JAX Mice Database - Growth Factors/Receptors/Cytokines

Search Criteria: Research Area is "Cancer Research: Growth Factors/Receptors/Cytokines"

Strains from the Research Colonies of Jackson Laboratory Scientists
New Strains Under Development

JAX^® Mice Strains

Stock Number	Strain Name Strain Description	Standard Supply
002287	B6.129S7-Ifng^tm1Ts/J	Level 2
	Mice homozygous for the Ifng^tm1Ts 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.
100410	WBB6F1/J-Kit^W/Kit^W-v/J	Level 2
	Kit mutant mice possess pleiotropic defects in pigment-forming cells, germ cells, RBC's and mast cells. In addition, they exhibit impaired resistance to parasitic infection and an intrinsic progenitor cell defect. Kit^W-v homozygotes resemble Kit^W homozygotes in color, anemia, and germ cells, but many of them survive to maturity. The lack of germ cells in mutant mice leads to the development of some ovarian tumors (mesotheliomas and granulosa cell), associated with an overproduction of pituitary gonadotropic hormone. Kit^W/Kit^W-v double heterozygotes are viable but sterile because of germ cell deficiency. They are also mast cell deficient. Kit^W/Kit^W-v double heterozygotes lack intermediate cells, derived from melanoblasts, in the stria vascularis resulting in endocochlear degeneration, loss of endocochlear potential, and hearing impairment.
002251	B6.129P2-Il10^tm1Cgn/J	Level 3
	Mice homozygous for the Il10^tm1Cgn targeted mutation are viable and fertile when housed under specific pathogen free (SPF) conditions. Under conventional housing conditions, Il10-deficiency is associated with altered lymphocyte and myeloid profiles, elevated serum amyloid A levels, altered responses to inflammatory or autoimmune stimuli (both endogenous and induced), increased prevalence of colorectal adenocarcinoma (especially on 129/Sv and, to a lesser extent, BALB/c genetic background), and spontaneous development of chronic enterocolitis (see below). As The Jackson Laboratory Repository maintains these mice at high health status conditions (high SPF), the observed or experimentally-induced Il10-deficient phenotype may vary from that previously published using mice from conventional mouse rooms. These IL-10 mutant mice may be useful studying inflammatory bowel disease (IBD) (Crohn's disease (CD) and/or colitis), cancer, innate and adaptive immunity, a ..... For more information please see the full descriiption on the strain data sheet
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.
004326	C3Bir.129P2(B6)-Il10^tm1Cgn/Lt	Level 3
	Mice homozygous for the Il10^tm1Cgn targeted mutation are viable and fertile when housed under specific pathogen free (SPF) conditions. Under conventional housing conditions, Il10-deficiency is associated with altered lymphocyte and myeloid profiles, elevated serum amyloid A levels, altered responses to inflammatory or autoimmune stimuli (both endogenous and induced), increased prevalence of colorectal adenocarcinoma (especially on 129/Sv and, to a lesser extent, BALB/c genetic background), and spontaneous development of chronic enterocolitis (see below). As The Jackson Laboratory Repository maintains these mice at high health status conditions (high SPF), the observed or experimentally-induced Il10-deficient phenotype may vary from that previously published using mice from conventional mouse rooms. These IL-10 mutant mice may be useful studying inflammatory bowel disease (IBD) (Crohn's disease (CD) and/or colitis), cancer, innate and adaptive immunity, a ..... For more information please see the full descriiption on the strain data sheet
005557	NOD.Cg-Prkdc^scid Il2rg^tm1Wjl/SzJ	Level 3
	The NOD.Cg-Prkdc^scid Il2rg^tm1Wjl/SzJ mice, commonly known as NOD scid gamma (NSG), do not express the Prkdc gene nor the X-linked Il2rg gene. NSG 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. NSG mice 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 mutant 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. Please note that the NSG carries the tr ..... For more information please see the full descriiption on the strain data sheet
002818	B6.129-Tnfrsf1a^tm1Mak/J	Level 4
	Mice homozygous for the Tnfrsf1a^tm1Mak targeted mutation (formerly Tnfr1^tm1Mak) have normal thymocyte development, lymphocyte populations and clonal deletion of potentially self-reactive T cells. TNF signaling is largely abolished, with no TNF induction of NF-kB. Homozygous mutant mice are resistant to lethal dosages of either lipopolysaccharides or S. aureus enterotoxin but succumb to L. monocytogenes infection. TNFRSF1an may also protect against atherosclerotic lesion development in mice fed an atherogenic diet.
002693	B6.129S1-Il12b^tm1Jm/J	Level 4
	Mice homozygous for the Il12b^tm1Jmtargeted mutation have a severely restricted ability to mount a TH1 response to in vivo endotoxin administration as evidenced by decreased interferon-gamma production although IL2 (IL-2) production is not compromised. The TH2 response is enhanced as evidenced by increased secretion of IL4 (IL-4). Delayed type hypersensitivity (DTH) responses are reduced. Also see the Il12a-deficient strains (Stock No. 002691 & 002692).
004434	B6.129S4-Ccl2^tm1Rol/J	Level 4
	Mice that are homozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. No gene product is detected in lipopolysaccharide (LPS) -stimulated peritoneal macrophages isolated from homozygous mice. The numbers of peritoneal macrophages, Kupffer cell and alveolar macrophages were similar to levels found in wildtype mice. Thioglycollate induced peritonitis results in impaired recruitment of monocytes and macrophages to peritoneal cavity. Cellular recruitment to delayed-type hypersensitivity challenges and secondary granulomata is reduced. This mutant mouse strain represents a model that may be useful in studies related to leukocyte trafficking.
003288	B6.129S7-Ifngr1^tm1Agt/J	Level 4
	Mice homozygous for the Ifngr1^tm1 targeted mutation are viable and fertile with no overt abnormalities. They have normal T cell responses but are defective in natural resistance, evidenced by an increased susceptibility to infection by Listeria monocytogenes and vaccinia virus.
003008	B6;129S-Tnf^tm1Gkl/J	Level 4
	Mice homozygous for the Tnf^tm1Gkl targeted mutation are viable and fertile. Development of both lymph nodes and Peyer's patches is normal, and homozygous mutant mice show no apparent phenotypic abnormalities. Homozygous mice completely lack splenic primary B cell follicles and cannot form organized follicular dendritic cell networks and germinal centers. TNF-deficient mice treated to induce skin carcinogenesis develop significantly less benign and malignant tumors than treated wildtype mice. Nonobese homozygous mutant mice show modest decreases in body weight, epididymal fat depot weight, and percent body fat (statistically significant in males at 28 weeks of age). Further characterization indicates that 28 week old male mutant mice display lower insulin, triglyceride, and leptin levels compared to wildtype controls. Characterization of TNF deficient homozygotes injected with gold-thioglucose (GTG) to induce hyperphagic obesity indicates that the presence of TNF does ..... For more information please see the full descriiption on the strain data sheet
003243	B6;129S-Tnfrsf1a^tm1Imx Tnfrsf1b^tm1Imx/J	Level 4
	Mice homozygous for both the Tnfrsf1a^tm1Imx and Tnfrsf1b^tm1Imx targeted mutations (p55 and p75 deficient) are viable and fertile. Double homozygous mutant mice fail to bind TNF. Thymus, spleen, and other lymphoid tissue are normal, indicating that TNF is not required for normal development of these organs.
002286	C.129S7(B6)-Ifng^tm1Ts/J	Level 4
	Mice homozygous for the Ifng^tm1Ts 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.
000049	C57BL/6J-Kit^W-v/J	Level 4
	Kit mice possess pleiotropic defects in pigment-forming cells, germ cells, RBC's and mast cells. In addition, they exhibit impaired resistance to parasitic infection and an intrinsic progenitor cell defect. Kit^W-v homozygotes resemble Kit^W homozygotes in color, anemia, and germ cells, but many of them survive to maturity. The lack of germ cells in mutant mice leads to the development of some ovarian tumors (mesotheliomas and granulosa cell), associated with an overproduction of pituitary gonadotropic hormone.
000692	WB/ReJ Kit^W/J	Level 4
	Kit mice possess pleiotropic defects in pigment-forming cells, germ cells, RBC's and mast cells. In addition, they exhibit impaired resistance to parasitic infection and an intrinsic progenitor cell defect. The lack of germ cells in homozygous mutant mice leads to the development of some ovarian tumors (mesotheliomas and granulosa cell), associated with an overproduction of pituitary gonadotropic hormone.
004368	129(B6)-Il10^tm1Cgn/J	Repository- Live
	Mice homozygous for the Il10^tm1Cgn targeted mutation are viable and fertile when housed under specific pathogen free (SPF) conditions. Under conventional housing conditions, Il10-deficiency is associated with altered lymphocyte and myeloid profiles, elevated serum amyloid A levels, altered responses to inflammatory or autoimmune stimuli (both endogenous and induced), increased prevalence of colorectal adenocarcinoma (especially on 129/Sv and, to a lesser extent, BALB/c genetic background), and spontaneous development of chronic enterocolitis (see below). As The Jackson Laboratory Repository maintains these mice at high health status conditions (high SPF), the observed or experimentally-induced Il10-deficient phenotype may vary from that previously published using mice from conventional mouse rooms. These IL-10 mutant mice may be useful studying inflammatory bowel disease (IBD) (Crohn's disease (CD) and/or colitis), cancer, innate and adaptive immunity, a ..... For more information please see the full descriiption on the strain data sheet
002702	129-Ifngr1^tm1Agt/J	Repository- Live
	Mice homozygous for the Ifngr1^tm1Agt targeted mutation are viable and fertile with no overt abnormalities. They have normal T cell responses but are defective in natural resistance, evidenced by an increased susceptibility to infection by Listeria monocytogenes; and vaccinia virus.
004293	129-Shh^tm2Amc/J	Repository- Live
	Mice that are homozygous for the Shh^tm2Amc targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. This conditional mutant contains two loxP sites flanking exon 2 of the targeted allele. Cre-mediated recombination excises exon 2 and some surrounding intronic sequence, generating a null allele. When the conditional mutant is crossed with a ubiquitously-expressing Cre recombinase carrier to remove Shh activity in the early embryo, the resulting phenotype resembles the Shh null mutation. These conditional mutant mice may be mated to strains expressing Cre recombinase to study the effects of temporal and tissue-specific ablation of the targeted allele. This mutant mouse strain represents a model that may be useful in studies of developmental defects resulting from disruption of Shh-dependent pathways. When bred to a strain expressing Cre recombinase under the control of a tet ..... For more information please see the full descriiption on the strain data sheet
002250	B10.129P2(B6)-Il10^tm1Cgn/J	Repository- Live
	Mice homozygous for the Il10^tm1Cgn targeted mutation are viable and fertile when housed under specific pathogen free (SPF) conditions. Under conventional housing conditions, Il10-deficiency is associated with altered lymphocyte and myeloid profiles, elevated serum amyloid A levels, altered responses to inflammatory or autoimmune stimuli (both endogenous and induced), increased prevalence of colorectal adenocarcinoma (especially on 129/Sv and, to a lesser extent, BALB/c genetic background), and spontaneous development of chronic enterocolitis (see below). As The Jackson Laboratory Repository maintains these mice at high health status conditions (high SPF), the observed or experimentally-induced Il10-deficient phenotype may vary from that previously published using mice from conventional mouse rooms. These IL-10 mutant mice may be useful studying inflammatory bowel disease (IBD) (Crohn's disease (CD) and/or colitis), cancer, innate and adaptive immunity, a ..... For more information please see the full descriiption on the strain data sheet
006412	B6.129-Il12b^tm1Lky/J	Repository- Live
	Mice homozygous for this bicistronic "yet40" allele are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. The IRES-EYFP is inserted downstream of the endogenous stop codon, allowing for normal expression of the endogenous gene and simultaneous EYFP reporter expression. ELISA assays confirm that p40 protein is expressed at similar levels in homozygous mutant and wildtype mice. The EYFP reporter marks dendritic cell (DC) and macrophage lineage cells that produce p40 following stimulation with toll-like receptor (TLR) ligands both in vivo and in vitro. These mice may be useful for labeling activated IL12/23 p40 expressing cells in studies of immunology and immunity, TLR signal cascades, cancer immunity, and vaccine development.
006860	B6.129-Ins2^Akita Bdkrb2^tm1Jfh/SmiJ	Repository- Live
	Mice homozygous for the targeted mutation and heterozygous for the Ins2^Akita spontaneous mutation are viable and fertile. Similar to mice only heterozygous for the Ins2^Akita mutation, the double mutant mice are severely diabetic: their body weights are 70% of wildtype, they consume over 3-fold the normal amount of food, and their urinary output is approximately 20-fold more than that of wildtype mice. Double mutant mice have markedly enlarged kidneys. Urinary albumin excretion in double mutants is almost 4-fold that of either single mutant, and double mutants experience more severe nephropathy than mice that are heterozygous for the Akita mutation alone. Megsin and nephrin expression is markedly increased in double mutant mice when compared to wildtype or to mice with either single mutation alone. By 12 months of age, double mutant mice experience hair loss due to a reduction in hair follicle numbers and thinning of the dermis. Double mutants ..... For more information please see the full descriiption on the strain data sheet
008451	B6.129P(Cg)-Ptprc^a Cx3cr1^tm1Litt/LittJ	Repository- Live
	Mice that are homozygous for the CX3CR1-GFP targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. RT-PCR analysis of lymphoid tissue from homozygotes detects mutant gene product (mRNA) and no wild type gene product (mRNA). Flow cytometric analysis of peripheral blood cells identified a subset of green fluorescent cells not observed in wild type mice. Enhanced Green Fluorescent Protein (EGFP), but not the endogenous gene, is expressed in monocytes, dendritic cells, NK cells, and brain microglia, mimicking endogenous gene expression. The same subset of peripheral blood cells isolated from heterozygote mice express detectable levels of EGFP. Immunohistochemical analysis of spleen and peripheral nerve tissue from homozygotes does not detect EGFP. These mice also express the CD45.1 (Ly5.1 or Ptprc^a) allele, which is atypical for the C57BL/6 congenic background, and this marker may be used to track donor cell popul ..... For more information please see the full descriiption on the strain data sheet
005582	B6.129P-Cx3cr1^tm1Litt/J	Repository- Live
	Mice that are homozygous for the CX3CR1-GFP targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. RT-PCR analysis of lymphoid tissue from homozygotes detects mutant gene product (mRNA) and no wild type gene product (mRNA). Flow cytometric analysis of peripheral blood cells identified a subset of green fluorescent cells not observed in wild type mice. Enhanced Green Fluorescent Protein (EGFP), but not the endogenous gene, is expressed in monocytes, dendritic cells, NK cells, and brain microglia, mimicking endogenous gene expression. The same subset of peripheral blood cells isolated from heterozygote mice express detectable levels of EGFP. Immunohistochemical analysis of spleen and peripheral nerve tissue from homozygotes does not detect EGFP. These CX3CR1-GFP mutant mice may be useful in studies of leukocyte migration and trafficking, as well as for transplantation studies. Of note, CX3CR1-GFP mice are also avail ..... For more information please see the full descriiption on the strain data sheet
007572	B6.129P2(Cg)-Rorc^tm2Litt/J	Repository- Live
	Mice homozygous for this Rorc(γt^GFP (or RORγt)^GFP) mutant allele are viable and fertile. While Rorcγ mRNA is detected in liver in Rorc(γ)t^GFP homozygotes, mRNA and protein for the thymus-specific isoform (Rorcγt) encoded by the targeted allele are not detected in the thymus. EGFP expression reports Rorc(γt) transcription in the thymi of adult Rorc(γt)GFP mice. Homozygous mice exhibit abnormal lymph node, Peyer's patch, and lymphoid tissue inducer (LTi) cell development. Mice with Rorcγt-deficient T cells lack tissue-infiltrating proinflammatory T-helper cells (Th17 cells), and are protected from induced autoimmune disease (EAE) on this genetic background. The donating investigator also reports increased thymoma incidence with age in homozygotes. These RorcγtGFP mutant mice may be useful in studying immune system homeostasis, T cell repertoire selection, CD4/CD8 double positive (CD4⁺/CD8 ..... For more information please see the full descriiption on the strain data sheet
002687	B6.129P2-Ccl3^tm1Unc/J	Repository- Live
	Mice homozygous for the Scya3^tm1Unc targeted 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. Also known as macrophage inflammatory protein 1a, Mip1a.
005427	B6.129P2-Ccr5^tm1Kuz/J	Repository- Live
	At birth, mice homozygous for the targeted allele are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. No transcript is detected in splenocytes or peritoneal macrophages. Thioglycollate-elicited peritoneal macrophages from homozygotes exhibit a delayed period before reaching peak mobilization (72 hours vs. 36 for wild type mice). 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 5427. 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.
002928	B6.129P2-Cd40^tm1Kik/J	Repository- Live
	Mice homozygous for the targeted mutation are viable and fertile. Homozygous mutant mice exhibit impaired immunoglobulin class switching and germinal center formation.
002252	B6.129P2-Il2^tm1Hor/J	Repository- Live
	Homozygous mutant mice show no apparent deficit in thymocyte differentiation or selection, types and numbers of T cells from spleens and lymph nodes are comparable to those of wild-type. They do have an impaired response to polyclonal T cell activators in the absence of additional IL2, deficits in their helper function and a reduction in natural killer cell activity. There is significant pre-weaning and post-weaning loss of homozygotes on the C3H/HeJCrlBR and C57BL/6J genetic backgrounds. In addition, homozygous mice develop inflammatory bowel disease between six and 15 weeks of age and reportedly die within 10-25 weeks under conventional housing conditions. Homozygotes on the C57BL/6J genetic background show an atrophied pancreas with apparently intact islets. Homozygotes on the BALB/c genetic background do not develop inflammatory bowel disease symptoms but rather die three to five weeks postnatally of a form of hemolytic anemia. For a more detailed description please refer to the ..... For more information please see the full descriiption on the strain data sheet
002253	B6.129P2-Il4^tm1Cgn/J	Repository- Live
	Mice homozygous for the Il4^tm1Cgn targeted mutation are viable and fertile. T and B cell development is normal but IgGl and IgE levels and the ability of homozygous mutant mice to produce Th2-derived cytokines are significantly reduced.
005540	B6.129S-Tnf^tm1Gkl/J	Repository- Live
	Mice homozygous for the targeted mutation are viable and fertile. Development of both lymph nodes and Peyer's patches is normal, and homozygous mutant mice show no apparent phenotypic abnormalities. Homozygous mice completely lack splenic primary B cell follicles and cannot form organized follicular dendritic cell networks and germinal centers. TNF-deficient mice treated to induce skin carcinogenesis develop significantly less benign and malignant tumors than treated wildtype mice. Nonobese homozygous mutant mice show modest decreases in body weight, epididymal fat depot weight, and percent body fat (statistically significant in males at 28 weeks of age). Further characterization indicates that 28 week old male mutant mice display lower insulin, triglyceride, and leptin levels compared to wildtype controls. Characterization of TNF deficient homozygotes injected with gold-thioglucose (GTG) to induce hyperphagic obesity indicates that the presence of TNF does not affect the degree of obe ..... For more information please see the full descriiption on the strain data sheet
002692	B6.129S1-Il12a^tm1Jm/J	Repository- Live
	Mice homozygous for the Il12a^tm1Jm targeted mutation on a normally resistant 129/Sv genetic background are unable to restrict the progression of Leishmania major infection, demonstrating the importance of this cytokine for developing such resistance. Homozygotes are unable to mount a delayed-type hypersensitivity (DTH) reaction but a TH2 response is induced. Also known as p35. Please refer to the Il12b-deficient related targeted mutations (Stock No. 002693 and 002694). 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 a ..... For more information please see the full descriiption on the strain data sheet
003248	B6.129S1-Il12rb2^tm1Jm/J	Repository- Live
	Mice homozygous for the Il12rb2^tm1Jm targeted mutation are viable and fertile. Homozygous mutant mice do not show an increased susceptibility to infections. 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.
006848	B6.129S2(C)-Il8rb^tm1Mwm/J	Repository- Live
	The donating investigator reports that homozygous mice are viable and fertile but few pups are produced, and they need a gnotobiotic facility to thrive. Homozygous mice have several abnormalities, including neurological defects, impaired wound healing, impaired angiogenesis, and altered growth of induced/implanted tumors. Homozygotes may also exhibit splenomegaly, lymphadenopathy, and increased susceptibility to various pathogens due to impaired neutrophil recruitment and decreased pathogen clearance during innate immune responses. These mutant mice may be useful in studies of inflammation and immunology and cancer biology. 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 becom ..... For more information please see the full descriiption on the strain data sheet
002258	B6.129S2-Lta^tm1Dch/J	Repository- Live
	Mice homozygous Lta^tm1Dch targeted mutation are viable and fertile. Homozygous mutant mice show abnormal development of peripheral lymphoid organs with no detectable popliteal, inguinal, para-aortic, mesenteric, axillary, or cervical lymph nodes, and no detectable Peyer's patches. Morphological changes in the spleen white pulp were accompanied by alterations in T and B cell content. CD4⁺ and CD8⁺ T cells counts in peripheral blood are normal but there is a four-fold increase in B cells. Neutrophil, monocyte, and platelet counts are normal. The thymus contains normal numbers of CD4⁺CD8⁺, CD4⁺, CD8⁺, and CD4^-CD8^- T cells. Splenic T cells develop normal MHC class I and class II-restricted allocytotoxic responses. Also known as tumor necrosis factor beta, Tnfb.
002620	B6.129S2-Tnfrsf1b^tm1Mwm/J	Repository- Live
	Mice homozygous for a Tnfrsf1b^tm1Mwm targeted mutation (formerly Tnfr2^tm1Mwm, p75 deficient) are viable and fertile. Homozygous mutant mice show normal T-cell development and activity, but are resistant to TNF-induced cell death. Subcutaneous injections of TNF into homozygotes elicit much less tissue necrosis.
002952	B6.129S4-Il2ra^tm1Dw/J	Repository- Live
	Mice homozygous for the Il2ra^tm1Dw targeted mutation are are characterized by a lymphoproliferative disorder, hemolytic anemia, and an inflammatory bowel disease beginning at approximately 9 weeks of age; also known as p55 gene chain, Ly43, CD25.
003174	B6.129S4-Il2rg^tm1Wjl/J	Repository- Live
	Mice homozygous for the Il2rg^tm1Wjl 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.
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
003245	B6.129S7-Il1r1^tm1Imx/J	Repository- Live
	Mice homozygous for the Il1r^tm1Imx targeted mutation fail to respond to IL1. They display normal acute phase response to systemic LPS challenge, but have defective responses to local turpentine induced inflamation. Homozygotes display increased frequency and severity of S. aureus septic arthritis.
002295	B6.129S7-Il7r^tm1Imx/J	Repository- Live
	Mice homozygous for the Il7r^tm1Imx targeted mutation are viable and fertile. Newborn and young adult homozygous mutant mice have dramatically reduced thymic and splenic lymphoid cellularity in both B and T cell compartments. T cell development is affected prior to surface expression of CD4 and CD8 and prior to the initiation of T cell receptor beta chain rearrangement. B cell development is through pre-pro-B cells (Cd43⁺ HSA^dull). The phenotype in the mouse resembles human interleukin-2 receptor gamma deficiency (XSCID). IL2Rgamma has been shown to be a necessary component of the IL7R providing the biochemical basis for this condition.
006112	B6.129X1-Ela2^tm1Sds/J	Repository- Live
	Homozygous mice are viable, fertile and phenotypically normal in the absence of inflammatory stress. Homozygotes do not express the targeted gene in bone marrow myeloid cells. Homozygous mice have increased susceptibility to sepsis, morbidity, and mortality following intraperitoneal injection of Gram-negative (e.g. (K. pneumoniae and E. coli), but not Gram-positive (e.g. (S. aureus), bacteria. Despite this, mutant mice are not at increased risk to spontaneous infection. Although neutrophil, T cell, and macrophage migration/recruitment to the site of infection is unaffected in homozygous mutant mice, neutrophils show impaired bactericidal activity. Further, homozygous mice treated with a broad-spectrum inflammatory stimulus (zymosan) have impaired leukocyte firm adhesion and transmigration as well as reduced pro-inflammatory cytokine production. Upon exposure to cigarette smoke, homozygous mice are protected from the accumulation of neutrophils and macrophages in th ..... 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.
007745	B6.Cg-Mirn155^tm1.1Rsky/J	Repository- Live
	Mice homozygous for this loss-of-function/reporter allele (bic/mir-155-/-) are viable and fertile. The lacZ reporter allows the detection of bic promoter transcriptional activity using fluorescence activated cell sorting (FACS). In homozygotes, miR-155 expression is undetectable in activated splenic B cells. In heterozygotes, approximately 60% of germinal center (GC) B cells express the lacZ reporter whereas the vast majority of the non-GC B cells do not. Homozygous mice exhibit a reduced fraction of GC B cells in the gut-associated lymphoid tissue (GALT; including Peyer's patches (PPs) and mesenteric lymph nodes (mLNs)). In addition, bic/miR-155-/- B cells exhibit deficient tumor necrosis factor (TNF) and lymphotoxin-α (LT-α) cytokine production. Homozygous mice show impaired T cell-dependent antibody responses, and their T cells show a TH2 cytokine bias (an increased percentage of interleukin-4 (IL-4) producing cells and a decreased percentage of interferon-γ (IFN-& ..... For more information please see the full descriiption on the strain data sheet
000160	B6.D2-Kitl^Sl-d/J	Repository- Live
	The multiple steel mutations (Kitl^Sl) 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, steel-Dickie homozygotes (Kitl^Sl-d/Kitl^Sl-d) and compounds of steel and steel Dickie (Kitl^Sl/Kitl^Sl-d) are viable, black-eyed white, are usually sterile in one or both sexes, and have severe macrocytic anemia. 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. Primordial germ cells are absent in the nonviable steel homozygotes and severely reduced in steel Dickie and steel heterozygotes. Mast cells are virtually absent in skin and other tissu ..... For more information please see the full descriiption on the strain data sheet
008041	B6;129-Sirt1^tm1Ygu/J	Repository- Live
	Mice homozygous for this targeted allele (SirT1^co/co) are viable and fertile. A loxP-flanked neomycin cassette just upstream of exon 4 and a third loxP site downstream of exon 4 were inserted to create this targeted mutant Sirt1 allele. The floxed mutation does not affect SIRT1 protein expression in MEFs or mammary gland tissue in homozygotes. When bred to mice that express Cre recombinase, the resulting offspring have exon 4 (encoding an evolutionarily conserved Sir2 motif) deleted in cre-expressing tissue(s); (the donating investigator reports only one recombination event: complete removal of the neomycin cassette and exon 4, leaving a single loxp). These SirT1^co/co mice may be useful in generating conditional mutants for studying transcriptional regulation and the role of estrogen, insulin growth factor-1 (IGF-1), and transcription factors (including NF-kappaB) in mammary gland development, mammary cancer, apoptosis, and metabolic di ..... For more information please see the full descriiption on the strain data sheet
002782	B6;129P2-Ccr5^tm1Kuz/J	Repository- Live
	At birth, mice homozygous for the targeted allele are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. No transcript is detected in splenocytes or peritoneal macrophages. Thioglycollate-elicited peritoneal macrophages from homozygotes exhibit a delayed period before reaching peak mobilization (72 hours vs. 36 for wild type mice).
003244	B6;129S-Tnfrsf1a^tm1Imx Il1r1^tm1Imx/J	Repository- Live
	Mice homozygous for both targeted mutations (called TNFRp55(-/-)-IL-1RI(-/-), TNFR1/IL1R1 or IL-1R1/TNFR1 KO) are viable and fertile, lacking both interlekin-1 beta type 1 receptor (IL1R1) and tumor necrosis factor alpha p55 (type 1) receptor (TNFR1). Double homozygotes exhibit characteristics of both the single "knockouts" including reduced inflammatory responses, reduced delayed-type hypersensitivity response, and remain highly susceptible to infection by Listeria monocytogenes. Homozygous mutant mice also have defects in Peyer's patch development, splenic architecture, formation of germinal centers and liver regeneration. Furthermore, IL-1R1/TNFR1 KO mice exhibit alterations in rapid eye movement sleep (REMS) and non-rapid eye movement sleep (NREMS) (a sleep phenotype different from that observed for mice singly homozygous for one or the other of these cytokine receptors), as well as differences in NREMS and REMS following sleep deprivation compared to control mice.
003018	B6;129S1-Il1r1^tm1Roml/J	Repository- Live
	Mice homozygous for the Il1r1^tm1Roml targeted mutation exhibit a reduced inflammatory response and no response to interleukin-1 alpha or beta. IL1 receptor type I deficient mice have a reduced delayed type hypersensitivity response and are highly susceptible to infection by Listeria monocytogenes.
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).
008080	B6;C3-Tg(CAG-SAC/EGFP)35Rang/J	Repository- Live
	Hemizygous SAC transgenic mice have normal fertility, viability, and aging. Widespread expression of the transgene is observed in all tested tissues (with some differential tissue-specific regulation of transgene expression or protein stability reported). The SAC-GFP fusion protein is composed of the cancer-specific proapoptotic effector domain (or SAC domain) of the Par-4 gene fused to an enhanced green fluorescent protein (EGFP). As a result, SAC-GFP transgenic mice have increased resistance to spontaneous liver/spleen and TRAMP-induced prostate tumor development. The protective nature of the transgene appears to be linked to inhibition of NF-kappaB activity and induction of apoptosis. Cells derived from SAC transgenic mice grow normally in short-term culture and presence of the SAC transgene prevents oncogene-mediated cellular transformation. The donating investigator reports that EGFP expression is appropriate for immunoblots, but not sufficient enough for fluorescence of flow cyto ..... For more information please see the full descriiption on the strain data sheet
000231	B6C3Fe a/a-Csf1^op/J	Repository- Live
	Mice homozygous for the osteopetrosis spontaneous mutation (Csf1^op) are viable and exhibit osteopetrosis. The osteoclasts are the primary cell type affected in homozygous mutant mice. This results in a generalized macrophage deficiency, monocytopenia, and defective bone remodeling. Homozygous mutant mice also have abnormal calcium regulation, impaired dental growth and female mice fail to lactate. Total leukocyte counts are reduced and marrow cells are decreased to one-tenth of normal control mice. Homozygous mutant mice have a deficient microglia and macrophage response, and therefore may be useful tools to study the role of glia in neurological disease if mated to transgenic models of neurodegenerative disease.
002496	BALB/c-Il4^tm2Nnt/J	Repository- Live
	Mice homozygous for the Il4^tm2Nnt targeted mutation are viable and fertile. T and B cell development is normal but IgGl and IgE levels and the ability of homozygous mutant mice to produce Th2-derived cytokines are significantly reduced. Susceptible to infection by Leishmania major despite deficiency in IL4.
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.
004333	C.129P2(B6)-Il10^tm1Cgn/J	Repository- Live
	Mice homozygous for the Il10^tm1Cgn targeted mutation are viable and fertile when housed under specific pathogen free (SPF) conditions. Under conventional housing conditions, Il10-deficiency is associated with altered lymphocyte and myeloid profiles, elevated serum amyloid A levels, altered responses to inflammatory or autoimmune stimuli (both endogenous and induced), increased prevalence of colorectal adenocarcinoma (especially on 129/Sv and, to a lesser extent, BALB/c genetic background), and spontaneous development of chronic enterocolitis (see below). As The Jackson Laboratory Repository maintains these mice at high health status conditions (high SPF), the observed or experimentally-induced Il10-deficient phenotype may vary from that previously published using mice from conventional mouse rooms. These IL-10 mutant mice may be useful studying inflammatory bowel disease (IBD) (Crohn's disease (CD) and/or colitis), cancer, innate and adaptive immunity, a ..... For more information please see the full descriiption on the strain data sheet
002691	C.129S1(B6)-Il12a^tm1Jm/J	Repository- Live
	Mice homozygous for the Il12a^tm1Jm targeted mutation on a normally resistant 129/Sv genetic background are unable to restrict the progression of Leishmania major infection, demonstrating the importance of this cytokine for developing such resistance. Homozygotes are unable to mount a delayed-type hypersensitivity (DTH) reaction but a TH2 response is induced. Also known as p35. Please refer to the Il12b-deficient related targeted mutations (002693 & 002694). 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.
002694	C.129S1-Il12b^tm1Jm/J	Repository- Live
	Mice homozygous for the Il12b^tm1Jm targeted mutation have a severely restricted ability to mount a TH1 response to in vivo endotoxin administration as evidenced by decreased interferon-gamma production although IL2 (IL-2) production is not compromised. The TH2 response is enhanced as evidenced by increased secretion of IL4 (IL-4). Delayed type hypersensitivity (DTH) responses are reduced. Also see the Il12a-deficient strains (002691 & 002692).
002724	C.129S2(B6)-Il8rb^tm1Mwm/J	Repository- Live
	Mice homozygous for the Il8rb^tm1Mwm targeted mutation are viable and fertile although the reproductive rate is lower than normal wildtype siblings. Homozygous mutant mice have splenomegaly, lymphadenopathy, and impaired neutrophil migration. Formerly referred to as Cmkar2, chemokine (C-X-C) receptor 2; also called Il8r, interleukin 8 receptor.
002518	C57BL/6-Il4^tm1Nnt/J	Repository- Live
	Mice homozygous for the Il4^tm1Nnt targeted mutation are viable and fertile. T and B cell development is normal but IgGl and IgE levels and the ability of homozygous mutant mice to produce Th2-derived cytokines are significantly reduced.
003242	C57BL/6-Tnfrsf1a^tm1Imx/J	Repository- Live
	Mice homozygous for the Tnfrsf1a^tm1Imx targeted mutation (formerly Tnfr1^tm1Imx, p55 deficient) show defects in resistance to intracellular pathogens and are resistant to the lethal effects of LPS administration in conjunction with D-galactosamine. Pulmonary inflammatory responses are diminished in p55 deficient mice. There are also defects in Peyer's patch development, splenic architecture, formation of germinal centers, and liver regeneration. TNFRSF1 deficient mice display increased susceptibility to atherosclerosis when maintained on a high fat diet.
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
007799	NOD.Cg-Rag1^tm1Mom Il2rg^tm1Wjl/SzJ	Repository- Live
	Females homozygous for both the Rag1^null and IL2rγ^null mutations (and males homozygous for Rag1^null and hemizygous for the X-linked IL2rγ^null mutation) are viable and fertile. When compared to NOD-scid IL2rg^null (Stock No. 005557), these NOD-Rag1^null IL2rγ^null mice tolerate much higher levels of irradiation conditioning. Additionally, NOD-Rag1^null IL2rγ^null mice support higher levels of both human cord blood stem cell engraftment following irradiation-conditioning (leading to multi-lineage hematopoietic cell populations and a complete repertoire of human immune cells, including human T cells) and human peripheral blood mononuclear cells engraftment in unconditioned adult mice with respect to NOD-Rag1^null (Stock No. For more information please see the full descriiption on the strain data sheet
000693	WC/ReJ Kitl^Sl/J	Repository- Live
	The multiple steel mutations (Kitl^Sl) 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. Kitl^Sl/Kitl^Sl-d) are viable, black-eyed white, are usually sterile in one or both sexes, and have severe macrocytic anemia. 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. 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 ..... For more information please see the full descriiption on the strain data sheet
100401	WCB6F1/J Kitl^Sl Kitl^Sl-d	Repository- Live
	The multiple steel mutations (Kitl^Sl) 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). Many steel alleles cause severe anemia resulting in death in utero of homozygous mutant mice. However, mice homozygous for some steel mutations and compound heterozygotes for two steel alleles (e.g., Kitl^Sl/Kitl^Sl-d) are viable and have black eyes and a white coat; they have severe macrocytic anemia, and both sexes are usually sterile due to failure of germ cells to migrate correctly during development. Mice heterozygous for a single steel mutation have diluted coat color with a small amount of white spotting, are viable and fertile, and may have a slight macrocytic anemia. Primordial germ cells are absent in the nonviable steel homozygotes and severely reduced in steel heterozygotes. Mast cells are virtuall ..... For more information please see the full descriiption on the strain data sheet
004166	129-Itgb5^tm1Des/J	Repository-Cryopreserved
	Mice that are homozygous for the Itgb5^tm1Des targeted mutation are viable, fertile, normal in size, and do not display any gross physical or behavioral abnormalities. No Itgb5 gene product (mRNA or protein) is detected. Homozygotes display defects in VEGF-mediated vascular permeability. Cultured keratinocytes derived from homozygous mutant animals display impaired adhesion and migration on vitronectin-coated surfaces.
002497	129-Ntf5^tm1Jae/J	Repository-Cryopreserved
	Mice homozygous for the targeted mutation are viable and fertile. Homozygous mutant mice lose sensory neurons in the nodose-petrosal and geniculate ganglia. However, they do not show loss of facial nucleus motor neurons, sympathetic neurons of the superior cervical ganglion, or dopaminergic neurons in the substantia nigra.
000090	129S1/Sv-Oca2⁺ Tyr⁺ Kitl^Sl-J/J	Repository-Cryopreserved
	The multiple steel mutations (Kitl^Sl) 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. Kitl^Sl/Kitl^Sl-d) are viable, black-eyed white, are usually sterile in one or both sexes, and have severe macrocytic anemia. 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. 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 a ..... For more information please see the full descriiption on the strain data sheet
000004	ABP/LeJ	Repository-Cryopreserved
	Mice homozygous for the Tgfa^wa1 spontaneous mutation are recognizable at 2 or 3 days of age by their curly whiskers. The first coat is strongly waved and straight in later coats. Most of the whiskers also become straight, but the guard hairs are curved and shorter than normal. Some homozygotes have eyelids open at birth. Mice homozygous for the recessive Adamts20^bt mutation have a dorsal and a ventral unpigmented patch posterior to the midline of the trunk with the dorsal patch usually being larger than the ventral patch. These patches run in a more transverse orientation across the mouse than lengthwise and often extend around the sides of the mouse to form a white belt. The size of the patches can vary from approximately 1 to 20 percent of the surface. Unlike other spotting mutations, no variability in phenotype was identified when belted was transferred onto the C57BL/6J or JU/CtLm backgrounds (Lamoreaux 1999). Murray and Snell reported findin ..... For more information please see the full descriiption on the strain data sheet
000599	B6 x B6CBCa A^w-J/A-T(5;13)264Ca Kit^W-v/J	Repository-Cryopreserved

006564	B6(C)-Kit^W-41J Gusb^mps/BrkJ	Repository-Cryopreserved
	Mice homozygous for the "mps" (mucopolysaccharidosis type VII or MPS VII) mutation are devoid of expression of the lysosomal enzyme beta glucuronidase. Homozygous animals are viable, but females have a deficiency in lactation. Skeletal and connective tissue anomalies in both males and females are believed to prevent successful breeding. As this mutation is recessive, heterozygous mice are phenotypically similar to wildtype. Homozygotes exhibit short and thickened long bones (smaller than heterozygous or wildtype littermates), "pug type" appearance of the nose, hepatomegaly, splenomegaly, corneal clouding, and deafness. In appearance, homozygous Kit^W-41J mice are mostly white with black eyes and brown or grey spots. MPS VII mice are a model of the beta glucuronidase enzyme deficiency in humans called Sly Disease. They may be useful in developing new therapies (enzyme replacement, cell transplantation, gene therapy) broadly applicable to other lysosomal storage disease ..... For more information please see the full descriiption on the strain data sheet
003509	B6.129-Blmh^tm1Geh/J	Repository-Cryopreserved
	Bleomycin (BLM) is a clinically used glycopeptide anticancer agent. It is deaminated in vitro by BLMH. Blmh null mice have decreased viability and fertitility. Only about 65% of the expected number survive the neonatal period. Mice lacking Blmh exhibit variably penetrant tail dermatitis that resembles rodent ringtail. This resembles skin lesions in humans with pellagra, necrolytic migratory erythema, and acrodermatitis enteropathica. Null mice also are more sensitive to acute BLM lethality and develop pulmonary fibrosis following BLM treatment.
002938	B6.129-Kdr^tm1Jrt/J	Repository-Cryopreserved
	Mice homozygous for the Kdr^tm1Jrt targeted mutation (formerly called Flk1) die at ~E8.5-E9.5 due to defects in hematopoietic and endothelial development. Embryos lack blood islands at E7.5 and fail to form organized blood vessels. There is severe reduction in hematopoietic progenitor cells.
002619	B6.129-Tgfb3^tm1Doe/J	Repository-Cryopreserved
	Mice homozygous for the Tgfb3^tm1Doe mutation are not viable. Mice exhibit cleft palate and possibly developmental defects in the lung.
002816	B6.129P2-Il2rb^tm1Mak/J	Repository-Cryopreserved
	Mice homozygous for the Il2rb^tm1Mak targeted mutation have dysfunctional T and B cell compartments. Effects of the mutation include myeloproliferative disorder, splenomegaly and lymphoadenopathy by 3 weeks of age. Mice have high serum immunoglobulins G1 and E and autoantibodies leading to hemolytic anemia. Lifespan is approximately 12 weeks.
002405	B6.129P2-Ncam1^tm1Cgn/J	Repository-Cryopreserved
	Mice homozygous for the Ncam1^tm1Cgn targeted mutation show a 10% reduction in overall brain weight and 36% reduction in olfactory bulb size. Motor end plates were 14% smaller in NCAM-deficient mice compared to controls, and the formation of junctional folds was delayed. They also show deficits in spatial learning and in the amount of protein-bound alpha-(2,8)-linked polysialic acid. Both homozygous and heterozygous mutant mice are reportedly more aggressive than wildtype controls.
003142	B6.129P2-Prlr^tm1Cnp/J	Repository-Cryopreserved
	There is complete female sterility due to abberant estrous cycles, abnormal preimplantation development of eggs, no implantation of blastocysts, lack of pseudopregnancy. Males show slightly delayed fertility. Mammary development is markedly affected. Homozygotes have no mammary development and do not lactate. Heterozygotes are unable to lactate after the first pregnancies, but attain some degree of lactation as they age or after multiple pregnancies. Serum prolactin levels are increased 60 - 100 fold in both males and females. Maternal behavior is diminished in pimiparous and nulliparous animals. Bone remodelling is decreased in homozygote mutants.
002219	B6.129P2-Tgfa^tm1Ard/J	Repository-Cryopreserved
	Mice homozygous for the Tgfa^tm1Ard mutation develop normally, are of normal size, weight, and health, and are fertile. They display a pronounced waviness in the coat and whiskers, and dramatic derangement of the hair follicles. Older homozygous mice occasionally show some corneal inflammation that may be the result of a defect in wound healing.
002984	B6.129S1-Il12rb1^tm1Jm/J	Repository-Cryopreserved
	Mice homozygous for the Il12rb^tm1Jm targeted mutation are viable and fertile. Con A-activated splenocytes from homozygous mutant mice express only low affinity IL12-binding sites and fail to proliferate or produce interferon gamma in response to IL12. In addition, NK lytic activity in response to IL12 is defective. In vivo immune responses to endotoxin are also impaired.
002612	B6.129S2-Bmp4^tm1Blh/J	Repository-Cryopreserved
	Mice homozygous for the Bmp4^tm1Blh targeted mutation mutation die early in embryogenesis. Fifteen to twenty percent of heterozygous mice show developmental defects including polydactyly, craniofacial defects, and cystic kidneys. Heterozygotes have also been reported to show eye abnormalities.
002248	B6.129S2-Gzmb^tm1Ley/J	Repository-Cryopreserved
	Mice homozygous for the Gzmb^tm1Ley mutation are viable and fertile. Lymphopoiesis and peripheral lymphoid tissue development is normal. T cell responses to mitogenic (Con A and IL2) and allogeneic (mixed lymphocyte culture) stimulation are unaffected. There is a 10-fold reduction in condensation of chromatin resulting in nuclear crescents and pyknosis when Gzmb^tm1Ley CTL are used as effectors. Thus, activated CTL from homozygous mice are deficient in the early induction of DNA fragmentation and apoptosis in allogeneic target cells. Formerly called Ctla1.
003098	B6.129S2-Ntrk2^tm1Bbd/J	Repository-Cryopreserved
	Mice homozygous for this Ntrk2^tm targeted mutation (commonly referred to as trkB) die by 2-3 weeks of age. Homozygous mutant mice show a complete lack of nodose, vestibular, and cochlear neurons. In addition, mice display CNS deficits including cell death in dentate gyrus, cortical layers II-III and V-VI, striatum and thalamus.
002220	B6.129S2-Tgfb1^tm1Doe/J	Repository-Cryopreserved
	It has been reported that mice homozygous for Tgfb1^tm1Doe mutation develop normally but die approximately two to three weeks after birth. It was also reported that this strain shows a lower than expected number of homozygous births (~14% from heterozygous matings on a mixed genetic background) suggesting that in utero death may occur (See Husbandry). Homozygous mice usually die within a few days of the onset of a wasting syndrome. Death is due to a massive inflammatory cell response and tissue necrosis. A multifocal mixed inflammatory cell infiltration occurs into numerous organs, particularly the heart and stomach. Heterozygous mice do not differ from normal wildtype littermates. This strain may provide a model for human immune and inflammatory diseases such as autoimmune disease, transplant rejection and graft versus host reactions.
002275	B6.129S4-Ntf3^tm1Jae/J	Repository-Cryopreserved
	Mice homozygous for the Ntf3^tm1Jae targeted mutation are smaller than their normal littermates and most die shortly after birth. Survivors die prior to weaning. They display limb ataxia, an inability to position the limbs properly when attempting to move, and there is a tendency for all four limbs to intermittently stiffen in an extensor posture. Autopsy showed all peripheral ganglia markedly smaller in the mutant. Spinal proprioceptive afferents and their peripheral sense organs are completely absent. Heterozygous mice appear normal; however, the number of muscle spindles in heterozygotes is half that of normal wildtype siblings. There is approximately a 50% reduction in the sympathetic superior cervical ganglion (SCG) neurons caused by excessive apoptosis of sympathetic neuroblasts during neurogenesis.
003541	B6.129S4-Ntf3^tm2Jae/J	Repository-Cryopreserved
	This strain has loxP sites located on either side of the Ntf3 exon 2. Mice homozygous for this allele are viable, fertile and without behavioral abnormalities. If this strain is crossed with a transgenic strain bearing Cre recombinase, expression of the Ntf3 gene in offspring can be blocked in a tissue-specific manner depending on the promoter controlling the recombinase. Strains under the control of the rat nestin promoter block expression in the central nervous system; see strains 002275 and 002276.
003312	B6.129S7-Ngf^tm1Gne/J	Repository-Cryopreserved
	Mice homozygous for the disrupted Ngfb gene are born alive, but are smaller, on average, than wild type or heterozygous individuals. They fail to thrive and have a life span of 4 weeks or less, often dying within the first three days of life. Mutant mice are developmentally delayed and exhibit severe cell loss in sympathetic ganglia. They exhibit a more selective cell loss in sensory ganglia, revealing a reduced number of small cells in the dorsal root ganglia (DRG) at 3 days of age, while large cell numbers in the DRG are comparable to wild type mice. Mutant mice also display a decreased responsiveness to pain in comparison to +/+ or +/- littermates. During the first month of life, survival of cholinergic neurons in the basal forebrain does not appear to be affected by absence of NGF, as these cells were observed to differentiate and maintain their phenotype throughout the life span of homozygous mutant mice. Mice heterozygous for the Ngfb gene disruption exhibit normal ..... For more information please see the full descriiption on the strain data sheet
003246	B6.129S7-Tnfrsf1b^tm1Imx/J	Repository-Cryopreserved
	Mice homozygous for a Tnfrsf1b^tm1Imx targeted mutation (formerly Tnfr2^tm1Imx, p75 deficient) are viable and fertile. T cells from homozygous mutant mice display defects in activation induced cell death in vitro and dramatically elevated levels of circulating Tnf following systemic challenge with LPS. Pulmonary neutrophil influx is exacerbated in p75 deficient mice in a model of hypersensitivity pneumonitis.
003126	B6.129X1-Grpr^tm1Jfb/J	Repository-Cryopreserved
	Mice homozygous (females) or hemizygous (males) for the X-linked Grpr^tm1Jfb targeted mutation are viable with no gross phenotypic abnormalities observed. There is a deficiency in bombesin-induced mediation of satiety as measured by glucose intake. A modest increase in body weight is observed in older animals. At 18-20 months of age, hemizygous males (N = 8) are 44.5g ± 5.1 (mean ± std dev) and wildtype littermates (N = 8) are 38.3g ± 5.1 (L. Hampton, unpublished observation). We have recently observed head tilts and bobbing in the hemizygous males in our production colony. The donating investigator of this strain has also observed this phenotype and considers it a mutation not related to the gene. We are working to remove this phenotype, but we will continue to ship from the colony while we finish this process.
000495	B6.C-H38^c/By-Kit^W-56J/J	Repository-Cryopreserved

000560	B6.C-H7^b/By Kit^W-50J/J	Repository-Cryopreserved

000122	B6.C3-Kit^W-44J/J	Repository-Cryopreserved
	Kit^W-44J heterozygotes have white-tipped feet and a white tail tip although the belly spot standardly found in Kit^W* mutations is very small in this mutant, sometimes restricted to only a few hairs. Homozygotes have a flecked pelt that is predominantly white, especially ventrally, with pigmented patches particularly at the lateral borders. The pigmentation fades with age yielding black-eyed white mice by approximately 9 months of age. While many Kit^W-44J homozygotes are viable, fertility is diminished. Homozygous females have greatly reduced fertility and gonads that are smaller in size with reduced activity. Homozygous males are sterile although spermatogenesis occurs. The Kit^W-44J allele does not produce anemia in either its heterozygous or homozygous state. The red blood cell count, white blood cell count, hematocrit, and mean cell volume are normal. However, bone marrow transplantation experiments reveal that t ..... For more information please see the full descriiption on the strain data sheet
000991	B6.C58-Kit^W-57J/J	Repository-Cryopreserved

005912	B6.Cg-Il10^tm1Cgn (D3Mit49-D3Mit348)/Lt	Repository-Cryopreserved
	Homozygous mice are IL10-deficient and develop spontaneous colitic lesions in the cecum and large intestine as early as 6-8 weeks of age. The severity and age of onset of colitis varies with the donor type and location of the cytokine deficiency colitis susceptibility 1 (Cdcs1) interval. Generally, the C3H/HeJBir region encompassed by D3Mit348 through D3Mit254 (127.7-132.5 megabases) confers increased colitis susceptibility on the B6.129P2-Il10^tm1Cgn background (Beckwith J, et al., 2005). Mice on the B6.129P2-Il10^tm1Cgn background are prone to rectal prolapse particularly when carrying susceptibility alleles from Chromosome 3. Granulocyte populations in peripheral blood increase upon lesion development and provide a robust non-lethal assessment of colitis severity.
000133	B6.Cg-Kit^W-24J/J	Repository-Cryopreserved

000139	B6.Cg-Kit^W-25J/J	Repository-Cryopreserved

000164	B6.Cg-Kit^W/J	Repository-Cryopreserved

002993	B6.Cg-Kitl^Sl-18H/EiJ	Repository-Cryopreserved

000124	B6.Cg-Kitl^Sl Krt71^Ca/J	Repository-Cryopreserved
	The multiple steel mutations (Kitl^Sl) 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. Kitl^Sl/Kitl^Sl-d are viable, black-eyed white, are usually sterile in one or both sexes, and have severe macrocytic anemia. 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. 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 adva ..... For more information please see the full descriiption on the strain data sheet
000194	B6.Cg-Lx Kit^W-v/J	Repository-Cryopreserved
	Kit mice possess pleiotropic defects in pigment-forming cells, germ cells, RBC's and mast cells. In addition, they exhibit impaired resistance to parasitic infection and an intrinsic progenitor cell defect. Kit^W-v homozygotes resemble Kit^W homozygotes in color, anemia, and germ cells, but many of them survive to maturity. The lack of germ cells in mutant mice leads to the development of some ovarian tumors (mesotheliomas and granulosa cell), associated with an overproduction of pituitary gonadotropic hormone. Heterozygous lx mice show preaxial polydactyly (including hyperphalangy of the first digit) of the hindfeet. Homozygotes show preaxial polydactyly or oligodactyly of the hindfeet, reduction of the tibia, loss of part of the femur and pubis, decrease in number of presacral vertebrae, and anomalies of the urogenital system including horseshoe kidney, hydronephrosis, and hydroureter. Although homozygous Kit^W-v/ ..... For more information please see the full descriiption on the strain data sheet
002863	B6.Cg-Tgfa^wa1/J	Repository-Cryopreserved
	Mice homozygous for the Tgfa^wa1 spontaneous mutation are recognizable at 2 or 3 days of age by their curly whiskers. The first coat is strongly waved and straight in later coats. Most of the whiskers also become straight, but the guard hairs are curved and shorter than normal. Some homozygotes have eyelids open at birth. Ventricular enlargement and striatal reduction is observed in adult homozygous wa1 mice. The phenotype is more severe in males. In addition, adult males exhibit reduced hippocampal volume and impaired auditory and contextural fear learning. Both sexes demonstrate an abnormal fear response. Peripubertal mice do not exhibit behavioral deficits despite slight forebrain structural abnormalities. (Koshibu K, et al., 2005)
000171	B6.D2-Kit^W-45J/J	Repository-Cryopreserved

001563	B6.D2-Kit^W-73J/J	Repository-Cryopreserved

001177	B6.LP-Kit^W-49J/J	Repository-Cryopreserved

002398	B6;129P2-Csf3^tm1Ard/J	Repository-Cryopreserved
	Mice homozygous for the Csf3^tm1Ard targeted mutation are viable and fertile but are characterized by chronic neutropenia. Peripheral blood neutrophil levels of homozygotes are 20 to 30% of wildtype. There is a 50% reduction of granulocyte, macrophage and blast progenitor cells in marrow of homozygous mice and an impaired resistance to infection with Listeria monocytogenes.
003284	B6;129S1-Il1rap^tm1Roml/J	Repository-Cryopreserved
	Interleukin-1 receptor accessory protein (Il1rap)-null mice are viable and fertile. They exhibit loss of Il-1 receptor mediated signal transduction. Treatment of these mutant mice with IL-1 Alpha or IL-1 Beta results in no detectable increase in IL-6 levels in serum and fails to induce increased expression of E-selectin mRNA.
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.
002247	B6;129S2-Gzmb^tm1Ley/J	Repository-Cryopreserved
	Mice homozygous for the Gzmb^tm1Ley mutation are viable and fertile. Lymphopoiesis and peripheral lymphoid tissue development is normal. T cell responses to mitogenic (Con A and IL2) and allogeneic (mixed lymphocyte culture) stimulation are unaffected. There is a 10-fold reduction in condensation of chromatin resulting in nuclear crescents and pyknosis when Gzmb^tm1Ley CTL are used as effectors. Thus, activated CTL from homozygous mice are deficient in the early induction of DNA fragmentation and apoptosis in allogeneic target cells. Formerly called Ctla1.
002257	B6;129S2-Lta^tm1Dch/J	Repository-Cryopreserved
	Mice homozygous Lta^tm1Dch targeted mutation are viable and fertile. Homozygous mutant mice show abnormal development of peripheral lymphoid organs with no detectable popliteal, inguinal, para-aortic, mesenteric, axillary, or cervical lymph nodes, and no detectable Peyer's patches. Morphological changes in the spleen white pulp were accompanied by alterations in T and B cell content. CD4⁺ and CD8⁺ T cells counts in peripheral blood are normal but there is a four-fold increase in B cells. Neutrophil, monocyte, and platelet counts are normal. The thymus contains normal numbers of CD4⁺CD8⁺, CD4⁺, CD8⁺, and CD4^-CD8^- T cells. Splenic T cells develop normal MHC class I and class II-restricted allocytotoxic responses. Also known as tumor necrosis factor beta, Tnfb.
002544	B6;129S2-Ntrk2^tm1Bbd/J	Repository-Cryopreserved
	Mice homozygous for this Ntrk2^tm targeted mutation (commonly referred to as trkB) die by 2-3 weeks of age. Homozygous mutant mice show a complete lack of nodose, vestibular, and cochlear neurons. In addition, mice display CNS deficits including cell death in dentate gyrus, cortical layers II-III and V-VI, striatum and thalamus.
002481	B6;129S2-Ntrk3^tm1Bbd/J	Repository-Cryopreserved
	Mice homozygous for this Ntrk3^tm1 targeted mutation (commonly referred to as trkC) die by 2-3 weeks of age. Homozygous mutant mice lack proprioceptive and cochlear neurons and have a reduction in vestibular neurons.
002462	B6;129S4-Il2ra^tm1Dw/J	Repository-Cryopreserved
	Mice homozygous for the Il2ra^tm1Dw targeted mutation are are characterized by a lymphoproliferative disorder, hemolytic anemia, and an inflammatory bowel disease beginning at approximately 9 weeks of age; also known as p55 gene chain, Ly43, CD25.
002296	B6;129S7-Il7r^tm1Imx/J	Repository-Cryopreserved
	Mice homozygous for the Il7r^tm1Imx targeted mutation are viable and fertile. Newborn and young adult homozygous mutant mice have dramatically reduced thymic and splenic lymphoid cellularity in both B and T cell compartments. T cell development is affected prior to surface expression of CD4 and CD8 and prior to the initiation of T cell receptor beta chain rearrangement. B cell development is through pre-pro-B cells (Cd43⁺ HSA^dull). The phenotype in the mouse resembles human interleukin-2 receptor gamma deficiency (XSCID). IL2Rgamma has been shown to be a necessary component of the IL7R providing the biochemical basis for this condition.
002402	B6;129S7-Lifr^tm1Imx/J	Repository-Cryopreserved

006147	B6;FVB-Tg(Sfpi1,-EGFP)7Dgt/J	Repository-Cryopreserved
	Hemizygous mice are viable and fertile with no gross or behavioral abnormalities. Flow cytometry identifies enhanced green fluorescent protein (EGFP) reporter expression in a pattern similar to the endogenous gene; in bone marrow, high expression is observed in myeloid cells, and to a lesser degree in B lymphocytes and erythroid cells. Expression in spleen is consistent with B cells and natural killer cells, while no expression is observed in thymus. These mice may be useful in studies of hematopoietic cell development, transcription factor pathways, and leukemia (including erythroleukemia).
000350	B6By.Cg-Kit^W-v Mitf^Mi-wh T/J	Repository-Cryopreserved
	Kit mice possess pleiotropic defects in pigment-forming cells, germ cells, RBC's and mast cells. In addition, they exhibit impaired resistance to parasitic infection and an intrinsic progenitor cell defect. Kit^W-v homozygotes resemble Kit^W homozygotes in color, anemia, and germ cells, but many of them survive to maturity. The lack of germ cells in mutant mice leads to the development of some ovarian tumors (mesotheliomas and granulosa cell), associated with an overproduction of pituitary gonadotropic hormone. Mutations at the Mitf locus affect eye size, pigmentation, and the capacity for secondary bone resorption. Mice homozygous for the white allele (Mitf^Mi-wh) display an overall absence of pigment cells with the exception of the retina which expresses a few giving the eye a small amount of pigment. Homozygotes show slight microphthalmia but a normal skeleton. Heterozygotes (Mitf^Mi-wh/+) have a dilut ..... For more information please see the full descriiption on the strain data sheet
000553	B6EiC3Sn a/A-Egfr^wa2 Wnt3a^vt/J	Repository-Cryopreserved
	Mice homozygous for the spontaneous waved 2 mutation (Egfr^wa2) are recognizable at 2 to 3 days by curly whiskers. The first coat is waved but later coats are not; vibrissae usually remain curled and the guard hairs curved. Some homozygotes have eyelids open at birth. Fertile mutant females have impaired lactation. Mice homozygous for the vestigial tail spontaneous mutation (Wnt3a^vt) have very short tails, few presacral vertebrae, and abnormal formation of the lumbar vertebrae.
002229	C.129P2(B6)-Il2^tm1Hor/J	Repository-Cryopreserved
	Homozygous mutant mice for the Il2^tm1Hor targeted mutation show no apparent deficit in thymocyte differentiation or selection, types and numbers of T cells from spleens and lymph nodes are comparable to those of wildtype. They do have an impaired response to polyclonal T cell activators in the absence of additional IL2, deficits in their helper function and a reduction in natural killer cell activity. There is significant pre-weaning and post-weaning loss of homozygotes on the C3H/HeJCrlBR and C57BL/6J genetic backgrounds. In addition, homozygous mice develop inflammatory bowel disease between 6 and 15 weeks of age and reportedly die within 10-25 weeks under conventional housing conditions. Homozygotes on the C57BL/6J genetic background show an atrophied pancreas with apparently intact islets. Homozygotes on the BALB/c genetic background do not develop inflammatory bowel disease symptoms but rather die 3-5 weeks postnatally of a form of hemolytic anemia. For a more de ..... For more information please see the full descriiption on the strain data sheet
003017	C.129S1-Il12rb1^tm1Jm/J	Repository-Cryopreserved
	Mice homozygous for the Il12rb^tm1Jm targeted mutation are viable and fertile. Con A-activated splenocytes from homozygous mutant mice express only low affinity IL12-binding sites and fail to proliferate or produce interferon gamma in response to IL12. In addition, NK lytic activity in response to IL12 is defective. In vivo immune responses to endotoxin are also impaired.
003480	C.129S2(B6)-Il4^tm1Gru/J	Repository-Cryopreserved
	This strain was made using gene targeting in embryonic stem cells to modify the Il4 locus by knocking-in a transmembrane domain. Expression of Il4 in a membrane-bound form provides a novel method for the identification and characterization of Il4-producing cells.
003169	C.129S4-Il2rg^tm1Wjl/J	Repository-Cryopreserved
	Mice homozygous for the Il2rg^tm1Wjl 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.
002228	C3.129P2(B6)-Il2^tm1Hor/J	Repository-Cryopreserved
	Homozygous mutant mice for the Il2^tm1Hor targeted mutation show no apparent deficit in thymocyte differentiation or selection, types and numbers of T cells from spleens and lymph nodes are comparable to those of wildtype. They do have an impaired response to polyclonal T cell activators in the absence of additional IL2, deficits in their helper function and a reduction in natural killer cell activity. There is significant pre-weaning and post-weaning loss of homozygotes on the C3H/HeJCrlBR and C57BL/6J genetic backgrounds. In addition, homozygous mice develop inflammatory bowel disease between 6 and 15 weeks of age and reportedly die within 10-25 weeks under conventional housing conditions. Homozygotes on the C57BL/6J genetic background show an atrophied pancreas with apparently intact islets. Homozygotes on the BALB/c genetic background do not develop inflammatory bowel disease symptoms but rather die 3-5 weeks postnatally of a form of hemolytic anemia. For a more de ..... For more information please see the full descriiption on the strain data sheet
003968	C3Bir.129P2(B6)-Il10^tm1Cgn/LtJ	Repository-Cryopreserved
	Mice homozygous for the Il10^tm1Cgn targeted mutation are viable and fertile when housed under specific pathogen free (SPF) conditions. Under conventional housing conditions, Il10-deficiency is associated with altered lymphocyte and myeloid profiles, elevated serum amyloid A levels, altered responses to inflammatory or autoimmune stimuli (both endogenous and induced), increased prevalence of colorectal adenocarcinoma (especially on 129/Sv and, to a lesser extent, BALB/c genetic background), and spontaneous development of chronic enterocolitis (see below). As The Jackson Laboratory Repository maintains these mice at high health status conditions (high SPF), the observed or experimentally-induced Il10-deficient phenotype may vary from that previously published using mice from conventional mouse rooms. These IL-10 mutant mice may be useful studying inflammatory bowel disease (IBD) (Crohn's disease (CD) and/or colitis), cancer, innate and adaptive immunity, a ..... For more information please see the full descriiption on the strain data sheet
000291	C3FeLe.Cg-a/a Hm Kitl^Sl Krt71^Ca-J/J	Repository-Cryopreserved
	The multiple steel mutations (Kitl^Sl) 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. Kitl^Sl/Kitl^Sl-d) are viable, black-eyed white, are usually sterile in one or both sexes, and have severe macrocytic anemia. 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. 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 adva ..... For more information please see the full descriiption on the strain data sheet
000627	C3H/HeJ-Kit^W-x/J	Repository-Cryopreserved

000847	C3Sn.B6-Kit^W-39J/J	Repository-Cryopreserved

001380	C3Sn.Cg-Kitl^Sl-con/J	Repository-Cryopreserved
	Both homozygous and heterozygous mice with the contrasted induced mutation (Kitl^Sl-con) are viable. Male homozygous mutant mice are fertile but females are usually sterile. Mice heterozygous for the contrasted mutation are recognizable soon after birth by dark pigmentation of the genital papilla with the adult coat being slightly lighter than normal. Homozygous mutant mice also have dark genitalia and a markedly diluted coat and mild macrocytic anemia.
003175	C57BL/6-Il5^tm1Kopf/J	Repository-Cryopreserved
	Mice homozygous for the Il5^tm1Kopf targeted mutation are viable and fertile. Surprisingly, IL5 deficient mice show no defects in conventional B (B-2) cells, T cell dependent antibody production, or cytotoxic T cell responses. Eosinophilia response to infection is lacking in homozygous mutant mice. They also exhibit impaired CD5⁺ B-1 cell development.
002980	C57BL/6-Tg(Cd152Ig)1Jbs/J	Repository-Cryopreserved
	A soluble form of the CD152 antigen (CTLA4Ig)is expressed under the control of the K14 promoter that is primarily active in the skin, but also thymus and tongue. The animal produces blood circulating levels of CTLA4Ig that are easily detectable by ELISA or functional assays.
000166	C57BL/6J-Kit^W-17J/J	Repository-Cryopreserved

000167	C57BL/6J-Kit^W-18J/J	Repository-Cryopreserved

000169	C57BL/6J-Kit^W-20J/J	Repository-Cryopreserved

000117	C57BL/6J-Kit^W-34J/J	Repository-Cryopreserved

000128	C57BL/6J-Kit^W-35J/J	Repository-Cryopreserved

000134	C57BL/6J-Kit^W-37J/J	Repository-Cryopreserved

000062	C57BL/6J-Kit^W-39J/J	Repository-Cryopreserved

000121	C57BL/6J-Kit^W-40J/J	Repository-Cryopreserved

000119	C57BL/6J-Kit^W-41J/J	Repository-Cryopreserved

000127	C57BL/6J-Kit^W-42J/J	Repository-Cryopreserved

000129	C57BL/6J-Kit^W-43J/J	Repository-Cryopreserved

000990	C57BL/6J-Kit^W-55J/J	Repository-Cryopreserved

001179	C57BL/6J-Kit^W-62J/J	Repository-Cryopreserved

003252	C57BL/6J-Kitl^Sl-20J/J	Repository-Cryopreserved
	Kitl^Sl-20J is a dominant allele. On the C57BL/6J background heterozygotes have a light black coat color with lighter tail and feet and a steel colored belly with a belly spot. Heterozygotes of both sexes are viable and fertile.
000118	C57BL/6J-Ph/J	Repository-Cryopreserved

002226	C57BL/6J-Tg(Alb1HBV)44Bri/J	Repository-Cryopreserved
	This strain is referred to as "50-4" or "Tg(Alb1-HBV)Bri44" in the primary reference.
002230	C57BL/6J-Tg(LckIl4)1315Dbl/J	Repository-Cryopreserved
	Transgenic mice overexpressing the IL4 transgene under the control of the Lck promoter show severe osteoporosis of both cortical and trabecular bone by 2 months in both males and females. There is decreased bone formation by osteoblasts and kyphosis; characterized by long snout ("weasel face") by 6 weeks of age.
002499	C57BL/6J-Tg(WapIGFBP3)67Dlr/J	Repository-Cryopreserved
	Mice homozygous for the WapIGFBP3 transgene are viable and fertile. The transgene is expressed at high levels during lactation and post-lactation. There were no obvious changes in mammary gland histomorphology during lactation, but at 5 to 10 days post-laction, there was a delay in involution and decreased apoptosis. This phenotype is identical to that of the C57BL/6J-TgN(WapIgf1)39Dlr strain mice.
000965	CBACa.C3-Kit^W-x/J	Repository-Cryopreserved

003642	CBy.129S1-Il12rb2^tm1Jm/J	Repository-Cryopreserved
	Mice homozygous for the Il12rb2^tm1Jm targeted mutation are viable and fertile. Homozygous mutant mice do not show an increased susceptibility to infections. 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.
002927	CNCr.129P2-Cd40^tm1Kik/J	Repository-Cryopreserved
	Mice homozygous for the targeted mutation are viable and fertile. Homozygous mutant mice exhibit impaired immunoglobulin class switching and germinal center formation.
005879	D1Lac.Cg-Il4^tm1Cgn/J	Repository-Cryopreserved
	Mice homozygous for the targeted mutation are viable, fertile, normal in size, and do not display any gross physical or behavioral abnormalities. No endogenous gene product is detectable in splenocyte supernatants. Mutant mice crossed to the DBA/1LacJ background (I-A^q haplotype) are susceptible to collagen-induced arthritis. Deletion of the endogenous gene exacerbates both the incidence and severity of collagen-induced arthritis, which is accompanied with increased IgG2 and decreased IgG1 in sera. Following type II collagen (CII) tolerization of mutant mice, splenocytes cultured with CII have increased Th2 (IL-5, IL-9, IL-10, IL-13) and Th1 (IFNgamma, IL-6) cytokines. Mutant mice may be useful in other studies of collagen-induced arthritis, rheumatoid arthritis, mechanisms of tolerance, regulation of autoimmune disease, and T helper cell immune responses. On the C57BL/6 background (see Stock No. 002253) from which this mouse was created, T and B cell development is nor ..... For more information please see the full descriiption on the strain data sheet
000092	FL/1Re-Kit^W/J	Repository-Cryopreserved

006125	FVB-Tg(H2-D-Il15)3304Clgr/J	Repository-Cryopreserved
	Mice hemizygous for this transgene are viable and fertile. The transgene was designed to optimize the overexpression of secreted, mature interleukin-15. Transgenic IL-15 expression has a similar tissue distribution as the endogenous gene, but at a significantly higher level. IL-15 protein is detectable in the serum from most mutant, but not from wildtype, mice. Mutant mice develop a progressive alopecia by as early as 5-6 weeks of age, with skin lesions appearing over time. While all transgenic mice exhibit early polyclonal/benign expansion of natural killer and memory CD8⁺ T lymphocytes (T/NK), two distinct phenotypes emerge over time: approximately 70% of the transgenic mice will exhibit polyclonal T/NK progression in multiple tissues, while the remaining 30% are characterized by T/NK clonal expansion in multiple tissues and acute lymphoblastic leukemia (T/NK ALL). Both T/NK phenotypes are fatal within the first year of life. Mice harboring this transgene may be useful in ..... For more information please see the full descriiption on the strain data sheet
003268	FVB-Tg(IRS1)1Mhep/J	Repository-Cryopreserved
	Mice transgenic for human insulin receptor substrate-1 (hIRS-1) are viable. Overexpression of hIRS-1 is liver specific. The hIRS-1 protein interacts with several SH2-containing molecules in hIRS-1 transgenic mouse liver, including PIK3, Grb2 and SHP2. PI3K activity and MAPK activity are higher in transgenic mouse liver in comparison to wild type liver, indicating that hIRS-1 overexpression activates downstream signaling pathways in vivo. Mutant mice show enhanced liver growth associated with increased hepatocyte proliferation within the first three months of life.
005144	NOD.129(B6)-Ctla4^tm1All/DoiJ	Repository-Cryopreserved
	Heterozygous Ctla4^tm1All mice are viable, fertile, and normal in size and exhibit diabetes incidence comparable to NOD. Ctla4^tm1All homozygous mice on various backgrounds, including C57BL/6, BALB/c, 129 and NOD, die at 3-4 weeks of age due to massive polyclonal expansion of T-cells and massive lymphocyte infiltration into non-lymphoid organs, such as heart, liver, lung and pancreas. Treatment with murine Ctla4Ig or depletion of CD4⁺ T-cells blocks this lymphoproliferative disease. Splenic and lymph node T-cells display an activated phenotype characterized as CD69⁺, CD25⁺, CD44^hi, Mel14^lo, CD45RB^lo and Sca1^hi and have down regulated the TCR. Lymph node and spleen cells cultured from Ctla4^tm1All homozygous mice spontaneously proliferate while wild-type controls do not. Cells from whole lymph nodes or purified T-cells are unresponsive to anti CD28mAb stimu ..... For more information please see the full descriiption on the strain data sheet
002573	NOD.129P2(B6)-Il2^tm1Hor/DvsJ	Repository-Cryopreserved

004222	NOD.129P2(B6)-Il4^tm1Cgn/DvsJ	Repository-Cryopreserved
	Complete Freund's adjuvant (CFA) induced suppression of diabetes in NOD mice has been associated with a shift to Th2 cytokine production. NOD mice deficient in IL4 were created to investigate the role of IL4 in this shift. Mice homozygous for the Il4^tm1Cgn targeted mutation are viable and fertile. T and B cell development is normal but IgG1and IgE levels and the ability of homozygous mutant mice to produce Th2-derived cytokines are significantly reduced. IL4 deficient NOD mice develop IDDM with the same incidence as standard NOD/Lt controls, and there is no change between IL4 deficient and wildtype NOD in disease protection conferred by treatment of bacillus Calmette-Guerin vaccine (BCG) or CFA. Both IL4 deficient and wildtype NOD mice are significantly protected from insulitis by treatment of CFA but not by treatment of BCG. (Serreze et al 2001)
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.
002575	NOD.129S7(B6)-

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