JAX Mice Database - Intracellular Signaling Molecules

Search Criteria: Research Area is "Immunology and Inflammation Research: Intracellular Signaling Molecules"

JAX^® Mice Strains

Stock Number	Strain Name Strain Description	Standard Supply
002650	B6.129S2-Il6^tm1Kopf/J	Level 3
	Mice homozygous for the targeted mutation are viable and fertile. No gene product (mRNA) is detected by RT-PCR analysis of lipopolysaccharide (LPS) challenged macrophages. Bioassay and enzyme-linked immunosorbent assay (ELISA) analysis of serum from LPS-challenged homozygotes reveals no detectable protein activity. These interleukin 6 (IL6) mutant mice show defects in responses to various viruses and in inflammatory responses to tissue damage or infection. Of note, IL6-mutant mice may be available on different genetic backgrounds including mixed B6;129S2 (Stock No. 002254), C57BL/6J (Stock No. 002650), and BALB/cByJ.
000629	C57BL/6J-Lyst^bg-J/J	Level 4
	Mice homozygous for the beige-J spontaneous mutation (Lyst^bg-J) are identical to the original beige mutation (Lyst^bg). The phenotype closely resembles Chediak-Higashi disease in man and similar conditions in mink and cattle. Abnormal giant lysosomal granules occur in all tissues with granule-containing cells, including granulocytes, lymphocytes, cells of the liver, kidney, central nervous system, pancreas, and thyroid, and the ducts of most glands; in type II pneumocytes; in mast cells; and in retinal pigment epithelium. Granulocytes from beige homozygous mutant mice mice show defective chemotaxis and reduced bactericidal activity. Beige mice are more susceptible than controls to pneumonitis and to various viral, bacterial, and parasitic infections. Natural killer (NK) cells from beige mice exhibit decreased endogenous cytotoxic activity. Beige mice also have a defective cytotoxic T-cell and cytotoxic antibody response to allogeneic tumor cells. Syn ..... For more information please see the full descriiption on the strain data sheet
006102	B10.Cg-H2^k Tg(Il2/NFAT-luc)83Rinc/J	Repository- Live
	Hemizygous transgenic mice are viable, fertile, normal in size, and do not display any gross physical or behavioral abnormalities. The donating investigator reports that homozygous females in their colony are subfertile. These transgenic mice express luciferase under the regulation of the Il2 minimal promoter and 3 binding sites for the NFAT inducible nuclear factor involved in the regulation of interleukin-2 and other cytokine expression. Luciferase activity in these transgenic mice identifies NFAT-mediated transcription. These NFAT-luc transgenic mice may be useful be useful as reporters for NFAT-mediated expression during thymocyte development and selection and in studies related to signal transduction, apoptosis, and transcriptional regulation.
006910	B6.129-Crkl^tm1Hkp/J	Repository- Live
	While heterozygous mice are viable and fertile, mice homozygous for this targeted allele die in utero. Immunoblots from homozygous tissues show no protein expression from the targeted gene. The prenatal lethality exhibited by homozygotes on this C57BL/6J congenic background (and also on a 129Sv genetic background) likely results from heart, liver, and placental defects. Please note that homozygous mutants on a mixed/outbred genetic background (129/Sv X Black Swiss) are viable and fertile. These mutant mice may be useful in studying the role of Crkl tyrosine-phosphorylation in Bcr/Abl (Philadelphia chromosome) chronic myelogenous leukemia (CML), acute lymphoblastic leukemia (ALL), Digeorge Syndrome (DGS) and Velocardiofacial Syndrome.
008462	B6.129P2-Trp53^tm1Brn/J	Repository- Live
	Exons 2-10 are flanked by loxP sites in this conditional targeted mutation. Mice homozygous for the floxed allele do not show any increase in disease incidence for at least a year. When bred to mice with a cre recombinase gene under the control of a promoter of interest, expression is deleted in the tissue of interest. For example, when crossed to a strain expressing Cre recombinase in the nervous system (see Stock No. 003771), this mutant mouse strain may be useful in studies of medulloblastoma formation.
004525	B6.129S1-Bcl2l11^tm1.1Ast/J	Repository- Live
	Mice that are homozygous for the targeted mutation are viable, normal in size and do not display any gross physical or behavioral abnormalities. No full length gene product (protein) is immunodetected in spleen cells from homozygous mutant mice. Homozygous mice have lympho-myeloid hyperplasia and reduced platelet number. Lymphocytes are insensitive to certain apoptotic stimuli. Both homozygous and heterozygous mice exhibit progressive systemic autoimmune disease. This mutant mouse strain may be useful in studies of apoptosis, degenerative and autoimmune diseases, including lupus erythematosus and autoimmune kidney disease.
006233	B6.129S1-Casp3^tm1Flv/J	Repository- Live
	On this C57BL/6 congenic background, homozygotes are viable, fertile, and reach adulthood, but females reported display suboptimal mothering instincts. Functional endogenous protein and mRNA are absent from all tissues tested. Homozygous mice are resistant to in vivo cerebral ischemia/reperfusion and in vitro oxygen-glucose deprivation. Ovaries from female homozygotes show aberrant atretic follicles associated with a granulosa cell-intrinsic defect in apoptosis as well as defective corpus luteum regression. Homozygous mice are congenitally deaf with hair cell defects in the Organ of Corti. Optic lens formation/morphology also is abnormal with cataracts at the anterior lens pole. Of note, these mice lack the embryonic/perinatal-lethal brain pathology observed in mutant mice on the 129 and mixed B6;129 genetic backgrounds. These mutant mice may be useful in studies of apoptosis, ovarian follicle and corpus luteum development, and eye and ear development.
004319	B6.129S1-Mapk8^tm1Flv/J	Repository- Live
	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.
005763	B6.129S1-Nod2^tm1Flv/J	Repository- Live
	Homozygous mice are viable and fertile with normal lymphoid and myeloid cellularity and no intestinal inflammation up to 6 months of age. Homozygotes do not express the targeted gene in spleen or intestinal crypts. Null mice, as well as antigen presenting cells derived from them, lack the protective immunity (IgG1, interleukin-6, and NF-kappaB-related responses) normally afforded by endogenous protein recognition of its ligand, bacterial muramyl dipeptide (MDP). Mice homozygous for the mutation have increased susceptibility to oral (intragastric) bacterial challenge and diminished cryptdins. This mouse may be useful in studies of Crohn's disease and other inflammatory bowel diseases, innate immunity, signal transduction, and bacterial susceptibility.
005977	B6.129S2(C)-Stat6^tm1Gru/J	Repository- Live
	Homozygous mice are viable and fertile with no behavioral abnormalities. Homozygotes do not express the endogenous protein in thymus and peripheral lymphoid organs. In contrast to controls, IL-4 treated lymphocytes show no induction of MHC class II or IL-4 receptor genes and have severly impaired proliferative responses. Further, homozygous mice have a defective IgE response. While T-helper 1 (Th1) cell differentiation is unimpaired in homozygous splenocytes, Th2 cell differentiation is almost completely abrogated despite IL-4 or IL-13 incubation. Myelin oligodendrocyte glycoprotein (MOG)-induced experimental autoimmune encephalomyelitis (EAE) is more severe in homozygous mice compared to wildtype. This mouse may be useful in studies of Th2 cell differentiation, Th2-mediated diseases, asthma, cytokine/chemokine function, signal transduction and transcription factors, and diseases of the central nervous system such as multiple sclerosis.
002101	B6.129S2-Trp53^tm1Tyj/J	Repository- Live
	Mice homozygous for the Trp53^tm1Tyj mutation show no visible phenotype but most develop tumors (principally lymphomas and osteosarcoma) at three to six months of age. Heterozygous mice develop tumors at about 10 months of age. These mice model some of the features of human Li-Fraumeni syndrome, a form of familial breast cancer with mutations in TRP53. Homozygous mice may produce a litter before succumbing to tumors.
003610	B6.129S4-Cd80^tm1Shr Cd86^tm2Shr/J	Repository- Live
	Cd80/Cd86-mediated signaling is critical to germinal center formation and Ig class switching in vivo. Mice homozygous for both the Cd80 (B7-1) and Cd86 (B7-2) targeted mutations are viable, fertile and have a normal life span. Homozygous null Cd80/Cd86 mice fail to generate antigen specific IgG1 and IgG2a responses. During the postimmunization period (seven-10 days) they have smaller spleens devoid of germinal centers. Unimmunized null mice exhibit a three to five fold reduction in total serum immunoglobulin and IgG2a. Levels of IgG1 are also reduced five to 10 fold. Levels of IgM and IgG3 are elevated three to five fold. When immunized, antigen specific IgG1 and IgG2a isotype levels are 0.1% that of wild-type levels. Levels remain low even when immunization is performed with adjuvent. This strain is also resistant to myelin oligodendrocyte glycoprotein (MOG) 35-55 peptide-induced experimental autoimmune encephalomyelitis (EAE), a T cell-mediat ..... For more information please see the full descriiption on the strain data sheet
003611	B6.129S4-Cd80^tm1Shr/J	Repository- Live
	Cd80 (B7-1) null mice are viable and fertile. They possess normal numbers of B and T lymphocytes but exhibit a diminished mixed lymphocyte response. Following immunization, antigen specific IgG1, IgG2a and IgM isotypes are 25%-50% that of wild type levels. Survival of certain tissue allografts are slightly prolonged in Cd80 null mice.
003609	B6.129S4-Cd86^tm1Shr/J	Repository- Live
	Cd86 (B7-2) null mice are viable and fertile. Unimmunized mice have normal levels of serum immunoglobulin and normal numbers of B and T lymphocytes. Upon intravenous immunization without adjuvant, they fail to form germinal centers or undergo isotype switching and antigen specific IgG1 and IgG2a isotypes are found to be 5% that of wild type levels. When the immunization route is subcutaneous, IgG1 and IgG2a levels are the same as in wild type mice.
008076	B6.129S4-Traf1^tm1Tsi/J	Repository- Live
	Mice homozygous for the TRAF1 mutant allele (TRAF1^-/-) are viable and fertile. No protein expression from the targeted gene is observed in CD40-stimulated splenocytes isolated from homozygous mice. Homozygous mice on a C57BL/6 congenic background (B6-TRAF1^-/-) have abnormal memory T cell survival and impaired influenza virus CD8 T cell responses. Activated B6-TRAF1^-/- T cells accumulate increased levels of proapoptotic BH3-only family member Bim, particularly the most toxic isoform, Bim_s. The donating investigator reports that B6-TRAF1 mutant mice may be difficult to breed and gain more weight than BALB/c-TRAF1 mutant mice. Homozygous mice on a BALB/c congenic background (BALB/c-TRAF1^-/-) exhibit acute liver injury and elevated serum liver enzymes following intratracheal TNF-alpha treatment. Furthermore, activated TRAF1^-/- T cells have significantly increased expression of Th2 cytokines (IL-4, IL-5 and IL-13) that el ..... For more information please see the full descriiption on the strain data sheet
006236	B6.129S6-Casp6^tm1Flv/J	Repository- Live
	Homozygous mice are viable and fertile with no gross morphological or behavioral abnormalities. These mutant mice may be useful in studies of mitochondrial events of apoptosis (especially when paired with other executioner caspase mutant models) and lens development.
006237	B6.129S6-Casp7^tm1Flv/J	Repository- Live
	Homozygous mice are viable and fertile with normal appearance, organ morphology, and lymphoid development. Endogenous protein expression is absent in all tissues tested (including brain, thymus, heart, lung, liver, spleen, kidney, and skeletal muscle). Mouse embryonic fibroblasts (MEFs) from homozygotes exhibit a slight survival advantage when treated with apoptosis inducers, but other cell subsets undergo normal apoptosis (including activated T cells death following T cell receptor stimulation, thymocyte apoptosis, and Fas-mediated B cell and hepatocyte cell death). These mutant mice may be useful in studies of mitochondrial events of apoptosis, especially when paired with other executioner caspase mutant models.
007218	B6.129S6-Trp53^tm2Xu/J	Repository- Live
	Mice homozygous for this targeted mutation are viable and fertile. They carry two phosphorylation site disruptions: Ser18 to Ala (S18A), and Ser23 to Ala (S23A). Trp53-dependent apoptosis is essentially abolished in thymocytes. These mice develop spontaneous tumors at approximately 1.5 years of age and also develop a range of malignancies that are distinct from those found in animals carrying either a single S23A mutation or a complete knockout of the gene. This mutant mouse strain may be useful in studies of phosphorylation events, cancer development and apoptosis. In an attempt to offer alleles on well-characterized or multiple genetic backgrounds, alleles are frequently moved to a genetic background different from that on which an allele was first characterized. It should be noted that the phenotype could vary from that originally described. We will modify the strain description if necessary as published results become available.
002994	B6.129X1-Bax^tm1Sjk/J	Repository- Live
	Mice homozygous for the Bax^tm1Sjk 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. Used in conjunction with strain B6.129-Bak1^tm1Thsn/J (see Stock No. 004183), to generate the double knock-out Bak/Bax, a model for demonstrating severe defects in the regulation of apoptosis during development and tissue homeostasis. *Coat color of Bax^tm1Sjk* mice** The coat color loci tyrosinase (Tyr) and pink-eyed dilution (p) are linked to the Bcl2-associated X pr ..... For more information please see the full descriiption on the strain data sheet
006606	B6.129X1-Camkk1^tm1Tch/J	Repository- Live
	Homozygotes are viable and fertile. Immunoblots using antibodies against both carboxy- and amino-terminal peptide sequences confirms the absence of wildtype protein in brain tissue. These CaMKKalpha-deficient mice exhibit deficits in context fear during both conditioning and long-term follow-up testing. This is accompanied by impaired activation of other kinases and substrates downstream in the Ca²⁺/calmodulin kinase (CaMK) cascade. Homozygous mice have normal long-term spatial memory formation, cued fear conditioning, long-term potentiation and anxiety-like behavior levels. These mutant mice may be useful in neurological studies involving the CaMK cascade, neuronal gene transcription, synaptic plasticity, contextual fear and long-term memory consolidation.
004088	B6.Cg-Foxp3^sf/J	Repository- Live
	Scurfy mice develop an X-linked lymphoproliferative disease resulting from defective T cell tolerance. Phenotypes associated with these mice include runting, scaly, crusty skin on the eyelids, ears and tails, dermal thickening, squinted eyes, cachexia, reddening and swelling of the genital papilla, and small testicles that are retained in the abdominal cavity. This disorder, which parallels X-linked autoimmunity-allergic disregulation syndrome (XLAAD) in humans, results in Coombs' test-positive anemia, hypergammaglobulinemia, a small, thin thymus, and lymphohistiocytic proliferation in the skin and lymphoid organs, with splenomegaly, lymphadenomegaly, and hepatomegaly. Foxp3^sf/Y males generally die by 16-25 days of age. Transgenic expression of Foxp3 prevents scurfy disease in Foxp3^sf/Y mice. Neonatal thymectomy of scurfy males ameliorates disease and increases lifespan; athymic nude Foxp3^sf/Y mice do not develop scurfy ..... For more information please see the full descriiption on the strain data sheet
006908	B6.Cg-Ikbke^tm1Tman/J	Repository- Live
	Homozygous IKKepsilon mutant mice are viable and fertile. Homozygous deletion results in a complete loss of the endogenous kinase function in lung, spleen, and embryonic fibroblasts. These mice have increased susceptibility to viral infection due to defective inteferon (IFN) signaling. These IKKepsilon mutant mice may be useful in immunological studies involving IFN signaling and host responses to infection.
006098	B6.Cg-Tg(Il2/NFAT-luc)83Rinc/J	Repository- Live
	Hemizygous mice are viable, fertile, normal in size, and do not display any gross physical or behavioral abnormalities. Homozygous females are subfertile. These transgenic mice express luciferase under the regulation of the Il2 minimal promoter and 3 binding sites for NFAT, an inducible nuclear factor involved in the regulation of interleukin-2 and other cytokine expression. Luciferase activity in these transgenic mice identifies NFAT-mediated transcription. These mice may be useful as reporters for NFAT-mediated expression during thymocyte development and selection and in studies related to signal transduction, apoptosis, and transcriptional regulation.
008045	B6;129-Trp53^tm2Holl/J	Repository- Live
	In this mutant strain, exons 4-9 of the endogenous mouse Trp53 gene have been replaced with the homologous human TRP53 region. Transcription of the human sequence is under the control of the endogenous mouse promoter. The inserted human sequence segment encodes the DNA binding domain and the TRP53 polyproline domain. This latter domain contains a polymorphism at codon 72 that encodes either arginine or proline in human populations. This mutant strain expresses the proline variant at codon 72 and the related strain, 129-Trp53^tm1Holl/J (Stock No. 004301) expresses the arginine variant. Mice that are homozygous for this mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Immortalized cell lines derived from primary embryonic fibroblasts harvested from these mice frequently harbor a TRP53 (p53) mutation in the DNA binding domain t ..... For more information please see the full descriiption on the strain data sheet
006980	B6;129-Trp53^tm2Xu/J	Repository- Live
	Mice homozygous for this targeted mutation are viable and fertile. They carry two phosphorylation site disruptions: Ser18 to Ala (S18A), and Ser23 to Ala (S23A). Trp53-dependent apoptosis is essentially abolished in thymocytes. These mice develop spontaneous tumors at approximately 1.5 years of age and a range of malignancies that are distinct from those found in animals carrying either a single S23A mutation or a complete knockout of the gene. This mutant mouse strain may be useful in studies of phosphorylation events in cancer development and apoptosis.
002254	B6;129S2-Il6^tm1Kopf/J	Repository- Live
	Mice homozygous for the targeted mutation are viable and fertile. No gene product (mRNA) is detected by RT-PCR analysis of lipopolysaccharide (LPS) challenged macrophages. Bioassay and enzyme-linked immunosorbent assay (ELISA) analysis of serum from LPS-challenged homozygotes reveals no detectable protein activity. These interleukin 6 (IL6) mutant mice show defects in responses to various viruses and in inflammatory responses to tissue damage or infection. Of note, IL6-mutant mice may be available on different genetic backgrounds including mixed B6;129S2 (Stock No. 002254), C57BL/6J (Stock No. 002650), and BALB/cByJ (Stock No. 001026).
002785	B6;129S4-E2f1^tm1Meg/J	Repository- Live
	Mice homozygous for defective E2f1 are viable and fertile. They show thymocyte maturation defects due to a failure of apoptosis, eventually resulting in increased proliferation and increased tumorigenesis. As mutant mice age, they show exocrine gland dysplasia and testicular atrophy. Mutant mice develop a broad spectrum of cancers, although mammary carcinomas were not observed on this genetic background. Mutant mice are also protected from experimental autoimmune encephalomyelitis (EAE). These mice may be useful in studies of apoptosis, cancer, thymocyte development/selection, diabetes, autoimmunity, and multiple sclerosis.
002852	B6;129S4-Jak3^tm1Ljb/J	Repository- Live
	Mice homozygous for the Jak3^tm1Ljb mutation are viable and fertile. B cell development is blocked at pre-B resulting in a significant decrease in peripheral IgM⁺ B cells. The thymus is small but T cell development is relatively normal. There are increased numbers of CD4⁺ Cd8^- cells in some homozygotes. Proliferative responses to mitogenic signals are defective and Il2 receptor signaling is blocked. The overall phenotype results in a severely immunocompromised mouse.
003514	BALB/c-Il4ra^tm1Sz/J	Repository- Live
	Mice homozygous for the Il4ra ^tm1Sz targeted mutation are viable and fertile. While homozygous mutant mice show no overt phenotypic abnormalities they do exhibit a loss of Il4 signal transduction. This lack of response to Il4 results in a diminished TH2 helper T cell response to helminthic parasite infections. Il4ra-deficient mice provide a tool for analyzing the physiological pathways through which priming for TH2 responses are induced and the role of Il4 in a wide variety of infectious and other pathological conditions.
004190	C.129-Il4^tm1Lky/J	Repository- Live
	Mice homozygous for the targeted allele are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. A knockin replaces the endogenous gene with an Il4/IRES/EGFP gene (IL4 activity remains intact). This leads to generation of a bicistronic transcript under the control of endogenous regulatory elements. Cells activated to express IL4 will express EGFP, allowing reliable in vivo tracking of both innate and adaptive immune cells, and/or enabling their isolation without further stimulation. As the IRES element promotes translational competence capable of revealing low-level transcription otherwise not apparent from the canonical 5'-cap of the mRNA, cells from these mice can also be used to report competence for IL4 production upon stimulation.
007810	C.129-Stat5b^tm1Hwd/J	Repository- Live
	Mice that are heterozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. No gene product (mRNA or protein) is detected by Northern and immunoblot analysis of liver, spleen, mammary gland, thymus, kidney or skeletal muscle from homozygous animals. Levels of the closely related Stat5a gene products (mRNA and protein) are unaffected in thymus and spleen. At 4 - 5 weeks of age, male homozygotes are smaller in size and have a reduced body weight (27% lighter than wildtype controls) when compared to wildtype. Female homozygotes exhibit spontaneous abortion between day 8 and 17 of pregnancy and have impaired lactation. Pups (independent of genotype) born to heterozygous females have higher perinatal death than pups born to wildtype females. Some homozygotes have pale and enlarged livers. Homozygotes have less adipose tissue than wildtype controls, exhibit abnormal gene expression in liver, reduced insuli ..... For more information please see the full descriiption on the strain data sheet
007806	C.129S(B6)-Stat5a^tm1Mam/J	Repository- Live
	Mice homozygous for the targeted mutation are viable, develop normally, and are fertile, but females do not lactate. Mammary ductal development through pregnancy is normal, but lobuloalveolar development is severely reduced, and milk is not secreted even after prolonged suckling. Levels of the closely-related STAT5B protein are also markedly reduced in STAT5A-deficient mice, but STAT5B protein levels increase and phosphorylation is evident after 3 days of suckling. Expression of several milk protein genes is unaffected in homozygous mutants, but whey acidic protein expression is severely reduced. Homozygous males exhibit abnormal prostate morphology and an increase in probasin secretion. Immmunological defects exhibited by homozygotes include a reduced number of peritoneal mast cells, decreased IL-3-dependent development of bone marrow-derived mast cells, defective bone marrow-derived macrophage GM-CSF (Granulocyte-Macrophage Colony-Stimulating Factor)-induced proliferation, decreased ..... For more information please see the full descriiption on the strain data sheet
002826	C.129S2-Stat4^tm1Gru/J	Repository- Live
	Mice homozygous for the Stat4^tm1Gru mutation are viable and fertile. IL12 induced interferon-gamma secretion and stimulation of lymphocytes are defective. Development of Th1 cells in response to either IL12 or Listeria monocytogenes is also defective with propensity towards Th2 cells.
002828	C.129S2-Stat6^tm1Gru/J	Repository- Live
	Mice homozygous for the Stat6^tm1Gru 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.
007680	C.129X1-Il4ra^tm1Tch/J	Repository- Live
	Mice homozygous for this "IL4Rα Y500F" mutant allele are viable and fertile. The mice express a mutant IL4Rα chain with a phenylalanine substitution at the proximal tyrosine residue (Y500F) in the cytoplasmic tail. This residue is a critical component of the insulin/interleukin-4 receptor (I4R) motif, and is required for binding by phosphotyrosine-binding domain (PTB) adaptor proteins and for initiating subsequent downstream signaling cascades in response to IL-4. Allele-specific PCR verifies the amino acid substitution. The Y500F mutation abrogates insulin receptor substrate-2 (IRS-2) phosphorylation, and impairs IL-4-induced CD4+ lymphocyte proliferation with no reported effect on Stat6 activation, IL-4-responsive gene product up-regulation, or Th cell differentiation under Th2 polarizing conditions. In vivo, the Y500F mutation is associated with increased allergen-induced IgE production, airway hyper-responsiveness (AHR), tissue eosinophilia, goblet cell metaplasi ..... For more information please see the full descriiption on the strain data sheet
007225	FVB.129(B6)-Usp18^tm1Dzh/J	Repository- Live
	Homozygous Usp18 (or Ubp43) mutant mice on the FVB/N genetic background are viable and fertile, exhibiting none of the severe neurologic disorders that lead to embryonic lethality or early death reported for Ubp43-deficient mice on a C57BL/6 or mixed B6;129 genetic background. In contrast to wildtype mice, thymi from homozygous mice injected with LPS exhibit no protein from the targeted gene. Expression of the lacZ cassette is observed in both heterozygous and homozygous brain tissues. Homozygous mice are hypersensitive to type I interferon (IFN) and undergo apoptosis upon IFN stimulation. Ubp43-deficiency results in enhanced and prolonged STAT1 phosphorylation, DNA binding, and increased induction of hundreds of interferon stimulated genes (ISGs). Homozygous mice exhibit greater resistance to the cytopathic effects caused by a number of viruses (including lymphocytic choriomeningitis virus (LCMV), vesicular stomatitis virus (VSV), and Sindbis virus (SNV)). Ubp43-defici ..... For more information please see the full descriiption on the strain data sheet
004301	129-Trp53^tm1Holl/J	Repository-Cryopreserved
	In this mutant mouse strain, the endogenous murine sequence for exons 4-9 of the targeted gene, which encode the DNA binding domain of the tumor suppressor protein, have been replaced with the homologous normal human sequence. Transcription is under the control of the endogenous mouse promoter. Mice that are homozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Homozygous mutant mice exhibit normal expression and functional activity of the chimeric gene. Homozygous mutant mice have normal immunodetectable levels of p53 protein accumulation in nuclei in response to UV-induced DNA damage. Thymocytes from mutant mice are as susceptible to gamma-irradiation-induced and dexamethaxone-induced apoptosis as wildtype thymocytes. This mutant mouse strain may be useful in studies related to in vivo spontaneous and induced mutation of the human TRP53 gene sequence, and pharmacological agents for alt ..... For more information please see the full descriiption on the strain data sheet
002080	129-Trp53^tm1Tyj/J	Repository-Cryopreserved
	Mice homozygous for the Trp53^tm1Tyj mutation show no visible phenotype but most develop tumors (principally lymphomas and osteosarcoma) at 3-6 months of age. Heterozygous mice develop tumors at about 10 months of age. These mice model some of the features of human Li-Fraumeni syndrome, a form of familial breast cancer with mutations in TRP53. Homozygous mice may produce a litter before succumbing to tumors.
002082	129S-Rb1^tm1Tyj/J	Repository-Cryopreserved
	Mice homozygous for this targeted mutation die in utero, apparently from a failure to produce erythrocytes in the liver, demonstrating that the endogenous gene is essential for normal development. Heterozygous mice, which are analogous to human carrier individuals, do not develop retinal tumors, but do develop pituitary tumors by 8 months of age.
003082	129S1/SvImJ-Bcl2^tm1Mpin/J	Repository-Cryopreserved
	Heterozygous mice exhibit expression of beta-galactosidase in populations of large sensory neurons. Mice homozygous for the Bcl2^tm1Mpin targeted mutation do not produce either the a or b form of the Bcl2 protein. Bcl2 is a major regulator of programmed cell death, a critical process in shaping the developing nervous system. The absence of the Bcl2 does not significantly influence the development of motor neurons before or during the main period of physiological cell death. Rather, Bcl2 exerts its influence beyond this period, subsequent to the phase where the majority of neuronal loss normally takes place. Polycystic kidney disease is less severe in this strain compared to the Bcl2^tm1Sjk targeted mutation (Stock No. 002265).
003292	129S6/SvEvTac-Was^tm1Sbs/J	Repository-Cryopreserved
	WAS-deficient mice are viable and fertile. Mutant mice show normal lymphocyte development, serum immunoglobulin (Ig) levels and antibody responses. However, peripheral blood lymphocyte counts and platelet numbers are reduced in these mice. Development of chronic colitis is also observed. In vitro, WAS-deficient T cells show markedly impaired proliferative responses to anti-CD3e mediated stimulation. The Was gene is X-linked, so hemizygous males are WAS deficient.
006100	B10.Cg-H2^k Tg(NFkB/Fos-luc)26Rinc/J	Repository-Cryopreserved
	Hemizygous mice are viable, fertile, normal in size, and do not display any gross physical or behavioral abnormalities. Mutant mice have the luciferase gene driven by two copies of the NF-kappaB (NF-kB or NFkB) regulatory element. The presence of nuclear NF-kB DNA binding activity (as detected by electrophoretic mobility shift assay [EMSA]) is consistent with luciferase reporter activity; these reporter mice identify NF-kB transcriptional activity in any tissue. These transgenic mice may be useful in studies of immunology, cellular signaling, signal transduction, apoptosis, and transcription factor function.
005711	B6.129P2-Prkcq^tm1Litt/J	Repository-Cryopreserved
	Mice homozygous for the targeted allele are viable, fertile, normal in size, and do not display any behavioral abnormalities. No endogenous or truncated protein product was detected in thymocytes or T cells. Mature T lymphocytes from null mice have blunted proliferative responses with decreased levels of both IL-2 and IL-2 receptor, and defective T cell receptor-initiated IkappaB-degradation/NF-kappaB activation. Homozygous mice exhibit severely impaired Th2, but normal Th1, immune responses as well as abnormal insulin signaling and glucose transport. Mutant mice also have defective regulatory T cell development (very low CD25 expression). This mutant may be suitable for use in studies related to T cell proliferation/signal transduction/immunodeficiency, Th2-mediated disease, asthma, and diabetes.
007017	B6.129S1-Ripk2^tm1Flv/J	Repository-Cryopreserved
	Homozygotes are viable and fertile and do not display any gross physical or behavioral abnormalities. Cytokine production in macrophages is reduced upon stimulation with lipopolysaccharide, peptidoglycan and double-stranded RNA, but not with bacterial DNA. Deficient cells are also hyporesponsive to signalling through IL1 and IL18 interleukin receptors, and deficient for signalling through NOD (nucleotide-binding oligomerization domain) proteins. T cells show severely reduced NFKB (nuclear factor of kappa light chain gene enhancer in B-cells) activation, IL2 production and proliferation on T cell receptor (TCR) engagement, and impaired differentiation to T-helper subtype 1 (T_H1)cells. Western blot analysis of thymocytes demonstrates the absence of protein in homozygous mutant mice.
002102	B6.129S2-Rb1^tm1Tyj/J	Repository-Cryopreserved
	Mice homozygous for this targeted mutation die in utero, apparently from a failure to produce erythrocytes in the liver, demonstrating that the endogenous gene is essential for normal development. Heterozygous mice, which are analogous to human carrier individuals, do not develop retinal tumors, but do develop pituitary tumors by 8 months of age. In an attempt to offer alleles on well-characterized or multiple genetic backgrounds, alleles are frequently moved to a genetic background different from that on which an allele was first characterized. This is the case for this strain. It should be noted that the phenotype could vary from that originally described. We will modify the strain description if necessary as published results become available.
008183	B6.129S4(Cg)-Trp53^tm2.1Tyj/J	Repository-Cryopreserved
	Mice carrying this Trp53 (p53) R172H point mutation mimic human Li-Fraumeni Syndrome, both genotypically and phenotypically. Heterozygotes develop a broad spectrum of tumors with a mean survival time of 16 months. Prominent tumor types include osteosarcomas (often metastatic), hemangiosarcomas, B-cell lymphomas and a variety of carcinomas. Homozygous mice also develop a broad spectrum of tumors, particularly T-cell lymphomas, hemangiosarcomas, soft-tissue sarcomas, osteosarcomas, primitive tumors (particularly male teratocarcinomas), and a variety of epithelial carcinomas. Mutant protein is expressed at high levels in mouse embryonic fibroblasts, as determined by Western blotting.
008182	B6.129S4-Trp53^tm3.1Tyj/J	Repository-Cryopreserved
	These targeted mutant mice carry a R270H missense mutation in exon 8 of the gene. Heterozygous mice develop a broad spectrum of tumors with a mean survival time of 16 months. Prominent tumor types include osteosarcomas (often metastatic), hemangiosarcomas, B-cell lymphomas and a variety of carcinomas. Homozygous mice also develop an array of tumor types including a variety of hematological tumors (particularly T-cell lymphomas), hemangiosarcomas, soft-tissue sarcomas, ostersarcomas, primitive tumors (particularly male teratocarcinomas), and a variety of epithelial carcinomas. Homozygotes have a mean survival time of 4.5 months. Mutant protein is expressed in all of the places that wildtype protein is expressed in normal tissues. Irradiation or DNA damage leads to substantially increased protein levels. Expression is also upregulated in some tumor types. This strain may be useful in studies of cancer and Li-Fraumeni Syndrome.
004197	B6.129S6-Rac2^tm1Mddw/J	Repository-Cryopreserved
	Mice that are homozygous for the targeted mutation are viable, fertile, and normal in size but exhibit phagocytic immunodeficiency. No endogenous gene product (mRNA or protein) was detected by Northern blot analysis, RT-PCR or Western blot analysis. The Rac proteins are a subclass of the Rho family of GTPases, and are involved in actin cytoskeletal organization in cell movement, cell proliferation, kinase signaling pathways, and in superoxide production in phagocytic cells. Neutrophils and mast cells derived from homozygous mice display abnormal actin-based functions: cytoskeleton remodeling ability, adhesion, migration, degranulation, and phagocytosis. Diminished superoxide production in response to some agonists, and reduced total number of leukocytes and neutrophils in peritoneal exudate is observed. As result of functional deficiencies in neutrophil and mast cell populations, these mutant mice are more vulnerable to invasive infection. Slowed growth of mast cells, accompanying redu ..... For more information please see the full descriiption on the strain data sheet
000204	B6.Cg-Lyst^bg/J	Repository-Cryopreserved
	Mice homozygous for the beige spontaneous mutation (Lyst^bg) are characterized by a condition that closely resembles Chediak-Higashi disease in man and similar conditions in mink and cattle. Abnormal giant lysosomal granules occur in all tissues with granule-containing cells, including granulocytes, lymphocytes, cells of the liver, kidney, central nervous system, pancreas, and thyroid, and the ducts of most glands; in type II pneumocytes; in mast cells; and in retinal pigment epithelium. Granulocytes from beige homozygous mutant mice mice show defective chemotaxis and reduced bactericidal activity. Beige mice are more susceptible than controls to pneumonitis and to various viral, bacterial, and parasitic infections. Natural killer (NK) cells from beige mice exhibit decreased endogenous cytotoxic activity. Beige mice also have a defective cytotoxic T-cell and cytotoxic antibody response to allogeneic tumor cells. Syngeneic tumor cells grow better in beige mice than in l ..... For more information please see the full descriiption on the strain data sheet
002319	B6.Cg-Tg(BCL2)22Wehi/J	Repository-Cryopreserved
	Expression of the human BCL2 transgene is restricted to B cell lineage (no T cell expression) in which it enhances cell survival. Hemizygotes show increased numbers of B lymphocytes, Ig-secreting cells and serum Ig, as well as a heightened and prolonged antibody response to immunization. This phenotype is somewhat greater on the BALB/c than on the C57BL/6 background. Hemizygotes on a mixed B6,SJL background (but not on the BALB/c background) develop autoimmune disease characterized by immune complex glomerulonephritis, anti-nuclear antibodies, lymphadenopathy and myocardial infarction. These mice serve as a robust source for the production of B cells and antibodies. Although mice bearing this allele exhibit a mild increase in spontaneous lymphoma and plasmacytoma occurrence (<10% to 18 months) on a (C57BL/6 x SJL)F2 background, on the BALB/c and C57BL/6 backgrounds tumor incidence is insignificant. When this transgene is crossed with an Emu-myc transgene bearing strain (Stock ..... For more information please see the full descriiption on the strain data sheet
002320	B6.Cg-Tg(BCL2)25Wehi/J	Repository-Cryopreserved
	Expression of the human BCL2 transgene restricted to the T cell lineage (no B-cell expression). Thymocytes, peripheral T-cells and activated T cells from these mice withstand prolonged culture in the absence of growth factors. Cells are resistant to killing by gamma-radiation, glucocorticoids, ionomycin, PMA and sodium azide but NOT complement, cytotoxic T cells or Fas ligand. Hemizygotes have a normal total T-cell count and thymic involution rate but show an enhanced response to immunization. This transgenic line displays no detectable autoimmunity. These mice serve as a robust source for the production of T-cell lines or hybridomas. Also known as 25Wehi or Emu-bcl-2-25.
002321	B6.Cg-Tg(BCL2)36Wehi/J	Repository-Cryopreserved
	Expression of the human BCL2 transgene in both T cell and B cell lineages. This transgenic line combines the characteristics of both Tg(BCL2)22Wehi and the Tg(BCL2)25Wehi lines. Hemizygotes show increased numbers of B lymphocytes, Ig-secreting cells and serum Ig, as well as a heightened and prolonged antibody response to immunization. T-cells withstand prolonged culture in the absence of growth factors and are resistant to killing by gamma-radiation, glucocorticoids, ionomycin, PMA and sodium azide but NOT complement, cytotoxic T cells, or Fas ligand. Hemizygotes have a normal total T-cell count and thymic involution rate but show an enhanced response to immunization. These mice serve as a robust source for the production of B-cells, antibodies T-cell lines or hybridomas. Although mice bearing this allele exhibit a mild increase in spontaneous lymphoma and plasmacytoma occurrence (<10% to 18 months) on a (C57BL/6 x SJL)F2 background, on the BALB/c and C57BL/6 backgrounds tumor incid ..... For more information please see the full descriiption on the strain data sheet
006101	B6.Cg-Tg(TRE/Prl-luc)31FlvRinc/J	Repository-Cryopreserved
	Hemizygous mice are viable, fertile, normal in size, and do not display any gross physical or behavioral abnormalities. Naïve (unstimulated) cells from transgenic mice show no luciferase activity. When activated via addition of phorbol myristate acetate (PMA) plus ionomycin, cell populations from hemizygous mice exhibit high luciferase transcriptional activity in CD4⁺ T cells. Identically treated single-positive CD8⁺ T cells have lower transcriptional activity, while no luciferase is observed in B cell populations. Interleukin-2 transcriptional activators (anti-CD3 and ConA) also promote similar cell-specific patterns of reporter transcription. Luciferase expression is cyclosporine sensitive. Nuclear proteins isolated from hemizygous splenocytes show AP-1 specific binding to the transgenic TRE domain. This reporter transgene faithfully identifies AP-1 transcriptional activity both in vivo and in vitro. These mice may be useful in studies of immu ..... For more information please see the full descriiption on the strain data sheet
003666	B6;129S1-Map2k4^tm1Liz/J	Repository-Cryopreserved
	Mice that are homozygous null for the Map2k4(SEK1, JNKK, or MKK4) gene exhibit liver abnormalities and suffer lethality before embryonic day 14.5. Histological examination reveals a reduced number of hepatocytes and enlarged, hemorrhaging sinuses. The donating investigator speculates that embryo death results from anemia brought on by massive bleeding. SEK1 is an enzyme in the stress-activated MAP kinase pathway.
002265	B6;129S2-Bcl2^tm1Sjk/J	Repository-Cryopreserved
	Mice homozygous for the Bcl2^tm1Sjk targeted mutation appear normal at birth; however, growth retardation is evident by one week of age with considerable heterogeneity in weight compared to normal wildtype siblings (30% to 90%). There is some pre-weaning loss. Homozygotes succumb to renal failure as a result of polycystic kidney disease. Hematopoiesis, including lymphocyte differentiation is initially normal but the thymus and spleen decrease in size due to increased apoptosis. The coat color of homozygotes turns grey with the second hair follicle cycle.
008191	B6;129S2-Trp53^tm1Tyj Nf1^tm1Tyj/J	Repository-Cryopreserved
	These mice carry Trp53 and Nf1 targeted mutations on the same chromosome (cis). Double homozygotes are embryonic lethal. Double heterozygotes survive an average of five months and exhibit a significant increase in the percentage of soft tissue sarcomas compared with mice of other genotypes (Nf1 +/-, 5%; p53, 57%; Nf1/Trp53 trans, 36%; Nf1/Trp53 cis, 81%). Furthermore, although Nf1/Trp53 trans mice exclusively develop osteo-, fibro-, rhabdomyo-, and hemangiosarcomas, about 30% of tumors from the Nf1/Trp53 cis animals stain positively for S100 (consistent with glial cell origin) and exhibit classic histological features of malignant peripheral nerve sheath tumors (MPNSTs). This strain may be useful in studies of astrocytomas/glioblastomas and tumor suppressor genes.
002103	B6;129S2-Trp53^tm1Tyj/J	Repository-Cryopreserved
	Mice homozygous for the Trp53^tm1Tyj mutation show no visible phenotype but most develop tumors (principally lymphomas and osteosarcoma) at 3-6 months of age. Heterozygous mice develop tumors at about 10 months of age. These mice model some of the features of human Li-Fraumeni syndrome, a form of familial breast cancer with mutations in TRP53. Homozygous mice may produce a litter before succumbing to tumors.
008181	B6;129S4-Trp53^tm4Tyj/J	Repository-Cryopreserved
	Mice homozygous for this S23A point mutation are viable and fertile. Cells from the mice, including thymocytes and neurons in the cerebellum, exhibit defective apoptosis in response to DNA damage and exhibit partially impaired TRP53 (p53) stabilization. Mice develop increased lymphomas (especially B-cell lineage) and other tumors between one and two years of age.
002833	B6;129S6-Stat5a^tm1Mam/J	Repository-Cryopreserved
	Mice homozygous for the targeted mutation are viable, develop normally, and are fertile, but do not lactate. Mammary ductal development through pregnancy is normal, but lobuloalveolar development is severely reduced and there is no milk secretion even after prolonged suckling. Levels of the closely related STAT5B signalling molecule are also markedly reduced in STAT5A-deficient mice, but levels increase and phosphorylation is evident after three days of suckling. Expression of several milk protein genes is unaffected in homozygous mutants, whereas whey acidic protein expression is severely reduced. Homozygous males exhibit abnormal prostate morphology and an increase in probasin secretion. Immmunological defects exhibited by homozygotes include a reduced number of peritoneal mast cells, decreased IL-3 dependent development of bone marrow-derived mast cells, defective bone marrow-derived macrophage GM-CSF (Granulocyte-Macrophage Colony-Stimulating Factor) induced proliferation, decreas ..... For more information please see the full descriiption on the strain data sheet
003330	B6;D2-Tg(LCK-NFKBIA)5Dwb/J	Repository-Cryopreserved
	Mice hemizygous for TgN(LCK-NFKBIA)5Dwb transgene exhibit a complete inactivation of the NFKB signalling pathway. The T cell lineage expresses a trans-dominant form of IkBa that constitutively represses the activity of multiple NFKB/Rel proteins. Transgenic cells expressing this inhibitor exhibit a significant proliferative defect. Mitogenic stimulation of splenocytes leads to increased apoptosis of transgenic T cells. Transgene expression also impairs the development of normal T cell populations as evidenced by diminished numbers of TCR ^hiCD8 single-positive thymocytes. This defect is significantly amplified in the periphery and is accompanied by a decrease in CD4 ⁺ T cells.
000604	B6C3 a/A-T(10;13)199H +/+ Lyst^bg-J/J or Lyst^bg-2J/J	Repository-Cryopreserved

002526	C.129S2(B6)-Trp53^tm1Tyj/J	Repository-Cryopreserved
	Mice homozygous for the Trp53^tm1Tyj mutation show no visible phenotype but most develop tumors (principally lymphomas and osteosarcoma) at 3-6 months of age. Heterozygous mice develop tumors at about 10 months of age. These mice model some of the features of human Li-Fraumeni syndrome, a form of familial breast cancer with mutations in TRP53. Homozygous mice may produce a litter before succumbing to tumors. In an attempt to offer alleles on well-characterized or multiple genetic backgrounds, alleles are frequently moved to a genetic background different from that on which an allele was first characterized. This is the case for the strain above. It should be noted that the phenotype could vary from that originally described. We will modify the strain description if necessary as published results become available.
003750	C.129S2-Stat4^tm1Gru Stat6^tm1Gru/J	Repository-Cryopreserved
	Mice homozygous for both the Stat4^tm1Gru and Stat6^tm1Gru targeted mutations are viable and fertile. Mutant mice display characteristics of both STAT4 and STAT6 deficient mice. They are defective in both IL-12 mediated signaling as well as IL-4 induced responses. They do not generate functional Th2 cells, a characteristic of STAT6 deficient mice. However, while STAT4 deficient mice do not produce interferon gamma secreting Th1 cells, the STAT4/STAT6 double deficient mice do exhibit a functional Th1 response, producing significant amounts of IFN-{\f 23 g}. The presence of a functional Th1 response in double deficient mice indicates that there is a STAT4 independent pathway for the production of Th1 cells when STAT6 signaling is not activated.
002318	C.Cg-Tg(BCL2)22Wehi/J	Repository-Cryopreserved
	Expression of the human BCL2 transgene is restricted to B cell lineage (no T cell expression) in which it enhances cell survival. Hemizygotes show increased numbers of B lymphocytes, Ig-secreting cells and serum Ig, as well as a heightened and prolonged antibody response to immunization. This phenotype is somewhat greater on the BALB/c than on the C57BL/6 background. Hemizygotes on a mixed B6,SJL background (but not on the BALB/c background) develop autoimmune disease characterized by immune complex glomerulonephritis, anti-nuclear antibodies, lymphadenopathy and myocardial infarction. These mice serve as a robust source for the production of B cells and antibodies. Although mice bearing this allele exhibit a mild increase in spontaneous lymphoma and plasmacytoma occurrence (<10% to 18 months) on a (C57BL/6 x SJL)F2 background, on the BALB/c and C57BL/6 backgrounds tumor incidence is insignificant. When this transgene is crossed with an Emu-myc transgene bearing strain (Stock ..... For more information please see the full descriiption on the strain data sheet
002427	C3H/He-Tg(LCKprBCL2)36Sjk/J	Repository-Cryopreserved
	Hemizygotes carrying the human LCKprBCL2 transgene display normal architecture of all lymphoid organs to 10 weeks of age. They show an increased percentage of CD3^hi/TCR^hi and CD4^-8⁺ thymocytes with a decreased percentage in CD3^lo T cells. CD8⁺ cells and the total percentage of T cells are increased in the spleen and lymph nodes. Mice are resistant to apoptosis induced by glucocorticoid treatment, by radiation treatment, or by anti-CD3 treatment. Malignant lymphoma develop in hemizygotes at approximately 18 months of age.
000509	C3H/HeJ-Lyst^bg-2J/J	Repository-Cryopreserved
	Mice homozygous for the beige 2J spontaneous mutation (Lyst^bg-2J) display characteristics very similar to the original beige mutation (Lyst^bg). The mouse phenotype closely resembles Chediak-Higashi syndrome in man and similar conditions in mink and cattle. Abnormal giant lysosomal granules occur in all tissues with granule-containing cells, including granulocytes, lymphocytes, cells of the liver, kidney, central nervous system, pancreas, and thyroid, and the ducts of most glands; in type II pneumocytes; in mast cells; and in retinal pigment epithelium. Granulocytes from beige homozygous mutant mice show defective chemotaxis and reduced bactericidal activity. Beige mice are more susceptible than controls to pneumonitis and to various viral, bacterial, and parasitic infections. Natural killer (NK) cells from beige mice exhibit decreased endogenous cytotoxic activity. Beige mice also have a defective cytotoxic T-cell and cytotoxic antibody response to a ..... For more information please see the full descriiption on the strain data sheet
002547	C3Ou.129S2(B6)-Trp53^tm1Tyj/J	Repository-Cryopreserved
	Mice homozygous for the Trp53^tm1Tyj mutation show no visible phenotype but most develop tumors (principally lymphomas and osteosarcoma) at 3-6 months of age. Heterozygous mice develop tumors at about 10 months of age. These mice model some of the features of human Li-Fraumeni syndrome, a form of familial breast cancer with mutations in TRP53. Homozygous mice may produce a litter before succumbing to tumors.
002546	C3Ou.129S2-Rb1^tm1Tyj/J	Repository-Cryopreserved
	Mice homozygous for this targeted mutation die in utero, apparently from a failure to produce erythrocytes in the liver, demonstrating that the endogenous gene is essential for normal development. Heterozygous mice, which are analogous to human carrier individuals, do not develop retinal tumors, but do develop pituitary tumors by 8 months of age. In an attempt to offer alleles on well-characterized or multiple genetic backgrounds, alleles are frequently moved to a genetic background different from that on which an allele was first characterized. This is the case for this strain. It should be noted that the phenotype could vary from that originally described. We will modify the strain description if necessary as published results become available.
003652	C57BL/6-Ptprcap^tm1Tho/J	Repository-Cryopreserved
	Homozygous knockout mice are viable and fertile and exhibit no gross defects. Thymocyte function and numbers appear normal, as do the percentages of CD4 and CD8 subsets. No gross abnormality in T- and B-cell antigen receptor signaling was detected.
003567	C57BL/6-Tg(LCK-NFKBIA)5Dwb/J	Repository-Cryopreserved
	Mice hemizygous for TgN(LCK-NFKBIA)5Dwb transgene exhibit a complete inactivation of the NFKB signalling pathway. The T cell lineage expresses a trans-dominant form of IkBa that constitutively represses the activity of multiple NFKB/Rel proteins. Transgenic cells expressing this inhibitor exhibit a significant proliferative defect. Mitogenic stimulation of splenocytes leads to increased apoptosis of transgenic T cells. Transgene expression also impairs the development of normal T cell populations as evidenced by diminished numbers of TCR^hiCD8 single-positive thymocytes. This defect is significantlly amplified in the periphery and is accompanied by a decrease in CD4⁺ T cells.
002900	FVB.129S2(B6)-Rb1^tm1Tyj/J	Repository-Cryopreserved
	Mice homozygous for this targeted mutation die in utero. Homozygous embryos are morphologically indistinguishable from normal embryos at 12.5 days post coitum, but then die between 13.5 d.p.c and 14.5 d.p.c. Defects are seen in fetal liver hematopoiesis as well as in lens and nervous system development. Heterozygous mice, which are analogous to human carrier individuals, do not develop retinal tumors, but do develop pituitary tumors by 8 months of age. In an attempt to offer alleles on well-characterized or multiple genetic backgrounds, alleles are frequently moved to a genetic background different from that on which an allele was first characterized. This is the case for this strain. It should be noted that the phenotype could vary from that originally described. We will modify the strain description if necessary as published results become available.
002899	FVB.129S2(B6)-Trp53^tm1Tyj/J	Repository-Cryopreserved
	Mice homozygous for the Trp53^tm1Tyj mutation show no visible phenotype but most develop tumors (principally lymphomas and osteosarcoma) at 3-6 months of age. Heterozygous mice develop tumors at about 10 months of age. These mice model some of the features of human Li-Fraumeni syndrome, a form of familial breast cancer with mutations in TRP53. Homozygous mice may produce a litter before succumbing to tumors.
003502	FVB.129S6-Stat5a^tm1Mam/J	Repository-Cryopreserved
	Mice homozygous for the targeted mutation are viable, develop normally, and are fertile, but do not lactate. Mammary ductal development through pregnancy is normal, but lobuloalveolar development is severely reduced and there is no milk secretion even after prolonged suckling. Levels of the closely related STAT5B signalling molecule are also markedly reduced in STAT5A-deficient mice, but levels increase and phosphorylation is evident after 3 days of suckling. Expression of several milk protein genes is unaffected in homozygous mutants, whereas whey acidic protein expression is severely reduced. Homozygous males exhibit abnormal prostate morphology and an increase in probasin secretion. Immmunological defects exhibited by homozygotes include a reduced number of peritoneal mast cells, decreased IL-3 dependent development of bone marrow-derived mast cells, defective bone marrow-derived macrophage GM-CSF (Granulocyte-Macrophage Colony-Stimulating Factor) induced proliferation, decreased ..... For more information please see the full descriiption on the strain data sheet
002659	FVB/N-Tg(Trp53R172H)8512Jmr/J	Repository-Cryopreserved
	The FVB/NTgN(Trp53R172H)8512Jmr express TRP53 with both dominant-negative and a gain-of function properties, i.e. this mutant is capable of inducing multiple drug resistance(MDR) promoter-driven reporter gene expression in transfection studies performed in p53 null cells. Transgene expression alone exerts no apparent effect on normal mammary gland development. Mice treated with the chemical carcinogen, dimethylbenz(a)anthracine (DMBA) or crossed with mice overexpressing erb-B2 develop tumors with significantly shorter latencies than controls. These tumors are characterized by large pleiomorphic nuclei and genomic instability. Spontaneous tumors are rarely observed in multiply bred animals in the first year of life.
002660	FVB/N-Tg(Trp53R172L)4491Jmr/J	Repository-Cryopreserved
	The FVB/N-TgN(Trp53R172L)4491Jmr express TRP53 with pseudo-wildtype properties capable of inducing p21 and mdm-2 expression. Lobuloalveolar development is altered and apoptosis is increased during late pregnancy. The few normal lobules observed during early lactation did not express the Trp53 transgene suggesting that they arose by clonal expansion of cells not expressing the transgene during mid-pregnancy. Transgenic mice fail to lactate. There is no apparent alteration in ductal development. Mice expressing a dominant negative 172Arg-His mutation do not exhibit any detectable alterations in mammary gland development and have a very low incidence of spontaneous mammary tumors. Mice bearing the 172Arg-Leu transgene and a pituitary isograft displayed a marked increase in apoptosis and a significant delay in DMBA-induced tumorigenesis, while those bearing the 172Arg-His dominant negative p53 transgene were more susceptible to DMBA-induced tumorigenesis.
000494	J.Cg-Oca2⁺ Tyr⁺ Lyst^bg/J	Repository-Cryopreserved
	Mice homozygous for the beige spontaneous mutation (Lyst^bg) are characterized by a condition that closely resembles Chediak-Higashi disease in man and similar conditions in mink and cattle. Abnormal giant lysosomal granules occur in all tissues with granule-containing cells, including granulocytes, lymphocytes, cells of the liver, kidney, central nervous system, pancreas, and thyroid, and the ducts of most glands; in type II pneumocytes; in mast cells; and in retinal pigment epithelium. Granulocytes from beige homozygous mutant mice mice show defective chemotaxis and reduced bactericidal activity. Beige mice are more susceptible than controls to pneumonitis and to various viral, bacterial, and parasitic infections. Natural killer (NK) cells from beige mice exhibit decreased endogenous cytotoxic activity. Beige mice also have a defective cytotoxic T-cell and cytotoxic antibody response to allogeneic tumor cells. Syngeneic tumor cells grow better in beige mice than in l ..... For more information please see the full descriiption on the strain data sheet
004673	NOD.129(B6)-Rag1^tm1Mom Cd80^tm1Shr/JbsJ	Repository-Cryopreserved
	The NOD.129(B6)Rag1^tm1MomCd80^tm1Shr/JbsJ homozygous mice fail to produce T or B cells. Mice homozygous for both Rag1^tm1Mom and Cd80^tm1Shr are viable and fertile and exhibit no signs of diabetes due to the absence of lymphocytes. On the NOD background Cd80^tm1Shr alone exacerbates diabetes onset when compared to standard NOD controls. When injected with proteolipid protein in Complete Freund's Adjuvant, NOD mice homozygous for the Cd80^tm1Shr/JbsJ mutation alone develop similar though slightly milder, experimental autoimmune encephalomyelitis (EAE) when compared with NOD controls. NOD.129(B6)-Rag1^tm1MomCd80^tm1Shr/JbsJ are valuable for unraveling the co-stimulatory pathways of T cell activation as it relates to autoimmune diseases and organ transplantation.
004672	NOD.129S2(Cg)-Stat6^tm1Gru/JbsJ	Repository-Cryopreserved
	NOD mice homozygous for the Stat6^tm1Gru mutation exhibit an increased diabetes incidence compared to NOD controls and 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. This strain can be used to look at the role of Il4 in diabetes development.
004671	NOD.129S2-Stat4^tm1Gru/JbsJ	Repository-Cryopreserved
	Stat4^tm1Gru homozygous mice are viable, fertile, normal in size, and do not display any gross physical or behavioral abnormalities. NOD female mice homozygous for the Stat4^tm1Grumutation are reported to exhibit significantly decreased diabetes, approximately 20% diabetic by 30 weeks of age, compared to Approximately 45% of the female NOD controls (Chatenoud et al, 2001). There is no detectable STAT4 protein in purified splenocytes. IL12 mediated interferon-gamma secretion, natural killer cytolytic function and Th1 cell differentiation are defective. Analysis by ELISA indicates reduction of interferon gamma and IL2 when compared to diabetic and non-diabetic NOD. Phenotype of this stock is similar to the Yang et al, model reported to have a shorter congenic interval on Chromosome 1 including an NOD-derived Idd5. This model is useful for looking at the role of IL12 in diabetes development.
004762	NOD.129S4-Cd86^tm1Shr/JbsJ	Repository-Cryopreserved
	The NOD.129S4-Cd86^tm1Shr/JbsJ homozygous mice fail to produce functional protein in T cells. Mice carrying this allele are protected from diabetes. Some homozygote mice have delayed onset peri-insulitis, which does not progress to severe insulitis. Beginning at 20 weeks of age, homozygous mice begin developing spontaneous autoimmune peripheral polyneuropathy marked by symmetrical mild hind limb paralysis. By 32 weeks of age 100% female and 30% males are severely affected with hind limb paralysis and moderate foreleg paralysis. Histological evaluation shows severe inflammation and mononuclear infiltrates in the peripheral nervous system. Skeletal muscle of severely affected mice showed focal neurogenic atrophy, but no cellular infitration. No detectable lesions were found in the brain or spinal cord. This phenotype has not been observed on C57BL/6 or 129 backgrounds (Salomon et al, 2001). NOD.129S4- Cd86^tm1Shr /JbsJ provides a useful model for studyin ..... For more information please see the full descriiption on the strain data sheet
006698	NOD.Cg-Il4^tm1Lky/JbsJ	Repository-Cryopreserved
	A "knock-in" replaces the endogenous gene with an Il4/IRES/EGFP bicistronic construct, which places both IL4 and EGFP expression under the control of the endogenous Il4 gene regulatory elements. IL4 activity in these mutant mice remains intact. Cells activated to express IL4 also express EGFP allowing reliable in vivo tracking of both innate and adaptive immune cells and enabling their isolation without further stimulation. Because the IRES element promotes translational competence capable of revealing low-level transcription otherwise not apparent from the canonical 5'-cap of the mRNA, cells from these mice also can be used to report competence for IL4 production upon stimulation. This knock-in allele has been backcrossed to NOD for 15 generations. Diabetes incidence in mutant mice is reported to be about 60%, which is not statistically different from wild-type cohorts or NOD inbred mice.
005273	NOD.Cg-Rag1^tm1Mom Cd86^tm2Shr Cd80^tm1Shr/JbsJ	Repository-Cryopreserved
	Mice homozygous for the Cd80^tm1Shr and Cd86^tm2Shr mutations are deficient in both CD80 and CD86. NOD mice defiecient for CD80, CD86 and Rag1 are viable and fertile, fail to produce T or B cells, and exhibit no signs of diabetes due to the absence of lymphocytes. In an immunocompetent NOD background, the Cd86^tm2Shr and Cd80^tm1Shr mutations exacerbate diabetes onset as well as a variety of other autoimmune diseases including thyroiditis, sialitis, exocrine pancreas disease and neuropathy when compared to normal NOD controls. These mice have also been observed, by the donating investigator, to be Treg-deficient. NOD.129(B6)-Rag1^tm1Mom Cd86^tm2ShrCd80^tm1Shr/JbsJ are valuable for unraveling the co-stimulatory pathways of T cell activation and Treg function as they relate to autoimmune diseases and organ transplantation.
000269	SB/LeJ	Repository-Cryopreserved
	The SB/Le inbred strain is homozygous for both the satin (Foxq1^sa) and beige (Lyst^bg) mutations. Most of the immunological phenotype is due to the beige mutation. Homozygous mutant beige mice are characterized by a condition that closely resembles Chediak-Higashi disease in man and similar conditions in mink and cattle. Abnormal giant lysosomal granules occur in all tissues with granule-containing cells, including granulocytes, lymphocytes, cells of the liver, kidney, central nervous system, pancreas, and thyroid, and the ducts of most glands; in type II pneumocytes; in mast cells; and in retinal pigment epithelium. Granulocytes from beige mice show defective chemotaxis and reduced bactericidal activity. Beige mice are more susceptible than controls to pneumonitis and to various viral, bacterial, and parasitic infections. They have a severe deficiency of natural killer (NK) cells. Beige mice also have a defective cytotoxic T-cell and cytotoxic antibo ..... For more information please see the full descriiption on the strain data sheet
003534	STOCK Inpp5d^tm1Dmt/J	Repository-Cryopreserved
	Inpp5d (commonly called SHIP) -deficient mice are viable and fertile. However, fertility rate is 10% lower in homozygotes and lifespan is shortened in comparison to controls. Inpp5d -deficient mice exhibit dramatic chronic hyperplasia of myeloid cells resulting in splenomegaly, lymphadenopathy and myeloid infiltration of vital organs. Histological and flow studies demonstrate a substantial increase in granulocyte-macrophage/monocyte populations in bone marrow, spleen and lymph nodes. Spleens and lymph nodes are severely enlarged compared to wildtype. The difference in spleen size is apparent as early as 4 weeks of age, and by 16 weeks of age, spleens from null mice are 10 fold greater than those of wildtype mice. Neutrophils and bone marrow-derived mast cells from these mice appear to be less susceptible to apoptotic stimuli.
003262	STOCK Tg(Trp53A135V)L3Ber/J	Repository-Cryopreserved
	Mice homozygous for the (Trp53A135V)2Ber transgene are viable and fertile, but show a high incidence of tumors, particularly lung adenocarcinomas, osteosarcomas, and lymphomas. This strain may serve as a model for Li-Fraumeni syndrome.

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Stock Number	Strain Name Strain Description	Standard Supply
006775	NOD.Cg-Foxp3^sf/DoiJ	On Hold
Scurfy mice develop an X-linked lymphoproliferative disease resulting from defective T cell tolerance. By 3 weeks of age, Foxp3-deficient NOD mice suffer massive lymphoproliferation and inflammatory infiltration in lungs, liver, skin, pancreas, kidneys, stomach, colon, fat and muscles and die by three weeks of age. At 14 days of age, NOD.Foxp3-deficient mice developed exocrine pancreatitis and occasional peri-insulitis; however invasive insulitis and diabetes were not observed. In a NOD.Foxp3-deficient, BDC2.5 TCR transgenic model, mice experienced markedly decreased lymphoproliferation, yet 100% were diabetic by 20 days of age. This congenic NOD scurfy model is useful to study the role of Foxp3-dependent regulatory T cells on diabetes development.
007899	B6.129S4-Casp2^tm1Yuan/J	Under Development for Production
Mice homozygous for this caspase-2 targeted mutation are viable and fertile. As the mutation deletes the QACRG active site and the caspase-2_S sequence of the endogenous enzyme, this deletion was shown to inactivate both the long and short form of caspase-2. As such, homozygous mice exhibit defects in regulation of apoptosis; including an enlarged oocyte reserve attributed to a germ cell-intrinsic death defect during prenatal ovarian development (resistance to oocyte cell death following complete cytokine starvation or exposure to an anticancer drug), as well as accelerated motor neuron cell death and defective B lymphoblast apoptosis. In addition, caspase-2-deficient mice exhibit characteristics of premature aging (including shortened maximum lifespan, impaired hair growth, increased bone loss, reduced body fat content, and higher hepatic levels of oxidized proteins). As caspase-2 acts as an upstream regulator of cell death in many cell types, caspase-2-deficient mice may b ..... For more information please see the full description on the strain data sheet
008240	B6.129S6-Eif2ak4^tm1.2Dron/J	Under Development for Production
Mice homozygous for the GCN2.KO4 mutant locus (also called GCN2.KO4^-, GCN2^-, GCN2.KO4^ex, or GCN2-KO) are viable, fertile and overtly indistinguishable from wild-type mice, with little if any mRNA expressed from the mutant locus. Homozygous GCN2-deficiency is associated with altered inflammatory responses and altered stress responses, including sensitivity to nutritional deficiencies and aberrant eating behavior. As GCN2 is a protein kinase that phosphorylates eIF2 (eukaryotic initiation factor 2) in response to environmental stresses (amino acid starvation, proteasome inhibition and UV irradiation) to reduce global translation and activate stress-related transcription factors (such as NF-kappaB) to alleviate cellular injury or alternatively induce apoptosis, these GCN2.KO4 mutant mice may be useful for such immunology, inflammatory, immunity cell biology, or neurobiology research. Of note, mice with a conditional allele (loxP-flanked exon XII ..... For more information please see the full description on the strain data sheet
008691	B6.129X1-Ebi3^tm1Rsb/J	Under Development for Production
Mice homozygous for this Ebi3-mutant allele are viable and fertile with the donating investigator reporting no overt autoimmunity or inflammatory disease associated with the mutation. No RNA from the targeted gene is observed in splenocytes isolated from homozygotes. Ebi3-deficiency leads to impaired T_reg activity with failure to control homeostatic proliferation. Homozygotes exhibit decreased numbers and function of invariant natural killer T cells (iNKT); stimulated iNKT cells show impaired IL-4 production both in vivo and in vitro. Homozygotes are resistant to oxazolone-induced colitis (mediated primarily by T helper (Th) 2-type cytokine production by iNKT cells), whereas Ebi3-deficiency shows no affect on trinitrobenzene sulfonic acid-induced colitis (a predominantly Th1-mediated colitis model). These Ebi3-mutant strains may be useful in studying T_reg function, IL12 heterodimeric cytokines (such as IL-35 and IL-27),IFNgamma production, and Th1/Th ..... For more information please see the full description on the strain data sheet
007962	B6.FVB-Tg(MMTV-neu/OT-I/OT-II)CBnel Tg(Trp53R172H)8512Jmr/J	Under Development for Production
These compound transgenic mice carry a rat Erbb2/HER-2/neu oncogene tagged with ovalbumin epitopes OT-I and OT-II, which are recognized by T cell receptors, under the control of the MMTV promoter (termed fusion protein neu^OT-I/OT-II). In addition, this strain carries a mouse Trp53 mini-gene, harboring a G to A point mutation in codon 172 (changing Arg to His; R172H) driven by the rat whey acidic protein promoter. Approximately 85% of compound mutant females develop focal mammary tumors at 6-10 months of age. Both virgin and breeder mice develop tumors. Approximately 37% of tumor-bearing mice develop metastatic disease to the lung. High expression of neu is detected in tumor tissue while very low levels are found in lung and ovary. Female mice carrying only the neu^OT-I/OT-II mutation develop focal mammary tumors at approximately 18 months of age. This strain may be useful in studies of cancer immunotherapy.
008452	B6;129-Eif2ak4^tm1.1Dron/J	Under Development for Production
Mice homozygous for the GCN2.KO4^conditional allele (also called GCN2.KO4c) are viable and fertile, with loxP sites flanking exon XII of the targeted gene. When bred to mice that express Cre recombinase, the resulting offspring will have this region (containing amino acid residues 606-648 encoding the critical lysine 618 required for kinase activity) deleted in the cre-expressing tissue(s). GCN2 is a protein kinase that phosphorylates eIF2 (eukaryotic initiation factor 2) in response to environmental stresses (amino acid starvation, proteasome inhibition and UV irradiation) resulting in a reduction of global translation and activation of stress-related transcription factors (such as NF-kappaB). These GCN2.KO4^conditional mice may be useful in studies related to eIF2 phosphorylation in response to environmental stresses. Of note, mice with a traditional "knockout" (deletion of exon XII) are also available (see Stock No. For more information please see the full description on the strain data sheet
008074	C.129S4-Traf1^tm1Tsi/TsiPryhJ	Under Development for Production
Mice homozygous for the TRAF1 mutant allele (TRAF1^-/-) are viable and fertile. No protein expression from the targeted gene is observed in CD40-stimulated splenocytes isolated from homozygous mice. Homozygous mice on a BALB/c congenic background (BALB/c-TRAF1^-/-) exhibit acute liver injury and elevated serum liver enzymes following intratracheal TNF-alpha treatment. Furthermore, activated TRAF1^-/- T cells have significantly increased expression of Th2 cytokines (IL-4, IL-5 and IL-13) that elicit enhanced Th2 responses in vivo. BALB/c-TRAF1^-/- T cells exhibit elevated nuclear expression of NFAT-interacting protein (NIP45) and also induce significantly more intense pulmonary inflammation and higher airway hyper-responsiveness in OVA allergic inflammation models. Pulmonary leukocyte recruitment is attenuated following inhalation of lipopolysaccharide in BALB/c-TRAF1^-/- mice. Homozygous mice on a C57BL/6 congenic background ( ..... For more information please see the full description on the strain data sheet
008701	C.129X1(B6)-Ebi3^tm1Rsb/J	Under Development for Production
Mice homozygous for this Ebi3-mutant allele are viable and fertile with the donating investigator reporting no overt autoimmunity or inflammatory disease associated with the mutation. No RNA from the targeted gene is observed in splenocytes isolated from homozygotes. Ebi3-deficiency leads to impaired T_reg activity with failure to control homeostatic proliferation. Homozygotes exhibit decreased numbers and function of invariant natural killer T cells (iNKT); stimulated iNKT cells show impaired IL-4 production both in vivo and in vitro. Homozygotes are resistant to oxazolone-induced colitis (mediated primarily by T helper (Th) 2-type cytokine production by iNKT cells), whereas Ebi3-deficiency shows no affect on trinitrobenzene sulfonic acid-induced colitis (a predominantly Th1-mediated colitis model). These Ebi3-mutant strains may be useful in studying T_reg function, IL12 heterodimeric cytokines (such as IL-35 and IL-27) and IFNgamma production, and Th ..... For more information please see the full description on the strain data sheet
008242	C57BL/6-Gt(ROSA)26Sor^{tm1(Ikbkb)Rsky}/J	Under Development for Production
Mice homozygous for the R26Stop^FLikk2ca conditional allele are viable and fertile, with a loxP-flanked STOP cassette preventing transcription of the downstream bicistronic sequences (a FLAG-tagged, constitutively active form of IKbkb (IKK2ca) and EGFP). When bred to mice that express Cre recombinase, the resulting offspring will have the STOP cassette deleted in the cre-expressing tissue(s); resulting in expression of the IKK2ca as well as EGFP fluorescence. Expression of IKK2ca leads to constitutively active NF-kappaB transcription factor activity. These R26Stop^FLikk2ca mice allow inducible expression of an activated form of Ikbkb (IKK2 or IKK-beta) and subsequent activation of the NF-kappaB transcription factor pathways. For example, when bred to a strain with a Cd19 null allele and expressing Cre recombinase during the B lymphocyte development (Stock No. 006785), this ..... For more information please see the full description on the strain data sheet

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The Jackson Laboratory serves as a worldwide distributor and national repository for common and rare strains of inbred mice and mice carrying spontaneous mutations or induced mutations (i.e., transgenic, targeted/"knockout", or chemically induced mutations). At any one time, we have over 100 strains at various stages of development and colony expansion. Strains "Under Development" fall into two categories depending on the anticipated demand from the scientific community.
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