1|MGI:2681136|natural killer T cell numbers 1; C57BL/6J|Nktcn1|MGI:2681149|1|Mice that are homozygous for this allele are viable, fertile and normal in size.Congenic Nk Cell Marker. Congenic Marker for NKT1 region. Congenic Marker for Slam1d region. Increased Nkt cell numbers.||NOD/Lt|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|10|||No|11-Dec-2017|Cryopreserved sperm|||Unknown||Nk1.1, TCR, NK cell, autoimmunity|Yes| 8377.0|NOD.Nkrp1b.Slam1D|NOD-Klrb1b Nkt1 Slam1D/Bax||Recessive|||||||||||||||||||||||||||||signaling lymphocytic activation molecule family member 1|Slamf1|||MGI:1351314||||1|Mice that are homozygous for this allele are viable, fertile and normal in size.Congenic Nk Cell Marker. Congenic Marker for NKT1 region. Congenic Marker for Slam1d region. Increased Nkt cell numbers.||NOD/Lt|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|10|||No|11-Dec-2017|Cryopreserved sperm|||Unknown||Nk1.1, TCR, NK cell, autoimmunity|Yes| 170.0|RetTGM|C57BL/6-Ret||Recessive|ret proto-oncogene|Ret|Nil|RET51, RET9|MGI:97902|targeted mutation 1, Jeffrey Milbrandt|Ret|MGI:2449909|6||||||||||||||||Yes|||||||||||||All cells expressing Ret express GFP in both the nucleus and cytoplasm. Homozygous null mice die at birth, probably from gut motility defects.|None reported|C57BL/6|No|No|No|No|No|Yes|No|Unknown||||No|17-Apr-2006||0.0|0.0|Unknown||GFP, kidney, neuron, agenesis|Yes| 206.0|Tbx20 KO|Tbx20||Recessive|T-box 20|Tbx20|Nil|Tbx12|MGI:1888496|targeted mutation 1.1, Richard P Harvey|Tbx20|MGI:3579836|9||||||||||||||||No|||||||||||||Embryonic lethal ~E10.5. Abnormal cardiac and yolk sac development.Failure of looping morphogenesis-looping is blocked.|None reported|C57BL/6 x 129|No|No|Yes|No|No|Yes|No|Unknown||||No|24-Apr-2006||0.0|0.0|Unknown||cardiac, embryonic lethal, yolk sac, looping, heart, transcription factor|Yes| 214.0|Cryptic|C57BL/6-Cfc1||Recessive|cripto, FRL-1, cryptic family 1|Cfc1|Nil|cryptic|MGI:109448|targeted mutation 1, Michael M Shen|Cfc1|MGI:2179530|1||||||||||||||||Yes|||||||||||||Embryonic lethal. postnatal lethality (J:58104)homozygous mutant mice died within the first 2 weeks after birth, probably because of cardiac abnormalitieslife span/agingpremature death (J:58104)five homozygotes (from >90) survived past weaningcardiovascular systemabnormal direction of looping morphogenesis (J:58104)at 8.5-9.5 dpc, mutant embryos exhibited randomization of cardiac loopingat these stages, abnormal cardiac looping and embryo turning were highly correlateddextrocardia (J:58104)in 36% of mutant mice, the cardiac apex pointed to the right as opposed to the normal leftmesocardia (J:58104)in 12% of mutant mice, the cardiac apex pointed to the middle as opposed to the normal leftabnormal atrial septum morphology (J:58104)88% of mutant mice displayed septal defectsabnormal aorta morphology (J:58104)in wild-type mice, the aorta is dorsal to the pulmonary artery and connects to the left ventricle; in contrast, the mutant aorta was ventral to the pulmonary artery and connected to the right ventricleabnormal patterning of the aortic arch (J:58104)the mutant azygos vein could be located on the left side while the aorta arched to the left (as in wild-type), on the right while the aorta arched rightward, or bilaterally while the aorta arched leftwarddigestive/alimentary systemabnormal stomach morphology (J:58104)many newborn homozygotes exhibited a milk spot on their right side, instead of the leftembryogenesisabnormal direction of embryo turning (J:58104)at 8.5-9.5 dpc, homozygous mutant embryos exhibited randomization of embryo turningabnormal left-right axis patterning (J:58104)E18.5 and neonatal mutant mice (<1 week of age) displayed left-right laterality defects including heterotaxia, randomization of organ situs, and isomerism of bilaterally asymmetric tissuesgrowth/sizeright pulmonary isomerism (J:58104)100% of mutant mice displayed right pulmonary isomerismsitus inversus (J:58104)approximately 50% of homozygotes exhibited inverted situs of visceral organs including the stomach, spleen, and pancreashematopoietic systemabsent spleen (J:58104)100% homozygotes exhibited asplenia or severe hyposplenia|Viable and fertile|C57BL/6|No|No|Yes|No|No|Yes|No|Unknown||||No|24-Apr-2006||0.0|0.0|Yes||Left-right axis, Cardiac, aorta, pulmonary, liver|Yes| 220.0|Z/AP|Tg(CAG-Bgeo/ALPP)1Lbe||Dominant||||||||||||||||||||||||||transgene insertion 1, Corrinne Lobe|CMV enhancer/chicken beta-actin promoter|||||||||||Prenatal lethality|No information is available|C57BL/6|No|No|Yes|No|No|Yes|No|Unknown||||No|25-Apr-2006||0.0|0.0|Unknown||LacZ, alkaline phosphatase, reporter|Yes| 224.0|11Bal|C57BL/6-Trp53||Semi-dominant||||||||||||||||||||||||||||||||||||||Die in utero. Wildtype are black.Tumour incidence is similar to other Trp53 alleles.|Pale ears and tail but have black fur.|C57BL/6|No|No|Yes|No|No|Yes|No|Unknown||||No|25-Apr-2006||0.0|0.0|Unknown||Balancer, inversion, mutagenesis, drosophila, chromosome|Yes| 226.0|129.ZEG|129-Tg(CAG-Bgeo/GFP)21Lbe||Dominant||||||||||||||||||||||||||transgene insertion 21, Corrinne Lobe|CMV enhancer/chicken beta actin promoter|||||||||||Mice that are homozygous for the transgenic insert are viable, fertile, normal in size and do not display any gross physical or behavioural abnormalities. Expression of lacZ in transgenic mice is widespread, with notable exceptions being liver and lung tissue. This expression is observed throughout all embryonic and adult stages.Expresses enhanced GFP upon Cre-mediated excision.Used as a reporter of Cre-recombinase activity, for either stage-or tissue-specificity, following the excision of the floxed target and activation of the EGFP transgene.||129|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|25-Apr-2006||0.0|0.0|Unknown||LacZ, Green Fluorescent Protein (GFP), embryonic development|Yes| 1551.0||BALB/c-IL13 Tg(iFABPp-IL9)||Recessive|interleukin 13|Il13|Unknown|Il-13|MGI:96541|targeted mutation 2, Andrew NJ McKenzie|Il13|MGI:1931804|11||||||||||||||||Yes|interleukin 9|rat intestinal fatty acid binding protein (nucleotides -1178 - +28) - iFABP , i-FABP linked to nucleotides 3–2,150 of the human growth hormone (hGH) gene (except for its 5' regulatory sequences).|High||||||||||Restricted expression of IL9 transgene to intestine - duodenum and proximal jejunum.||BALB/c|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|06-Jul-2007|Cryopreserved sperm|100.0|0.0|Unknown||T cell, infection, IL-4, IL-5, allergy, mast cell|Yes| 1552.0||BALB/c-IL4R Tg(iFABPp-IL9)||Recessive|interleukin 4 receptor, alpha|Il4ra|Unknown|CD124, IL-4 receptor alpha chain, Il4r|MGI:105367||||7||||||||||||||||Yes|Interleukin 9|rat intestinal fatty acid binding protein (nucleotides -1178 - +28) - iFABP , i-FABP linked to nucleotides 3–2,150 of the human growth hormone (hGH) gene (except for its 5' regulatory sequences). |High||||||||||Restricted expression of IL9 transgene to intestine - duodenum and proximal jejunum.||BALB/c|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|06-Jul-2007|Cryopreserved sperm|130.0|0.0|Unknown||T cell, lymphocyte, immunoglobulin, interleukin|Yes| 1554.0||BALB/c-Stat6 Tg(iFABPp-IL9) ||Recessive|signal transducer and activator of transcription 6|Stat6|Unknown||MGI:103034|signal transducer and activator of transcription 6; targeted mutation 1, Shizuo Akira|Stat6|MGI:2386746|10||||||||||||||||No|interleukin 9|rat intestinal fatty acid binding protein (nucleotides -1178 - +28) - iFABP , i-FABP linked to nucleotides 3–2,150 of the human growth hormone (hGH) gene (except for its 5' regulatory sequences). |High||||||||||Restricted expression of IL9 transgene to intestine - duodenum and proximal jejunum.||BALB/c|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|06-Jul-2007|Cryopreserved sperm|95.0|0.0|Unknown||IL-4, T cell, B cell, immunoglobulin, infection, mast cell, allergy, anaphylaxis|Yes| 2354.0|Azharrudin|B6.129S2-Cd28 Tg(TcraTcrb)1100Mjb||Recessive|CD28 antigen|CD28|Nil|OT-1, OT-I, OT-I(OVA)TCR, OT-ITCR, OT1, OTI, OVA-tcr-I, OVA-Tg, TCR-OT-I, Tg(OT-I), Tg(TcrOva)1100Mjb|MGI:88327|targeted mutation 1, Tak Mak|Cd28|MGI:1857150|1||||||||||||||||Yes|transgene insertion 1100, Michael J Bevan||||||||||||The OT-1 strain carries a transgenic T cell receptor that recognizes ovalbumin residues 257-264 (SIINFEKL) in the context of H2K||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|11-Dec-2007|Cryopreserved sperm|150.0|0.0|Unknown||T cell, immunoglobulin, ovalbumin, lymphocyte|Yes| 2354.0|Azharrudin|B6.129S2-Cd28 Tg(TcraTcrb)1100Mjb||Recessive|||Unknown||||Tg(TcraTcrb)1100Mjb|MGI:3054907|Unknown|||||||||||||||||||||||||||||The OT-1 strain carries a transgenic T cell receptor that recognizes ovalbumin residues 257-264 (SIINFEKL) in the context of H2K||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|11-Dec-2007|Cryopreserved sperm|||Unknown||T cell, immunoglobulin, ovalbumin, lymphocyte|Yes| 2395.0||C57BL/6-Tnf Tnfrsf1a Tnfrsf1b||Recessive|tumor necrosis factor|Tnf|Normal|DIF, TNF alpha, TNF-alpha, Tnfa, TNFalpha, Tnfsf1a, tumor necrosis factor-alpha|MGI:104798|targeted mutation 2, Jonathon D Sedgwick|Tnf|MGI:3578747|17||||||||||||||||Yes|||||||||||||||C57BL/6 x 129|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|20-Dec-2007|Cryopreserved sperm|100.0|301.0|Unknown||lymphocyte, inflammation, lipopolysaccharide, neutrophil, innate immunity|Yes| 2395.0||C57BL/6-Tnf Tnfrsf1a Tnfrsf1b||Recessive|tumor necrosis factor receptor superfamily, member 1a|Tnfrsf1a|Nil|CD120a, p55, p55-R, TNF receptor alpha chain, TNF-alpha-R1, TNF-alphaR1, TNF-R-I, TNF-R1, TNF-R55, TNFalpha-R1, TNFAR, Tnfr-2, Tnfr1, TNFR60, TNFRI, TNFRp55|MGI:1314884|targeted mutation 1, Immunex Research and Development Corporation|Tnfrsf1a|MGI:1857468|6|||||||||||||||||||||||||||||||C57BL/6 x 129|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|20-Dec-2007|Cryopreserved sperm|||Unknown||lymphocyte, inflammation, lipopolysaccharide, neutrophil, innate immunity|Yes| 2395.0||C57BL/6-Tnf Tnfrsf1a Tnfrsf1b||Recessive|tumor necrosis factor receptor superfamily, member 1b|Tnfrsf1b|Nil|CD120b, p75, p75 TNFR, TNF-alphaR2, TNF-R-II, TNF-R2, TNF-R75, TNFalpha-R2, TNFBR, Tnfr-1, Tnfr2, TNFR80, TNFRII|MGI:1314883|targeted mutation 1, Immunex Research and Development Corporation|Tnfrsf1b|MGI:1860087|4|||||||||||||||||||||||||||||||C57BL/6 x 129|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|20-Dec-2007|Cryopreserved sperm|||Unknown||lymphocyte, inflammation, lipopolysaccharide, neutrophil, innate immunity|Yes| 3389.0|EphA1 conditional full knockout (EA1C KO)|B6.129-Epha1||Recessive|Eph receptor A1|Epha1|Normal|5730453L17Rik, Eph, Esk|MGI:107381|targeted mutation 2, Shannon L Duffy|Epha1||6||||||||||||||||Yes|||||||||||||Normal|Normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|3|5|Hom x Hom|No|11-Jul-2008|Cryopreserved sperm|255.0|0.0|Unknown||Receptor Tyrosine Kinase, ephrin, epithelium, uterus, tail, embryonic|Yes| 4513.0|ENU10B6a:007|C57BL/6JAnu-Tnfrsf1a/AnuApb||Dominant|tumor necrosis factor receptor superfamily, member 1a|Tnfrsf1a||CD120a, p55, p55-R, TNF receptor alpha chain, TNF-alpha-R1, TNF-alphaR1, TNF-R-I, TNF-R1, TNF-R55, TNFalpha-R1, TNFAR, Tnfr-2, Tnfr1, TNFR60, TNFRI, TNFRp55|MGI:1314884||||6|ENSMUSG00000030341|ENSMUST00000032491|Tnfrsf1a-001|152|453|A to G|ENSMUSE00000242873|2|50|Histidine to Arginine|||||TAGCTTGTGTCCCCAAGGAAAGTATGTCCATTCTAAGAACAATTCCATCTGCTGCACCAAG|Yes|||||||||||||Increased susceptibility to tuberculosis. Failure to limit multiplication of Mycobacterium tuberculosis in lung after inhalation. ||C57BL/6JAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|||Sib x Sib|No|26-Feb-2009|Cryopreserved sperm|29.0|0.0|Unknown||tuberculosis, infection, lung, ENU, Wellcome Trust|Yes| 4888.0||129-Ctsg/H||Dominant|cathepsin G|Ctsg|Nil||MGI:88563|targeted mutation 1.1, Jurgen Roes|Ctsgtm1.1Roes|MGI:2182170|14|||||||||||||||||||||||||||||Decreased susceptibility to bacterial infection: median survival time is increased to 560 +/- 47 min compared to 435 +/- 8 min in wild-type miceIncreased susceptibility to fungal infection: after infection with 500,000 A. fumigatus spores median survival time was only 13 +/- 4 days compared to wild-type mice which all survive6 days after infection kidney fungal load (457 mean CFU) is higher than in wild-type (16 mean CFU) but lower than in Ctsg and Ela double homozygotes (1009 mean CFU)||129/Sv|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|28-Sep-2009|Cryopreserved sperm|89.0|0.0|Unknown||Neutrophil, serine protease, reactive oxygen intermediates, endotoxin, LPS, TNF alpha, elastase|Yes| 4950.0|Light -/- IFNgR -/-|C57BL/6-Tnfsf14 Ifngr1||Recessive|tumor necrosis factor (ligand) superfamily, member 14|Tnfsf14|Nil|HVEM-L, LIGHT|MGI:1355317|tumor necrosis factor (ligand) superfamily, member 14; targeted mutation 1, Klaus Pfeffer|Tnfsf14|MGI:2671122|17|||||||||||||||||||||||||||||In the experimental model of Active EAE we found no significant difference between the LIGHT-/-IFN GAMMA R-/-BL6 strain and the IFN GAMMA R -/-BL6 strain in both the EAE disease development and daily clinical score. At the time of termination of experimentation the mice from both the experimental groups were of a similar severe level of EAE disease in comparison with the significantly lower level of EAE in the C57/BL6/Wt control mice. There was also no histopathological difference in the brain and spinal cord samples of the two experimental groups at the completion of the EAE experiment.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|04-Dec-2009|Cryopreserved sperm|100.0|0.0|Unknown||TNF, T cell, IL2, costimulation, lymphotoxin beta receptor|Yes| 4950.0|Light -/- IFNgR -/-|C57BL/6-Tnfsf14 Ifngr1||Recessive|interferon gamma receptor 1|Ifngr1|Unknown|CD119, Ifgr, IFN-gamma R, IFN-gammaR, Ifngr, Nktar|MGI:107655|interferon gamma receptor 1; targeted mutation 1, Michel Aguet|Ifngr1|MGI:1857286|Unknown|||||||||||||||||||||||||||||In the experimental model of Active EAE we found no significant difference between the LIGHT-/-IFN GAMMA R-/-BL6 strain and the IFN GAMMA R -/-BL6 strain in both the EAE disease development and daily clinical score. At the time of termination of experimentation the mice from both the experimental groups were of a similar severe level of EAE disease in comparison with the significantly lower level of EAE in the C57/BL6/Wt control mice. There was also no histopathological difference in the brain and spinal cord samples of the two experimental groups at the completion of the EAE experiment.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|04-Dec-2009|Cryopreserved sperm|||Unknown||TNF, T cell, IL2, costimulation, lymphotoxin beta receptor|Yes| 4968.0|IL-15NΔ|NOD.B6-Il15||Recessive|interleukin 15|Il15|Unknown||MGI:103014||||8||||||||||||||||No|||||||||||||Unknown|Unknow|NOD|Yes|Yes|Yes|Yes|Yes|Yes|No|Excellent|14|||No|15-Jan-2010|Cryopreserved sperm|100.0|0.0|Unknown||IL-15, diabetes, cytokine|Yes| 2375.0|Eddie ; ENU6WTNIH:028|CBA;B6JSfdAnu-Kcnn2/AnuApb||Recessive|potassium intermediate/small conductance calcium-activated channel, subfamily N, member 2|Kcnn2||SK2, small conductance calcium-activated potassium channel 2|MGI:2153182|eddie|||18|ENSMUSG00000054477|ENSMUST00000066890|Kcnn2-201|||||||||||||No|||||||||||||Generalised shaking, mild hypermetria, jerky movements, non progressive. First noted at weaning.||C57BL/6 x CBA|Yes|No|Yes|Yes|No|Yes|No|Unknown||||No|14-Dec-2007|Cryopreserved sperm|95.0|0.0|Unknown||shaking, ataxia, ENU|No| 2454.0||ENU6PH:043||Recessive|interferon regulatory factor 4|Irf4|Unknown|IRF-4, Spip|MGI:1096873||||13||||||||||||||||No|||||||||||||Hypo IgE response following allergic challenge.||C57BL/6 x C57BL/10|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|14-Jan-2008|Cryopreserved sperm|60.0|0.0|Unknown||T cell, B cell, lymphocyte, allergy, autoimmune, immunoglobulin, IgE|No| 3936.0|APN1|B6.129-Rbbp7/MIMR||Recessive|retinoblastoma binding protein 7|Rbbp7|Nil|mRbAp46|MGI:1194910|retinoblastoma binding protein 7; gene trap AD0754, Wellcome Trust Sanger Institute|Rbbp7|MGI:3856325|X||||||||||||||||Yes|||||||||||||Not bred to homozygocity|Normal|C57BL/6|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|16-Oct-2008|Cryopreserved sperm|135.0|0.0|Unknown||retinoblastoma, Gene trap, chromatin remodelling|Yes| 3937.0|APN2|B6.129-Stx16/MIMR||Recessive|syntaxin 16|Stx16|Unknown|SYN16|MGI:1923396|syntaxin 16; gene trap CD0253, Wellcome Trust Sanger Institute|Stx16|MGI:3864547|2||||||||||||||||Yes|||||||||||||Unknown at this time|Normal|C57BL/6|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown|1|||No|16-Oct-2008|Cryopreserved sperm|45.0|0.0|Unknown||ES cell genetrap, APN|Yes| 4076.0||ENU6PH:016||Recessive|||||||||Unknown||||||||||||||||Yes|||||||||||||Hypo IgG1 and IgE response following allergic challenge.||B6 B10 Balb/b|Yes|Yes|Yes|Yes|Yes|Yes|No|Poor||3||No|04-Dec-2008|Cryopreserved sperm|15.0|0.0|Unknown||allergic challenge, ENU, Immunoglobulin, IgE|No| 4180.0|mNET|C3H.FVB-Tg(Foxa2enhancer.β-globin-LacZ) ||Dominant||||||||||||||||||||||||||lacZ (Beta-galactosidase)|mouse notochord Foxa2 enhancer element, β-globin minimal promoter|||||||||||Normal. LacZ expressed in the 8.0 dpc notochord|Normal. LacZ expressed in the 8.0 dpc notochord|C3H/HeH|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|18-Dec-2008|Cryopreserved sperm|50.0|0.0|Unknown||Notochord, transcription factor, enhancer|Yes| 3384.0|Histamine receptor type 1 -/-|B6.129P2-Hrh1|B6.129P2-Hrh1|Recessive|histamine receptor H1|Hrh1|Nil|Bphs|MGI:107619|targeted mutation 1, Takeshi Watanabe|Hrh1|MGI:2182945|6||||||||||||||||Yes|||||||||||||Homozygous null mutants show decrease in exploratory behavior, diurnal activity, aggression, anxiety, serotonin release, respiratory reaction to temperature and leptin response. Natural variants affect B. pertussis induced vasoactive amine sensitization. Increased responses to papain sensitisation.Increased brown adipose tissue amount:* the amount of brown adipose tissue at 48 weeks of age is increased relative to in wild-type mice.* insulin levels during a 4 week feeding schedule are lower than in mice fed ad libitum.* however, the levels of brown adipose tissue at 12 weeks of age is normal.Increased white adipose tissue amount: at 28 weeks of age, white adipose tissue is increased by 23%, 48% and 40% in the epididymmal, mesenteric and retroperitoneal fat pads, respectively, compared to wild-type mice.Decreased adipose tissue amount: unlike in wild-type mice, intraperitoneal administration of the histamine agonist methyl(2[2-pyridyl]ethyl)amine dyhydrochloride (1 ug/g for 7 days) results in decreased in adiposity.Increased fat cell size:* adipocytes in the epididymal white adipose tissue are larger than in wild-type mice at 48 weeks of age.* however, adipocyte size at 12 weeks of age is normal.Decreased circulating insulin level:* at 48 weeks of age, serum insulin levels are increased relative to in wild-type mice.* however, at 12 weeks of age serum insulin levels are normal.Increased circulating leptin level:* at 48 weeks of age, leptin levels are increased by 66% compared to in wild-type mice.* however, at 12 weeks of age leptin levels are normalIncreased circulating free fatty acid level:* at 48 weeks of age, free fatty acid levels are increased relative to in wild-type mice.* however, at 12 weeks of age free fatty acid levels are normal.Increased triglyceride level: mice exhibit 45% and 20% more triglycerides in the liver and skeletal muscle, respectively, compared to wild-type mice.Abnormal response/metabolism to endogenous compounds: following intracerebroventricular administration of 0.5 ug leptin or intraperitoneal injection of 50 ug of leptin, mice exhibit a smaller decrease in food consumption and body mass relative to wild-type.Decreased body weight:* during 4 week on a feeding schedule, mice fail to gain weight as do wild-type mice despite equivalent food consumption.* unlike in wild-type mice, intraperitoneal administration of the histamine agonist methyl(2[2-pyridyl]ethyl)amine dyhydrochloride (1 ug/g for 7 days) results in decreased body mass.* however, intracerebroventricular administration of methyl(2[2-pyridyl]ethyl)amine dyhydrochloride has no effect on mice.Increased body weight: after 28 weeks of age mice exhibit increased body mass relative to wild-type mice.Increased IgG level: following ovalbumin challenge, IgG1, IgG2a and IgG2b levels are increased relative to similarly treated wild-type mice.Increased IgM level: following ovalbumin challenge, IgM levels are increased relative to similarly treated wild-type mice.Decreased interferon-gamma secretion: antigen stimulation of splenocytes results in the production of less interferon-gamma compared to in similarly treated wild-type mice.Decreased interleukin-13 secretion: antigen stimulation of splenocytes results in the production of less IL-13 compared to in similarly treated wild-type mice.Decreased interleukin-5 secretion: antigen stimulation of splenocytes results in the production of less IL-5 compared to in similarly treated wild-type mice.Decreased inflammatory response:* following challenge with ovalbumin, mice fail to develop lung inflammation as do wild-type mice with fewer eosinophils and lymphocytes detected in the bronchoalveolar lavage.* however, mice exhibit normal B cell immune responses and inhalation of IL-4 or IL-13 induces lung inflammation.Abnormal behavior:* during passive avoidance testing, mice display more frequent urination and defecation and decreased movement compared to wild-type mice.* however, passive avoidance behavior is normal.Abnormal circadian rhythm:* mice exhibit increased locomotor activity during early portions of the light phase and decreased ambulation during the dark phase of a 12 hours light 12 hour dark cycle relative to similarly treated wild-type mice.* the ratio of ambulation during the light phase to total ambulation during 24 hours is increased compared to in wild-type mice.* however, total ambulation during a 24 hours period is normal.Decreased exploration in new environment: despite normal motor coordination, mice exhibit decreased ambulation and time of rearing for the first 30 minutes when placed in a new environment.Decreased vertical activity: mice rear less when placed in a new environment compared to wild-type mice.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|09-Jul-2008|Cryopreserved sperm|150.0|0.0|Unknown||behaviour, aggression, leptin, respiration, serotonin|Yes| 3383.0|K14-Grhl3|B6-Tg(K14-Grhl3) ||Dominant||||||||||||||||||||||||||grainyhead-like 3 (Drosophila) (Grhl3)|keratin 14 (K14)|||||||||||Normal|Normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|||transgenic x transgenic|No|09-Jul-2008|Cryopreserved sperm|150.0|0.0|Unknown||Transcription Factor, epidermis, keratin|Yes| 3938.0|HtrA3-KO (MP10 Cre55)|C57BL/6-Htra355||Recessive|HtrA serine peptidase 3|Htra3|Nil||MGI:1925808||||5||||||||||||||||No|||||||||||||Normal||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|16-Oct-2008|Cryopreserved sperm|100.0|0.0|Unknown||placenta, pregnancy, serine protease, placental insufficiency|Yes| 4080.0||ENU6PH:078||Recessive|||||||||Unknown||||||||||||||||Yes|||||||||||||Hypo IgE response following allergic challenge.||C57BL/6 x C57BL/10 x Balb/b|Yes|Yes|Yes|Yes|Yes|Yes|No|Poor||||No|04-Dec-2008|Cryopreserved sperm|60.0|0.0|Unknown||Allergic challenge, ENU, Immunoglobulin, IgE|No| 4081.0||ENU6PH:094||Recessive|||||||||Unknown||||||||||||||||Yes|||||||||||||Hypo IgE response following allergic challenge.||C57BL/6 x C57BL/10|Yes|Yes|Yes|Yes|Yes|Yes|No|Poor||||No|04-Dec-2008|Cryopreserved sperm|60.0|0.0|Unknown||Allergic challenge, ENU, Immunoglobulin, IgE|No| 4082.0||ENU7PMH:036||Recessive|||||||||Unknown||||||||||||||||Yes|||||||||||||Hypo IgE response following allergic challenge.||C57BL/6 x C57BL/10|Yes|Yes|Yes|Yes|Yes|Yes|No|Poor||||No|04-Dec-2008|Cryopreserved sperm|45.0|0.0|Unknown||Allergic challenge, ENU, Immunoglobulin, IgE|No| 4176.0|APN3|B6;129-Uba2/MIMR||Recessive|ubiquitin-like modifier activating enzyme 2|Uba2|Unknown|anthracycline-associated resistance, Arx, SAE2, Sumo-1 activating enzyme subunit 2, UBA2, Uble1b|MGI:1858313|ubiquitin-like modifier activating enzyme 2; gene trap RRO015, BayGenomics|Uba2|MGI:4329423|7||||||||||||||||No|||||||||||||Unknown|Normal|C57BL/6 x NODk|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||1|chimera x C57BL/6|No|18-Dec-2008|Cryopreserved sperm|40.0|0.0|Unknown||ES cell genetrap, APN|Yes| 4178.0|APN4|B6;129-Rbbp4/MIMR||Recessive|retinoblastoma binding protein 4|Rbbp4|Unknown|CAF-1 p48 subunit, mRbAp48|MGI:1194912|retinoblastoma binding protein 4; gene trap AD0773, Wellcome Trust Sanger Institute|Rbbp4|MGI:3863854|4||||||||||||||||Yes|||||||||||||Unknown|Normal|C57BL/6|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown|1||Chimera x C57BL/6|No|18-Dec-2008|Cryopreserved sperm|45.0|0.0|Unknown||Gene trap, retinoblastoma, Rb, APN, ES cell|Yes| 4179.0|APN7|B6;29-Ifrd1/MIMR||Recessive|interferon-related developmental regulator 1|Ifrd1|Unknown|Ifnl, PC4, Tis7|MGI:1316717|interferon-related developmental regulator 1; gene trap AZ0065, Wellcome Trust Sanger Institute|Ifrd1|MGI:3857584|12||||||||||||||||Yes|||||||||||||Unknown. Note: Homozygous null mice display impaired muscle regeneration and myogenic differentiation and decreased body weight in older mice.|Normal|C57BL/6|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown|1||Chimera x C57BL/6|No|18-Dec-2008|Cryopreserved sperm|30.0|0.0|Unknown||Gene trap, APN, ES cell|Yes| 4603.0|mIMPα2FL|C57BL/6-Tg(EGFP-Kpna2 full length) ||Recessive|karyopherin (importin) alpha 2|Kpna2|Unknown|Importin alpha, m-importin, m-importin-alpha-P1, pendulin, Rch1|MGI:103561||||11||||||||||||||||Yes|EGFP fused to full length Kpna2|Protamine 1|||||||||||Unknown|Normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|13-Mar-2009|Cryopreserved sperm|40.0|0.0|Unknown||nuclear transport, importin, testis|No| 4719.0|TgAPP751 (Tg80.1 line)|B6.SJL-Tg(APP751)80.1Aust ||Dominant|amyloid beta (A4) precursor protein|APP|Unknown|Abeta, Adap, appican, betaAPP, Cvap, E030013M08Rik, protease nexin II, A4, AD1|MGI:88059||||16||||||||||||||||Yes|amyloid beta (A4) precursor protein|? moPrP, hamster prion protein promotor|||||||||||? Transgene primarily expressed in brain. No overt phenotype, normal growth and breeding.||? C57BL/6 x SJL|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|08-Apr-2009|Cryopreserved sperm|70.0|0.0|Yes||Amyloid precursor protein, amyloid Aβ, Alzheimer's disease, early onset Australian FAD mutation|No| 9447.0|Bake 4|C57BL/6NCrlAnu-Zfp64em3Anu Zfp64em4Anu/Anu||Recessive|zinc finger protein 64|Zfp64|||MGI:107342|Zfp64:F0#4-g1 / 7-28kDel; Zfp64:F0#4-g3-39bpDel|||2|||||||||||||||||||||||||||||Unknown|Unknown|C57Bl/6N|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|02-Nov-2022|Cryopreserved sperm|55.0|0.0|Unknown|||Possibly| 8306.0|AMPK a2(T485A/S491A) KI|C57BL/6-Prkaa2||Recessive|protein kinase, AMP-activated, alpha 2 catalytic subunit|Prkaa2|Unknown|2310008I11Rik, AMPKalpha2|MGI:1336173||||4|||||||||||||||||||||||||||||Normal|Normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|19-Sep-2017|Cryopreserved sperm|50.0|0.0|Unknown|||Possibly| 9453.0||C57Bl/6N-Klhdc3/Apb||Semi-dominant|Klhdc3|||||Klhdc3+/-|||Unknown|||||||||||||||||||||||||||||May be homozygous viable to ~30 days of age (low numbers to date)|Heterozygous animals appear normal - fertile, normal weights on C57BL/6 background|C57Bl/6J|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|11-Nov-2022|Cryopreserved sperm|40.0|0.0|Unknown|||Possibly| 10457.0|Tlr9 KO|C57BL/6J-Tlr9/Mgmp||Dominant|Tlr9|||||Tlr9:endonuclease-mediated mutation2, Monash Genome Modification Platform|Tlr9:KO(em2)||Unknown|||||||||||||||||||||||||||||Expect immune deficiency|Unknown||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|16-Oct-2024||0.0|0.0|Unknown|||No| 8899.0|DmdS3059E|C57BL/6-Dmd/Apb||Recessive|Dystrophin, muscular dystrophy|Dmd|Unknown|Dp427, Dp71, Duchenne muscular dystrophy, dys, mdx, pke, X-linked muscular dystrophy|MGI:94909||||X|||||||||||||||||||||||||||||Unknown|Unknown|C57BL/6|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|18-Mar-2020|Cryopreserved sperm|40.0|0.0|Yes|Muscular dystrophy||Yes| 8463.0|ASD598:Albiol:AireKO|B6.129-Aire Hivep2/AnuApb||Recessive|autoimmune regulator (autoimmune polyendocrinopathy candidiasis ectodermal dystrophy)|Aire|Nil||MGI:1338803|autoimmune regulator (autoimmune polyendocrinopathy candidiasis ectodermal dystrophy); targeted mutation 1, Leena Peltonen|Aire|MGI:2182940|10|||||||||||||||||||||||||||||Unknown|Unknown|B10.BR|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|06-Apr-2018|Cryopreserved sperm|24.0|0.0|Unknown||T cell|Yes| 8463.0|ASD598:Albiol:AireKO|B6.129-Aire Hivep2/AnuApb||Recessive|human immunodeficiency virus type I enhancer binding protein 2|Hivep2||Gm20114, MIBP1, Schnurri-2, Shn-2|MGI:1338076|Hivep2, endonuclease-mediated mutation 1, Australian National University|Hivep2||10||||||||||Unknown to Unknown|||||||||||||||||||Unknown|Unknown|B10.BR|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|06-Apr-2018|Cryopreserved sperm|||Unknown||T cell|Yes| 4436.0||C57BL/6-Tg(PDHA2-eGFP-MAP2cN)||Recessive||||||||||||||||||||||||||Enhanced green fluorescent protein (GFP) fused to microtubule-associated protein 2 (human) (EGFP-MAP2cN)|pyruvate dehydrogenase E1 alpha 2 (PDHA2)|||||||||||Appears to be infertile|||Yes|Yes|Yes|No|No|No|No|Poor||||No|17-Feb-2009|Cryopreserved sperm|18.0|0.0|Unknown||infertility, testis|Yes| 4448.0|APN16|B6;129-Dusp4/MIMR||Recessive|Dual specificity phosphatase 4|Dusp4|Unknown|MKP2|MGI:2442191|dual specificity phosphatase 4; gene trap XG164, BayGenomics|Dusp4|MGI:4127030|8||||||||||||||||Yes|||||||||||||Unknown|Normal|C57BL/6|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown|1|0||No|20-Feb-2009|Cryopreserved sperm|70.0|0.0|Unknown||somite, clock, signal transduction, ES cell genetrap, APN|Yes| 4490.0|EphA1 conditional transgenic|B6.129-Tg(Ubc-Epha1)1Sld||Dominant||||||||||||||||||||||||||Eph receptor A1|Ubiquitin C|2.5x wildtype in tissue tested by QPCR||||||||||||C57BL/6 x 129|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|||hemizygote x wildtype|No|24-Feb-2009|Cryopreserved sperm|100.0|0.0|Unknown||receptor tyrosine kinase, migration, adhesion, embryonic|Yes| 4604.0|mIMPα2delta|C57BL/6-Tg(EGFP-Kpna2 dominant negative) ||Dominant|karyopherin (importin) alpha 2|Kpna2|Unknown|Importin alpha, m-importin, m-importin-alpha-P1, pendulin, Rch1|MGI:103561||||11||||||||||||||||Yes|EGFP fused to dominant negative Kpna2|Protamine 1|||||||||||Fertility maybe affected||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|13-Mar-2009|Cryopreserved sperm|30.0|0.0|Unknown||importin, testis, protamine 1, fertility, nuclear transport|No| 4733.0||B6;B10Br;129-Cblb Tg(MLsHEL)Ccg ||Recessive|Casitas B-lineage lymphoma b|Cblb|Nil|Cbl-b|MGI:2146430|targeted mutation 1, Josef M Penninger|Cblb|MGI:2180570|16||||||||||||||||Yes|soluble Hen Egg Lysozyme (HEL)|H-2K|high||||||||||Defect in T cell signalling||C57BL/6 x C57BL/10.Br x 129|Yes|Yes|Yes|Yes|Yes|Yes|No|Poor|1|2||No|19-Apr-2009|Cryopreserved sperm|30.0|0.0|No||T cell, Hen Egg Lysozyme, signal transduction|Yes| 8382.0|Ighg1-cre Igk KO|B6.129P2(Cg)-Ighg1 Igk/UbAnu||Recessive|immunoglobulin kappa chain complex|Igk|Nil|kappa|MGI:96494|immunoglobulin kappa chain complex; targeted mutation 1, Dennis Huszar|Igk|MGI:2429510|6|||||||||||||||||||||||||||||Unknown||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|12-Dec-2017|Cryopreserved sperm|11.0|0.0|Unknown||B cell, Germinal Centre, Immunoglobulin|Yes| 8382.0|Ighg1-cre Igk KO|B6.129P2(Cg)-Ighg1 Igk/UbAnu||Recessive|immunoglobulin heavy constant gamma 1 (G1m marker)|Ighg1||IgG1, Igh-4|MGI:96446|immunoglobulin heavy constant gamma 1 (G1m marker); targeted mutation 1, University of Cologne|Ighg1|MGI:3652526|12|||||||||||||||||||||||||||||Unknown||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|12-Dec-2017|Cryopreserved sperm|||Unknown||B cell, Germinal Centre, Immunoglobulin|Yes| 8356.0|ASD666:Ramos:TtoC|C57BL/6NCrlAnu-Tlr7/AnuApb||X-linked|toll-like receptor 7|Tlr7|||MGI:2176882|Tlr7, endonuclease-mediated mutation 2, Australian National University|Tlr7/Anu||X||||||||||Unknown to Unknown|||||||||||||||||||Unknown||C57BL/6NCrlAnu|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|27-Nov-2017|Cryopreserved sperm|33.0|108.0|Unknown|||Yes| 8552.0|Fut7 KO (line 1) |C57BL/6-Fut7/Apb||Recessive|fucosyltransferase 7|Fut7|Unknown|FTVII, Fuc-TVII, FucT-VII|MGI:107692||||2|||||||||||||||||||||||||||||Unknown. These mice have a defect in immune cell migration, which may make them more susceptible to infections. Regular monitoring is important to establish phenotype of these CRISPR mice. |Unknown. These mice have a defect in immune cell migration, which may make them more susceptible to infections. Regular monitoring is important to establish phenotype of these CRISPR mice. |C57BL/6|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|28-Aug-2018|Cryopreserved sperm|20.0|0.0|Unknown|||Yes| 4438.0|APN14|B6.129-Kdm1a/MIMR||Recessive|lysine (K)-specific demethylase 1A|Kdm1a|Unknown|Aof2, Kdm1, LSD1, mKIAA0601|MGI:1196256|lysine (K)-specific demethylase 1A; gene trap XP0207, Wellcome Trust Sanger Institute|Kdm1a|MGI:3858605|4||||||||||||||||No|||||||||||||Unknown for genetrap. Germline deletion of Aof2 causes early embryonic lethality (E7.5) probably due to defects in pituitary development and hormone production.||C57BL/6|No|No|Yes|No|No|Yes|No|Unknown|1|||No|17-Feb-2009|Cryopreserved sperm|40.0|0.0|Unknown||ES cell genetrap, APN, pituitary, embryonic lethal|Yes| 4952.0|APN 15|B6.129-Slc2a3/MIMR||Recessive|solute carrier family 2 (facilitated glucose transporter), member 3|Slc2a3|Reduced|Glut-3, Glut3|MGI:95757|solute carrier family 2 (facilitated glucose transporter), member 3; gene trap XG611, BayGenomics|Slc2a3|MGI:3822325|6||||||||||||||||||||||||||||||Nervous system phenotype:* no paroxysmal EEG activity* no epileptic seizuresAbnormal brain wave pattern: absolute EEG power densities show a slight but significant elevation.Decreased prepulse inhibition:* significant reduction in inhibition by a low intensity prepulse* inhibition due to a high intensity prepulse is normalBehavior/neurological phenotype:* performance normal in rotarod, open field, and shuttle box tests.* normal performance in a Morris water maze.* generally normal responses in anxiety related tests although some trends are noted.Increased anxiety-related response:* preference for closed compartment in elevated maze.* increased tendency to stay in illuminated areas in light/dark avoidance tests.Increased startle reflex: increased startle response.|C57BL/6 x 129|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|14-Dec-2009|Cryopreserved sperm|81.0|0.0|Unknown||GLUT3, behaviour, anxiety|No| 4974.0|C151 CD9 DKO|C57BL/6-CD151 CD9||Recessive|Cd151 antigen|Cd151|Nil|PETA-3, SFA-1, Tspan24|MGI:1096360|targeted mutation 1, Leonie K Ashman|Cd151|MGI:3050539|7||||||||||||||||Yes|||||||||||||||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|22-Jan-2010|Cryopreserved sperm|60.0|0.0|Unknown||epithelium, integrin, fibroblast, wound, migration|Yes| 4974.0|C151 CD9 DKO|C57BL/6-CD151 CD9||Recessive|CD19 antigen|Cd9|Nil|Tspan29|MGI:88348|targeted mutation 1, Claude Boucheix|Cd9|MGI:2180795|6||||||||||Unknown to Unknown|||||||||||||||||||||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|22-Jan-2010|Cryopreserved sperm|||Unknown||epithelium, integrin, fibroblast, wound, migration|Yes| 8528.0|17NF|B6.Cg-Tg(Cyp17a1-NGF)2456Oje/AnuApb||Dominant||||||||||||||||||||||||||transgene insertion 2456, Sergio R Ojeda|17alpha-hydroxylase promoter|thecal-interstitial cells||||||||||Polycystic ovary disease|||Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|29-Jun-2018|Cryopreserved sperm|44.0|0.0|Yes|polycystic ovarian syndrome (PCOS)|ovarian nerve growth factor (NGF), ovulation|Yes| 4905.0|Stiliom; ENU4AT:032|C57BL/6JSfdAnu-Tomm40/AnuApb||Semi-dominant|translocase of outer mitochondrial membrane 40 homolog (yeast)|Tomm40|Nil|Tom40|MGI:1858259|Stiliom|Stil||7|ENSMUSG00000002984|ENSMUST00000093552|Tomm40-202|977|1048|C to T|ENSMUSE00000582554|10|326|Alanine to Valine|||||CTCTGTGAACAGTAACTGGATCGTGGGCGCCACGCTGGAGAAGAAGCTTCCGCCCTTGCCC|Yes|||||||||||||Lethal lung haemorrhage at 4 – 6 weeks, blood vessel fragility may be caused by suspected transdifferentiation of smooth muscle cells into skeletal muscle (a physiological process in the oesophagus) occurring throughout the body.TOM complex is absent in Blue-native PAGE analysis|Blue-native PAGE shows reduced levels of TOM complex in mitochondria in HETs; Monomeric Tomm40 is detected, but the mutant version of the protein migrates faster on SDS-PAGE than the wild-type protein (data from Diana Stojanovski and Mike Ryan at Latrobe.|C57BL/6SfdAnu x B10.BR x CBA|Yes|No|Yes|Yes|No|Yes|No|Unknown||||No|09-Oct-2009|Cryopreserved sperm|32.0|0.0|Unknown||lung, haemorrhage, smooth muscle, mitochondrial myopathy, skeletal muscle, differentiation, blood vessel, transdifferentiation, JDRF, ENU|Yes| 5045.0|APN27|B6;129P2/OlaHsd-Rbm5/MAS||Recessive|RNA binding motif protein 5|Rbm5|Unknown||MGI:1933204|RNA binding motif protein 5; gene trap PST20293, Mammalian Functional Genomics Centre|Rbm5|MGI:3902497|9||||||||||||||||No|||||||||||||Unknown|Unknown|C57BL/6 x 129P2/OlaHsd|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Good||||No|25-Feb-2010|Cryopreserved sperm|54.0|0.0|Unknown||RNA, ES cell|Yes| 5047.0|NOD.pIgR-/- R2 N13|NOD.B6(pIgR-D1Mit348)N13-Pigr||Recessive|polymeric immunoglobulin receptor|Pigr|Unknown||MGI:103080|polymeric immunoglobulin receptor; targeted mutation 1, Richard A Strugnell|Pigrtm1|MGI:2651659|1||||||||||||||||No|||||||||||||Like B6.pIgR-/- mice (described in Uren et al., 2003), this mouse strain does not produce functional pIgR, and therefore lacks IgA in secretions and has increased levels of IgA in serum. The incidence of diabetes in female mice is about 40% after 43-weeks, which is significantly lower than the incidence of diabetes in NOD/Lt mice in host facility (~60% at 43-weeks of age).|Like B6.pIgR+/- mice, heterozygotes of this mouse strain produce functional pIgR, and have normal levels of IgA in secretions, however the levels of IgA in serum are intermediate between NOD/Lt and NOD.pIgR-/-. The incidence of diabetes has not been tested in heterozygotes of this mouse strain.|NOD/Lt|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|13|8|Hom x Hom|No|26-Feb-2010|Cryopreserved sperm|45.0|0.0|Yes|Type 1 Diabetes|IgA, IgM, Idd5.4, B cell|Yes| 5048.0|NOD.pIgR-/- R0 N10|NOD.B6(D1Mit48-D1Mit348)N10-Pigr||Recessive|polymeric immunoglobulin receptor|Pigr|Unknown||MGI:103080|||MGI:2651659|1||||||||||||||||No|||||||||||||Like B6.pIgR-/- mice (described in Uren et al., 2003), this mouse strain does not produce functional pIgR, and therefore lacks IgA in secretions and has increased levels of IgA in serum. The incidence of diabetes in female mice is 75-85% after 43-weeks, which is significantly higher than the incidence of diabetes in female NOD/Lt mice in our facility (50-60% at 43-weeks of age). The incidence of diabetes in male mice is 25-50% after 43 weeks of age, which is significantly higher than the incidence of diabetes in male NOD/Lt mice in our facility (5-10% at 43-weeks of age).|Like B6.pIgR+/- mice, heterozygotes of this mouse strain produce functional pIgR, and have normal levels of IgA in secretions, however the levels of IgA in serum are intermediate between NOD/Lt and NOD.pIgR-/-. The incidence of diabetes in heterozygous females is 70%, and heterozygous males is 30%. |NOD/Lt|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|10|8|Hom x Hom|No|26-Feb-2010|Cryopreserved sperm|45.0|0.0|Yes|Type 1 Diabetes|IgA, IgM, Idd5.4, B cell|Yes| 5049.0|NOD.pIgR-/- R1 N10|NOD.B6(D1Mit495-D1Mit348)N10-Pigr||Recessive|polymeric immunoglobulin receptor|Pigr|Unknown||MGI:103080|||MGI:2651659|1||||||||||||||||No|||||||||||||Like B6.pIgR-/- mice (described in Uren et al., 2003), this mouse strain does not produce functional pIgR, and therefore lacks IgA in secretions and has increased levels of IgA in serum. The incidence of diabetes in female mice is 60-65% after 43-weeks, which is consistently, but not significantly higher than the incidence of diabetes in NOD/Lt mice in host facility (50-60% at 43-weeks of age). The incidence of diabetes in mice of this strain is not significantly different from NOD/Lt males in our facility.|Like B6.pIgR+/- mice, heterozygotes of this mouse strain produce functional pIgR, and have normal levels of IgA in secretions, however the levels of IgA in serum are intermediate between NOD/Lt and NOD.pIgR-/-. The incidence of diabetes of heterozygote females is 63% at 40-weeks of age.|NOD/Lt|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|10|8|Hom x Hom|No|26-Feb-2010|Cryopreserved sperm|45.0|0.0|Yes|Type 1 Diabetes|IgA, IgM, Idd5.4, B cell|Yes| 5050.0|NOD.pIgR-/- R1 N14|NOD.B6(D1Mit495-D1Mit348)N14-Pigr||Recessive|polymeric immunoglobulin receptor|Pigr|Unknown||MGI:103080|||MGI:2651659|1||||||||||||||||No|||||||||||||Like B6.pIgR-/- mice (described in Uren et al., 2003), this mouse strain does not produce functional pIgR, and therefore lacks IgA in secretions and has increased levels of IgA in serum. The incidence of diabetes has not been tested for this strain but it is expected that it would be the same as the NOD.pIgR-/- R1 N10 strain (female mice is 60-65% after 43-weeks, the incidence of diabetes in NOD/Lt mice in host facility is 50-60% at 43-weeks of age). |Like B6.pIgR+/- mice, heterozygotes of this mouse strain produce functional pIgR, and have normal levels of IgA in secretions, however the levels of IgA in serum are intermediate between NOD/Lt and NOD.pIgR-/-. |NOD/Lt|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|14|8|Hom x Hom|No|26-Feb-2010|Cryopreserved sperm|45.0|0.0|Yes|Type 1 Diabetes|IgA, IgM, Idd5.4, B cell|Yes| 5054.0|NOD.B6 R11 N12|NOD.B6(D1Mit495-D1Mit286)N12||Recessive||||||||||||||||||||||||||||||||||||||The incidence of diabetes has not been tested in this mouse strain as yet but may prove useful in the dissection of the Idd5.4 susceptibility locus.|The incidence of diabetes has not been tested in heterozygotes of this mouse strain.|NOD/Lt|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|12|8|Hom x Hom|No|26-Feb-2010|Cryopreserved sperm|45.0|0.0|Yes|Type 1 Diabetes|IgA, IgM, Idd5.4, B cell|Yes| 5079.0|Fzd5|C57BL/6-Fzd5||Recessive|frizzled homolog 5 (Drosophila)|Fzd5|Normal|Fz5|MGI:108571|frizzled homolog 5 (Drosophila); targeted mutation 1, Hans Clevers|Fzd5|MGI:3583769|1||||||||||||||||Yes|||||||||||||Normal|Normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|20||Maintained as heterozygous by crossing to C57BL/6|No|25-Mar-2010|Cryopreserved sperm|50.0|0.0|Unknown||Wnt pathway, Cre recombinase|Yes| 8417.0|Egr2-GFP|B6.Cg-Egr2/Anu||Recessive|early growth response 2|Egr2||Egr-2, Krox20, Krox-20, NGF1-B, Zfp-25|MGI:95296||||10||||||||||||||||||||||||||||||||Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|16-Jan-2018|Cryopreserved sperm|55.0|0.0|Unknown|||Yes| 9462.0|Adidias, D865G|C57Bl/6N-Nfkb2/Apb||Semi-dominant|nuclear factor of kappa light polypeptide gene enhancer in B cells 2, p49/p100|Nfkb2|||MGI:1099800||||19|||||||||||||||||||||||||||||Unknown|Unknown|C57Bl/6N|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|05-Dec-2022||0.0|0.0|Unknown|||Possibly| 5051.0|NOD.pIgR-/- R2 N15|NOD.B6(pIgR-D1Mit348)N15-Pigr||Recessive|polymeric immunoglobulin receptor|Pigr|Unknown||MGI:103080|||MGI:2651659|1||||||||||||||||No|||||||||||||Like B6.pIgR-/- mice (described in Uren et al., 2003), this mouse strain does not produce functional pIgR, and therefore lacks IgA in secretions and has increased levels of IgA in serum. The incidence of diabetes in female mice is about 40% after 43-weeks, which is significantly lower than the incidence of diabetes in NOD/Lt mice in our facility (~60% at 43-weeks of age).|Like B6.pIgR+/- mice, heterozygotes of this mouse strain produce functional pIgR, and have normal levels of IgA in secretions, however the levels of IgA in serum are intermediate between NOD/Lt and NOD.pIgR-/-. The incidence of diabetes has not been tested in heterozygotes of this mouse strain.|NOD/Lt|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|15|8|Hom x Hom|No|26-Feb-2010|Cryopreserved sperm|45.0|0.0|Yes|Type 1 Diabetes|IgA, IgM, Idd5.4, B cell|Yes| 5064.0|Zic5 K363R:C3H/HeH|C3H/HeH-Zic5||Recessive|Zinc finger protein of the cerebellum 5|Zic5|Unknown|odd-paired related, Opr|MGI:1929518||||14||||||||||||||||Yes|||||||||||||Viable and fertile|Viable and fertile|C3H/HeH|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|10||Homozygote male paired with homozygote female|No|25-Mar-2010|Cryopreserved sperm|30.0|0.0|Unknown||zinc finger, ENU|Yes| 5114.0|ENU7B6:039 (CD8)|C57BL/6JSfdAnu-Senp2/AnuApb|C57BL/6JSfdAnu-Senp2/AnuApb|Recessive|SUMO/sentrin specific peptidase 2|Senp2|Unknown||MGI:1923076|SUMO/sentrin specific peptidase 2; mutation 1, The Australian National University|Senp2|MGI:5563407|16|ENSMUSG00000022855|ENSMUST00000023561| Senp2-201|939|1097|A to G|ENSMUSE00000131327|11|313|Glycine to Glycine|||||CTCCGATTTGAAAAGGAAGGTACAAGAGGACACCAAATGGAGCCTGATCTGTCAGAAGAAG|Yes|||||||||||||Subclinical autoimmune susceptibility. Antinuclear autoantibodies: homogeneous nuclear.Low CD8 protein expression and reduced T cell numbers.||C57BL/6JSfdAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|11-May-2010|Cryopreserved sperm|60.0|0.0|Unknown||autoimmunity, antinuclear antibodies (ANA), ENU, Wellcome Trust, T cell, CD8|Yes| 5097.0|Hic1lox|C57BL/6-Hic1/MarpApb||Dominant|Hypermethylated in Cancer-1|Hic1|Normal||1338010|Hic1lox|Hic1||11|||||||||||||||||||||||||||||Normal|Normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|3||homozygote to homozygote|No|27-Apr-2010|Cryopreserved sperm|43.0|0.0|Unknown||Hic1, epigenetics, development, cancer|Possibly| 5105.0|APN23, RRR232|B6;129-Tbc1d15/Marp||Recessive|TBC1 domain family, member 15|Tbc1d15|Unknown|Ly6dl|MGI:1913937|TBC1 domain family, member 15; gene trap RRR232, BayGenomics|Tbc1d15|MGI:4397430|10||||||||||||||||No|||||||||||||Unknown|Unknown|C57BL/6|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|30-Apr-2010|Cryopreserved sperm|50.0|0.0|Unknown||Genetrap, ES cell|Yes| 5198.0|tghFS315(mFS WT)|Transgenic Human Follistatin 315 on mouse wildtype follistatin background||Dominant||||||||||||||||||||||||||Human follistatin-315 splice variant|endogenous human promoter|unknown||||||||||Unknown|Hemizygous: normal Note: An abnormal phenotype is not observed until these mice are bred onto a mouse follistatin knockout background|129 x C57BL/6J|Yes|Yes|Yes|Yes|Yes|Yes|No|Excellent||||No|04-Aug-2010|Cryopreserved sperm|50.0|0.0|No||FST315, FST288, angiogenesis, ovary|Possibly| 5220.0|Lyn|C57BL/6-Lyn||Semi-dominant|Yamaguchi sarcoma viral (v-yes-1) oncogene homolog|Lyn|Normal|Hck-2|MGI:96892|Yamaguchi sarcoma viral (v-yes-1) oncogene homolog; targeted mutation 2, Margaret Hibbs|Lyn||4||||||||||||||||Yes|||||||||||||The mice carry a mutation in the ATP-binding site of Lyn kinase (K275M) which renders the kinase catalytically inactive. Lyn mice have reduced numbers of recirculating B cells, their B cells have an activated phenotype and they are hyper-responsive to B cell antigen receptor cross-linking. Lyn mice develop titres of circulating autoantibodies with age but they are reduced compared to age-matched Lyn<-/-> mice. The findings to date demonstrate considerable phenotypic similarity between this Lyn kinase-dead strain and Lyn<-/-> mice. |Similar to homozygous state but with reduced severity.|C67BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|16-Sep-2010|Cryopreserved sperm|100.0|0.0|Unknown||signal transduction, phosphatase, tyrosine, myeloid, neutrophil, B cell, src family, lymphocyte|Yes| 5224.0|BALB.Lyn up/up STAT6 knockout mice; BALB.Lyn-Y508FSTAT6 -/-|BALB/c-Lyn Stat6/Apb||Recessive|Yamaguchi sarcoma viral (v-yes-1) oncogene homolog|Lyn|Reduced|Hck-2|MGI:96892|Yamaguchi sarcoma viral (v-yes-1) oncogene homolog; targeted mutation 1, Margaret Hibbs|Lyn|MGI:2157016|4|||||||||||||||||||||||||||||Not well defined|Not defined|BALB/c|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|01-Oct-2010|Cryopreserved sperm|50.0|0.0|Unknown||src family, signal transduction, inflammation, lung, tyrosine kinase, phosphorylation|Yes| 5224.0|BALB.Lyn up/up STAT6 knockout mice; BALB.Lyn-Y508FSTAT6 -/-|BALB/c-Lyn Stat6/Apb||Recessive|signal transducer and activator of transcription 6|Stat6|Nil||MGI:103034|signal transducer and activator of transcription 6; targeted mutation 1, Shizuo Akira|Stat6|MGI:2386746|10||||||||||||||||No|||||||||||||Not well defined|Not defined|BALB/c|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|01-Oct-2010|Cryopreserved sperm|||Unknown||src family, signal transduction, inflammation, lung, tyrosine kinase, phosphorylation|Yes| 5314.0|BALB.Lyn up/up |BALB/c-Lyn/Apb||Semi-dominant|Yamaguchi sarcoma viral (v-yes-1) oncogene homolog|Lyn|Reduced|Lyn, Lyn|MGI:96892|Yamaguchi sarcoma viral (v-yes-1) oncogene homolog; targeted mutation 1, Margaret Hibbs|Lyn|MGI:2157016|4||||||||||||||||Yes|||||||||||||The mice carry a gene-targeted gain-of-function mutation in the Lyn tyrosine kinase (Y508F). The mice display a severe diminution of mature B cells but have increased numbers of B1a B cells. Their B cells display marked down-regulation of surface IgM, Ig-beta, CD19, CD21 and CD22, and they are poorly responsive to B cell receptor cross-linking. Unlike mixed genetic background Lyn mice, BALB/c background mice are not autoimmune-prone. Due to the dominant nature of the gain-of-function Lyn mutation, Lyn-expressing cells from Lyn mice show hyper-phosphorylation of many signaling proteins.On the BALB/c genetic background, the mice develop a severe inflammatory lung disease that resembles bullous emphysema. The disease is obvious in 12 wk old mice.|Lyn<+/up> mice show a reduction in numbers of B cells and Lyn-expressing cells show hyper-phosphorylation of many signaling proteins.|Balb/c|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|10|||No|09-Nov-2010|Cryopreserved sperm|50.0|0.0|Unknown||kinase, phosphorylation, signal transduction, ITIM, tyrosine|Yes| 5317.0|Kamu ; ENU14WT:020|C57BL/6JAnu-Pde2a/AnuApb|C57BL/6JAnu-Pde2a/AnuApb|Recessive|phosphodiesterase 2A, cGMP-stimulated|Pde2a|||MGI:2446107|phosphodiesterase 2A, cGMP-stimulated; mutation 1, The Australian National University|Pde2a|MGI:5563440|7|ENSMUSG00000030653|ENSMUST00000084894|Pde2a-202|2198|2425|T to C|ENSMUSE00000633282|26|733|Leucine to Proline|||||GCACCACTTTGCTCAAGCCATTGCTATCCTCAACACCCACGGCTGCAATATCTTTGACCAC|Yes|||||||||||||Pale embryos at E14.5 with hematopoetic development defect manifesting in a tiny/absent fetal liver and increase in primitive red blood cells|Unknown|C57BL/6JAnu|No|No|Yes|No|No|Yes|No|Good||||No|12-Nov-2010|Cryopreserved sperm|10.0|0.0|Unknown||ENU, haemopoiesis, stem cell|Yes| 5496.0|A33:Lgp130YFKQ ; TgNA33L-gp130YFKQ (line 10) (ME-216)|CB;129-Tg(Gpa33-Il6st*)10Ern/Lud||Dominant||||||||||||||||||||||||||transgene insertion 10, Matthias Ernst|glycoprotein A33 (transmembrane)|||||||||||Unknown|Unknown|CBA x 129|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|02-May-2011|Cryopreserved sperm|50.0|0.0|Unknown||stat, epithelium, colon|Yes| 5333.0|ENU16FOX:020 B6.129-Tg(FoxP3-GFP)|B6.129-Zap70 Foxp3/AnuApb||Recessive|zeta-chain (TCR) associated protein kinase|Zap70||Srk, TZK, ZAP-70|MGI:99613||||1|ENSMUSG00000026117|ENSMUST00000027291|Zap70‐201|728|830|C to T|ENSMUSE00000155943|5|243|Alanine to Valine|||||GCAGCTGGTGGAGTACCTGAAGCTGAAGGCGGATGGACTAATTTACCGCTTGAAGGAGGTC|Unknown|||||||||||||Elevated regulatory T cell population. Phenotype detected by peripheral blood FACS.Cells from the Foxp3-gfp background strain that express FoxP3 fluoresce green, predominantly T cells|Normal |129 x C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|||Affected x affected|Yes|26-Nov-2010|Cryopreserved sperm|45.0|0.0|Unknown||regulatory T cells, immunology|Possibly| 5333.0|ENU16FOX:020 B6.129-Tg(FoxP3-GFP)|B6.129-Zap70 Foxp3/AnuApb||Recessive|forkhead box P3|Foxp3|Normal|JM2, scurfin|MGI:1891436|forkhead box P3; targeted mutation 2, Alexander Y Rudensky|Foxp3|MGI:3574964|X|||||||||||||||||||||||||||||Elevated regulatory T cell population. Phenotype detected by peripheral blood FACS.Cells from the Foxp3-gfp background strain that express FoxP3 fluoresce green, predominantly T cells|Normal |129 x C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|||Affected x affected|Yes|26-Nov-2010|Cryopreserved sperm|||Unknown||regulatory T cells, immunology|Possibly| 5389.0|Ndufs6gt/+|B6.129P2-Ndufs6/Mrch|B6.129P2-Ndufs6/Mrch|Recessive|NADH dehydrogenase (ubiquinone) Fe-S protein 6|Ndufs6|Reduced|IP13|MGI:107932|NADH dehydrogenase (ubiquinone) Fe-S protein 6; gene trap AR0138, Wellcome Trust Sanger Institute|Ndufs6|MGI:4346527|13||||||||||||||||Yes|||||||||||||Ndufs6gt/gt mice are fertile. For the first 4 months of life, Ndufs6gt/gt mice have no overt phenotype, with normal weight gain and survival. After 4 months of age, Ndufs6gt/gt mice develop cardiac hypertrophy, which can lead to sudden weight loss, lethargy and death. Ndufs6gt/gt males are more severely affected than females. |Normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|11|3|heterogygote X heterozygote|No|18-Jan-2011||0.0|0.0|Yes|Mutations in human gene, NDUFS6, encoding one of the 45 subunits of Complex I, are one cause of Complex I deficiency. NDUFS6-/- patients suffer from seizures, hypotonia and abnormal eye movements and die in the first month of life. Currently, no effective treatment is available. |Mitochondria, Cardiac , Complex I, Oxidative phosphorylation, ES cell|Possibly| 5470.0|APN 82|C57BL/6N-Gkn2/Marp||Recessive|gastrokine 2|Gkn2|Unknown||MGI:1913534|gastrokine 2; targeted mutation 1, Velocigene|Gkn2|MGI:4399717|6||||||||||||||||Yes|||||||||||||Unknown - Not bred to homozygocity |Normal |C57BL/6N|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|25-Mar-2011|Cryopreserved sperm|50.0|0.0|Unknown||ES cell|Yes| 5472.0|APN 87 ; Golga4|B6;129/Ola-Golga4/Marp||Recessive|golgi autoantigen, golgin subfamily a, 4|Golga4|Nil|golgin-245, Olp-1 |MGI:1859646 |golgi autoantigen, golgin subfamily a, 4; gene trap XG298, BayGenomics|Golga4|MGI:4125759|9||||||||||||||||Yes|||||||||||||Not bred to homozygocity|Normal|C57BL/6N|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|25-Mar-2011|Cryopreserved sperm|50.0|0.0|Unknown||Gene trap, ES cell|Yes| 5475.0|ENU1WT:049|C57BL/6JAnu-Knyn/Anu||Recessive|||Unknown|||kanyon|knyn|MGI:5510719|7||||||||||||||||Yes|||||||||||||Skeletal defect, exencephaly at embryonic day 13.5.Facial clefts.|Normal|C57BL/6JAnu|No|No|Yes|No|No|Yes|Yes|Unknown|||het x het|No|06-Apr-2011|Cryopreserved sperm|50.0|0.0|Yes|frontonasal dysplasias (OMIM 136760)|exencephaly, skeletal, bone, development, embryonic, ENU|Possibly| 5486.0|ENU20FLT3-ITD:G1(#37)|ENU20FLT3-ITD:G1||Dominant|FMS-like tyrosine kinase 3|Flt3|Increased|CD135, Flk-2, Flk2, Flt-3|MGI:95559|FMS-like tyrosine kinase 3; targeted mutation 1, D Gilliland|Flt3|MGI:3763385|5||||||||||||||||Yes|||||||||||||Accelerated onset of Acute Myeloid leukaemia.|Accelerated onset of Acute Myeloid leukaemia.|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Poor||G1||No|19-Apr-2011|Cryopreserved sperm|10.0|0.0|Yes|Myelomonocytic Leukaemia|AML, myeloid, lymphocyte, CML, ENU|Possibly| 5486.0|ENU20FLT3-ITD:G1(#37)|ENU20FLT3-ITD:G1||Dominant|Unknown||Unknown||||||Unknown|||||||||||||||||||||||||||||Accelerated onset of Acute Myeloid leukaemia.|Accelerated onset of Acute Myeloid leukaemia.|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Poor||G1||No|19-Apr-2011|Cryopreserved sperm|||Yes|Myelomonocytic Leukaemia|AML, myeloid, lymphocyte, CML, ENU|Possibly| 5485.0|ENU18FLT3-ITD:G2 #58|ENU18FLT3-ITD:G2||Dominant|FMS-like tyrosine kinase 3|Flt3|Increased|CD135, Flk-2, Flk2, Flt-3|MGI:95559|FMS-like tyrosine kinase 3; targeted mutation 1, D Gilliland|Flt3|MGI:3763385|5||||||||||||||||Yes|||||||||||||Accelerated onset of Acute Myeloid leukaemia.|Accelerated onset of Acute Myeloid leukaemia.|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Poor||G2||No|19-Apr-2011|Cryopreserved sperm|20.0|0.0|Yes|Myelomonocytic Leukaemia|AML, myeloid, lymphocyte, CML, ENU|Possibly| 5485.0|ENU18FLT3-ITD:G2 #58|ENU18FLT3-ITD:G2||Dominant|Unknown||Unknown||||||Unknown|||||||||||||||||||||||||||||Accelerated onset of Acute Myeloid leukaemia.|Accelerated onset of Acute Myeloid leukaemia.|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Poor||G2||No|19-Apr-2011|Cryopreserved sperm|||Yes|Myelomonocytic Leukaemia|AML, myeloid, lymphocyte, CML, ENU|Possibly| 4085.0||ENU7PMH:139, Metabolic Lean 3||Recessive|||||||||Unknown||||||||||||||||Yes|||||||||||||Low percentage of body fat when fed on a high fat diet.||C57BL/6 x C57BL/10|Yes|Yes|Yes|Yes|Yes|Yes|No|Poor||3||No|04-Dec-2008|Cryopreserved sperm|40.0|0.0|No||ENU, Obesity, Diet, Fat, Adipose|No| 4087.0||ENU8PH:139, Metabolic Obese 1||Recessive|||||||||Unknown||||||||||||||||Yes|||||||||||||High percentage of body fat on a low fat diet||C57BL/6 x C57BL/10|Yes|Yes|Yes|Yes|Yes|Yes|No|Poor||3||No|04-Dec-2008|Cryopreserved sperm|30.0|0.0|Unknown||ENU, Obesity, Diet, Fat, Adipose|Possibly| 4772.0|4AT31|ENU4AT:031||Recessive||||||||||||||||||||||||||transgene insertion 3, Christopher C Goodnow|Rat insulin promoter|||||||||||Heightened susceptibility to autoimmune diabetes on the transgenically sensitized TCR x insHEL background (see figure). Phenotype Screen: Urine glucose|Normal|C57BL/6 x B10BR x CBA|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|06-Sep-2009|Cryopreserved sperm|50.0|0.0|Yes|Type I Diabetes|ENU, JDRF, T cell, autoimmunity|Possibly| 4772.0|4AT31|ENU4AT:031||Recessive||||||||||||||||||||||||||transgene insertion 1, Mark M Davis||||||||||||Heightened susceptibility to autoimmune diabetes on the transgenically sensitized TCR x insHEL background (see figure). Phenotype Screen: Urine glucose|Normal|C57BL/6 x B10BR x CBA|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|06-Sep-2009|Cryopreserved sperm|||Yes|Type I Diabetes|ENU, JDRF, T cell, autoimmunity|Possibly| 5442.0|81.BR ; (ADAR2—/—/AGluR-B)|B6;129-Adarb1 Gria2||Recessive|adenosine deaminase, RNA-specific, B1|Adarb1|Reduced|ADAR2, D10Bwg0447e, RED1|MGI:891999|adenosine deaminase, RNA-specific, B1; targeted mutation 1, Peter H Seeburg|Adarb1|MGI:2178079|10||||||||||||||||No|||||||||||||No abnormal phenotype detected: double homozygous null mice appear normal at all ages, as judged by food intake, weight increase, postnatal development, breeding and general behavior (full rescue)|Adarb1/Adarb1Gria2/Gria2<+>Postnatal lethality: compound mutant mice survive up to P35 (partial rescue; extended postnatal survival).|C57BL/6|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown|Unknown|||No|17-Feb-2011|Cryopreserved sperm|49.0|0.0|Unknown||AMPA receptor, ion channel, motor neuron, RNA, deamination|Yes| 5442.0|81.BR ; (ADAR2—/—/AGluR-B)|B6;129-Adarb1 Gria2||Recessive|glutamate receptor, ionotropic, AMPA2 (alpha 2)|Gria2||Glur-2, GluR-B, GluR2, Glur2|MGI:95809|glutamate receptor, ionotropic, AMPA2 (alpha 2); targeted mutation 1.1, Peter H Seeburg|Gria2|MGI:2178125|3||||||||||||||||Yes|||||||||||||No abnormal phenotype detected: double homozygous null mice appear normal at all ages, as judged by food intake, weight increase, postnatal development, breeding and general behavior (full rescue)|Adarb1/Adarb1Gria2/Gria2<+>Postnatal lethality: compound mutant mice survive up to P35 (partial rescue; extended postnatal survival).|C57BL/6|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown|Unknown|||No|17-Feb-2011|Cryopreserved sperm|||Unknown||AMPA receptor, ion channel, motor neuron, RNA, deamination|Yes| 5542.0|Wonggan (Wong); ENU14nih 002|ENU14NIH:002||Recessive|Unknown|Unknown|||||||Unknown|||||||||||||||||||||||||||||Embryos @14.5 appear smaller than normal, have increased KLS cell in fetal liver, increased primitive RBCs and decreased definitive RBCs.|normal|C57BL/6JAnu x C57BL/10|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Good||||No|19-Jul-2011|Cryopreserved sperm|18.0|0.0|Unknown||red blood cell|Possibly| 5546.0|ENU15China:072a|C57BL/6JAnu-Ptpn6/AnuApb|C57BL/6JAnu-Ptpn6/AnuApb|Dominant|protein tyrosine phosphatase, non-receptor type 6|Ptpn6 |Reduced|hcp, Hcph, Ptp1C, SHP-1, Spin|MGI:96055|protein tyrosine phosphatase, non-receptor type 6; mutation 1, The Australian National University|Ptpn6|MGI:5563436|6|ENSMUSG00000004266|ENSMUST00000004377|Ptpn6-003|1385|1498|C to T|ENSMUSE00000195628|12|462|Threonine to Methionine|||||TGTGCATTGCAGCGCTGGCATCGGCCGCACGGGCACCATCATCGTCATTGATATGCTTATG||||||||||||||Homozygous mice are unhealthy at weaning and are usually euthanised.Mice that survive to 8 weeks have a reduced percent of B cells and few mature B cells. Phenotype measured by flow cytometry using antibodies against the following antigens: B220, CD3, CD4, CD44, KLRG1, NK1.1, IgM, IgD|Reduced IgM expression on mature B cells as measured by flow cytometry.Phenotype measured by flow cytometry using antibodies against the following antigens: B220, CD3, CD4, CD44, KLRG1, NK1.1, IgM, IgD|C57BL/6JAnu|Yes|No|Yes|Yes|No|Yes|No|Good|4-6|4|Affected x B6|No|01-Aug-2011|Cryopreserved sperm|58.0|0.0|Unknown||B cell, IgM|Possibly| 5566.0|ENU20Bcl2.05 VavP-BCL2-69; C57BL/6-Tg(Vav-BCL2)1Jad/Wehi|B6(Cg)-Nin Tg(Vav-BCL2)1Jad/WehiAnuApb||Dominant|ninein|Nin||3110068G20Rik, mKIAA1565|MGI:105108||||12|ENSMUSG00000021068|ENSMUST00000085314|Nin-001|1240|1240|A to G|ENSMUSE00000114325|9|414|Asparagine to Glycine|||||TGGACGATCACCACGCGGCCATTGAGCGGAGGAATGAATACAACCTCAGGAAACTGGATGA||transgene insertion 1, Jerry M Adams|mouse Vav promoter|High, haemopoietic cells||||||||||Increased numbers of Monocytes and Granulocytes in peripheral blood|Abnormal lymphocyte cell number:* the ratio of CD4 cells per B cell is 25% to 50% lower than in wild-type mice.Increased B cell number: 5-fold higher in the spleen at 18 weeksIncreased T cell number:* mice exhibit higher splenic T cell numbers than in wild-type and Tg(BCL2)22Wehi or Tg(BCL2)36Wehi mice.Increased CD4-positive T cell number:* the increase in CD4+ T cells is greater than the increase in CD8+ T cells.Increased CD8-positive T cell number:* the increase in CD4+ T cells is greater than the increase in CD8+ T cells.Abnormal class switch recombination:* the total number of B cells that undergo class switching is 50-fold higher than in wild-type mice.Abnormal somatic hypermutation frequency:* 22 of 23 clones isolated from class-switching cells harbor on average about 6 somatic mutations compared to in wild-type cells where no mutations are found.Enlarged spleen:Abnormal spleen germinal center morphology:* mice exhibit a larger pool of cycling B cells with a germinal center phenotype than in wild-type mice.* at 18 weeks, mice exhibit an increased in germinal center size and number compared to in wild-type mice.* however, expansion of germinal centers is dependent on CD4 T cell help.Increased spleen germinal center number: at 18 weeks.Increased spleen germinal center size: at 18 weeks.Enlarged lymph nodes.Glomerulonephritis:* at 40 weeks, 15% to 25% of mice develop autoimmune glomerulonephritis.Increased tumor incidence:* 12% of mice develop plasma cell tumorsLymphoma: less than 10% of mice develop lymphoblastic lymphomas.B cell derived lymphoma:* less than 10% of mice develop large cell B lymphomasFollicular lymphoma:* at 18 months, 37% to 50% of mice develop monoclonal follicular lymphoma.Thymic lymphoma: in less than 10% of miceHistiocytic sarcoma: in less than 10% of mice.|C57BL/6JAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|19-Aug-2011|Cryopreserved sperm|12.0|0.0|Unknown||B cell, bcl-2, vav, Progenitor, lymphoma, germinal centre, granulocyte|Yes| 4773.0|4AT62|ENU4AT:062||Recessive||||||||||||||||||||||||||transgene insertion 3, Christopher C Goodnow|Rat insulin promoter|||||||||||Heightened susceptibility to autoimmune diabetes on the transgenically sensitized TCR x insHEL background (see figure). Phenotype Screen: Urine glucose|Normal|C57BL/6 x B10BR x CBA|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|06-Sep-2009|Cryopreserved sperm|90.0|0.0|Yes|Type I Diabetes|ENU, JDRF, T cell, autoimmunity|Possibly| 4773.0|4AT62|ENU4AT:062||Recessive||||||||||||||||||||||||||transgene insertion 1, Mark M Davis||||||||||||Heightened susceptibility to autoimmune diabetes on the transgenically sensitized TCR x insHEL background (see figure). Phenotype Screen: Urine glucose|Normal|C57BL/6 x B10BR x CBA|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|06-Sep-2009|Cryopreserved sperm|||Yes|Type I Diabetes|ENU, JDRF, T cell, autoimmunity|Possibly| 4775.0|5AT142|ENU5AT:142||Recessive||||||||||||||||||||||||||transgene insertion 3, Christopher C Goodnow|Rat insulin promoter|||||||||||Heightened susceptibility to autoimmune diabetes on the transgenically sensitized TCR x insHEL background (see figure). Phenotype Screen: Urine glucose|Normal|C57BL/6 x B10BR x CBA|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|06-Sep-2009|Cryopreserved sperm|50.0|0.0|Yes|Type I Diabetes|ENU, JDRF, T cell, autoimmunity|Possibly| 4775.0|5AT142|ENU5AT:142||Recessive||||||||||||||||||||||||||transgene insertion 1, Mark M Davis||||||||||||Heightened susceptibility to autoimmune diabetes on the transgenically sensitized TCR x insHEL background (see figure). Phenotype Screen: Urine glucose|Normal|C57BL/6 x B10BR x CBA|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|06-Sep-2009|Cryopreserved sperm|||Yes|Type I Diabetes|ENU, JDRF, T cell, autoimmunity|Possibly| 4810.0|Burnum|ENU8BAT:061||Recessive|||||||||Unknown|||||||||||||||||transgene insertion 3, Christopher C Goodnow|Rat insulin promoter|Expression of the inserted sequence specifically to pancreatic islet beta cells||||||||||Mice carrying the ins-HEL gene have a subclinical predisposition to diabetes due to islet cell failure. Mice carrying the insHEL and TCR transgenes have asubclinical predisposition to autoimmune destruction of the beta cell. Screening mice by urine glucose test. High glucose levels indicate diabetes and thus autoimmunity. "Early onset diabetes" definition changed during screen from approx 80 days to 40 days.||C57BL/6 x CBA x C57BL/10BR|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|||Breed diabetic Double transgenic with a non transgenic sib for next generation|No|24-Sep-2009|Cryopreserved sperm|30.0|0.0|Yes|Type I Diabetes|ENU, Singapore, autoimmunity, T cell, B cell, glucose|Possibly| 4810.0|Burnum|ENU8BAT:061||Recessive||||||||||||||||||||||||||transgene insertion 1, Mark M Davis||||||||||||Mice carrying the ins-HEL gene have a subclinical predisposition to diabetes due to islet cell failure. Mice carrying the insHEL and TCR transgenes have asubclinical predisposition to autoimmune destruction of the beta cell. Screening mice by urine glucose test. High glucose levels indicate diabetes and thus autoimmunity. "Early onset diabetes" definition changed during screen from approx 80 days to 40 days.||C57BL/6 x CBA x C57BL/10BR|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|||Breed diabetic Double transgenic with a non transgenic sib for next generation|No|24-Sep-2009|Cryopreserved sperm|||Yes|Type I Diabetes|ENU, Singapore, autoimmunity, T cell, B cell, glucose|Possibly| 4814.0|Alba|ENU8BAT:079||Recessive|||||||||Unknown|||||||||||||||||transgene insertion 3, Christopher C Goodnow|Rat insulin promoter|Expression of the inserted sequence specifically to pancreatic islet beta cells||||||||||Mice carrying the ins-HEL gene have a subclinical predisposition to diabetes due to islet cell failure. Mice carrying the insHEL and TCR transgenes have asubclinical predisposition to autoimmune destruction of the beta cell. Screening mice by urine glucose test. High glucose levels indicate diabetes and thus autoimmunity. "Early onset diabetes" definition changed during screen from approx 80 days to 40 days.||C57BL/6 x CBA x C57BL/10BR|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|||Breed diabetic Double transgenic with a non transgenic sib for next generation|No|24-Sep-2009|Cryopreserved sperm|45.0|0.0|Yes|Type I Diabetes|ENU, Singapore, autoimmunity, T cell, B cell, glucose|Possibly| 4814.0|Alba|ENU8BAT:079||Recessive||||||||||||||||||||||||||transgene insertion 1, Mark M Davis||||||||||||Mice carrying the ins-HEL gene have a subclinical predisposition to diabetes due to islet cell failure. Mice carrying the insHEL and TCR transgenes have asubclinical predisposition to autoimmune destruction of the beta cell. Screening mice by urine glucose test. High glucose levels indicate diabetes and thus autoimmunity. "Early onset diabetes" definition changed during screen from approx 80 days to 40 days.||C57BL/6 x CBA x C57BL/10BR|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|||Breed diabetic Double transgenic with a non transgenic sib for next generation|No|24-Sep-2009|Cryopreserved sperm|||Yes|Type I Diabetes|ENU, Singapore, autoimmunity, T cell, B cell, glucose|Possibly| 6904.0|APN125|C57Bl/6N-Ptcra/Marp||Recessive|pre T cell antigen receptor alpha|Ptcra|Unknown|pT-alpha, pT[a], pTalpha|MGI:104857|pre T cell antigen receptor alpha; targeted mutation 2a, Helmholtz Zentrum Muenchen GmbH|Ptcratm2a(EUCOMM)Hmgu|MGI:4434686|17|||||||||||||||||||||||||||||Unknown|Normal|C57Bl/6N|Unknown|Unknown|Unknown|Unknown|Unknown|Yes|No|Good||||No|31-May-2012|Cryopreserved sperm|50.0|0.0|Unknown|||Possibly| 4804.0|Mallee|ENU8BAT:018||Recessive|||||||||Unknown|||||||||||||||||transgene insertion 3, Christopher C Goodnow|Rat insulin promoter|Expression of the inserted sequence specifically to pancreatic islet beta cells||||||||||Mice carrying the ins-HEL gene have a subclinical predisposition to diabetes due to islet cell failure. Mice carrying the insHEL and TCR transgenes have asubclinical predisposition to autoimmune destruction of the beta cell. Screening mice by urine glucose test. High glucose levels indicate diabetes and thus autoimmunity. "Early onset diabetes" definition changed during screen from approx 80 days to 40 days.||C57BL/6 x CBA x C57BL/10BR|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|||Breed diabetic Double transgenic with a non transgenic sib for next generation|No|24-Sep-2009|Cryopreserved sperm|40.0|0.0|Yes|Type I Diabetes|ENU, Singapore, autoimmunity, T cell, B cell, glucose|Possibly| 4804.0|Mallee|ENU8BAT:018||Recessive||||||||||||||||||||||||||transgene insertion 1, Mark M Davis||||||||||||Mice carrying the ins-HEL gene have a subclinical predisposition to diabetes due to islet cell failure. Mice carrying the insHEL and TCR transgenes have asubclinical predisposition to autoimmune destruction of the beta cell. Screening mice by urine glucose test. High glucose levels indicate diabetes and thus autoimmunity. "Early onset diabetes" definition changed during screen from approx 80 days to 40 days.||C57BL/6 x CBA x C57BL/10BR|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|||Breed diabetic Double transgenic with a non transgenic sib for next generation|No|24-Sep-2009|Cryopreserved sperm|||Yes|Type I Diabetes|ENU, Singapore, autoimmunity, T cell, B cell, glucose|Possibly| 4805.0|Akama|ENU8BAT:022||Recessive|||||||||Unknown|||||||||||||||||transgene insertion 3, Christopher C Goodnow|Rat insulin promoter|Expression of the inserted sequence specifically to pancreatic islet beta cells||||||||||Mice carrying the ins-HEL gene have a subclinical predisposition to diabetes due to islet cell failure. Mice carrying the insHEL and TCR transgenes have asubclinical predisposition to autoimmune destruction of the beta cell. Screening mice by urine glucose test. High glucose levels indicate diabetes and thus autoimmunity. "Early onset diabetes" definition changed during screen from approx 80 days to 40 days.||C57BL/6 x CBA x C57BL/10BR|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|||Breed diabetic Double transgenic with a non transgenic sib for next generation|No|24-Sep-2009|Cryopreserved sperm|45.0|0.0|Yes|Type I Diabetes|ENU, Singapore, autoimmunity, T cell, B cell, glucose|Possibly| 4805.0|Akama|ENU8BAT:022||Recessive||||||||||||||||||||||||||transgene insertion 1, Mark M Davis||||||||||||Mice carrying the ins-HEL gene have a subclinical predisposition to diabetes due to islet cell failure. Mice carrying the insHEL and TCR transgenes have asubclinical predisposition to autoimmune destruction of the beta cell. Screening mice by urine glucose test. High glucose levels indicate diabetes and thus autoimmunity. "Early onset diabetes" definition changed during screen from approx 80 days to 40 days.||C57BL/6 x CBA x C57BL/10BR|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|||Breed diabetic Double transgenic with a non transgenic sib for next generation|No|24-Sep-2009|Cryopreserved sperm|||Yes|Type I Diabetes|ENU, Singapore, autoimmunity, T cell, B cell, glucose|Possibly| 4806.0|Koora|ENU8BAT:032||Recessive|||||||||Unknown|||||||||||||||||transgene insertion 3, Christopher C Goodnow|Rat insulin promoter|Expression of the inserted sequence specifically to pancreatic islet beta cells||||||||||Mice carrying the ins-HEL gene have a subclinical predisposition to diabetes due to islet cell failure. Mice carrying the insHEL and TCR transgenes have asubclinical predisposition to autoimmune destruction of the beta cell. Screening mice by urine glucose test. High glucose levels indicate diabetes and thus autoimmunity. "Early onset diabetes" definition changed during screen from approx 80 days to 40 days.||C57BL/6 x CBA x C57BL/10BR|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|||Breed diabetic Double transgenic with a non transgenic sib for next generation|No|24-Sep-2009|Cryopreserved sperm|25.0|0.0|Yes|Type I Diabetes|ENU, Singapore, autoimmunity, T cell, B cell, glucose|Possibly| 4806.0|Koora|ENU8BAT:032||Recessive||||||||||||||||||||||||||transgene insertion 1, Mark M Davis||||||||||||Mice carrying the ins-HEL gene have a subclinical predisposition to diabetes due to islet cell failure. Mice carrying the insHEL and TCR transgenes have asubclinical predisposition to autoimmune destruction of the beta cell. Screening mice by urine glucose test. High glucose levels indicate diabetes and thus autoimmunity. "Early onset diabetes" definition changed during screen from approx 80 days to 40 days.||C57BL/6 x CBA x C57BL/10BR|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|||Breed diabetic Double transgenic with a non transgenic sib for next generation|No|24-Sep-2009|Cryopreserved sperm|||Yes|Type I Diabetes|ENU, Singapore, autoimmunity, T cell, B cell, glucose|Possibly| 4807.0|Jayne|ENU8BAT:023||Recessive|||||||||Unknown|||||||||||||||||transgene insertion 3, Christopher C Goodnow|Rat insulin promoter|Expression of the inserted sequence specifically to pancreatic islet beta cells||||||||||Male infertility. Mutant found in HEL:TCR ENU library.HEL:TCR transgenes not required for mutant phenotype||C57BL/6 x CBA x C57BL/10BR|Yes|Yes|Yes|Yes|No|Yes|No|Poor||||No|24-Sep-2009|Cryopreserved sperm|45.0|0.0|Yes|Male Infertility|ENU, fertility, sperm|Possibly| 4807.0|Jayne|ENU8BAT:023||Recessive||||||||||||||||||||||||||transgene insertion 1, Mark M Davis||||||||||||Male infertility. Mutant found in HEL:TCR ENU library.HEL:TCR transgenes not required for mutant phenotype||C57BL/6 x CBA x C57BL/10BR|Yes|Yes|Yes|Yes|No|Yes|No|Poor||||No|24-Sep-2009|Cryopreserved sperm|||Yes|Male Infertility|ENU, fertility, sperm|Possibly| 4907.0|ENUstrain:005|High Five||Recessive||||||||||||||||||||||||||transgene insertion 3, Christopher C Goodnow|Rat insulin promoter|||||||||||Heightened susceptibility to autoimmune diabetes on the transgenically sensitized TCR x insHEL background. Phenotype Screen: Urine glucose|Normal|C57BL/6 x B10BR x CBA|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|09-Oct-2009|Cryopreserved sperm|100.0|0.0|Yes|Type I Diabetes|ENU, JDRF, T cell, autoimmunity|Possibly| 4907.0|ENUstrain:005|High Five||Recessive||||||||||||||||||||||||||transgene insertion 1, Mark M Davis||||||||||||Heightened susceptibility to autoimmune diabetes on the transgenically sensitized TCR x insHEL background. Phenotype Screen: Urine glucose|Normal|C57BL/6 x B10BR x CBA|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|09-Oct-2009|Cryopreserved sperm|||Yes|Type I Diabetes|ENU, JDRF, T cell, autoimmunity|Possibly| 7578.0|Inpp5efl|C57BL/6-Inpp5e/Marp||Dominant|inositol polyphosphate-5-phosphatase E|Inpp5e|Normal|1200002L24Rik, 72kDa, mKIAA0123|MGI:1927753|inositol polyphosphate-5-phosphatase E; targeted mutation 1, Christina A Mitchell|Inpp5e|MGI:5823279|2||||||||||Unknown to Unknown|||||||||||||||||||Normal|Normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|24-Jan-2014|Cryopreserved sperm|50.0|0.0|Unknown||cilia|Possibly| 4809.0|Cooee|ENU8BAT:044||Recessive|||||||||Unknown|||||||||||||||||transgene insertion 3, Christopher C Goodnow|Rat insulin promoter|Expression of the inserted sequence specifically to pancreatic islet beta cells||||||||||Mice carrying the ins-HEL gene have a subclinical predisposition to diabetes due to islet cell failure. Mice carrying the insHEL and TCR transgenes have asubclinical predisposition to autoimmune destruction of the beta cell. Screening mice by urine glucose test. High glucose levels indicate diabetes and thus autoimmunity. "Early onset diabetes" definition changed during screen from approx 80 days to 40 days.||C57BL/6 x CBA x C57BL/10BR|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|||Breed diabetic Double transgenic with a non transgenic sib for next generation|No|24-Sep-2009|Cryopreserved sperm|75.0|0.0|Yes|Type I Diabetes|ENU, Singapore, autoimmunity, T cell, B cell, glucose, JDRF|Possibly| 4809.0|Cooee|ENU8BAT:044||Recessive||||||||||||||||||||||||||transgene insertion 1, Mark M Davis||||||||||||Mice carrying the ins-HEL gene have a subclinical predisposition to diabetes due to islet cell failure. Mice carrying the insHEL and TCR transgenes have asubclinical predisposition to autoimmune destruction of the beta cell. Screening mice by urine glucose test. High glucose levels indicate diabetes and thus autoimmunity. "Early onset diabetes" definition changed during screen from approx 80 days to 40 days.||C57BL/6 x CBA x C57BL/10BR|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|||Breed diabetic Double transgenic with a non transgenic sib for next generation|No|24-Sep-2009|Cryopreserved sperm|||Yes|Type I Diabetes|ENU, Singapore, autoimmunity, T cell, B cell, glucose, JDRF|Possibly| 4812.0|ENU8BAT:070:Wash|C57BL/6JSfdAnu-Henmt1/AnuApb||Recessive|HEN1 methyltransferase homolog 1 (Arabidopsis)|Henmt1|Unknown|4921515J06Rik, Hen1|MGI:1913965||||3|ENSMUSG00000045662|ENSMUST00000106586|4921515J06Rik-204||||||||108745775|3|||ATTTAGTGGATCGCCATGAACCCAAGAAGGTAATTATTATTATTATTATTGTTATTATTA|Yes|||||||||||||Male infertility. Mutant found in HEL:TCR ENU library.HEL:TCR transgenes not required for mutant phenotype||C57BL/6 x CBA x C57BL/10BR|Yes|Yes|Yes|Yes|No|Yes|No|Poor||||No|24-Sep-2009|Cryopreserved sperm|125.0|0.0|Yes|Male Infertility|ENU, fertility, sperm|Possibly| 4983.0|6AT:HELxTCR:14:non-lactation:G5|ENU6AT:14:non-lactation||Recessive|Unknown||Unknown||||||Unknown|||||||||||||||||||||||||||||Mothers fail to lactate|Normal|C57BL/6 x CBA|Yes|No|Yes|Yes|Yes|Yes|No|Unknown||||No|22-Jan-2010|Cryopreserved sperm|25.0|0.0|Unknown||ENU, lactation, fertility, milk|Yes| 5082.0|Slc2a6 (Glut6) KO|C57BL/6-Slc2a6||Recessive|solute carrier family 2 (facilitated glucose transporter), member 6|Slc2a6|Normal|Glut6, Glut9|MGI:2443286||||2||||||||||||||||Yes|||||||||||||Unknown|Normal|C57BL/6|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Good||||No|25-Mar-2010|Cryopreserved sperm|30.0|0.0|Unknown||transporter, glucose, channel|Possibly| 5089.0|Mulberry ; Mulkirri|B10;B6JAnu-Pde2a/AnuApb||Recessive|phosphodiesterase 2A, cGMP-stimulated|Pde2a|||MGI:2446107||||7|ENSMUSG00000030653|ENSMUST00000084894|Pde2a-202|1964|2191|A to T|ENSMUSE00000633285|23|655|Histidine to Leucine|||||CCGGGATCCACCCTACCACAACTGGATGCACGCCTTCTCTGTCTCTCATTTTTGCTACCTG|Yes|||||||||||||Reduced fetal liver size in embryos at E14.5.Increase % of primitive RBCs and HSCs.|Normal|C57BL/6 x C57BL/10|No|No|Yes|No|No|Yes|No|Good||||No|12-Apr-2010|Cryopreserved sperm|19.0|0.0|Unknown||ENU, haemopoietic stem cell, RBC|Possibly| 5090.0|ALZ17|C57BL/6-Tg(Thy1-MAPT)ALZ17Godt||Dominant||||||||||||||||||||||||||transgene insertion ALZ17, Michel Goedert|murine Thy1||||||||||||Neuron-specific expression of the longest human brain isoform 17 of MAPT.Transgenic mice aged 3 weeks to 25 months overexpressed human tau protein in nerve cells of brain and spinal cord. Numerous abnormal, tau-immunoreactive nerve cell bodies and dendrites were seen. In addition, large numbers of pathologically enlarged axons containing neurofilament- and tau-immunoreactive spheroids were present, especially in spinal cord. Signs of Wallerian degeneration and neurogenic muscle atrophy were observed. When motor function was tested, transgenic mice showed signs of muscle weakness. Taken together, these findings demonstrate that overexpression of human four-repeat tau leads to a central and peripheral axonopathy that results in nerve cell dysfunction and amyotrophy. |C57BL/6|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|15-Apr-2010|Cryopreserved sperm|40.0|0.0|Yes|Frontotemporal dementia and parkinsonism|frontotemporal dementia, parkinson disease, axonopathy, amyotrophy, nerve, tau|Possibly| 4815.0|Hanya|ENU8BAT:083||Recessive|||||||||Unknown|||||||||||||||||transgene insertion 3, Christopher C Goodnow|Rat insulin promoter|Expression of the inserted sequence specifically to pancreatic islet beta cells||||||||||Mice carrying the ins-HEL gene have a subclinical predisposition to diabetes due to islet cell failure. Mice carrying the insHEL and TCR transgenes have asubclinical predisposition to autoimmune destruction of the beta cell. Screening mice by urine glucose test. High glucose levels indicate diabetes and thus autoimmunity. "Early onset diabetes" definition changed during screen from approx 80 days to 40 days.||C57BL/6 x C57BL/10BR|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|||Breed diabetic Double transgenic with a non transgenic sib for next generation|No|24-Sep-2009|Cryopreserved sperm|15.0|0.0|Yes|Type I Diabetes|ENU, Singapore, autoimmunity, T cell, B cell, glucose|Possibly| 4815.0|Hanya|ENU8BAT:083||Recessive||||||||||||||||||||||||||transgene insertion 1, Mark M Davis||||||||||||Mice carrying the ins-HEL gene have a subclinical predisposition to diabetes due to islet cell failure. Mice carrying the insHEL and TCR transgenes have asubclinical predisposition to autoimmune destruction of the beta cell. Screening mice by urine glucose test. High glucose levels indicate diabetes and thus autoimmunity. "Early onset diabetes" definition changed during screen from approx 80 days to 40 days.||C57BL/6 x C57BL/10BR|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|||Breed diabetic Double transgenic with a non transgenic sib for next generation|No|24-Sep-2009|Cryopreserved sperm|||Yes|Type I Diabetes|ENU, Singapore, autoimmunity, T cell, B cell, glucose|Possibly| 8448.0|W140S|C57BL/6NCrlAnu-Arpc1b/Anu||Recessive|actin related protein 2/3 complex, subunit 1B|Arpc1b|Normal|L72, p41-ARC, SOP2Hs|MGI:1343142|actin related protein 2/3 complex, subunit 1B; endonuclease-mediated mutation 1, Australian National University|Arpc1b||5||||||||||Unknown to Unknown|||||||||||||||||||Unknown||C57BL/6NCrlAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|19-Mar-2018|Cryopreserved sperm|12.0|0.0|Unknown|||Yes| 8616.0|Aicda fl:Flpe|C57BL/6N(Cg)-Aicda/MarpAnuApb||Recessive|activation-induced cytidine deaminase|Aicda|Normal|Aid|MGI:1342279|activation-induced cytidine deaminase; targeted mutation 1c, Helmholtz Zentrum Muenchen GmbH|Aicda|MGI:4460367|6|||||||||||||||||||||||||||||Normal||C57BL/6N|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||4||No|29-Nov-2018|Cryopreserved sperm|66.0|0.0|Unknown||EuCOMM|Yes| 8560.0|ASD542:Busquets:C57Bl/6crlAnu|C57BL/6NCrlAnu-Bank1/AnuApb||Recessive|B cell scaffold protein with ankyrin repeats 1|Bank1|Unknown|A530094C12Rik|MGI:2442120|Bank1, endonuclease-mediated mutation 1, Australian National University |Bank1||3||||||||||Unknown to Unknown|||||||||||||||||||Normal|Normal|C57BL/6NCrlAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|18-Sep-2018|Cryopreserved sperm|55.0|0.0|Unknown|||Yes| 8477.0|Traj18 KO|BALB/c-Traj18/Apb||Recessive|T cell receptor alpha joining 18|Traj18|Nil|Gm17009|MGI:4440521||||14|||||||||||||||||||||||||||||Normal|Normal|BALB/c|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|27-Apr-2018|Cryopreserved sperm|30.0|0.0|Unknown|||Yes| 8748.0|S1ECN*Smad1-ERT-cre-neu|STOCK Smad1 Tg(Elf5-rtTa-TetO) Tg(MMTVneu)202Mul/Apb||Recessive|SMAD family member 1|Smad1||Madh1, Madr1, Smad 1|MGI:109452|SMAD family member 1; targeted mutation 2, Elizabeth J Robertson|Smad1|MGI:2155484|8|||||||||||||||||Elf5-rtTa-TetO||||||||||||These mice are normal and breed well, and develop normally. Adult mice older than 6 month may develop multiple tumours in mammary glands.Younger mice seem to be more active than wild type mice. At the moment the phenotype of smad1 CRE/ERT mediated deletion is unknown.Doxycycline is required from a young age for effective knockout of Smad1.|ERT/CRE and NEU modifications are active in heterozygous setting, so the above phenotype is the same. Smad1 flox is required in the homozygous state for effective knockout.|mixed-mainly BALBc and FVB/N|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|04-Jul-2019|Cryopreserved sperm|50.0|0.0|Unknown|||Yes| 8748.0|S1ECN*Smad1-ERT-cre-neu|STOCK Smad1 Tg(Elf5-rtTa-TetO) Tg(MMTVneu)202Mul/Apb||Recessive||||||||||||||||||||||||||transgene insertion 202, William Muller|MMTV|||||||||||These mice are normal and breed well, and develop normally. Adult mice older than 6 month may develop multiple tumours in mammary glands.Younger mice seem to be more active than wild type mice. At the moment the phenotype of smad1 CRE/ERT mediated deletion is unknown.Doxycycline is required from a young age for effective knockout of Smad1.|ERT/CRE and NEU modifications are active in heterozygous setting, so the above phenotype is the same. Smad1 flox is required in the homozygous state for effective knockout.|mixed-mainly BALBc and FVB/N|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|04-Jul-2019|Cryopreserved sperm|||Unknown|||Yes| 8447.0|Arpc1b fl|C57BL/6N-Arpc1b Tg(ACTFLPe)9205Dym/Anu||Recessive|actin related protein 2/3 complex, subunit 1B|Arpc1b|Normal|L72, p41-ARC, SOP2Hs|MGI:1343142|actin related protein 2/3 complex, subunit 1B; targeted mutation 1c, Wellcome Trust Sanger Institute|Arpc1b||5|||||||||||||||||transgene insertion 9205, Susan Dymecki||||||||||||Normal||C57BL/6NCrlAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|19-Mar-2018|Cryopreserved sperm|22.0|0.0|Unknown|||Yes| 4976.0|ENU14:G1 ; Chokerre|ENU14China:014||Recessive|||||||||Unknown|||||||||||||||||||||||||||||Embryonic lethal.E14 embryos are alive but look sick.Increase in primitive RBCDecrease in definitive RBC|Possible embryonic blood defect|C57BL/6|No|No|Yes|No|No|Yes|No|Unknown||||No|22-Jan-2010|Cryopreserved sperm|10.0|0.0|Unknown||Haemopoietic stem cell, red blood cell, differentiation, proliferation, ENU, embryonic lethal|Yes| 5011.0|Ova BCR|B6.129-Ova BCR Tg1||Dominant||||||||||||||||||||||||||||||||||||||||10|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|22-Feb-2010|Cryopreserved sperm|150.0|0.0|Unknown|||Possibly| 5121.0|GDNF+/-|C57BL/6-Gdnf||Recessive|glial cell line derived neurotrophic factor|Gdnf|Unknown|glial cell line-derived neurotrophic factor|MGI:107430|glial cell line derived neurotrophic factor; targeted mutation 1, Laboratory of Mammalian Genes and Development, Heiner Westphal|Gdnf|MGI:2136846|15||||||||||||||||No|||||||||||||Neonatal lethality: die 12-24 hours after birthAbnormal kidney development: * severe renal dysgenesis or renal agenesis * metanephric development is halted between E11 and E14.5Abnormal ureteric bud morphology: ureteric bud is absent in most mice.Absent kidney.Abnormal ureter development: delayed or total absence of ureteric branching in cultured urogenital blocks.Abnormal enteric cholinergic neuron morphology: devoid of enteric parasympathetic cholinergic ganglion cells.Absent enteric neurons: neurons of the myenteric plexus are absent from the intestine.Hypoperistalsis: presence of milk in the oesophagus and reduced progression of food into the gastrointestinal tract.|On 129 background:Abnormal kidney morphology: 35% possess a wide range of renal defects between 3 to 5 months of age.Abnormal kidney development: 12% have severe bilateral kidney dysgenesis.Abnormal ureteric bud morphology: ureteric bud defects.Abnormal ureteric bud branching morphogenesis: reduced ureteric branching in cultured urogenital blocks.Small kidney: 23% have unilateral small kidneys with abnormal shape and/or cortical cysts or rough surface.Single kidney: unilateral kidney agenesis.On 129 x C57BL/6 backgroundPostnatal lethality: * Background Sensitivity: 17.1% preweaning lethality on the C57BL/6 background and 8.4% preweaning lethality on the CD-1 background which increased to 16.7% after interbreeding of offspring on the CD-1 background. * low, but highly significant, preweaning lethalitySingle kidney: 10% exhibit unilateral kidney agenesisAbnormal enteric ganglia morphology * hypoganglionisis, as indicated by reduced numbers and mesh density of ganglionic cells in both the myenteric and the submucosal plexus formations of the gastrointestinal tract. * 64% reduction of ganglionic cells in the ileocecum and colon and 50% reduction in the stomach and small intestine. * exhibit aganglionic regions interspersed along the hypoganglionic regions of the intestine.Megacolon: 84% have varying degrees of colon dilationAbnormal stomach morphology: 38.5% exhibit stomach distention.Chronic constipation: 74% exhibit fecal retention, a sign of chronic constipation.Hypoperistalsis: delayed gastric emptying of milk in newborns, indicating impaired intestinal motility.|C57BL/6|No|No|Yes|No|No|Yes|No|Poor||||No|12-May-2010|Cryopreserved sperm|40.0|0.0|Yes|Hirschsprung Disease, Susceptibility to, 1; HSCR1 OMIM ID: 142623|neuron, migration, enteric, colon, lethal|Yes| 5128.0|152|B6-Tg(Thy1-APPSwe,Prnp-PSEN2*N141I)152HLaoz||Dominant||||||||||||||||||||||||||transgene insertion 152H, Laurence Ozmen|Thy1 promoter driving expression of the human APP ; Prnp promoter driving the expression of human PSEN2||||||||||||Abnormal spatial learning: * in a Morris water maze, mice exhibit increased swim speed during cued acquisition at 2 and 4 months compared with wild-type mice. * in a Morris water maze, mice exhibit exhibited decreased spatial learning at 4 and 12 months compared with wild-type mice.Impaired coordination: on at rotarod at 4 months.Amyloid beta deposits: * from 4 to 16 months, mice exhibit amyloid beta deposits unlike wild-type mice. * amyloid beta deposits worsen with age.Increased body weight: at 4 to 12 months|C57BL/6|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|20-May-2010|Cryopreserved sperm|30.0|0.0|Yes|Alzheimer's disease (AD)|amyloid, Abeta plaques, tau, neuron|Yes| 5129.0|H2g7apf|KRN:241:H2g7apf:B10||Recessive|histocompatibility-2, MHC|H2|Unknown|H-2, MHC-II|MGI:95894|histocompatibility-2, MHC; g7 variant|H2|MGI:3579321|17||||||||||||||||Yes|||||||||||||Normal.Spontaneous recombinant incorporating a short length of the C57BL/10 derived H2 into the congenic H2g7. Alters the H2 expressed resulting in change to presentation that was using the g7 allele.|Normal|C57BL/10|Yes|Yes|Yes|Yes|Yes|Yes|No|Excellent|2||het x het|No|21-May-2010|Cryopreserved sperm|50.0|0.0|Unknown||Histocompatability, H2, presentation, T cell|Possibly| 5142.0|16FOX 009 B6.129-Tg(FoxP3-GFP)|ENU16FOX:009 Foxp3||Recessive|forkhead box P3|Foxp3|Normal|JM2, scurfin|MGI:1891436|||MGI:3574964|X||||||||||||||||No|||||||||||||Grey coloured coat.Cells from the background strain that express FoxP3 fluoresce green, predominantly T cells|Normal |129 x C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|||Affected x affected|No|27-May-2010|Cryopreserved sperm|20.0|0.0|Unknown||grey, coat, colour, melanocyte|Yes| 5142.0|16FOX 009 B6.129-Tg(FoxP3-GFP)|ENU16FOX:009 Foxp3||Recessive|Unknown|Unknown|||||||Unknown|||||||||||||||||||||||||||||Grey coloured coat.Cells from the background strain that express FoxP3 fluoresce green, predominantly T cells|Normal |129 x C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|||Affected x affected|No|27-May-2010|Cryopreserved sperm|||Unknown||grey, coat, colour, melanocyte|Yes| 5144.0|ENU15CHINA:002|C57BL/6JAnu-Gmds/AnuApb|C57BL/6JAnu-Gmds/AnuApb|Recessive|GDP-mannose 4, 6-dehydratase|Gmds|||MGI:1891112|GDP-mannose 4, 6-dehydratase; mutation 1, The Australian National University|Gdpd3|MGI:5563465|13|ENSMUSG00000038372|ENSMUST00000041859|Gmds-001|561|692|T to A|ENSMUSE00000282995|6|187|Tyrosine to STOP|||||CCCTATGGAGCAGCCAAACTCTATGCCTATTGGATTGTGGTGAATTTCCGTGAAGCTTATA|Yes|||||||||||||Highly activated T cells, expansion of myeloid cells.High CD44<+> B and T cells, Low T cells, Low NK cells.|Unknown|C57BL/6JAnu|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Poor||2||No|28-May-2010|Cryopreserved sperm|53.0|0.0|Unknown||T cell, ENU|Possibly| 5538.0|APN 112|C57BL/6N-Ptpn22/Marp||Recessive|protein tyrosine phosphatase, non-receptor type 22 (lymphoid) |Ptpn22|Unknown|70zpep, Ptpn8 |MGI:107170 |protein tyrosine phosphatase, non-receptor type 22 (lymphoid); targeted mutation 1a, Wellcome Trust Sanger Institute |Ptpn22tm1a(EUCOMM)Wtsi|MGI:4434268|3||||||||||||||||Yes|||||||||||||Unknown - Not bred to homozygocity |Normal |C57BL/6N|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|15-Jul-2011|Cryopreserved sperm|50.0|0.0|Unknown||ES cell|Yes| 6828.0|APN 241|C57Bl/6N-Rnpc3/Marp||Recessive|RNA-binding region (RNP1, RRM) containing 3|Rnpc3|Unknown|2810441O16Rik, AI447568, C030014B17Rik|1914475|RNA-binding region (RNP1, RRM) containing 3; targeted mutation 1a, Wellcome Trust Sanger Institute |Rnpc3 |MGI:4433222|3|||||||||||||||||||||||||||||Unknown|Normal|C57BL/6N|Unknown|Unknown|Unknown|Unknown|Unknown|Yes|No|Unknown||||No|01-Mar-2012|Cryopreserved sperm|50.0|0.0|Unknown|||Possibly| 5547.0|Snoopy ; ENU12WT009:B6G2|C57BL/6JAnu-Crkl/AnuMarpApb||Recessive|v-crk sarcoma virus CT10 oncogene homolog (avian)-like|Crkl|Unknown|1110025F07Rik, Crkol|MGI:104686||Snoopy|MGI:5510713|16||||||||||Unknown to Unknown|||||||||||||||||||Abnormal eye development:• poorly developed at E13.5Cyclopia:• in some miceOcular hypotelorism:• at E13.5Absent mandible:• hypoplasia/aplasia at E13.5Mandible hypoplasia:• hypoplasia/aplasia at E13.5Holoprosencephaly:• some mice exhibit complete failure of forebrain vesicle separationAbnormal forebrain morphology:• at E13.5|Normal|C57BL/6JAnu|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|03-Aug-2011|Cryopreserved sperm|10.0|0.0|Unknown||ENU, mandible, holoprosencephaly|Possibly| 5550.0|ENU16China:071a|C57BL/6JAnu-Pax5/AnuApb|C57BL/6JAnu-Pax5/AnuApb|Recessive|paired box gene 5|Pax5 |Reduced|EBB-1, Pax-5 |MGI:97489 |paired box gene 5; mutation 2, The Australian National University|Pax5|MGI:5563442|4|ENSMUSG00000014030|ENSMUST00000014174|Pax5-001|233|1271|T to A|ENSMUSE00000527453|3|78|Isoleucine to Asparagine|||||TCTTGGCAGGTATTATGAGACAGGAAGCATCAAGCCGGGGGTGATTGGAGGATCCAAACCA||||||||||||||Mice have severely reduced numbers of B cells|Some Het mice seem to have increased immature B cells|C57BL/6JAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|4-6|5|Sib x sib|No|09-Aug-2011|Cryopreserved sperm|55.0|0.0|Unknown||B cell, lymphocyte, ENU|Yes| 5571.0|Zic5 V504G: C57BL/6|B6.C(C3H)-Zic5/HAnu|B6.C(C3H)-Zic5/HAnu|Recessive|Zinc finger protein of the cerebellum 5|Zic5|Unknown|odd-paired related, Opr|MGI:1929518||||14||||||||||||||||Yes|||||||||||||Viable and fertile|Viable and fertile|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|10|0|Heterozygote animal paired with C57BL/6 animal|No|31-Aug-2011|Cryopreserved sperm|50.0|0.0|Unknown||zinc finger, ENU|Yes| 6616.0|APN 113|CPT1a||Recessive|carnitine palmitoyltransferase 1a, liver |Cpt1a||Cpt1, CPTI, L-CPT I |MGI:1098296 ||||19|Cpt1a|ENSMUST00000025835|Cpt1a-201||||||||||||||||||||||||||Unknown|Normal|C57BL/6J|Unknown|Unknown|No|Unknown|Unknown|Unknown|No|Excellent||||No|13-Oct-2011|Cryopreserved sperm|50.0|0.0|Unknown|||Possibly| 6649.0|APN 116|C57BL/6N-Cish/Marp||Recessive|cytokine inducible SH2-containing protein |Cish ||Cis, CIS1, cytokine-inducible SH2 protein, F23 |MGI:103159 |cytokine inducible SH2-containing protein; targeted mutation 1e, Wellcome Trust Sanger Institute |Cishtm1e(KOMP)Wtsi|MGI:4363203|9|||||||||||||||||||||||||||||Unknow - Not bred to homozygocity|Normal|C57Bl/6N|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|22-Nov-2011|Cryopreserved sperm|50.0|0.0|Unknown|||Possibly| 6653.0|VavP-BCL2-69; C57BL/6-Tg(Vav-BCL2)1Jad/Wehi|ENU22Bcl2.006||Dominant|Unknown||||||||Unknown|||||||||||||||||transgene insertion 1, Jerry M Adams|mouse Vav promoter|High, haemopoietic cells|||||||||||Abnormal lymphocyte cell number:* the ratio of CD4 cells per B cell is 25% to 50% lower than in wild-type mice.Increased B cell number: 5-fold higher in the spleen at 18 weeksIncreased T cell number:* mice exhibit higher splenic T cell numbers than in wild-type and Tg(BCL2)22Wehi or Tg(BCL2)36Wehi mice.Increased CD4-positive T cell number:* the increase in CD4+ T cells is greater than the increase in CD8+ T cells.Increased CD8-positive T cell number:* the increase in CD4+ T cells is greater than the increase in CD8+ T cells.Abnormal class switch recombination:* the total number of B cells that undergo class switching is 50-fold higher than in wild-type mice.Abnormal somatic hypermutation frequency:* 22 of 23 clones isolated from class-switching cells harbor on average about 6 somatic mutations compared to in wild-type cells where no mutations are found.Enlarged spleen:Abnormal spleen germinal center morphology:* mice exhibit a larger pool of cycling B cells with a germinal center phenotype than in wild-type mice.* at 18 weeks, mice exhibit an increased in germinal center size and number compared to in wild-type mice.* however, expansion of germinal centers is dependent on CD4 T cell help.Increased spleen germinal center number: at 18 weeks.Increased spleen germinal center size: at 18 weeks.Enlarged lymph nodes.Glomerulonephritis:* at 40 weeks, 15% to 25% of mice develop autoimmune glomerulonephritis.Increased tumor incidence:* 12% of mice develop plasma cell tumorsLymphoma: less than 10% of mice develop lymphoblastic lymphomas.B cell derived lymphoma:* less than 10% of mice develop large cell B lymphomasFollicular lymphoma:* at 18 months, 37% to 50% of mice develop monoclonal follicular lymphoma.Thymic lymphoma: in less than 10% of miceHistiocytic sarcoma: in less than 10% of mice.|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|01-Dec-2011|Cryopreserved sperm|10.0|0.0|Unknown||B cell, bcl-2, vav, Progenitor, lymphoma, germinal centre|Yes| 6763.0|APN 150|C57BL/6N-Acss1/Marp||Recessive|acyl-CoA synthetase short-chain family member 1 |Acss1|Unknown|1110032O15Rik, Acas2, Acas2l, AceCS2 |MGI:1915988 |acyl-CoA synthetase short-chain family member 1; targeted mutation 1a, Wellcome Trust Sanger Institute |Acss1tm1a(EUCOMM)Wtsi|MGI:4441709|2||||||||||||||||Yes|||||||||||||Unknown - Not bred to homozygocity |Normal |C57BL/6N|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|15-Dec-2011|Cryopreserved sperm|50.0|0.0|Unknown||ES cell|Yes| 6617.0|ENU23 MDX:::B6:F1|ANU:ENU23MDX:F1||X-linked|dystrophin, muscular dystrophy|Dmd|Unknown|Dp427, Duchenne muscular dystrophy, mdx, pke, X-linked muscular dystrophy|MGI:94909|X linked muscular dystrophy|Dmd|MGI:1856328|X||||||||||||||||No|||||||||||||Abnormal muscle morphology.dilated sarcoplasmic reticulum.Abnormal skeletal muscle fiber morphology: * development of electron-dense bodies in the mitochondria resulting in swelling and degenerating mitochondria, and disruption of the plasmalemma basal lamina. * the normal myofibrillar architecture of bands and lines disappears and myofilaments disintegrate and become misaligned.Increased variability of skeletal muscle fiber size: variable muscle fiber size; progressive starting at 3 weeks of age.Skeletal muscle fibrosis: exhibit mild muscle fibrosis, however there is no replacement of lost muscle by fat cells.Skeletal muscle necrosis: progressive starting at 9 weeks of age.Muscle degeneration: progressive starting at 3 weeks of age.Abnormal muscle physiology: increased intracellular sodium concentration in muscle; increased severity with age.Muscular atrophy: progressive starting at 3 weeks of age.Dystrophic muscle.Myopathy: progressive degenerative myopathy; increased severity with age.Abnormal circulating enzyme level: exhibit elevated blood levels of muscle creatine kinase and pyruvate kinase.Reduced female fertility: slight reduction in fertility.||C57BL/6 x C57BL/10|Unknown|Unknown|Yes|Unknown|Unknown|Yes|Yes|Unknown||||No|14-Oct-2011|Cryopreserved sperm|220.0|0.0|Yes||Muscular dystrophy, Duchenne Type, muscle, necrosis, degeneration|Possibly| 6617.0|ENU23 MDX:::B6:F1|ANU:ENU23MDX:F1||X-linked|Unknown||||||||Unknown|||||||||||||||||||||||||||||Abnormal muscle morphology.dilated sarcoplasmic reticulum.Abnormal skeletal muscle fiber morphology: * development of electron-dense bodies in the mitochondria resulting in swelling and degenerating mitochondria, and disruption of the plasmalemma basal lamina. * the normal myofibrillar architecture of bands and lines disappears and myofilaments disintegrate and become misaligned.Increased variability of skeletal muscle fiber size: variable muscle fiber size; progressive starting at 3 weeks of age.Skeletal muscle fibrosis: exhibit mild muscle fibrosis, however there is no replacement of lost muscle by fat cells.Skeletal muscle necrosis: progressive starting at 9 weeks of age.Muscle degeneration: progressive starting at 3 weeks of age.Abnormal muscle physiology: increased intracellular sodium concentration in muscle; increased severity with age.Muscular atrophy: progressive starting at 3 weeks of age.Dystrophic muscle.Myopathy: progressive degenerative myopathy; increased severity with age.Abnormal circulating enzyme level: exhibit elevated blood levels of muscle creatine kinase and pyruvate kinase.Reduced female fertility: slight reduction in fertility.||C57BL/6 x C57BL/10|Unknown|Unknown|Yes|Unknown|Unknown|Yes|Yes|Unknown||||No|14-Oct-2011|Cryopreserved sperm|||Yes||Muscular dystrophy, Duchenne Type, muscle, necrosis, degeneration|Possibly| 6643.0|IPO5 FL/FL|C57BL/6-Ipo5||Dominant|importin 5|Ipo5|Normal|1110011C18Rik, 5730478E03Rik, IMB3, Kpnb3, Ranbp5|MGI:1917822||||14|||||||||||||||||||||||||||||Normal|Normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|||FL/FL x FL/FL|No|07-Nov-2011|Cryopreserved sperm|40.0|0.0|Unknown|||Possibly| 6650.0|APN 119|C57BL/6N-PYY/Marp||Recessive|peptide YY |Pyy ||MGC:19143 |MGI:99924 |peptide YY; targeted mutation 1, Wellcome Trust Sanger Institute |Pyytm1(KOMP)Wtsi|MGI:4363090|11|||||||||||||||||||||||||||||Unknown - Not bred to homozygocity|Normal|C57Bl/6N|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|22-Nov-2011|Cryopreserved sperm|50.0|0.0|Unknown|||Possibly| 6761.0|ENU17FOX:008|C57BL/6JAnu-Il17f Foxp3/AnuApb||Recessive|interleukin 17F|Il17f|||MGI:2676631||||1|ENSMUSG00000041872|ENSMUST00000039046|Il17f-201|158|229|C to A|ENSMUSE00000308433|2|53|Valine to Leucine|||||GAACTGTCCTCCCCTGGAGGATAACACTGTGAGAGTTGACATTCGAATCTTCAACCAAAAC||||||||||||||N/A|Hyper IgE, high numbers of monocytes and low numbers of B cells in peripheral blood.|C57BL/6JAnu|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|07-Dec-2011|Cryopreserved sperm|50.0|0.0|Unknown||B cell, lymphocyte|Possibly| 6761.0|ENU17FOX:008|C57BL/6JAnu-Il17f Foxp3/AnuApb||Recessive|forkhead box P3|Foxp3|Normal|JM2, scurfin|MGI:1891436|forkhead box P3; targeted mutation 2, Alexander Y Rudensky|Foxp3|MGI:3574964|X|||||||||||||||||||||||||||||N/A|Hyper IgE, high numbers of monocytes and low numbers of B cells in peripheral blood.|C57BL/6JAnu|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|07-Dec-2011|Cryopreserved sperm|||Unknown||B cell, lymphocyte|Possibly| 6769.0|APN 154|C57BL/6N-Hspa5/Marp||Recessive|heat shock protein 5 |Hspa5|Unknown|78kDa, Bip, D2Wsu141e, D2Wsu17e, Grp78, Hsce70, mBiP, Sez7, XAP-1 antigen 98 |MGI:95835 |heat shock protein 5; targeted mutation 1, Velocigene |Hspa5tm1(KOMP)Vlcg|MGI:4399453|2||||||||||||||||Yes|||||||||||||Unknown - Not bred to homozygocity |Normal |C57BL/6N|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|20-Dec-2011|Cryopreserved sperm|50.0|0.0|Unknown||ES cell|Possibly| 6783.0|APN 103|C57BL/6N-F2rl1/Marp||Recessive|coagulation factor II (thrombin) receptor-like 1 |F2rl1 |Unknown|Gpcr11, PAR-2, Par2, Protease-activated receptor-2, proteinase-activated receptor-2 |MGI:101910|coagulation factor II (thrombin) receptor-like 1; targeted mutation 1a, Wellcome Trust Sanger Institute |F2rl1tm1a(EUCOMM)Wtsi|MGI:4460480|13||||||||||||||||Yes|||||||||||||Unknown - Not bred to homozygocity |Normal |C57BL/6N|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|18-Jan-2012|Cryopreserved sperm|50.0|0.0|Unknown||ES cell|Yes| 6785.0|APN 122|C57BL/6N-Plin5/Marp||Recessive|perilipin 5 |Plin5 |Unknown|2310076L09Rik, Lsdp5, MLDP |MGI:1914218|perilipin 5; targeted mutation 2a, Wellcome Trust Sanger Institute |Plin5tm2a(KOMP)Wtsi|MGI:4455577|17||||||||||||||||Yes|||||||||||||Unknown - Not bred to homozygocity |Normal |C57BL/6N|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|18-Jan-2012|Cryopreserved sperm|50.0|0.0|Unknown||ES cell|Yes| 8446.0|Choir|C57BL/6NCrlAnu-Fcho1/AnuApb||Recessive|FCH domain only 1|Fcho1|Unknown|3322402E17Rik|MGI:1921265|Fcho1, endonuclease-mediated mutation 1, Australian National University|Fcho1||8||||||||||Unknown to Unknown|||||||||||||||||||Unknown||C57BL/6NCrlAnu|Yes|Yes|Yes|Yes|Unknown|Yes|No|Unknown||||No|19-Mar-2018|Cryopreserved sperm|55.0|0.0|Unknown|||Yes| 8501.0|ASD798:Sapote:2|C57BL/6NCrlAnu-Ifit3b/AnuApb||Recessive|interferon-induced protein with tetratricopeptide repeats 3B|Ifit3b|Unknown|I830012O16Rik|MGI:3698419|Ifit3b, endonuclease-mediated mutation 2, Australian National University|Ifit3b||19||||||||||Unknown to Unknown|||||||||||||||||||Unknown||C57BL/6NCrlAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|05-Jun-2018|Cryopreserved sperm|46.0|0.0|Unknown|||Yes| 6786.0|APN 149|C57BL/6N-Acss1/Marp||Recessive|acyl-CoA synthetase short-chain family member 1 |Acss1|Unknown|1110032O15Rik, Acas2, Acas2l, AceCS2 |MGI:1915988 |acyl-CoA synthetase short-chain family member 1; targeted mutation 1a, Wellcome Trust Sanger Institute |Acss1tm1a(EUCOMM)Wtsi|MGI:4441709|2||||||||||||||||Yes|||||||||||||Unknown - Not bred to homozygocity |Normal |C57BL/6N|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|18-Jan-2012|Cryopreserved sperm|60.0|0.0|Unknown||ES cell|Yes| 6787.0|APN 94|C57BL/6N-Inpp4a /Marp||Recessive|inositol polyphosphate-4-phosphatase, type I |Inpp4a |Unknown|107kDa |MGI:1931123 |inositol polyphosphate-4-phosphatase, type I; targeted mutation 1a, Helmholtz Zentrum Muenchen GmbH |Inpp4atm1a(EUCOMM)Hmgu|MGI:4434756|1||||||||||||||||Yes|||||||||||||Unknown - Not bred to homozygocity |Normal |C57BL/6N|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|18-Jan-2012|Cryopreserved sperm|50.0|0.0|Unknown||ES cell|Yes| 6792.0|A33CreERt2/LacZ13 (ME-223)|STOCK Tg(Gpa33-cre/ERT2) Tg(Pgk1-lacZ)13Vmel/LudApb||Dominant||||||||||||||||||||||||||cre recombinase|glycoprotein A33 (transmembrane)|||||||||||Unknown|Unknown|Mixed|No|Unknown|Yes|No|Unknown|Yes|No|Unknown||||No|18-Jan-2012|Cryopreserved sperm|45.0|0.0|Unknown||LacZ, cre recombinase|Yes| 6792.0|A33CreERt2/LacZ13 (ME-223)|STOCK Tg(Gpa33-cre/ERT2) Tg(Pgk1-lacZ)13Vmel/LudApb||Dominant||||||||||||||||||||||||||transgenic insertion 13, Harald von Melchner|mouse Pgk1 promoter|||||||||||Unknown|Unknown|Mixed|No|Unknown|Yes|No|Unknown|Yes|No|Unknown||||No|18-Jan-2012|Cryopreserved sperm|||Unknown||LacZ, cre recombinase|Yes| 6832.0|APN 185|C57Bl/6N-Plin5/MarpApb||Recessive|perilipin 5|Plin5|Unknown|2310076L09Rik, Lsdp5, MLDP|MGI:1914218|perilipin 5; targeted mutation 1a, Wellcome Trust Sanger Institute|Plin5 |MGI:4364899|17|||||||||||||||||||||||||||||Unknown|Normal|C57Bl/6N|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|01-Mar-2012|Cryopreserved sperm|50.0|0.0|Unknown|||Possibly| 6833.0|APN 207|C57Bl/6NTac-Gpr183/MarpApb||Recessive|G protein-coupled receptor 183 |Gpr183 |Unknown|Ebi2 |MGI:2442034 |G protein-coupled receptor 183; targeted mutation 1, Velocigene |Gpr183tm1(KOMP)Vlcg |MGI:3808449|14|||||||||||||||||||||||||||||Unknown|Normal|C57Bl/6N|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|01-Mar-2012|Cryopreserved sperm|50.0|0.0|Unknown|||Possibly| 6834.0|APN 267|C57Bl/6J-Gkn3/Marp||Recessive|gastrokine 3 |Gkn3|Unknown|1190003M12Rik |MGI:1916138 |gastrokine 3; targeted mutation 1a, Wellcome Trust Sanger Institute |Gkn3tm1a(EUCOMM)Wtsi |MGI:4433233|6|||||||||||||||||||||||||||||Unknown|Normal|C57Bl/6N|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|01-Mar-2012|Cryopreserved sperm|50.0|0.0|Unknown|||Possibly| 6870.0|APN126|C57Bl/6N-Ptcra/MarpApb||Recessive|pre T cell antigen receptor alpha|Ptcra|Unknown|pT-alpha, pT[a], pTalpha|MGI:104857|pre T cell antigen receptor alpha; targeted mutation 2a, Helmholtz Zentrum Muenchen GmbH|Ptcratm2a(EUCOMM)Hmgu|MGI:4434686|17|||||||||||||||||||||||||||||Unknown|Normal|C57Bl/6N|Unknown|Unknown|Unknown|Unknown|Unknown|Yes|No|Good||||No|05-Apr-2012|Cryopreserved sperm|50.0|0.0|Unknown|||Possibly| 6874.0|DBC1 Clone 5C8B|C57BL/6-Dbc1/Marp||Recessive|deleted in bladder cancer 1 (human)|Dbc1||Dbccr1, Fam5a|MGI:1928478||||4|||||||||||||||||||||||||||||Normal|Normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|23-Apr-2012|Cryopreserved sperm|50.0|0.0|Unknown|||Possibly| 6899.0|B6.BlGpA ; B6.TgN(HUFUT1-HUGTA-MUSMICAM2)|C57BL/6-Tg(Icam2-FUT1, GTA)/StV||Dominant||||||||||||||||||||||||||human H-transferase and human A-transferase|ICAM2|||||||||||Expression of human blood group A on vascular endothelium and on a subset of polymorphonuclear cells|Expression of human blood group A on vascular endothelium and on a subset of polymorphonuclear cells|C57BL/6|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Excellent|20|||No|24-May-2012|Cryopreserved sperm|50.0|0.0|No||Blood group A, Transgenic|Possibly| 6877.0|Abca1fl/fl Abcg1fl/fl|C57BL/6-Abca1Abcg1/Marp ||Semi-dominant|ATP-binding cassette, sub-family A (ABC1), member 1|Abca1|Unknown|Abca1|MGI:99607||||4|||||||||||||||||||||||||||||Normal|Normal|C57BL/6J|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|24-Apr-2012|Cryopreserved sperm|50.0|0.0|Unknown|||Possibly| 6877.0|Abca1fl/fl Abcg1fl/fl|C57BL/6-Abca1Abcg1/Marp ||Semi-dominant|ATP-binding cassette, sub-family G (WHITE), member 1|Abcg1||Abc8, White|MGI:107704||||17|||||||||||||||||||||||||||||Normal|Normal|C57BL/6J|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|24-Apr-2012|Cryopreserved sperm|||Unknown|||Possibly| 6905.0|APN 259|C57BL/6N-Ift140/Marp||Recessive|intraflagellar transport 140 homolog (Chlamydomonas)|Ift140 |Unknown|mKIAA0590, Tce5, Wdtc2 |MGI:2146906 | intraflagellar transport 140 homolog (Chlamydomonas); targeted mutation 1a, Wellcome Trust Sanger Institute |Ift140tm1a(KOMP)Wtsi|MGI:4363217|17||||||||||||||||Yes|||||||||||||Unknown - Not bred to homozygocity |Normal |C57BL/6N |Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|01-Jun-2012|Cryopreserved sperm|50.0|0.0|Unknown||ES cell|Possibly| 8542.0|Rab32.3|C57BL/6-Rab32/Apb||Recessive|RAB32, member RAS oncogene family|Rab32||2810011A17Rik|MGI:1915094||||10|||||||||||||||||||||||||||||Normal|Normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|30-Jul-2018|Cryopreserved sperm|50.0|0.0|Unknown||Ras, CRISPR/Cas9|Yes| 6907.0|ENU15NIH49a|C57BL/6JAnu-Satb1/AnuApb|C57BL/6JAnu-Satb1/AnuApb|Dominant|special AT-rich sequence binding protein 1|Satb1|Unknown|2610306G12Rik |MGI:105084|special AT-rich sequence binding protein 1; mutation 1, The Australian National University|Satb1|MGI:5563413|17|ENSMUSG00000023927|ENSMUST00000144331|Satb1-001|1179|1416|T to A|ENSMUSE00000322390|7|393|Phenylalanine to Leucine|||||AAACGAGCCGGAATCTCACAGGCAGTATTTGCACGCGTGGCTTTTAACCGAACTCAGGGAT||||||||||||||Reduced expression of CD44 on CD4<+> and CD8<+> T cells|Intermediate phenotype of reduced expression of CD44 on CD4<+> and CD8<+> T cells|C57BL/6JAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||7||No|08-Jun-2012|Cryopreserved sperm|50.0|0.0|Unknown||lymphocyte, T cell, CD44, CD4, CD8, ENU|Possibly| 6908.0|BAC(A33:M2rtTA)|B6;129-Tg(Gpa33-rtTAS*M2)1||Dominant|||||||||||||||||||||||||||glycoprotein A33 (transmembrane), Gpa33|Mosaic activity in intestinal epithelium||||||||||Not described|The M2rtTA tet transactivator is expressed in the epithelium of the intestine and colon under the control of the intestine-specific A33 promoter. The expression/activety of the transactivator is mosaic, most likely due to stochastic transgene silencing. Approximately 1 to 5 crypts in the proximal small intestine express the transgene, fewer in the distral intestine and colon.|C57BL/6 x 129|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|14-Jun-2012|Cryopreserved sperm|50.0|0.0|No||intestine, epithelium, tetracycline|Possibly| 6910.0|MPS IIIA/MIP KO|B6.Cg-Ccl3 Sgsh/J||Recessive|N-sulfoglucosamine sulfohydrolase (sulfamidase)|Sgsh|Reduced|sulphamidase|MGI:1350341|N-sulfoglucosamine sulfohydrolase (sulfamidase); mucopolysaccharidosis IIIA|Sgsh|MGI:2151181|11|||||||||||||||||||||||||||||The phenotype of the MPSIIIA/MIPKO mice has not been fully characterized but is anticipated to be similar to that of the MPSIIIA Mice (Crawley et al (2006) Brain res 1104:1-17). |Normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|Generation 14 (MPSIIIA strain)||Brother x Sister (MPSIIIA strain and MIP KO strain), Non-brother X Sister for MPS/MIP crosses|No|20-Jun-2012|Cryopreserved sperm|50.0|0.0|Yes|MPSIIIA is a progressive neurodegenerative disorder|Lysosomal storage disorder, Mucopolysaccharidosis, Neuroinflammation, Macrophage Inflammatory Protein|Yes| 6910.0|MPS IIIA/MIP KO|B6.Cg-Ccl3 Sgsh/J||Recessive|chemokine (C-C motif) ligand 3|Ccl3|Nil|CCL3, G0S19-1, LD78alpha, macrophage inflammatory protein-1alpha, Mip1a, MIP1-(a), MIP-1alpha, MIP-1 alpha, MIP1-alpha, Scya3|MGI:98260|chemokine (C-C motif) ligand 3; targeted mutation 1, University of North Carolina|Ccl3|MGI:1857243|11|||||||||||||||||||||||||||||The phenotype of the MPSIIIA/MIPKO mice has not been fully characterized but is anticipated to be similar to that of the MPSIIIA Mice (Crawley et al (2006) Brain res 1104:1-17). |Normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|Generation 14 (MPSIIIA strain)||Brother x Sister (MPSIIIA strain and MIP KO strain), Non-brother X Sister for MPS/MIP crosses|No|20-Jun-2012|Cryopreserved sperm|||Yes|MPSIIIA is a progressive neurodegenerative disorder|Lysosomal storage disorder, Mucopolysaccharidosis, Neuroinflammation, Macrophage Inflammatory Protein|Yes| 7022.0|APN152|C57BL/6N-A Ptafr/Marp||Recessive|platelet-activating factor receptor|Ptafr|Unknown|PAFR, PAF receptor|MGI:106066|platelet-activating factor receptor; targeted mutation 1a, Wellcome Trust Sanger Institute |Ptafr |MGI:4460278|4|||||||||||||||||||||||||||||Unknown|Normal|C57BL/6N|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|19-Jul-2012|Cryopreserved sperm|50.0|0.0|Unknown||ES cell clone|Possibly| 7034.0||ENU22 Bcl2:015||Dominant|unknown|unknown|||||||Unknown|||||||||||||||||||||||||||||High Platelet phenotype. Phenotyping technique by Advia. Not: Even though sperm freezing shows medium to low concentration and motility these mice breed extremely well.|Normal.Not: Even though sperm freezing shows medium to low concentration and motility these mice breed extremely well.|C57BL/6NCrl|Unknown|Unknown|Unknown|Unknown|Yes|Yes|No|Excellent|Mice will be frozen at G4||Affected by B6|No|31-Jul-2012|Cryopreserved sperm|45.0|0.0|Unknown||ENU|Possibly| 7076.0|APN159|C57BL/6N-A-Recql4/Marp|MGI:5050948|Recessive|RecQ protein-like 4|Recql4|Unknown||MGI:1931028|RecQ protein-like 4; targeted mutation 3, Wellcome Trust Sanger Institute |Recql4/Marp |MGI:5050948|15|||||||||||||||||||||||||||||Unknown|Normal|C57BL/6N|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|05-Sep-2012|Cryopreserved sperm|50.0|0.0|Unknown||ES cell clone|Possibly| 7213.0|NOD-SBmut12|NOD/ShiLt-Slc16a10/Svi||Recessive|solute carrier family 16 (monocarboxylic acid transporters), member 10|Slc16a10|Unknown|2610103N14Rik, Mct10, PRO0813, TAT1|MGI:1919722|solute carrier family 16 (monocarboxylic acid transporters), member 10; transgenic transposon insertion 12, Thomas Brodnicki|Tn(sb-lacZ,GFP)12Tcb||10|||||||||||||||||||||||||||||Unknown|Unknown|NOD/ShiLt|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|NA|||No|15-Nov-2012|Cryopreserved sperm|50.0|0.0|Unknown|||Possibly| 7214.0|ENU15WT007b|C57BL/6JAnu-Tec/Apb|C57BL/6JAnu-Tec/Apb|Recessive|tec protein tyrosine kinase|Tec|Unknown||MGI:98662||||5|ENSMUSG00000029217|ENSMUST00000071944|Tec-001|1309|1503|A to G|ENSMUSE00001280689|15|437|Isoleucine to Threonine|||||TCTATGGTGTATGCACCCAGCAGAAGCCCATCTACATCGTTACCGAGTTCATGGAACGGGG||||||||||||||Increased susceptibility to infection with TB|Unknown|C57BL/6JAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|None|10|Het x Het and Hom x Hom|No|16-Nov-2012|Cryopreserved sperm|20.0|0.0|Unknown||ENU, infection|Possibly| 7229.0|APN310|C57Bl/6NTac-Ptcd1/Marp||Recessive|pentatricopeptide repeat domain 1|Ptcd1|Unknown|1110069M14Rik|MGI:1919049|pentatricopeptide repeat domain 1; targeted mutation 1, Velocigene/Marp|Ptcd<1tm1(KOMP)Vlcg/Marp>|MGI:4951221|5|||||||||||||||||||||||||||||Unknown|Normal|C57Bl6N|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Good||||No|22-Nov-2012|Cryopreserved sperm|50.0|0.0|Unknown|||Possibly| 7249.0|APN319|C57Bl/6N-A Sppl2a||Recessive|signal peptide peptidase like 2A|Sppl2a|Unknown|2010106G01Rik, C130089K23Rik|MGI:1913802|signal peptide peptidase like 2A; targeted mutation 1a, Helmholtz Zentrum Muenchen GmbH|Sppl2atm1a(EUCOMM)Hmgu|MGI:4887673|2|||||||||||||||||||||||||||||Unknown|Normal|C57Bl/6N|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Good||||No|12-Dec-2012|Cryopreserved sperm|50.0|0.0|Unknown|||Possibly| 7250.0|ENU18China:68b|C57BL/6JAnu-Ptpn6/AnuApb|C57BL/6JAnu-Ptpn6/AnuApb|Dominant|protein tyrosine phosphatase, non-receptor type 6|Ptpn6 |Reduced|hcp, Hcph, Ptp1C, SHP-1, Spin|MGI:96055|protein tyrosine phosphatase, non-receptor type 6; mutation 2, The Australian National University|Ptpn6|MGI:5563434|6|ENSMUSG00000004266|ENSMUST00000112484|Ptpn6-002|4|205|C to T|ENSMUSE00000691827|1|2|Valine to Methionine|||||ATGGTGAGGTGGTTTCACCGGGACCTCAGCGGGCC||||||||||||||Reduced IgM expression on mature B cells. Reduced percentage of mature B cells. Adult homozygous mice are healthy.|Mild reduction in the percent of mature B cells and mild reduction of IgM on mature B cells|C57BL/6JAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||7|homozygous x homozygous|No|13-Dec-2012|Cryopreserved sperm|47.0|0.0|Unknown||B cell, IgM, signaling, ENU|Possibly| 7261.0|APN246|C57BL/6N(Ag)-Casp9MarpApb||Recessive|caspase 9|Casp9 ||Caspase-9, ICE-LAP6, Mch6 |MGI:1277950 |caspase 9; targeted mutation 1a, Helmholtz Zentrum Muenchen GmbH |Casp9tm1a(EUCOMM)Hmgu|MGI:4950193|4|||||||||||||||||||||||||||||Unknown|Normal|C57Bl/6N|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|17-Jan-2013|Cryopreserved sperm|50.0|0.0|Unknown|||Possibly| 7274.0|Primurus:swHEL:HcLc:Ly5a x EGFP|C57BL/6-Dock8 Igh Ptprc Tg(IgkHyHEL10)1Rbr Tg(nZeg EGFP)||Dominant|immunoglobulin heavy chain complex|Igh|||MGI:96442|immunoglobulin heavy chain complex; targeted mutation 1, Robert Brink|Igh|MGI:3800383|12||||||||||||||||Yes|transgene insertion 1, Robert Brink||||||||||||Unknown||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|13-Feb-2013|Cryopreserved sperm|70.0|0.0|Unknown||Immunoglobulin, Hen Egg lysozyme (HEL), self-tolerance, autoimmunity, B cell, ENU, memory|Yes| 7274.0|Primurus:swHEL:HcLc:Ly5a x EGFP|C57BL/6-Dock8 Igh Ptprc Tg(IgkHyHEL10)1Rbr Tg(nZeg EGFP)||Dominant|dedicator of cytokinesis 8|Dock8||1200017A24Rik, 5830472H07Rik, A130095G14Rik|MGI:1921396|primurus|Dock8|MGI:3835421|19|||||||||||||||||nZEG EGFP||||||||||||Unknown||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|13-Feb-2013|Cryopreserved sperm|||Unknown||Immunoglobulin, Hen Egg lysozyme (HEL), self-tolerance, autoimmunity, B cell, ENU, memory|Yes| 7274.0|Primurus:swHEL:HcLc:Ly5a x EGFP|C57BL/6-Dock8 Igh Ptprc Tg(IgkHyHEL10)1Rbr Tg(nZeg EGFP)||Dominant|protein tyrosine phosphatase, receptor type, C|Ptprc|Unknown|B220, CD45, Ly-5, Lyt-4, T200|MGI:97810|protein tyrosine phosphatase, receptor type, C; a variant|Ptprc|MGI:4819849|1|||||||||||||||||||||||||||||Unknown||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|13-Feb-2013|Cryopreserved sperm|||Unknown||Immunoglobulin, Hen Egg lysozyme (HEL), self-tolerance, autoimmunity, B cell, ENU, memory|Yes| 7275.0|B6.SJL.RIIa Tg|B6.SJL Fcgr 2a Tg|HOGA|Semi-dominant|Human Fcgamma r2a|FcgR2a|Normal||||||Unknown|||||||||||||||||human FcyR2a|human FcyR2a|normal|FcyR2a|FcyR2a||FcyRIIa, CD32a||FcyR2a high responder|FcyR2a HR||Unknown|spontaneous development of autoimmune disease including distructive arthritis in 40% of animals|not known|inbred|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||Yes|15-Feb-2013|Cryopreserved sperm|50.0|0.0|Yes|Rheumatoid arthritis, inflamation of joints|Fc receptor, antibody, immune complex, inflammation, arthritis|Possibly| 7277.0|SJL.RIIa Tg|SJL.Fcgr2a Tg|HOGA|Semi-dominant|Fcgamma r2a|FcgR2a|Normal||||||Unknown|||||||||||||||||human FcyR2a|human FcyR2a|normal||||||||||spontaneous arthritis|not known|SJL|Yes|Yes|Yes|Yes|Yes|Yes|Yes|Good|12|||Yes|15-Feb-2013|Cryopreserved sperm|45.0|0.0|Yes|immune complex disease|Fc receptor, antibody, immune complex, inflammation, arthritis, thrombocytopenia|Possibly| 7354.0|Lck-Cre:Foxo1-flox|B6.129-Foxo1 Tg(Lck-cre)157Jxm/Anu||Recessive|forkhead box O1|Foxo1|Normal|Afxh, FKHR, Fkhr1, Foxo1a|MGI:1890077|forkhead box O1; targeted mutation 1, Richard A Flavell|Foxo1|MGI:3840910|3|||||||||||||||||targeted mutation I57, Jamey Marth; transgene insertion I57, Jamey Marth|mouse proximal Lck promoter|active in thymocytes and splenocytes||||||||||||C57BL/6JAnu|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|19-Jun-2013|Cryopreserved sperm|30.0|0.0|Unknown||T cell, transcription|Possibly| 7420.0|Ankyrin1 ; ENU20_44b|C57BL/6NCrlAnu-Ank1/Apb||Recessive|Ankyrin 1|Ank1|Unknown|Ank-1, pale|MGI:88024||||8|||||||||||||||||||||||||||||Increased levels of reticulocytes - high, Low RBC number, low hematocrit, low haemoglobin, low MCV|Normal|C57BL/6NCrlAnu|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|Yes|Poor||4|het x het|No|26-Aug-2013|Cryopreserved sperm|20.0|0.0|Unknown||Reticulocyte, Anaemia|Possibly| 7461.0|Hes7|B6.Cg-Hes7||Recessive|hairy and enhancer of split 7 (Drosophila)|Hes7|Nil|bHLHb37|MGI:2135679|hairy and enhancer of split 7 (Drosophila); targeted mutation 1, Ryoichiro Kageyama|Hes7|MGI:2652222|11||||||||||||||||No|||||||||||||Null pups die perinatally with vertebal segmentation defects.|Some heterozygous mice have tail kinks|C57BL/6|No|No|Yes|No|No|Yes|No|Good|10|0|Hes7 +/- (heterozygous) mated with C57BL/6|No|22-Oct-2013|Cryopreserved sperm|80.0|0.0|Unknown|Spondylocostal dysostosis|Hes7, Somitogenesis, Notch signalling|Possibly| 8761.0|TBXAS- B6129P2|B6.129P2-Tg(TbxAS)||Dominant||||||||||||||||||||||||||TbxAS||||||||||||Unknown||C57BL/6|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|05-Aug-2019|Cryopreserved sperm|30.0|0.0|Unknown|||Yes| 8664.0|C169 (Gabrg2 PM)|C57BL/6J-Gabrg2/Mgmp||Recessive|gamma-aminobutyric acid (GABA) A receptor, subunit gamma 2|Gabrg2||GABAA-R, Gabrg-2, gamma2|MGI:95623||||11|||||||||||||||||||||||||||||Unknown|Normal|C57BL/6J|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|26-Feb-2019|Cryopreserved sperm|50.0|0.0|Unknown|||Yes| 2.0|Unmodulated|C57BL/6JSfdAnu-Card11/AnuApb|C57BL/6JSfdAnu-Card11/AnuApb|Recessive|caspase recruitment domain family, member 11|Card11|Normal|CARMA1, BIMP3|MGI:1916978|caspase recruitment domain family, member 11; unmodulated|Card11|MGI:3045963|5|ENSMUSG00000036526|ENSMUST00000085786|Card11-201|914|1235|T to A|ENSMUSE00000431473|7|305|Leucine to Glutamine|||||TGACTCAGACAAGGCCATCTTGGACATCCTGGAACATGACCGGAAGGAGGCGCTAGAGGAC|Yes|||||||||||||Diminished antibody formation upon T cell-independent type 2 and T cell-dependent immunization. Diminished B cell NFκB activation and proliferation to antigen receptor engagement, but normal proliferation to TLR4 stimulation. Failure to form normal IgMlow IgDhi follicular B cells, and failure to form peritoneal B1 B cells. Diminished T cell NFκB activation and proliferation to TCR+CD28 stimulation. Spontaneous dermatitis accompanied by dermal mastocytosis and hyper-IgE syndrome.||C57BL/6JSfdAnu|Yes|Yes|Yes|Yes|Yes|Yes|Yes|Poor||||No|25-Nov-2005|Cryopreserved sperm|125.0|0.0|Unknown||B cell, T cell, dermititis, ENU, Wellcome Trust|Yes| 173.0||C57BL/6-Tau-GFP||Dominant|microtubule-associated protein tau|Mapt ||Tau|MGI:97180||||11|ENSMUSG00000018411|ENSMUST00000106989|||||||||||||||transgene insertion |CMV intermediate early enhancer coupled to the chicken beta actin promoter|||||||||||Every cell expresses a tau-GFP fusion protein, enabling visualization of microtubules and long cell processes (including axons). Mice homozygous for the transgene do not survive. ||C57BL/6|No|No|Yes|No|No|Yes|No|Unknown||||No|17-Apr-2006||0.0|0.0|No||GFP, microtubules, tau, axon|Yes| 10461.0|OT-II_B6N|B6.Cg-Tg(TcraTcrb)425Cbn/Anu||Recessive|transgene insertion 425, Frank Carbone|Tg:Tg(TcraTcrb)425Cbn||OT2, OT-II|MGI:3046083|Tg(TcraTcrb)425Cbn|Tg:OT2||Unknown|||||||||||||||||transgene insertion 425, Frank Carbone||||||||||||OVA-specif Cd4 T cells ||C57Bl/6N|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|07-Nov-2024|Cryopreserved sperm|22.0|0.0|Unknown|||Yes| 8907.0|Flk2CremTmG|B6-Tg(Flt3-Cre)#Ccb Gt(ROSA)26Sor/Apb||Semi-dominant|gene trap ROSA 26, Philippe Soriano|Gt(ROSA)26Sor||beta geo, Gtrgeo26, Gtrosa26, R26, ROSA26, Thumpd3as1|MGI:104735|gene trap ROSA 26, Philippe Soriano; targeted mutation 4, Liqun Luo|Gt(ROSA)26Sor|MGI:3716464|6|||||||||||||||||transgene insertion, Conrad C Bleul|Flt3|||||||||||Normal|Normal|C57BL/6|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Excellent||||No|20-Mar-2020|Cryopreserved sperm|50.0|0.0|Unknown|||Possibly| 7430.0|APN 369|C57BL/6N-A Katna1MarpApb||Recessive|katanin p60 (ATPase-containing) subunit A1|Katna1 |||MGI:1344353 |katanin p60 (ATPase-containing) subunit A1; targeted mutation 1a, Wellcome Trust Sanger Institute |Katna1tm1a(KOMP)Wtsi|MGI:4458514|10|||||||||||||||||||||||||||||Unknown|Normal|C57Bl/6N|Unknown|Unknown|Unknown|Unknown|Unknown|Yes|No|Unknown||||No|05-Sep-2013|Cryopreserved sperm|20.0|0.0|Unknown|||Possibly| 7479.0|dll1|C57BL/6J-Dll1|C57BL/6J-Dll1|Recessive|delta-like 1 (Drosophila)|Dll1|Nil|Delta1|MGI:104659|delta-like 1 (Drosophila); targeted mutation 1, Michael J Owen|Dll1|MGI:3044907|17||||||||||||||||No|||||||||||||None|None|C57BL/6J|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|10|0|D1flox homozygous intercross|No|13-Nov-2013|Cryopreserved sperm|80.0|0.0|No||Dll1, Notch, receptor, B cell, marginal zone|Possibly| 9118.0|Fancl-del336_337|C57BL/6J-Fancl/Richard Dandrea||Semi-dominant|Fanconi anemia, complementation group L|Fancl||2010322C19Rik, B230118H11Rik, gcd, Phf9, Pog |MGI:1914280|endonuclease mediated targeting 1; Richard D'Andrea|Fancl-del336_337||Unknown|||||||||||||||||||||||||||||Slightly smaller than wild type, microphtalmia in one or both eyes.|Normal|C57Bl/6J|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|18-Jan-2021|Cryopreserved sperm|50.0|0.0|Unknown|||Possibly| 9122.0|Adh5-48|C57Bl6/J/ApbAnu||Semi-dominant|alcohol dehydrogenase 5 (class III), chi polypeptide|Adh5|Unknown|Adh3, Adh-5, GSNOR, S-nitrosoglutathione reductase|MGI:87929||||3|||||||||||||||||||||||||||||Homozygotes might be susceptible to endotoxic shock and low blood pressure under anaesthesia.|Normal.|C57Bl/6J|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|19-Jan-2021|Cryopreserved sperm|50.0|0.0|Unknown|||Possibly| 7534.0|ENU20Flt3ITD:37|ENU20FLT3-ITD:037||Dominant|FMS-like tyrosine kinase 3|Flt3|Increased|CD135, Flk-2, Flk2, Flt-3|MGI:95559|FMS-like tyrosine kinase 3; targeted mutation 1, D Gilliland|Flt3|MGI:3763385|5||||||||||||||||Yes|||||||||||||Accelerated onset of Acute Myeloid leukaemia.|Accelerated onset of Acute Myeloid leukaemia.|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Poor||G2||No|10-Dec-2013|Cryopreserved sperm|74.0|0.0|Yes|Myelomonocytic Leukaemia|AML, myeloid, lymphocyte, CML, ENU|Possibly| 7534.0|ENU20Flt3ITD:37|ENU20FLT3-ITD:037||Dominant|Unknown||Unknown||||||Unknown|||||||||||||||||||||||||||||Accelerated onset of Acute Myeloid leukaemia.|Accelerated onset of Acute Myeloid leukaemia.|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Poor||G2||No|10-Dec-2013|Cryopreserved sperm|||Yes|Myelomonocytic Leukaemia|AML, myeloid, lymphocyte, CML, ENU|Possibly| 7557.0|ENU27:002:PIK3IP1:B6|C57BL/6NCrlAnu-Pik3ip1/AnuApb|C57BL/6NCrlAnu-Pik3ip1/AnuApb|Recessive|phosphoinositide-3-kinase interacting protein 1|Pik3ip1|Unknown|1500004A08Rik, 5830455E04Rik|MGI:1917016|phosphoinositide-3-kinase interacting protein 1; mutation 1, The Australian National University|Pik3ip1|MGI:5563439|11|ENSMUSG00000034614|ENSMUST00000045153|Pik3ip1-001|313|847|A to G|ENSMUSE00000314294|4|105|Serine to Alanine|||||CCTGCGAGGACGTGAGTTGCCCAGAGACCACTTCCCAAGCACCACCGCCATCCTCTGCCAT||||||||||||||Normal blood lymphocyte populations as measured by expression of following proteins: B220, CD3, CD4, CD44, KLRG1, NK1.1, IgM, IgD by flow cytometry.|Normal blood lymphocyte populations as measured by expression of following proteins: B220, CD3, CD4, CD44, KLRG1, NK1.1, IgM, IgD by flow cytometry.|C57BL/6NCrlAnu|Yes|Unknown|Yes|Yes|Unknown|Yes|No|Unknown||||No|19-Dec-2013|Cryopreserved sperm|30.0|0.0|Unknown||ENU|Yes| 7565.0|ENU27:020:Katnal2:B6|C57BL/6NCrlAnu-Katnal2/AnuApb||Recessive|Katanin p60 subunit A-like 2|Katnal2|Unknown|3110023G01Rik, 4933439B08Rik|MGI:1924234|katanin p60 subunit A-like 2; mutation 1, Australian National University|Katnal2|MGI:6164198|18|ENSMUSG00000025420|ENSMUST00000026486|Katnal2-005|257|329|T to C|ENSMUSE00001268471|3|86|Tyrosine to Cysteine|||||GAGCTATTATTTTGTAAAGTTCCAGAAGTACCCCAAAGTGGTTAAGAAGGCCCCGGACCCA||||||||||||||Unknown|Unknown|C57BL/6NCrlAnu|Unknown|Unknown|Unknown|Unknown|No|Yes|Yes|Unknown||||No|14-Jan-2014|Cryopreserved sperm|52.0|0.0|Unknown||ENU, missense, mutation, MMP|Possibly| 7600.0|APN 366|C57BL/6N-A Prrt2MarpApb||Recessive|proline-rich transmembrane protein 2|Prrt2 |||MGI:1916267 |proline-rich transmembrane protein 2; targeted mutation 1a, Wellcome Trust Sanger Institute|Prrt2tm1a(KOMP)Wtsi|MGI:4362325|7|||||||||||||||||||||||||||||Unknown|Normal|C57Bl/6N|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|21-Feb-2014|Cryopreserved sperm|40.0|0.0|Unknown|||Possibly| 7600.0|APN 366|C57BL/6N-A Prrt2MarpApb||Recessive|nonagouti|a||agouti, agouti signal protein, As, ASP|MGI:87853|nonagouti; targeted mutation 1, Allan Bradley|A|MGI:3842513|2|||||||||||||||||||||||||||||Unknown|Normal|C57Bl/6N|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|21-Feb-2014|Cryopreserved sperm|||Unknown|||Possibly| 7651.0|RBC10|C;B6-Slc12a4/WehiMarpApb||Dominant|solute carrier family 12, member 4|slc12a4|Unknown|KCC1, K-Cl Co-transporter-1|MGI:1309465|solute carrier family 12, member 4; red blood cell mutant 10|Slc12a4|MGI:5703920|8||||||||||Unknown to Unknown|||||||||||||||||||Homozygotes are viable and fertile. They display microcytic anaemia.|Intermediate between homozygotes and wild types.|BALB/c|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|||heterozygous intercrosses or homozygous intercrosses|No|08-Apr-2014|Cryopreserved sperm|60.0|0.0|Unknown||KCC1, Gain of function, ENU|Possibly| 7661.0|ENU26:014:Setx|C57BL/6NCrlAnu-Setx/AnuApb|C57BL/6NCrlAnu-Setx/AnuApb|Recessive|senataxin|Setx||A930037J23Rik, Als4|MGI:2443480|senataxin; mutation 1, The Australian National University|Setx|MGI:5563422|2|ENSMUSG00000043535|ENSMUST00000061578|Setx-001|140|823|A to G|ENSMUSE00001221495|3|47|Tyrosine to Cysteine|||||CTGCTACTGCTTAGAGTGTGTGGCTGAGTACCACCGAGCCAGAGATGAGGTGCCGTTCTTG||||||||||||||Increased numbers of IgM IgD expressing B cells.|Normal|C57BL/6NCrlAnu|Yes|Unknown|Yes|Yes|Unknown|Yes|No|Unknown||||No|11-Apr-2014|Cryopreserved sperm|33.0|0.0|Unknown||ENU, B cell, lymphocyte|Possibly| 7668.0|ASCIZ CD23 Bcl6|B6.Cg-Atmin Ighm Tg(Fcer2a-cre)5Mbu/SviApb||Dominant|ATM interactor|Atmin|||MGI:2682328|ATM interactor; targeted mutation 1.2, Jorg Heierhorst|Atmin|MGI:5463937|8|||||||||||||||||transgene insertion 5, Meinrad Busslinger|Fcer2a |||||||||||Normal|Normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|more than 10|||No|30-Apr-2014|Cryopreserved sperm|50.0|0.0|No|||Possibly| 7668.0|ASCIZ CD23 Bcl6|B6.Cg-Atmin Ighm Tg(Fcer2a-cre)5Mbu/SviApb||Dominant|immunoglobulin heavy constant mu|Ighm||BCR, Igh6, Igh-M, IgM, Ig mu, muH, muMT|MGI:96448|immunoglobulin heavy constant mu; targeted mutation 1, Riccardo Dalla-Favera|Ighm|MGI:3581517|12|||||||||||||||||||||||||||||Normal|Normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|more than 10|||No|30-Apr-2014|Cryopreserved sperm|||No|||Possibly| 7672.0||C57BL/6NCrlAnu-Pikfyve/AnuApb||Recessive|phosphoinositide kinase, FYVE finger containing|Pikfyve|Unknown|5230400C17Rik, Pip5k3, PipkIII|MGI:1335106||||1|||||||||||||||||||||||||||||Unknown|Unknown|C57BL/6NCrlAnu|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|05-May-2014|Cryopreserved sperm|11.0|0.0|Unknown||ENU|Yes| 7698.0|R26 WT-Hoxa1 ki|C57BL/6-Gt(ROSA)26Sor||Semi-dominant|gene trap ROSA 26, Philippe Soriano|Gt(ROSA)26Sor|Unknown|beta geo, Gtrgeo26, Gtrosa26, R26, ROSA26|MGI:104735|gene trap ROSA 26, Philippe Soriano; targeted mutation 3237, TaconicArtemis|Gt(ROSA)26Sor||6|||||||||||||||||||||||||||||Unknown|Unknown|C57BL/6|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Excellent||||No|12-Jun-2014|Cryopreserved sperm|50.0|0.0|Unknown|||Possibly| 8581.0|Fn14 KO/C57BL/6 |C57BL/6-Tnfrsf12a/Apb||Recessive|tumor necrosis factor receptor superfamily, member 12a|Tnfrsf12a|Unknown|Fn14, TweakR, TWEAK-R|MGI:1351484||||17|||||||||||||||||||||||||||||Normal|Normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|02-Oct-2018|Cryopreserved sperm|50.0|0.0|Unknown|||Yes| 8833.0|AMPK A2(S345A) KI|C57BL/6 Prkaa2(S345A)||Recessive|protein kinase, AMP-activated, alpha 2 catalytic subunit|Prkaa2||AMPKalpha2|MGI:1336173||||4|ENSMUSG00000028518|ENSMUST00000030243|||||||||||||||||||||||||||Normal|Normal|C57BL/6J|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|10-Dec-2019|Cryopreserved sperm|50.0|0.0|Unknown|||Yes| 7617.0|Helios floxed|B6.Cg-Ikzf2 Tg(CD4-Cre)/Anu||Recessive|IKAROS family zinc finger 2|Ikzf2||A730095J18Rik, Helios, Zfpn1a2|MGI:1342541|IKAROS family zinc finger 2; targeted mutation 1.1, Ethan M Shevach|Ikzf2|MGI:4456473|1|||||||||||||||||transgene insertion 1, Christopher B Wilson|CD4|||||||||||Abnormal regulatory T cell physiology:• regulatory T cells fail to respond to TCR stimulation or IL2 unlike wild-type cells• however, regulatory T cells respond normally to anti-CD3 and IL2 and are as suppressive as wild-type regulatory T cells||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|07-Mar-2014|Cryopreserved sperm|9.0|0.0|Unknown||CD4, T cell, Treg, FoxP3|Possibly| 7625.0|Srsf7-KO|B6NTac;B6N-A Srsf7/WtsiMarp||Dominant|serine/arginine-rich splicing factor 7|Srsf7||9430065L19Rik, 9G8, NX-96, Sfrs7|MGI:1926232|serine/arginine-rich splicing factor 7; targeted mutation 1a, Wellcome Trust Sanger Institute|Srsf7|MGI:4433826|17|||||||||||||||||||||||||||||Embryonic lethal|Uncharacterised|C57BL/6NTacMarp|No|No|Yes|No|No|Yes|No|Good|na|na||No|24-Mar-2014|Cryopreserved sperm|50.0|0.0|Unknown|||Possibly| 7654.0|Hbbtm2(HBG1,HBB*)Tow|C57BL/6-Hba Hbb Hbb/MarpApb||Dominant|hemoglobin alpha chain complex|Hba|Nil||MGI:96014|hemoglobin alpha chain complex; targeted mutation 1, Timothy Townes|Hba|MGI:3790755|11|||||||||||||||||||||||||||||Display sickle cell disease. Mice develop anemia from 3 weeks of age. Lethality occurs at variable rates (after 3 months). |Normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|||heterozygous intercrosses|No|08-Apr-2014|Cryopreserved sperm|60.0|0.0|Unknown||Sickle cell disease, haematology|Yes| 7654.0|Hbbtm2(HBG1,HBB*)Tow|C57BL/6-Hba Hbb Hbb/MarpApb||Dominant|hemoglobin beta chain complex|Hbb|Nil||MGI:96020|hemoglobin beta chain complex; targeted mutation 2, Timothy Townes|Hbb|MGI:3790753|7|||||||||||||||||||||||||||||Display sickle cell disease. Mice develop anemia from 3 weeks of age. Lethality occurs at variable rates (after 3 months). |Normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|||heterozygous intercrosses|No|08-Apr-2014|Cryopreserved sperm|||Unknown||Sickle cell disease, haematology|Yes| 7654.0|Hbbtm2(HBG1,HBB*)Tow|C57BL/6-Hba Hbb Hbb/MarpApb||Dominant|hemoglobin beta chain complex|Hbb|||MGI:96020|hemoglobin beta chain complex; targeted mutation 3, Timothy Townes|Hbb|MGI:3790756|7|||||||||||||||||||||||||||||Display sickle cell disease. Mice develop anemia from 3 weeks of age. Lethality occurs at variable rates (after 3 months). |Normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|||heterozygous intercrosses|No|08-Apr-2014|Cryopreserved sperm|||Unknown||Sickle cell disease, haematology|Yes| 7677.0|Egr2-GFP|C57BL/6-Egr2/JhmiAnu||Dominant|early growth response 2|Egr2||Egr-2, Krox20, Krox-20, NGF1-B, Zfp-25|MGI:95296||||10|||||||||||||||||||||||||||||Normal||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|09-May-2014|Cryopreserved sperm|11.0|0.0|Unknown|||Yes| 7714.0|UK dep|C57BL/6-Zdhhc21/MarpApb||Recessive|zinc finger, DHHC domain containing 21| Zdhhc21|Unknown|9130404H11Rik, D130004H04Rik, dep|MGI:1915518|zinc finger, DHHC domain containing 21; depilated|Zdhhc21|MGI:1856841|4|||||||||||||||||||||||||||||Abnormal coat appearance:• identifiable at about 1 week of age when first coat appearsabnormal hair shaft melanin granule morphology• clumps of pigment appear to be the remains of degenerating follicles• excessive accumulation and clumping of pigment in the hairAbnormal hair growth.Premature hair loss:• some mice are nearly hairless at 3 weeks of age; others may have a nearly normal coat.Short hair.Sparse hair.Matted coat.Greasy coat.Abnormal hair medullary septa cells:• 20% of coat hairs show an irregular arrangement of septa or complete interruption of septa.Abnormal hair follicle morphology.Abnormal hair follicle orientation.Abnormal hair cycle.Abnormal epidermal layer morphology:• dermal-epidermal recombination grafts of embryonic skin shows this allele acts in the epidermis.Enlarged sebaceous gland:• enlarged sebaceous glands with an excess of sebumSebaceous gland hyperplasia:• mild sebaceous gland hyperplasia at P5Abnormal sebaceous gland physiology:• increase in the percentage of BrdU positive, proliferating cells that are observed in sebaceous glandsAbnormal sebaceous lipid secretion:• excess of sebum|Wildtype|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||11||No|02-Jul-2014|Cryopreserved sperm|40.0|0.0|Unknown||palmitoylation, hair follicles|Possibly| 7815.0|MPS IIIA Knock out|C57BL/6-Sgsh/LdruApb|ldru|Recessive|N-sulfoglucosamine sulfohydrolase (sulfamidase)|Sgsh|Unknown|4632406A19Rik, sulphamidase|MGI:1350341||||11|||||||||||||||||||||||||||||We anticipate that the phenotype of MPS IIIA knock-out mice will be similar to our well-characterised present mouse model of MPS IIIA that expresses ~3% residual sulphamidase activity. This includes storage of heparan sulphate in tissues and fluids and behavioural changes such as altered locomotor activity and anxiety-related behaviours, memory and learning defects and changes in the walking pattern (gait) of the mice.|Expected to be normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|0|8|brother X sister|No|15-Dec-2014|Cryopreserved sperm|50.0|0.0|Yes|Sanfilippo syndrome (Mucopolysaccharidosis IIIA)||Possibly| 7716.0|Fras1|B6.Cg-Fras1/MarpApb||Dominant|Fraser syndrome 1 homolog (human)|Fras1|Unknown|bl, E130113P14Rik, mKIAA1500|MGI:2385368|Fraser syndrome 1 homolog (human); blebbed|Fras1|MGI:1856691|5|||||||||||||||||||||||||||||Embryonic lethal.• most homozygotes die before birth• however, a few reach adulthood with no signs of skin blisteringSyndactyly:• adult homozygotes exhibit distal limb defects, such as syndactyly of the hind limbs.Clubfoot:• homozygotes may exhibit clubbed feet or hands.Abnormal kidney development:• at E11.5-E15.5, homozygotes show a range of defects in metanephric kidney development, followed by degeneration of early metanephric rudiments• however, 20% of homozygous mutant embryos display a relatively normal metanephric development, including formation of glomeruli by E15.5Abnormal metanephric mesenchyme morphology:• by E13.5-E14.5, the metanephric mesenchyme is poorly differentiated with many cells containing pyknotic nuclei suggestive of apoptosis.Increased metanephric mesenchyme apoptosis:• by E13.5-E14.5, many cells contain pyknotic nuclei suggesting apoptosis.Abnormal metanephros morphology:• at E11.5-E15.5, some homozygotes display small and pooorly differentiated metanephroi, followed by degeneration of early metanephric rudiments.Delayed kidney development:• by E13.5-E14.5, mutant kidneys appear developmentally delayed and are much smaller than those of wild-type mice.Small kidney:• at E13.5-E14.5Absent kidney:• homozygotes may lack one or both kidneys.Kidney cysts:• 2 of 146 live-born survivors display grossly cystic kidneysSingle kidney:• homozygotes may exhibit only one kidney.• 20 of 146 live-born survivors display complete unilateral renal agenesis.Abnormal ureteric bud morphology:• at E11.5-E12.5, homozygous mutant embryos exhibit a dilated uteric bud.Impaired branching involved in ureteric bud morphogenesis:• at E11.5-E12.5, homozygous mutant embryos display reduced ureteric bud branching relative to wild-type embryos.Microphthalmia:• homozygotes display reduced eyesCryptophthalmos:• adult homozygotes display cryptophthalmosAbnormal hair growth:• homozygotes often display abnormal hair development between the eyesBleb:• blebs are still visible at birthFetal bleb:• at E14.5, homozygotes display prominent blebs over the rump and smaller blebs over the head and forelimb• however, homozygotes that survive and are live-born show no signs of skin blistering.|wildtype|C57BL/6|No|No|Yes|No|No|Yes|No|Good|7|4||No|02-Jul-2014|Cryopreserved sperm|80.0|0.0|Yes|Fraser Syndrome|Fraser Syndrome|Possibly| 7732.0|A/J - Joey-RSA|A/J.B6-Rbm5/MarpApb||Recessive|RNA binding motif protein 5|Rbm5|Unknown||MGI:1933204|RNA binding motif protein 5; spermatid differentiation arrest|Rbm5|MGI:5563424|9|ENSMUSG00000032580|ENSMUST00000035199|Rbm5-201|788|940|G to C|ENSMUSE00000251397|10|63|Arginine to Proline|||||CTATGCTTCCTTAGCTGTCAATAACATTCGCCTCATAAAAGACAAACAGACACAACAGAAC|Yes|||||||||||||Embryonic lethal|Round spermatid arrest.|A/JMarp|No|No|Yes|No|No|Yes|No|Unknown|8|||No|05-Sep-2014|Cryopreserved sperm|50.0|0.0|Unknown||infertility, sperm, arrest, ENU|Yes| 7739.0|Pax5-Exon 8|C57BL/6NJAnu-Pax5/AnuApb||Recessive|paired box 5|Pax5||EBB-1, Pax-5|MGI:97489||||4|||||||||||||||||||||||||||||B cell||C57BL/6JAnu|Yes|Unknown|Yes|Yes|Unknown|Yes|No|Unknown||||No|12-Sep-2014|Cryopreserved sperm|22.0|0.0|Unknown|||Yes| 7799.0|Krt76 tm1a|B6(Cg)-Krt76/MarpApb||Dominant|keratin 76|Krt76|Reduced|2310001L23Rik|MGI:1924305|keratin 76; targeted mutation 1a, Wellcome Trust Sanger Institute|Krt76|MGI:4363117|15|||||||||||||||||||||||||||||Unkempt, dull coats and smaller body size, scaling of skin of the tail, abnormal paw pad hyperpigmentation |Abnormal sebaceous gland morphology, abnormal hair cycle, abnormal epidermis stratum basale morphology, hyperkerotosis, parakerotosis|C57BL/6J|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|2|6||No|26-Nov-2014|Cryopreserved sperm|50.0|0.0|No||Keratin 76, tight junctions, CLDN1, inflammation, skin|Possibly| 8155.0|NODlga|NOD-Ifngr1||Recessive|Interferon gamma receptor 1|Ifngr1|Unknown|CD119, Ifgr, IFN-gammaR, IFN-gamma R, Ifngr, Nktar|MGI:107655||em10Tcb||10|||||||||||||||||||||||||||||Unknown|Unknown|NOD/LtJ|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|16-Dec-2016|Cryopreserved sperm|50.0|0.0|Yes|Type 1 diabetes||Possibly| 7816.0|Heterozygote MPS IIIA KO / Transgenic control|C57BL/6-Sgsh Sgsh/Apb|ldru|Recessive|N-sulfoglucosamine sulfohydrolase (sulfamidase)|Sgsh|Unknown|4632406A19Rik, sulphamidase|MGI:1350341||||11||||||||||Unknown to Unknown|||||||||||||||||||We anticipate that the phenotype of MPS IIIA knock-out mice will be similar to our well-characterised present mouse model of MPS IIIA that expresses ~3% residual sulphamidase activity. This includes storage of heparan sulphate in tissues and fluids and behavioural changes such as altered locomotor activity and anxiety-related behaviours, memory and learning defects and changes in the walking pattern (gait) of the mice.|Expected to be normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|0|4|brother X sister|No|15-Dec-2014|Cryopreserved sperm|49.0|0.0|Yes|Sanfilippo syndrome (Mucopolysaccharidosis IIIA)|MPS IIIA , Sanfilippo syndrome, Knockout|Possibly| 7816.0|Heterozygote MPS IIIA KO / Transgenic control|C57BL/6-Sgsh Sgsh/Apb|ldru|Recessive|N-sulfoglucosamine sulfohydrolase (sulfamidase)|Sgsh||4632406A19Rik, sulphamidase|MGI:1350341||||11|||||||||||||||||||||||||||||We anticipate that the phenotype of MPS IIIA knock-out mice will be similar to our well-characterised present mouse model of MPS IIIA that expresses ~3% residual sulphamidase activity. This includes storage of heparan sulphate in tissues and fluids and behavioural changes such as altered locomotor activity and anxiety-related behaviours, memory and learning defects and changes in the walking pattern (gait) of the mice.|Expected to be normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|0|4|brother X sister|No|15-Dec-2014|Cryopreserved sperm|||Yes|Sanfilippo syndrome (Mucopolysaccharidosis IIIA)|MPS IIIA , Sanfilippo syndrome, Knockout|Possibly| 7857.0|Sppl2a:Ctss KO|C57BL/6JAnu-Sppl2a Ctss/AnuApb|C57BL/6JAnu-Sppl2a Ctss/AnuApb|Recessive|signal peptide peptidase like 2A|Sppl2a|Unknown|2010106G01Rik, C130089K23Rik|MGI:1913802 |signal peptide peptidase like 2A; mutation 1, The Australian National University|Sppl2a|MGI:5432126|2|ENSMUSG00000027366|ENSMUST00000028844|2010106G01Rik-001||||||||126746052|7|||ATTCATAGGATGCCATGTGGACAGTGCACGTACGTATCTGTTAGCCTATGATGCAATTAG||||||||||||||Unknown|Normal|C57BL/6JAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|10-Mar-2015|Cryopreserved sperm|33.0|0.0|Unknown||lymphocyte, B cell, IgD, ENU, immunoglobulin|Yes| 7857.0|Sppl2a:Ctss KO|C57BL/6JAnu-Sppl2a Ctss/AnuApb|C57BL/6JAnu-Sppl2a Ctss/AnuApb|Recessive|cathepsin S|Ctss|Nil|Cat S|MGI:107341|cathepsin S; targeted mutation 1, Harold A Chapman|Ctss|MGI:2182133|3|||||||||||||||||||||||||||||Unknown|Normal|C57BL/6JAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|10-Mar-2015|Cryopreserved sperm|||Unknown||lymphocyte, B cell, IgD, ENU, immunoglobulin|Yes| 7860.0|Rosa26-Cryab floxed knockin|B6;C-Gt(ROSA)26Sor/KkhaApb||Recessive|gene trap ROSA 26, Philippe Soriano|Gt(ROSA)26Sor|Increased|beta geo, Gtrgeo26, Gtrosa26, R26, ROSA26|MGI:104735|Rosa26-Cryab-KI|Cryab-FLAG||6|||||||||||||||||||||||||||||Floxed mice are viable and fertile|floxed mice are viable and fertile|C57BL/6 and Balb/C mixed background|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|18-Mar-2015|Cryopreserved sperm|50.0|0.0|Unknown||crystallin|Possibly| 7871.0|Sppl2a KO1 conditional|B6.Cg-Sppl2a Tg(ACTFLPe)9205Dym/1MarpAnuApb||Recessive|signal peptide peptidase like 2A|Sppl2a|Unknown|2010106G01Rik, C130089K23Rik|MGI:1913802|signal peptide peptidase like 2A; targeted mutation 1a, Helmholtz Zentrum Muenchen GmbH|Sppl2a|MGI:4887673|2|||||||||||||||||transgene insertion 9205, Susan Dymecki|ACTB, actin, beta, human|The FLPe recombinase variant exhibits enhanced thermostability with recombination activity being 4X and 10X that of wildtype FLP at 37°C and 40°C, respectively||||||||||Normal|Normal|C57BL/6NCrlAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|16-Apr-2015|Cryopreserved sperm|66.0|0.0|Unknown||Conditional|Possibly| 7893.0|ENU31:014:Itgb2|C57BL/6NCrlAnu-Itgb2/AnuApb||Recessive|integrin beta 2|Itgb2||2E6, Cd18, Mac-1 beta|MGI:96611||||10|ENSMUSG00000000290|ENSMUST00000000299|Itgb2-001|857|1068|G to T|ENSMUSE00001306558|7|286|Cysteine to Phenylalanine|||||TGCCATCCTGACCCCCAATGATGGCCGCTGCCACCTGGAGGATAACATGTACAAGAGGAGC|Unknown|||||||||||||Activated T cells in blood|Normal|C57BL/6NCrlAnu|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||1||No|15-May-2015|Cryopreserved sperm|44.0|0.0|Unknown||ENU, random, mutagenesis, screen, T cell|Yes| 7903.0|APN 405; Immp2l|C57BL/6NTac-Immp2l/MarpApb||Recessive|IMP2 inner mitochondrial membrane peptidase-like (S. cerevisiae)|Immp2l|Unknown|IMP2|MGI:2135611|IMP2 inner mitochondrial membrane peptidase-like (S. cerevisiae); gene trap IST11147G7, Texas A&M Institute for Genomic Medicine|Immp2l|MGI:3992884|12|||||||||||||||||||||||||||||Tourette like hyperactive and repetitive behaviour|Tourette like hyperactive and repetitive behaviour|C57BL/6NTacMarp|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|||Bro x sis; het x het and hom x het|No|10-Jun-2015|Cryopreserved sperm|100.0|0.0|Unknown|||Possibly| 7937.0|ENU29:005:Tmem30a|C57BL/6NCrlAnu-Tmem30a/AnuApb||Recessive|transmembrane protein 30A|Tmem30a|Unknown|2010200I23Rik, Cdc50a, D9Wsu20e|MGI:106402||Tmem30a||9|ENSMUSG00000032328|ENSMUST00000034878|Tmem30a-001||||||||79775100|6|||AAAAGAGAGCCTCGAAGAAAAGTTTAAAGGTAAAATATGATCAATATCCCTTCTTGTCTA||||||||||||||Embryonic Lethal|Normal|C57BL/6NCrlAnu|No|No|Yes|No|No|Yes|No|Unknown||||No|26-Jun-2015|Cryopreserved sperm|54.0|0.0|Unknown||Embryonic lethal, ENU|Yes| 8033.0|Foxn1-cre x Atg5 loxp|B6.129-Atg5 Foxn1/Wehi||Recessive|autophagy related 5|Atg5|Normal|2010107M05Rik, 3110067M24Rik, Apg5l, Paddy|MGI:1277186|autophagy related 5; targeted mutation 1, Minesuke Yokoyama|Atg5|MGI:3663625|10|||||||||||||||||||||||||||||Normal||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|04-Apr-2016|Cryopreserved sperm|10.0|0.0|Unknown||Autophagy, dendritic cell|Yes| 8033.0|Foxn1-cre x Atg5 loxp|B6.129-Atg5 Foxn1/Wehi||Recessive|forkhead box N1|Foxn1|Normal|D11Bhm185e, Hfh11, whn|MGI:102949|forkhead box N1; targeted mutation 3, Nancy R Manley|Foxn1|MGI:3760775|11|||||||||||||||||||||||||||||Normal||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|04-Apr-2016|Cryopreserved sperm|||Unknown||Autophagy, dendritic cell|Yes| 7984.0|Recql4 K525A|C57BL/6-Recql4||Dominant|RecQ protein-like 4|Recql4|Nil||MGI:1931028|Recql4|Recql4 K525A||15|||||||||||||||||||||||||||||As young mice no phenotype is yet apparent (8-12 week old) homozygous PM. Fertility unknown at this point|Hets appear normal and fertile|C57BL/6|Yes|Unknown|Yes|Yes|Unknown|Yes|No|Excellent|generated on pure C57BL/6 so not backcrossed. Only maintained on C57|NA|PM/+ to either PM/+ or WT|No|27-Oct-2015|Cryopreserved sperm|30.0|0.0|Yes|Rothmund-Thomson Syndrome|Recql4|Possibly| 8009.0|Dll1null|B6-DII1/DunwApb||Recessive|delta-like 1 (Drosophila)|Dll1|||MGI:104659|delta like canonical Notch ligand 1; targeted mutation 1.1, Michael J Owen|DII1|MGI:5431502|17||||||||||Unknown to Unknown|||||||||||||||||||Dll1 homozygous embryos die during gestation|Normal|C57BL/6J|No|No|No|No|No|No|Yes|Poor||||No|10-Dec-2015|Cryopreserved sperm|50.0|0.0|Unknown||Embryonic lethal|Possibly| 8077.0|Fcho1|B6(Cg)-Fcho1/AnuApb||Recessive|FCH domain only 1|Fcho1|Unknown|3322402E17Rik|MGI:1921265||||8|||||||||||||||||||||||||||||Unknown||C57BL/6NCrlAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|17-Jul-2016|Cryopreserved sperm|10.0|0.0|Unknown|||Yes| 8089.0|RHBDF1 KO|C57BL/6-Rhbdf1/MarpApb||Recessive|rhomboid 5 homolog 1|Rhbdf1||Dist, Dist1, Egfr-rs|MGI:104328||||11|||||||||||||||||||||||||||||Unknown|Unknown|C57BL/6|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|24-Aug-2016|Cryopreserved sperm|50.0|0.0|Unknown|||Yes| 8092.0|HoxB7-Cre|C57BL/6-Tg(Hoxb7-cre)13AmcMarpApb||Dominant||||||||||||||||||||||||||transgene insertion 13, Andrew P McMahon|Hoxb7, homeobox B7, mouse, laboratory|||||||||||Not viable|Mice hemizygous for the transgenic insert are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. |C57BL/6|No|No|Yes|No|No|Yes|No|Unknown||||No|31-Aug-2016|Cryopreserved sperm|50.0|0.0|Unknown||Cre recombinase|Yes| 8100.0|ASD601:Mertesacker|C57BL/6NCrlAnu-Vps51/AnuApb||Recessive|VPS51 GARP complex subunit|Vps51|Unknown|1110014N23Rik, 3110057M17Rik|MGI:1915755||||19|ENSMUSG00000024797|ENSMUST00000159832.7|Vps51-001|233|659|G to C|ENSMUSE00001277360|3|78|Arginine to Proline|||||CGACCCGGAAGTTTATCTTGACAAGCTGCGTAGAGAATGTCCTCTGGCCCAGCTGATGGAC||||||||||||||Embryonic lethal||C57BL/6NCrlAnu|No|No|Yes|No|No|Yes|No|Unknown||||No|09-Sep-2016|Cryopreserved sperm|55.0|0.0|Unknown|||Yes| 8121.0|Foxb1|B6.129X1-Foxb1/Anu||Dominant|forkhead box B1|Foxb1||C43, Fkh5, Foxb1a, Foxb1b, Hfh-e5.1, Mf3, TWH|MGI:1927549|forkhead box B1; targeted mutation 1, Gonzalo Alvarez-Bolado|Foxb1|MGI:3772366|9|||||||||||||||||||||||||||||No phenotypic analysis||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|27-Oct-2016|Cryopreserved sperm|43.0|0.0|Unknown||Cre recombinase|Yes| 9304.0|ENU34:001:62b:Foxp3GFP:F9|RelbL281Q ; ENU34-Relb||Dominant|only for L2 reder||||||||Unknown|||||||||||||||||||||||||||||||C57Bl/6N|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|17-Nov-2021||0.0|60.0|Unknown|||No| 8150.0|NODCrisprGzmA|NOD-Gzma||Recessive|granzyme A|Gzma|Unknown|BLT esterase, Ctla3, Ctla-3, Hanukah factor, Hf, H factor, SE1, serine esterase 1, TSP1, TSP-1|MGI:109266||em2Tcb||13|||||||||||||||||||||||||||||Unknown|Unknown|NOD/LtJ|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|15-Dec-2016|Cryopreserved sperm|50.0|0.0|Yes|Type 1 diabetes||Possibly| 8622.0|Zeb1 fl K5-creERt R26-YAP5SA|STOCK Zeb1 Gt(ROSA)26Sor<(CAGGS-Yap5SA,LacZ)Mao> Tg(KRT5-cre/ERT2)2Ipc||Recessive|gene trap ROSA 26, Philippe Soriano|Gt(ROSA)26Sor||beta geo, Gtrgeo26, Gtrosa26, R26, ROSA26, Thumpd3as1|MGI:104735||||6|||||||||||||||||transgene insertion 2, I Pierre Chambon||||||||||||Overexpression of activated YAP (NLS-YAP-5SA) with Keratin-5 (K5-CreERt) is sufficient to induce rapid formation of both SCC and spSCC in mice. spSCC tumours arise at sites of epithelial scratch wounding, where tumour-initiating epithelial cells undergo EMT to generate spSCC. Expression of the EMT transcription factor ZEB1 arises upon wounding and is a defining characteristic of spSCC in mice and humans. Thus, the wound healing response synergises with YAP to drive metaplastic transformation of SCC to spSCC.||C57BL/6J|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|18-Dec-2018|Cryopreserved sperm|55.0|106.0|Unknown||Hippo, epithelium, Squamous cell carcinoma (SCC) , epithelial-mesenchymal transition (EMT)|Yes| 8622.0|Zeb1 fl K5-creERt R26-YAP5SA|STOCK Zeb1 Gt(ROSA)26Sor<(CAGGS-Yap5SA,LacZ)Mao> Tg(KRT5-cre/ERT2)2Ipc||Recessive|zinc finger E-box binding homeobox 1|Zeb1|Unknown|3110032K11Rik, AREB6, [delta]EF1, MEB1, Nil2, Tcf18, Tcf8, Tw, ZEB, Zfhep, Zfhx1a, Zfx1a |MGI:1344313|zinc finger E-box binding homeobox 1; targeted mutation 1.1, Marc Stemmler|Zeb1|MGI:5901939|18|||||||||||||||||||||||||||||Overexpression of activated YAP (NLS-YAP-5SA) with Keratin-5 (K5-CreERt) is sufficient to induce rapid formation of both SCC and spSCC in mice. spSCC tumours arise at sites of epithelial scratch wounding, where tumour-initiating epithelial cells undergo EMT to generate spSCC. Expression of the EMT transcription factor ZEB1 arises upon wounding and is a defining characteristic of spSCC in mice and humans. Thus, the wound healing response synergises with YAP to drive metaplastic transformation of SCC to spSCC.||C57BL/6J|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|18-Dec-2018|Cryopreserved sperm|||Unknown||Hippo, epithelium, Squamous cell carcinoma (SCC) , epithelial-mesenchymal transition (EMT)|Yes| 326.0|spasmodic|B6.C3Fe a/a-Glra1||Recessive|glycine receptor, alpha 1 subunit|Glra1|Unknown|B230397M16Rik, nmf11, oscillator, ot|MGI:95747|spasmodic|Glra1|MGI:1856362|11||||||||||||||||Yes|||||||||||||Impaired righting response:exhibit difficulty in regaining an upright posture when turned on their sides.response improved in mice receiving IP injections of aminooxyacetic acid, 15 micrograms/gm body weightLimb grasping:tend to clasp their hind feet when picked up by the tail and spunTremors: at rest, in a quiet cage, appear normal but are hyperexcitable and shake rapidly when disturbed.Exhibit a rapid tremor when picked up by the tail, however show no differences in the levels of the major CNS and PNS myelin proteins of lipidsAbnormal posture: stiff postureHyperactivity: mimics sublethal strychnine intoxicationAbnormal gait: walk slowly and on their toesMale infertility: males appear unable to breedImpaired acrosome reaction: the zona pellucida-initiated acrosome reaction is significantly decreased compared to wild-typeImpaired fertilization: in mutants, the zona pellucida-initiated acrosome reaction is significantly decreased compared to wild-type||C57BL/6 x C3HeB/Fe|Yes|Yes|Yes|Yes|No|Yes|Yes|Poor||||No|05-May-2006||0.0|0.0|Yes||ataxia, tremors, Hyperekplexia, glycine receptor, hypertonia|Yes| 10290.0|BL6.Crisp1em2 MGMP Crisp2 em4 MGMP/MkobMarp/J|C57BL/6J-Crisp1<(em2) MGMP-Mkob>Crisp2<(em4)MGMP-Mkob>MarpApb||Recessive|cysteine-rich secretory protein 1|CRISP1 ||Aeg1, CRISP-1|MGI:102553||CRISP1/2 DKO||17|||||||||||||||||||||||||||||Infertile|Normal|C57Bl/6J|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|14-Feb-2023|Cryopreserved sperm|50.0|0.0|Unknown|||Possibly| 10290.0|BL6.Crisp1em2 MGMP Crisp2 em4 MGMP/MkobMarp/J|C57BL/6J-Crisp1<(em2) MGMP-Mkob>Crisp2<(em4)MGMP-Mkob>MarpApb||Recessive|cysteine-rich secretory protein 2|Crisp2||CRISP-2, GAPDL5, Tpx1, Tpx-1|MGI:98815||CRISP1/2 DKO||17|||||||||||||||||||||||||||||Infertile|Normal|C57Bl/6J|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|14-Feb-2023|Cryopreserved sperm|||Unknown|||Possibly| 10293.0||C57BL/6J-Crisp4/MarpApb||Semi-dominant|cysteine-rich secretory protein 4|CRISP4|||MGI:1925331||||1|||||||||||||||||||||||||||||Subfertile|Normal|C57Bl/6J|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|14-Feb-2023||0.0|0.0|Unknown|||Possibly| 8671.0|Il18 KO|B6.129P2-Il18/JAnu||Recessive|interleukin 18|Il18|Nil|Igif, Il-18|MGI:107936|interleukin 18; targeted mutation 1, Shizuo Akira|Il18|MGI:2136769|9|||||||||||||||||||||||||||||Impaired neutrophil chemotaxis: • less numbers of neutrophils are recruited to the lung both 6- and 24 hours after infection with Haemophilus influenzae.Increased susceptibility to induced colitis: • mice exhibit increased susceptibility to dextran sodium sulfate (DSS)-induced colitis compared with similarly treated wild-type mice• mice transmit increased susceptibility to DSS-induced colitis to co-housed wild-type mice.Increased susceptibility to bacterial infection: • bacterial counts in the lung are 20-fold higher one day after infection with Haemophilus influenzae• there is less inflammation present in the lungs 6- and 24- hours after infection with histological scores significantly reduced compared to wild-type mice• mice are able to clear infection from the lungs 10 days after infection, which is similar to wild-type mice.Abnormal gut flora balance: • mice and co-housed wild-type mice exhibit expanded bacterial phylotypes compared with wild-type mice||C57BL/6J|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|04-Mar-2019||0.0|0.0|Unknown||Cytokine, Macrophage, LPS|Yes| 8796.0|Casp1 KO|B6.Cg-Casp1/JAnuApb||Recessive|caspase 1|Casp1|Nil|Caspase-1, ICE, Il1bc, interleukin 1 beta-converting enzyme|MGI:96544|caspase 1; endonuclease-mediated mutation 1, Russell Vance|Casp1|MGI:6246541|9||||||||||||||||||||||||||||||||Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|30-Sep-2019||0.0|0.0|Unknown||Inflammasome, Caspase|Yes| 9201.0|ASD896:Eureka|C57Bl/6N-Setd5/Apb||Semi-dominant|SET domain containing 5|Setd5|||MGI:1920145|Setd5; endonuclease-mediated mutation 2, Australian National University|Setd5||6|||||||||||||||||||||||||||||may develop symptoms of autoimmune disease |may develop symptoms of autoimmune disease |Bcl6|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|07-Jun-2021|Cryopreserved sperm|24.0|0.0|Unknown|||Possibly| 5228.0||Osr-1 GFP||Dominant|odd-skipped related 1 (Drosophila)|Osr1||Odd1|MGI:1344424||||12||||||||||||||||Yes|||||||||||||Kidney abnormality|Normal|CD1|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|05-Oct-2010|Cryopreserved sperm|50.0|0.0|Unknown||kidney, nephron|No| 8234.0|Il21r KO_Smarta_Ly5a|B6.Cg-Il21r Ptprc Tg(TcrLCMV)Aox/MarpAnu||Semi-dominant|interleukin 21 receptor|Il21r|Nil|NILR|MGI:1890475|interleukin 21 receptor; targeted mutation 1, Warren J Leonard|Il21r|MGI:2446509|7|||||||||||||||||transgene insertion, Annette Oxenius|||protein tyrosine phosphatase, receptor type, C|Ptprc||B220, CD45, Ly-5, Lyt-4, T200|MGI:97810|protein tyrosine phosphatase, receptor type, C; a variant|Ptprc|MGI:4819849|1|Lack of Il21 receptor expression.Il21r KO mice have:Abnormal immunoglobulin level.Increased IgE level:• serum levels of IgE in nave mice are higher than in controls• ovalbumin immunized mice have variable total IgE levels with some mice having levels similar to wild-type and some mice having 3- to 6- fold higher amounts• total IgE production is increased about 50-fold after KLH immunization with similar increases with antigen specific antibody• IgE levels are 20- to 25- fold greater than controls 100 days after infection with toxoplasma gondiiDecreased IgG1 level:• serum levels of IgG1 in nave mice are lower than in controls• after immunization with ovalbumin, the normal increase in IgG1 seen in wild-type mice is markedly impaired in these mice• in immunized mice, total serum IgG1 is 4 to 5% of wild-type and levels of antigen-specific antibody is 0.1% of that in wild-type• an impaired IgG1 response is also observed after keyhole limpet hemocyanin (KLH) immunization, with antigen specific antibodies being 1/10 of that found in wild-type• IgG1 levels are third of controls 100 days after infection with toxoplasma gondiiDecreased IgG2a level:• IgG2a levels are lower than controls 100 days after infection with toxoplasma gondiiDecreased IgG2b level:• serum levels of IgG2b in nave mice are lower than in controls• after ovalbumin immunization, levels of antigen specific IgGb2 antibody are significantly lower• an impaired IgG2b response is also observed after KLH immunization, with antigen specific antibodies being 1/10 of that found in wild-type• IgG2b levels are lower than controls 100 days after infection with toxoplasma gondiiDecreased IgG3 level:• after ovalbumin immunization, levels of antigen specific IgG3 antibody are significantly lower• an impaired IgG3 response is also observed after KLH immunization, with antigen specific antibodies being 1/10 of that found in wild-type• IgG3 levels are lower than controls 100 days after infection with toxoplasma gondiiAbnormal CD8-positive, alpha-beta T cell physiology:• CD8+ T cell proliferation in vitro is not enhanced in the presence of IL-15 in the same manner as wild-type CD8+ T cells• the percentage of antigen-specific CD8+ T cells found in the spleen is a third lower than controls after vaccination• the percentage of CD8+ T cells making IFN-gamma one week after vaccination is about half that of wild-type controlsDecreased cytotoxic T cell cytolysis:• the cytotoxic activity of CD8+ T cells is significantly lower than wild-type cellsDecreased interleukin-17 secretion:• IL-17 production by CD4 T cells is much lower than controls when activated with IL-6 and TGF-beta in vitro• there is no IL-17 production from T cells when activated in vitro with IL-21 and TGF-beta compared to the robust production of controlsExpresses TCR specific for LCMV GP-derived epitpoe P13||C57BL/6J|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|28-Mar-2017|Cryopreserved sperm|20.0|0.0|Unknown||LCMV, TCR, IL21 receptor, immunoglobulin|Yes| 8847.0|Trpa1 KO|B6;129P-Trpa1/JAnu||Recessive|transient receptor potential cation channel, subfamily A, member 1|Trpa1|Nil|ANKTM1|MGI:3522699|transient receptor potential cation channel, subfamily A, member 1; targeted mutation 1, Kelvin Y Kwan|Trpa1|MGI:3624810|1|||||||||||||||||||||||||||||Hyporesponsive to tactile stimuli:• homozygous mutants are less sensitive to punctate mechanical stimuli relative to littermates; fewer mutants show a pain response than wild-type and the average threshold is higher in mutants• 2 hours after injection with bradykinin, the threshold for mechanical sensitivity is unchanged in mutants while it is reduce 5-fold in wild-typeAbnormal thermosensation:• mutants show reduced sensitivity to the cooling sensation elicited by a drop of acetone on the hindpaw compared with wild-type and heterozygotes: differences between wild-type and mutants is greater for females than malesIncreased thermal nociceptive threshold.Decreased threshold for auditory brainstem response:• at frequency of 32kHz in an ABR test, mutant mice are more sensitive than wild-type, however, results are similar to controls at all other frequencies tested• hearing and vestibular function are normal as assesed by behavioral tests• whole-cell transduction currents in mouse utricular hair cells are similar to controlsAbnormal taste sensitivity:• knockout mice consume more mustard oil-containing water than wild-type or heterozygotes; at the highest concentration, mutants consume more than one third of the normal amount||C57BL/6J|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|04-Feb-2020|Cryopreserved sperm|58.0|0.0|Unknown||nociceptor|Yes| 9021.0|Lang-EGFP|B6.129S2-Cd207tm2Mal/J||Dominant|CD207 antigen (Langerin)|CD207|Unknown|Clec4K|3581825|Cd207tm2Mal|||6|||||||||||||||||||||||||||||Lang-EGFP mutant mice contain an internal ribosome entry site (IRES) and an enhanced green fluorescent protein (EGFP) downstream of the internal stop codon of the CD207 antigen (Cd207 or Langerin) gene. Homozygotes are viable, fertile, and normal in size. Langerin is a transmembrane receptor produced by specialized antigen-presenting cells located in the skin called Langerhans cells (LCs), and other dendritic cells including dermal DCs and splenic CD8+ DCs. Langerin is specifically localized in the Birbeck granules, where it is necessary for their formation. In these mice, EGFP expression is evident in the cytosol of immature Langerin-derived DCs and CD8+ DCs and is decreased upon LC maturation. These mice may be useful for visualizing Langerhans cells and monitoring their movement during inflammation.|similar to homozygous|C57BL/6J (This mouse line was obtained from Bernard Malissen via William Heath (PDI, Melbourne)). An MTA was signed with B Malissen and his authorisation is required for anyone requesting the line)|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|should be more than 10 according to the source|unknown||No|23-Jun-2020||0.0|0.0|No||Langerin, Langerhans cells, Liver capsular macrophages, epidermis, dendritic cells |Possibly| 9022.0|Macblue|B6.Cg-Tg(Csf1r*-GAL4/VP16,UAS-ECFP)1Hume/JApb||Dominant||||||||||||||||||||||||||transgene insertion 1, David A Hume|CSF1R promoter lacking the 158 bp (-454 to -298 relative to ATG) trophoblast transcription start sites and a TATA-box |||||||||||MacBlue transgenic mice express enhanced cyan fluorescent protein (ECFP) from a truncated colony stimulating factor 1 receptor (Csf1r) promoter using the binary yeast Gal4-UAS system. The Gal4-UAS system utilizes a transgene that consists of both Gal4-expressing and Gal4-reporting modules to drive the expression of the ECFP reporter in Csf1r-expressing cells. In this strain, the Csf1r promoter lacks the 150 bp trophoblast and osteoclast-specific transcription start sites, directing reporter expression specifically in macrophages. Hemizygotes are viable and fertile. All ECFP+ cells in peripheral blood of MacBlue mice are CD11b-positive, and are negative for lymphocyte markers. 10% of granulocytes in peripheral blood and bone marrow express ECFP, as do Ly6C+ and Ly6C- monocytes. All ECFPhi leukocytes express the monocyte/macrophage marker F4/80. 7% of bone marrow cells are ECFP+. ECFP was also detected in adult dendritic cells and blood monocytes in the gut, microglia and Langerhans cells, Peyer’s patches and isolated lymphoid follicles. These mice may be bred to mice carrying tagged proteins under control of the Gal4-dependent promoter to direct expression of that protein in mononuclear phagocytes.|similar to homozygous mice|C57BL6/J|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|23-Jun-2020||0.0|0.0|Unknown|||Yes| 10466.0|NODk_TCH|NOD.Cg-H2/Anu||Dominant|histocompatibility-2, MHC|H2||MHC-II|MGI:95894|Histocompatibility H2k variant|H2k||17|||||||||||||||||||||||||||||This strain is prone to develop diabetes with western diet feeding|Not applicable|NOD|Yes|Yes|Unknown|Yes|Yes|Unknown|No|Poor|N5F10RF14|||No|20-Jan-2025||0.0|34.0|Unknown|||Possibly| 10468.0|Foz:NOD.B10:R97/16|NOD(Cg)-H2 Alms1/Anu||Dominant|ALMS1, centrosome and basal body associated|Alms1||Alstrom syndrome 1|MGI:1934606|Alms1:Fat Aussie|Alms1:Foz||6|ENSMUSG00000063810||||||||||||||||||||||||||||NOD.B10 mice homozygous for foz/foz mutation develop obesity and with high fat feeding fatty liver disease and diabetes.|Normal|NOD.B10 Hybrid|Unknown|Unknown|Unknown|Unknown|No|Unknown|No|Unknown||||No|20-Jan-2025||0.0|116.0|Unknown|||No| 10469.0|Maggott|Nod/K.B6-Slc6a19/Anu||Dominant|solute carrier family 6 (neurotransmitter transporter), member 19|Slc6a19|||MGI:1921588|Slc6a19:13g2-5Del|Slc6a19:13g2-5Del||13|||||||||||||||||||||||||||||NODk.Slc6a19+/+ (WT) mice develop a western diet induced obesity and type 2 diabetesHomozygous NODk.Slc6a19-/- (mutant) mice develop neutral aminoaciduria are less prone to develop western diet induced hyperglycaemia and diabetes|As for WT mice.|NOD.Cg-H2/Anu|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|20-Jan-2025||0.0|281.0|Unknown|||No| 10480.0|Csf1rflox|B6.Cg-Csf1r/J||Recessive|colony stimulating factor 1 receptor|Csf1r||Fim2, Fms|MGI:1339758|colony stimulating factor 1 receptor; targeted mutation 1.2, Jeffrey W Pollard| Csf1r|MGI:5780867|18|ENSMUSG00000024621 ||||||||||||||||||||||||||||These Csf1rfl/fl floxed mutant mice possess loxP sites flanking exon 5 of the colony stimulating factor 1 receptor (Csf1r) gene. Csf1r encodes Cd115 which acts as the receptor for colony stimulating factor 1, a cytokine which controls the production, differentiation, and function of macrophages. Expressed in macrophages, expression is also seen in oocytes, osteoclasts, trophoblasts, CNS microglia, and some myoblasts. Mice that are homozygous for this allele are viable and fertile. When these mutant mice are bred to mice that express Cre recombinase, resulting offspring will have exon 5 and the neo cassette deleted in cre-expressing tissues.|same as homozygous|C57Bl/6J|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|04-Feb-2025|Cryopreserved sperm|50.0|0.0|Unknown|||Possibly| 9307.0||C57Bl/6-Adar/Apb||Semi-dominant|adenosine deaminase, RNA-specific|Adar||ADAR1, Adar1p110, Adar1p150, mZaADAR|MGI:1889575|adenosine deaminase, RNA-specific; endonuclease-mediated mutation 1, Carl R Walkley|Adar|MGI:7514376|3||||||||||Unknown to Unknown|||||||||||||||||||Homozygous L196C/L196C is embryonic lethal at E11.5-E12.5. This mutation leads to the loss of the p150 isoform of ADAR1 specifically; p110 is expressed still. Phenotype similar to the full ADAR1 null mouse|Heterozygous animals are viable, fertile and normal|C57Bl/6N|No|Unknown|Unknown|No|Unknown|Unknown|No|Unknown||||No|26-Nov-2021|Cryopreserved sperm|40.0|0.0|Unknown|||Possibly| 10483.0|XCR1-DTRvenus|B6.Cg-Xcr1||Dominant|Chemokine receptor 1|Xcr1||GPR5, XCR1|MGI:1346338|chemokine (C motif) receptor 1; targeted mutation 2, Tsuneyasu Kaisho|Xcr1|MGI:5544058|9|ENSMUSG00000060509 ||||||||||||||||||||||||||||A chemokine receptor, XCR1, is a receptor for XCL1 and expressed dominantly in type 1 cDCs (cDC1s) one of the two main conventional dendritic cell subsets. XCR1-DTRvenus mice were generated by knocking the gene encoding a fusion protein consisting of human diphteria toxin receptor (DTR or HBEGF) and a fluorescence protein, venus (derived from Dr. Atsushi Miyawaki at BRI) into the murine XCR1 gene locus. In XCR1-DTRvenus mice, XCR1-expressing cells can be detected by venus expression and ablated transiently by the administration of diphteria toxin. Venus expression is very low and hard to detect. Homozygous mice do not express endogenous XCR1.|Same as homozygous mice except that heterozygous mice express endogenous XCR1.|C57Bl/6J|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|04-Feb-2025|Cryopreserved sperm|50.0|0.0|Unknown|||No| 9301.0|Jalapeno |B6.SJL-Ptprca Pepcb/BoyJ; Cx3cr1/J x Gt(ROSA)26Sor x B6129S7-Rag1/JAusb x Tg<(TcraHsv2.3,TcrbHsv2.3)L118-1Cbn> x Cxcr6/Apb ||Semi-dominant|protein tyrosine phosphatase receptor type C|Ptprc |||MGI:97810|protein tyrosine phosphatase receptor type C; a variant|Ptprc|MGI:4819849|1|||||||||||||||||transgene insertion L118-1, Frank Carbone||||||||||||TCR Transgenic mice expressing the transgenic gBT-1 TCR recognising the immunodominat epitope of HSV expressing the congenial marker CD45.1. These mice have been bred onto the RAG-1 ko background and also display restricted expression of GFP in CXCR6+ cells and Cre-dependent expression of Tomato in CX3CR1+ cells. In the homozygous state, they are CX3CR1-deficient, CXCR6-deficient, RAG1-/- deficient and Ly5.1+ Ly5.2- |In the heterozygous state (after breeding with B6 mice), het mice would be they express CX3CR1 and CXCR6 (one allele), RAG1 sufficient and Ly5.1+ Ly5.2+|C57Bl/6J|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|09-Nov-2021|Cryopreserved sperm|20.0|0.0|Unknown|||Possibly| 9301.0|Jalapeno |B6.SJL-Ptprca Pepcb/BoyJ; Cx3cr1/J x Gt(ROSA)26Sor x B6129S7-Rag1/JAusb x Tg<(TcraHsv2.3,TcrbHsv2.3)L118-1Cbn> x Cxcr6/Apb ||Semi-dominant|peptidase C|Pepc|||MGI:97541|peptidase C; b variant|Pepc|MGI:4819861|1|||||||||||||||||||||||||||||TCR Transgenic mice expressing the transgenic gBT-1 TCR recognising the immunodominat epitope of HSV expressing the congenial marker CD45.1. These mice have been bred onto the RAG-1 ko background and also display restricted expression of GFP in CXCR6+ cells and Cre-dependent expression of Tomato in CX3CR1+ cells. In the homozygous state, they are CX3CR1-deficient, CXCR6-deficient, RAG1-/- deficient and Ly5.1+ Ly5.2- |In the heterozygous state (after breeding with B6 mice), het mice would be they express CX3CR1 and CXCR6 (one allele), RAG1 sufficient and Ly5.1+ Ly5.2+|C57Bl/6J|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|09-Nov-2021|Cryopreserved sperm|||Unknown|||Possibly| 9301.0|Jalapeno |B6.SJL-Ptprca Pepcb/BoyJ; Cx3cr1/J x Gt(ROSA)26Sor x B6129S7-Rag1/JAusb x Tg<(TcraHsv2.3,TcrbHsv2.3)L118-1Cbn> x Cxcr6/Apb ||Semi-dominant|C-X3-C motif chemokine receptor 1|Cx3cr1|||MGI:1333815|C-X3-C motif chemokine receptor 1; targeted mutation 2.1, Steffen Jung|Cx3cr1tm2.1(cre/ERT2)Jung|MGI:5467985|9|ENSMUSG00000052336 ||||||||||||||||||||||||||||TCR Transgenic mice expressing the transgenic gBT-1 TCR recognising the immunodominat epitope of HSV expressing the congenial marker CD45.1. These mice have been bred onto the RAG-1 ko background and also display restricted expression of GFP in CXCR6+ cells and Cre-dependent expression of Tomato in CX3CR1+ cells. In the homozygous state, they are CX3CR1-deficient, CXCR6-deficient, RAG1-/- deficient and Ly5.1+ Ly5.2- |In the heterozygous state (after breeding with B6 mice), het mice would be they express CX3CR1 and CXCR6 (one allele), RAG1 sufficient and Ly5.1+ Ly5.2+|C57Bl/6J|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|09-Nov-2021|Cryopreserved sperm|||Unknown|||Possibly| 9301.0|Jalapeno |B6.SJL-Ptprca Pepcb/BoyJ; Cx3cr1/J x Gt(ROSA)26Sor x B6129S7-Rag1/JAusb x Tg<(TcraHsv2.3,TcrbHsv2.3)L118-1Cbn> x Cxcr6/Apb ||Semi-dominant|gene trap ROSA 26, Philippe Soriano|Gt(ROSA)26Sor||Gtrosa26, R26, ROSA26|MGI:104735|gene trap ROSA 26, Philippe Soriano; targeted mutation 9, Hongkui Zeng|Gt(ROSA)26Sor|MGI:3809523|6|ENSMUSG00000086429 ||||||||||||||||||||||||||||TCR Transgenic mice expressing the transgenic gBT-1 TCR recognising the immunodominat epitope of HSV expressing the congenial marker CD45.1. These mice have been bred onto the RAG-1 ko background and also display restricted expression of GFP in CXCR6+ cells and Cre-dependent expression of Tomato in CX3CR1+ cells. In the homozygous state, they are CX3CR1-deficient, CXCR6-deficient, RAG1-/- deficient and Ly5.1+ Ly5.2- |In the heterozygous state (after breeding with B6 mice), het mice would be they express CX3CR1 and CXCR6 (one allele), RAG1 sufficient and Ly5.1+ Ly5.2+|C57Bl/6J|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|09-Nov-2021|Cryopreserved sperm|||Unknown|||Possibly| 9301.0|Jalapeno |B6.SJL-Ptprca Pepcb/BoyJ; Cx3cr1/J x Gt(ROSA)26Sor x B6129S7-Rag1/JAusb x Tg<(TcraHsv2.3,TcrbHsv2.3)L118-1Cbn> x Cxcr6/Apb ||Semi-dominant|recombination activating 1|Rag1|||MGI:97848|recombination activating 1; targeted mutation 1, Peter Mombaerts|Rag1|MGI:1857241|2|ENSMUSG00000061311||||||||||||||||||||||||||||TCR Transgenic mice expressing the transgenic gBT-1 TCR recognising the immunodominat epitope of HSV expressing the congenial marker CD45.1. These mice have been bred onto the RAG-1 ko background and also display restricted expression of GFP in CXCR6+ cells and Cre-dependent expression of Tomato in CX3CR1+ cells. In the homozygous state, they are CX3CR1-deficient, CXCR6-deficient, RAG1-/- deficient and Ly5.1+ Ly5.2- |In the heterozygous state (after breeding with B6 mice), het mice would be they express CX3CR1 and CXCR6 (one allele), RAG1 sufficient and Ly5.1+ Ly5.2+|C57Bl/6J|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|09-Nov-2021|Cryopreserved sperm|||Unknown|||Possibly| 9301.0|Jalapeno |B6.SJL-Ptprca Pepcb/BoyJ; Cx3cr1/J x Gt(ROSA)26Sor x B6129S7-Rag1/JAusb x Tg<(TcraHsv2.3,TcrbHsv2.3)L118-1Cbn> x Cxcr6/Apb ||Semi-dominant|C-X-C motif chemokine receptor 6|Cxcr6||BONZO, STRL33|MGI:1934582|C-X-C motif chemokine receptor 6; targeted mutation 1, Daniel Littman|Cxcr6|MGI:3613526|9|ENSMUSG00000048521||||||||||||||||||||||||||||TCR Transgenic mice expressing the transgenic gBT-1 TCR recognising the immunodominat epitope of HSV expressing the congenial marker CD45.1. These mice have been bred onto the RAG-1 ko background and also display restricted expression of GFP in CXCR6+ cells and Cre-dependent expression of Tomato in CX3CR1+ cells. In the homozygous state, they are CX3CR1-deficient, CXCR6-deficient, RAG1-/- deficient and Ly5.1+ Ly5.2- |In the heterozygous state (after breeding with B6 mice), het mice would be they express CX3CR1 and CXCR6 (one allele), RAG1 sufficient and Ly5.1+ Ly5.2+|C57Bl/6J|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|09-Nov-2021|Cryopreserved sperm|||Unknown|||Possibly| 10472.0|Ubf1 KO bp20|C57BL/6NCrlAnu-Ubtf/ANU||Recessive|Upstream binding transcription factor, RNA polymerase I|Ubtf||Tcfubf, UBF, UBF1|MGI:98512|Ubtf|Ubf1 KO||11|ENSMUSG00000020923|ENSMUST00000174302|||||||||||||||||||||||||||Embryonic lethal|Normal|C57Bl/6N|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|21-Jan-2025|Cryopreserved sperm|55.0|0.0|Unknown|||No| 10422.0|ASD886:Cavendish:SwHEL|C57BL/6NCrlAnu-Sh2b3 Igh Tg(IgkHyHEL10)1Rbr/Anu||Dominant|SH2B adaptor protein 3|Sh2b3||Lnk|MGI:893598|Sh2b3; endonuclease-mediated mutation 2, Australian National University|Sh2b3||5|ENSMUSG00000042594|ENSMUST00000086310|||||||||||||||transgene insertion 1, Robert Brink||||||||||||BCR Transgenic|Normal|C57Bl/6N|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|02-May-2024|Cryopreserved sperm|31.0|0.0|Unknown|||Possibly| 10422.0|ASD886:Cavendish:SwHEL|C57BL/6NCrlAnu-Sh2b3 Igh Tg(IgkHyHEL10)1Rbr/Anu||Dominant|immunoglobulin heavy chain complex|Igh|||MGI:96442|immunoglobulin heavy chain complex; targeted mutation 1, Robert Brink|Igh|MGI:3800383|12|||||||||||||||||||||||||||||BCR Transgenic|Normal|C57Bl/6N|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|02-May-2024|Cryopreserved sperm|||Unknown|||Possibly| 10318.0||C57BL/6J-Gt(Rosa26)Sortm1(LPfCSPrev-mCherry)Anu/N||Semi-dominant|Rosa26|||||mCherry|||Unknown|||||||||||||||||||||||||||||N/A mouse maintained as Hets|Expression of mCherry|C57Bl/6J|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|25-Mar-2023||0.0|0.0|Unknown|||Possibly| 10347.0||B6.129-Nox4/Apb||Dominant|NADPH Oxidase 4 |Nox4|||MGI:1354184|NADPH oxidase 4; targeted mutation 1, Karl-Heinz Krause|Nox4|MGI:5502326|7|ENSMUSG00000030562 | ENSMUST00000068829|||||||||||||||||||||||||||Phenotype information includes data collected from the published literature. Nox4 deficiency reduced oxidative stress and apoptosis in alveolar epithelial cells stimulated with TGFb1. Bleomycin-treated mice demonstrate decreased bleomycin-induced weight loss, lung fibrosis, myofibroblasts accumulation and alveolar epithelial cell death compared to wild-type mice, however, bleomycin-induced inflammation is normal. Homozygous mice are viable and fertile. |Normal|C57Bl/6J|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|5x||homozygote x homozygote|No|30-Jun-2023|Cryopreserved sperm|50.0|0.0|Unknown|||Possibly| 10439.0|Lcp1 I232F (10)|C57Bl/6N-Lcp1Anu/Apb||Recessive|lymphocyte cytosolic protein 1 |Lcp1||D14Ertd310e, L-fimbrin, L-plastin, Pls2|MGI:104808|Lcp1:endonuclease-mediated mutation 3, Australian National University|Lcp1||14|ENSMUSG00000021998||||||||||||||||||||||||||||Leukopenic in the bloodT cell proliferation defect, cytokinesis arrest leading to polyploidy cells|Leukopenic in the bloodT cell proliferation defect, cytokinesis arrest leading to polyploidy cells|C57Bl/6N|Yes|Unknown|Yes|Yes|Unknown|Yes|No|Good||||No|28-Jun-2024|Cryopreserved sperm|20.0|0.0|Unknown|||No| 10355.0|JNK2-/- JNK1 fl/fl|B6.Mapk9 Mapk8/Mhn||Recessive|Mitogen-Activated Protein Kinase 9|MapK9||JNK2,|MGI:1346862|mitogen-activated protein kinase 9; targeted mutation 1, Richard Flavell|Mapk9|MGI:2176243|11|ENSMUSG00000020366 ||||||||||||||||||||||||||||Normal|Normal|C57Bl/6J|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|01-Sep-2023|Cryopreserved sperm|50.0|0.0|Unknown|||No| 10355.0|JNK2-/- JNK1 fl/fl|B6.Mapk9 Mapk8/Mhn||Recessive|mitogen-activated protein kinase 8|Mapk8||JNK1|MGI:1346861|mitogen-activated protein kinase 8; targeted mutation 1, Richard Flavell|Mapk8|MGI:2176239|14|ENSMUSG00000021936 ||||||||||||||||||||||||||||Normal|Normal|C57Bl/6J|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|01-Sep-2023|Cryopreserved sperm|||Unknown|||No| 10397.0|Drosha/NCrl|B6.129P2-Drosha/Anu||Recessive|drosha, ribonuclease type III|Drosha||Etohi2, Rnasen|MGI:1261425|drosha, ribonuclease type III; targeted mutation 1, Dan R Littman|Drosha|MGI:3801076|15|ENSMUSG00000022191|ENSMUST00000090292|||||||||||||||||||||||||||Normal|Normal|C57Bl/6N|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|20-Dec-2023|Cryopreserved sperm|54.0|0.0|Unknown|||No| 10473.0|Ubf1 KO bp12|C57BL/6NCrlAnu-Ubtf/ANU||Recessive|Upstream binding transcription factor, RNA polymerase I|Ubtf||Tcfubf, UBF, UBF1|MGI:98512|Ubtf|Ubf1 KO||11|ENSMUSG00000020923|ENSMUST00000174302|||||||||||||||||||||||||||Embryonic lethal|Normal|C57Bl/6N|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|21-Jan-2025|Cryopreserved sperm|59.0|0.0|Unknown|||No| 9324.0|Agxt/Apb||Semi-dominant|alanine-glyoxylate aminotransferase|Agxt|||MGI:1329033|Agxt: endonuclease-mediated mutation 1, Australian National University|Agxt||1|||||||||||||||||||||||||||||unknown|unknown|C57Bl/6N|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|20-Dec-2021|Cryopreserved sperm|10.0|0.0|Unknown|||Possibly| 10402.0|mPfCSPrev-mCherry|C57BL/6J-Gt(ROSA)26Sor/Anu||Recessive|Plasmodium falciparum circumsporozoite protein|PfCSPrev-mCherry|||Plasmodium falciparum circumsporozoite protein||||Unknown|||||||||||||||||mCherry red fluorescent protein||||||||||||Presence of gene trap indicated by mCherry expression|Presence of gene trap indicated by mCherry expression|C57Bl/6J|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Good|backcrossed to C57BL / 6NCrlAnu|||No|31-Jan-2024|Cryopreserved sperm|41.0|0.0|Unknown|||No| 5352.0|B6.SOD1.SOD3.Gpx1.Tg|C57BL/6-Tg(H2-K-GPX1,-SOD1,-SOD3/CD55)CCpj/Apb||Dominant||||||||||||||||||||||||||human CuZn superoxide dismutase (SOD1) tagged with a hemagglutinin epitope tag|H2-K|medium||||||||||Expression of all three enzymes was the only combination protective against hypoxia/reoxygenation. In contrast to single- and double-transgenic grafts, triple-transgenic grafts significantly improved control of blood glucose compared with wild type. In contrast to single- and double-transgenic grafts, triple-transgenic grafts significantly improved control of blood glucose compared with wild type.|Normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Excellent|10|||No|20-Dec-2010|Cryopreserved sperm|45.0|0.0|Unknown||reactive oxygen species (ROS), transplantation, islet, antioxidant, graft|No| 5352.0|B6.SOD1.SOD3.Gpx1.Tg|C57BL/6-Tg(H2-K-GPX1,-SOD1,-SOD3/CD55)CCpj/Apb||Dominant||||||||||||||||||||||||||human extracellular superoxide dismutase (SOD3) modified to include a glycosyl phosphatidylinositol (GPI) membrane linkage signal & tagged with a FLAG epitope tag|H2-K|||||||||||Expression of all three enzymes was the only combination protective against hypoxia/reoxygenation. In contrast to single- and double-transgenic grafts, triple-transgenic grafts significantly improved control of blood glucose compared with wild type. In contrast to single- and double-transgenic grafts, triple-transgenic grafts significantly improved control of blood glucose compared with wild type.|Normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Excellent|10|||No|20-Dec-2010|Cryopreserved sperm|||Unknown||reactive oxygen species (ROS), transplantation, islet, antioxidant, graft|No| 5352.0|B6.SOD1.SOD3.Gpx1.Tg|C57BL/6-Tg(H2-K-GPX1,-SOD1,-SOD3/CD55)CCpj/Apb||Dominant||||||||||||||||||||||||||human cellular glutathione peroxidase (Gpx-1) tagged with a histidine (6xHis) tag|H2-K|||||||||||Expression of all three enzymes was the only combination protective against hypoxia/reoxygenation. In contrast to single- and double-transgenic grafts, triple-transgenic grafts significantly improved control of blood glucose compared with wild type. In contrast to single- and double-transgenic grafts, triple-transgenic grafts significantly improved control of blood glucose compared with wild type.|Normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Excellent|10|||No|20-Dec-2010|Cryopreserved sperm|||Unknown||reactive oxygen species (ROS), transplantation, islet, antioxidant, graft|No| 10487.0|CK1D1 ROSA26 KI|B6.-Gt(ROSA)26Sor||Recessive|casein kinase 1 delta transcript variant 1 knock in|||||casein kinase 1 delta|CSNK1D||Unknown|||||||||||||||||||||||||||||Normal|Normal|C57Bl/6N|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|25-Feb-2025|Cryopreserved sperm|50.0|0.0|Unknown|||No| 10482.0|Cx3cr1CreER knock-in/knock-out|B6.129P2(C)-Cx3cr1/J||Recessive|chemokine (C-X3-C motif) receptor 1|Cx3cr1|||MGI:1333815|C-X3-C motif chemokine receptor 1; targeted mutation 2.1, Dan R Littman|Cx3cr1|MGI:5450813|9|ENSMUSG00000052336||||||||||||||||||||||||||||Cx3cr1CreER knock-in/knock-out mice express tamoxifen-inducible Cre recombinase under the direction of the Cx3cr1 promoter in the mononuclear phagocyte system making them useful for fate-mapping studies of the monocyte and macrophage compartment, as well as microglia. Insertion of the Cre-ER fusion protein knocks out endogenous CX3CR1 expression. Homozygous mice are viable and fertile. When Cx3cr1CreER mice are bred with mice containing loxP-flanked sequence, tamoxifen-inducible, Cre-mediated recombination will result in deletion of the floxed sequences.|Same as homozygous mice except that heterozygous express endogenous Cx3CR1 from the wt allele.|C57Bl/6N|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|04-Feb-2025|Cryopreserved sperm|40.0|0.0|Unknown|||Possibly| 10474.0|Ubf1 KO bp3|C57BL/6NCrlAnu-Ubtf/ANU||Recessive|Upstream binding transcription factor, RNA polymerase I|Ubtf||Tcfubf, UBF, UBF1|MGI:98512|Ubtf|Ubf1 KO||11|ENSMUSG00000020923|ENSMUST00000174302|||||||||||||||||||||||||||Embryonic lethal|Normal|C57Bl/6N|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|21-Jan-2025|Cryopreserved sperm|54.0|0.0|Unknown|||No| 9435.0|Brca2 KO|Balb/c-Brca2/Apb||Dominant|breast cancer 2, early onset|BRCA2|||MGI:109337|Brca2: endonuclease mutation 1, Australian National University|Brca2||5|||||||||||||||||||||||||||||Heterozygous - normalHomozygous - embryonic lethal|Normal|Balb/cJ|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|28-Sep-2022|Cryopreserved sperm|54.0|0.0|Unknown|||Possibly| 4939.0|B6.Asciz|C57BL/6-Atmin/Apb||Recessive|ATM interactor ; ATM substrate Chk2-interacting Zinc-finger protein|Atmin ; ASCIZ|Nil|Asciz, MGC:79206, mKIAA0431|MGI:2682328|ATM interactor; targeted mutation 1.1, Jorg Heierhorst|Atmin|MGI:4881337|8||||||||||||||||Yes|||||||||||||Embryonic lethal. late embryonic lethality (~E16.5) with complete absence of lungs and severe tracheal atresia (100% penetrance);Frequent exencephaly (~25% penetrance); Increased cellular DNA base damage sensitivity, including oxidative DNA damage and damage-dependent premature senescence; Highly reduced Dynll1 gene expression (>10-fold) in all tissues and cell types investigated.|Normal|C57BL/6|No|No|Yes|No|No|Yes|No|Excellent|2|||No|03-Dec-2009|Cryopreserved sperm|100.0|0.0|Unknown||Base excision repair, embryonic lethal, zinc finger, ATM kinase|Yes| 5030.0|Hulett 5B|C57BL/6J-Hpse/AnuApb||Recessive|heparanase|Hpse||Hpa|MGI:1343124|Hpse; targeted mutation 1, Australian National University|Hpse ||5||||||||||Unknown to Unknown|||||||||||||||||||Mice are anatomically normal and fertile.The trafficking of dendritic cells from the skin to the draining lymph nodes was markedly reduced in Hpse<−/−> mice. Impaired ability to generate an allergic inflammatory response in the airways.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|22-Feb-2010|Cryopreserved sperm|90.0|0.0|Unknown||migration, dendritic cell, trafficking|Possibly| 5270.0|Crouzon|STOCK Fgfr2/Apb|MGI:3053095|Dominant|fibroblast growth factor receptor 2|Fgfr2|Normal|Bek, Fgfr-2, Fgfr-7, Fgfr7, KGFRTr, svs|MGI:95523|fibroblast growth factor receptor 2; targeted mutation 4, Peter Lonai|Fgfr2|MGI:3053095|7||||||||||||||||No|||||||||||||Homozygous mutants display multiple joint fusions,cleft palate, and trachea and lung defects, and die shortly afterbirth.|Fgfr2cC342Y/+ heterozygote miceare viable and fertile with shortened face, protruding eyes, prematurefusion of cranial sutures, and enhanced Spp1 expression inthe calvaria. Prone to malocclusion.|C57BL/6 (not congenic)|No|No|Yes|No|No|Yes|No|Good||||No|25-Oct-2010|Cryopreserved sperm|50.0|0.0|Yes|Crouzon craniosynostosis|Craniosynostosis, fibroblast growth factor receptor, bone, suture, gain of function|Yes| 5323.0|NfiB Conditional|B6.129-Nfib/Apb||Dominant|nuclear factor I/B|NFib|Reduced||MGI:103188|nuclear factor I/B; targeted mutation 2, Richard M Gronostajski|Nfib|MGI:5052268|4|||||||||||||||||||||||||||||Apparently normal. Viable as homozygous mice when not crossed to a Cre expressing line.|Apparently normal. Viable as heterozygous mice when not crossed to a Cre expressing line.|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|17-Nov-2010|Cryopreserved sperm|44.0|0.0|Unknown||lung, epithelium|Possibly| 10488.0|CK1D Two R26 KI |B6.-Gt(ROSA)26Sortm1(CAG-CK1D2)HO||Recessive|casein kinase 1 delta transcript variant 2 knock in|||||casein kinase 1 delta|CSNK1D||Unknown|||||||||||||||||||||||||||||Normal|Normal|C57Bl/6N|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|25-Feb-2025|Cryopreserved sperm|50.0|0.0|Unknown|||No| 10489.0|CK1D2 KO |B6-Csnk1dHO||Recessive|casein kinase 1, delta|Csnk1d|||MGI:1355272|casein kinase 1 delta Knock out|CSNK1D||11|ENSMUSG00000025162 | ENSMUST00000239115|||||||||||||||||||||||||||Normal|Normal|C57Bl/6N|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|25-Feb-2025|Cryopreserved sperm|50.0|0.0|Unknown|||No| 10475.0|GLR|Tg(TcraHsv2.3,TcrbHsv2.3)L118-1Cbn B6.SJL-Ptprca Pepcb/BoyJ, B6.129S7-Rag1tm1Mom/J||Recessive|Tcra, Tcrb, RAG-1, ptprca|||||Tcra, Tcrb, RAG-1, ptprca|TCR, RAG-1 and Ly5.1||Unknown|||||||||||||||||TCR|2 kb fragment of the H-2Kb and a 700 bp fragment including the Igh enhancer.|||||||||||Tg mouse line in which all T cells express the rearranged Tcra and Tcrb derived from HSV-1 glycoprotein B specific CTL clone HSV2.3, under the control of a 2 kb fragment of the H-2Kb and a 700 bp fragment including the Igh enhancer. T C57BL/6 congenic strain carries the differential Ptprca pan leukocyte marker commonly known as CD45.1 or Ly5.1. This mouse line was backcrossed onto wildtype C57BL/6 inbred mice expressing the Ptprcb (CD45.2 or Ly5.2) allele and are also deficient for RAG-1 as mice are deficient for RAG, they lack B cells and all their T cells express the same transgenic TCR|Normal ||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|22-Jan-2025|Cryopreserved sperm|30.0|0.0|Unknown|||Possibly| 5386.0|Fat Aussie|NOD.B10-Alms1/AnuApb||Recessive|Alstrom syndrome 1 homolog (human)|Alms1|Unknown||MGI:1934606|Alstrom syndrome 1 homolog (human); fat aussie|Alms1|MGI:3621984|6||||||||||||||||Yes|||||||||||||Mice are hyperphagic leading to obesity and diabetes. Males are sterile. High fat feeding accelerates obesity and diabetes development, and leads to nonalcoholic steatohepatitis which progresses to liver fibrosis.Insulin resistance: female mice develop insulin resistance by 200 days of age.Increased eating behavior: mutants eat more than wild-type.Abnormal hepatocyte morphology: mutant livers show many hepatocytes with ballooning degeneration and extensive lobular inflammation with polymorphs and mononuclear cells.Enlarged liver: mice fed high-fat diet show hepatomegaly compared to wild-type (8.9g vs. 2g).Increased liver weight: liver weights in mutant are twice that of wild-type (3.4g vs. 1.6g).Liver fibrosis: mutant livers show pericellular and pericentral fibrosis.Hepatic steatosis: chow-fed mutants develop steatosis; mutants fed the high-fat diet develop severe steatohepatitis.|Normal|NOD.B10|Yes|Yes|Yes|Yes|No|Yes|Yes|Excellent|>10||heterozygote mating|No|17-Jan-2011|Cryopreserved sperm|50.0|0.0|Yes|Alstrom syndrome is a disorder of childhood obesity, diabetes development and infertility.|obesity, diabetes, nonalcoholic fatty liver disease, alstrom syndrome, cilia|Yes| 5387.0|Fat Aussie|C57BL/6-Alms1/AnuApb||Recessive|Alstrom syndrome 1 homolog (human)|Alms1|Unknown||MGI:1934606|Alstrom syndrome 1 homolog (human); fat aussie|Alms1|MGI:3621984|6||||||||||||||||Yes|||||||||||||Mice are hyperphagic leading to obesity. Males are sterile. High fat feeding accelerates obesity development, and leads to nonalcoholic steatohepatitis which progresses to liver fibrosis. Steatohepatitis also develops in chow-fed animals.Hyperglycemia: female mice are diabetic by 200 days of age.Increased circulating insulin level: female mice develop insulinemia (20ng/mL insulin vs. 2-5ng/mL in wild-type).Insulin resistance: female mice develop insulin resistance by 200 days of age.Increased eating behavior: mutants eat more than wild-type.Abnormal hepatocyte morphology: mutant livers show many hepatocytes with ballooning degeneration and extensive lobular inflammation with polymorphs and mononuclear cells.Enlarged liver: mice fed high-fat diet show hepatomegaly compared to wild-type (8.9g vs. 2g).Increased liver weight: liver weights in mutant are twice that of wild-type (3.4g vs. 1.6g).Liver fibrosis: mutant livers show pericellular and pericentral fibrosis.Hepatic steatosis: chow-fed mutants develop steatosis; mutants fed the high-fat diet develop severe steatohepatitis.|Normal|C57BL/6|Yes|Unknown|Yes|Yes|No|Yes|Yes|Good|>10||heterozygote mating|No|17-Jan-2011|Cryopreserved sperm|32.0|0.0|Yes|Alstrom syndrome is a disorder of childhood obesity, diabetes development and infertility.|obesity, diabetes, nonalcoholic fatty liver disease, alstrom syndrome, cilia|Yes| 10476.0|PLR|C57BL/6-Tg(H2-Kb-Tcra,-Tcrb)P25Ktk/J, B6.SJL-Ptprca Pepcb/BoyJ, B6.129S7-Rag1tm1Mom/J ||Recessive|TCR alpha and TCR beta chains|||||tcra,tcrb|tcra, tcrb||Unknown|||||||||||||||||transgene insertion P25, Kiyoshi Takatsu|H-2Kb promoter|||||||||||Mice have no T cells and B cells and all T cells express the same TCR displaying the same specificity|Same as above except that RAG heterozygosity means that mice will have B cells. T cells would also express an additional endogenous a and b chains. ||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|23-Jan-2025|Cryopreserved sperm|50.0|0.0|Unknown|||Possibly| 5391.0|MPS IIIA Congenic Strain|B6.Cg-Sgsh/Apb||Recessive|N-sulfoglucosamine sulfohydrolase (sulfamidase)|Sgsh|Reduced|sulphamidase|MGI:1350341|N-sulfoglucosamine sulfohydrolase (sulfamidase); mucopolysaccharidosis IIIA|Sgsh|MGI:2151181|11|||||||||||||||||||||||||||||General health and vigour is generally good, at least until 30 weeks of age. Newborn MPS IIIA mice are no different to their unaffected counterparts. It is not until around 10 weeks of age that we begin to see differences. From 10 weeks onwards, MPS IIIA males can be aggressive towards each other. If we test the mice in an open-field test of activity, they are less active. They are heavier (presumably due to slightly enlarged liver and spleen), plus urinary retention in some (but not all) mice. Affected females and males are both fertile. From around 18-20 weeks mice are less able to perform a test of learning and memory (Morris water maze) and can best be described as a little ‘duller’ than unaffected mice. Their fur is ruffled and rough looking. We do not often retain mice past around 30 weeks of age, however we might expect that some (but not all) will die younger than unaffected mice. The reason for this is not known, but may relate to liver dysfunction.We have primarily sought to characterise the brain disease in the MPS IIIA mice as this is the area of the body most affected in the mice/patients with this condition. Mice exhibit reduced anxiety, reduced activity, reduced cognition (memory and learning). Other deficits, which may have both a central nervous system and somatic organ/tissue involvement include mildly impaired gait, reduced grip strength. None of these observations are likely to have a major welfare impact. Fighting in affected male mice has been observed, and monitoring for this followed by separation is required. This has significant welfare implications. Early death is seen (40+ weeks). Monitoring more often after 30 weeks of age is recommended, so humane euthanasia can occur. |Normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|13||Brother Sister|No|20-Jan-2011|Cryopreserved sperm|50.0|0.0|Yes|Neurodegenerative lysosomal storage disorder characterised by mental decline, sleep disturbance and hyperactivity.|Lysosomal storage disorder, Mucopolysaccharidosis, Neurodegenerative|Yes| 5392.0|Adam22|B6;CBA-Adam22/Apb||Recessive|a disintegrin and metallopeptidase domain 22|Adam22|Nil|MDC2|MGI:1340046|a disintegrin and metallopeptidase domain 22; targeted mutation 1, Koji Sagane|Adam22|MGI:3584137|5||||||||||||||||Yes|||||||||||||Complete postnatal lethality: start to die after P10 and all die before P20.Ataxia: * all display severe ataxia after P10 * unable to support themselves on hindlimbs at P18Convulsive seizures: occasionally observe convulsive seizures.Decreased body size.Decreased body weight: average body weight is approximately half that of controls at P10.Abnormal Schwann cell morphology: higher density of pro-myelinating Schwann cells in the sciatic nerve and delay in differentiation of Schwann cells.Abnormal myelination: lack of myelin or thin myelin in the sciatic nerves and trigeminal nerves, however myelin formation in spinal cord and brain is normal.Abnormal glial cell morphology: enteric sections exhibit fewer glial cells than in wild-type mice.Abnormal neuron morphology: cultured primary neurons cannot be myelinated by Rat Schwann cells unlike similarly treated neurons from heterozygous mice.Demyelination: * in the sciatic nerve at P12 that is less severe than in Lgi4 homozygotes * of peripheral nerves|Normal|C57BL/6|No|No|Yes|No|No|Yes|No|Unknown||||No|24-Jan-2011|Cryopreserved sperm|20.0|0.0|Unknown||myelin, neuron, ataxia, integrin, adhesion|Yes| 5393.0|a33 b-neo/b-neo|C57BL/6-Gpa33/Apb||Dominant|glycoprotein A33 (transmembrane)|Gpa33||A33 antigen|MGI:1891703|glycoprotein A33 (transmembrane) targeted mutation 2, Matthias Ernst|Gpa33||1||||||||||||||||Yes|||||||||||||Unknown|Unknown|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|24-Jan-2011|Cryopreserved sperm|50.0|0.0|Unknown||A33, epithelium, b-catenin|Yes| 10478.0|Ai9 or Ai9(RCL-tdT)|B6.Cg-Gt(ROSA)26Sortm9(CAG-tdTomato)Hze/J||Dominant|Rosa26|||||gene trap ROSA 26, Philippe Soriano|Gt(ROSA)26Sor||Unknown|||||||||||||||||||||||||||||Ai9 is a Cre reporter tool strain designed to have a loxP-flanked STOP cassette preventing transcription of a CAG promoter-driven red fluorescent protein variant (tdTomato) - all inserted into the Gt(ROSA)26Sor locus. Ai9 mice express robust tdTomato fluorescence following Cre-mediated recombination. This strain is congenic on the C57BL/6J genetic background.|same as homozygous mice|C57Bl/6N|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|23-Jan-2025|Cryopreserved sperm|50.0|0.0|Unknown|||Yes| 8483.0|Scn2a R851X|C57BL/6-Scn2a/Apb||Recessive|sodium channel, voltage-gated, type II, alpha|Scn2a||A230052E19Rik, Nav1.2, Scn2a1|MGI:98248||Scn2a||2|||||||||||||||||||||||||||||Lethal before P5|Life expectancy is similar to wild type. No obvious abnormal phenotype.|C57BL/6|No|No|Yes|No|No|Yes|No|Unknown||||No|11-May-2018|Cryopreserved sperm|40.0|0.0|Unknown|||Yes| 5502.0|580S/TVA/Lacz ; Apc 580S/580S;tgNA33 TVA; Tgn(lacZ13)|STOCK Apc Tg(Gpa33-TVA)#Ern Tg(Pgk1-lacZ)13Vmel/LudApb||Dominant|adenomatosis polyposis coli|Apc|Reduced|CC1, Min|MGI:88039|adenomatosis polyposis coli; targeted mutation 1, Tetsuo Noda|Apc|MGI:1857966|18||||||||||||||||Yes|transgenic insertion 1, Matthias Ernst|glycoprotein A33 (transmembrane)|||||||||||Unknown|Unknown|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|09-May-2011|Cryopreserved sperm|50.0|0.0|Unknown||colon|Yes| 5502.0|580S/TVA/Lacz ; Apc 580S/580S;tgNA33 TVA; Tgn(lacZ13)|STOCK Apc Tg(Gpa33-TVA)#Ern Tg(Pgk1-lacZ)13Vmel/LudApb||Dominant||||||||||||||||||||||||||transgenic insertion 13, Harald von Melchner|mouse Pgk1 promoter|||||||||||Unknown|Unknown|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|09-May-2011|Cryopreserved sperm|||Unknown||colon|Yes| 10491.0|Tlr4-mVenus|B6CBA-Tlr4/SagenSah||Recessive|toll-like receptor 4|Tlr4||Lps, Rasl2-8|MGI:96824||||4|ENSMUSG00000039005||||||||||||||||||||||||||||Normal|Normal||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|28-Feb-2025||0.0|0.0|Unknown|||Possibly| 5388.0|Fat Aussie|BALB/c-Alms1/AnuApb||Recessive|Alstrom syndrome 1 homolog (human)|Alms1|Unknown||MGI:1934606|Alstrom syndrome 1 homolog (human); fat aussie|Alms1|MGI:3621984|6||||||||||||||||Yes|||||||||||||Mice are hyperphagic leading to obesity . Males are sterile. High fat feeding accelerates obesity development. Compared to foz/foz mice on NOD.B10 background, BALB/c foz/foz mice do not develop diabetes and liver disease is less severe.|normal|BALB/c|Yes|Unknown|Yes|Yes|No|Yes|Yes|Good|>10||heterozygote mating|No|17-Jan-2011|Cryopreserved sperm|39.0|0.0|Yes|Alstrom syndrome is a disorder of childhood obesity, diabetes development and infertility.|obesity, diabetes, nonalcoholic fatty liver disease, alstrom syndrome, cilia|Yes| 5394.0|A33/B-cat del/580's|Stock Gpa33 Ctnnb1 Apc/LudApb||Dominant|glycoprotein A33 (transmembrane)|Gpa33|||MGI:1891703|glycoprotein A33 (transmembrane) targeted mutation 2, Matthias Ernst|Gpa33||1|||||||||||||||||||||||||||||Unknown|Unknown||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|24-Jan-2011|Cryopreserved sperm|40.0|0.0|Unknown||Wnt, polyposis|Yes| 5394.0|A33/B-cat del/580's|Stock Gpa33 Ctnnb1 Apc/LudApb||Dominant|catenin (cadherin associated protein), beta 1|Ctnnb1||beta catenin, beta-catenin, Bfc, Catnb|MGI:88276|catenin (cadherin associated protein), beta 1; targeted mutation 4, Walter Birchmeier|Ctnnb1|MGI:2148594|9||||||||||||||||No|||||||||||||Unknown|Unknown||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|24-Jan-2011|Cryopreserved sperm|||Unknown||Wnt, polyposis|Yes| 5394.0|A33/B-cat del/580's|Stock Gpa33 Ctnnb1 Apc/LudApb||Dominant|adenomatosis polyposis coli|Apc|Reduced|CC1, Min|MGI:88039|adenomatosis polyposis coli; targeted mutation 1, Tetsuo Noda|Apc|MGI:1857966|18||||||||||||||||Yes|||||||||||||Unknown|Unknown||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|24-Jan-2011|Cryopreserved sperm|||Unknown||Wnt, polyposis|Yes| 5524.0|Gp130dstat/dstat(Balb/C)|C;(Cg)-Il6st/LudApb||Recessive|interleukin 6 signal transducer|Il6st|Unknown|CD130, D13Ertd699e, gp130|MGI:96560|interleukin 6 signal transducer; targeted mutation 1, Ashley R Dunn|Il6st|MGI:2388476|Unknown||||||||||||||||Yes|||||||||||||Postnatal lethality: * numbers deficient at weaning * ratio of homozygotes normal at E18.Premature death (J:79555): * 6 month life span for males * 8 month life span for femalesDecreased body length: 20-30% shorter trunk length at birth.Decreased body weight: 20-30% lower body weight at birth.Abnormal uterine environment: failure of implantation, blastocysts will develop to term in wild-type recipient femalesFemale infertility: females show no external signs of pregnancy regardless of male genotype.Gastrointestinal haemorrhage: faecal blood at 4 months of age.Abnormal digestive system morphology.Rectal prolapse.Gastrointestinal ulcer: * caecal ulcers * ulceration of the anorectal regionGgastric ulcer: ulceration of the gastric pylorus at 4 months of age.Large intestinal inflammation: caecal inflammation.Increased susceptibility to induced colitis: * severe erosion of the intestinal epithelium from exposure to 3.5% dextran sodium sulfate. * remain moribund when exposure is ended.Abnormal leukocyte cell number: white blood cell count significantly higher than in controls.Decreased immunoglobulin level.Decreased IgA level: * basal IgA levels are reduced * impaired ability to mount an intestinal IgA response after challenge * basal IgM is normalDecreased IgG level: impaired ability to mount an intestinal IgG response after challenge.Conjunctivitis.Increased susceptibility to parasitic infection: tend to carry higher parasitic loads.Abnormal common myeloid progenitor cell morphology: * colony forming cells elevated in the spleen but not in bone marrow * elevated "CFU-S" hematopoietic progenitor cells * hematopoietic progenitors elevated in the liver at E14 relative to controls.Abnormal megakaryocyte morphology.Abnormal thrombopoiesis: * impaired maturation of megakaryocytes to produce platelets * 40% reduction in the number of platelets produced per megakaryocyte.Decreased platelet cell number: platelet count reduced 30%.Decreased megakaryocyte cell number: by 23% in bone marrow.Increased megakaryocyte cell number: numbers in spleen increased 2 fold relative to controls.Skeleton phenotype: trabecular bone volume is normal.Abnormal femur morphology.Decreased diameter of femur: significantly reduced femoral width.Short femur.Abnormal joint morphology.Abnormal joint capsule morphology: * cartilaginous nodules in joint capsules that replace menisci and support cartilage in knee joints * erosion of articular surfaces in older mice.Joint swelling: * of weight bearing joints in 60% of adults * observed by 7 days of age * more severe in males than femalesAbnormal joint mobility: * flexion abnormalities of hindlimbs * reluctance to stand * restricted flexion and extension of ankles and wrists * stiffness of one or more limbsIncreased cell proliferation: proliferative response of fibroblasts in culture to Il6 is increased.Gastrointestinal hemorrhage: fecal blood at 4 months of age.||BALB/c|Yes|Unknown|Yes|Yes|Unknown|Yes|No|Unknown||||No|14-Jun-2011|Cryopreserved sperm|50.0|0.0|Unknown||signal transduction, kinase, STAT, IL6, gp130, joint|Yes| 5551.0|Krüppel-like Factor 8 (Klf8) Knockout |FVB/N.129P2-Klf8/Apb||X-linked|Kruppel-like factor 8|Klf8|Nil||MGI:2442430|Kruppel-like factor 8; gene trap AD0101, Wellcome Trust Sanger Institute|Klf8|MGI:4331301|X||||||||||||||||Yes|||||||||||||Largely normal.Some mice by 6 months of age.Mice exhibit normal full blood counts indicating normal erythroid parameters and platelet numbers and normal response to phenylhydrazine treatment |Normal.Premature death: • some mice by 6 months|FVB/N|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|09-Aug-2011|Cryopreserved sperm|49.0|0.0|Unknown||Kruppel-like Factor 8, KLF, Apoptosis, cell cycle|No| 6764.0|gp130/Stat3 (BJ-13)|STOCK Il6st Stat3/LudApb||Recessive|interleukin 6 signal transducer|Il6st|Normal|5133400A03Rik, CD130, D13Ertd699e, gp130|MGI:96560|interleukin 6 signal transducer; targeted mutation 1, Matthias Ernst|Il6st|MGI:2388478|13|||||||||||||||||||||||||||||Homozygous Stat3 mice are not viable. They are embryonic lethal.The Gp130 mutation will result in gastric polyp development, although this is significantly delayed in comparison to BJ-12 (Stat3 wt). Check for hunching and general disintrest.|Normal||No|No|Unknown|No|No|Unknown|No|Unknown||||No|16-Dec-2011|Cryopreserved sperm|50.0|0.0|Unknown||signal transduction|Yes| 6764.0|gp130/Stat3 (BJ-13)|STOCK Il6st Stat3/LudApb||Recessive|signal transducer and activator of transcription 3|Stat3|Nil|1110034C02Rik, Aprf|MGI:103038|signal transducer and activator of transcription 3; targeted mutation 1, Shizuo Akira|Stat3|MGI:1926814|11|||||||||||||||||||||||||||||Homozygous Stat3 mice are not viable. They are embryonic lethal.The Gp130 mutation will result in gastric polyp development, although this is significantly delayed in comparison to BJ-12 (Stat3 wt). Check for hunching and general disintrest.|Normal||No|No|Unknown|No|No|Unknown|No|Unknown||||No|16-Dec-2011|Cryopreserved sperm|||Unknown||signal transduction|Yes| 10321.0|ENU58:G3|ANU:ENU58:G3||Recessive|Unknown||||||||Unknown||||||||||||||||||||||||||||| | |C57Bl/6N|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|01-Apr-2023|Cryopreserved sperm|166.0|0.0|Unknown|||Possibly| 5490.0|Hck(129sv/ter) ;Hck up mutant.129sv/ter|129T1/Sv-Hck/LudApb||Dominant|hemopoietic cell kinase|Hck|Reduced|Bmk, Hck-1|MGI:96052|hemopoietic cell kinase; targeted mutation 1, Matthias Ernst|Hck|MGI:3663799|2||||||||||||||||Yes|||||||||||||Abnormal alveolar macrophage morphology: * there are large macrophages in mutant lungs despite specific pathogen-free (SPF) housing. * alveolar macrophages are frequently vacuolated with eosinophilic cytoplasm.Lung inflammation: * lungs have areas of infiltration into the interstitium and alveoli at 3-4 months of age and older * lungs are characterized by areas of accumulation of mononuclear inflammatory cells around airways and blood vessels * areas of pulmonary consolidations become evident around 5-6 weeks of age and progress from that pointPulmonary hyperplasia: lungs are consistently characterized by increased cellularity within the parenchymaAbnormal pulmonary alveolus morphology: alveolar spaces contain eosinophilic matter accompanied by degranulated eosinophilic proteinOverexpanded pulmonary alveoli: lungs show some areas of enlarged airspaces at 3-4 months of age and older.Thick pulmonary interalveolar septum: excessive fibrotic deposits of extracellular matrix in the alveolar septa.Emphysema: lungs show areas of emphysema, with loss of orderly appearance of acinus.Pulmonary fibrosis: lungs display signs of fibrosis characterized by depostion of extracellular matrix material in the alveolar septa.Abnormal respiratory epithelium morphology: epithelial cells lining the conducting airways exhibit extensive mucus cell metaplasia resulting in mucus aggregates in the airway lumen.Respiratory epithelium hypertrophy: epithelium lining conducting airways is frequently hypertrophic and many epithelial cells are enlarged due to excessive production/accumulation of mucus material.Decreased lung elastance: mutants show decreased tissue elastance of the lung tissue at baseline compared with wild-type.Respiratory distress: aging mice show signs of respiratory distress, evident by use of accessory muscles.Atelectasis: in 3-4 month-old and older mutants, lungs show areas of atelectasis.Increased eosinophil cell number: eosinophils are most prominent cell type in infiltrates in lungs (30% of total bronchoalveolar lavage fluid (BALF) from mutants compared to 2% in wild-type.||129T1/Sv|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|29-Apr-2011|Cryopreserved sperm|80.0|0.0|Unknown||kinase, macrophage, hyperplasia, pulmonary, eosinophil, SRC|Yes| 5503.0|Gp130stat|Stock Il6st/LudApb||Dominant|interleukin 6 signal transducer|Il6st|Unknown|CD130, D13Ertd699e, gp130|MGI:96560|interleukin 6 signal transducer; targeted mutation 1, Ashley R Dunn|Il6st|MGI:2388476|13||||||||||||||||Yes|||||||||||||Postnatal lethality: * numbers deficient at weaning * ratio of homozygotes normal at E18.Premature death (J:79555): * 6 month life span for males * 8 month life span for femalesDecreased body length: 20-30% shorter trunk length at birth.Decreased body weight: 20-30% lower body weight at birth.Abnormal uterine environment: failure of implantation, blastocysts will develop to term in wild-type recipient femalesFemale infertility: females show no external signs of pregnancy regardless of male genotype.Gastrointestinal haemorrhage: faecal blood at 4 months of age.Abnormal digestive system morphology.Rectal prolapse.Gastrointestinal ulcer: * caecal ulcers * ulceration of the anorectal regionGgastric ulcer: ulceration of the gastric pylorus at 4 months of age.Large intestinal inflammation: caecal inflammation.Increased susceptibility to induced colitis: * severe erosion of the intestinal epithelium from exposure to 3.5% dextran sodium sulfate. * remain moribund when exposure is ended.Abnormal leukocyte cell number: white blood cell count significantly higher than in controls.Decreased immunoglobulin level.Decreased IgA level: * basal IgA levels are reduced * impaired ability to mount an intestinal IgA response after challenge * basal IgM is normalDecreased IgG level: impaired ability to mount an intestinal IgG response after challenge.Conjunctivitis.Increased susceptibility to parasitic infection: tend to carry higher parasitic loads.Abnormal common myeloid progenitor cell morphology: * colony forming cells elevated in the spleen but not in bone marrow * elevated "CFU-S" hematopoietic progenitor cells * hematopoietic progenitors elevated in the liver at E14 relative to controls.Abnormal megakaryocyte morphology.Abnormal thrombopoiesis: * impaired maturation of megakaryocytes to produce platelets * 40% reduction in the number of platelets produced per megakaryocyte.Decreased platelet cell number: platelet count reduced 30%.Decreased megakaryocyte cell number: by 23% in bone marrow.Increased megakaryocyte cell number: numbers in spleen increased 2 fold relative to controls.Skeleton phenotype: trabecular bone volume is normal.Abnormal femur morphology.Decreased diameter of femur: significantly reduced femoral width.Short femur.Abnormal joint morphology.Abnormal joint capsule morphology: * cartilaginous nodules in joint capsules that replace menisci and support cartilage in knee joints * erosion of articular surfaces in older mice.Joint swelling: * of weight bearing joints in 60% of adults * observed by 7 days of age * more severe in males than femalesAbnormal joint mobility: * flexion abnormalities of hindlimbs * reluctance to stand * restricted flexion and extension of ankles and wrists * stiffness of one or more limbsIncreased cell proliferation: proliferative response of fibroblasts in culture to Il6 is increased.Gastrointestinal hemorrhage: fecal blood at 4 months of age.|Unknown||Yes|No|Yes|Yes|Yes|Yes|No|Unknown|||Mate homozygous males with heterozygote females|No|09-May-2011|Cryopreserved sperm|50.0|0.0|Unknown||signal transduction, kinase, STAT, IL6, gp130, joint|Yes| 5570.0|MCC floxed|B6.Cg-Mcc/AusbApb|Maija|Recessive|mutated in colorectal cancers|Mcc|||MGI:96930|mutated in colorectal cancers; targeted mutation 1, Maija Kohonen-Corish|Mcc|MGI:6810152|18||||||||||Unknown to Unknown|||||||||||||||||||Normal|Normal|C57BL/6J|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|29-Aug-2011|Cryopreserved sperm|50.0|0.0|Unknown||tumour suppressor, phosphorylation, nuclear localization, signal transduction|Possibly| 6640.0|NOD.HinsA|NOD-Tg(Tcra/Tcrb) Tg(Ins2-INS1)1/StvApb||Dominant||||||||||||||||||||||||||T-cell receptor alpha chain /T-cell receptor beta chain||||||||||||Unknown|Normal|NOD/Lt|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Good|||Intercrossing|No|03-Nov-2011|Cryopreserved sperm|45.0|0.0|Yes|NOD/Lt mice develop type 1 diabetes. These transgenic mice were made to study this disease.|Diabetes, Tolerance, Autoantigen, Autoimmunity, insulin|Yes| 6640.0|NOD.HinsA|NOD-Tg(Tcra/Tcrb) Tg(Ins2-INS1)1/StvApb||Dominant||||||||||||||||||||||||||human insulin|rat insulin promoter (RIP) (Ins2)|||||||||||Unknown|Normal|NOD/Lt|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Good|||Intercrossing|No|03-Nov-2011|Cryopreserved sperm|||Yes|NOD/Lt mice develop type 1 diabetes. These transgenic mice were made to study this disease.|Diabetes, Tolerance, Autoantigen, Autoimmunity, insulin|Yes| 6849.0|BomKI ; Grhl2 knockin|B6.129-Grhl3/MarpApb||Recessive|grainyhead-like 3 (Drosophila)|Grhl3||ct, Get1, nmf231, Som|MGI:2655333|grainyhead-like 3 (Drosophila); targeted mutation 2.1, Stephen M Jane|Grhl3|MGI:4836382|4|||||||||||||||||||||||||||||All homozygous mice have neural tube defects including spina bifida (in the lumbo-sacral region in almost all embryos) and curly tail.Complete lethality during fetal growth through weaning:• die between E18.5 and weaning|Normal, small percentage displays neural tube defects such as curlytail and spina-bifida.|C57BL/6|No|No|Yes|No|No|Yes|No|Good|||KI/+ x +/+|No|14-Mar-2012|Cryopreserved sperm|50.0|0.0|Unknown||spine, embryonic lethal, closure|Possibly| 6850.0|Grhl1KO|C57BL/6-Grhl1/MarpApb||Recessive|grainyhead-like 1 (Drosophila)|Grhl1|Nil|LBP-32, p61 MGR, p70 MGR, Tcfcp2l2|MGI:2182540|grainyhead-like 1 (Drosophila); targeted mutation 1, Stephen M Jane|Grhl1|MGI:3778923|2|||||||||||||||||||||||||||||Homozygous mice are small and have a variable hair phenotype leading to hair loss.Postnatal growth retardation: similar in size at birth and at 2 months of age but significantly smaller than littermate controls at weaning.Cardiovascular system phenotype: unlike human patients with striate palmoplantar keratoderma disorder, no evidence of cardiomyopathy is detected.Alopecia: * over 30% of mice lack hair at weaning with the remainder having sparse coats * extensive regional hair loss is seen when mice are housed with other mice with regrowth when mice are housed alone * despite the thinner coat, in a tape-stripping test more hairs are removed compared to wild-type controls.Delayed hair appearance: delay in coat growth that may be the result of maternal grooming.Sparse hair: * over 30% of mice lack hair at weaning with the remainder having sparse coats * coat remains sparse throughout lifeAbnormal hair follicle morphology: * sections of skin from hypotrichotic regions contain empty cysts in telogen follicles * cleft between the inner and outer root sheath * depilated hairs have a naked anagen bulb lacking the inner and outer root sheathAbnormal epidermal layer morphology: fewer desmosomes are identified in the interfolicular epidermis and unlike in wild-type mice, this number is further reduced after EGTA treatment.Hyperkeratosis: marked thickening of the stratum corneum on the palmoplantar surfaces of the paws.|Normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|||+/- x +/-|No|14-Mar-2012|Cryopreserved sperm|50.0|0.0|Yes|Keratosis Palmoplantaris Striata I; PPKS1 ; Loose Anagen Hair Syndrome|Hair, Coat, follicle|Possibly| 6851.0|Grhl2KO|B6.129S1-Grhl2/MarpApb||Recessive|grainyhead-like 2 (Drosophila)|Grhl2|Nil|0610015A08Rik, BOM, Tcfcp2l3|MGI:2182543|grainyhead-like 2 (Drosophila); targeted mutation 1.1, Stephen M Jane|Grhl2|MGI:4836381|15|||||||||||||||||||||||||||||Homozygous mice are embryonic lethal, dying around E12.5.Complete embryonic lethality during organogenesis: die at approximately E11.5.Abnormal neural tube closure: the posterior neuropore remains open at E10.5.Cranioschisis.Facial cleft: fully penetrant split face malformation.Abnormal neural fold elevation formation: * the dorso-lateral hinge points fail to form in the cephalic region by the 15 - 25 somite stage * however, in areas of the spinal cord above the neural tube defect dorso-lateral hinge formation is seen.|Normal|C57BL/6|No|No|Yes|No|No|Yes|No|Good|||+/- x +/+|No|14-Mar-2012|Cryopreserved sperm|50.0|0.0|Unknown||neural fold, split-face malformation, exencephaly, neuro-epithelial folding, neural tube|Possibly| 7754.0|GFP|BALB/c-Tg(CAG-GFP)/MarpApb||Dominant||||||||||||||||||||||||||Green fluorescent protein|B-actin (CAG)|||||||||||Wildtype are normal.These mice express the GFP reporter gene under the beta-actin promoter. All cells are fluorescent green under UV light. GPF expressed in all cells where beta-actin in transcribed.|These mice express the GFP reporter gene under the beta-actin promoter. All cells are fluorescent green under UV light. GPF expressed in all cells where beta-actin in transcribed.|BALB/c|Yes|Yes|Yes|Yes|Yes|Yes|No|Excellent|not applicable|Over 5 years|Heterozygote with wildtype (either sex)|No|07-Oct-2014|Cryopreserved sperm|40.0|0.0|No||stem cells|Yes| 7989.0|Muc13 knockout|B6.129-Muc13||Dominant|mucin 13, epithelial transmembrane|Muc13|Nil|114/A10, Ly64|MGI:103190||||16|||||||||||||||||||||||||||||No unchallenged phenotype and more severe intestinal inflammation and epithelial apoptosis under stress.|Normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Excellent|12||This strain can be maintained by het x het or hom x hom.|No|04-Nov-2015|Cryopreserved sperm|48.0|0.0|No||mucin, Muc13, colonic cancer, epithelial transmembrane, inflammation, colitis|Yes| 7999.0|Y-GFPd2 ; Ddx3y_cl.115_GFP|129-Ddx3y/KalpApb|Ygfpd2|Semi-dominant|DEAD (Asp-Glu-Ala-Asp) box polypeptide 3, Y-linked|Ddx3y|Normal|8030469F12Rik, D1Pas1-rs1, Dby|MGI:1349406||||Y|||||||||||||||||||||||||||||Normal|Most tissues express the green fluorescent protein gene. There is variation in expression between tissues.|12951/Sv1mJ |Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|04-Dec-2015|Cryopreserved sperm|60.0|0.0|No||GFP, reporter|Yes| 6922.0|Recql4+/-|C57BL/6-Recql4/Apb||Dominant|RecQ protein-like 4|Recql4|Nil||MGI:1931028|Recql4 germ-line knockout|||15|||||||||||||||||||||||||||||homozygous lethal at or before E10.5|apparently normal - viable, fertile|C57BL/6|No|No|Yes|No|No|Yes|No|Excellent|generated on pure C57Bl/6 so not backcrossed. Only maintained on C57||+/- to +/-|No|27-Jun-2012|Cryopreserved sperm|64.0|0.0|Yes|Rothmund-Thomson Syndrome||Possibly| 6852.0|Grhl3KO|B6.129S1-Grhl3/MarpApb||Recessive|grainyhead-like 3 (Drosophila)|Grhl3|Nil|ct, Get1, nmf231, Som|MGI:2655333|grainyhead-like 3 (Drosophila); targeted mutation 1, Stephen M Jane|Grhl3|MGI:2684328|4|||||||||||||||||||||||||||||Homozygous mice die at birth from severe spina bifida.Complete preweaning lethality: mutant embryos were represented in Mendelian ratios up to E18.5; no mice survived to weaning.Decreased embryo size: embryos show growth retardationSpina bifida: * all embryos had thoracolumbosacral spina bifida and curled tails * the neural plate appeared to furrow normally, but neural foled elevation did not occur * the incidence of spina bifida could not be reduced with folate treatment.Kinked tail.Kyphosis.Abnormal vertebrae morphology: full body skeletal preparations showed abnormalities in the vertebral column.Abnormal vertebral spinous process morphology: splayed spinal processes.Absent vertebral arch: lack of vertebral arch formation.Exencephaly: 2% of mutants had coincident exencephaly|Normal|C57BL/6|No|No|Yes|No|No|Yes|No|Good|||+/- x +/+|No|14-Mar-2012|Cryopreserved sperm|50.0|0.0|Yes|Spina Bifida|transcription factor, epidermis, lipid, neural tube, spina bifida|Possibly| 7979.0|Nrp1:Cre/EGFP|C57BL/6-Tg(Nrp1-cre/Egfp)||Dominant||||||||||||||||||||||||||Cre recombinase/EGFP|Nrp1|low||||||||||Normal|Normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|09-Oct-2015|Cryopreserved sperm|50.0|0.0|No||Neuropilin 1, Nrp1, Cre recombinase|Possibly| 8000.0|Y-RFP ;Ddx3y_cl.106_RFP|129-Ddx3y/106KalpApb|Yrfp|Semi-dominant|DEAD (Asp-Glu-Ala-Asp) box polypeptide 3, Y-linked|Ddx3y|Normal||MGI:1349406||||Y|||||||||||||||||||||||||||||Normal|Most tissues express the mKate2 red fluorescent protein gene. There is some variation in expression between tissues.|12951/Sv1mJ |Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|04-Dec-2015|Cryopreserved sperm|50.0|0.0|No||RFP|Yes| 6909.0|BAC(A33:M2rtTA)|B6;129-Tg(Gpa33-rtTAS*M2)2/LudApb||Dominant|||||||||||||||||||||||||||glycoprotein A33 (transmembrane), Gpa33|Mosaic activity in intestinal epithelium||||||||||Not described|The M2rtTA tet transactivator is expressed in the epithelium of the intestine and colon under the control of the intestine-specific A33 promoter. The expression/activety of the transactivator is mosaic, most likely due to stochastic transgene silencing. Approximately 1 to 5 crypts in the proximal small intestine express the transgene, fewer in the distral intestine and colon.|C57BL/6 x 129|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|20-Jun-2012|Cryopreserved sperm|50.0|0.0|No||intestine, epithelium, tetracycline|Possibly| 7035.0|Osx-Cre p53fl/fl pRbfl/fl|STOCK Rb1 Trp53 Tg(Sp7-tTA,tetO-EGFP/cre)1Amc/StvApb||Dominant|transformation related protein 53|Trp53|Nil|p53|MGI:98834|transformation related protein 53; targeted mutation 1, Anton Berns|Trp53|MGI:1931011|11|||||||||||||||||Osx-Cre:GFP - transgene insertion 1, Andrew P McMahon|Osterix (Sp7)|medium||||||||||Generate osteosarcoma (bone cancer)Conditional mouse osteosarcoma, dependent on p53 loss and potentiated by loss of Rb, mimics the human disease.|Slightly smaller, susceptible to malocclusion. Generate osteosarcoma if p53fl/+ but at long latency (1yr)|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|5||Cre+ve males to Cre-ve females, homozygous pRb and p53|No|03-Aug-2012|Cryopreserved sperm|27.0|0.0|Yes|Osteosarcoma|osteosarcoma, Osx-Cre, p53fl/fl, pRbfl/fl|Yes| 7035.0|Osx-Cre p53fl/fl pRbfl/fl|STOCK Rb1 Trp53 Tg(Sp7-tTA,tetO-EGFP/cre)1Amc/StvApb||Dominant|retinoblastoma 1|Rb1|Nil|pRb, Rb, Rb-1|MGI:97874|retinoblastoma 1; targeted mutation 3, Tyler Jacks|Rb1|MGI:2450162|14|||||||||||||||||||||||||||||Generate osteosarcoma (bone cancer)Conditional mouse osteosarcoma, dependent on p53 loss and potentiated by loss of Rb, mimics the human disease.|Slightly smaller, susceptible to malocclusion. Generate osteosarcoma if p53fl/+ but at long latency (1yr)|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|5||Cre+ve males to Cre-ve females, homozygous pRb and p53|No|03-Aug-2012|Cryopreserved sperm|||Yes|Osteosarcoma|osteosarcoma, Osx-Cre, p53fl/fl, pRbfl/fl|Yes| 7792.0|LacIR|B6.FVB/N-Tg(ACTB-lacI*)1Scrb/AnuApb||Dominant||||||||||||||||||||||||||transgene insertion 1, Heidi Scrable|Human beta-actin rabbit beta-globin fusion promoter|ubiquitous||||||||||Normal|Normal|C57BL/6JAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Excellent| more than 8|3|Standard|No|20-Nov-2014|Cryopreserved sperm|84.0|0.0|Unknown|||Possibly| 7039.0|Osx-Cre p53.1224 pRbfl/fl|C57BL/6-Rb1 Tg(Sp7-tTA,tetO-EGFP/cre)1Amc Tg(tetO-GFP/RNAi:Trp53)Slowe/CrwApb||Dominant|retinoblastoma 1|Rb1|Nil|pRb, Rb, Rb-1|MGI:97874|retinoblastoma 1; targeted mutation 3, Tyler Jacks|Rb1|MGI:2450162|14|||||||||||||||||transgene insertion 1, Andrew P McMahon|Osterix (Sp7)|medium||||||||||Mice generate osteosarcoma (bone cancer) which is the osteoblastic subtype (Cre:lox line generated a fibroblastic OS).|Mice are slightly smaller, susceptible to malocclusion. long latency, highly metastatic OS. |C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|5||Cre+ve males to Cre-ve females, homozygous pRb and p53.1224 +ve|No|06-Aug-2012|Cryopreserved sperm|54.0|0.0|Yes|Osteosarcoma|osteosarcoma, Osx-Cre, TRE-p53.1224, pRbfl/fl, shRNA|Yes| 7039.0|Osx-Cre p53.1224 pRbfl/fl|C57BL/6-Rb1 Tg(Sp7-tTA,tetO-EGFP/cre)1Amc Tg(tetO-GFP/RNAi:Trp53)Slowe/CrwApb||Dominant||||||||||||||||||||||||||TRE-p53.1224|tet-responsive TRE-CMV promoter|good||||||||||Mice generate osteosarcoma (bone cancer) which is the osteoblastic subtype (Cre:lox line generated a fibroblastic OS).|Mice are slightly smaller, susceptible to malocclusion. long latency, highly metastatic OS. |C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|5||Cre+ve males to Cre-ve females, homozygous pRb and p53.1224 +ve|No|06-Aug-2012|Cryopreserved sperm|||Yes|Osteosarcoma|osteosarcoma, Osx-Cre, TRE-p53.1224, pRbfl/fl, shRNA|Yes| 7053.0|A33 hfneo|B6;129/Sv-Gpa33/LudApb||Recessive|glycoprotein A33 (transmembrane)|Gpa33|Unknown|2010310L10Rik, 2210401D16Rik, A33 antigen|MGI:1891703||||1|||||||||||||||||||||||||||||This strain shows no phenotypic signs different from wildtype|Normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|21-Aug-2012|Cryopreserved sperm|50.0|0.0|Unknown|||Possibly| 7236.0|K5rTA-TetOmOVA 0413|C57BL/6-Tg(K5-rTA)04Cbn Tg(TetOmOVA)13Cbn/Apb||Dominant||||||||||||||||||||||||||tetracycline-regulated transcriptional transactivator|bovine keratin-5|||||||||||In these mice following oral doxycyline treatment, rTA expresssion induced in the skin activates the TetO promoter for mOVA expression in the skin.In the absence of doxycyline treatment the mice are normal for lifespan and breeding.|As for homozygous mice.|C57Bl/6|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Good||||No|28-Nov-2012|Cryopreserved sperm|45.0|0.0|No||autoimmunity, ovalbumin, doxycyline inducible|Yes| 7236.0|K5rTA-TetOmOVA 0413|C57BL/6-Tg(K5-rTA)04Cbn Tg(TetOmOVA)13Cbn/Apb||Dominant||||||||||||||||||||||||||transferrin receptor membrane domain and ovalbumin residues 139-385)|CMV minimal promoter and 7 TetO sequences|||||||||||In these mice following oral doxycyline treatment, rTA expresssion induced in the skin activates the TetO promoter for mOVA expression in the skin.In the absence of doxycyline treatment the mice are normal for lifespan and breeding.|As for homozygous mice.|C57Bl/6|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Good||||No|28-Nov-2012|Cryopreserved sperm|||No||autoimmunity, ovalbumin, doxycyline inducible|Yes| 7237.0|K5rTA-TSLP 0419|C57BL/6-Tg(K5-rTA)04Cbn Tg(TetO-TSLP)19Cbn/Apb||Dominant||||||||||||||||||||||||||tetracycline-regulated transcriptional transactivator|bovine keratin-5|||||||||||In these mice following oral doxycyline treatment, rTA expresssion induced in the skin activates the TetO promoter driving TSLP expression in the skin.In the absence of doxycyline treatment the mice are normal for lifespan and breeding.|As for homozygous mice.|C57Bl/6|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Good|||Tg/+ +/+ x +/+ Tg/+|No|28-Nov-2012|Cryopreserved sperm|50.0|0.0|Yes||thymic stromal lymphopoietin, dermatitis, doxycyline inducible|Possibly| 7237.0|K5rTA-TSLP 0419|C57BL/6-Tg(K5-rTA)04Cbn Tg(TetO-TSLP)19Cbn/Apb||Dominant||||||||||||||||||||||||||thymic stromal lymphopoietin|CMV minimal promoter and 7 TetO sequences|||||||||||In these mice following oral doxycyline treatment, rTA expresssion induced in the skin activates the TetO promoter driving TSLP expression in the skin.In the absence of doxycyline treatment the mice are normal for lifespan and breeding.|As for homozygous mice.|C57Bl/6|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Good|||Tg/+ +/+ x +/+ Tg/+|No|28-Nov-2012|Cryopreserved sperm|||Yes||thymic stromal lymphopoietin, dermatitis, doxycyline inducible|Possibly| 7100.0|Osx-Cre Rb|B6(Cg)-Rb1 Tg(Sp7-tTA,tetO-EGFP/cre)1Amc/StvApb||Dominant|retinoblastoma 1|Rb1|Normal|pRb, Rb, Rb-1|MGI:97874|retinoblastoma 1; targeted mutation 3, Tyler Jacks|Rb1|MGI:2450162|14|||||||||||||||||transgene insertion 1, Andrew P McMahon|Osterix (Sp7)|good in osteoblast precursors||||||||||No obvious phenotype. No effect on lifespan, breeding or skeleton|None observed. Osx-Cre mice have phenotypes due to teh Osx-Cre - malocclusion, slightly smaller than a truw wild-type. No other effect of loss of Rb|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|5|unknown/not collected|Osx-Cre+ve pRBfl/+ male to Osx-Cre-ve pRBfl/+ female|No|04-Oct-2012|Cryopreserved sperm|40.0|0.0|Yes|hereditary retinoblastoma - bone specifc model|Rb, Osx-Cre, osteosarcoma|Yes| 7240.0|ADAR1 E861A|C57BL/6-Adar/SviApb||Dominant|adenosine deaminase, RNA-specific|Adar |Unknown|ADAR1, mZaADAR|MGI:1889575 |adenosine deaminase, RNA-specific; targeted mutation 2184, TaconicArtemis|Adar1|MGI:5805648|3|||||||||||||||||||||||||||||Homozygous lethal at ~E12.5|heterozygous animals are normal and fertile with no apparent abnormalities|C57BL/6|No|Yes|Yes|No|Yes|Yes|No|Good|on pure C57BL/6 - was derived on C57 ES line||ki/+ crossed to ki/+|No|03-Dec-2012|Cryopreserved sperm|36.0|0.0|Yes|Aicardi-Goutières syndrome||Possibly| 7304.0|PbT-II-129|C57BL/6-Tg(H-2K-TcraD78TcrbD78)129Cbn/Apb||Dominant||||||||||||||||||||||||||transgene insertion 129, Francis Carbone|H-2Kb|||||||||||Majority of CD4 T cells express the transgenic T cell recepter Va2Vb12 specific for Plasmodium berghei (Pb) parasites.|As for homozygous|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Excellent||4|brother-sister or Tg positive to C57BL/6|No|05-Apr-2013|Cryopreserved sperm|45.0|0.0|Yes|Used to model cerebral/severe malaria|malaria, Plasmodium berghei, CD4 TCR transgenic|Yes| 7309.0|K5rTA-Rae1-29|C57BL/6-Tg(K5-rTA)04Cbn Tg(TetO-RaeT1e)29Cbn/Apb||Dominant||||||||||||||||||||||||||tetracycline-regulated transcriptional transactivator|bovine keratin-5|||||||||||In these mice following oral doxycyline treatment, rTA expresssion induced in the skin activates the TetO promoter driving RaeT1e expression in the skin.|As for homozygous mice.|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||5|Tg Tg x Tg Tg|No|09-Apr-2013|Cryopreserved sperm|45.0|0.0|Yes||etinoic acid early transcript 1E, doxycyline inducible|Yes| 7309.0|K5rTA-Rae1-29|C57BL/6-Tg(K5-rTA)04Cbn Tg(TetO-RaeT1e)29Cbn/Apb||Dominant||||||||||||||||||||||||||transgene insertion 29, Frank Carbone|CMV minimal promoter and 7 TetO sequences|||||||||||In these mice following oral doxycyline treatment, rTA expresssion induced in the skin activates the TetO promoter driving RaeT1e expression in the skin.|As for homozygous mice.|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||5|Tg Tg x Tg Tg|No|09-Apr-2013|Cryopreserved sperm|||Yes||etinoic acid early transcript 1E, doxycyline inducible|Yes| 7467.0|Bm1.OT-1|B6.C-H2 Tg(TcraTcrb)1100Mjb/Apb||Dominant||||||||||||||||||||||||||transgene insertion 1100, Michael J Bevan|H-2K promoter||histocompatibility 2, K region|H2-K|||MGI:3040519|histocompatibility 2, K region; b haplotype mutation 1|H2-K|MGI:3618114|17|Transgenic mice on a C57BL/6 background are somewhat immunodeficient, and may be used to study the role of peptides in positive selection and the response of CD8+ T cells to antigen.Carry OVA-specific, H-2K-restricted T cell receptor|Normal|B6.C-H2/ByJ|Yes|Yes|Yes|Yes|Yes|Yes|No|Excellent|10|||No|29-Oct-2013|Cryopreserved sperm|50.0|0.0|No||T cell, receptor, ovalbumin, CD8|Yes| 7589.0||C57BL/6-Grb10-global||Dominant|growth factor receptor bound protein 10|Grb10|Reduced|5730571D09Rik, maternally expressed gene 1, Meg1, mKIAA0207|MGI:103232||Grb10Δ||11|||||||||||||||||||||||||||||Homozygotes are rare. If produced, they have the phenotype of being very large at birth|Paternal heterozygotes - normalMaternal heterozygotes - large during embryogenesis and large at birth|C57BL/6|Unknown|No|Yes|Unknown|Unknown|Yes|No|Good|||paternal heterozygotes x WT to be used for breeding|No|14-Feb-2014|Cryopreserved sperm|50.0|0.0|Unknown||imprinting, development, muscle, growth|Yes| 7263.0|R26-CreERT2 Recql4fl/fl|B6.129-Gt(ROSA)26Sor Recql4/SviApb||Dominant|gene trap ROSA 26, Philippe Soriano|Gt(ROSA)26Sor |Unknown|Gt(ROSA)26Sor, R26, Rosa26|MGI:104735|gene trap ROSA 26, Philippe Soriano; targeted mutation 1, Tyler Jacks|Gt(ROSA)26Sor|MGI:3699244|6|||||||||||||||||||||||||||||Non tamoxifen treated animals are viable, fertile and are slightly smaller than wild-type controls|No apparent phenotype|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|generated on C57 (Recql4fl/fl); 129S4/SvJae-derived J1 embryonic stem (ES) cells and backcrossed 8 times to C57BL/6 by the donating laboratory|1|R26-CreERT2 ki/ki Recql4fl/+ male crossed to Recql4fl/+ female|No|18-Jan-2013|Cryopreserved sperm|50.0|0.0|Yes|Rothmund-Thomson Syndrome|Recql4, R26-CreERT2|Possibly| 7263.0|R26-CreERT2 Recql4fl/fl|B6.129-Gt(ROSA)26Sor Recql4/SviApb||Dominant|RecQ protein-like 4|Recql4|Nil|RECQ4|MGI:1931028|RecQ protein-like 4; targeted mutation 1.1, TaconicArtemis|Recql4|MGI:5645319|15|||||||||||||||||||||||||||||Non tamoxifen treated animals are viable, fertile and are slightly smaller than wild-type controls|No apparent phenotype|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|generated on C57 (Recql4fl/fl); 129S4/SvJae-derived J1 embryonic stem (ES) cells and backcrossed 8 times to C57BL/6 by the donating laboratory|1|R26-CreERT2 ki/ki Recql4fl/+ male crossed to Recql4fl/+ female|No|18-Jan-2013|Cryopreserved sperm|||Yes|Rothmund-Thomson Syndrome|Recql4, R26-CreERT2|Possibly| 7291.0|floxed AR Neo-|B6.129-Ar/Apb||X-linked|androgen Receptor|Ar|Normal||MGI:88064|androgen receptor; targeted mutation 1, Jeffrey D Zajac|Ar|MGI:3717246|X|||||||||||||||||||||||||||||Normal|Normal|C57BL/6J|Yes|Yes|Yes|Unknown|Unknown|Yes|No|Excellent|>20|||No|19-Mar-2013|Cryopreserved sperm|50.0|0.0|Unknown||androgen, fertility|Possibly| 7303.0|PbT-II-157|C57BL/6-Tg(TcraD78TcrbD78)157Cbn/Apb||Dominant||||||||||||||||||||||||||transgene insertion 157, Francis Carbone|H-2Kb|||||||||||Majority of CD4 T cells express the transgenic T cell recepter Va2Vb12 specific for Plasmodium berghei (Pb) parasites.|As for homozygous|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Excellent||4|brother-sister or Tg positive to C57BL/6|No|05-Apr-2013|Cryopreserved sperm|45.0|0.0|Yes|Used to model cerebral/severe malaria|malaria, Plasmodium berghei, CD4 TCR transgenic|Yes| 7331.0|ADAR1 +/-|B6.129-Adar/TacStvApb||Dominant|adenosine deaminase, RNA-specific|Adar|Nil|ADAR1, mZaADAR|MGI:1889575|adenosine deaminase, RNA-specific; targeted mutation 1, Peter H Seeburg |Adar|MGI:3029789|3|||||||||||||||||||||||||||||Homozygous animals die at E11.5.|Heterozygous animals normal and healthy|C57BL/6|No|Yes|Yes|No|Yes|Yes|No|Excellent|more than 6|unknown/not collected|+/- to +/-|No|09-May-2013|Cryopreserved sperm|30.0|0.0|Yes|Mutations in ADAR1 cause Aicardi-Goutières syndrome associated with a type I interferon signature. Nat Genet. 2012 Sep 23. doi: 10.1038/ng.2414|ADAR1, RNA editing|Yes| 7480.0|PbT-I-25/Ly5.1 ; C57BL/6-Tg(TCRaB4-46TcrbB4-46)25Cbn|C57BL/6-Ptprc Tg(H2-K-Tcra,-Tcrb)25Cbn/AnuApb||Dominant||||||||||||||||||||||||||transgene insertion 25, Francis Carbone|H-2Kb||protein tyrosine phosphatase, receptor type, C|Ptprc||B220, CD45, Ly-5, Lyt-4, T200|MGI:97810|protein tyrosine phosphatase, receptor type, C; a variant|Ptprc|MGI:4819849|1|Majority of CD8 T cells express the transgenic T cell recepter Va8Vb10 specific for Plasmodium berghei (Pb) parasites.|As for homozygous|C57BL/6|Yes|Yes|Yes|Unknown|Unknown|Unknown|No|Excellent||4|brother-sister|No|14-Nov-2013|Cryopreserved sperm|20.0|107.0|Yes|Used to model cerebral/severe malaria|malaria, Plasmodium berghei, CD8 TCR transgenic|Yes| 7294.0|B6NCrl redev - Yellow G7|C57BL/6NCrlAnu-redev - YellowG7||Dominant||||||||||||||||||||||||||||||||||||||Normal||C57BL/6NCrlAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|21-Mar-2013|Cryopreserved sperm|18.0|0.0|Unknown|||No| 5230.0|Mincle F / MNB|C57BL/6J-Clec4e/Apb||Semi-dominant|C-type lectin domain family 4, member e|Clec4e|Nil|Clecsf9, Mincle|MGI:1861232|C-type lectin domain family 4, member e; targeted mutation 1, Peter Sobieszczuk|Clec4e|MGI:3618604|6||||||||||||||||Yes|||||||||||||Approx 20% decrease in white blood cell count, though still within normal range. Heart valves with increased amounts of extracellular matrix.|Unknown|C57BL/6J|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|not known|4 years||No|06-Oct-2010|Cryopreserved sperm|40.0|0.0|Yes|oral and vaginal candidiasis (thrush)|C-type lectin, Pattern recognition receptor, Innate immunity, Macrophage, Tuberculosis, Yeast infection|Yes| 5382.0|Clone 4|BALB/c-Tg(TcraCl4,TcrbCl4)1Shrm/Apb||Dominant||||||||||||||||||||||||||transgene insertion 1, Linda Sherman|Tcra, Tcrb|||||||||||Normal|Normal|BALB/c|Yes|Yes|Yes|Yes|Yes|Yes|No|Poor|||Clone 4 males with clone 4 females or BALB/c females|No|07-Jan-2011|Cryopreserved sperm|10.0|0.0|Unknown||TCR transgenic, CD8, influenza A virus|Possibly| 10506.0|CK1D1 ROSA26 KI|B6.-Gt(ROSA)26Sor||Recessive|gene trap ROSA 26, Philippe Soriano|Gt(ROSA)26Sor|||MGI:104735|casein kinase 1 delta transcript variant 1 knock in|Gt(ROSA)26Sor||6|||||||||||||||||||||||||||||Normal|Normal||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|31-Mar-2025||0.0|0.0|Unknown|||No| 7536.0|Tpcn1∆|B6.129S5-Tpcn1/Ausb||Dominant|two pore channel 1|Tpcn1|Unknown||MGI:2182472|two pore channel 1; gene trap OST359423, Lexicon Genetics|Tpcn1|MGI:3529820|5||||||||||||||||No|||||||||||||Unknown|Unknown|C57Bl/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|12-Dec-2013|Cryopreserved sperm|40.0|0.0|Unknown||channel, Pore|Possibly| 7829.0|MDA5-/-|B6(Cg).129X1-Ifih1/JStVApb|Ifih1tm1.1Cln|Dominant|interferon induced with helicase C domain 1|Ifih1|Nil|9130009C22Rik, Helicard, MDA5, MDA-5|MGI:1918836|interferon induced with helicase C domain 1; targeted mutation 1.1, Marco Colonna|Ifih1|MGI:3663677|2|||||||||||||||||||||||||||||Increased sensitivity to induced morbidity/mortality:*mice die sooner than wild-type following encephalomyocarditis virus infection.Abnormal cytokine secretion:*both naked and transfected polyI:C induced cytokine secretion is reduced 2- to 3-fold.*IFN-alpha, IL-6 and MCP-1 secretion in response to encephalomyocarditis virus infection (EMCV) is abrogated.Decreased interferon-alpha secretion:*IFN-alpha production following polyI:C induction is abrogated.*IFN-alpha induction by recombinant influenza A with the R38A NS1 mutation, West Nile wirus, Sindbus virus and herpes simplex virus-1 is reduced 2-fold.Decreased interleukin-6 secretion:* polyI:C induction of IL-6 is reduced in a limited fashion.Increased susceptibility to viral infection:*following encephalomyocarditis virus infection (EMCV), mice develop symptoms of hindlimb paralysis earlier (at 24 to 72 hours) and die sooner.* IFN-alpha, IL-6 and MCP-1 secretion in response to EMCV is abrogated.* IFN-alpha induction by recombinant influenza A with the R38A NS1 mutation, West Nile virus, Sindbus virus and herpes simplex virus-1 is reduced 2-fold.* however, response to murine cytomegalovirus (MCMV) and reovirus is normal.|Hets are normal and have a normal immune response|C57BL/6N, C57BL/6J|Yes|Yes|Yes|Yes|Yes|Yes|No|Excellent|directly purchased form Jackson Labs Dec 2014 and interbred with each other|directly purchased form Jackson Labs Dec 2014 and interbred with each other|KO male to KO female|No|08-Jan-2015|Cryopreserved sperm|40.0|0.0|Yes|Aicardi-Goutieres Syndrome 7; AGS7|Ifih1, MDA5, infection, receptor, encephalomyocarditis picornavirus|Possibly| 10507.0|Wnt9b-SpotTag|C57Bl/6J-Wnt9b/Apb||Dominant|wingless-type MMTV integration site family, member 9B|Wnt9b||clf1, Wnt14b, Wnt15|MGI:1197020|Wnt9b:endonuclease-mediated mutation 1, Alexander N. Combes|Wnt9b||11|ENSMUSG00000018486 ||||||||||||||||||||||||||||Normal|Normal|C57Bl/6J|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|14-Apr-2025|Cryopreserved sperm|50.0|0.0|Yes|understanding of the mechanisms of kidney development and disease in mouse and human kidney organoid models||Yes| 7295.0|B6NCrl redev - White G8|C57BL/6NCrlAnu-redev - WhiteG8||Dominant||||||||||||||||||||||||||||||||||||||Normal||C57BL/6NCrlAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|21-Mar-2013|Cryopreserved sperm|16.0|0.0|Unknown|||No| 7300.0|B6/JAnu-redev - Purple G19|C57BL/6JAnu-redev-PurpleG19||Dominant||||||||||||||||||||||||||||||||||||||||C57BL/6JAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|28-Mar-2013|Cryopreserved sperm|10.0|0.0|Unknown|||No| 5416.0|APC (580s) ; MF-01|STOCK Apc/Apb||Dominant|adenomatosis polyposis coli|Apc|Reduced|CC1, Min|MGI:88039|adenomatosis polyposis coli; targeted mutation 1, Tetsuo Noda|Apc|MGI:1857966|18||||||||||||||||Yes|||||||||||||Normal until:Hepatocellular carcinoma: * all mutant mice (n=15) develop hepatocellular carcinomas by 450 days of age * hepatic tumor volumes in homozygous mice are larger than in heterozygous mice * no intestinal polyps (>18 month, n=24)|Normal||Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|04-Feb-2011|Cryopreserved sperm|50.0|0.0|Yes|Familial adenomatous polyposis coli (FAP)|Familial adenomatous polyposis coli (FAP), colorectal adenomas, epithelium|Yes| 7544.0|Tlr2 KO|B6.129-Tlr2/AnuApb|B6.129-Tlr2/AnuApb|Recessive|toll-like receptor 2|Tlr2|Nil|Ly105|MGI:1346060|toll-like receptor 2; targeted mutation 1, Shizuo Akira|Tlr2|MGI:2178675|3||||||||||||||||Yes|||||||||||||Homozygous null mice demonstrate abnormal responses to bacterial and viral infections.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|13-Dec-2013|Cryopreserved sperm|40.0|0.0|Unknown||infection, bacterial, viral infection, macrophage|Yes| 9073.0|Scl-Cre-ERT|C57BL/6J-Tg/Jrg||Dominant|||||||||Unknown|||||||||||||||||ERT Inducible Cre|Tal enhancer|Unknown||||||||||Normal|Normal|C57BL/6J|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|Unknown|||No|04-Sep-2020|Cryopreserved sperm, Live|67.0|0.0|No||CRE, SCL, TAL1, Tamoxifen-inducible, Hematopoietic stem cells|Yes| 10492.0|Tlr4-mVenus|B6CBA-Tlr4/SagenSah||Dominant|toll-like receptor 4|Tlr4||Lps, Rasl2-8|MGI:96824||Tlr4||6|ENSMUSG00000039005 ||||||||||||||||||||||||||||Normal|Normal||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|03-Mar-2025|Cryopreserved sperm|30.0|0.0|Unknown|||Possibly| 10496.0|APP/PS1/IFNAR1-/-|APP/PS1/IFNAR1-/-||Dominant|APP - amyloid precursor protein||||||||Unknown|||||||||||||||||||||||||||||This mouse develops amyloid plaques and lacks the type-I interferon receptor.|Unknown|C57Bl/6J|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|20-Mar-2025|Cryopreserved sperm|40.0|0.0|Unknown|||Possibly| 128.0|Deirdre ; IgMdE|C57BL/6JSfdAnu-Tg(IgMdEHEL)Ccg/AnuApb|C57BL/6JSfdAnu-Tg(IgMδEHEL)Ccg/AnuApb|Dominant||||||||||||||||||||||||||chimeric anti-Hen Egg Lysozyme Ig molecule, the extracellular spacer of IgM was substituted for IgD.||H and L genes are cointegrated||||||||||B cells express chimeric IgM/D molecule with affinity for Hen Egg Lysozyme||C57BL/6JAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||10|sib x sib|No|06-Feb-2006|Cryopreserved sperm|20.0|0.0|No||B cell, Hen Egg Lysozyme (HEL), Immunoglobulin, tolerance, glycosylation|Yes| 5523.0|NOD-SBmut8|NOD/Lt-Tg(sb-pTrans-SA-IRESLacZ-CAG-GFP-SD:Neo)8TCB/Apb||Recessive||||||||||||||||||||||||||TgTn(sb-pTrans-SA-IRESLacZ-CAG-GFP-SD:Neo)2TCB||||||||||||Unknown|Unknown|NOD/Lt|Unknown|Unknown|Yes|Unknown|Unknown|Unknown|No|Unknown||||No|10-Jun-2011|Cryopreserved sperm|50.0|0.0|Unknown|||No| 7804.0|R26CreER RARaRARg R26eYFP|B6.Cg-Gt(ROSA)26Sor RARa RARg Gt(ROSA)26Sor/Apb||Recessive|gene trap ROSA 26, Philippe Soriano|Gt(ROSA)26Sor ||Gtrosa26, R26|MGI:104735||Gt(ROSA)26Sor|gene trap ROSA 26, Philippe Soriano; targeted mutation 1, Tyler Jacks|6|ENSMUSG00000086429 ||||||||||||||||||||||||||||In absence of tamoxifen cells are wildtype, when treated with tamoxifen loss of the vitamin A receptors, RARa and RARg occur, causing different phenotypes in distinct cell types.|Unknown|C57BL/6|Yes|Unknown|Unknown|Yes|Unknown|Unknown|No|Excellent|At least 10|||No|03-Dec-2014|Cryopreserved sperm|50.0|0.0|Unknown|||Possibly| 7804.0|R26CreER RARaRARg R26eYFP|B6.Cg-Gt(ROSA)26Sor RARa RARg Gt(ROSA)26Sor/Apb||Recessive|retinoic acid receptor, alpha|Rara|||MGI:97856|retinoic acid receptor, alpha; targeted mutation 1, Pierre Chambon|Rara|MGI:1857622|11|ENSMUSG00000037992 ||||||||||||||||||||||||||||In absence of tamoxifen cells are wildtype, when treated with tamoxifen loss of the vitamin A receptors, RARa and RARg occur, causing different phenotypes in distinct cell types.|Unknown|C57BL/6|Yes|Unknown|Unknown|Yes|Unknown|Unknown|No|Excellent|At least 10|||No|03-Dec-2014|Cryopreserved sperm|||Unknown|||Possibly| 7804.0|R26CreER RARaRARg R26eYFP|B6.Cg-Gt(ROSA)26Sor RARa RARg Gt(ROSA)26Sor/Apb||Recessive|retinoic acid receptor, gamma|Rarg||RARgamma2|MGI:97858|retinoic acid receptor, gamma; targeted mutation 1, Pierre Chambon|Rarg|MGI:1931079|15|||||||||||||||||||||||||||||In absence of tamoxifen cells are wildtype, when treated with tamoxifen loss of the vitamin A receptors, RARa and RARg occur, causing different phenotypes in distinct cell types.|Unknown|C57BL/6|Yes|Unknown|Unknown|Yes|Unknown|Unknown|No|Excellent|At least 10|||No|03-Dec-2014|Cryopreserved sperm|||Unknown|||Possibly| 7804.0|R26CreER RARaRARg R26eYFP|B6.Cg-Gt(ROSA)26Sor RARa RARg Gt(ROSA)26Sor/Apb||Recessive|gene trap ROSA 26, Philippe Soriano|Gt(ROSA)26Sor ||Gtrosa26, R26, ROSA26|MGI:104735|gene trap ROSA 26, Philippe Soriano; targeted mutation 1, Frank Costantini|Gt(ROSA)26Sor|MGI:2449038|6|ENSMUSG00000086429||||||||||||||||||||||||||||In absence of tamoxifen cells are wildtype, when treated with tamoxifen loss of the vitamin A receptors, RARa and RARg occur, causing different phenotypes in distinct cell types.|Unknown|C57BL/6|Yes|Unknown|Unknown|Yes|Unknown|Unknown|No|Excellent|At least 10|||No|03-Dec-2014|Cryopreserved sperm|||Unknown|||Possibly| 10493.0|B-Arrestin-mVenus|B6;CBA-Arrb2/SahgenSah||Recessive|arrestin, beta 2|Arrb2||beta arr2, beta-arrestin-2|MGI:99474||||11|ENSMUSG00000060216 ||||||||||||||||||||||||||||Normal|Normal||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|03-Mar-2025|Cryopreserved sperm|30.0|0.0|Unknown|||Possibly| 10481.0|Cx3cr1-Cre knock-in/knock-out|B6J.B6N(Cg)-Cx3cr1/J||Recessive|chemokine (C-X3-C motif) receptor 1|Cx3cr1|||MGI:1333815|C-X3-C motif chemokine receptor 1; targeted mutation 1.1, Steffen Jung|Cx3cr1|MGI:5467983|9|ENSMUSG00000052336 ||||||||||||||||||||||||||||Cx3cr1-Cre mice express Cre recombinase under the direction of the Cx3cr1 promoter in the mononuclear phagocyte system making them useful for fate-mapping studies of the monocyte and macrophage compartment, as well as microglia. Homozygous mice are viable and fertile. When Cx3cr1-Cre are bred with mice containing loxP-flanked sequence, cre-mediated recombination will result in deletion of the floxed sequences in the cre-expressing cells of the offspring. Homozygous mice do not express endogenous Cx3cr1.|same as homozygous mice except that heterozygous mice express endogenous CX3CR1.|C57Bl/6N|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|04-Feb-2025|Cryopreserved sperm|30.0|0.0|Unknown|||Possibly| 7839.0|C-alphaKO:Ly5aa:B6-JAX::G9|C57BL/6J-Ptprc Tcra ||Recessive| T cell receptor alpha chain|Tcra|||MGI:98553|T cell receptor alpha chain; targeted mutation 1, Peter Mombaerts|Tcra |MGI:1857255|14|||||||||||||||||||||||||||||TCR Calpha knockout mice on B6 background were obtained from Jackson labs in 1996. They have been maintained as B10.BR Ly5a with TCR transgene. Absence of Calpha gene prevents endogenous TCR alpha chain rearrangments. T cell development is blocked at the DP thymocyte stage and no T cell can be found in the periphery of homozygote mice. ||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|25-Jan-2015|Cryopreserved sperm|33.0|0.0|Unknown||T cell, receptor, rearrangement|Yes| 7839.0|C-alphaKO:Ly5aa:B6-JAX::G9|C57BL/6J-Ptprc Tcra ||Recessive|protein tyrosine phosphatase receptor type C|Ptprc|||MGI:97810|protein tyrosine phosphatase receptor type C; a variant|Ptprc|MGI:4819849|1|||||||||||||||||||||||||||||TCR Calpha knockout mice on B6 background were obtained from Jackson labs in 1996. They have been maintained as B10.BR Ly5a with TCR transgene. Absence of Calpha gene prevents endogenous TCR alpha chain rearrangments. T cell development is blocked at the DP thymocyte stage and no T cell can be found in the periphery of homozygote mice. ||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|25-Jan-2015|Cryopreserved sperm|||Unknown||T cell, receptor, rearrangement|Yes| 7865.0|TRAMP|C57BL/6-Tg(TRAMP)8247Ng/Apb||Recessive||||||||||||||||||||||||||transgene insertion 8247, Norman M Greenberg|rat Probasin promoter|||||||||||Transgenic mice on a C57BL6 background develop progressive forms of prostate cancer with distant site metastasis. Forms of disease range from mild intraepithelial hyperplasia to large multinodular malignant neoplasia. Tumors are detected in the prostate as early as 10 weeks of age. The tumors have elevated levels of nuclear TRP53 and decreased androgen receptor expression.|Transgenic mice on a C57BL6 background develop progressive forms of prostate cancer with distant site metastasis. Forms of disease range from mild intraepithelial hyperplasia to large multinodular malignant neoplasia. Tumors are detected in the prostate as early as 10 weeks of age. The tumors have elevated levels of nuclear TRP53 and decreased androgen receptor expression.|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Excellent||||Yes|08-Apr-2015|Cryopreserved sperm|50.0|0.0|Yes|Prostate Adenocarcinoma|TRAMP, Prostate cancer, preclinical trials|Yes| 7241.0|R26eYFP Recql4fl/fl|C57BL/6-Recql4 Gt(ROSA)26Sor/Apb||Dominant|RecQ protein-like 4|Recql4|||MGI:1931028|RecQ protein-like 4; targeted mutation 1.1, TaconicArtemis|Recql4|MGI:5645319|15|||||||||||||||||||||||||||||Homozygous animals are normal, fertile and viable (floxed line with eYFP reporter of cre activity)|Normal, fertile and viable (floxed line with eYFP reporter of cre activity)|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|generated on pure C57Bl/6 so not backcrossed. Only maintained on C57||homozygous R26eYFP Recql4fl/fl in breeding|No|06-Dec-2012|Cryopreserved sperm|50.0|0.0|Yes|Rothmund-Thomson Syndrome|Recql4, R26eYFP, Rothmund-Thomson Syndrome|Yes| 7241.0|R26eYFP Recql4fl/fl|C57BL/6-Recql4 Gt(ROSA)26Sor/Apb||Dominant|gene trap ROSA 26, Philippe Soriano|Gt(ROSA)26Sor|||MGI:104735|gene trap ROSA 26, Philippe Soriano; targeted mutation 1, Frank Costantini|Gt(ROSA)26Sor|MGI:2449038|6|||||||||||||||||||||||||||||Homozygous animals are normal, fertile and viable (floxed line with eYFP reporter of cre activity)|Normal, fertile and viable (floxed line with eYFP reporter of cre activity)|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|generated on pure C57Bl/6 so not backcrossed. Only maintained on C57||homozygous R26eYFP Recql4fl/fl in breeding|No|06-Dec-2012|Cryopreserved sperm|||Yes|Rothmund-Thomson Syndrome|Recql4, R26eYFP, Rothmund-Thomson Syndrome|Yes| 9221.0|B6.(Cg)-Drosha|Drosha CD4-cre Foxp3-GFP||Dominant|drosha, ribonuclease type III|Drosha |||MGI:1261425|drosha, ribonuclease type III; targeted mutation 1, Dan R Littman|Drosha|MGI:3801076|15|ENSMUSG00000022191||||||||||||||||CD4-cre|CD4 promoter/enhancer/silencer|||||||||||Reduction of certain T cell populations. All Treg cells are labelled with GFP. Older animals (at least 6 months) can develop spontaneous inflammatory disease, which reduces lifespan|Normal. However, in females there are heterozygous for the Foxp3-GFP knockin, only half of the Treg cells in the animal will be labelled with GFP.|C57BL/6 (backcrossed >10 generations)|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|08-Jul-2021|Cryopreserved sperm|49.0|0.0|Unknown|||Possibly| 9221.0|B6.(Cg)-Drosha|Drosha CD4-cre Foxp3-GFP||Dominant|forkhead box P3|Foxp3||JM2, scurfin|MGI:1891436|forkhead box P3; targeted mutation 2, Alexander Y Rudensky|Foxp3|MGI:3574964|X|ENSMUSG00000039521 ||||||||||||||||||||||||||||Reduction of certain T cell populations. All Treg cells are labelled with GFP. Older animals (at least 6 months) can develop spontaneous inflammatory disease, which reduces lifespan|Normal. However, in females there are heterozygous for the Foxp3-GFP knockin, only half of the Treg cells in the animal will be labelled with GFP.|C57BL/6 (backcrossed >10 generations)|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|08-Jul-2021|Cryopreserved sperm|||Unknown|||Possibly| 9221.0|B6.(Cg)-Drosha|Drosha CD4-cre Foxp3-GFP||Dominant|CD4 antigen|Cd4|||MGI:88335||CD4-cre||6|ENSMUSG00000023274||||||||||||||||||||||||||||Reduction of certain T cell populations. All Treg cells are labelled with GFP. Older animals (at least 6 months) can develop spontaneous inflammatory disease, which reduces lifespan|Normal. However, in females there are heterozygous for the Foxp3-GFP knockin, only half of the Treg cells in the animal will be labelled with GFP.|C57BL/6 (backcrossed >10 generations)|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|08-Jul-2021|Cryopreserved sperm|||Unknown|||Possibly| 10456.0|B6N GSTO1 ko mice|C57B6;129/Sv-Gsto1/TacAnu||Recessive|glutathione S-transferase omega 1|Gsto1||GSTX, p28|MGI:1342273|glutathione S-transferase omega 1; targeted mutation 1, TaconicArtemis|Gsto1|MGI:6258601|19|||||||||||||||||||||||||||||Normal|Normal|C57Bl/6N|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|08-Oct-2024|Cryopreserved sperm|50.0|0.0|Unknown|||No| 10495.0|Relb KO (6)|C57BL6/NCrl-Relb/AnuApb||Recessive|avian reticuloendotheliosis viral (v-rel) oncogene related B|Relb||shep|MGI:103289|Relb:endonuclease-mediated mutation 4, Australian National University|Relb||7|ENSMUSG00000002983 ||||||||||||||||||||||||||||Unknown|Unknown|C57Bl/6N|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|20-Mar-2025|Cryopreserved sperm|22.0|0.0|Unknown|||No| 7840.0|SCN2A Ki/Ki|C57BL/6-Scn2a1/Apb||Dominant|sodium channel, voltage-gated, type II, alpha 1|Scn2a1||A230052E19Rik, Nav1.2|MGI:98248||||2|||||||||||||||||||||||||||||significant increases in action potential firing in NaV1.2 neurons and in seizure susceptibility of NaV1.2 mice, supporting our hypothesis. At postnatal day 15 (P15), when 17% of the WT NaV1.2 is 'neonatal', the firing properties of NaV1.2 and WT neurons converged. However, inhibitory postsynaptic currents in NaV1.2 neurons were larger and the expression level of Scn2a mRNA was 24% lower compared with the WT. The enhanced seizure susceptibility of the NaV1.2 mice persisted into adult age. The adult NaV1.2 mice also exhibited greater risk-taking behaviour. |unknown|C57BL/6|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|27-Jan-2015|Cryopreserved sperm|60.0|0.0|Unknown||sodium channel, neuron, seizure|Possibly| 9345.0|Arjuna:TCR:B10.BR |B10.BR-Tg(ILK3mHEL)3Ccg Tg(TcrHEL3A9)1Mmd/Anu||Dominant|TCR3A9,InsHEL transgenes||||||||Unknown|||||||||||||||||transgene insertion 1, Mark M Davis||||||||||||Mice express the TCR3A9 transgene, which recognizes HEL petide in the context of H2K(K)and the noe-self antigen HEL under the insulin promotor|mice are hemizygous only|B10BR|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|28-Feb-2022|Cryopreserved sperm|17.0|0.0|Unknown|||Possibly| 9345.0|Arjuna:TCR:B10.BR |B10.BR-Tg(ILK3mHEL)3Ccg Tg(TcrHEL3A9)1Mmd/Anu||Dominant||||||||||||||||||||||||||transgene insertion 3, Christopher C Goodnow||||||||||||Mice express the TCR3A9 transgene, which recognizes HEL petide in the context of H2K(K)and the noe-self antigen HEL under the insulin promotor|mice are hemizygous only|B10BR|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|28-Feb-2022|Cryopreserved sperm|||Unknown|||Possibly| 10458.0|Tlr9 S12P|C57BL/6J-Tlr9/Mgmp||Recessive|toll-like receptor 9|Tlr9|||MGI:1932389|Tlr9:endonuclease-mediated mutation1, Monash Genome Modification Platform|Tlr9||9|ENSMUSG00000045322||||||||||||||||||||||||||||Unknown|Unknown|C57Bl/6J|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|16-Oct-2024||0.0|36.0|Unknown|||No| 10420.0||B6(Cg)-Trex1 Ifnar1/Anu||Recessive|three prime repair exonuclease 1|Trex1|||MGI:1328317|Trex1: mutation 1, the Australian National University|Trex1||9|ENSMUSG00000049734 ||||||||||||||||||||||||||||Ifnar1 KO rescue Trex1 hom phenotype, which is an extensive type 1 interferon mediated inflammatory response.|Normal|C57Bl/6N|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|02-May-2024|Cryopreserved sperm|32.0|0.0|Unknown|||Possibly| 10420.0||B6(Cg)-Trex1 Ifnar1/Anu||Recessive|interferon (alpha and beta) receptor 1|Ifnar1||IFN-alpha/betaR, Ifrc|MGI:107658|interferon (alpha and beta) receptor 1; targeted mutation 1, Michel Aguet|Ifnar1|MGI:1930950|16|||||||||||||||||||||||||||||Ifnar1 KO rescue Trex1 hom phenotype, which is an extensive type 1 interferon mediated inflammatory response.|Normal|C57Bl/6N|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|02-May-2024|Cryopreserved sperm|||Unknown|||Possibly| 10484.0|huBTN Tg|B6.CD45.1-Tg(BTN3A2-BTN)/J||Recessive|human Butyrophilin subfamily 3 member A1|human Btn3A2||CD277, BTF5|||||Unknown|||||||||||||||||Tg(BTN3A2-BTN)||||||||||||Normal|Normal|C57Bl/6J|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|05-Feb-2025||0.0|0.0|Unknown|||No| 10497.0|Pura F232 KO|C57BL/6J-Pura/Apb||Recessive|purine rich element binding protein A |Pura||CAGER-1|MGI:103079|Pura, endonuclease-mediated mutation 1, Monash Genome Modification Platform|Pura||18|ENSMUSG00000043991|ENSMUST00000051301|||||||||||||||||||||||||||unknown, but suspected to be lethal|expected phenotype:seizure model with a limited lifespan.Line is not fully characterised at submission||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|21-Mar-2025|Cryopreserved sperm|40.0|0.0|Unknown|||Possibly| 10508.0|Irf4:Blimp-GFP|B6N;B6-Irf4 Prdm1/Anu||Dominant|interferon regulatory factor 4|Irf4||IRF-4, Spip|MGI:1096873|Irf4:endonuclease-mediated mutation 1, Monash Genome Modification Platform|Irf4||13|||||||||||||||||||||||||||||Reduced antibody production, GCs and plasma cells|Reduced antibody production, normal GC responses.|C57Bl/6N|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|05-May-2025||0.0|55.0|Unknown|||No| 10508.0|Irf4:Blimp-GFP|B6N;B6-Irf4 Prdm1/Anu||Dominant|PR domain containing 1, with ZNF domain|Prdm1||Blimp-1, Blimp1, PRDI-BF1|MGI:99655|PR domain containing 1, with ZNF domain; targeted mutation 1, Stephen L Nutt|Prdm1|MGI:3510704|10|||||||||||||||||||||||||||||Reduced antibody production, GCs and plasma cells|Reduced antibody production, normal GC responses.|C57Bl/6N|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|05-May-2025||||Unknown|||No| 10447.0|GSTO1KOB6N|B6N;129/Sv-Gsto1/TacAnu||Recessive|glutathione S-transferase omega 1|Gsto1 ||GSTX, p28|MGI:1342273||Gsto1||19|ENSMUSG00000025068||||||||||||||||||||||||||||normal|normal|C57Bl/6N|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|19-Aug-2024||0.0|0.0|Unknown|||Possibly| 10460.0|Irf4|C57BL/6NCrl-Irf4||Recessive|interferon regulatory factor 4|Irf4||Spip|MGI:1096873|Irf4:endonuclease-mediated mutation 1, Monash Genome Modification Platform|Irf4||13|ENSMUSG00000021356|ENSMUST00000021784|||||||||||||||||||||||||||Broad abnormalities in B and T cell development and function.|Broad abnormalities in B and T cell development and function.|C57Bl/6N|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|24-Oct-2024||0.0|0.0|Unknown|||No| 8244.0|Ai32:ePet-cre|B6.Cg-Gt(ROSA)26Sor Tg(Fev-cre)1Esd/JAusb||Recessive|gene trap ROSA 26, Philippe Soriano|Gt(ROSA)26Sor||beta geo, Gtrgeo26, Gtrosa26, R26, ROSA26, Thumpd3as1|MGI:104735|gene trap ROSA 26, Philippe Soriano; targeted mutation 32, Hongkui Zeng|Gt(ROSA)26Sor|MGI:5013789|6|||||||||||||||||transgene insertion 1, Evan S Deneris|ETS oncogene family|serotonergic-specific||||||||||No analysis performed||C57BL/6J|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|06-Apr-2017|Cryopreserved sperm|60.0|0.0|Unknown|||Yes| 10490.0|Clockdelta19 |B6.Cg-Tg(tet0-Clock)CL57Jt/J||Recessive|CLOCK|||||CLOCK|CLOCK||Unknown|||||||||||||||||transgene insertion CL57, Joseph S Takahashi|tetracycline-responsive promoter element|||||||||||Normal|Normal|C57Bl/6J|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|25-Feb-2025|Cryopreserved sperm|50.0|0.0|Unknown|||No| 10503.0|Rdh5 KO B6J|C57BL/6JAnu-Rdh5/7Anu||Recessive|retinol dehydrogenase 5|Rdh5|||MGI:1201412|Rdh5:endonuclease-mediated mutation 4, Australian National University|Rdh5||10|ENSMUSG00000025350 ||||||||||||||||||||||||||||Possible retinal degenerative phenotype|unknown|C57Bl/6J|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|28-Mar-2025||0.0|0.0|Unknown|||Possibly| 9161.0|ASD1015:Pea:2|C57BL/6NCrlANu-Gbp3em2Anu/Anu||Semi-dominant|guanylate binding protein 3|Gbp3|||MGI:1926263||||3|||||||||||||||||||||||||||||Normal|Normal|C57Bl/6N|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|12-Mar-2021|Cryopreserved sperm|60.0|0.0|Unknown|||Possibly| 10343.0|Defb41tm1(icre)Psip|C6:129Sv-Defb41/Apb|5439010|Dominant|Defensin beta 41|Defb41|Nil||MGI:1924923|defensin beta 41; targeted mutation 1, Petra Sipila|Defb41|MGI:5439010|1|||||||||||||||||cre recombinase(iCre) |Defensin beta 41 (Defb41)|||||||||||normal|normal|129/Sv * C57BL/6N|Yes|Yes|Yes|Yes|Yes|Yes|Yes|Good||||No|21-Jun-2023|Cryopreserved sperm|50.0|0.0|Unknown|||Possibly| 10509.0|Adar1mNeonGreen+. strain 1|C57BL/6J-Adar/Apb||Dominant||||||||||||||||||||||||||||||||||||||Would be expected to be embryonic lethal (not tested prior to cryopreservation)|Normal, fertile and health. No discernable phenotype|C57Bl/6J|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|12-May-2025|Cryopreserved sperm|40.0|0.0|Unknown|||Yes| 10510.0|Adar1mNeonGreen+. strain 2|C57BL/6J-Adar/Apb||Dominant|adenosine deaminase, RNA-specific |Adar||Adar1p110, Adar1p150|MGI:1889575|adenosine deaminase, RNA-specific; endonuclease-mediated mutation 4, Carl R Walkley|Adar||3|ENSMUSG00000027951||||||||||||||||||||||||||||Would be expected to be embryonic lethal (not tested prior to cryopreservation)|Normal, fertile and health. No discernable phenotype|C57Bl/6J|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Good|made on C57Bl/6J background|||No|12-May-2025|Cryopreserved sperm|50.0|0.0|Unknown|||Yes| 8271.0|nZegEGFP:Hamlet|C57BL/6JSfdAnu-Tg(IghelMD4)4Ccg/AnuApb||Dominant||||||||||||||||||||||||||transgene insertion 4, Christopher C Goodnow||low copy number||||||||||Bone marrow contains fewer combined numbers of combined pro-pre B cells than on a B6 background. Transgenic mice, more than 90% of B-cells in the spleen are derived from the transgene (a allotype) and are predominantly IgM and IgD. There is a moderate reduction in B cell frequency and number in spleen and lymph node. B cells did not express Ly-1 or Mac-1. The Ig phenotype of splenic B cells in adult mice (IgMhiIgDlo-hi) resembled that of splenic B cells in non-transgenic 1 - 2-week-old mice.||C57BL/6JAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||17||No|05-Jul-2017|Cryopreserved sperm|22.0|0.0|No||immunoglobulin, T cell, B cell, Hen Egg Lysozyme (HEL), tolerance, autoimmunity|Yes| 8271.0|nZegEGFP:Hamlet|C57BL/6JSfdAnu-Tg(IghelMD4)4Ccg/AnuApb||Dominant||||||||||||||||||||||||||nZEG||||||||||||Bone marrow contains fewer combined numbers of combined pro-pre B cells than on a B6 background. Transgenic mice, more than 90% of B-cells in the spleen are derived from the transgene (a allotype) and are predominantly IgM and IgD. There is a moderate reduction in B cell frequency and number in spleen and lymph node. B cells did not express Ly-1 or Mac-1. The Ig phenotype of splenic B cells in adult mice (IgMhiIgDlo-hi) resembled that of splenic B cells in non-transgenic 1 - 2-week-old mice.||C57BL/6JAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||17||No|05-Jul-2017|Cryopreserved sperm|||No||immunoglobulin, T cell, B cell, Hen Egg Lysozyme (HEL), tolerance, autoimmunity|Yes| 9326.0|Stag2 c2533|C57Bl/6N-Stag2Anu/Apb||Semi-dominant|STAG2 cohesin complex component|Stag2|||MGI:1098583||||X|||||||||||||||||||||||||||||unknown|unknown|C57Bl/6N|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|20-Dec-2021|Cryopreserved sperm|11.0|0.0|Unknown|||Possibly| 10512.0|Sgsh(R245H)|B6.Cg-Sgsh||Recessive|N-sulfoglucosamine sulfohydrolase (sulfamidase)|Sgsh |||MGI:1350341|Mucopolysaccharidosis IIIA|Sgsh||11|ENSMUSG00000005043 ||||||||||||||||||||||||||||SgshR245H / SgshR245H mice provide a model for the human disease Mucopolysaccharidosis type IIIA (MPS IIIA), also known as Sanfilippo syndrome (OMIM#252900). R245H mutations have been reported with frequencies of 57%, 41% and 35% in The Netherlands, Australia and Germany, respectively (Weber et al., 1998; Bunge et al., 1999; Yogalingam and Hopwood, 2001).Mice homozygous for the SgshR245H mutation have <2% of the wild-type level of N-sulfoglucosamine sulfohydrolase (sulfamidase) activity and display progressive accumulation of incompletely degraded heparan sulfate (HS) in brain tissue. Accumulation of HS fragments in other tissues and fluids is anticipated. The general health and vigour of MPS IIIA mice is good until at least ~30 weeks of age. Affected males and females are both fertile. From ~5 months of age, MPS IIIA mice and are less able to remember the location of the hidden platform in the Morris Water Maze test of learning and memory. Male/female R245H MPS IIIA mice also show reduced anxiety-related measures in the Elevated Plus Maze test and short-term memory defects in the Y-maze test.|Unknown|C57Bl/6J|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|19-May-2025|Cryopreserved sperm|50.0|0.0|Unknown|||Possibly| 8453.0|ASD866:F2|C57BL/6NCrlAnu:Green:F2||Dominant||||||||||||||||||||||||||||||||||||||Normal|||Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||2||No|06-Apr-2018||0.0|343.0|Unknown|||Yes| 9188.0|Drosha|B6.129P2-Drosha/AnuApb||Recessive|drosha, ribonuclease type III|Drosha|Nil|1110013A17Rik, Etohi2, Rnasen|MGI:1261425|drosha, ribonuclease type III; targeted mutation 1, Dan R Littman|Drosha|MGI:3801076|15|||||||||||||||||||||||||||||When bred to mice with a cre recombinase gene under the control of a promoter of interest, exon 9 is excised in the tissue of interest. Full knockouts of this gene are embryonic lethal before embryonic day 10.5 (E10.5).|These mice possess loxP sites on either side of exon 9 of the ribonuclease III, nuclear gene. Mice that are homozygous for this allele are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. |C57BL/6J |No|Yes|Yes|No|Yes|Yes|No|Unknown|Unknown|||Yes|14-May-2021|Live|0.0|30.0|Unknown||miRNA biogenesis, T reg cells, Drosha, Dicer, Foxp3|Yes| 2396.0|B6.TnfRI-/-RII-/-|B6.129S-Tnfrsf1a Tnfrsf1b/J||Recessive|tumor necrosis factor receptor superfamily, member 1a|Tnfrsf1a|Nil|CD120a, p55, p55-R, TNF receptor alpha chain, TNF-R-I, TNF-R1, TNF-R55, TNFAR, Tnfr-2, Tnfr1, TNFR60, TNFRI, TNFRp55|MGI:1314884|targeted mutation 1, Immunex Research and Development Corporation|Tnfrsf1a|MGI:1857468|6||||||||||||||||No|||||||||||||Increased circulating tumor necrosis factor level: two hours post lipopolysaccharide (LPS) challenge serum levels are 15-20 fold higher than controls, however, TNF kinetics and activity are not altered.Decreased susceptibility to endotoxin shock: exhibits resistance to a lethal LPS dose plus hepatoxin D-gal (increases sensitivity to LPS).Decreased inflammatory response: M. faeni- induced neutrophil accumulation in the lung is decreased as compared to control, however monocyte and lymphocyte levels are comparable to control.Osteomyelitis:* osteolytic lesions of molars are significantly larger in these mice 2 weeks after bacterial inoculation of the dental pulp* the osteolytic lesions continue to be larger for at least 38 days after innoculation.Increased susceptibility to bacterial infection: mice have 3 log greater bacterial penetration of the dental pulp eight days after experimental bacterial infection.Necrosis:* mice have significantly higher necrosis scores of the dental pulp seven days after bacterial inoculation.* complete necrosis of the dental pulp is observed by 21 days after inoculation compared to control mice that still have intact dental pulp at 38 days post-innoculation.Increased bone resorption:* there is significantly more osteoclastogenesis that occurs in molars between 7 and 21 days after bacterial infection of the dental pulp.* osteoclast activity of the molars is almost 2-fold higher than in wild-types 7 days after bacterial inoculation.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|20-Dec-2007|Cryopreserved sperm|70.0|0.0|Unknown||inflammation, lipopolysaccharide (LPS), neutrophil, lymphocyte, innate immunity|Yes| 2396.0|B6.TnfRI-/-RII-/-|B6.129S-Tnfrsf1a Tnfrsf1b/J||Recessive|tumor necrosis factor receptor superfamily, member 1b|Tnfrsf1b|Nil|CD120b, p75, p75 TNFR, TNF-R-II, TNF-R2, TNF-R75, TNFBR, Tnfr-1, Tnfr2, TNFR80, TNFRII|MGI:1314883|targeted mutation 1, Immunex Research and Development Corporation|Tnfrsf1b|MGI:1860087|4|||||||||||||||||||||||||||||Increased circulating tumor necrosis factor level: two hours post lipopolysaccharide (LPS) challenge serum levels are 15-20 fold higher than controls, however, TNF kinetics and activity are not altered.Decreased susceptibility to endotoxin shock: exhibits resistance to a lethal LPS dose plus hepatoxin D-gal (increases sensitivity to LPS).Decreased inflammatory response: M. faeni- induced neutrophil accumulation in the lung is decreased as compared to control, however monocyte and lymphocyte levels are comparable to control.Osteomyelitis:* osteolytic lesions of molars are significantly larger in these mice 2 weeks after bacterial inoculation of the dental pulp* the osteolytic lesions continue to be larger for at least 38 days after innoculation.Increased susceptibility to bacterial infection: mice have 3 log greater bacterial penetration of the dental pulp eight days after experimental bacterial infection.Necrosis:* mice have significantly higher necrosis scores of the dental pulp seven days after bacterial inoculation.* complete necrosis of the dental pulp is observed by 21 days after inoculation compared to control mice that still have intact dental pulp at 38 days post-innoculation.Increased bone resorption:* there is significantly more osteoclastogenesis that occurs in molars between 7 and 21 days after bacterial infection of the dental pulp.* osteoclast activity of the molars is almost 2-fold higher than in wild-types 7 days after bacterial inoculation.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|20-Dec-2007|Cryopreserved sperm|||Unknown||inflammation, lipopolysaccharide (LPS), neutrophil, lymphocyte, innate immunity|Yes| 5083.0|Bn|B6;BNT/LeJ-Zic3/AnuApb||X-linked|zinc finger protein of the cerebellum 3|Zic3|||MGI:106676 |zinc finger protein of the cerebellum 3; bent tail|Zic3|MGI:1856679|X||||||||||||||||Yes|||||||||||||Hemizygous males and homozygous females have a shortened as well as a bent tail.|Heterozygous females have a variable bent tail ranging from an almost imperceptible bend, to extreme cases where the tail is curled up and pressed against the body.|C57BL/6 (backcross N1 - N3)|No|No|Yes|No|No|Yes|Yes|Poor|1 to 3||Hemizygous male to C57BL/6 female. Heterozygous female to C57BL/6 male.|No|08-Apr-2010|Cryopreserved sperm|100.0|0.0|Yes|Neural tube defects, exencephaly, laterality defects, embryonic lethality|Neural tube defect, situs defects, exencephaly, embryonic lethality, gastrulation|Yes| 2428.0|H2KK|B6.AK-H2/FlaEgJAnuApb|B6.AK-H2/FlaEgJAnuApb|Recessive||||||||||||||||||||||||||||||||||||||The H2 complex contains 3 major classes of highly polymorphic gene sets: class I (H2-K, H2-D, Q, H2-T18 genes), class II (H2-I genes), and class III (H2-S genes). These genes are involved in many processes, including graft rejection, immune response, antigen presentation and complement component.||C57BL/6JFlaEg|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|11-Jan-2008|Cryopreserved sperm|25.0|0.0|No||MHC, T cell, antigen presentation, H2|Yes| 7818.0|CD74 KO|B6.129-Cd74/JAnuApb||Recessive|CD74 antigen (invariant polypeptide of major histocompatibility complex, class II antigen-associated)|Cd74|Nil|CLIP, Ii|MGI:96534|CD74 antigen (invariant polypeptide of major histocompatibility complex, class II antigen-associated); targeted mutation 1, Elizabeth Bikoff|Cd74|MGI:1927530|18|||||||||||||||||||||||||||||Decreased B cell number:• in the spleen and lymph nodeDecreased CD4-positive, alpha beta T cell number:• significant reduction in numbers of mature CD4+CD8- thymocytes in thymus and periphery is seen compared to wild-typeDecreased T cell proliferation:• lymph node cells show significantly lower proliferative responses to immunization with keyhole limpet cyanin (KLH) compared to wild-typeAbnormal T-helper 1 physiology:• in vivo, Th1 response to MOG is absent unlike in wild-type mice• in vitro, lymph node cells from mice receiving wild-type MOG T cells exhibit reduced Th1 recall response compared with similarly treated wild-type mice• in vivo, Th1 response to PLP is reduced compared to in wild-type mice• in vitro, the frequency of Th1 recall response is greater than in H2-Dma homozygotesDecreased susceptibility to type IV hypersensitivity reaction:• dramatically compared to in wild-type mice when wild-type MOG T cells are transferredAbnormal antigen presentation:• antigen presenting cells cannot process and present recombinant MOG protein unlike wild-type cellsAbnormal antigen presentation via MHC class II:• class II molecules are relatively ineffective for presentation of native protein antigensAbnormal level of surface class II molecules:• mutants expressed greatly reduced amounts of class II on spleen cells compared to wild-typeDefective assembly of class II molecules:• in spleen cells, immature alpha and beta chains exhibiting no evidence of having been exported past the cis-Golgi are observed, whereas compact alpha/beta dimers efficiently transported past the cis-Golgi are produced by Cd74-deficient cells; floppy conformers are seen, compared to compact dimers in wild-typeDecreased susceptibility to experimental autoimmune encephalomyelitis:• whether MOG-primed or adoptively transferred with MOG-specific T blasts, mice fail to develop symptoms of experimental autoimmune encephalomyelitis (EAE) unlike wild-type mice• PLP-treated mice fail to develop EAE unlike similarly treated wild-type mice||C57BL/6J|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|03-Jan-2015|Cryopreserved sperm|31.0|0.0|Unknown||MHC II, T cell, B cell, CD4|No| 7968.0|iNOSΔ|B6.129P2-Nos2/JAusbAnuApb||Recessive|nitric oxide synthase 2, inducible|Nos2|Nil|iNOS, Nos-2, NOS-II, Nos2a|MGI:97361|nitric oxide synthase 2, inducible; targeted mutation 1, Victor E Laubach|Nos2|MGI:1857228|11|||||||||||||||||||||||||||||Abnormal surfactant physiology:*Following infection with mycoplasma, the numbers of large surfactant aggregates is decreased and higher protein to lipid ratios are present in the bronchoalveolare lavage fluid compared to similarly infected wild-type mice.*Following infection with mycoplasma, the minimal surface area on the pulsating bubble is increased and the levels of surfactant protein are decreased compared to similarly infected wild-type mice.Abnormal circadian rhythm:*Mice display a more pronounced diurnal variation of sleep-wake activity.Abnormal sleep pattern:*Mice spend more time in REM sleep during the light phase as a result of an increased number of REM episodes and shortened duration of the inter REM intervals.*Mice display a more pronounced diurnal variation of sleep-wake activity.*Mice spend less time in non-REM sleep during the dark phase.*During the light phase mice spend the same amount of time in non-REM sleep but have a higher number of non-REM episodes of shorter average duration.Abnormal brain wave pattern:*During non-REM sleep the absolute value of slow wave activity is increased.Abnormal inflammatory response:*Unlike in wild-type mice, LPS injection fails to reduce nighttime body temperature relative to saline injected controls. Decreased inflammatory response: *Fever in response to LPS injection is partially reduced compared to wild-type controls. *The fever response to LPS is initiated but not sustained. *However, fever in response to turpentine injection is not different from controls.||unknown|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|17-Sep-2015|Cryopreserved sperm, Embryo|45.0|0.0|Unknown||iNOS, Inflammatory disorders|Yes| 6784.0|APPPS1B6C3|B6.C3-Tg(APPswe,PSEN1dE9)85Dbo/JAusb|B6.C3-Tg(APPswe,PSEN1dE9)85Dbo/JAusb|Dominant||||||||||||||||||||||||||transgene insertion 85, David R Borchelt|mouse prion protein |Predominantly to CNS neurons||||||||||Unknown|Mice develop beta amyloid deposits in brain by 6 or 7 months of age. The humanized Mo/HuAPP695swe transgene allows the mice to secrete a human A-beta peptide.A slight alteration in the tail can occur due to mixed background.|B6/C3|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown|||Maintained as a hemizygote by crossing transgenic mice to B6C3F1/J mice|No|18-Jan-2012|Cryopreserved sperm|2.0|0.0|Yes|Alzheimers|CNS neurons, hippocampus, amyloid beta peptide , astrocytosis|Yes| 8053.0|JNK1 -/-, JNK1 KO|B6.129S1-Mapk8/JApb||Recessive|mitogen-activated protein kinase 8|Mapk8 |Nil|c-Jun N-terminal kinase, JNK1, Prkm8 |MGI:1346861|mitogen-activated protein kinase 8; targeted mutation 1, Richard Flavell|Mapk8|MGI:2176239|14|||||||||||||||||||||||||||||Mice that are homozygous for the targeted mutation are viable, normal in size, do not display any gross physical or behavioral abnormalities and are fertile but poor breeders. No gene product, protein or mRNA, is detected. Lymphocyte development, T cell to B cell ratio and CD4 to CD8 ratio are normal. Naive Th cells activated in vitro preferentially differentiate into Th2 cells. Mutant mice are susceptible to infection when challenged with the intracellular pathogen, Leishmania major. Primary murine embryonic fibroblasts prepared from mutant embryos are partially protected from UV-induced apoptosis. This mutant mouse strain represents a model that may be useful in studies related to signal transduction.|Normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Poor|5||Heterozygote x Heterozygote|No|23-May-2016|Cryopreserved sperm|55.0|0.0|Unknown|||No| 8143.0|Alcam KO|B6.129(FVB)-Alcam/JAnu||Recessive|activated leukocyte cell adhesion molecule|Alcam|Nil|BEN, CD166, DM-GRASP, MGC:27910, MuSC, SC1|MGI:1313266|activated leukocyte cell adhesion molecule; targeted mutation 1, Joshua A Weiner|Alcam|MGI:3056579|16|||||||||||||||||||||||||||||Abnormal retina morphology: • in 75% of mutant eyes retinal dysplasia is seen with finger like projections of photoreceptor cells protruding into the outer nuclear layer and/or invagination of the retina without disrupting the cell layers• dysplasia can be detected on P1Abnormal photoreceptor outer segment morphology: • photoreceptor outer segments appear elongated and disorganizedAbnormal retinal ganglion layer morphology: • axons are loosely bundled and occasionally have aberrant trajectories however all exit the optic disc normallyAbnormal motor neuron innervation pattern: • motor neurons are loosely bundled with some axons exiting the bundles at a right angle to the adjacent nerve and ending blindly or forming bridges to neighboring bundles||C57BL/6J|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|24-Nov-2016|Cryopreserved sperm|44.0|0.0|Unknown||BEN, retina, motor, axon|No| 8279.0|Tet2fl/fl|B6.129-Tet2/J||Recessive|tet methylcytosine dioxygenase 2|Tet2||Ayu17-449, E130014J05Rik, mKIAA1546|MGI:2443298|tet methylcytosine dioxygenase 2; targeted mutation 1.1, Iannis Aifantis|Tet2|MGI:5141120|3|||||||||||||||||||||||||||||Normal (conditional line)|Normal (conditional line)|C57Bl/6|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|09-Aug-2017|Cryopreserved sperm|40.0|0.0|Unknown||Myeloid, stem cell|Yes| 8981.0|progesterone receptor; Isoform A (PRAKO)|B6;129S7-Pgr/J||Recessive|progesterone receptor|Pgr||9930019P03Rik, ENSMUSG00000074510, NR3C3, PR, PR-A, PR-B|MGI:97567|progesterone receptor; targeted mutation 1, Orla M Conneely|Pgr|MGI:2183208|9|||||||||||||||||||||||||||||Uterus hyperplasia:• treatment of female homozygotes with estrogen plus progesterone results in a progesterone-dependent increase in uterine epithelial proliferation over that observed with estrogen alone.Abnormal ovulation:• following treatment with pregnant mare serum gonadotropin and human chorionic gonadotropin, female homozygotes produce a reduced number of oocytes relative to superovulated wild-type females.Abnormal uterine environment:• defective uterine implantation is associated with loss of progesterone-regulated expression of a subset of uterine epithelial target genes associated with receptivity.Abnormal decidualization:• uteri of superovulated female homozygotes fail to exhibit decidualization of stromal cells in response to traumal stimulation.Female infertility:• female homozygotes appear normal but are infertile• matings between superovulated female homozygotes and wild-type males fail to result in successful pregnancies although a small number of oocytes is released in mutant femalesEndocrine/exocrine gland phenotype:N • following estrogen and progesterone treatment, ovariectomized female homozygotes display normal thoracic mammary gland development with extensive hormone-dependent ductal branching and multiple alveolar lobules, as well as normal proliferation and differentiation of the mammary epithelium in response to progesterone• also, estrogen- and progesterone-treated ovariectomized female homozygotes exhibit normal thymic involution relative to similarly-treated wild-type females||C57BL/6|Yes|No|Yes|Yes|Yes|Yes|No|Unknown||||No|23-Apr-2020|Cryopreserved sperm|50.0|0.0|Unknown|||Yes| 9230.0|ASD712:Cx3cr1-cre:Dicer fl/fl:RFP fl/fl|B6.129P2(Cg)-Cx3cr1 Dicer1 Gt(ROSA)26Sor/JAnuApb||Semi-dominant|dicer 1, ribonuclease type III|Dicer1||1110006F08Rik, D12Ertd7e, Dicer1, mKIAA0928|MGI:2177178|dicer 1, ribonuclease type III; targeted mutation 1, Brian D Harfe|Dicer1|MGI:3589208|12|||||||||||||||||LoxP Cre recombinase|Cx3cr1|||||||||||Newly developed stain, phenotype unknown. Expected phenotype; Dicer deficient, YFP microglia, RFP with tamoxifen administration.|As above.|C57BL6J (ANU)|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|19-Jul-2021|Cryopreserved sperm|22.0|0.0|Unknown|||Possibly| 9230.0|ASD712:Cx3cr1-cre:Dicer fl/fl:RFP fl/fl|B6.129P2(Cg)-Cx3cr1 Dicer1 Gt(ROSA)26Sor/JAnuApb||Semi-dominant|C-X3-C motif chemokine receptor 1|Cx3cr1|||MGI:1333815|Cx3cr1:targeted mutation 2.1, Dan R Littman|Cx3cr1|MGI:5450813|9|ENSMUSG00000052336 ||||||||||||||||||||||||||||Newly developed stain, phenotype unknown. Expected phenotype; Dicer deficient, YFP microglia, RFP with tamoxifen administration.|As above.|C57BL6J (ANU)|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|19-Jul-2021|Cryopreserved sperm|||Unknown|||Possibly| 9230.0|ASD712:Cx3cr1-cre:Dicer fl/fl:RFP fl/fl|B6.129P2(Cg)-Cx3cr1 Dicer1 Gt(ROSA)26Sor/JAnuApb||Semi-dominant|gene trap ROSA 26, Philippe Soriano|Gt(ROSA)26Sor||Gtrosa26, R26, ROSA26,|MGI:104735|gene trap ROSA 26, Philippe Soriano; targeted mutation 14, Hongkui Zeng|Gt(ROSA)26Sor|MGI:3809524|6|||||||||||||||||||||||||||||Newly developed stain, phenotype unknown. Expected phenotype; Dicer deficient, YFP microglia, RFP with tamoxifen administration.|As above.|C57BL6J (ANU)|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|19-Jul-2021|Cryopreserved sperm|||Unknown|||Possibly| 8136.0|Ai32; ChR2(H134R)-EYFP|B6.129S6-Gt(ROSA)26Sor/JAusb||Recessive|gene trap ROSA 26, Philippe Soriano|Gt(ROSA)26Sor||beta geo, Gtrgeo26, Gtrosa26, R26, ROSA26, Thumpd3as1|MGI:104735|gene trap ROSA 26, Philippe Soriano; targeted mutation 32, Hongkui Zeng|Gt(ROSA)26Sor|MGI:5013789|6|||||||||||||||||||||||||||||No analysis performed||C57BL/6J|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|16-Nov-2016|Cryopreserved sperm|88.0|0.0|Unknown|||Yes| 8265.0|Edn3 KO|B6.129-Edn3/J||Recessive|endothelin 3|Edn3|Nil|114CH19, 114-CH19, tmgc48|MGI:95285|endothelin 3; targeted mutation 1, Masashi Yanagisawa|Edn3|MGI:1857160|2|||||||||||||||||||||||||||||This mutation is alleleic with the lethal spotting spontaneous mutation in the endothelin 3 gene (Edn3; ET-3). Homozygous mice are viable at birth. In original 129-Edn3/J mice most die within about a month. However, these have been backcrossed onto C57BL/6 and once backcrossed, aganglionosis is right up to small intestine resulting in early postnatal lethality. They show a disruption in neural crest lineage development. They die from peritonitis subsequent to aganglionic megacolon. They may serve as a model for human Hirschsprung's disease.|Hets have no phenotype|C57BL/6|Yes|Unknown|Yes|Yes|Unknown|Yes|No|Unknown||||No|06-Jun-2017|Cryopreserved sperm|50.0|0.0|Yes|Hirschprung's Disease ; Waardenburg syndrome type 4B|enteric neuron, epidermal melanocyte|Yes| 281.0|B6.IfngTm1 Ts|B6.129-Ifng/Apb||Recessive|interferon gamma|Ifng|Nil|Ifg, IFN-gamma|MGI:107656|targeted mutation 1, Timothy Stewart|Ifng|MGI:1857184|10||||||||||||||||Yes|||||||||||||Immune systemincreased splenocyte proliferation:splenocytes from BCG infected mice exhibit increased proliferation in response to Con Aabnormal macrophage physiology:macrophages from BCG infected mice fail to produce nitric oxide in response to LPS challengemacrophages from BCG infected mice exhibit reduced production of superoxide anion in response to PMA challengeabnormal MHC II cell surface expression on macrophages:macrophages from BCG infected mice exhibit reduced class II expressionabnormal NK cell physiology:significantly lower resting splenic NK cell activityincreased susceptibility to bacterial infection:increased mortality following a sublethal dose of Mycobacterium bovis (BCG )tumorigenesisincreased resistance to tumor development:tumor-bearing mice treated with Th-17-polarized cells from Tg(Tcra,Tcrb)9Rest cells show increased tumor rejection compared to controlshematopoietic systemincreased splenocyte proliferation:splenocytes from BCG infected mice exhibit increased proliferation in response to Con A||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|10|||No|02-May-2006|Cryopreserved sperm|114.0|0.0|Unknown||macrophage, MHC, Mycobacterium bovis, T cell, cytotoxic|Yes| 8982.0|Progesterone receptor; Isoform B (PRBKO)|B6;129S7-Pgr/J||Recessive|progesterone receptor|Pgr|Nil|9930019P03Rik, ENSMUSG00000074510, NR3C3, PR, PR-A, PR-B|MGI:97567|progesterone receptor; targeted mutation 2, Orla M Conneely|Pgr|MGI:2674932|9|||||||||||||||||||||||||||||Abnormal mammary gland growth during pregnancy: • reduction in both ductal sidebranching and development of alveolar lobules during pregnancy, seen as early as 7.5 days of pregnancy.Abnormal mammary gland epithelium morphology: • mammary glands supplemented for 21 days with pregnancy levels of estrogen and progesterone exhibit a 30% decrease in proliferation of the ductal epithelium• mammary glands supplemented for 21 days with pregnancy levels of estrogen and progesterone exhibit an increase in apoptosis in the alveolar epithelium.Abnormal branching of the mammary ductal tree:• reduction in the ductal sidebranching during pregnancy• mammary glands from ovariectomized mutants supplemented for 21 days with pregnancy levels of estrogen and progesterone display a decrease in ductal sidebranching.Abnormal mammary gland alveolus morphology:• reduction in the development of alveolar lobules during pregnancy• at day 1 of lactation, glands show lower density of alveolar lobules than wild-type glands, however they do not appear underdeveloped• mammary glands from ovariectomized mutants supplemented for 21 days with pregnancy levels of estrogen and progesterone display a decrease in lobuloalveolar development.Abnormal lactation:• even though females are able to lactate, offspring of homozygous mothers are growth retarded independent of their genotype, indicating lactational defectsReproductive system phenotype:N • in contrast to female mice lacking isoform A, female mice ovulate normally and are fertile.Abnormal mammary gland growth during pregnancy:• reduction in both ductal sidebranching and development of alveolar lobules during pregnancy, seen as early as 7.5 days of pregnancy||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|23-Apr-2020|Cryopreserved sperm|50.0|0.0|Unknown|||Yes| 10414.0|Nox 2 KO|B6.129S6-Cybb/J||X-linked|cytochrome b-245, beta polypeptide|Cybb||Cgd, gp91phox, gp91phox, Nox2|MGI:88574|cytochrome b-245, beta polypeptide; targeted mutation 1, Mary C Dinauer|Cybb|MGI:1857284|X|ENSMUSG00000015340 ||||||||||||||||||||||||||||Nox2 KO mice have a compromised immune system|Heterozygous female mice are normal. Hemizygous male mice are KO or WT as the Nox2 gene is X-linked, and as a KO male it has a compromised immune system.|C57Bl/6J|Unknown|Unknown|Yes|Unknown|Unknown|Unknown|No|Unknown||||No|14-Mar-2024|Cryopreserved sperm|50.0|0.0|Unknown|||No| 630.0|T3RKO|B6;129S1-Tlr3/Apb|B6;129S1-Tlr3/Apb|Recessive|toll-like receptor 3|Tlr3|Normal||MGI:2156367|targeted mutation 1, Richard A Flavell|Tlr3|MGI:2653138|8||||||||||||||||No|||||||||||||Lymph node enlargement.Normal lymphocyte development.Normal expression of CD3, B220, CD4, and CD8 in thymocytes and splenocytesAbnormal B cell physiology.Impaired expression of CD69, CD80, and CD86 in response to poly(I:C), but not LPSImpaired expression of CD69 in response to viral genomic dsRNA from Type I Lang mammalian reovirusAbnormal macrophage physiology.Impaired ability to produce IL6, IL12 and TNF-alpha in response to poly(I:C), a synthetic dsRNA analogueproduction of IL6, IL12, and TNF-alpha in response to LPS, PGN, LTA, zymosan, mannan, or CpG DNA was comparable to wild type controlsDecreased inflammatory response.Resistant to poly(I:C)-induced shock compared to wild type mice produced less IL12 after poly(I:C) i.p. injection.Upregulation of costimulatory molecules, CD40 and CD86, by peritoneal macrophages in response to dsRNA was preserved on C57BL/6 background.Impaired ability to produce type I interferon and TNF-alpha in response to dsRNA, but not in response to LPS.|Normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|Yes|Excellent|||Hom x Hom|Yes|25-Apr-2007|Cryopreserved sperm|100.0|0.0|No||B cell, lymphocyte, Macrophage, inflammatory response, LPS|Yes| 842.0|Sap KO|B6;129-Sh2d1a/Apb|B6;129-Sh2d1a/Apb|X-linked|SH2 domain protein 1A|Sh2d1a|Nil|Duncan disease homolog, SAP|MGI:1328352|targeted mutation 1, Pamela L Schwartzberg|Sh2d1a|MGI:2388241|X||||||||||||||||No|||||||||||||Decreased IgE level: * after immunization with ovalbumin, severe deficit in IgE is observed with little or no Ig E detected.Abnormal lymphocyte cell number:* although lymphocyte numbers were generally normal, occasional animals had increased T cell and NK cell numbers together with decreased B cell numbers in the spleen.Increased T cell proliferation:* tendency for T-cell proliferation to be increased even in the absence of infection.Abnormal T-helper 1 cell morphology:* biased toward the production of the Th1 cytokines Il-2 and IFN-gamma.Abnormal T-helper 2 cell morphology:* biased toward decreased production of the Th2 cytokine Il-4Decreased IgE level:* although levels of IgM, IgG, and IgA were normal, IgE levels were reduced.Increased susceptibility to infection.Increased susceptibility to parasitic infection:* elevated T-cell response to Toxoplasma gondii infectionlower titers of Ig isotypes directed against Toxoplasma antigensIncreased susceptibility to viral infection:* increased T-cell response to infection with lymphocyte choriomeningitis virus (LCMV).* Elevated activity of CD8+ cytotoxic T lymphocytes in spleenCD4+ cells also increased 2-3X.* decrease in antibody secreting cells in spleen and bone marrow.* more virulent strains led to increased morbidity.||C57BL/6 x MLB|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|23-May-2007|Cryopreserved sperm|200.0|0.0|Yes||T cell, lymphoproliferative disease, X-linked, lymphocyte, B cell|Yes| 10464.0|nor-1 Nr4a3|B6;129-Nr4a3/J||Dominant|nuclear receptor subfamily 4, group A, member 3|Nr4a3||MINOR, Nor1, NOR-1, TEC|MGI:1352457|nuclear receptor subfamily 4, group A, member 3; targeted mutation 1, Orla M Conneely|Nr4a3|MGI:3037444|4|ENSMUSG00000028341|ENSMUST00000153369|||||||||||||||||||||||||||Normal|Normal|C57Bl/6J|Yes|Unknown|Yes|Yes|Unknown|Yes|No|Unknown||||No|03-Dec-2024||0.0|30.0|Unknown|||No| 860.0|B10.A(5R)|B10.A-H2(R5)/AnuApb|B10.A-H2(R5)/AnuApb|Recessive|histocompatibility-2, MHC|H2|Normal|H-2|MGI:95894|i5 variant|H2|MGI:3628763|17||||||||||||||||No|||||||||||||||C57BL/10|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|||sib x sib|No|24-May-2007|Cryopreserved sperm|100.0|0.0|Unknown||histocompatibility, H2, MHC, T cell, lymphocyte|Yes| 1504.0|B6.IL-18-/-|B6.129P2-Il18/AnuApb|B6.129P2-Il18/AnuApb|Recessive|interleukin 18|Il18|Nil|Igif, Il-18|MGI:107936|targeted mutation 1, Shizuo Akira|Il18|MGI:2136769|9||||||||||||||||No|||||||||||||In Propionibacterium acnes (P. acnes)-primed IL-18-deficient mice, LPS-induced IFNgamma production was markedly reduced, despite normal IL-12 induction. Natural killer cell activity was significantly impaired. Th1 cell response after injection of P. acnes or Mycobacterium bovis (bacillus Calmette-Guerin [BCG]) was significantly reduced.||C57BL/6 x 129P2|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|||Brother x Sister|No|04-Jul-2007|Cryopreserved sperm|110.0|0.0|Unknown||T cell, interferon, Natural Killer, IL-12, IL12|Yes| 2420.0|Nos1 -/-|B6;129S4-Nos1/AnuApb|B6;129S4-Nos1|Recessive|nitric oxide synthase 1, neuronal|Nos1|Nil|bNOS, nNOS, NO, Nos-1|MGI:97360|targeted mutation 1, Paul L Huang|Nos1|MGI:1857227|5||||||||||||||||Yes|||||||||||||The neurons normally expressing NOS appear intact, and the mutant NOS mice are viable, fertile, and without evident histopathological abnormalities in the central nervous system. The most evident effect of disrupting the neuronal NOS gene is the development of grossly enlarged stomachs, with hypertrophy of the pyloric sphincter and the circular muscle layer. This phenotype resembles the human disorder infantile pyloric stenosis, in which gastric outlet obstruction is associated with the lack of NDP neurons in the pylorus.||C57BL/6 x 129|Yes|Yes|Yes|Yes|Yes|Yes|No|Poor||||No|10-Jan-2008|Cryopreserved sperm|90.0|0.0|Yes||Pyloric Stenosis, hypertrophy, stomach, neurogenesis|Yes| 4477.0||B6.129-Hcn1/AnuApb||Recessive|hyperpolarization-activated, cyclic nucleotide-gated K+ 1|Hcn1|Nil|Bcng1, HAC2|MGI:1096392|targeted mutation 2, Eric R Kandel|Hcn1|MGI:2686951|13||||||||||||||||Yes|||||||||||||Behavior/neurological phenotype* basic motor functions were all normalIncreased thigmotaxis * observed during water maze testsAbnormal eye blink conditioning behavior * a deficiency was observed in latency to peak conditioned responseAbnormal learning/ memory Abnormal motor learning* there is a learned motor skill deficit in a rotorod test* impairment apparently involves learning and memory of relatively fast coordinated movementsAbnormal spatial learning* impaired learning in a water maze test||C57BL/6 x 129|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|22-Feb-2009|Cryopreserved sperm|120.0|0.0|Unknown||motor, Purkinje cell, cerebellar, retina, earning|Yes| 5072.0|Flt3-ITD|B6.129-Flt3/Apb||Dominant|FMS-like tyrosine kinase 3|Flt3||CD135, Flk2, Flk-2, Flt-3, wmfl|MGI:95559|FMS-like tyrosine kinase 3; targeted mutation 1, D Gilliland|Flt3|MGI:3763385|5|||||||||||||||||||||||||||||Onset of Acute Myeloid leukaemia.Abnormal hematopoiesis: * bone marrow cells exhibit a two-fold increase in the Lin-Sca1+cKit+ (LSK) compartment compared to in wild-type and heterozygous mice. * monocytes are present in the bone marrow and liver in a background of increased number of maturing myeloid cells is increased compared to in wild-type mice. * the relative percentage of immunophenotypic granulocyte-monocyte progenitors is expanded while the percent of megakaryocyte-erythroid progenitors is decreased. * the proportion of LSK cells in S/G2/M phase is increased while the proportion in G0/G1 is increased compared to in wild-type mice. * fewer LSK cells undergo apoptosis compared to in wild-type and heterozygous mice. * however, the total number of myeloid progenitor cells is the same as in wild-type mice.Abnormal common myeloid progenitor cell morphology: * when cultured on methylcellulose, bone marrow cells produce more colonies than wild-type cells with a greater number of monocytes and fewer erythroid burst forming units and granulocyte-erythroid burst forming units compared to wild-type and heterozygous mice. * however, re-plated colonies do not exhibit increased self-renewal properties.Decreased B cell number: the rise in monocytes in the bone marrow and spleen is accompanied by a decrease in the percentage of T and B lymphoid cells.Decreased mature B cell number: the number of mature B cells in the bone marrow and spleen is decreased compared to in wild-type mice.Decreased T cell number: the rise in monocytes in the bone marrow and spleen is accompanied by a decrease in the percentage of T and B lymphoid cells.Increased leukocyte cell number: mice exhibit leukocytosis and monocytosis with a reversal in the neutrophil to lymphocyte ratio compared to in wild-type mice.Increased granulocyte number: granulocyte populations are increased in peripheral blood compared to in wild-type mice.Increased monocyte cell number: * monocyte populations are increased in peripheral blood. * monocytes are present in the bone marrow and liver in a background of increased number of maturing myeloid cells is increased compared to in wild-type mice.Abnormal B cell differentiation: B cell maturation is blocked at the pre-B stage.Increased spleen red pulp amount: expanded red pulp is comprised of mainly mature myeloid and ad-mixed erythroid elements.Enlarged spleen: mice develop a variable and progressive splenomegaly that is more severe than in heterozygous miceIncreased spleen white pulp amount: expanded white pulp is comprised of cells resembling maturing monocytes.|Onset of Acute Myeloid leukaemia.Abnormal hematopoiesis: * bone marrow cells exhibit a two-fold increase in the Lin-Sca1+cKit+ (LSK) compartment compared to in wild-type mice * fewer LSK cells undergo apoptosis compared to in wild-type. * monocytes are present in the bone marrow and liver in a background of increased number of maturing myeloid cells is increased compared to in wild-type mice.Decreased B cell number: the rise in monocytes in the bone marrow and spleen is accompanied by a decrease in the percentage of T and B lymphoid cells.Decreased mature B cell number: the number of mature B cells in the bone marrow and spleen is decreased compared to in wild-type mice.Decreased T cell number: the rise in monocytes in the bone marrow and spleen is accompanied by a decrease in the percentage of T and B lymphoid cells.Increased leukocyte cell number: mice exhibit leukocytosis and monocytosis with a reversal in the neutrophil to lymphocyte ratio compared to in wild-type mice.Increased granulocyte number: granulocyte populations are increased in peripheral blood compared to in wild-type mice.Increased monocyte cell number: * monocyte populations are increased in peripheral blood. * monocytes are present in the bone marrow and liver in a background of increased number of maturing myeloid cells is increased compared to in wild-type mice.Abnormal B cell differentiation: B cell maturation is blocked at the pre-B stage.Increased spleen red pulp amount: expanded red pulp is comprised of mainly mature myeloid and ad-mixed erythroid elements.Enlarged spleen: mice develop a variable and progressive splenomegaly that is not as severe as in homozygous mice.Increased spleen white pulp amount: expanded white pulp is comprised of cells resembling maturing monocytes.|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Poor||||No|25-Mar-2010|Cryopreserved sperm|75.0|0.0|Yes|Myelomonocytic Leukaemia|AML, myeloid, lymphocyte, CML|Yes| 2421.0|B10.H2g7|B10.NOD-H2/AnuApb|B10.NOD-H2/AnuApb|Recessive|histocompatibility-2, MHC|H2|Normal|H-2, MHC-II|MGI:95894|g7 variant|H2|MGI:3579321|17||||||||||||||||Yes|||||||||||||The H2 complex contains 3 major classes of highly polymorphic gene sets: class I (H2-K, H2-D, Q, H2-T18 genes), class II (H2-I genes), and class III (H2-S genes). These genes are involved in many processes, including graft rejection, immune response, antigen presentation and complement component. The g7 variant is found in NOD strain||C57BL/10|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|10-Jan-2008|Cryopreserved sperm|129.0|0.0|No||MHC, diabetes, autoimmune disease, insulitis|Yes| 3385.0|Histamine receptor type 2 -/- |B6.129P2-Hrh2|B6.129P2-Hrh2|Recessive|histamine receptor H2|Hrh2|Nil||MGI:108482|histamine receptor H2; targeted mutation 1, Takeshi Watanabe|Hrh2|MGI:2182949|13||||||||||||||||No|||||||||||||Homozygotes for a targeted null mutation exhibit enlarged folds in gastric mucosa, elevated serum gastrin levels, increased numbers of parietal and enterochromaffin-like cells, and lack of secretion of gastric acid in response to histamine or gastrin.Abnormal gastric mucosa morphology:* enterochromaffin-like (ECL) cells are increased in number and are found not only in the basal region, but also in the neck region and isthmus.* increase in H+, K+-ATPase negative cells in the isthmus and neck region.* histamine content in the gastric mucosa is elevated.* young mice (4 weeks old) in which hypertrophy of the oxyntic mucosa is not yet seen, exhibit a significant increase in cell proliferation in the mucosa.Abnormal gastric parietal cell morphology: parietal cells are increased in number, are smaller and contain enlarged secretory canaliculi with a lower density of microvilli and few typical tubulovesicles in the narrow cytoplasm.Increased thickness of gastric mucosa:* thickness of the oxyntic mucosa in the glandular region is increased in 16-week old mutants resulting in the formation of enlarged gastric folds.* change in mucosal thickness is most prominent in the isthmus and neck region.Decreased digestive secretion: induction of gastric acid secretion by histamine or gastrin is completely abolished, however carbachol still induced secretion.Abnormal stomach pH: basal gastric pH is normal, however elevation of gastric pH by administration of an Hrh2 antagonist, famotidine, is not observed.Increased circulating gastrin level: 12- to 18-week old mutants exhibit elevated serum gastrin levels (hypergastrinemia).||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|||Brother x sister|No|09-Jul-2008|Cryopreserved sperm|150.0|0.0|Unknown||UV immunosuppression, resistance, mucosa, gastric, histamine, stomach, pH|Yes| 10513.0|Hck S431F|C57BL/6J-Hck/Anu||Recessive|hemopoietic cell kinase|Hck||Bmk, Hck-1|MGI:96052|hemopoietic cell kinase; endonuclease-mediated mutation 1,Monash Genome Modification Platform|Hck||2|ENSMUSG00000003283 ||||||||||||||||||||||||||||Unknown|Unknown||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|26-Jun-2025||0.0|0.0|Unknown|||No| 4576.0||B6.129S7-Ifngr1/AnuApb||Recessive|interferon gamma receptor 1|Ifngr1|Unknown|CD119, Ifgr, IFN-gamma R, IFN-gammaR, Ifngr, Nktar|MGI:107655|targeted mutation 1, Michel Aguet|Ifngr1|MGI:1857286|10||||||||||||||||Yes|||||||||||||abnormal immune cell physiology (J:99347)splenocytes proliferate against the antigen and a mitogen more vigorously than those from wild-typeincreased interferon-gamma secretion (J:99347)stimulation of splenocytes with an antigen or a mitogen induces a higher production of IFN-gamma than in wild-typeincreased interleukin-6 secretion (J:99347)stimulation of splenocytes with an antigen induces a higher production of IL-4, IL-6, IL-13 and IFN-gamma than in wild-typestimulation of splenocytes with a mitogen induces a higher production of IL-13increased susceptibility to experimental autoimmune uveoretinitis (J:99347)exhibit increased incidence and severity of induced experimental autoimmune uveoretinitis compared to wild-type (59.3% vs. 40% of wild-type)upon uveoretinitis induction, see a significant infiltration of eosinophils into the eyes compared to wild-typeliver/biliary systemliver/biliary system phenotype (J:120559)mice show no liver injury on treatment with HBsAg-specific Th1 cells and HBsAgtumorigenesisaltered tumor susceptibility (J:138466)tumor growth in tumor-bearing mice treated with Th-17-polarized cells from Tg(Tcra,Tcrb)9Rest cells is minimally delayed, and develop progressive disease||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|10|||No|08-Mar-2009|Cryopreserved sperm|58.0|0.0|Unknown||cytokine, interleukin, infection, immunoglobulin, macrophage|Yes| 10514.0|Hck KO|C57BL/6J-Hck/Anu||Recessive|hemopoietic cell kinase|Hck||Bmk, Hck-1|MGI:96052|hemopoietic cell kinase; endonuclease-mediated mutation 2, Monash Genome Modification Platform|Hck||2|ENSMUSG00000003283 ||||||||||||||||||||||||||||Abnormal neutrophil physiology - neutrophil degranulation following adhesion is decreased compared to wild type mice.|Unknown|C57Bl/6J|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|26-Jun-2025||0.0|0.0|Unknown|||No| 7044.0|Activin BA knockout ; Inhba-/-|B6;129S7-Inhba/MarpApb||Dominant|inhibin beta-A|Inhba||activin|MGI:96570|inhibin beta-A; targeted mutation 1, Martin M Matzuk|Inhba|MGI:1861957|13|||||||||||||||||||||||||||||Mice die at birth due to abnormal palate development, precluding feeding.|Delayed onset of fertility, no impact on general viability|C57BL/6 x 129S|No|No|Yes|No|No|Yes|Yes|Good|Unknown||Heterozygous matings|No|06-Aug-2012|Cryopreserved sperm|50.0|0.0|No||activin|Possibly| 10515.0||C57BL/6-Ins2Akita/J||Dominant|insulin II|Ins 2||Mody, Mody4|MGI:96573|insulin II; Akita|Ins2|MGI:1857572|7|ENSMUSG00000000215 ||||||||||||||||||||||||||||Untreated homozygotes rarely survive beyond 12 weeks of age.|Mice heterozygous for the Akita spontaneous mutation (Ins2Akita) are viable and fertile. Symptoms in heterozygous mutant mice include hyperglycemia, hypoinsulinemia, polydipsia, and polyuria, beginning around 3-4 weeks of age. The diabetic phenotype is more severe and progressive in the male than in the female. Obesity or insulitis does not accompany diabetes.||Yes|No|Yes|Yes|No|Yes|No|Unknown|||WT x Heterozygote; Breeding Summary: C57BL/6J female x Heterozygous male.|No|01-Jul-2025|Cryopreserved sperm|49.0|0.0|Yes|type 1 diabetes||Possibly| 7119.0|MNEI KO|B6.129S6-Serpinb1a/CbenMarpApb||Dominant|serine (or cysteine) peptidase inhibitor, clade B, member 1a|Serpinb1a|Nil|1190005M04Rik, EIA, ELANH2, LEI, MNEI, M/NEI, ovalbumin|MGI:1913472|serine (or cysteine) peptidase inhibitor, clade B, member 1a; targeted mutation 1, Charaf Benarafa|Serpinb1a|MGI:3761627|13|||||||||||||||||||||||||||||Normal.Increased susceptibility to infection with P. Aeruginosa. P. Aeruginosa infection results in abnormal neutrophil physiology, numbers in lungs.|Normal|C57B/6J|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|29-Oct-2012|Cryopreserved sperm|50.0|0.0|Unknown||neutrophil, infection, lung|Yes| 7392.0|B6.Nramp|B6.129-Slc11a1/Apb||Dominant|solute carrier family 11 (proton-coupled divalent metal ion transporters), member 1|Slc11a1|Normal|Bcg, host resistance locus Bcg/Ity/Lsh, ity, Ity, Lsh, Nramp, Nramp1|MGI:1345275|solute carrier family 11 (proton-coupled divalent metal ion transporters), member 1; host resistance (Bcg/Ity/Lsh)|Slc11a1|MGI:1857756|1|||||||||||||||||||||||||||||Decreased susceptibility to bacterial infection:the mutation results in Gly at position 105 substitution within predicted transmembrane domain 2 of Nramp.This results in resistance to infection with Mycobacteria, Salmonella and Leishmania|Similar to hom state but resistance is intermediate.|C57BL/6|Yes|Yes|Unknown|Yes|Yes|Unknown|No|Excellent|13|||Yes|06-Aug-2013|Cryopreserved sperm|50.0|0.0|Unknown||infection, resistance, bacteria|Yes| 7393.0|B6.TLR4 0/0|B6.C3-Tlr4/Apb||Semi-dominant|||||||||||||||||||||||||||||toll-like receptor 4|Tlr4||lipopolysaccharide response, Lps, Rasl2-8|MGI:96824|toll-like receptor 4; defective lipopolysaccharide response|Tlr4|MGI:1857718|4|The Lps-d allele renders the animals endotoxin-resistant. |unknown|C57BL/6|Yes|Yes|Unknown|Yes|Yes|Unknown|No|Excellent|13|||Yes|06-Aug-2013|Cryopreserved sperm|50.0|0.0|Unknown||LPS, endotoxin, TLR4|Yes| 9346.0|Arjuna:TCR:FoxP3-cre:B10.BR |B6.B10-H2 Foxp3 Tg(ILK3mHEL)3Ccg Tg(TcrHEL3A9)1Mmd/Anu||Dominant|histocompatibility-2, MHC|H2|||MGI:95894|histocompatibility-2, MHC; k2 variant|H2|MGI:4936842|17|||||||||||||||||transgene insertion 3, Christopher C Goodnow||||||||||||Mice carry the transgenes:1 Cre udner the foxp3 promotor2 TCR3A9, which recognises HEL in the context of H2K(K)|mice are hemizygous only|B10BR N5|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|28-Feb-2022|Cryopreserved sperm|21.0|0.0|Unknown|||No| 9346.0|Arjuna:TCR:FoxP3-cre:B10.BR |B6.B10-H2 Foxp3 Tg(ILK3mHEL)3Ccg Tg(TcrHEL3A9)1Mmd/Anu||Dominant|forkhead box P3|Foxp3||scurfin|MGI:1891436|forkhead box P3; targeted mutation 4, Alexander Y Rudensky|Foxp3|MGI:3790499|X|ENSMUSG00000039521||||||||||||||||transgene insertion 1, Mark M Davis||||||||||||Mice carry the transgenes:1 Cre udner the foxp3 promotor2 TCR3A9, which recognises HEL in the context of H2K(K)|mice are hemizygous only|B10BR N5|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|28-Feb-2022|Cryopreserved sperm|||Unknown|||No| 10518.0|OT-I:CD45.1|B6.Cg-Ptprc Tg(TcraTcrb)1100Mjb/Anu||Dominant|protein tyrosine phosphatase receptor type C|Ptprc ||CD45, Ly-5, Lyt-4, T200|MGI:97810|protein tyrosine phosphatase receptor type C; a variant|Ptprc|MGI:4819849|1|ENSMUSG00000026395||||||||||||||||transgene insertion 1100, Michael J Bevan||||||||||||Normal|Normal|C57BL/6|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|09-Jul-2025||0.0|69.0|Unknown|||Yes| 9363.0|C3AC (CX3CR1-Cre x Ai9 x CSF1Ffl/fl )|B6.(Cg)-Cx3cr1 Gt(ROSA)26Sor Csf1r/J||Semi-dominant|C-X3-C motif chemokine receptor 1|CX3Cr1|||MGI:1333815|C-X3-C motif chemokine receptor 1; targeted mutation 1.1, Steffen Jung|Cx3cr1|MGI:5467983|9|ENSMUSG00000052336 ||||||||||||||||||||||||||||Mice in which all CX3CR1+ cells and their progeny express Cre and Tomato and are constitutively deficient for CSF1R. This mouse line results from the cross of 3 mouse lines imported from Jackson labs. Ai9 (B6.Cg-Gt(ROSA)26Sortm9(CAG-tdTomato)Hze/J): a Cre reporter tool strain designed to have a loxP-flanked STOP cassette preventing transcription of a CAG promoter-driven red fluorescent protein variant (tdTomato) - all inserted into the Gt(ROSA)26Sor locus. Ai9 mice express robust tdTomato fluorescence following Cre-mediated recombination. This strain is congenic on the C57BL/6J genetic background. CX3CR1-Cre (B6J.B6N(Cg)-Cx3cr1tm1.1(cre)Jung/J) : a knock-in mouse line express Cre recombinase under the direction of the emgogenous Cx3cr1 promoter in the mononuclear phagocyte system making them useful for fate-mapping studies of the monocyte and macrophage compartment, as well as microglia. Mice that are homozygous for the do not express endogenous Cx3cr1.CSF1R fl/fl (B6.Cg-Csf1rtm1.2Jwp/J): a floxed mutant mice possess loxP sites flanking exon 5 of the colony stimulating factor 1 receptor (Csf1r) gene and may be useful in studying the role of CSF1R in development.Mice homozygous for the 3 mutations are CX3CR-1 deficient, while all CX3CR1+ cells and their progeny express Tomato and are constitutively deficient for CSF1R|Mice heterozygous for the 3 mutations are hemyzygous for CX3CR1 and CSF1R and express Tomato in all CX3CR1+ cells. Mice appear normal|C57Bl/6N|Yes|Unknown|Yes|Yes|Unknown|Yes|No|Unknown|more than 10|||No|21-Mar-2022|Cryopreserved sperm|60.0|0.0|Unknown|||Possibly| 9363.0|C3AC (CX3CR1-Cre x Ai9 x CSF1Ffl/fl )|B6.(Cg)-Cx3cr1 Gt(ROSA)26Sor Csf1r/J||Semi-dominant|gene trap ROSA 26, Philippe Soriano|Gt(ROSA)26So||Gtrosa26, R26, ROSA26|MGI:104735|gene trap ROSA 26, Philippe Soriano; targeted mutation 9, Hongkui Zeng|Gt(ROSA)26Sor|MGI:3809523|6|ENSMUSG00000086429||||||||||||||||||||||||||||Mice in which all CX3CR1+ cells and their progeny express Cre and Tomato and are constitutively deficient for CSF1R. This mouse line results from the cross of 3 mouse lines imported from Jackson labs. Ai9 (B6.Cg-Gt(ROSA)26Sortm9(CAG-tdTomato)Hze/J): a Cre reporter tool strain designed to have a loxP-flanked STOP cassette preventing transcription of a CAG promoter-driven red fluorescent protein variant (tdTomato) - all inserted into the Gt(ROSA)26Sor locus. Ai9 mice express robust tdTomato fluorescence following Cre-mediated recombination. This strain is congenic on the C57BL/6J genetic background. CX3CR1-Cre (B6J.B6N(Cg)-Cx3cr1tm1.1(cre)Jung/J) : a knock-in mouse line express Cre recombinase under the direction of the emgogenous Cx3cr1 promoter in the mononuclear phagocyte system making them useful for fate-mapping studies of the monocyte and macrophage compartment, as well as microglia. Mice that are homozygous for the do not express endogenous Cx3cr1.CSF1R fl/fl (B6.Cg-Csf1rtm1.2Jwp/J): a floxed mutant mice possess loxP sites flanking exon 5 of the colony stimulating factor 1 receptor (Csf1r) gene and may be useful in studying the role of CSF1R in development.Mice homozygous for the 3 mutations are CX3CR-1 deficient, while all CX3CR1+ cells and their progeny express Tomato and are constitutively deficient for CSF1R|Mice heterozygous for the 3 mutations are hemyzygous for CX3CR1 and CSF1R and express Tomato in all CX3CR1+ cells. Mice appear normal|C57Bl/6N|Yes|Unknown|Yes|Yes|Unknown|Yes|No|Unknown|more than 10|||No|21-Mar-2022|Cryopreserved sperm|||Unknown|||Possibly| 9363.0|C3AC (CX3CR1-Cre x Ai9 x CSF1Ffl/fl )|B6.(Cg)-Cx3cr1 Gt(ROSA)26Sor Csf1r/J||Semi-dominant|colony stimulating factor 1 receptor|Csf1r||CD115, CSF-1R, Csfmr, Fim-2|MGI:1339758|colony stimulating factor 1 receptor; targeted mutation 1.2, Jeffrey W Pollard|Csf1r|MGI:5780867|18|ENSMUSG00000024621||||||||||||||||||||||||||||Mice in which all CX3CR1+ cells and their progeny express Cre and Tomato and are constitutively deficient for CSF1R. This mouse line results from the cross of 3 mouse lines imported from Jackson labs. Ai9 (B6.Cg-Gt(ROSA)26Sortm9(CAG-tdTomato)Hze/J): a Cre reporter tool strain designed to have a loxP-flanked STOP cassette preventing transcription of a CAG promoter-driven red fluorescent protein variant (tdTomato) - all inserted into the Gt(ROSA)26Sor locus. Ai9 mice express robust tdTomato fluorescence following Cre-mediated recombination. This strain is congenic on the C57BL/6J genetic background. CX3CR1-Cre (B6J.B6N(Cg)-Cx3cr1tm1.1(cre)Jung/J) : a knock-in mouse line express Cre recombinase under the direction of the emgogenous Cx3cr1 promoter in the mononuclear phagocyte system making them useful for fate-mapping studies of the monocyte and macrophage compartment, as well as microglia. Mice that are homozygous for the do not express endogenous Cx3cr1.CSF1R fl/fl (B6.Cg-Csf1rtm1.2Jwp/J): a floxed mutant mice possess loxP sites flanking exon 5 of the colony stimulating factor 1 receptor (Csf1r) gene and may be useful in studying the role of CSF1R in development.Mice homozygous for the 3 mutations are CX3CR-1 deficient, while all CX3CR1+ cells and their progeny express Tomato and are constitutively deficient for CSF1R|Mice heterozygous for the 3 mutations are hemyzygous for CX3CR1 and CSF1R and express Tomato in all CX3CR1+ cells. Mice appear normal|C57Bl/6N|Yes|Unknown|Yes|Yes|Unknown|Yes|No|Unknown|more than 10|||No|21-Mar-2022|Cryopreserved sperm|||Unknown|||Possibly| 7394.0|B6.ICE-/-|B6.129S2-Casp1/Apb||Recessive|caspase 1|Casp1|Nil|Caspase-1, ICE, Il1bc, interleukin 1 beta-converting enzyme|MGI:96544|caspase 1; targeted mutation 1, Richard Flavell|Casp1|MGI:2158744|9|||||||||||||||||||||||||||||mice lack expression of interleukin-1 converting enzyme (or caspase-1) and therefore cannot proteolytically cleave interleukin 1β and interleukin 18 into active mature peptides. |unknown|C57BL/6|Yes|Yes|Unknown|Yes|Yes|Unknown|No|Excellent|13|||Yes|06-Aug-2013|Cryopreserved sperm|50.0|0.0|Unknown||caspase-1, IL-1b, IL-18|Yes| 7568.0|Mt3KO:ANU|B6.129-Mt3/Apb||Recessive|metallothionein 3|Mt3|Nil|MT-3|MGI:97173|metallothionein 3; targeted mutation 1, Richard D Palmiter|Mt3|MGI:2389488|8|||||||||||||||||||||||||||||Mice homozygous for a knock-out allele exhibit a zinc deficiency in several brain regions, abnormal astrocyte morphology, increased susceptibility to kainic acid induced seizures, and altered zinc accumulation and neuronal death in certain brain areas following seizure-induced or acute brain injury.|Unknown|C57BL/6|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Excellent||||No|17-Jan-2014|Cryopreserved sperm|50.0|0.0|Unknown||zinc, metals, seizures|Possibly| 10443.0|JAX Swiss Outbred|J:ARC(s)||Recessive|N/A|N/A|||||||Unknown|||||||||||||||||||||||||||||Normal|Normal|Swiss|Yes|Yes|Yes|Yes|Yes|Yes|No|Excellent|||Outbred|No|06-Aug-2024||0.0|1066.0|Unknown|||No| 7531.0|R-DTA|B6.129-Gt(ROSA)26Sor/MelbAnuApb||Dominant|gene trap ROSA 26, Philippe Soriano|Gt(ROSA)26Sor||beta geo, Gtrgeo26, Gtrosa26, R26, ROSA26|MGI:104735|gene trap ROSA 26, Philippe Soriano; targeted mutation 1, Richard M Locksley|Gt(ROSA)26Sor|MGI:3829362|6|||||||||||||||||||||||||||||Mice heterozygous or homozygous for the ROSA26 retroviral insertion display no distinguishing phenotype. lacZ is expressed in all tissues of the developing embryo and in most tissues of the adult mouse.Removal of flexed stuffer sequence by Cre recombinase results in diphtheria expression and cell death.Abnormal cell death:• T cells infected with a retroviral cre exhibit cell death without inducing cell death in uninfected cells||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|04-Dec-2013|Cryopreserved sperm|36.0|0.0|Unknown||diphtheria toxin|Yes| 7823.0|ENU15NIH:085:a:HamletxCharles:G7|B6.129-Sppl2a Tg(IghelMD4)4Ccg Tg(MLsHEL)Ccg/AnuApb||Recessive|signal peptide peptidase like 2A|Sppl2a|Nil|cbl-b|MGI:1913802 |signal peptide peptidase like 2A; mutation 1, The Australian National University|Sppl2a|MGI:5432126|2|ENSMUSG00000027366|ENSMUST00000028844|2010106G01Rik-001|||||||||7||||Yes|transgene insertion 4, Christopher C Goodnow||||||||||||Defect in T cell signalling||C57BL/6 x 129|Yes|Yes|Yes|Yes|Yes|Yes|No|Poor||10||No|03-Jan-2015|Cryopreserved sperm|20.0|0.0|No||T cell, Hen Egg Lysozyme (HEL), signal transduction, ENU|Yes| 7823.0|ENU15NIH:085:a:HamletxCharles:G7|B6.129-Sppl2a Tg(IghelMD4)4Ccg Tg(MLsHEL)Ccg/AnuApb||Recessive||||||||||||||||||||||||||immunoglobulin kappa chain complex, immunoglobulin heavy chain complex. (IgM and IgD). Genomic clones of H+L genes with normal control elements. soluble HEL (hen egg lysozyme)|H-2K|||||||||||Defect in T cell signalling||C57BL/6 x 129|Yes|Yes|Yes|Yes|Yes|Yes|No|Poor||10||No|03-Jan-2015|Cryopreserved sperm|||No||T cell, Hen Egg Lysozyme (HEL), signal transduction, ENU|Yes| 8213.0|Ifnar KO|B6.129-Ifnar1/AnuApb||Recessive|interferon (alpha and beta) receptor 1|Ifnar1|Unknown|CD118, Ifar, Ifrc, INF-a receptor, Infar|MGI:107658|targeted mutation 1, Michel Aguet|Ifnar1|MGI:1930950|16||||||||||||||||Yes|||||||||||||Homozygotes for targeted null mutations exhibit increased susceptibility to viral infection, elevated levels of myeloid lineage cells in the peripheral blood and bone marrow, and reduced immune response to immunostimulatory DNA.||C57BL/6NCrlAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|08-Mar-2017|Cryopreserved sperm|48.0|0.0|Unknown||interferon, infection, immunity, T cell|Yes| 10400.0||C57Bl/6N-Klhdc3/Apb||Dominant|kelch domain containing 3|Klhdc3||Peas|MGI:2651568|Klhdc3:endonuclease-mediated mutation 2, Carl Walkley|Klhdc3||17|ENSMUSG00000063576 ||||||||||||||||||||||||||||no phenotype (Klhdc3 fl/fl or fl/+ mice). Conditional allele of Klhdc3|no phenotype (Klhdc3 fl/fl or fl/+ mice). Conditional allele of Klhdc3|C57Bl/6N|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|17-Jan-2024|Cryopreserved sperm|40.0|0.0|Unknown|||No| 7981.0|Nrp1Sema|B6.129P2-Nrp1/DdgApb||Recessive|neuropilin 1|Nrp1|Normal|Neuropilin-1, NP-1, Npn1, NPN-1|MGI:106206|neuropilin 1; targeted mutation 1, David D Ginty|Nrp1|MGI:3512099|8|||||||||||||||||||||||||||||Mutant embryos from het X het matings have axonal guidance defects in a range of central and peripheral neurons. Adults mutants are smaller than littermates and also have axonal defasciculation. Postnatal lethality:• 40% die by P7Dilated heart atrium:• exhibited bilateral atrial enlargement, however no vascular branching defects were observedPostnatal growth retardation:• 70% of P7 survivors are growth retardedAbnormal axon guidance:• guidance of ophthalmic nerve axons and cutaneous sensory neurons was abnormal so that projections extended beyond their normal zonesAbnormal corpus callosum morphology:• callosal axons displayed varying degrees of defasciculation with agenesis of corpus callosum resulting in the formation of Probst bundles in extreme cases.Abnormal hippocampus morphology:• entorhinohippocampal axons were no longer restricted in the stratum lacunosum-moleculare of the ipsilateral hippocampus with many fibers innervating ectopic layers.Abnormal cranial nerve morphology:Abnormal trigeminal nerve morphology:• defasciculated and abnormally extended ophthalmic branch of the trigeminal nerve, however defects were less severe than in Nrp1.Abnormal vestibulocochlear nerve morphology:• E12.5 mutants have additional smaller fiber bundles that extend beyond their normal termination zones within the sensory end organs with projection defects persisting at E14.5 and E15.5Abnormal dorsal root ganglion morphology:• many cutaneous afferent axons entered the gray matter a E14.5 with some projections extending into the most ventral regions of the spinal cord.• at P2, some axons were outside their normal termination zones, along the midline and in the medial-ventral spinal cord.Abnormal spinal nerve morphology:• disorganized peripheral projections of spinal nerves in E11.5 mutants.Abnormal T cell physiology:• defective T-cell priming by antigenAbnormal dendritic cell physiology:• impaired dendritic cell migration|Normal|C57BL/6J|Yes|Unknown|Yes|Yes|Unknown|Yes|No|Good||||No|12-Oct-2015|Cryopreserved sperm|60.0|0.0|Unknown||Neuropilin, Nrp1, Npn1, Semaphorins, vascular endothelial growth factor|Possibly| 8015.0|CD122 KO|B6.129-Il2rb/AusbAnuApb||Recessive|interleukin 2 receptor, beta chain|Il2rb|Nil|CD122, IL15Rbeta, IL-15Rbeta, IL-15 receptor beta chain, IL-2/15Rbeta, Il-2Rbeta|MGI:96550|interleukin 2 receptor, beta chain; targeted mutation 1, Tak Mak|Il2rb|MGI:1857193|15|||||||||||||||||||||||||||||Increased susceptibility to autoimmune hemolytic anemia:• by 26 days of age• can be prevented with adoptive transfer at birth of 1 x 10<5> CD25-positive CD4 T cells from wild-type miceAbnormal lymphocyte morphology.Decreased regulatory T cell number:• there is a 2 to 5 fold reduction in the percentage of CD25-postive CD4 T cells in both the thymus and lymph nodes• transgeneic expression of Il2rb in the thymus rescues number of regulatory T cells.Enlarged spleen:• in mice by 26 days of age• can be prevented with adoptive transfer at birth of 1 x 10<5> CD25-positive CD4 T cells from wild-type miceabnormal spleen periarteriolar lymphoid sheath morphology ( J:113547 )• increased in size at 26 days of age• can be prevented with adoptive transfer at birth of 1 x 105 CD25-positive CD4 T cells from wild-type miceAbnormal T cell activation:• percentage of CD4 and CD8 T cells that express high levels of activation markers is increased• T cells are hyporesponsive to inflammatory cytokines as measured by in vitro proliferation assays• expression of activation markers is normalized upon transfer of 1 x 10<5> CD25-positive CD4 T cells from wild-type miceDecreased T cell proliferation:• in mice by 26 days of age• can be prevented with adoptive transfer at birth of 1 x 10<5> CD25-positive CD4 T cells from wild-type miceEnlarged lymph nodes:• in mice by 26 days of age• can be prevented with adoptive transfer at birth of 1 x 10<5> CD25-positive CD4 T cells from wild-type miceIncreased anti-double stranded DNA antibody level:• can be prevented with adoptive transfer at birth of 1 x 10<5> CD25-positive CD4 T cells from wild-type mice• in mice by 26 days of ageAbnormal response to transplant:• adoptively transfered regulatory T cell expand at least 15 to 20 times until they make up 3-5% of the total cells in the lymph nodes and spleen• regulatory T cells were unable to engraft in wild-type mice.||C57BL/6|Unknown|Yes|Yes|Unknown|Yes|Yes|No|Unknown||||No|21-Dec-2015|Cryopreserved sperm|22.0|0.0|Unknown||T cell, Lymphocyte|Yes| 9000.0||B6.129-F2rl1 Tg(Sp7-tTA,tetO-EGFP/cre)1Amc/Apb||Recessive|coagulation factor II (thrombin) receptor-like 1|F2rl1||Gpcr11, Par2, PAR-2, Protease-activated receptor-2, proteinase-activated receptor-2|MGI:101910|coagulation factor II (thrombin) receptor-like 1; targeted mutation 1c, Wellcome Trust Sanger Institute|F2rl1|MGI:6151132|13|||||||||||||||||transgene insertion 1, Andrew P McMahon|SP7|||||||||||Homozygous B6.129-F2rl1tm1c(EUCOMM)Wtsi mice that are positive for the transgene Sp7-tTA,tetO-EGFP/cre are viable and fertile. Like B6.Cg-Tg(Sp7-tTA,tetO-EGFP/cre)1Amc/J mice, slow longitudinal bone growth is noticeable. This appears to last up to 13 weeks of age.|Like homozygous.|C57BL/6J|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|05-Jun-2020|Cryopreserved sperm|40.0|0.0|Unknown|||Yes| 10428.0|Nox2 KO |C57Bl/6J-Cybb/Apb||Dominant|cytochrome b-245, beta polypeptide|Cybb||gp91phox, Nox2, NADPH Oxidase 2|MGI:88574|cytochrome b-245, beta polypeptide, targeted mutation 1, Mary C Dinauer|Cybb|MGI:1857284|X|||||||||||||||||||||||||||||Nox2 KO/ deficient mice have compromised immune system. Homozygous mice are viable and fertile. |Heterozygous female mice- Normal.Hemizygous Nox2 male mice are WT or KO.Nox2 null gene is X-linked. Affected Nox2 KO male mice have compromised immune system, lacks phagocyte superoxide production, and increased susceptibility to infection. |C57Bl/6J|Yes|Yes|Yes|Yes|Yes|Unknown|No|Unknown||||No|31-May-2024|Cryopreserved sperm|50.0|0.0|Unknown|||No| 8103.0|Kca3.1|B6.129-Kcnn4/Apb||Recessive|potassium intermediate/small conductance calcium-activated channel, subfamily N, member 4|Kcnn4|Unknown|IK1, IKCa1, KCa3.1, mIKCa1, SK4|MGI:1277957|potassium intermediate/small conductance calcium-activated channel, subfamily N, member 4; targeted mutation 1, James E Melvin|Kcnn4|MGI:3521668|7|||||||||||||||||||||||||||||Increased parotid gland size:• in homozygous males the weight of the parotid gland is significantly increased, however no change in salivary flow or composition is seenAbnormal hematopoietic system physiology:• A23187-stimulated, clotrimazole sensitive uptake of 86Rb into red blood cells is nearly eliminated in homozygous mutants and A23187 has no effect on the tonicity at which 50% of mutant red cells lyseAbnormal T cell physiology:• shrinkage of T lymphocytes induced by the Ca2+ ionophore, ionomycin, is greatly reduced||C57BL/6J|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|15-Sep-2016|Cryopreserved sperm|45.0|0.0|Unknown||Potassium channel|Yes| 8469.0|Sphingosine kinase 2 Knockout |B6.129S6-Sphk2/RlpUsaApb||Recessive|sphingosine kinase 2|Sphk2|||MGI:1861380|sphingosine kinase 2; targeted mutation 1, Richard L Proia|Sphk2|MGI:3611080|7|||||||||||||||||||||||||||||Normal|Normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|12-Apr-2018|Cryopreserved sperm|50.0|0.0|Unknown||Vascular development, Angiogenesis|Yes| 9190.0|Ago2|B6.129P2(129S4)-Ago2/AnuApb||Recessive|argonaute RISC catalytic subunit 2|Ago2|Nil|1110029L17Rik, 2310051F07Rik, argonaute 2, Eif2c2, mKIAA1567|MGI:2446632|argonaute RISC catalytic subunit 2; targeted mutation 1.1, Alexander Tarakhovsky|Ago2|MGI:4839762|15|||||||||||||||||||||||||||||These mice possess loxP sites on either side of exons 9-11 in the Eif2c2 (eukaryotic translation initiation factor 2C, 2) gene, also known as Ago2. Mice that are homozygous for this floxed allele are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. When crossed with a Cre recombinase-expressing strain, the Mid domain is deleted and Ago2 expression is lost, causing functional inactivation of the gene.|Unknown|C57BL/6J |Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|Unknown|||Yes|21-May-2021|Live|0.0|0.0|Unknown||miRNA biogenesis, T reg cells, Ago2, Argonaute|Yes| 10358.0|Ubc-CreER R26-Adar1p150 |C57BL/6J-Gt(ROSA)26Sor Ndor1/Apb||Dominant|gene trap ROSA 26, Philippe Soriano|Gt(ROSA)26Sor||Ubc-CreER R26-Adar1p150|MGI:104735|Gt(ROSA)26Sor; Endonuclease-mediated mutation 1.1, Melbourne Advanced Gene Editing Centre|Gt(ROSA)26Sor||6|||||||||||||||||NADPH dependent diflavin oxidoreductase 1; transgene insertion 1, Eric J Brown||||||||||||No phenotype unless tamoxifen treated. Tamoxifen induces CreER activation which leads to overexpression of the ADAR1 p150 isoform from the R26 locus. Also leads to GFP expression.|No phenotype unless tamoxifen treated. Tamoxifen induces CreER activation which leads to overexpression of the ADAR1 p150 isoform from the R26 locus. Also leads to GFP expression.|C57Bl/6N|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|20-Sep-2023|Cryopreserved sperm|40.0|0.0|Unknown|||No| 10364.0|Ubc-CreER R26-Adar1|C57BL/6J-Gt(ROSA)26Sor Ndor1/Apb||Dominant|gene trap ROSA 26, Philippe Soriano|Gt(ROSA)26Sor||Ubc-CreER R26-Adar1|MGI:104735|Gt(ROSA)26Sor; Endonuclease-mediated mutation 1.1, Melbourne Advanced Gene Editing Centre|Gt(ROSA)26Sor||6|ENSMUSG00000086429 ||||||||||||||||NADPH dependent diflavin oxidoreductase 1; transgene insertion 1, Eric J Brown||||||||||||no phenotype when homozygous. Requires tamoxifen treatment to induce ectopic expression of murine ADAR1.|no phenotype when homozygous. Requires tamoxifen treatment to induce ectopic expression of murine ADAR1.|C57Bl/6N|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|27-Sep-2023|Cryopreserved sperm|50.0|0.0|Unknown|||No| 9227.0|ASD816:TCF-Lef:H2B-GFP|B6.129-Tg(TCF/Lef1-HIST1H2BB/EGFP)61Hadj/Apb||Dominant|TCF/Lef:H2B/GFP||||||||Unknown|||||||||||||||||transgene insertion 61, Anna-Katerina Hadjantonakis|Hspa1b, heat shock protein 1B, mouse, laboratory|||||||||||No externally observable phenotype. GFP expression in cells with active canonical WNT signalling. GFP expression is evident in cells of the extraembryonic visceral endoderm, the primitive streak, the mature node, presomitic mesoderm and newly formed somites, posterior neural plate, cranial neural crest, face, and branchial arches. By E12.5 fluorescence is also seen in the kidney, gonads, and some neuronal subsets in the brain.|No externally observable phenotype. GFP expression in cells with active canonical WNT signalling. GFP expression is evident in cells of the extraembryonic visceral endoderm, the primitive streak, the mature node, presomitic mesoderm and newly formed somites, posterior neural plate, cranial neural crest, face, and branchial arches. By E12.5 fluorescence is also seen in the kidney, gonads, and some neuronal subsets in the brain.|C57BL.6|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|15-Jul-2021|Cryopreserved sperm|60.0|0.0|Unknown|||Possibly| 10519.0|cNLRC4 Villin-Cre|B6N.Cg-Nlrc4 Tg(Vil1-cre)1000Gum/JAnu||Dominant|NLR family, CARD domain containing 4|Nlrc4 ||Card12, Ipaf|MGI:3036243|Nlrc4:endonuclease-mediated mutation 2, Australian National University|Nlrc4 ||17|||||||||||||||||transgene insertion 1000, Deborah L Gumucio||||||||||||Normal|Normal||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|29-Jul-2025||0.0|0.0|Unknown|||No| 10357.0||ANU:ENU59:G3||Recessive|Unknown||||||||Unknown||||||||||||||||||||||||||||| | |C57Bl/6N|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|11-Sep-2023|Cryopreserved sperm|25.0|0.0|Unknown|||Possibly| 10517.0|cNLRC4 (50)|C57BL/6NCrlAnu-Nlrc4/AnuApb||Dominant|NLR family, CARD domain containing 4|Nlrc4||Card12, Ipaf|MGI:3036243|Nlrc4:endonuclease-mediated mutation 2, Australian National University|Nlrc4||17|ENSMUSG00000039193||||||||||||||||||||||||||||Normal|Normal||Yes|Yes|Unknown|Yes|Yes|Unknown|No|Good|||hom x hom|No|08-Jul-2025|Cryopreserved sperm|23.0|0.0|Unknown|||No| 10521.0|cNLRC4 (50)|C57BL/6NCrlAnu-Nlrc4/AnuApb||Dominant|NLR family, CARD domain containing 4|Nlrc4||Card12, Ipaf|MGI:3036243|Nlrc4:endonuclease-mediated mutation 2, Australian National University|Nlrc4||17|ENSMUSG00000039193||||||||||||||||||||||||||||Normal|Normal||Yes|Yes|Unknown|Yes|Yes|Unknown|No|Good|||hom x hom|No|18-Aug-2025||0.0|0.0|Unknown|||No| 8305.0|APPPS1|B6.C3-Tg(APPswe,PSEN1dE9)85Dbo/JAusbAnu|B6.C3-Tg(APPswe,PSEN1dE9)85Dbo/JAusbAnu|Dominant||||||||||||||||||||||||||transgene insertion 85, David R Borchelt|mouse prion protein |Predominantly to CNS neurons||||||||||Unknown|Mice develop beta amyloid deposits in brain by 6 or 7 months of age. The humanized Mo/HuAPP695swe transgene allows the mice to secrete a human A-beta peptide.A slight alteration in the tail can occur due to mixed background.|C57BL/6JAnu|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown|1|1|Maintained as a hemizygote by crossing transgenic mice to B6C3F1/J mice|No|14-Sep-2017|Cryopreserved sperm|15.0|187.0|Yes|Alzheimers|CNS neurons, hippocampus, amyloid beta peptide , astrocytosis|Yes| 7582.0|B1-8 High Affinity +/-, (ROSA)td Tomato -/- KI|B6.129-IgH Gt(ROSA)26Sor/JMnzAnu||Recessive|immunoglobulin heavy chain complex|Igh|||MGI:96442|immunoglobulin heavy chain complex; targeted mutation 1, Michel C Nussenzweig|Igh|MGI:3712224|12|||||||||||||||||||||||||||||All cells express red colour from Tomato||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|Tomato - 8x to B6; B1-8 high >15x to B6|||No|05-Feb-2014|Cryopreserved sperm|32.0|0.0|Unknown||T cell, Germinal centre, B cell|Possibly| 7582.0|B1-8 High Affinity +/-, (ROSA)td Tomato -/- KI|B6.129-IgH Gt(ROSA)26Sor/JMnzAnu||Recessive|gene trap ROSA 26, Philippe Soriano|Gt(ROSA)26Sor||beta geo, Gtrgeo26, Gtrosa26, R26, ROSA26 |MGI:104735|gene trap ROSA 26, Philippe Soriano; targeted mutation 9, Hongkui Zeng|Gt(ROSA)26Sor|MGI:3809523|6|||||||||||||||||||||||||||||All cells express red colour from Tomato||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|Tomato - 8x to B6; B1-8 high >15x to B6|||No|05-Feb-2014|Cryopreserved sperm|||Unknown||T cell, Germinal centre, B cell|Possibly| 10479.0|Csf1rflox|B6.Cg-Csf1r/J||Recessive|colony stimulating factor 1 receptor|Csf1r||Fim2, Fms|MGI:1339758|colony stimulating factor 1 receptor; targeted mutation 1.2, Jeffrey W Pollard|Csf1r|MGI:5780867|18|ENSMUSG00000024621 ||||||||||||||||||||||||||||These Csf1rfl/fl floxed mutant mice possess loxP sites flanking exon 5 of the colony stimulating factor 1 receptor (Csf1r) gene. Csf1r encodes Cd115 which acts as the receptor for colony stimulating factor 1, a cytokine which controls the production, differentiation, and function of macrophages. Expressed in macrophages, expression is also seen in oocytes, osteoclasts, trophoblasts, CNS microglia, and some myoblasts. Mice that are homozygous for this allele are viable and fertile. When these mutant mice are bred to mice that express Cre recombinase, resulting offspring will have exon 5 and the neo cassette deleted in cre-expressing tissues.|same as homozygous|C57Bl/6J|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|04-Feb-2025||0.0|0.0|Unknown|||Possibly| 10486.0|Wnt4GCE-nTnG|B6.Cg-Wnt4-Gt(ROSA)26Sor/Apb||Dominant|wingless-type MMTV integration site family, member 4|Wnt4|||MGI:98957|wingless-type MMTV integration site family, member 4; targeted mutation 2, Andrew P McMahon|Wnt4|MGI:3845544|4|ENSMUSG00000036856||||||||||||||||||||||||||||Homozygous mice die in utero or in early postnatal life due to a lack of kidney function and other abnormalities arising from the loss of Wnt4 function.|Heterozygous mice are viable and fertile|C57Bl/6J|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|05-Feb-2025|Cryopreserved sperm|50.0|0.0|Unknown|||Possibly| 10486.0|Wnt4GCE-nTnG|B6.Cg-Wnt4-Gt(ROSA)26Sor/Apb||Dominant|gene trap ROSA 26, Philippe Soriano|Gt(ROSA)26Sor||Gtrosa26, R26|MGI:104735|gene trap ROSA 26, Philippe Soriano; targeted mutation 1, Edward E Schmidt|Gt(ROSA)26Sor|MGI:5504463|6|ENSMUSG00000086429 ||||||||||||||||||||||||||||Homozygous mice die in utero or in early postnatal life due to a lack of kidney function and other abnormalities arising from the loss of Wnt4 function.|Heterozygous mice are viable and fertile|C57Bl/6J|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|05-Feb-2025|Cryopreserved sperm|||Unknown|||Possibly| 10522.0|Esyt1-Pmel (cKO)|C57BL/6J-Esyt1 Pmel||Dominant|extended synaptotagmin-like protein 1|Esyt1||Fam62a, Mbc2, vp115|MGI:1344426|Esyt1:endonuclease-mediated mutation 1, Mgmp|Esyt1||10|ENSMUSG00000025366 ||||||||||||||||||||||||||||Normal (requires Cre Recombinase for phenotype)|Normal (requires Cre Recombinase for phenotype)||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|18-Aug-2025||0.0|0.0|Unknown|||No| 10522.0|Esyt1-Pmel (cKO)|C57BL/6J-Esyt1 Pmel||Dominant|premelanosome protein|Pmel||Pmel17, Si|MGI:98301|Pmel:endonuclease-mediated mutation 1, Mgmp|Pmel||10|ENSMUSG00000025359||||||||||||||||||||||||||||Normal (requires Cre Recombinase for phenotype)|Normal (requires Cre Recombinase for phenotype)||Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|18-Aug-2025||||Unknown|||No| 4889.0||129-Elane Ctsg/HApb||Dominant|cathepsin G|Ctsg|Nil||MGI:88563|targeted mutation 1.1, Jurgen Roes|Ctsgtm1.1Roes|MGI:2182170|14|||||||||||||||||Cre recombinase||myeloid precursor cells||||||||||Decreased susceptibility to endotoxin shock: after injection of 100ng LPS along with D-galactosamine 54% of double homozygotes survive compared to only 9% of wild-type mice and median survival time is increased to 935 +/- 227 min compared to 435 +/- 8 min in wild-type mice.LPS-induced increases in serum TNF, recruitment of neutrophils into the liver, and liver damage are all normal; however vascular and lung damage are reduced.Increased susceptibility to fungal infection: after infection with 500,000 A. fumigatus spores median survival time was only 10 +/- 3 days compared to wild-type mice which all survive.Infection with a lower concentration of spores, at which all single homozygotes survive, resulted in the death of 60% of double homozygotes.6 days after infection kidney fungal load is 1009 mean CFU much higher than wild-type (16 mean CFU) or either single homozygote.||129/Sv|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|28-Sep-2009|Cryopreserved sperm|99.0|0.0|Unknown||Neutrophil, serine protease, reactive oxygen intermediates, endotoxin, LPS, TNF alpha, elastase|Yes| 4889.0||129-Elane Ctsg/HApb||Dominant|elastase, neutrophil expressed|Elane|Nil|Ela2, F430011M15Rik, NE, neutrophil elastase|MGI:2679229|targeted mutation 1, Jurgen Roes|Elane|MGI:2182177|10|||||||||||||||||||||||||||||Decreased susceptibility to endotoxin shock: after injection of 100ng LPS along with D-galactosamine 54% of double homozygotes survive compared to only 9% of wild-type mice and median survival time is increased to 935 +/- 227 min compared to 435 +/- 8 min in wild-type mice.LPS-induced increases in serum TNF, recruitment of neutrophils into the liver, and liver damage are all normal; however vascular and lung damage are reduced.Increased susceptibility to fungal infection: after infection with 500,000 A. fumigatus spores median survival time was only 10 +/- 3 days compared to wild-type mice which all survive.Infection with a lower concentration of spores, at which all single homozygotes survive, resulted in the death of 60% of double homozygotes.6 days after infection kidney fungal load is 1009 mean CFU much higher than wild-type (16 mean CFU) or either single homozygote.||129/Sv|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|28-Sep-2009|Cryopreserved sperm|||Unknown||Neutrophil, serine protease, reactive oxygen intermediates, endotoxin, LPS, TNF alpha, elastase|Yes| 7262.0|LysM-Cre Rb|B6(Cg)-Lyz2 Rb1/StvApb||Dominant|retinoblastoma 1|Rb1|Normal|pRb, Rb, Rb-1|MGI:97874|retinoblastoma 1; targeted mutation 3, Tyler Jacks|Rb1|MGI:2450162|14|||||||||||||||||||||||||||||No obvious phenotype. No effect on lifespan, breeding or skeleton|None observed. LysM-Cre mice are ok as both heterozygous and homozygous alleles|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|5|unknown/not collected|LysM-Creki/+ pRBfl/+ male to LysM-Creki/+ pRBfl/+ female|No|18-Jan-2013|Cryopreserved sperm|50.0|0.0|No|hereditary retinoblastoma - bone specifc model|Rb, LysM-Cre|Yes| 7262.0|LysM-Cre Rb|B6(Cg)-Lyz2 Rb1/StvApb||Dominant|lysozyme 2|Lyz2 |Nil|Lys, Lysm, Lyzs, Lzm, Lzm-s1, Lzp |MGI:96897|lysozyme 2; targeted mutation 1, Irmgard Forster |Lyz2tm1(cre)Ifo|MGI:1934631|10|||||||||||||||||||||||||||||No obvious phenotype. No effect on lifespan, breeding or skeleton|None observed. LysM-Cre mice are ok as both heterozygous and homozygous alleles|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|5|unknown/not collected|LysM-Creki/+ pRBfl/+ male to LysM-Creki/+ pRBfl/+ female|No|18-Jan-2013|Cryopreserved sperm|||No|hereditary retinoblastoma - bone specifc model|Rb, LysM-Cre|Yes| 10341.0|JNK1 -/-, JNK1 KO|B6.129S1-Mapk8/JMhn||Recessive|mitogen-activated protein kinase 8|Mapk8 |Nil|c-Jun N-terminal kinase, JNK1, Prkm8 |MGI:1346861|mitogen-activated protein kinase 8; targeted mutation 1, Richard Flavell|Mapk8|MGI:2176239|14|||||||||||||||||||||||||||||Mice that are homozygous for the targeted mutation are viable, normal in size or can be a little smaller, do not display any gross physical or behavioral abnormalities and are fertile but poor breeders. No gene product, protein or mRNA, is detected. Lymphocyte development, T cell to B cell ratio and CD4 to CD8 ratio are normal. Naive Th cells activated in vitro preferentially differentiate into Th2 cells. Mutant mice are susceptible to infection when challenged with the intracellular pathogen, Leishmania major. Primary murine embryonic fibroblasts prepared from mutant embryos are partially protected from UV-induced apoptosis. |Normal|C57Bl/6J|Yes|Yes|Yes|Yes|Yes|Yes|No|Poor|5||Heterozygote x Heterozygote|No|19-Jun-2023|Cryopreserved sperm|50.0|0.0|Unknown|||No| 8546.0|Foz:Jnk1 KO|B6(Cg)-Alms1 Mapk8/AnuApb||Recessive|Alstrom syndrome 1 homolog (human)|Alms1|Unknown||MGI:1934606|Alstrom syndrome 1 homolog (human); fat aussie|Alms1|MGI:3621984|6||||||||||||||||Yes|||||||||||||Mice are hyperphagic leading to obesity. Males are sterile. High fat feeding accelerates obesity development, and leads to nonalcoholic steatohepatitis which progresses to liver fibrosis. Steatohepatitis also develops in chow-fed animals.Hyperglycemia: female mice are diabetic by 200 days of age.Increased circulating insulin level: female mice develop insulinemia (20ng/mL insulin vs. 2-5ng/mL in wild-type).Insulin resistance: female mice develop insulin resistance by 200 days of age.Increased eating behavior: mutants eat more than wild-type.Abnormal hepatocyte morphology: mutant livers show many hepatocytes with ballooning degeneration and extensive lobular inflammation with polymorphs and mononuclear cells.Enlarged liver: mice fed high-fat diet show hepatomegaly compared to wild-type (8.9g vs. 2g).Increased liver weight: liver weights in mutant are twice that of wild-type (3.4g vs. 1.6g).Liver fibrosis: mutant livers show pericellular and pericentral fibrosis.Hepatic steatosis: chow-fed mutants develop steatosis; mutants fed the high-fat diet develop severe steatohepatitis.Jnk1 KO mice are susceptible to infection when challenged with the intracellular pathogen, Leishmania major. Primary murine embryonic fibroblasts prepared from mutant embryos are partially protected from UV-induced apoptosis.|Normal|C57BL/6|Yes|Unknown|Yes|Yes|No|Yes|Yes|Good|>10||heterozygote mating|No|06-Aug-2018|Cryopreserved sperm|55.0|0.0|Yes|Alstrom syndrome is a disorder of childhood obesity, diabetes development and infertility.|obesity, diabetes, nonalcoholic fatty liver disease, alstrom syndrome, cilia, infection, T cell|Yes| 8546.0|Foz:Jnk1 KO|B6(Cg)-Alms1 Mapk8/AnuApb||Recessive|mitogen-activated protein kinase 8|Mapk8|Nil|c-Jun N-terminal kinase, JNK1, Prkm8 |MGI:1346861|mitogen-activated protein kinase 8; targeted mutation 1, Richard Flavell|Mapk8|MGI:2176239|14|||||||||||||||||||||||||||||Mice are hyperphagic leading to obesity. Males are sterile. High fat feeding accelerates obesity development, and leads to nonalcoholic steatohepatitis which progresses to liver fibrosis. Steatohepatitis also develops in chow-fed animals.Hyperglycemia: female mice are diabetic by 200 days of age.Increased circulating insulin level: female mice develop insulinemia (20ng/mL insulin vs. 2-5ng/mL in wild-type).Insulin resistance: female mice develop insulin resistance by 200 days of age.Increased eating behavior: mutants eat more than wild-type.Abnormal hepatocyte morphology: mutant livers show many hepatocytes with ballooning degeneration and extensive lobular inflammation with polymorphs and mononuclear cells.Enlarged liver: mice fed high-fat diet show hepatomegaly compared to wild-type (8.9g vs. 2g).Increased liver weight: liver weights in mutant are twice that of wild-type (3.4g vs. 1.6g).Liver fibrosis: mutant livers show pericellular and pericentral fibrosis.Hepatic steatosis: chow-fed mutants develop steatosis; mutants fed the high-fat diet develop severe steatohepatitis.Jnk1 KO mice are susceptible to infection when challenged with the intracellular pathogen, Leishmania major. Primary murine embryonic fibroblasts prepared from mutant embryos are partially protected from UV-induced apoptosis.|Normal|C57BL/6|Yes|Unknown|Yes|Yes|No|Yes|Yes|Good|>10||heterozygote mating|No|06-Aug-2018|Cryopreserved sperm|||Yes|Alstrom syndrome is a disorder of childhood obesity, diabetes development and infertility.|obesity, diabetes, nonalcoholic fatty liver disease, alstrom syndrome, cilia, infection, T cell|Yes| 5512.0|c-myc fl/fl|B6.129S6-Myc/Apb||Semi-dominant|myelocytomatosis oncogene|Myc|Normal|c-myc, Myc2, Niard, Nird|MGI:97250|myelocytomatosis oncogene; targeted mutation 2, Frederick W Alt|Myc|MGI:2178233|15||||||||||||||||No|||||||||||||Normal|Normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Excellent||||No|24-May-2011|Cryopreserved sperm|50.0|0.0|Unknown||myc|Possibly| 7755.0|Flt3-ITD|B6.129-Flt3/AnuApb||Dominant|FMS-like tyrosine kinase 3|Flt3|Increased|CD135, Flk-2, Flk2, Flt-3|MGI:95559|FMS-like tyrosine kinase 3; targeted mutation 1, D Gilliland|Flt3|MGI:3763385|5||||||||||||||||Yes|||||||||||||these mice bearing a knocked in FLT3-ITD allele develop only a mild myeloproliferative disease (MPD) at 3 to 6 months. FLT3-ITD has been shown to cooperate with known oncogenes to induce overt AML. Onset of Acute Myeloid leukaemia.Abnormal hematopoiesis: * bone marrow cells exhibit a two-fold increase in the Lin-Sca1+cKit+ (LSK) compartment compared to in wild-type and heterozygous mice. * monocytes are present in the bone marrow and liver in a background of increased number of maturing myeloid cells is increased compared to in wild-type mice. * the relative percentage of immunophenotypic granulocyte-monocyte progenitors is expanded while the percent of megakaryocyte-erythroid progenitors is decreased. * the proportion of LSK cells in S/G2/M phase is increased while the proportion in G0/G1 is increased compared to in wild-type mice. * fewer LSK cells undergo apoptosis compared to in wild-type and heterozygous mice. * however, the total number of myeloid progenitor cells is the same as in wild-type mice.Abnormal common myeloid progenitor cell morphology: * when cultured on methylcellulose, bone marrow cells produce more colonies than wild-type cells with a greater number of monocytes and fewer erythroid burst forming units and granulocyte-erythroid burst forming units compared to wild-type and heterozygous mice. * however, re-plated colonies do not exhibit increased self-renewal properties.Decreased B cell number: the rise in monocytes in the bone marrow and spleen is accompanied by a decrease in the percentage of T and B lymphoid cells.Decreased mature B cell number: the number of mature B cells in the bone marrow and spleen is decreased compared to in wild-type mice.Decreased T cell number: the rise in monocytes in the bone marrow and spleen is accompanied by a decrease in the percentage of T and B lymphoid cells.Increased leukocyte cell number: mice exhibit leukocytosis and monocytosis with a reversal in the neutrophil to lymphocyte ratio compared to in wild-type mice.Increased granulocyte number: granulocyte populations are increased in peripheral blood compared to in wild-type mice.Increased monocyte cell number: * monocyte populations are increased in peripheral blood. * monocytes are present in the bone marrow and liver in a background of increased number of maturing myeloid cells is increased compared to in wild-type mice.Abnormal B cell differentiation: B cell maturation is blocked at the pre-B stage.Increased spleen red pulp amount: expanded red pulp is comprised of mainly mature myeloid and ad-mixed erythroid elements.Enlarged spleen: mice develop a variable and progressive splenomegaly that is more severe than in heterozygous miceIncreased spleen white pulp amount: expanded white pulp is comprised of cells resembling maturing monocytes.|Onset of Acute Myeloid leukaemia.Abnormal hematopoiesis: * bone marrow cells exhibit a two-fold increase in the Lin-Sca1+cKit+ (LSK) compartment compared to in wild-type and heterozygous mice. * monocytes are present in the bone marrow and liver in a background of increased number of maturing myeloid cells is increased compared to in wild-type mice. * the relative percentage of immunophenotypic granulocyte-monocyte progenitors is expanded while the percent of megakaryocyte-erythroid progenitors is decreased. * the proportion of LSK cells in S/G2/M phase is increased while the proportion in G0/G1 is increased compared to in wild-type mice. * fewer LSK cells undergo apoptosis compared to in wild-type and heterozygous mice. * however, the total number of myeloid progenitor cells is the same as in wild-type mice.Abnormal common myeloid progenitor cell morphology: * when cultured on methylcellulose, bone marrow cells produce more colonies than wild-type cells with a greater number of monocytes and fewer erythroid burst forming units and granulocyte-erythroid burst forming units compared to wild-type and heterozygous mice. * however, re-plated colonies do not exhibit increased self-renewal properties.Decreased B cell number: the rise in monocytes in the bone marrow and spleen is accompanied by a decrease in the percentage of T and B lymphoid cells.Decreased mature B cell number: the number of mature B cells in the bone marrow and spleen is decreased compared to in wild-type mice.Decreased T cell number: the rise in monocytes in the bone marrow and spleen is accompanied by a decrease in the percentage of T and B lymphoid cells.Increased leukocyte cell number: mice exhibit leukocytosis and monocytosis with a reversal in the neutrophil to lymphocyte ratio compared to in wild-type mice.Increased granulocyte number: granulocyte populations are increased in peripheral blood compared to in wild-type mice.Increased monocyte cell number: * monocyte populations are increased in peripheral blood. * monocytes are present in the bone marrow and liver in a background of increased number of maturing myeloid cells is increased compared to in wild-type mice.Abnormal B cell differentiation: B cell maturation is blocked at the pre-B stage.Increased spleen red pulp amount: expanded red pulp is comprised of mainly mature myeloid and ad-mixed erythroid elements.Enlarged spleen: mice develop a variable and progressive splenomegaly that is more severe than in heterozygous miceIncreased spleen white pulp amount: expanded white pulp is comprised of cells resembling maturing monocytes.|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Poor||||No|08-Oct-2014|Cryopreserved sperm|55.0|0.0|Yes|Myelomonocytic Leukaemia|AML, myeloid, lymphocyte, CML|Yes| 9028.0||B6.Cg-Tg(Csf1r*-GAL4/VP16,UAS-ECFP)1Hume Gt(ROSA)26Sor Tg(Alb1-cre)1Dlr/JApb||Recessive|gene trap ROSA 26, Philippe Soriano|Gt(ROSA)26Sor|||MGI:104735|gene trap ROSA 26, Philippe Soriano; targeted mutation 4, Liqun Luo|Gt(ROSA)26Sor|MGI:3716464|6|||||||||||||||||transgene insertion 1, David A Hume||||||||||||These mice result from a triple cross between Mac blue, Alb-Cre and mT/mG mousse lines in which hepatocytes (but also biliary duct) is membrane GFP+, monocytes and monocyte-derived cells (CD11b+) are CFP+ and all cells but hepatocytes are membrane Tomato+. Detailed descriptions of the 3 lines are below:MacBlue transgenic mice express enhanced cyan fluorescent protein (ECFP) from a truncated colony stimulating factor 1 receptor (Csf1r) promoter using the binary yeast Gal4-UAS system. The Gal4-UAS system utilizes a transgene that consists of both Gal4-expressing and Gal4-reporting modules to drive the expression of the ECFP reporter in Csf1r-expressing cells. In this strain, the Csf1r promoter lacks the 150 bp trophoblast and osteoclast-specific transcription start sites, directing reporter expression specifically in macrophages. Hemizygotes are viable and fertile. All ECFP+ cells in peripheral blood of MacBlue mice are CD11b-positive, and are negative for lymphocyte markers. 10% of granulocytes in peripheral blood and bone marrow express ECFP, as do Ly6C+ and Ly6C- monocytes. All ECFPhi leukocytes express the monocyte/macrophage marker F4/80. 7% of bone marrow cells are ECFP+. ECFP was also detected in adult dendritic cells and blood monocytes in the gut, microglia and Langerhans cells, Peyer’s patches and isolated lymphoid follicles.The Alb1-cre transgene was designed with a Cre recombinase gene under control of albumin (Alb) promoter/enhancer elements. Hemizygous Alb1-cre mice are viable, fertile, and normal in size, with cre expression directed specifically to the liver. When these transgenic mice are bred with mice containing a loxP-flanked sequence, Cre-mediated recombination is expected to result in deletion of the floxed sequences in the Cre recombinase-expressing hepatic cells of the offspring. For example, when these mice are bred to Igf1tm1Dlr-containing mice, the removal of IGF1 expression in the liver causes a 75% reduction in serum IGF-1levels. These mice may be useful for studying the liver specific deletion of target genes.mT/mG mice (Stock No. 007676) have the same allele as Stock No. 007576 but has a C57BL/6J congenic background. ROSAmT/mG is a cell membrane-targeted, two-color fluorescent Cre-reporter allele. Prior to Cre recombination, cell membrane-localized tdTomato (mT) fluorescence expression is widespread in cells/tissues. Cre recombinase expressing cells (and future cell lineages derived from these cells) have cell membrane-localized EGFP (mG) fluorescence expression replacing the red fluorescence. ROSAmT/mG mice (Stock No. 007576 and Stock No. 007676) function similarly to ROSAnT-nG mice (Stock No. 023035 and Stock No. 023537), with ROSAmT/mG directed to cell membrane and ROSAnT-nG directed to nuclei.|Similar to homozygous|C57BL6/J|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|24-Jun-2020|Cryopreserved sperm|50.0|0.0|Unknown|||Yes| 9028.0||B6.Cg-Tg(Csf1r*-GAL4/VP16,UAS-ECFP)1Hume Gt(ROSA)26Sor Tg(Alb1-cre)1Dlr/JApb||Recessive||||||||||||||||||||||||||transgene insertion 1, Derek LeRoith|Albumin|||||||||||These mice result from a triple cross between Mac blue, Alb-Cre and mT/mG mousse lines in which hepatocytes (but also biliary duct) is membrane GFP+, monocytes and monocyte-derived cells (CD11b+) are CFP+ and all cells but hepatocytes are membrane Tomato+. Detailed descriptions of the 3 lines are below:MacBlue transgenic mice express enhanced cyan fluorescent protein (ECFP) from a truncated colony stimulating factor 1 receptor (Csf1r) promoter using the binary yeast Gal4-UAS system. The Gal4-UAS system utilizes a transgene that consists of both Gal4-expressing and Gal4-reporting modules to drive the expression of the ECFP reporter in Csf1r-expressing cells. In this strain, the Csf1r promoter lacks the 150 bp trophoblast and osteoclast-specific transcription start sites, directing reporter expression specifically in macrophages. Hemizygotes are viable and fertile. All ECFP+ cells in peripheral blood of MacBlue mice are CD11b-positive, and are negative for lymphocyte markers. 10% of granulocytes in peripheral blood and bone marrow express ECFP, as do Ly6C+ and Ly6C- monocytes. All ECFPhi leukocytes express the monocyte/macrophage marker F4/80. 7% of bone marrow cells are ECFP+. ECFP was also detected in adult dendritic cells and blood monocytes in the gut, microglia and Langerhans cells, Peyer’s patches and isolated lymphoid follicles.The Alb1-cre transgene was designed with a Cre recombinase gene under control of albumin (Alb) promoter/enhancer elements. Hemizygous Alb1-cre mice are viable, fertile, and normal in size, with cre expression directed specifically to the liver. When these transgenic mice are bred with mice containing a loxP-flanked sequence, Cre-mediated recombination is expected to result in deletion of the floxed sequences in the Cre recombinase-expressing hepatic cells of the offspring. For example, when these mice are bred to Igf1tm1Dlr-containing mice, the removal of IGF1 expression in the liver causes a 75% reduction in serum IGF-1levels. These mice may be useful for studying the liver specific deletion of target genes.mT/mG mice (Stock No. 007676) have the same allele as Stock No. 007576 but has a C57BL/6J congenic background. ROSAmT/mG is a cell membrane-targeted, two-color fluorescent Cre-reporter allele. Prior to Cre recombination, cell membrane-localized tdTomato (mT) fluorescence expression is widespread in cells/tissues. Cre recombinase expressing cells (and future cell lineages derived from these cells) have cell membrane-localized EGFP (mG) fluorescence expression replacing the red fluorescence. ROSAmT/mG mice (Stock No. 007576 and Stock No. 007676) function similarly to ROSAnT-nG mice (Stock No. 023035 and Stock No. 023537), with ROSAmT/mG directed to cell membrane and ROSAnT-nG directed to nuclei.|Similar to homozygous|C57BL6/J|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|24-Jun-2020|Cryopreserved sperm|||Unknown|||Yes| 7678.0|ENU18.FLT3-ITD.0.24.B6|B6.129-Flt3 Ndufa10/AnuApb||Recessive|NADH dehydrogenase (ubiquinone) 1 alpha subcomplex 10|Ndufa10||2900053E13Rik|MGI:1914523||||1|||||||||||||||||||||||||||||FLT3 hom's have myeloid proliferation Ndufa10 is unknown, contact Tom Gonda. |no phenotype in hetrozygous mice||Yes|Yes|Unknown|Yes|Yes|Unknown|Yes|Poor|BC7||het by het is best|No|12-May-2014|Cryopreserved sperm|64.0|0.0|Unknown||AML|Possibly| 7678.0|ENU18.FLT3-ITD.0.24.B6|B6.129-Flt3 Ndufa10/AnuApb||Recessive|FMS-like tyrosine kinase 3|Flt3||CD135, Flk2, Flk-2, Flt-3, wmfl|MGI:95559|FMS-like tyrosine kinase 3; targeted mutation 1, D Gilliland|Flt3|MGI:3763385|5|||||||||||||||||||||||||||||FLT3 hom's have myeloid proliferation Ndufa10 is unknown, contact Tom Gonda. |no phenotype in hetrozygous mice||Yes|Yes|Unknown|Yes|Yes|Unknown|Yes|Poor|BC7||het by het is best|No|12-May-2014|Cryopreserved sperm|||Unknown||AML|Possibly| 4581.0|Hamlet:kk|B10.BR-H2 Tg(IghelMD4)4Ccg/AnuApb||Dominant||||||||||||||||||||||||||transgene insertion 4, Christopher C Goodnow||low copy number|histocompatibility-2, MHC|H2||H-2, MHC-II|MGI:95894|histocompatibility-2, MHC; k variant|H2|MGI:3579322|17|bone marrow contains fewer combined numbers of combined pro-pre B cells than on a B6 background. transgenic mice, more than 90% of B-cells in the spleen are derived from the transgene (a allotype) and are predominantly IgM and IgD. There is a moderate reduction in B cell frequency and number in spleen and lymph node. B cells did not express Ly-1 or Mac-1. The Ig phenotype of splenic B cells in adult mice (IgMhiIgDlo-hi) resembled that of splenic B cells in non-transgenic 1 - 2-week-old mice.||B10.BR-H2|Yes|No|Yes|Yes|Yes|Yes|No|Unknown||||No|08-Mar-2009|Cryopreserved sperm|150.0|0.0|No||immunoglobulin, T cell, B cell, Hen Egg Lysozyme (HEL), tolerance, autoimmunity|Yes| 4745.0|Lyn:Hamlet|B6.129-Lyn Tg(IghelMD4)4Ccg/AnuApb||Recessive|Yamaguchi sarcoma viral (v-yes-1) oncogene homolog|Lyn|Unknown|Hck-2|MGI:96892|targeted mutation 1, Ashley R Dunn|Lyn|MGI:2157129|4||||||||||||||||Yes|transgene insertion 4, Christopher C Goodnow||||||||||||||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||15||No|27-Apr-2009|Cryopreserved sperm|150.0|0.0|No||Hen Egg Lysozyme, signal transduction, T cell, B cell, immunoglobulin|Yes| 8467.0|Slp2 KO:Hamlet|B6.129P2-Sytl2 Tg(IghelMD4)4Ccg/AnuApb||Recessive|synaptotagmin-like 2|Sytl2|Nil|Slp2, Slp2-a, Slp2-b, Slp2-c, Slp2-d|MGI:1933366|synaptotagmin-like 2; targeted mutation 1, Mitsunori Fukuda|Sytl2|MGI:3693881|7|||||||||||||||||transgene insertion 4, Christopher C Goodnow||low copy number||||||||||Abnormal gastric surface mucous cell morphology:• the number of mucus granules is decreased, 2.8-fold fewer granules are docked with the apical membrane, mucus granule size is increased, and irregular apical membranes are frequently observed• however, no clear abnormalities are seen in the thickness of the epithelia or the numbers of parietal, neck, or chief cellsDecreased digestive secretion:• reduced basal mucin secretion by gastric epithelial cells; however when stimulated with A23187 mucus secretion is similar to wild-type cells Transgenic mice, more than 90% of B-cells in the spleen are derived from the transgene (a allotype) and are predominantly IgM and IgD. There is a moderate reduction in B cell frequency and number in spleen and lymph node. B cells did not express Ly-1 or Mac-1. The Ig phenotype of splenic B cells in adult mice (IgMhiIgDlo-hi) resembled that of splenic B cells in non-transgenic 1 - 2-week-old mice.||C57BL/6NCrlAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|09-Apr-2018|Cryopreserved sperm|55.0|0.0|Unknown||Rab27, mucus granules, HEL|Yes| 6614.0|CD45KO:Hamlet|C57BL/6JAnu-Ptprc Tg(IghelMD4)4Ccg/AnuApb|C57BL/6JAnu-Ptprc Tg(IghelMD4)4Ccg/AnuApb|Recessive|protein tyrosine phosphatase, receptor type, C|Ptprc|Reduced|B220, CD45, Cd45, Ly-5, Lyt-4, T200|MGI:97810|targeted mutation 1, Tak W Mak|Ptprc|MGI:2181288|1|||||||||||||||||transgene insertion 4, Christopher C Goodnow||low copy number|||||||||| Transgenic mice, more than 90% of B-cells in the spleen are derived from the transgene (a allotype) and are predominantly IgM and IgD. There is a moderate reduction in B cell frequency and number in spleen and lymph node. B cells did not express Ly-1 or Mac-1. The Ig phenotype of splenic B cells in adult mice (IgMhiIgDlo-hi) resembled that of splenic B cells in non-transgenic 1 - 2-week-old mice.||C57BL/6JAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|11-Oct-2011|Cryopreserved sperm|54.0|0.0|No||immunoglobulin, T cell, B cell, Hen Egg Lysozyme (HEL), tolerance, autoimmunity|Yes| 149.0|Syk -/- :Hamlet|B6.129-Sykb Tg(IghelMD4)4Ccg/AnuApb|B6.129-Sykb Tg(IghelMD4)4Ccg/AnuApb|Recessive|spleen tyrosine kinase|Syk|Nil||MGI:99515|targeted mutation 1, Tony Pawson|Syk|MGI:1857421|13||||||||||||||||No|transgene insertion 4, Christopher C Goodnow |Ig|||||||||||Homozygous syk mutants suffered severe haemorrhaging as embryos and died perinatally, indicating that Syk has a critical role in maintaining vascular integrity or in wound healing during embryogenesis. Analysis of syk-/- lymphoid cells showed that the syk mutation impaired the differentiation of B-lineage cells, apparently by disrupting signalling from the pre-BCR complex and thereby preventing the clonal expansion, and further maturation, of pre-B cells. ||C57BL/6|No|No|Yes|No|No|Yes|No|Good||13||No|06-Feb-2006|Cryopreserved sperm|25.0|0.0|Unknown||B cell, kinase, vascular, hen egg lysozyme, lymphocyte|Yes| 138.0|Mev:Hamlet|C57BL/6JSfdAnu-Ptpn6 Tg(IghelMD4)4Ccg/AnuApb|C57BL/6JSfdAnu-Ptpn6 Tg(IghelMD4)4Ccg/AnuApb|Recessive|protein tyrosine phosphatase, non-receptor type 6|Ptpn6|Nil|hcp, Hcph, Ptp1C, SHP-1, Spin|MGI:96055|viable motheaten|Ptpn6|MGI:1856074|6||||||||||||||||Yes|transgene insertion 4, Christopher C Goodnow ||Low||||||||||||C57BL/6JSfdAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||5||No|06-Feb-2006|Cryopreserved sperm|100.0|0.0|No||motheaten, phosphatase, SHP, B cell, lymphocyte, tyrosine kinase, signal transduction|Yes| 145.0|RAMA:Hamlet|C57BL/6JSfdAnu-Tg(H2-sHEL)Ccg Tg(IghelMD4)4Ccg/AnuApb|C57BL/6JSfdAnu-Tg(H2-sHEL)Ccg Tg(IghelMD4)4Ccg/AnuApb|Recessive||||||||||||||||||||||||||soluble Hen Egg Lysozyme dimeric molecule|H-2k|Low||||||||||||C57BL/6JAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||13||No|06-Feb-2006|Cryopreserved sperm|99.0|0.0|No||hen egg lysozyme HEL, soluble, dimeric, B cell, lymphocyte|Yes| 145.0|RAMA:Hamlet|C57BL/6JSfdAnu-Tg(H2-sHEL)Ccg Tg(IghelMD4)4Ccg/AnuApb|C57BL/6JSfdAnu-Tg(H2-sHEL)Ccg Tg(IghelMD4)4Ccg/AnuApb|Recessive||||||||||||||||||||||||||transgene insertion 4, Christopher C Goodnow||||||||||||||C57BL/6JAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||13||No|06-Feb-2006|Cryopreserved sperm|||No||hen egg lysozyme HEL, soluble, dimeric, B cell, lymphocyte|Yes| 132.0|Hamlet ; MD4|C57BL/6JSfdAnu-Tg(IghelMD4)4Ccg/AnuApb|C57BL/6JSfdAnu-Tg(IghelMD4)4Ccg/AnuApb|Dominant||||||||||||||||||||||||||transgene insertion 4, Christopher C Goodnow||low copy number||||||||||Bone marrow contains fewer combined numbers of combined pro-pre B cells than on a B6 background. Transgenic mice, more than 90% of B-cells in the spleen are derived from the transgene (a allotype) and are predominantly IgM and IgD. There is a moderate reduction in B cell frequency and number in spleen and lymph node. B cells did not express Ly-1 or Mac-1. The Ig phenotype of splenic B cells in adult mice (IgMhiIgDlo-hi) resembled that of splenic B cells in non-transgenic 1 - 2-week-old mice.||C57BL/6JSfdAnu|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||17||No|06-Feb-2006|Cryopreserved sperm|133.0|0.0|No||immunoglobulin, T cell, B cell, Hen Egg Lysozyme (HEL), tolerance, autoimmunity|Yes| 7911.0|B6.p53|B6.129-Trp53/AnuApb||Dominant|transformation related protein 53|Trp53|Nil|p44, p53|MGI:98834|transformation related protein 53; targeted mutation 1, Tyler Jacks|Trp53|MGI:1857263|11|||||||||||||||||||||||||||||Premature death:* 90% had succumbed to tumors and died by 7 months of age.*average life span 160 days.Increased tumor incidence.Adenoma.Lymphoma.Thymic lymphoma: 75% of observed tumors were thymic lymphomasCarcinoma.Sarcoma.Abnormal apoptosis.Chromosome breakage: aneuploidyIncreased cellular sensitivity to ionizing radiation:* at P10, pattern and extent of oocyte loss in ovaries of mutants after exposure to 0.45 Gy radiation on P5 is similar to wild-type and much more sever than Trp63 mutants|Increased tumor incidence: age of onset 9 monthsLymphoma.Sarcoma|C57BL/6|Yes|Unknown|Yes|Yes|Unknown|Yes|No|Unknown||||No|18-Jun-2015|Cryopreserved sperm|120.0|0.0|Unknown|||Yes| 6488.0|p53 delta|B6.129S2-Trp53/WehiAusbApb||Semi-dominant|transformation related protein 53|Trp53|Nil|p44, p53|MGI:98834|transformation related protein 53; targeted mutation 1, Tyler Jacks|Trp53|MGI:1857263|11|||||||||||||||||||||||||||||Abnormal retinal vasculature morphology:*Background Sensitivity: abnormal blood vessels are found to extend from the peripapillary inner retina through the posterior vitreous and into the retrolental membranes.*Abnormally dilated peripheral retinal blood vessels.Abnormal posterior eye segment morphology:*Background Sensitivity: on the C57BL/6J background aberrant ocular phenotypes are observed as early as 14 days of age. Abnormal optic nerve morphology: *Background Sensitivity: the pial septae in many areas are disorganized on the C57BL/6J background but not the 129 or F1 backgrounds. Optic nerve degeneration: *Background Sensitivity: degeneration is found to varying degrees on the C57BL/6J background, but not the 129 background. Optic nerve hypoplasia: *Background Sensitivity: bilateral or unilateral optic nerve hypoplasia is found on the C57BL/6J background, but not on the 129 or F1 background. Abnormal ocular fundus morphology: *Background Sensitivity: pigmented or nonpigmented fibrous retrolental tissue is commonly found in homozygotes on the C57BL/6J background. Abnormal retina morphology: *Background Sensitivity: retinal folds are found in some homozygotes on the C57BL/6J background. Abnormal retinal vasculature morphology: *Background Sensitivity: abnormal blood vessels are found to extend from the peripapillary inner retina through the posterior vitreous and into the retrolental membranes. *Abnormally dilated peripheral retinal blood vessels. Opacity of vitreous body: *Background Sensitivity: fine snowflake-like vitreal opacities can be found on the C57BL/6J background by 21 days of age and may result from the accumulation of fibrous and vascular debris in the vitreous.Abnormal optic nerve morphology:*Background Sensitivity: the pial septae in many areas are disorganized on the C57BL/6J background but not the 129 or F1 backgrounds. Optic nerve degeneration: *Background Sensitivity: degeneration is found to varying degrees on the C57BL/6J background, but not the 129 background. Optic nerve hypoplasia: *Background Sensitivity: bilateral or unilateral optic nerve hypoplasia is found on the C57BL/6J background, but not on the 129 or F1 background.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|13-Sep-2011|Cryopreserved sperm|50.0|0.0|Unknown||p53, DNA damage, Sulindac|Yes| 10348.0|Ubc-CreER R26-Adar1-Za |C57BL/6J-Gt(ROSA)26Sor Ndor1/Apb||Recessive|gene trap ROSA 26, Philippe Soriano|Gt(ROSA)26Sor||ADAR1, Adar1p110, Adar1p150, mZaADAR|MGI:104735|Gt(ROSA)26Sor; Endonuclease-mediated mutation 1.1, Melbourne Advanced Gene Editing Centre|Gt(ROSA)26Sor||6|ENSMUSG00000086429 ||||||||||||||||NADPH dependent diflavin oxidoreductase 1; transgene insertion 1, Eric J Brown|Ubiquitin C|||||||||||no phenotype when homozygous. Requires tamoxifen treatment to activate expression of ADAR1 Za mutant from the Rosa26 locus|no phenotype when homozygous. Requires tamoxifen treatment to activate expression of ADAR1 Za mutant from the Rosa26 locus|C57Bl/6N|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|07-Jul-2023|Cryopreserved sperm|40.0|0.0|Unknown|||No| 1536.0|p53 KO|C.129-Trp53/AnuApb||Dominant|transformation related protein 53|Trp53|Nil|p53|MGI:98834|transformation related protein 53; targeted mutation 1, Tyler Jacks|Trp53|MGI:1857263|11||||||||||||||||No|||||||||||||Premature death:* 90% had succumbed to tumors and died by 7 months of age.*average life span 160 days.Increased tumor incidence.Adenoma.Lymphoma.Thymic lymphoma: 75% of observed tumors were thymic lymphomasCarcinoma.Sarcoma.Abnormal apoptosis.Chromosome breakage: aneuploidyIncreased cellular sensitivity to ionizing radiation:* at P10, pattern and extent of oocyte loss in ovaries of mutants after exposure to 0.45 Gy radiation on P5 is similar to wild-type and much more sever than Trp63 mutants|Increased tumor incidence: age of onset 9 monthsLymphoma.Sarcoma|BALB/c|Yes|No|Yes|Yes|No|Yes|No|Poor|14||Het x Het|No|05-Jul-2007|Cryopreserved sperm|40.0|0.0|Yes||tumourigenesis, cell cycle, DNA damage|Yes| 10383.0|Ubc-CreER R26-Adar1p110|C57BL/6J-Gt(ROSA)26Sor Ndor1/Apb||Dominant|gene trap ROSA 26, Philippe Soriano|Gt(ROSA)26Sor||Ubc-CreER R26-Adar1p110|MGI:104735|Gt(ROSA)26Sor; Endonuclease-mediated mutation 1.1, Melbourne Advanced Gene Editing Centre|Gt(ROSA)26Sor||Unknown|ENSMUSG00000086429 ||||||||||||||||NADPH dependent diflavin oxidoreductase 1; transgene insertion 1, Eric J Brown|human ubiquitin C (UBC) promoter|||||||||||No phenotype; requires tamoxifen treatment to induce overexpression of mouse ADAR1p110 from Rosa26 locus.|No phenotype; requires tamoxifen treatment to induce overexpression of mouse ADAR1p110 from Rosa26 locus.|C57Bl/6N|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|29-Nov-2023|Cryopreserved sperm|50.0|0.0|Unknown|||No| 278.0|R-double|129-Ifnar Ifngr/Apb||Recessive|interferon (alpha and beta) receptor 1|Ifnar1|Unknown|CD118, Ifar, Ifrc, INF-a receptor, Infar|MGI:107658|targeted mutation 1, Michel Aguet|Ifnar1|MGI:1930950|16||||||||||||||||Yes|||||||||||||increased susceptibility to viral infection mice are 100,000-fold more susceptible to MCMV viral infection than controlsacutely sensitive to Sindbis viral infection; as little as one pfu will induce mortality as opposed to wild type, which can withstand doses of 100,000 pfu||129|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|02-May-2006|Cryopreserved sperm|130.0|0.0|Unknown||receptor, infection|Yes| 278.0|R-double|129-Ifnar Ifngr/Apb||Recessive|interferon gamma receptor 1|Ifngr1|Unknown|CD119, Ifgr, IFN-gamma R, Ifngr, INF-g receptor, Nktar|MGI:107655|targeted mutation 1, Michel Aguet|Ifngr1|MGI:1857286|10|||||||||||||||||||||||||||||increased susceptibility to viral infection mice are 100,000-fold more susceptible to MCMV viral infection than controlsacutely sensitive to Sindbis viral infection; as little as one pfu will induce mortality as opposed to wild type, which can withstand doses of 100,000 pfu||129|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|02-May-2006|Cryopreserved sperm|||Unknown||receptor, infection|Yes| 6525.0|CD122?|B6.129P2-Il2rb/JScrAusb||Recessive|interleukin 2 receptor, beta chain|Il2rb|Nil|CD122, IL-15 receptor beta chain, IL-15Rbeta, IL-2/15Rbeta, Il-2Rbeta, IL15Rbeta|MGI:96550|interleukin 2 receptor, beta chain; targeted mutation 1, Tak Mak|Il2rb|MGI:1857193|15|||||||||||||||||||||||||||||Increased susceptibility to autoimmune hemolytic anemia:*By 26 days of age.*Can be prevented with adoptive transfer at birth of 1 x 10<5> CD25-positive CD4 T cells from wild-type mice.Abnormal lymphocyte morphology: Decreased regulatory T cell number: *There is a 2 to 5 fold reduction in the percentage of CD25-postive CD4 T cells in both the thymus and lymph nodes. *Transgeneic expression of Il2rb in the thymus rescues number of regulatory T cells. Abnormal T cell activation: *Percentage of CD4 and CD8 T cells that express high levels of activation markers is increased. *T cells are hyporesponsive to inflammatory cytokines as measured by in vitro proliferation assays. *Expression of activation markers is normalized upon transfer of 1 x 105 CD25-positive CD4 T cells from wild-type mice. Decreased T cell proliferation: *In mice by 26 days of age. *Can be prevented with adoptive transfer at birth of 1 x 10<5> CD25-positive CD4 T cells from wild-type mice.Enlarged spleen:*In mice by 26 days of age.*Can be prevented with adoptive transfer at birth of 1 x 105 CD25-positive CD4 T cells from wild-type mice.Abnormal spleen periarteriolar lymphoid sheath morphology:*Increased in size at 26 days of age.*Can be prevented with adoptive transfer at birth of 1 x 10<5> CD25-positive CD4 T cells from wild-type mice.Enlarged lymph nodes:*In mice by 26 days of age.*Can be prevented with adoptive transfer at birth of 1 x 10<5> CD25-positive CD4 T cells from wild-type mice.Increased anti-double stranded DNA antibody level:*In mice by 26 days of age.*Can be prevented with adoptive transfer at birth of 1 x 10<5> CD25-positive CD4 T cells from wild-type mice.Abnormal response to transplant:*Adoptively transfered regulatory T cell expand at least 15 to 20 times until they make up 3-5% of the total cells in the lymph nodes and spleen.*Regulatory T cells were unable to engraft in wild-type mice.||C57BL6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown||IL-2R beta, Hemolytic anemia, Granulocytopoiesis, Autoimmunity|Yes| 8294.0|Sparc KO|B6.129S-Sparc||Recessive|secreted acidic cysteine rich glycoprotein|Sparc|Nil|BM-40, osteonectin|MGI:98373|secreted acidic cysteine rich glycoprotein; targeted mutation 1, Chin Chen Howe|Sparc|MGI:1888383|11|||||||||||||||||||||||||||||Early onset of cataract formation. Otherwise normal|Normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|29-Aug-2017|Cryopreserved sperm|50.0|0.0|Unknown||cortex, eye, cataracts|Yes| 1510.0|Dhoni, GOTIT|C57BL/6-Infng Tg(TcraTcrb)1100Mjb/AnuApb||Recessive|interferon gamma|Ifng|Nil|Ifg, IFN-gamma|MGI:107656|targeted mutation 1, Timothy Stewart|Ifng|MGI:1857184|10||||||||||||||||Yes|transgene insertion 1100, Michael J Bevan|||||||||||||||Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|04-Jul-2007|Cryopreserved sperm|65.0|0.0|Unknown||T cell, receptor, ovalbumin, CD8, interferon|Yes| 6399.0|SAP KO|B6.129-Sh2d1a/Ausb||X-linked|SH2 domain protein 1A|Sh2d1a|Nil|Duncan disease homolog, SAP|MGI:1328352|SH2 domain protein 1A; targeted mutation 1, Pamela L Schwartzberg|Sh2d1a|MGI:2388241|X|||||||||||||||||||||||||||||Decreased IgE level:*After immunization with ovalbumin, severe deficit in IgE is observed with little or no Ig E detected.Abnormal CD4-positive T cell physiology:*Pronounced defect in production of IL-4 upon stimulation with anti-CD3 or anti-CD3 plus anti-CD28.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|13-Sep-2011||0.0|0.0|Unknown||XLP, SLAM-associated protein (SAP), Lymphocyte choriomeningitis virus (LCMV), Toxoplasma gondii|Yes| 8219.0|Sap KO:Ly5a|B6.Cg-Ptprc Sh2d1a/AnuApb||X-linked|SH2 domain protein 1A|Sh2d1a|Nil|Duncan disease homolog, SAP|MGI:1328352|targeted mutation 1, Pamela L Schwartzberg|Sh2d1a|MGI:2388241|X||||||||||||||||No||||protein tyrosine phosphatase, receptor type, C|Ptprc||B220, CD45, Ly-5, Lyt-4, T200|MGI:97810|protein tyrosine phosphatase, receptor type, C; a variant|ptprc|MGI:4819849|1|Decreased IgE level: * after immunization with ovalbumin, severe deficit in IgE is observed with little or no Ig E detected.Abnormal lymphocyte cell number:* although lymphocyte numbers were generally normal, occasional animals had increased T cell and NK cell numbers together with decreased B cell numbers in the spleen.Increased T cell proliferation:* tendency for T-cell proliferation to be increased even in the absence of infection.Abnormal T-helper 1 cell morphology:* biased toward the production of the Th1 cytokines Il-2 and IFN-gamma.Abnormal T-helper 2 cell morphology:* biased toward decreased production of the Th2 cytokine Il-4Decreased IgE level:* although levels of IgM, IgG, and IgA were normal, IgE levels were reduced.Increased susceptibility to infection.Increased susceptibility to parasitic infection:* elevated T-cell response to Toxoplasma gondii infectionlower titers of Ig isotypes directed against Toxoplasma antigensIncreased susceptibility to viral infection:* increased T-cell response to infection with lymphocyte choriomeningitis virus (LCMV).* Elevated activity of CD8+ cytotoxic T lymphocytes in spleenCD4+ cells also increased 2-3X.* decrease in antibody secreting cells in spleen and bone marrow.* more virulent strains led to increased morbidity.||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|19-Mar-2017|Cryopreserved sperm|60.0|0.0|Yes||T cell, lymphoproliferative disease, X-linked, lymphocyte, B cell|Yes| 7738.0|IFNAR-/- IFNGR-/- ADAR1-/-|B6-Ifnar1 Ifngr1 Adar||Dominant|interferon (alpha and beta) receptor 1|Ifnar1||IFN-alpha/betaR, Ifrc|MGI:107658|interferon (alpha and beta) receptor 1; targeted mutation 1, Michel Aguet|Ifnar1|MGI:1930950|16|ENSMUSG00000022967 ||||||||||||||||||||||||||||Homozygous triple nulls are not viable (embryonic lethal - time point not determined yet).IFNAR-/- IFNGR-/- ADAR1+/- are viable and fertile and are similar to the IFNAR-/-IFNGR-/- line.|viable, fertile and apparently normal|C57BL/6|No|No|Yes|No|No|Yes|No|Good|all on C57 when intercrossed|4|IFNAR-/-IFNGR-/- ADAR1+/- x IFNAR-/-IFNGR-/- ADAR1+/-|No|08-Sep-2014|Cryopreserved sperm|40.0|0.0|No||ADAR1, IFNAR, IFNGR, IFNAR IFNGR ADAR1|Possibly| 7738.0|IFNAR-/- IFNGR-/- ADAR1-/-|B6-Ifnar1 Ifngr1 Adar||Dominant|interferon gamma receptor 1|Ifngr1||IFN-gammaR, Ifngr, Nktar|MGI:107655|interferon gamma receptor 1; targeted mutation 1, Michel Aguet|Ifngr1|MGI:1857286|10|ENSMUSG00000020009||||||||||||||||||||||||||||Homozygous triple nulls are not viable (embryonic lethal - time point not determined yet).IFNAR-/- IFNGR-/- ADAR1+/- are viable and fertile and are similar to the IFNAR-/-IFNGR-/- line.|viable, fertile and apparently normal|C57BL/6|No|No|Yes|No|No|Yes|No|Good|all on C57 when intercrossed|4|IFNAR-/-IFNGR-/- ADAR1+/- x IFNAR-/-IFNGR-/- ADAR1+/-|No|08-Sep-2014|Cryopreserved sperm|||No||ADAR1, IFNAR, IFNGR, IFNAR IFNGR ADAR1|Possibly| 7738.0|IFNAR-/- IFNGR-/- ADAR1-/-|B6-Ifnar1 Ifngr1 Adar||Dominant|adenosine deaminase, RNA-specific|Adar||Adar1p150, mZaADAR|MGI:1889575|adenosine deaminase, RNA-specific; targeted mutation 1, Peter H Seeburg|Adar|MGI:3029789|3|ENSMUSG00000027951 ||||||||||||||||||||||||||||Homozygous triple nulls are not viable (embryonic lethal - time point not determined yet).IFNAR-/- IFNGR-/- ADAR1+/- are viable and fertile and are similar to the IFNAR-/-IFNGR-/- line.|viable, fertile and apparently normal|C57BL/6|No|No|Yes|No|No|Yes|No|Good|all on C57 when intercrossed|4|IFNAR-/-IFNGR-/- ADAR1+/- x IFNAR-/-IFNGR-/- ADAR1+/-|No|08-Sep-2014|Cryopreserved sperm|||No||ADAR1, IFNAR, IFNGR, IFNAR IFNGR ADAR1|Possibly| 8260.0|Ck6/ECFP|B6.129-Tg(CAG-ECFP)CK6Nagy||Dominant||||||||||||||||||||||||||transgene insertion CK6, Andras Nagy|cytomegalovirus (CMV) immediate early enhancer coupled to the chicken beta actin promoter|||||||||||Expression of enhanced cyan fluorescent protein||C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|24-May-2017|Cryopreserved sperm|24.0|0.0|Unknown||ECFP|Yes| 8586.0|Mx1Cre.Sphk1floxed.Spk2KO|B6.129-Sphk1 Sphk2 Tg(Mx1-cre)1Cgn/UsaApb||Recessive|sphingosine kinase 1|Sphk1|Unknown|1110006G24Rik, SK1|MGI:1316649|sphingosine kinase 1; targeted mutation 2, Shaun R Coughlin|Sphk1|MGI:3707997|11|||||||||||||||||transgene insertion 1, University of Cologne|Mx dynamin-like GTPase 1 (Mx1)|||||||||||Whilst the Cre is inactivated these mice are normal|Whilst the Cre is inactivated these mice are normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|12-Oct-2018|Cryopreserved sperm|40.0|0.0|Unknown||Endothelial, Lymphocytes|Yes| 8586.0|Mx1Cre.Sphk1floxed.Spk2KO|B6.129-Sphk1 Sphk2 Tg(Mx1-cre)1Cgn/UsaApb||Recessive|sphingosine kinase 2|Sphk2|Nil||MGI:1861380|sphingosine kinase 2; targeted mutation 1, Richard L Proia|Sphk2|MGI:3611080|7|||||||||||||||||||||||||||||Whilst the Cre is inactivated these mice are normal|Whilst the Cre is inactivated these mice are normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|12-Oct-2018|Cryopreserved sperm|||Unknown||Endothelial, Lymphocytes|Yes| 4778.0|Rathbone|C.B6(129)-Ifng/AnuApb||Recessive|interferon gamma|Ifng|Nil|Ifg, IFN-gamma|MGI:107656|targeted mutation 1, Timothy Stewart|Ifng|MGI:1857184|10||||||||||||||||Yes|||||||||||||Mutants show immune system abnormalities including decreased inflammatory response in one line, and uncontrolled splenocyte proliferation and susceptibility to intracellular pathogens in another. Mice homozygous for the Ifngtm1Ts targeted mutation are viable and fertile. Homozygotes appear normal in a "clean" environment but display reduced macrophage function in response to pathogens. Specifically, macrophages show impaired production of antimicrobial products and reduced expression of MHC II antigens. There is also uncontrollable proliferation of splenocytes from homozygotes in response to mitogens and alloantigens and a reduced resting natural killer cell activity.||BALB/c x C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown||||No|06-Sep-2009|Cryopreserved sperm|120.0|0.0|Unknown||macrophage, MHC, Mycobacterium bovis, T cell, cytotoxic|Yes| 5498.0|Twist-delBp|B6;129-Twist1/WchriApb||Semi-dominant|twist gene homolog 1 (Drosophila)|Twist1|Nil|charlie chaplin, M-Twist, pdt, Pluridigite, Skam10Jus, Ska10|MGI:98872|targeted mutation 1, Richard R Behringer|Twist1|MGI:1857265|12||||||||||||||||Yes|||||||||||||Homozygous mutant embyros have neural tube defects and die around E11.|Heterozygous mutants are viable and exhibit features of human Saethre-Chotzen syndrome, including hindlimb polydactyly, craniofacial defects, long bone abnormalities, an abnormal gait and a small size.|C57BL/6|No|No|Yes|No|No|Yes|No|Unknown|2|||No|04-May-2011|Cryopreserved sperm|10.0|0.0|Yes||polydactyly, neural tube, mesenchyme, cranial, morphogenesis|Yes| 7585.0|Epo-R-Cre R26eYFPki/ki pRbfl/fl|B6.129-Epor Gt(ROSA)26Sor Rb1/StvApb||Dominant|retinoblastoma 1|Rb1|Unknown|pRb, Rb, Rb-1|MGI:97874|targeted mutation 3, Tyler Jacks|Rb1|MGI:2450162|14||||||||||||||||Yes|||||||||||||Compound mutant: Mild anaemia. Single Epo-R-Cre – lethal as homozygous, heterozygous maintained only. Single pRbfl/fl – no phenotype until Cre exposedeYFP reporter for tracking of deleted cells in vivo|heterozygous mice are normal, viable and non-anaemic (only pRbfl/fl are anaemic)|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Excellent|5||Epor -ve Gt(ROSA)26Sortm1(EYFP)Cos Rb1 female x Epor +ve Gt(ROSA)26Sortm1(EYFP)Cos Rb1 het male|No|14-Feb-2014|Cryopreserved sperm|40.0|0.0|Yes|refractory anaemia of MDS|anaemia, MDS, mitochondria, erythroid differentiation|Yes| 7585.0|Epo-R-Cre R26eYFPki/ki pRbfl/fl|B6.129-Epor Gt(ROSA)26Sor Rb1/StvApb||Dominant|erythropoietin receptor|Epor|Unknown||MGI:95408|erythropoietin receptor; targeted mutation 1, Ursula Klingmuller|Epor|MGI:3052727|9|||||||||||||||||||||||||||||Compound mutant: Mild anaemia. Single Epo-R-Cre – lethal as homozygous, heterozygous maintained only. Single pRbfl/fl – no phenotype until Cre exposedeYFP reporter for tracking of deleted cells in vivo|heterozygous mice are normal, viable and non-anaemic (only pRbfl/fl are anaemic)|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Excellent|5||Epor -ve Gt(ROSA)26Sortm1(EYFP)Cos Rb1 female x Epor +ve Gt(ROSA)26Sortm1(EYFP)Cos Rb1 het male|No|14-Feb-2014|Cryopreserved sperm|||Yes|refractory anaemia of MDS|anaemia, MDS, mitochondria, erythroid differentiation|Yes| 7585.0|Epo-R-Cre R26eYFPki/ki pRbfl/fl|B6.129-Epor Gt(ROSA)26Sor Rb1/StvApb||Dominant|gene trap ROSA 26, Philippe Soriano|Gt(ROSA)26Sor|Increased|beta geo, Gtrgeo26, Gtrosa26, R26, ROSA26|MGI:104735|gene trap ROSA 26, Philippe Soriano; targeted mutation 1, Frank Costantini|Gt(ROSA)26Sor|MGI:2449038|6|||||||||||||||||||||||||||||Compound mutant: Mild anaemia. Single Epo-R-Cre – lethal as homozygous, heterozygous maintained only. Single pRbfl/fl – no phenotype until Cre exposedeYFP reporter for tracking of deleted cells in vivo|heterozygous mice are normal, viable and non-anaemic (only pRbfl/fl are anaemic)|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Excellent|5||Epor -ve Gt(ROSA)26Sortm1(EYFP)Cos Rb1 female x Epor +ve Gt(ROSA)26Sortm1(EYFP)Cos Rb1 het male|No|14-Feb-2014|Cryopreserved sperm|||Yes|refractory anaemia of MDS|anaemia, MDS, mitochondria, erythroid differentiation|Yes| 10285.0|ASK-1 KO|B6J.B6N-Map3k5/Apb||Recessive|mitogen-activated protein kinase kinase kinase 5|Map3k5||ASK1|MGI:1346876|mitogen-activated protein kinase kinase kinase 5; targeted mutation 1a, Helmholtz Zentrum Muenchen GmbH |Map3k5|MGI:4434801|10||||||||||Unknown to Unknown|||||||||||||||||||Normal|Normal|C57Bl/6J|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|N6+|||No|01-Feb-2023|Cryopreserved sperm|50.0|0.0|Unknown|||Possibly| 10286.0|ASK-1 flox|B6J.B6N-Map3k5/Apb||Recessive|mitogen-activated protein kinase kinase kinase 5|Map3k5||ASK1|MGI:1346876|mitogen-activated protein kinase kinase kinase 5; targeted mutation 1a, Helmholtz Zentrum Muenchen GmbH |Map3k5||10|ENSMUSG00000071369|||||||||Unknown to Unknown|||||||||||||||||||Normal|Normal|C57Bl/6J|Yes|Yes|Yes|Yes|Yes|Yes|No|Good|N6+|||No|01-Feb-2023|Cryopreserved sperm|50.0|0.0|Unknown|||No| 7073.0|B6-ASCIZ-Nkx2.1-eYFP|C57BL/6-Atmin Gt(ROSA)26Sor Tg(Nkx2.1-cre)2Sand/J||Recessive|ATM interactor|Atmin||Asciz, MGC:79206, mKIAA0431|MGI:2682328|targeted mutation 1, Jorg Heierhorst|Atmin||8|||||||||||||||||transgene insertion 2, Stewart Anderson|Nkx2-1||||||||||6|Normal|Normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|03-Sep-2012|Cryopreserved sperm|40.0|0.0|Unknown|||Possibly| 7073.0|B6-ASCIZ-Nkx2.1-eYFP|C57BL/6-Atmin Gt(ROSA)26Sor Tg(Nkx2.1-cre)2Sand/J||Recessive|gene trap ROSA 26, Philippe Soriano|Gt(ROSA)26Sor||beta geo, Gtrgeo26, Gtrosa26, R26, ROSA26|MGI:104735|gene trap ROSA 26, Philippe Soriano; targeted mutation 1, Frank Costantini|Gt(ROSA)26Sor|MGI:2449038|6|||||||||||||||||||||||||||||Normal|Normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|03-Sep-2012|Cryopreserved sperm|||Unknown|||Possibly| 7313.0|Epo-R-CreERT2 R26eYFP pRbfl/fl|C57BL/6-Epor Gt(ROSA)26Sor Rb1/SviApb||Dominant|retinoblastoma 1|Rb1|Nil|pRb, Rb, Rb-1 |MGI:97874|retinoblastoma 1; targeted mutation 3, Tyler Jacks |Rb1|MGI:2450162|14|||||||||||||||||||||||||||||Epo-R-CreER is lethal as a homozygous allele as it discrupts expression of endogenous Epo-R|none - tamoxifen inducible Cre knockin to Epo-R locus. |C57BL/6|No|No|Yes|No|No|Yes|No|Excellent|on pure C57BL/6 - was derived on C57 ES line||Epo-R-CreERT2 ki/+ to Epo-R-CreERT2+/+ (homozygous for all other alleles)|No|10-Apr-2013|Cryopreserved sperm|30.0|0.0|No|||Possibly| 7313.0|Epo-R-CreERT2 R26eYFP pRbfl/fl|C57BL/6-Epor Gt(ROSA)26Sor Rb1/SviApb||Dominant|gene trap ROSA 26, Philippe Soriano|Gt(ROSA)26Sor |Unknown|beta geo, Gtrgeo26, Gtrosa26, R26, ROSA26|MGI:104735|gene trap ROSA 26, Philippe Soriano; targeted mutation 1, Frank Costantini |Gt(ROSA)26Sor|MGI:2449038|6|||||||||||||||||||||||||||||Epo-R-CreER is lethal as a homozygous allele as it discrupts expression of endogenous Epo-R|none - tamoxifen inducible Cre knockin to Epo-R locus. |C57BL/6|No|No|Yes|No|No|Yes|No|Excellent|on pure C57BL/6 - was derived on C57 ES line||Epo-R-CreERT2 ki/+ to Epo-R-CreERT2+/+ (homozygous for all other alleles)|No|10-Apr-2013|Cryopreserved sperm|||No|||Possibly| 7313.0|Epo-R-CreERT2 R26eYFP pRbfl/fl|C57BL/6-Epor Gt(ROSA)26Sor Rb1/SviApb||Dominant|erythropoietin receptor|Epor |Nil||MGI:95408|C57BL/6-Epor|Epo-R-CreERT2||9|||||||||||||||||||||||||||||Epo-R-CreER is lethal as a homozygous allele as it discrupts expression of endogenous Epo-R|none - tamoxifen inducible Cre knockin to Epo-R locus. |C57BL/6|No|No|Yes|No|No|Yes|No|Excellent|on pure C57BL/6 - was derived on C57 ES line||Epo-R-CreERT2 ki/+ to Epo-R-CreERT2+/+ (homozygous for all other alleles)|No|10-Apr-2013|Cryopreserved sperm|||No|||Possibly| 4971.0|Fzd7|C57BL/6-Fzd7||Recessive|frizzled homolog 7 (Drosophila)|Fzd7|Normal|Fz7|MGI:108570||||1||||||||||||||||Yes|||||||||||||Normal|Normal|C57BL/6|Yes|Yes|Yes|Yes|Yes|Yes|No|Unknown|10||Het x C57BL/6|No|21-Jan-2010|Cryopreserved sperm|96.0|0.0|Unknown||Frizzled -7, Wnt pathway, conditional gene deletion, LoxP, Cre recombinase|Possibly| 10279.0|ENU57:G3|ANU:ENU57:G3||Recessive|Unknown||||||||Unknown||||||||||||||||||||||||||||| | |C57Bl/6N|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|08-Jan-2023|Cryopreserved sperm|45.0|0.0|Unknown|||Possibly| 8146.0|LAT3_KO|C57BL/6JMarp-Slc43a1/Marp||Recessive|solute carrier family 43, member 1|Slc43a1||2610016F07Rik, Lat3, PB39, Pov1|MGI:1931352||||Unknown|||||||||||||||||||||||||||||Unknown|Unknown|C57BL/6|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Unknown||||No|29-Nov-2016|Cryopreserved sperm|50.0|0.0|Unknown|||Yes| 10280.0|iDMPcre.Ai9|B6.Cg-Tg(Dmp1-cre/ERT2)D77Pdp Gt(ROSA)26Sor/Apb||Semi-dominant|gene trap ROSA 26, Philippe Soriano|Gt(ROSA)26Sor||R26, ROSA26, Thumpd3as1|MGI:104735||||6|||||||||||||||||transgene insertion D77, Paola Divieti Pajevic|Dmp1-cre/ERT2|||||||||||Normal|Normal|C57Bl/6J|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|16-Jan-2023|Cryopreserved sperm|50.0|0.0|Unknown|||Possibly| 10287.0|Adidas:indel07, S866fs|C57BL/6NCrlAnu-Nfkb2/Anu||Recessive|nuclear factor of kappa light polypeptide gene enhancer in B cells 2, p49/p100|Nfkb2|||MGI:1099800 |Nfkb2: endonuclease-mediated mutation 2, Australian National University|Nfkb2||19|||||||||||||||||||||||||||||Unknown|Unknown|C57Bl/6N|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|08-Feb-2023|Cryopreserved sperm|22.0|0.0|Unknown|||Possibly| 7849.0|Spi6-/-ROSA26eYFP+/+CreERT2+|B6(Cg)-SerpinB9a Gt(ROSA)26Sor Tg(Gzmb-Cre/ERT2)1Dtf/MarpApb||Recessive|serine (or cysteine) peptidase inhibitor, clade B, member 9|Serpinb9||ovalbumin, PI-9, Spi6|MGI:106603|serine (or cysteine) peptidase inhibitor, clade B, member 9; targeted mutation 2, Phillip I Bird|SerpinB9a||13|||||||||||||||||transgene insertion 1, Douglas T Fearon||||||||||||Unknown||C57BL/6|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|26-Feb-2015|Cryopreserved sperm|50.0|0.0|Unknown||Granzyme B|Yes| 7849.0|Spi6-/-ROSA26eYFP+/+CreERT2+|B6(Cg)-SerpinB9a Gt(ROSA)26Sor Tg(Gzmb-Cre/ERT2)1Dtf/MarpApb||Recessive|gene trap ROSA 26, Philippe Soriano|Gt(ROSA)26Sor ||beta geo, Gtrgeo26, Gtrosa26, R26, ROSA26|MGI:104735|gene trap ROSA 26, Philippe Soriano; targeted mutation 1, Frank Costantini|Gt(ROSA)26Sor|MGI:2449038|6|||||||||||||||||||||||||||||Unknown||C57BL/6|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|26-Feb-2015|Cryopreserved sperm|||Unknown||Granzyme B|Yes| 10299.0||C57BL/6J-Mdh1bMGMP/Apb||Semi-dominant|malate dehydrogenase 1B, NAD (soluble)|Mdh1b|||MGI:1923918||||1|||||||||||||||||||||||||||||Subfertile|Normal|C57Bl/6J|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|27-Feb-2023||0.0|0.0|Unknown|||Possibly| 10292.0||BL6.Crisp2MGMP/MkobMarp/J||Semi-dominant|cysteine-rich secretory protein 2|Crisp2|||MGI:98815||||17|||||||||||||||||||||||||||||Subfertile|Normal|C57Bl/6J|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|14-Feb-2023|Cryopreserved sperm|50.0|0.0|Unknown|||Possibly| 10298.0||C57BL/6J-Mroh9MAGEC/Apb||Semi-dominant|maestro heat-like repeat family member 9|Mroh9|||MGI:1925508|Mroh9KO|||1|||||||||||||||||||||||||||||Subfertile|Normal|C57Bl/6J|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|24-Feb-2023|Cryopreserved sperm|50.0|0.0|Unknown|||Possibly| 10296.0||C57Bl/6-TFF3(CreGFP)-Rosa26-Td(tomato)/Apb||Semi-dominant|trefoil factor 3, intestinal|Tff3||ITF, mITF|MGI:104638||||17|ENSMUSG00000024029|||||||||Unknown to Unknown|||||||||||||||||||Normal|Normal|C57Bl/6J|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|22-Feb-2023|Cryopreserved sperm|44.0|0.0|Unknown|||Possibly| 10294.0|Irf4c.127AG (1)|C57BL/6NCrlAnu-Irf4em12Anu/ANU||Recessive|IRF4||||||||Unknown|||||||||||||||||||||||||||||unknown|unknown|C57Bl/6N|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|17-Feb-2023|Cryopreserved sperm|54.0|0.0|Unknown|||Possibly| 10295.0|Ccdc89em1MAGEC|C57BL/6J-Ccdc89MAGEC/Apb||Recessive|coiled-coil domain containing 89|Ccdc89|||MGI:1917304|CCDC89 KO|||7|||||||||||||||||||||||||||||Subfertile|Normal|C57Bl/6J|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|21-Feb-2023|Cryopreserved sperm|50.0|0.0|Unknown|||Possibly| 10297.0||C57BL/6J-Mdh1bMGMP/Apb||Semi-dominant|malate dehydrogenase 1B, NAD (soluble)|Mdh1b|||MGI:1923918|Mdh1b KO|||1|||||||||||||||||||||||||||||Subfertile|Normal|C57Bl/6J|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|24-Feb-2023|Cryopreserved sperm|50.0|0.0|Unknown|||Possibly| 10289.0||C57BL/6N-Dnajb11<(em1)Anu>/Apb||Semi-dominant|DnaJ heat shock protein family (Hsp40) member B11|Dnajb11|||MGI:1915088 ||||16|||||||||||||||||||||||||||||Unknown|Unknown|C57Bl/6N|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|09-Feb-2023|Cryopreserved sperm|22.0|0.0|Unknown|||Possibly| 10288.0|Lyn R464C|C57BL/6NCrlAnu-Lynem1Anu/Anu||Recessive|LYN proto-oncogene, Src family tyrosine kinase|Lyn|||MGI:96892 |Lyn |||4||||||||||Unknown to Unknown|||||||||||||||||||Unknown|Unknown|C57Bl/6N|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|09-Feb-2023|Cryopreserved sperm|54.0|0.0|Unknown|||Possibly| 10301.0||C57BL/6J-Mroh9MAGEC||Semi-dominant|maestro heat-like repeat family member 9|Mroh9||4921528O07Rik, Armc11|MGI:1925508||||1|||||||||||||||||||||||||||||Subfertile|Normal|C57Bl/6J|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|27-Feb-2023||0.0|0.0|Unknown|||Possibly| 10291.0||BL6.Crisp1 MGMP /MkobMarp/J||Semi-dominant|cysteine-rich secretory protein 1|Crisp1|||MGI:102553||||17|||||||||||||||||||||||||||||Subfertile|Normal|C57Bl/6J|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|14-Feb-2023|Cryopreserved sperm|50.0|0.0|Unknown|||Possibly| 7314.0|Epo-R-CreERT2 R26eYFP ADAR1fl/fl|C57BL/6-Epor Gt(ROSA)26Sor Adar/SviApb||Dominant|adenosine deaminase, RNA-specific|Adar |Nil|ADAR1, mZaADAR|MGI:1889575|adenosine deaminase, RNA-specific; targeted mutation 1.1, Peter H Seeburg|Adar|MGI:3828307|3|||||||||||||||||||||||||||||Epo-R-CreER is hmozygous lethal due to loss of endogenous Epo-R expression|normal, viable, fertile|C57BL/6|No|No|Yes|No|No|Yes|No|Excellent|generated on pure C57BL/6 so not backcrossed. Only maintained on C57|||No|10-Apr-2013|Cryopreserved sperm|40.0|0.0|No|||No| 7314.0|Epo-R-CreERT2 R26eYFP ADAR1fl/fl|C57BL/6-Epor Gt(ROSA)26Sor Adar/SviApb||Dominant|gene trap ROSA 26, Philippe Soriano|Gt(ROSA)26Sor |Unknown|beta geo, Gtrgeo26, Gtrosa26, R26, ROSA26|MGI:104735|gene trap ROSA 26, Philippe Soriano; targeted mutation 1, Frank Costantini |Gt(ROSA)26Sor|MGI:2449038|6|||||||||||||||||||||||||||||Epo-R-CreER is hmozygous lethal due to loss of endogenous Epo-R expression|normal, viable, fertile|C57BL/6|No|No|Yes|No|No|Yes|No|Excellent|generated on pure C57BL/6 so not backcrossed. Only maintained on C57|||No|10-Apr-2013|Cryopreserved sperm|||No|||No| 7314.0|Epo-R-CreERT2 R26eYFP ADAR1fl/fl|C57BL/6-Epor Gt(ROSA)26Sor Adar/SviApb||Dominant|erythropoietin receptor|Epor|Nil|EpoR|MGI:95408|C57BL/6-Epor|Epo-R-CreERT2||9|||||||||||||||||||||||||||||Epo-R-CreER is hmozygous lethal due to loss of endogenous Epo-R expression|normal, viable, fertile|C57BL/6|No|No|Yes|No|No|Yes|No|Excellent|generated on pure C57BL/6 so not backcrossed. Only maintained on C57|||No|10-Apr-2013|Cryopreserved sperm|||No|||No| 10302.0|Katnal1 flox|C57BL6/J-Katnal1MGMP/MkobMarp||Semi-dominant|katanin p60 subunit A-like 1|Katnal1 flox|||MGI:2387638||||5|||||||||||||||||||||||||||||Normal|Normal|C57Bl/6J|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|27-Feb-2023|Cryopreserved sperm|50.0|0.0|Unknown|||Possibly| 10300.0|AireK115N (21)|C57BL/6NCrl-Aire/Anu||Recessive|autoimmune regulator|Aire|||MGI:1338803|Aire |||10|ENSMUSG00000000731||||||||||||||||||||||||||||Unknown|Unknown|C57Bl/6N|Unknown|Unknown|Yes|Unknown|Unknown|Yes|No|Good||||No|27-Feb-2023|Cryopreserved sperm|55.0|0.0|Unknown|||Possibly| 10305.0|Tubd1KO|C57BL6/J-Tubd1 /MkobMarp||Recessive|Tubd1||||||||Unknown|||||||||||||||||||||||||||||Subfertile|Normal|C57Bl/6J|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|28-Feb-2023|Cryopreserved sperm|50.0|0.0|Unknown|||Possibly| 5159.0|NODEYFP|NOD.129-Gt(ROSA)26Sor/MarpApb||Dominant|gene trap ROSA 26, Philippe Soriano|Gt(ROSA)26Sor|Normal|beta geo, Gtrgeo26, Gtrosa26, R26, ROSA26|MGI:104735|gene trap ROSA 26, Philippe Soriano; targeted mutation 1, Frank Costantini|Gt(ROSA)26Sor|MGI:2449038|6|||||||||||||||||||||||||||||Normal NOD mouse: reporter mouse for cre expression|Normal NOD mouse: reporter mouse for cre expression|NOD|No|Unknown|Yes|No|Unknown|Yes|No|Unknown|10+|||No|28-Jun-2010|Cryopreserved sperm|50.0|0.0|Unknown||Cre recombinase, expression, reporter, fluorescence|Possibly| 10303.0||C57BL/6J-Tex9<(em4)MAGEC>/Apb||Semi-dominant|testis expressed gene 9|Tex9||tsec-1|MGI:1201610||||Unknown|||||||||||||||||||||||||||||subfertile|Normal|C57Bl/6J|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|27-Feb-2023|Cryopreserved sperm|50.0|0.0|Unknown|||Possibly| 10304.0|M1ap/MkobMarp|C57BL/6J-M1ap<(em4)Mkob>/MarpApb||Recessive|meiosis 1 associated protein|M1ap||D6Mm5e|MGI:1315200||M1apMkob||6|||||||||||||||||||||||||||||Subfertile|Normal|C57Bl/6J|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|27-Feb-2023|Cryopreserved sperm|50.0|0.0|Unknown|||Possibly| 10306.0||C57BL/6N/J-Katna1Katnal1/Marp||Semi-dominant|katanin p60 (ATPase-containing) subunit A1|Katnal1|||MGI:1344353|Katanin p60 (ATPase-containing) subunit A1; targeted mutation 1e, Wellcome Trust Sanger Institute|Katna1|MGI:4458618|Unknown|||||||||||||||||||||||||||||Normal|Normal|C57Bl/ 6n/J|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|28-Feb-2023|Cryopreserved sperm|50.0|0.0|Unknown|||Possibly| 10306.0||C57BL/6N/J-Katna1Katnal1/Marp||Semi-dominant||P60|||||||Unknown|||||||||||||||||||||||||||||Normal|Normal|C57Bl/ 6n/J|Unknown|Unknown|Unknown|Unknown|Unknown|Unknown|No|Unknown||||No|28-Feb-2023|Cryopreserved sperm|||Unknown|||Possibly| 10307.0|Jun flox|C57BL/6J-Jun/Mhn||Recessive|jun proto-oncogene|c-Jun||c-jun, Junc|MGI:96646||||4|||||||||||||||||||||||||||||Normal|Normal|C57Bl/6J|Yes|Yes|Yes|Yes|Yes|Yes|No|Good||||No|01-Mar-2023|Cryopreserved sperm|50.0|0.0|Unknown|||Possibly|