Search Criteria: Research Area is "Cancer Research"
Strains from the Research Colonies of Jackson Laboratory Scientists
New Strains Under Development
| Stock Number |
Strain Name Phenotype |
Standard Supply |
| 001026 | BALB/cByJ | Level 1 |
| BALB/c mice are particularly well known for the production of plasmacytomas following injection with mineral oil, forming the basis for the production of monoclonal antibodies. Although not all BALB/c substrains have been examined for plasmacytoma induction, substrains derived from the Andervont (An) lineage (which includes BALB/cByJ) typically are susceptible, while those descended from BALB/cJ are resistant (see: Potter M ,1985). Mammary tumor incidence is normally low, but infection with mammary tumor virus by fostering to MMTV+ C3H mice dramatically increases tumor number and age of onset. BALB/c mice develop other cancers later in life including reticular neoplasms, primary lung tumors, and renal tumors. Rare spontaneous myoepitheliomas arising from myoepithelial cells of various exocrine glands have been observed in both BALB/cJ and BALB/cByJ substrains. BALB/cByJ has a deletion in the Qa2 subregion of the murine MHC. | ||
| 000651 | BALB/cJ | Level 1 |
| BALB/c mice are particularly well known for the production of plasmacytomas following injection with mineral oil forming the basis for the production of monoclonal antibodies. Although not all BALB/c substrains have been examined for plasmacytoma induction, substrains derived from the Andervont (An) lineage (which includes BALB/cByJ) typically are susceptible, while those descended from BALB/cJ are resistant (see: Potter M ,1985). Mammary tumor incidence is normally low but infection with mammary tumor virus by fostering to MMTV+ C3H mice dramatically increases tumor number and age of onset. BALB/c mice develop other cancers later in life including reticular neoplasms, primary lung tumors, and renal tumors. Rare spontaneous myoepitheliomas arising from myoepithelial cells of various exocrine glands have been observed in both BALB/cJ and BALB/cByJ substrains.
White et al. reported a variation in thioglycolate medium-induced peritoneal leukocyte recruitment in 4 analyzed s
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| 000659 | C3H/HeJ | Level 1 |
| C3H/HeJ mice are used as a general purpose strain in a wide variety of research areas including cancer, immunology and inflammation, sensorineural, and cardiovascular biology. C3H/HeJ mice and all other Jackson substrains are homozygous for the retinal degeneration 1 mutation (Pde6brd1), which causes blindness by weaning age. There is also a high incidence of hepatomas in C3H mice (reportedly 72-91% in males at 14 months, 59% in virgin females, 30-38% in breeding females). Despite the lack of exogenous mouse mammary tumor virus (MMTV), virgin and breeding females may still develop some mammary tumors later in life. C3H/HeJ mice, fed an atherogenic diet (1.25% cholesterol, 0.5% cholic acid and 15% fat), fail to develop atherosclerotic aortic lesions in contrast to several highly susceptible strains of mice (e.g. C57BL/6J, Stock No. 000664; C57L/J, Stock No. 00066
..... For more information please see the full phenotype on the strain data sheet | ||
| 001303 | NOD.CB17-Prkdcscid/J | Level 1 |
| Mice homozygous for the severe combined immune deficiency spontaneous mutation (Prkdcscid, commonly referred to as scid) are characterized by an absence of functional T cells and B cells, lymphopenia, hypogammaglobulinemia, and a normal hematopoietic microenvironment. Normal antigen-presenting cell, myeloid, and NK cell functions are strain dependent. scid mice carry a DNA repair defect and a defect in the rearrangement of genes that code for antigen-specific receptors on lymphocytes. Most homozygotes have no detectable IgM, IgG1, IgG2a, IgG2b, IgG3, or IgA. Thymus, lymph nodes, and splenic follicles are virtually devoid of lymphocytes. scid mice accept allogeneic and xenogeneic grafts making them an ideal model for cell transfer experiments. Some scid mice will spontaneously develop partial immune reactivity. scid mice that have serum Ig levels greater than 1 ug/ml are considered "leaky." scid leakiness is highly strain depen
..... For more information please see the full phenotype on the strain data sheet | ||
| 002448 | 129S1/SvImJ | Level 2 |
| Historically, the 129 inbred mice are known for the high incidence of spontaneous testicular teratomas, though the incidence differs between substrains.(1-3% in 129 parental substrains; 30% in teratoma substrains.) More recently, 129 mice are widely used in the production of targeted mutations due to the availability of multiple embryonic stem cell lines derived from them. There is major genetic variation within the 129 "family", which has led to an update of the nomenclature and a division of the substrains into three major groups: parental substrains (129P), steel substrains (129S) and "teratoma" substrains (129T). Investigators using 129 substrains for targeted mutagenesis should be careful in the selection of the appropriate 129 substrain to match the embryonic stem cell line. For a complete history of the numerous 129 substrains, see Simpson, et al., 1997.
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| 000691 | 129X1/SvJ | Level 2 |
| Historically, the 129 inbred mice are known for the high incidence of spontaneous testicular teratomas, though the incidence differs between substrains. (1-3% in 129 parental substrains; 30% in teratoma substrains.) More recently 129 mice are widely used in the production of targeted mutations due to the availability of multiple embryonic stem cell lines derived from them. There is major genetic variation within the 129 "family", which has led to an update of the nomenclature and a division of the substrains into three major groups: parental substrains (129P), steel substrains (129S) and "teratoma" substrains (129T). Investigators using 129 substrains for targeted mutagenesis should be careful in the selection of the appropriate 129 substrain to match the embryonic stem cell line. For a complete history of the numerous 129 substrains, see Simpson, et al., 1997.
In response to challenge, 129S1/SvImJ mice develop immune-mediated nephritis characterized by proteinuria, glome
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| 000646 | A/J | Level 2 |
| Developed by LC Strong in 1921 from a cross between a Cold Spring Harbor albino and a Bagg albino, the A inbred strain is used widely used in cancer and immunology research. It is highly susceptible to cortisone-induced congenital cleft palate. It has a high incidence of spontaneous lung adenomas, and lung tumors readily develop in response to carcinogens. A high percentage of mammary adenocarcinomas (a large proportion of acinar-type) develop in multiparous females. Rare spontaneous myoepitheliomas arising from myoepithelial cells of various exocrine glands have been observed in The Jackson Laboratory substrains. A/J mice fed an atherogenic diet (1.25% cholesterol, 0.5% cholic acid, and 15% fat) fail to develop atherosclerotic aortic lesions in contrast to several highly susceptible strains of mice (e.g. C57BL/6J, Stock No. 000664; C57L/J, Stock No. 000668, C57BR/cdJ, Sto
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| 000648 | AKR/J | Level 2 |
| Originally inbred at the Rockefeller Institute, AKR mice are widely used in cancer research for their high leukemia incidence (60-90%) and in immunology as a source of the Thy1.1 (theta AKR) antigen. AKR/J mice are viremic from birth, and express the ecotropic retrovirus AKV in all tissues. The hair interior defect (hid) mutation, a strain characteristic of AKR mice, causes alterations in hair development that is only evident microscopically. Adrenocortical lipid depletion (ald) in AKR mice is caused by a mutation in sterol O-acyltransferase 1 (Soat1), and leads to a truncated SOAT1 protein. AKR/J mice are relatively resistant to aortic lesion formation on a semi-synthetic high fat diet and are hyporesponsive to diets containing high levels of fat and cholesterol. | ||
| 002287 | B6.129S7-Ifngtm1Ts/J | Level 2 |
| Mice homozygous for the Ifngtm1Ts targeted mutation are viable and fertile. Homozygotes appear normal in a "clean" environment but display reduced macrophage function in response to pathogens. Specifically, macrophages show impaired production of antimicrobial products and reduced expression of MHC II antigens. There is also uncontrollable proliferation of splenocytes from homozygotes in response to mitogens and alloantigens and a reduced resting natural killer cell activity. | ||
| 000635 | C3H/HeOuJ | Level 2 |
| C3H/HeOuJ mice are used as a general purpose strain in a wide variety of research areas including cancer and sensorineural, research. C3H/HeOuJ mice and all other C3H substrains at The Jackson Laboratory are homozygous for the retinal degeneration 1 mutation (Pde6brd1), causing blindness by weaning age. There is also a high incidence of hepatomas in C3H mice (reportedly 72-91% in males at 14 months, 59% in virgin females, 30-38% in breeding females). Despite the lack of exogenous mouse mammary tumor virus (MMTV), virgin and breeding females may still develop some mammary tumors later in life. | ||
| 000654 | CBA/CaJ | Level 2 |
| The CBA inbred strain was initially bred for longevity and a low incidence of spontaneous mammary tumors (compared with C3H). Burdette and Strong reported that CBA mice were comparatively susceptible to tumor induction after a single subcutaneous injection of methylcholanthrene. The tumor types identified in this early work in CBA mice included spindle cell sarcoma, rhabdomyosarcoma, and epidermoid carcinoma. Strong and Smith reported finding benign hepatomas in aging CBA mice. Several groups confirmed this finding, and the majority of studies found a higher frequency of spontaneous hepatomas in males than in females.
CBA/Ca mice are commonly used for leukemogenesis research because this strain has a low spontaneous incidence of leukemia but has a relatively high inducibility of myeloid leukemia in response to benzene and radiation exposure. Multiple reports using CBA, its F1 hybrids, and other strains, have indicated that deletions in a specific segment of chromosome 2 are linked
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| 000686 | SJL/J | Level 2 |
| SJL mice display a very high incidence of reticulum cell sarcomas resembling Hodgkin's disease by approximately one year of age. Sarcomas first appear in the Peyer's patches and mesenteric lymph nodes and later in the spleen, liver, thymus and other lymph nodes. Most of the tumors are mixed-cell types classified as type B reticulum cell neoplasms, but a few are type A histiocytomas. This strain is also characterized by extreme aggression in males and its susceptibility to experimental autoimmune encephalomyelitis (EAE) for multiple sclerosis research. SJL/J mice develop a spontaneous myopathy resulting from a splice-site mutation in the Dysferlin gene. This Dysfim allele has been shown to result in decreased levels of dysferlin protein in SJL/J mice and makes this strain a good model for limb girdle muscular dystrophy 2B. This spontaneous myopathy is characterized by a progressive loss of muscle mass and strength corresponding with an increase in muscle pathology incl
..... For more information please see the full phenotype on the strain data sheet | ||
| 100410 | WBB6F1/J-KitW/KitW-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. KitW-v homozygotes resemble KitW 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. KitW/KitW-v double heterozygotes are viable but sterile because of germ cell deficiency. They are also mast cell deficient. KitW/KitW-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-Il10tm1Cgn/J | Level 3 |
| Mice homozygous for the Il10tm1Cgn 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 phenotype on the strain data sheet | ||
| 002650 | B6.129S2-Il6tm1Kopf/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 (Stock No. 007078). | ||
| 002216 | B6.129S7-Rag1tm1Mom/J | Level 3 |
| Mice homozygous for the Rag1tm1Mom mutation produce no mature T cells or B cells. Their phenotype can be described as a "non-leaky" severe combined immune deficiency (Prkdcscid/Prkdcscid) (Prkdcscid mice produce some B cells and IgM). They have no CD3+ or T cell receptor (TCR) alpha-beta positive cells. The thymus of the mutant mice contains 15 to 130 times fewer cells than heterozygous or wildtype siblings. The thymocytes are CD8-CD4- and most are IL2 receptor-positive. Neither the spleen nor the bone marrow contain any IgM or IgD staining cells, indicating an absence of mature B cells. These and other data suggest that B cell and T cell development has been arrested at an early stage. Macroscopically, the mutants are indistinguishable from heterozygotes or normal wildtype siblings. | ||
| 000482 | B6.MRL-Faslpr/J | Level 3 |
| Mice homozygous for the lymphoproliferation spontaneous mutation (Faslpr) show systemic autoimmunity, massive lymphadenopathy associated with proliferation of aberrant T cells, arthritis, and immune complex glomerulonephrosis. Onset and severity of symptoms associated with the Faslpr allele is strain-dependent. For example, lymphoproliferation varies greatly with congenic strain C57BL/6J-Faslpr/Faslpr at a 24 fold increase over control lymph node weight, MRL/Mp-Faslpr/Faslpr at 75 fold and congenic strain C3H/HeJ-Faslpr/Faslpr highest at 116 fold increase over control lymph node weight (Morse et al 1985). Variance in renal pathology ranks from extensive in MRL/Mp-Faslpr/Faslpr at 4 to 7 months to negligible at 14 to 16 months in mice with C57BL/6J and C3H/HeJ backgrounds and homozygous for Faslpr
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..... For more information please see the full phenotype on the strain data sheet | ||
| 004326 | C3Bir.129P2(B6)-Il10tm1Cgn/Lt | Level 3 |
| Mice homozygous for the Il10tm1Cgn 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 phenotype on the strain data sheet | ||
| 002020 | C57BL/6J-ApcMin/J | Level 3 |
| The C57BL/6J-ApcMin/J strain is highly susceptible to spontaneous intestinal adenoma formation. Homozygous mice are not viable. It was initially reported that one hundred percent of the C57BL/6J-ApcMin heterozygous mice raised on a high fat diet develop in excess of 30 adenomas throughout the intestinal tract and most die by 120 days of age. Heterozygotes also develop anemia. (Moser et al., 1990, Su et al., 1992). A small number of C57BL/6J-ApcMin heterozygous female mice develop mammary tumors. A subsequent publication indicates that this strain may carry a dominant modifier (Mom2) gene that reduces the number and incidence of polyp formation in C57BL/6J-ApcMin heterozygous mice (Silverman et al., 2002). | ||
| 002376 | FVB/N-Tg(MMTVneu)202Mul/J | Level 3 |
| Mice homozygous for the MMTVneu (rat) transgene are viable and fertile. There is no phenotypic effect in males. The transgene is expressed at low levels in normal mammary epithelium, salivary gland, and lung. Higher expression is detected in tumor tissue. Focal mammary tumors first appear at 4 months, with a median incidence of 205 days. Both virgin and breeder mice develop tumors. Tumors arise as foci in hyperplastic, dysplastic mammary glands. Seventy-two percent of tumor-bearing mice that live to 8 months or longer develop metastatic disease to the lung. The phenotype of MMTV/unactivated neu transgenic mice differs from that of the MMTV/activated neu produced by Phil Leder, in which multifocal tumors involving the entire mammary epithelium arise. | ||
| 000676 | LP/J | Level 3 |
| LP/J mice display a high susceptibility to audiogenic seizures. This strain is also reported to have a fairly high incidence of tumors that develop later in life, including mammary tumors, lymphoma, lung and soft-tissue sarcomas. LP/J mice are also homozygous for the spontaneous mutation piebald in the endothelin receptor type B gene (Ednrbs). The piebald spontaneous mutation is the result of a mutation in the endothelin receptor type B gene, Ednrb. Mice show irregular white spotting, the amount of which is greatly influenced by minor modifying genes. They also have dark eyes. The white areas of the coat are completely lacking in neural crest-derived melanocytes, and there is a reduction in the number of melanocytes in the choroid layer of the eye is reduced. | ||
| 005557 | NOD.Cg-Prkdcscid Il2rgtm1Wjl/SzJ | Level 3 |
| The NOD.Cg-Prkdcscid Il2rgtm1Wjl/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 phenotype on the strain data sheet | ||
| 000680 | PL/J | Level 3 |
| PL/J mice show a moderate susceptibility to experimental allergic encephalitis (EAE) with late onset and high mortality. Reports of leukemia incidence vary from 50% in females and 19% in males to 80-90%. In addition to a low threshold to electroconvulsive seizures, PL/J mice are susceptible to handling and rhythmic tossing-induced seizures (Kitami T, et al, 2004). | ||
| 000689 | SWR/J | Level 3 |
| SWR/J mice are used widely in research as a general purpose strain. Aging mice exhibit a high incidence of lung and mammary gland tumors. They also develop extreme polydipsia and polyuria (nephrogenic diabetes insipidus) with increasing age. SWR/J mice are highly susceptible to experimental allergic encephalomyelitis (EAE). Germline deletion of about 50% of T-cell receptor V beta-chain gene segments and a T-cell receptor V alpha polymorphism are responsible for the resistance of SWR/J mice to collagen type II-induced arthritis. SWR/J mice show an intermediate susceptibility to developing atherosclerotic aortic lesions (1670 to 1690 um2 atherosclerotic aortic lesions/aortic cross-section) following 14 weeks on an atherogenic diet (1.25% cholesterol, 0.5% cholic acid and 15% fat). SWR/J mice have been recommended for generation and propogation of transgenic mice because they are high responders to exogenous hormones, have large and prominant pronuclei with good resistance to l
..... For more information please see the full phenotype on the strain data sheet | ||
| 000690 | 129P3/J | Level 4 |
| Historically, the 129 inbred mice are known for the high incidence of spontaneous testicular teratomas, though the incidence differs between substrains. (1-3% in 129 parental substrains; 30% in teratoma substrains.) More recently, 129 mice are widely used in the production of targeted mutations due to the availability of multiple embryonic stem cell lines derived from them. There is major genetic variation within the 129 "family", which has led to an update of the nomenclature and a division of the substrains into three major groups: parental substrains (129P), steel substrains (129S) and "teratoma" substrains (129T). Investigators using 129 substrains for targeted mutagenesis should be careful in the selection of the appropriate 129 substrain to match the embryonic stem cell line. For a complete history of the numerous 129 substrains, see Simpson, et al., 1997. | ||
| 002065 | 129T2/SvEmsJ | Level 4 |
| Historically, the 129 inbred mice are known for the high incidence of spontaneous testicular teratomas, though the incidence differs between substrains. (1-3% in 129 parental substrains; 30% in teratoma substrains.) More recently 129 mice are widely used in the production of targeted mutations due to the availability of multiple embryonic stem cell lines derived from them. There is major genetic variation within the 129 "family", which has led to an update of the nomenclature and a division of the substrains into three major groups: parental substrains (129P), steel substrains (129S) and "teratoma" substrains (129T). Investigators using 129 substrains for targeted mutagenesis should be careful in the selection of the appropriate 129 substrain to match the embryonic stem cell line. For a complete history of the numerous 129 substrains, see Simpson, et al., 1997. | ||
| 000645 | A/HeJ | Level 4 |
| Developed by LC Strong in 1921 from a cross between a Cold Spring Harbor albino and a Bagg albino, the A inbred strain is used widely used in cancer and immunology research. It is highly susceptible to induction of congenital cleft palate by cortisone. It has a high incidence of spontaneous lung adenomas and lung tumors readily develop in response to carcinogens. High percentage of mammary adenocarcinomas (a large proportion acinar type) develop in multiparous females. Rare spontaneous myoepitheliomas arising from myoepithelial cells of various exocrine glands have been observed in The Jackson Laboratory substrains. A small percent (4%) of nonproductive males are hermaphrodites. An additional 17% of nonproductive males have abnormally small testes containing no sperm. | ||
| 002818 | B6.129-Tnfrsf1atm1Mak/J | Level 4 |
| Mice homozygous for the Tnfrsf1atm1Mak targeted mutation (formerly Tnfr1tm1Mak) 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-Il12btm1Jm/J | Level 4 |
| Mice homozygous for the Il12btm1Jmtargeted 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). | ||
| 002101 | B6.129S2-Trp53tm1Tyj/J | Level 4 |
| Mice homozygous for the Trp53tm1Tyj 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. | ||
| 004434 | B6.129S4-Ccl2tm1Rol/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-Ifngr1tm1Agt/J | Level 4 |
| Mice homozygous for the Ifngr1tm1 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-Tnftm1Gkl/J | Level 4 |
| Mice homozygous for the Tnftm1Gkl 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 phenotype on the strain data sheet | ||
| 003243 | B6;129S-Tnfrsf1atm1Imx Tnfrsf1btm1Imx/J | Level 4 |
| Mice homozygous for both the Tnfrsf1atm1Imx and Tnfrsf1btm1Imx 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. | ||
| 001021 | B6Smn.C3-Faslgld/J | Level 4 |
| Mice homozygous for the Faslgld mutation display lymphadenopathy and systemic autoimmunity similar to that in Fasllpr homozygous mice. There is significant enlargement of all lymph nodes to 50 times the control weight by 20 weeks of age. Homozygotes also have an enlarged spleen, greatly increased numbers of T, B, and null lymphocytes and develop immune complex glomerulonephrosis. Onset of symptoms is dependent on genetic background with the C3H/HeJ strain having the earliest onset exhibiting glomerulonephritis by 22 weeks. 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. The Cryaa
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| 002286 | C.129S7(B6)-Ifngtm1Ts/J | Level 4 |
| Mice homozygous for the Ifngtm1Ts targeted mutation are viable and fertile. Homozygotes appear normal in a "clean" environment but display reduced macrophage function in response to pathogens. Specifically, macrophages show impaired production of antimicrobial products and reduced expression of MHC II antigens. There is also uncontrollable proliferation of splenocytes from homozygotes in response to mitogens and alloantigens and a reduced resting natural killer cell activity. | ||
| 003145 | C.129S7(B6)-Rag1tm1Mom/J | Level 4 |
| Mice homozygous for the Rag1tm1Mom mutation produce no mature T cells or B cells. Their phenotype can be described as a "non-leaky" severe combined immune deficiency (Prkdcscid/Prkdcscid) (Prkdcscid mice produce some B cells and IgM). They have no CD3+ or T cell receptor (TCR) alpha-beta positive cells. The thymus of the mutant mice contains 15 to 130 times fewer cells than heterozygous or wildtype siblings. The thymocytes are CD8-CD4- and most are IL-2 receptor positive. Neither the spleen nor bone marrow contain any IgM or IgD staining cells, indicating an absence of mature B cells. These and other data suggest that B cell and T cell development has been arrested at an early stage. Macroscopically, the mutants are indistinguishable from heterozygotes or wildtype siblings. | ||
| 000049 | C57BL/6J-KitW-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. KitW-v homozygotes resemble KitW 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. | ||
| 004104 | FVB.Cg-Mmp9tm1Tvu/J | Level 4 |
| Mice that are homozygous null for the Mmp9 gene are viable and fertile. No Mmp9 activity is detected in spleen cell lysates. Long bones (tibia, femur) are 10% shorter in homozygous null mice. Histological examination of 3-week-old mice reveals a dramatically lengthened zone of hypertrophic cartilage (6 to 8 times larger vs. wildtype) due to delayed apoptosis, vascularization, and ossification. Subsequent remodeling resolves the condition, resulting in normal appearing bones by 8 weeks of age. Null mice show altered responses to repair of injury in skin, cornea, central nervous system and bone marrow reconstitution, and altered inflammatory responses. | ||
| 000485 | MRL/MpJ-Faslpr/J | Level 4 |
| Mice homozygous for the lymphoproliferation spontaneous mutation (Faslpr) show systemic autoimmunity, massive lymphadenopathy associated with proliferation of aberrant T cells, arthritis, and immune complex glomerulonephrosis. Starting at about three months of age, levels of circulating immune complexes rise greatly in the MRL-lpr/lpr mouse but not the MRL normal (Hewicker 1990). Onset and severity of symptoms associated with the Faslpr gene is strain-dependent. For example, lymphoproliferation varies greatly with congenic strain C57BL/6J-Faslpr/Faslpr at a 24 fold increase over control lymph node weight, MRL/Mp-Faslpr/Faslpr at 75 fold and congenic strain C3H/HeJ-Faslpr/Faslpr highest at 116 fold increase over control lymph node weight (Morse et al 1985). Variance in renal pathology ranks from extensive in MRL/Mp-Faslpr
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..... For more information please see the full phenotype on the strain data sheet | ||
| 000692 | WB/ReJ KitW/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. | ||
| 008215 | (C57BL/6-Tg(TRAMP)8247Ng/J X FVB/NJ)F1/J | Repository- Live |
| Mice carrying the TRAMP (Transgenic Adenocarcinoma of Mouse Prostate) transgene develop progressive forms of prostate cancer with distant site metastasis, primarily to the lymph nodes and lungs. These transgenic mice express the simian virus 40 (SV40) large tumor T antigen (Tag) under the control of the rat probasin promoter. Expression of the transgene is specific to the prostate epithelium. Transgenic mice exhibit various forms of disease from mild intraepithelial hyperplasia to large multinodular malignant neoplasia. The median survival time for these F1 transgenic mice is 19 weeks, very few mice survive past 33 weeks of age, which is significantly shorter than the lifespan of transgenic mice on the C57BL/6 background. Comparative histological analysis of tumors from these F1 transgenic mice and from transgenic mice on the C57BL/6 background reveals that the tumors found in these F1 mutants arise from the dorsolateral and ventral lobes of the prostate and are more spherical, hig
..... For more information please see the full phenotype on the strain data sheet | ||
| 004368 | 129(B6)-Il10tm1Cgn/J | Repository- Live |
| Mice homozygous for the Il10tm1Cgn 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 phenotype on the strain data sheet | ||
| 002702 | 129-Ifngr1tm1Agt/J | Repository- Live |
| Mice homozygous for the Ifngr1tm1Agt 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-Shhtm2Amc/J | Repository- Live |
| Mice that are homozygous for the Shhtm2Amc 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
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| 006050 | 129-Sirt6tm1Fwa/J | Repository- Live |
| Homozygous neonates are smaller than their wildtype and heterozygous littermates. They develop normally until approximately 21 days of age, when they develop an acute and rapid, aging-like degenerative pathology resulting in death by postnatal day 24. Homozygous mutant mice exhibit subcutaneous fat loss, lordokyphosis (hunchbacked spine) with osteopenia (30% loss of bone mineral density), colitis, and severe lymphopenia due to increased lymphocyte apoptosis. At day 12, mice have reduced insulin-like growth factor I (IGF-1) levels in serum, and develop severe hypoglycemia. Mouse embryonic fibroblasts (MEFs) prepared from homozygous embryos exhibit reduced proliferation, defective base excision repair function, as indicated by increased sensitivity to alkylating agents and ionizing radiation, and increased chromosomal aberrations. The donating investigators report that no gene product (mRNA or protein) is detected by RT-PCR or immuoblot analysis of tissues, MEFs or embryonic stem cells f
..... For more information please see the full phenotype on the strain data sheet | ||
| 001137 | 129P1/ReJ | Repository- Live |
| For a complete history of the numerous 129 substrains please refer to Simpson, et al., 1997. Historically, the 129 inbred mice are known for the high incidence of spontaneous testicular teratomas, though the incidence differs between substrains. Most recently 129 mice are widely used strain in the production of targeted mutations due to the availability of several lines of embryonic stem cells. There is major genetic variation within the 129 "family", which has led to an update of the nomenclature and a division of substrains into three major groups: parental substrains, steel substrains and "ter" substrains. Investigators using 129 substrains for targeted mutagenesis should be careful in the selection of the appropriate 129 substrain to match the embryonic stem cell line. | ||
| 002779 | 129S-Parp1tm1Zqw/J | Repository- Live |
| Mice that are homozygous null for the targeted gene are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Although a shortened transcript is generated, no enzymatic activity is detected in tissues. Proliferation of homozygous-null fibroblasts and thymocytes is impaired following gamma-radiation in comparison to cells derived from wild-type mice. Older mice are susceptible to spontaneous development of skin disease. A significant portion of older mice ( ~30%) can be expected to exhibit epidermal hyperplasia. Null mice are also less susceptible to damage induced by the neurotoxin MPTP. | ||
| 006661 | 129S.B6-Tg(KRT14-RAF1/ESR1)1Pkha/J | Repository- Live |
| Mice hemizygous for this "K14-Raf:ER" transgene are viable and fertile. Inducible expression of the human Raf1(Raf-1 [DD]):estrogen receptor (ER) fusion protein is observed in the epidermis following topical application of 4-hydroxytamoxifen (4OHT). Prolonged (4 weeks) induction of human Raf-1[DD] activity promotes the undifferentiated, proliferative phenotypic characteristics observed in epidermal cancer; including hyperplasia, increased mitotic index, decreased expression of differentiation markers and increased expression of beta-1 and beta-4 integrin subunits. Raf-1[DD]-induced skin abnormalities are entirely reversed within one month after 4OHT cessation. These mice have a similar 4OHT-inducible skin phenotype as the transgenic mice expressing human H-RasG12V (Stock No. 006403) or human Mek1R4F (Stock No. 006822), and may be useful in studies of the
..... For more information please see the full phenotype on the strain data sheet | ||
| 002753 | 129S6/SvEvTac-Atmtm1Awb/J | Repository- Live |
| Mice homozygous for the Atmtm1Awb targeted mutation display many of the characteristics of ataxia telangiectasia, including growth retardation, neurologic dysfunction, infertility, defects in T lymphocyte maturation, and extreme sensitivity to gamma-irradiation. Most homozygotes develop thymic lymphoma between 2 and 4 months of age. Heterozygous mice display no abnormalities through eight months of age. | ||
| 001649 | A.BY H2bc H2-T18f/SnJ-Dstncorn1/J | Repository- Live |
| Mice homozygous for the recessive Dstncorn1 mutation have abnormally proliferative basal corneal epithelial cells. Focal areas of corneal epithelial hyperplasia are found by one week of age, and neovascularization is found by 14 days of age when the eyes open. This neovascularization, which progresses during the first two months of age, is not found in mice homozygous for the Dstncorn-2J allele (which is a point mutation leading to a change in a single amino acid residue). In both mutants the corneal epithelial cells show increased levels and altered organizational pattern of filamentous actin. The areas of thickened cortical epithelia yield a roughened, opaque corneal surface. At 4 weeks of age in Dstncorn1 homozygotes, expression of keratin 14 and involucrin extend into the suprabasal layer in the areas of hyperplastic corneal epithelia. There is also an increase in the levels of expression of cofilin 1, lumican and kerat
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| 000647 | A/WySnJ | Repository- Live |
| Developed by LC Strong in 1921 from a cross between a Cold Spring Harbor albino and a Bagg albino, the A inbred strain is used widely used in cancer and immunology research. It is highly susceptible to induction of congenital cleft palate by cortisone. It has a high incidence of spontaneous lung adenomas and lung tumors readily develop in response to carcinogens. High percentage of mammary adenocarcinomas (a large proportion acinar type) develop in multiparous females. Rare spontaneous myoepitheliomas arising from myoepithelial cells of various exocrine glands have been observed in The Jackson Laboratory substrains. Unlike A/J mice, A/WySnJ mice carry a spontaneous mutation in Tnfrsf13c and exhibit a significant loss of mature B cells (Miller, et al., 1991, Lentz et al., 1996, Shulga-Morskaya et al., 2004). | ||
| 002250 | B10.129P2(B6)-Il10tm1Cgn/J | Repository- Live |
| Mice homozygous for the Il10tm1Cgn 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 phenotype on the strain data sheet | ||
| 005895 | B10.Cg-Thy1a H2d Tg(TcraCl1,TcrbCl1)1Shrm/J | Repository- Live |
| Male mice that are hemizygous for the Clone-1 TCR (also called Clone 1 Thy1.1 TCR or Cl.1 TCR) transgene are viable, fertile, and normal in size. Females are very weak and have low fecundity. The donating investigator reports that all transgenic mice are prone to tumor development by 5-6 months of age. The transgene encodes a rearranged low avidity T cell receptor that recognizes an influenza virus hemagglutinin epitope (HA518-526) restricted by MHC class I H-2Kd. Flow cytometric analysis shows appropriate skewing towards the CD8+ T cell compartment in thymocytes and peripheral lymphocytes. Both naive and activated clone 1 T cells exhibit decreased responsiveness when presented with their cognate antigen in vitro and when transferred into mice expressing HA on pancreatic beta cells. CD8+ T cells can be induced to exhibit both effector function and antitumor activity. This mouse is further modified with the Thy1.1 allele, rather than th
..... For more information please see the full phenotype on the strain data sheet | ||
| 006910 | B6.129-Crkltm1Hkp/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. | ||
| 006412 | B6.129-Il12btm1Lky/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-Ins2Akita Bdkrb2tm1Jfh/SmiJ | Repository- Live |
| Mice homozygous for the targeted mutation and heterozygous for the Ins2Akita spontaneous mutation are viable and fertile. Similar to mice only heterozygous for the Ins2Akita 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 phenotype on the strain data sheet | ||
| 008451 | B6.129P(Cg)-Ptprca Cx3cr1tm1Litt/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 Ptprca) 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 phenotype on the strain data sheet | ||
| 005582 | B6.129P-Cx3cr1tm1Litt/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
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| 007572 | B6.129P2(Cg)-Rorctm2Litt/J | Repository- Live |
| Mice homozygous for this Rorc(gtGFP (or RORgt)GFP) mutant allele are viable and fertile. While Rorcg mRNA is detected in liver in Rorc(g)tGFP homozygotes, mRNA and protein for the thymus-specific isoform (Rorcgt) encoded by the targeted allele are not detected in the thymus. EGFP expression reports Rorc(gt) transcription in the thymi of adult Rorc(gt)GFP mice. Homozygous mice exhibit abnormal lymph node, Peyer's patch, and lymphoid tissue inducer (LTi) cell development. Mice with Rorcgt-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 homozygo
..... For more information please see the full phenotype on the strain data sheet | ||
| 002687 | B6.129P2-Ccl3tm1Unc/J | Repository- Live |
| Mice homozygous for the Scya3tm1Unc 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-Ccr5tm1Kuz/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-Cd40tm1Kik/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-Il2tm1Hor/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 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 detailed description please refer to the For more information please see the full phenotype on the strain data sheet | ||
| 002253 | B6.129P2-Il4tm1Cgn/J | Repository- Live |
| Mice homozygous for the Il4tm1Cgn 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. | ||
| 005960 | B6.129S-Pecam1Gt(VICTR20)12Lex/J | Repository- Live |
| Mice that are homozygous for the gene-trapped allele are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. No gene product (protein) is detected by immunofluorescence in aorta endothelium from homozygotes, and endothelial nitric oxide synthase isoform (eNOS) is not detected in cell to cell junctions between aorta endothelial cells in these mice. Isolated skeletal muscle arterioles from homozygous mutant mice exhibit reduced vessel dilation and no significant change in wall shear stress responses when intraluminar flow is increased. This mutant mouse strain may be useful in studies of cellular adhesion, vascular integrity and physiology. | ||
| 005540 | B6.129S-Tnftm1Gkl/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 phenotype on the strain data sheet | ||
| 008087 | B6.129S1-Bchetm1Loc/J | Repository- Live |
| Mice homozygous for this BChE mutant allele are viable and fertile with no reported spontaneous abnormalities. All tissues and plasma from homozygous mice are devoid of BChE activity. As BChE (butyrylcholinesterase) is a bioscavenger molecule protecting acetylcholinesterase (AChE) activity against nerve agents and organophosphates, homozygous BChE-deficiency leads to impaired protection from toxic compounds. These BChE mutant mice are a model for human butyrylcholinesterase deficiency and may be useful for studying metabolic effects of organophosphorus toxicants or nerve agents, neurotransmitter function, and anti-Alzheimer's drug therapies.
Of note, the donating investigator has multiple strains available that may be useful for testing toxic compounds, including the AChE-deficient (Stock No. 005987), G117H BChE transgenic (Stock No. 007577), and BChE-deficient (see Stock
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| 004525 | B6.129S1-Bcl2l11tm1.1Ast/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. | ||
| 002692 | B6.129S1-Il12atm1Jm/J | Repository- Live |
| Mice homozygous for the Il12atm1Jm 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
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| 003248 | B6.129S1-Il12rb2tm1Jm/J | Repository- Live |
| Mice homozygous for the Il12rb2tm1Jm 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. | ||
| 007263 | B6.129S1-Ing1tm1Avg/J | Repository- Live |
| Mice homozygous for the targeted mutation are viable, fertile, and do not display any gross physical or behavioral abnormalities. Homozygotes are smaller than their wildtype littermates. Homozygous births from heterozygous crosses occur at a lower than expected frequency. During a 23 month period homozygotes exhibit increased morbidity or visible abnormalities including splenomegaly and an increased incidence of lymphomas (follicular center B-cell lymphomas) when compared to wild type littermates. When exposed to 6 consecutive daily doses of 2.34Gy total body gamma irradiation, mutant mice have a lower survival rate than wildtype controls. Mouse embryonic fibroblasts (MEFs) from homozygous animals are slightly more sensitive to UV-B exposure. This mutant mouse strain may be useful in studies of hypersensitivity to gamma irradiation and tumorigenesis. | ||
| 006221 | B6.129S1-Lyve1tm1Lhua/J | Repository- Live |
| Homozygotes are viable and fertile, and produce normal-sized litter. No gross phenotypic or behavioral abnormalities have been reported, even in older (2 year old) mice. Homozygous mutants express neither endogenous RNA or protein in liver tissue. Lymphatic capillary vessel morphology in the liver and intestines of homozygous mice is abnormal, with vessels having distended or rounded lumens in contrast to the smaller, typically collapsed, irregular shapes observed in wildtype controls. Intradermal interstitial-lymphatic flow also is increased. Syngenic tumor cell transplants into grow more rapidly and robustly in homozygous mutant mice compared with transplants into wildtype mice, and develop porous interstitial spaces. These mutant mice may be useful in studies of structural and functional characteristics of the lymphatic system, cell-surface retention sequence (CRS) motif-containing growth factor secretion, autocrine and paracrine regulation of cell growth, as well as of cancer and t
..... For more information please see the full phenotype on the strain data sheet | ||
| 006848 | B6.129S2(C)-Il8rbtm1Mwm/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
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| 002770 | B6.129S2-Cd40lgtm1Imx/J | Repository- Live |
| Mice homozygous for the targeted mutation are viable and fertile. Homozygous mutant mice show no overt phenotypic abnormalities. Percentages of B and T cell subpopulations is normal. Homozygotes do show selective deficiencies in humoral immunity (low basal serum isotype levels and undetectable IgE) as well as abnormal secondary antigen-specific responses to immunization with a thymus-dependent antigen. The phenotype of the mice resembles human X-linked hyper IgM syndrome. | ||
| 002258 | B6.129S2-Ltatm1Dch/J | Repository- Live |
| Mice homozygous Ltatm1Dch 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. | ||
| 002507 | B6.129S2-Serpine1tm1Mlg/J | Repository- Live |
| Mice homozygous for this mutation develop normally and are viable and fertile. Compared to wild type mice, pulmonary clot lysis is increased in the heterozygote and further increased in the homozygote. Endotoxin induced venous thrombosis is decreased compared to wild type mice. Thus, disruption of the Serpine1 gene induces a mild hyperfibrinolytic state. Hemostasis is normal in homozygous mutants. | ||
| 006141 | B6.129S2-Thbs1tm1Hyn/J | Repository- Live |
| Mice homozygous for this targeted mutation are viable and fertile, with an approximate 20% decrease in embryo/neonate viability and a mild and variable lordotic curvature of the spine apparent from birth. Homozygous mice have an abnormal, but no full length transcript in multiple tissues. Western analysis confirmed the absence of the protein in platelets. Homozygotes exhibit an increase in the number of circulating white blood cells. During the first four to ten weeks of life, homozygotes exhibit patches of acute and organizing pneumonia. At later time points, there is considerable hyperplasia of the various epithelial cell lineages. Mutant mice also have an increased number of retinal endothelial cells and inappropriate remodeling and maturation of retinal vasculature following injury. On the FVB/N background, spontaneous tumor growth and vasculature are significantly increased compared to wildtype. Mutant mice may be useful in studies of inflammatory responses in the lungs, eye, and
..... For more information please see the full phenotype on the strain data sheet | ||
| 002620 | B6.129S2-Tnfrsf1btm1Mwm/J | Repository- Live |
| Mice homozygous for a Tnfrsf1btm1Mwm targeted mutation (formerly Tnfr2tm1Mwm, 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. | ||
| 002781 | B6.129S4-Cdkn1btm1Mlf/J | Repository- Live |
| Mice deficient in p27kip are viable and larger than normal littermates, with increased cellularity of all tissues. The thymus and spleen are particularly enlarged. Nullizygous adult mice have a shortened lifespan due to the growth of benign intermediate lobe pituitary tumors. Female mice are infertile, with a follicular phase ovulatory block. Large doses of exogenous gonadotropin induce ovulation, but both implantation and intrauterine embryonic development is impaired. The mice demonstrate haploid-insufficient susceptibility to the development of adenomas in the pituitary, intestine and lung adenomas following exposure to gamma irradiation or chemical carcinogens. | ||
| 002952 | B6.129S4-Il2ratm1Dw/J | Repository- Live |
| Mice homozygous for the Il2ratm1Dw 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-Il2rgtm1Wjl/J | Repository- Live |
| Mice homozygous for the Il2rgtm1Wjl 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. | ||
| 008102 | B6.129S4-Ltb4r1tm1Adl/J | Repository- Live |
| Mice homozygous for this BLTR (BLT1)-deficient allele are viable and fertile. Northern blot analysis of neutrophils, macrophages, lymph nodes, lungs, and
spleens isolated from homozygous mice show absence of the normal transcript and presence of the expected larger transcript (due to the insertion of the neomycin resistance cassette in exon 2 of the targeted gene), albeit at lower levels than the wild type transcript. Homozygous disruption of this allele confers impaired leukocyte function (chemotaxis, recruitment, firm adhesion). For example, homozygotes exhibit substantially diminished recruitment of eosinophils in a model of peritonitis, effector T cells in a model of allergic pulmonary inflammation, and neutrophils in a model of rheumatoid arthritis. As the G protein-coupled receptor BLTR/BLT1 is expressed on myeloid leukocytes (including neutrophils, macrophages, eosinophils, T cell lymphomas, and effector T cells (TH1 CD4+ cells, TH2 CD4+ cells, and effecto
..... For more information please see the full phenotype on the strain data sheet | ||
| 006122 | B6.129S4-Mbl1tm1Kata Mbl2tm1Kata/J | Repository- Live |
| Mice homozygous for both mannose-binding lectin (MBL)-A and MBL-C targeted mutations (termed MBL-null) are viable, fertile, and normal in size with no obvious developmental defects. Histological examination of multiple organs from 6-10 week old mice shows no abnormalities. MBL-null mice have no endogenous gene expression in liver (the principal site of MBL synthesis) and no protein detectable in serum. While the classical complement pathway is unaffected in MBL-null mice, the lectin-dependent complement pathway is non-functional. MBL-null mice have increased mortality following intravenous injection of S. aureus associated with abnormal serum levels of TNFalpha and IL-6 (decreased at 2h, elevated at 24h post injection). Cyclophosphamide-induced febrile neutropenic MBL-null mice inoculated with S. aureus have greatly increased susceptibility to abscess formation in kidney, liver, and lung (but not spleen). These same treated mice also have persistent bacteremia despite a r
..... For more information please see the full phenotype on the strain data sheet | ||
| 005897 | B6.129S4-Ppardtm1Rev/J | Repository- Live |
| These mice possess loxP sites on either side of exon 4 of the targeted gene. Mice that are homozygous for this allele are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. When bred to mice with a cre recombinase gene under the control of a promoter of interest, exon 4 of the targeted gene is deleted in the tissue of interest, leading to premature termination of the translation product upstream of the DNA binding domain. This strain may be useful in generating tissue-specific mutants of the floxed allele for use in studies including embryo development, adipocyte physiology, fat metabolism and storage, inflammation, and cancer. | ||
| 006440 | B6.129S4-Ptentm1Hwu/J | Repository- Live |
| These mice possess loxP sites flanking exon 5 of the targeted gene. Mice homozygous for the"floxed" allele are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. When used in conjunction with a Cre recombinase-expressing strain, this strain is useful in generating tissue-specific mutants of the floxed allele. 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 as published results become available. | ||
| 008076 | B6.129S4-Traf1tm1Tsi/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, Bims. 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
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| 006447 | B6.129S6(CBA)-Cebpatm1Dgt/J | Repository- Live |
| Mice carrying this C/EBPalpha "floxed" allele (C/EBPalphaF) are viable and fertile. The floxed allele functions similarly to the wildtype allele. In mice homozygous for C/EBPalphaF and expressing an interferon-inducible Cre recombinase (introduced by breeding to a cre-expressing strain; see Stock No. 003556), C/EBPalpha activity is disrupted, leading to defective myeloid cell development, increased hematopoietic stem cell repopulating activity, and significantly increased myeloblast population in the bone marrow compartment. In combination with an appropriate Cre transgenic strain, these mutant mice may be useful in studies of hematopoietic cell (e.g. myeloid and basophil progenitor cell) development and function, cancer (e.g. acute myeloid leukemia), and alveolar cell differentiation. | ||
| 007218 | B6.129S6-Trp53tm2Xu/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. | ||
| 003245 | B6.129S7-Il1r1tm1Imx/J | Repository- Live |
| Mice homozygous for the Il1rtm1Imx 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-Il7rtm1Imx/J | Repository- Live |
| Mice homozygous for the Il7rtm1Imx 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+ HSAdull). 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. | ||
| 002994 | B6.129X1-Baxtm1Sjk/J | Repository- Live |
| Mice homozygous for the Baxtm1Sjk 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-Bak1tm1Thsn/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.
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| 006112 | B6.129X1-Ela2tm1Sds/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 phenotype on the strain data sheet | ||
| 004265 | B6.129X1-Mpotm1Lus/J | Repository- Live |
| Mice that are homozygous null for the targeted gene are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. No Mpo gene product (mRNA or protein) is detected. Mutant mice exhibit total white blood cell counts and differentials similar to wildtype mice. Neutrophils and monocytes in periperhal blood and bone marrow have no endogenous peroxidase activity. Superoxide production levels in peritoneal exudate cells of mutant mice are similar to levels found in wildtypes mice. Hypochlorous acid production is undetectable in both isolated leukocytes and peritoneal exudate cells. Mutant mice display impaired fungicidal activity due to myeloperoxidase deficiency. When maintained under hyperlipidemic conditions, mutant mice develop atherosclerotic lesions 50% larger than those seen in control mice. | ||
| 005085 | B6.Cg-Cd44tm1Hbg/J | Repository- Live |
| 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 (mRNA or protein) is detected. Although lymphocyte development appears unremarkable, irregularities are observed in lymphocyte trafficking. Tail-injected lymphocytes derived from null animals exhibit an impaired ability to traffic to peripheral lymph nodes, and to a much greater degree, the thymus. Transcription and translation of the targeted allele subsequently lead to the synthesis of the lacZ protein under control of the 5' regulatory elements of the endogenous locus in all cells and tissues normally expressing one or several of the CD44 isoforms. 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 f
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| 006230 | B6.Cg-Cebpatm1Dgt Tg(Mx1-cre)1Cgn/J | Repository- Live |
| Mice homozygous for this C/EBPalpha "floxed" allele (C/EBPalphaF) and hemizygous for the Mx1-cre transgene are viable and fertile, and exhibit no abnormalities in the hematopoietic system. In the absence of cre expression, the C/EBPalphaF allele functions similarly to the wildtype allele. Mx1-Cre transgene expression can be induced by administration of either interferon (alpha or beta) or synthetic double-stranded RNA (such as poly I:C), leading to deletion of the "floxed" gene. Following 3-4.5 weeks of poly I:C treatment, deletion efficiency is greater than 95% in hematopoietic tissues, and C/EBPalpha protein is undetectable in bone marrow. These poly I:C-treated, mice have defective myeloid cell development, increased hematopoietic stem cell repopulating activity, and a significantly increased myeloblast population in the bone marrow compartment. These mutant mice may be useful in studies of hematopoietic cell (e.g. myeloid and basophil progenitor cell) d
..... For more information please see the full phenotype on the strain data sheet | ||
| 006908 | B6.Cg-Ikbketm1Tman/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. | ||
| 004369 | B6.Cg-Rag1tm1Mom Ins2Akita/J | Repository- Live |
| Mice homozygous for the Rag1 targeted mutation and heterozygous for the Akita spontaneous display the diabetes phenotype in the absence of B and T cells and unlike single Akita mice, double mutants do not reject allografts. Mice heterozygous for only the Akita spontaneous mutation are viable and fertile. (Homozygotes typically die by 12 weeks of age from extreme hyperglycemia.) Symptoms in heterozygous mutant mice include hyperglycemia, hypoinsulinemia, polydipsia, and polyuria, beginning at approximately 3-4 weeks of age. The diabetic phenotype is more severe and progressive in heterozygous males than in females. Obesity and insulitis do not accompany diabetes. This double mutant strain is ideally suited for use in allogeneic or xenogeneic islet or stem cell transplantation protocols because the mice are severely immunocompromised and spontaneously develop diabetes at a young age. | ||
| 006922 | B6.Cg-Sfpi1tm2Dgt/J | Repository- Live |
| Mice that are homozygous for this "PU.1F" conditional allele are viable and fertile. When PU.1F mice are bred to mice expressing Cre recombinase, exons 4-5 of the targeted gene are deleted in the cre-expressing tissues in the offspring. These mice may be useful in studying T cell lymphoma, AML and other cancers, as well as transcription factors, hematopoiesis, and the development of multiple cell lineages. For example, when PU.1F mice are crossed with mice expressing the interferon- or dsRNA-inducible Mx1-cre transgenic mice (see Stock No. 003556), this mutant mouse strain may be useful in studies of hematopoietic stem cells. | ||
| 004132 | B6.Cg-Terctm1Rdp/J | Repository- Live |
| Early generation mice that are homozygous null for the Terc gene are phenotypically normal. No Terc transcript or telomerase activity is detected. If null mice are maintained as homozygotes, progressive adverse effects on the reproductive and hematopoietic systems are observed. By the fifth generation of homozygous intercrossing, fertility is significantly diminished. Testes size and weight is reduced by ~80%. Germ cells exhibit decreased rates in proliferation and increased rates of apoptosis resulting in a general state of germ cell depletion. Females exhibit smaller ovaries and diminished uterine horns. The proliferative capacity of hematopoietic cells derived from bone marrow and spleen is significantly compromised. Progressive generations of interbreeding the null mice results in progressive telomere shortening (4.8 +/- 2.4 kb per generation). Cells from the fourth generation onward possess chromosome ends lacking detectable telomere repeats, aneuploidy, and chromoso
..... For more information please see the full phenotype on the strain data sheet | ||
| 006200 | B6.Cg-Tnks2tm1.1Yjc/J | Repository- Live |
| Mice that are homozygous for the targeted mutation are viable and fertile. No gene product (mRNA) is detected by RT-PCR analysis of activated spleen lymphocytes. While neither telomere shortening nor chromosomal abnormalities (even across multiple generations) are observed, homozygous mice have significantly decreased body weight. These mutant mice may be useful in studies of both telomerase function and telomerase-independent pathways which affect development and metabolism. | ||
| 008111 | B6.Cg-Tg(CAG-Ub*G76V/GFP)1Dant/J | Repository- Live |
| Hemizygous transgenic mice are viable and fertile; they contain a green fluorescent protein (GFP) fused to a constitutively active degradation signal (UbG76V). Transgenic transcripts are detected in all tissues examined; however the G76V substitution leads to its ubiquitination and proteasomal degradation, rather than expression of the GFP fluorescent protein.
Following administration of proteasome inhibitors, UbG76V accumulates and GFP-derived fluorescence is readily apparent, evidence of an impaired ubiquitin/proteasome system. Both of the ubiquitin/proteasome system reporter founder lines, UbG76V-GFP/1 (Stock No. 008111) and UbG76V-GFP/2 (Stock No. 008112), may be useful for monitoring the role of ubiquitin/proteasome-dependent proteolysis in diverse disorders, and in efficacy trials for monitoring the effect of compounds on th
..... For more information please see the full phenotype on the strain data sheet | ||
| 008112 | B6.Cg-Tg(CAG-Ub*G76V/GFP)2Dant/J | Repository- Live |
| Hemizygous transgenic mice are viable and fertile; they contain the green fluorescent protein (GFP) fused to a constitutively active degradation signal (UbG76V). Transgenic transcripts are detected in all tissues examined; however no GFP protein expression is detected due to the G76V substitution which leads to its ubiquitination and proteasomal degradation. Following administration of proteasome inhibitors, UbG76V accumulates and GFP-derived fluorescence is readily apparent, evidence of an impaired ubiquitin/proteasome system. This strain and UbG76V-GFP/1 (Stock No. 008111) have similar expression patterns, but this line (UbG76V-GFP/2) shows lower transgene expression and is not reported to display background fluorescence. These strains may be useful for monitoring ubiquitin/proteasome-dependent proteolysis in diverse disorders, and in efficacy trials for monitoring the effect of compou
..... For more information please see the full phenotype on the strain data sheet | ||
| 005551 | B6.Cg-Tg(Cd4-TGFBR2)16Flv/J | Repository- Live |
| These transgenic mice express a dominant-negative form of the human transforming growth factor, beta receptor II (dnTGFBRII) under the direction of the mouse CD4 antigen promoter. Transgene expression is detected by RT-PCR analysis of thymus tissue, and is at a level sufficient to block TGF-beta signaling specifically in CD4+ and CD8+ T cells. At 3 to 4 months of age transgenic mice begin to display wasting and diarrhea. Histological examination reveals inflammatory bowel disease (IBD) and inflammatory infiltration of the large intestine, lungs, and liver. Less severe infiltration is observed in the stomach, duodenum, pancreas and kidney. The Donating Investigator indicates that the severity of and organs affected by the IBD is influenced by strain background. Western blot analysis detects circulating autoreactive antibodies. IgG immune deposits form in kidney glomeruli. There is a 3-fold increase in total cell numbers in peripheral lymphoid organs. T cells spontaneously differentiate
..... For more information please see the full phenotype on the strain data sheet | ||
| 006229 | B6.Cg-Tg(DRE-lacZ)2Gswz/J | Repository- Live |
| Hemizygous mice are viable, fertile, normal in size, and do not display any behavioral abnormalities. Following adult or in utero exposure with xenobiotic ligands (including 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) and polychlorinated biphenyls (PCBs)), lacZ expression is induced in tissues targeted by the toxic compounds; for example, embryonic tissues expressing beta-galactosidase following TCDD treatment in utero include hard and soft palates, genital tubercle, certain facial regions, shoulder, and other tissues). These mice may be useful in studies of toxicology, teratogenic and xenobiotic processes, Per-Arnt-Sim transcription factors, cleft-palate, and as a reporter strain to indicate the temporal and spatial context of transcriptionally active aryl hydrocarbon receptors following agonist exposure in vivo. | ||
| 002728 | B6.Cg-Tg(IghMyc)22Bri/J | Repository- Live |
| Expression of the mouse Myc transgene is restricted to the B cell lineage. Hemizygotes show increased pre-B cells in the bone marrow throughout life and a transient increase in large pre-B cells in the blood at 3-4 weeks of age. Spontaneous pre-B and B cell lymphomas reach an incidence of 50% at 15-20 weeks in hemizygous progeny of a wildtype female mated with a hemizygous male. The transgene synergizes with an TgN(BCL2)22Wehi transgene (Stock No. 02319) to produce primitive lymphoid tumors within 5 weeks of birth, and with an Emu-v-abl transgene to produce plasmacytomas by 8 weeks. | ||
| 000160 | B6.D2-KitlSl-d/J | Repository- Live |
| The multiple steel mutations (KitlSl) behave in a semidominant fashion and cause deficiencies in pigment cells, germ cells, and blood cells paralleling those caused by the Kit locus mutations (dominant spotting alleles). Most of the alleles at steel locus cause severe anemia in utero and death by 15 to 16 days of gestation in homozygous mutant mice. However, steel-Dickie homozygotes (KitlSl-d/KitlSl-d) and compounds of steel and steel Dickie (KitlSl/KitlSl-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 phenotype on the strain data sheet | ||
| 007084 | B6.FVB(Cg)-Mmp9tm1Tvu/J | Repository- Live |
| Mice that are homozygous null for the Mmp9 gene are viable and fertile. No Mmp9 activity is detected in spleen cell lysates. Long bones (tibia, femur) are 10% shorter in homozygous null mice. Histological examination of 3-week-old mice reveals a dramatically lengthened zone of hypertrophic cartilage (6 to 8 times larger vs. wildtype) due to delayed apoptosis, vascularization, and ossification. Subsequent remodeling resolves the condition, resulting in normal appearing bones by 8 weeks of age. Null mice show altered responses to repair of injury in skin, cornea, central nervous system and bone marrow reconstitution, and altered inflammatory responses.
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 ne
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| 006911 | B6;129-Gt(ROSA)26Sortm1(rtTA*M2)Jae Col1a1tm2(tetO-Pou5f1)Jae/J | Repository- Live |
| Mice heterozygous for both targeted mutations (R26-rtTA and Cola1a::tetO-Oct4) are viable and fertile. These "Oct-4/rtTA" mice express rtTA-M2, an optimized form of reverse tetracycline-controlled transactivator (rtTA) protein, in multiple tissues. In the absence of the tetracycline analog doxycycline (dox), Oct4 (Pou5f1) expression from the Col1a1 locus is not detected. Following dox administration, high Oct4 expression is induced in liver, bone marrow, stomach, intestine, and skin, with lower levels in the heart, lungs, kidney, spleen, and thymus; no expression was detected in the brain and testes. Dox-inducd activation of Oct4 results in dysplasia in epithelial tissues. These mutant mice may be useful for studies of tumorigenesis and pluripotent cells. | ||
| 008041 | B6;129-Sirt1tm1Ygu/J | Repository- Live |
| Mice homozygous for this targeted allele (SirT1co/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 SirT1co/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 phenotype on the strain data sheet | ||
| 008045 | B6;129-Trp53tm2Holl/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-Trp53tm1Holl/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 phenotype on the strain data sheet | ||
| 006980 | B6;129-Trp53tm2Xu/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. | ||
| 006495 | B6;129-Trp53bp1tm1Jc/J | Repository- Live |
| Homozygous "53BP1"-deficient mice are viable and fertile, but exhibit retarded growth and generate reduced litter sizes. Protein from the targeted gene is not detected in the testes (by immunoblot) or in mouse embryonic fibroblasts (MEFs) (by immunofluorescence). Homozygotes are immunocompromised, hypersensitive to whole-body irradiation, and develop thymic lymphomas with higher frequency (8%) compared to wildtype by 4-7 months of age. MEFs from homozygous mutant mice have a defective DNA damage response with impaired Chk2 activation. These mutant mice may be useful in studies of the immune system, cancer, tumor suppression, and DNA damage response pathways. | ||
| 005323 | B6;129P2 Pemttm1J-tnyw/J | Repository- Live |
| 002782 | B6;129P2-Ccr5tm1Kuz/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-Tnfrsf1atm1Imx Il1r1tm1Imx/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-Il1r1tm1Roml/J | Repository- Live |
| Mice homozygous for the Il1r1tm1Roml 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. | ||
| 003263 | B6;129S2-Cdkn1atm1Tyj/J | Repository- Live |
| Homozygotes are viable and fertile. p21, the product of the Cdkn1a gene, belongs to a family of regulators, known as cyclin-dependent kinase inhibitors, which modulate progression through the cell cycle. Following serum restimulation, expression of p21 is superinducible by cycloheximide in wild-type but not in p53-deficient cells. p53 appears to play a critical role in p21 induction following DNA damage. p21 can be regulated independently of p53 during normal tissue development, following serum stimulation, and during cellular differentiation. | ||
| 002254 | B6;129S2-Il6tm1Kopf/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 | |