JAX Mice Database - Increased Tumor Incidence

Search Criteria: Research Area is "Cancer Research: Increased Tumor Incidence"

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

JAX^® Mice Strains

Stock Number	Strain Name Strain Description	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 ..... For more information please see the full descriiption on the strain data sheet
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 (Pde6b^rd1), 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 descriiption on the strain data sheet
001303	NOD.CB17-Prkdc^scid/J	Level 1
	Mice homozygous for the severe combined immune deficiency spontaneous mutation (Prkdc^scid, 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 descriiption 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.
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, glomeru ..... For more information please see the full descriiption on the strain data sheet
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/c ..... For more information please see the full descriiption on the strain data sheet
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.
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 (Pde6b^rd1), 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 ..... For more information please see the full descriiption on the strain data sheet
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 Dysf^im 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 descriiption on the strain data sheet
100410	WBB6F1/J-Kit^W/Kit^W-v/J	Level 2
	Kit mutant mice possess pleiotropic defects in pigment-forming cells, germ cells, RBC's and mast cells. In addition, they exhibit impaired resistance to parasitic infection and an intrinsic progenitor cell defect. Kit^W-v homozygotes resemble Kit^W homozygotes in color, anemia, and germ cells, but many of them survive to maturity. The lack of germ cells in mutant mice leads to the development of some ovarian tumors (mesotheliomas and granulosa cell), associated with an overproduction of pituitary gonadotropic hormone. Kit^W/Kit^W-v double heterozygotes are viable but sterile because of germ cell deficiency. They are also mast cell deficient. Kit^W/Kit^W-v double heterozygotes lack intermediate cells, derived from melanoblasts, in the stria vascularis resulting in endocochlear degeneration, loss of endocochlear potential, and hearing impairment.
002020	C57BL/6J-Apc^Min/J	Level 3
	The C57BL/6J-Apc^Min/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-Apc^Min 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-Apc^Min 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-Apc^Min 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 (Ednrb^s). 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.
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 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 descriiption 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.
003008	B6;129S-Tnf^tm1Gkl/J	Level 4
	Mice homozygous for the Tnf^tm1Gkl targeted mutation are viable and fertile. Development of both lymph nodes and Peyer's patches is normal, and homozygous mutant mice show no apparent phenotypic abnormalities. Homozygous mice completely lack splenic primary B cell follicles and cannot form organized follicular dendritic cell networks and germinal centers. TNF-deficient mice treated to induce skin carcinogenesis develop significantly less benign and malignant tumors than treated wildtype mice. Nonobese homozygous mutant mice show modest decreases in body weight, epididymal fat depot weight, and percent body fat (statistically significant in males at 28 weeks of age). Further characterization indicates that 28 week old male mutant mice display lower insulin, triglyceride, and leptin levels compared to wildtype controls. Characterization of TNF deficient homozygotes injected with gold-thioglucose (GTG) to induce hyperphagic obesity indicates that the presence of TNF does ..... For more information please see the full descriiption on the strain data sheet
000049	C57BL/6J-Kit^W-v/J	Level 4
	Kit mice possess pleiotropic defects in pigment-forming cells, germ cells, RBC's and mast cells. In addition, they exhibit impaired resistance to parasitic infection and an intrinsic progenitor cell defect. Kit^W-v homozygotes resemble Kit^W homozygotes in color, anemia, and germ cells, but many of them survive to maturity. The lack of germ cells in mutant mice leads to the development of some ovarian tumors (mesotheliomas and granulosa cell), associated with an overproduction of pituitary gonadotropic hormone.
000668	C57L/J	Level 4
	C57L/J mice are used widely in research as a general purpose strain. Mice have a high incidence of Hodgkin's-like reticulum cell neoplasm at 18 months of age and pituitary tumors in old multiparous females. C57L/J mice are highly susceptible to experimental allergic encephalomyelitis (EAE). In addition, C57L/J mice are highly susceptible to developing atherosclerotic aortic lesions (4500 to 8000 um² atherosclerotic aortic lesions/aortic cross-section) following 14 weeks on an atherogenic diet (1.25% cholesterol, 0.5% cholic acid and 15% fat) (Paigen et al. 1990). On a lithogenic diet, C57L/J mice develop gallstones as a result of abnormal regulation of cholesterol synthesis (Xua et al. 2004). C57L/J mice carry no detectable endogenous ecotropic MuLV DNA sequences.
004104	FVB.Cg-Mmp9^tm1Tvu/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.
000692	WB/ReJ Kit^W/J	Level 4
	Kit mice possess pleiotropic defects in pigment-forming cells, germ cells, RBC's and mast cells. In addition, they exhibit impaired resistance to parasitic infection and an intrinsic progenitor cell defect. The lack of germ cells in homozygous mutant mice leads to the development of some ovarian tumors (mesotheliomas and granulosa cell), associated with an overproduction of pituitary gonadotropic hormone.
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 descriiption on the strain data sheet
004368	129(B6)-Il10^tm1Cgn/J	Repository- Live
	Mice homozygous for the Il10^tm1Cgn targeted mutation are viable and fertile when housed under specific pathogen free (SPF) conditions. Under conventional housing conditions, Il10-deficiency is associated with altered lymphocyte and myeloid profiles, elevated serum amyloid A levels, altered responses to inflammatory or autoimmune stimuli (both endogenous and induced), increased prevalence of colorectal adenocarcinoma (especially on 129/Sv and, to a lesser extent, BALB/c genetic background), and spontaneous development of chronic enterocolitis (see below). As The Jackson Laboratory Repository maintains these mice at high health status conditions (high SPF), the observed or experimentally-induced Il10-deficient phenotype may vary from that previously published using mice from conventional mouse rooms. These IL-10 mutant mice may be useful studying inflammatory bowel disease (IBD) (Crohn's disease (CD) and/or colitis), cancer, innate and adaptive immunity, a ..... For more information please see the full descriiption on the strain data sheet
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.
002753	129S6/SvEvTac-Atm^tm1Awb/J	Repository- Live
	Mice homozygous for the Atm^tm1Awb 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.
002065	129T2/SvEmsJ	Repository- Live
	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	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. A small percent (4%) of nonproductive males are hermaphrodites. An additional 17% of nonproductive males have abnormally small testes containing no sperm.
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).
008462	B6.129P2-Trp53^tm1Brn/J	Repository- Live
	Exons 2-10 are flanked by loxP sites in this conditional targeted mutation. Mice homozygous for the floxed allele do not show any increase in disease incidence for at least a year. When bred to mice with a cre recombinase gene under the control of a promoter of interest, expression is deleted in the tissue of interest. For example, when crossed to a strain expressing Cre recombinase in the nervous system (see Stock No. 003771), this mutant mouse strain may be useful in studies of medulloblastoma formation.
005540	B6.129S-Tnf^tm1Gkl/J	Repository- Live
	Mice homozygous for the targeted mutation are viable and fertile. Development of both lymph nodes and Peyer's patches is normal, and homozygous mutant mice show no apparent phenotypic abnormalities. Homozygous mice completely lack splenic primary B cell follicles and cannot form organized follicular dendritic cell networks and germinal centers. TNF-deficient mice treated to induce skin carcinogenesis develop significantly less benign and malignant tumors than treated wildtype mice. Nonobese homozygous mutant mice show modest decreases in body weight, epididymal fat depot weight, and percent body fat (statistically significant in males at 28 weeks of age). Further characterization indicates that 28 week old male mutant mice display lower insulin, triglyceride, and leptin levels compared to wildtype controls. Characterization of TNF deficient homozygotes injected with gold-thioglucose (GTG) to induce hyperphagic obesity indicates that the presence of TNF does not affect the degree of obe ..... For more information please see the full descriiption on the strain data sheet
007263	B6.129S1-Ing1^tm1Avg/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.
002101	B6.129S2-Trp53^tm1Tyj/J	Repository- Live
	Mice homozygous for the Trp53^tm1Tyj mutation show no visible phenotype but most develop tumors (principally lymphomas and osteosarcoma) at three to six months of age. Heterozygous mice develop tumors at about 10 months of age. These mice model some of the features of human Li-Fraumeni syndrome, a form of familial breast cancer with mutations in TRP53. Homozygous mice may produce a litter before succumbing to tumors.
002781	B6.129S4-Cdkn1b^tm1Mlf/J	Repository- Live
	Mice deficient in p27^kip 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.
008179	B6.129S4-Kras^tm4Tyj/J	Repository- Live
	This strain carries a point mutation (G12D) whose expression is blocked by the presence of a loxP-flanked stop codon. Homozygotes die in utero. Cre-mediated recombination can excise the stop codon and permit the oncogenic protein to be expressed. Intranasal infection with an adenovirus encoding Cre results in a very high frequency of lung tumors and permits controlled timing of tumor initiation and tumor multiplicity. This strain may be useful in studies of cancer and development. When bred to a strain expressing Cre recombinase under the control of a tetracycline-responsive promoter element and a strain expressing a tetracycline-controlled activator protein in lung epithelial cells (see Stock No. 006234 and 006235 respectively), this mutant mouse strain may be useful in studies of lung development. When bred to a strain expressing Cre recombinase in the male g ..... For more information please see the full descriiption on the strain data sheet
006447	B6.129S6(CBA)-Cebpa^tm1Dgt/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/EBPalpha^F 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-Trp53^tm2Xu/J	Repository- Live
	Mice homozygous for this targeted mutation are viable and fertile. They carry two phosphorylation site disruptions: Ser18 to Ala (S18A), and Ser23 to Ala (S23A). Trp53-dependent apoptosis is essentially abolished in thymocytes. These mice develop spontaneous tumors at approximately 1.5 years of age and also develop a range of malignancies that are distinct from those found in animals carrying either a single S23A mutation or a complete knockout of the gene. This mutant mouse strain may be useful in studies of phosphorylation events, cancer development and apoptosis. In an attempt to offer alleles on well-characterized or multiple genetic backgrounds, alleles are frequently moved to a genetic background different from that on which an allele was first characterized. It should be noted that the phenotype could vary from that originally described. We will modify the strain description if necessary as published results become available.
006230	B6.Cg-Cebpa^tm1Dgt Tg(Mx1-cre)1Cgn/J	Repository- Live
	Mice homozygous for this C/EBPalpha "floxed" allele (C/EBPalpha^F) 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/EBPalpha^F 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 descriiption on the strain data sheet
006922	B6.Cg-Sfpi1^tm2Dgt/J	Repository- Live
	Mice that are homozygous for this "PU.1F" conditional allele are viable and fertile. When PU.1^F 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.1^F 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.
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-Kitl^Sl-d/J	Repository- Live
	The multiple steel mutations (Kitl^Sl) behave in a semidominant fashion and cause deficiencies in pigment cells, germ cells, and blood cells paralleling those caused by the Kit locus mutations (dominant spotting alleles). Most of the alleles at steel locus cause severe anemia in utero and death by 15 to 16 days of gestation in homozygous mutant mice. However, steel-Dickie homozygotes (Kitl^Sl-d/Kitl^Sl-d) and compounds of steel and steel Dickie (Kitl^Sl/Kitl^Sl-d) are viable, black-eyed white, are usually sterile in one or both sexes, and have severe macrocytic anemia. Heterozygous steel mice have a diluted coat color with a small amount of white spotting, are viable and fertile, and may have a slight macrocytic anemia. Primordial germ cells are absent in the nonviable steel homozygotes and severely reduced in steel Dickie and steel heterozygotes. Mast cells are virtually absent in skin and other tissu ..... For more information please see the full descriiption on the strain data sheet
007084	B6.FVB(Cg)-Mmp9^tm1Tvu/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 three-week-old mice reveals a dramatically lengthened zone of hypertrophic cartilage (six to eight times larger vs. wild-type) due to delayed apoptosis, vascularization, and ossification. Subsequent remodeling resolves the condition, resulting in normal appearing bones by eight 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 de ..... For more information please see the full descriiption on the strain data sheet
008045	B6;129-Trp53^tm2Holl/J	Repository- Live
	In this mutant strain, exons 4-9 of the endogenous mouse Trp53 gene have been replaced with the homologous human TRP53 region. Transcription of the human sequence is under the control of the endogenous mouse promoter. The inserted human sequence segment encodes the DNA binding domain and the TRP53 polyproline domain. This latter domain contains a polymorphism at codon 72 that encodes either arginine or proline in human populations. This mutant strain expresses the proline variant at codon 72 and the related strain, 129-Trp53^tm1Holl/J (Stock No. 004301) expresses the arginine variant. Mice that are homozygous for this mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Immortalized cell lines derived from primary embryonic fibroblasts harvested from these mice frequently harbor a TRP53 (p53) mutation in the DNA binding domain t ..... For more information please see the full descriiption on the strain data sheet
006980	B6;129-Trp53^tm2Xu/J	Repository- Live
	Mice homozygous for this targeted mutation are viable and fertile. They carry two phosphorylation site disruptions: Ser18 to Ala (S18A), and Ser23 to Ala (S23A). Trp53-dependent apoptosis is essentially abolished in thymocytes. These mice develop spontaneous tumors at approximately 1.5 years of age and a range of malignancies that are distinct from those found in animals carrying either a single S23A mutation or a complete knockout of the gene. This mutant mouse strain may be useful in studies of phosphorylation events in cancer development and apoptosis.
006495	B6;129-Trp53bp1^tm1Jc/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.
002785	B6;129S4-E2f1^tm1Meg/J	Repository- Live
	Mice homozygous for defective E2f1 are viable and fertile. They show thymocyte maturation defects due to a failure of apoptosis, eventually resulting in increased proliferation and increased tumorigenesis. As mutant mice age, they show exocrine gland dysplasia and testicular atrophy. Mutant mice develop a broad spectrum of cancers, although mammary carcinomas were not observed on this genetic background. Mutant mice are also protected from experimental autoimmune encephalomyelitis (EAE). These mice may be useful in studies of apoptosis, cancer, thymocyte development/selection, diabetes, autoimmunity, and multiple sclerosis.
006238	B6;129S4-Thbs2^tm1Bst/J	Repository- Live
	Mice homozygous for this targeted mutation are viable and fertile. Multiple analyses has confirmed the absence of protein in embryonic and adult tissue of homozygous mice. Homozygotes exhibit skin disorders (abnormal collagen fiber patterns, reduced tensile strength, increased fragility) and skin fibroblasts have attachment defects. Mice also exhibit an increase in total density/cortical thickness of the long bones, abnormally long bleeding times, and a significant increase in blood vessel density. Homozygous mice exhibit accelerated wound healing after biopsy and accelerated/increased tumor formation following chemically-induced skin carcinogenesis. Mutant mice may be useful in studies of collagen fibrillogenesis in skin and tendons, angiogenesis and vascular pathophysiology, wound healing, chemically-induced tumor progression, and as a potential model for Ehlers Danlos syndrome. In an attempt to offer alleles on well-characterized or multiple genetic backgrounds, alleles are fre ..... For more information please see the full descriiption on the strain data sheet
004333	C.129P2(B6)-Il10^tm1Cgn/J	Repository- Live
	Mice homozygous for the Il10^tm1Cgn targeted mutation are viable and fertile when housed under specific pathogen free (SPF) conditions. Under conventional housing conditions, Il10-deficiency is associated with altered lymphocyte and myeloid profiles, elevated serum amyloid A levels, altered responses to inflammatory or autoimmune stimuli (both endogenous and induced), increased prevalence of colorectal adenocarcinoma (especially on 129/Sv and, to a lesser extent, BALB/c genetic background), and spontaneous development of chronic enterocolitis (see below). As The Jackson Laboratory Repository maintains these mice at high health status conditions (high SPF), the observed or experimentally-induced Il10-deficient phenotype may vary from that previously published using mice from conventional mouse rooms. These IL-10 mutant mice may be useful studying inflammatory bowel disease (IBD) (Crohn's disease (CD) and/or colitis), cancer, innate and adaptive immunity, a ..... For more information please see the full descriiption on the strain data sheet
008332	C.129S1-Igh^tm1Janz/J	Repository- Live
	These mutant mice carry a His₆-tagged Myc gene (cDNA) sequence inserted in the endogenous immunoglobulin heavy chain complex (Igh) locus, which mimics the human endemic Burkitt lymphoma t(8;14)(q24;q32) translocation and mouse plasmacytoma T(12;15) translocation. The His₆-tagged Myc is overexpressed in B-cells throughout B-cell development, as detected by FACS analysis. Tumor-free heterozygotes, 4 to 6 months of age, on a mixed B6;129X1 background, exhibit increased B-cell proliferation and apoptosis and have enlarged lymph nodes and spleen due to follicular hyperplasia. 68% of mutant mice between 6 and 21 months of age develop mature B-cell tumors that are IgM and BCL6 positive. Approximately half of the tumors detected are lymphoblastic B-cell lymphomas that are Burkitt-like in appearance and one fifth as plasmacytomas. The plasmacytomas occur in gut-associated lymphoid tissue (GALT), especially in the mesenteric lymph node and Peyer's ..... For more information please see the full descriiption on the strain data sheet
008372	C.B6-Tg(H2-L-IL6)1Kish/J	Repository- Live
	These transgenic mice express the human interleukin 6 (IL6) gene under the direction of the mouse histocompatibility 2, D region ( H-2L^D) promoter. The transgenic insert is located on Chromosome 9. Human IL6 protein is detected in serum by ELISA and mRNA is detected in the spleen, lymph nodes, thymus, heart, lung, liver, kidney, and intestine, but not in brain tissue. As early as three to four months of age, transgenic mice develop up to 10-fold enlarged lymph nodes (due to plasma cell accumulation), splenomegaly, and glomerulonephritis. Although homozygotes for this transgenic insert are viable and fertile, due to the early onset of plasma cell tumors, this strain is maintained as a hemizygote. This mutant mouse strain may be useful in studies of plasma cell neoplasms.
003135	C57BL/6-Tg(TRAMP)8247Ng/J	Repository- Live
	These mice harbor the Transgenic Adenocarcinoma of the Mouse Prostate (TRAMP); PB-Tag Line 8247 transgene. Mice hemizygous for the TRAMP transgene develop progressive forms of prostate cancer with distant site metastasis and exhibit various forms of disease from mild intraepithelial hyperplasia to large multinodular malignant neoplasia. TRAMP hemizygotes can exhibit prostatic epithelial neoplasia (PIN) by 12 weeks of age. Tumors, appearing as well differentiated adenocarcinoma, can arise by 24 weeks of age, mostly in the dorsal and lateral lobes of the prostate. By 30 weeks of age, most hemizygous mice will display evidence of metastatic spread to the lymph nodes and/or lungs, phylloides appearance of some tumors, and seminal vesicle invasion. Tumors exhibit elevated levels of nuclear TRP53 and decreased androgen receptor expression. Note that pure C57BL/6 TRAMP hemizygotes may live to 52 weeks of age or longer. TRAMP mice are also available on a mixed C57BL/6 x FVB/N genet ..... For more information please see the full descriiption on the strain data sheet
000669	C58/J	Repository- Live
	This strain was developed by MacDowell in 1921 from litter mates 58 and 52 of Miss Lathrop's stock. A mating of the same male but a different female gave rise to the commonly used C57BL group of strains. C58/J mice exhibit a high incidence of leukemia (>90% by one year of age). C58/J mice also exhibit 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).
001143	CBA/CaGnLeJ	Repository- Live

000655	CBA/CaH-T(14;15)6Ca/J	Repository- Live
	This strain carries the T(14;15)6Ca translocation which results in nondisjunction at a rate of 4.4% in males and 22.2% in females. CBA/CaH-T6 mice have been used in tandem with the CBA/H strain in foreign body tumorigenesis studies in which the T6 chromosome was used as a marker to distinguish donor cells from host.
000657	CE/J	Repository- Live
	CE/J mice are resistant to amyloid induction and development of amyloidosis. Amyloidosis is the extracellular deposition of the acute phase protein 'serum amyloid A' (SAA), which is induced in response to inflammation. CE/J mice express a single isoform of SAA designated SAA2.2, which is structurally unable to form amyloid fibrils. Viral expression of amyloidogenic proteins in CE/J mice does result in amyloid depostion, making this a useful model to examine the amyloid deposition potential of altered SAA proteins. Early studies by Dr. Margaret Dickie reported that approximately 1/3 of CE females and of reciprocal DBA x CE F1 hybrids were found to have ovarian tumors at 20 months of age. Virgin reciprocal DBA x CE F1 hybrids were found to develop hyperplasia of the uterus and an increased uterine sensitivity to estrogen that increases with age. This pathology results from a hormonal imbalance characteristic of this F1 cross and breeding the female can ameliorate this trait.< > ..... For more information please see the full descriiption on the strain data sheet
006132	DDD.GR-Mtv2^a/JmsJ	Repository- Live

005038	FVB-Tg(MMTV-Erbb2)NK1Mul/J	Repository- Live
	These transgenic mice express the activated rat Erbb2 (c-neu) oncogene under the direction of the mouse mammary tumor virus promoter. The activated, or transforming, version of the rat Erbb2 (c-neu) oncogene has a valine to glutamic acid substitution at acid 664, (Val⁶⁶⁴ to Glu⁶⁶⁴). Non-uniform and random transgene expression is detected by RNase protection assay in mammary gland epithelium from hemizygous mice. Tumor formation is multifocal, stochastic and matches the expression pattern of the transgene. While no transgene expression is detected at 5 and 8 weeks of age in normal mammary gland tissue, it is detected in adenocarcinomas from older (23 week old) mice. The donating investigator indicates that 50% of transgenic mice derived from the TG.NK founder line, develop tumors within 6-12 months of age. Mice that are homozygous for the targeted mutation are viable, fertile and normal in size. This mutant mouse strain may be useful in studies of bre ..... For more information please see the full descriiption on the strain data sheet
004363	FVB.Cg-Tg(MMTV-vHaras)SH1Led/J	Repository- Live
	These transgenic mice express the Harvey RAS (human) gene under the direction of the mouse mammary tumor virus promoter. The majority of expression of the transgene is detected in the mammary tissue and salivary glands. Both male and female transgenic mice develop malignant lymphoid tissue and mammary and salivary gland tumors as early as 5 weeks of age. Half of the female transgenic animals develop tumors by 6 months of age. Histological analysis of mammary tumors revealed most of the tumors were adenocarcinomas and were locally invasive with some cases of metastasis to liver and/or lung. The tumors were found to express the transgene transcript. Protein-tyrosine phosphatase epsilon mRNA and protein was found to be highly expressed only in mammary tumors. In 20% of the transgenic mice diffuse benign hyperplasia develops in the Harderian lacrimal gland causing bilateral exophthalmia. The donating investigator reports hemizygous females develop tumors by delivery of their first litter ( ..... For more information please see the full descriiption on the strain data sheet
002374	FVB/N-Tg(MMTV-PyVT)634Mul/J	Repository- Live
	Mice carrying the (MMTV-PyVT) transgene are viable, but show loss of lactational ability coincident with transgene expression. Female carriers develop palpable mammary tumors as early as 5 weeks of age. Adenocarcinomas arise in virgin and breeder females as well as males, which are multifocal, highly fibrotic, and involve the entire mammary fat pad. Males also develop adenocarcinoma of the seminal vesicles and hemangiomas. Pulmonary metastases are observed in 80-94% of tumor-bearing female mice. Transgene expression is detected at high levels in male and female mammary glands. Lower levels are detected in salivary gland, seminal vesicles, ovaries, and lungs (believed to be the result of pulmonary metastases).
004848	NOD.Cg-Rag1^tm1Mom Prf1^tm1Sdz/SzJ	Repository- Live
	Mice that are homozygous for both targeted mutations are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities when housed under specific pathogen free conditions. These double homozygote mutant mice have no mature T or B lymphocytes, no detectable NK cell cytotoxic activity, and lack serum immunoglobulin. The number of nucleated spleen cells is significantly reduced in double mutant mice, when compared to the single homozygote, NOD.129S7(B6)-Rag1^tm1Mom/J (Stock No. 003729). Although an increased number of DX5⁺CD122⁺ NK cells are found in the spleens of double mutants, these NK cells have impaired cytotoxic activity. The disruption of Prf1 ablates NK cell cytotoxic activity resulting in increased engraftment levels over that observed with Stock No. 003729. All mutant mice develop thymic lymphomas. This double mutant mouse strain may be useful in studies involving engraftment of human hematolympho ..... For more information please see the full descriiption on the strain data sheet
000679	P/J	Repository- Live
	P/J mice exhibit a high incidence of lymphatic leukaemia. They also show a high susceptibility to audiogenic and electroconvulsive seizures. P/J mice are also homozygous for a number of other mutations including nonagouti (a), brown (Tyrp1^b), pink-eyed dilution (Oca2^p), short ear (Bmp5^se), dilute Myo5a^d), and retinal degeneration 1 (Pdeb1^rd1).
005221	RIII/ImrNhsJ	Repository- Live
	The original RIII strain was known for its high incidence of hormone-dependent mammary tumors transmissible by milk-born MMTV. The RIII/ImrNhsJ substrain is reported to show a pattern of virus expression and tumor incidence similar to the RIII strain (Sarkar, et al. 2004). RIII/ImrNhsJ mice carry the following endogenous MMTV loci: Mtv-6, 8, 14, 17 and possibly 21 (Popken-Harris, et al. 2001). Exogenous MMTV infection leads to the deletion of CD4⁺ Vbeta-2 and Vbeta-8 peripheral and central T cells (Uz-Zaman, et al. 2003). It is possible to modulate mammary tumor incidence using high and low calorie diets (Li, et al. 1994). RIII/ImrNhsJ mice infected with exogenous MMTV may be useful for studies of human breast cancer activated by insertional mutagenesis. NOTE: Mice distributed by The Jackson Laboratory are not infected with MMTV. Regrettably, we do not have a source for the virus.
003081	STOCK Ptch1^tm1Mps/J	Repository- Live
	Mice homozygous for the targeted mutation die during embryogenesis and are found to have open and overgrown neural tubes. Heterozygous patched mice are larger than wild-type littermates and have a low incidence of hindlimb defects. Some heterozygotes develop brain tumors beginning around 5 weeks of age. Heterozygotes express lacZ in a pattern mimicking endogenous gene expression pattern. Homozygous embryos display derepressed lacZ expression starting at embryonic day 8.0.
006882	STOCK Tg(CAG-Bgeo,-AML1/ETO,-ALPP)1Lbe/J	Repository- Live
	Mice hemizygous for this "Z/AP-AML1-ETO" transgene (coding for the translocation t(8;21) present in 15% of acute myeloid leukemias (AML)) are viable and fertile. Homozygotes die in utero presumably due to high lacZ expression. Prior to cre-mediated excision of the "floxed" STOP sequence, expression of lacZ is observed in all tissues including bone marrow progenitor cells. When bred to Cre recombinase expressing mice, the STOP sequence (and beta-geo) is removed in the resulting offspring, allowing transcription/co-expression of both the human AML1-ETO fusion protein and placental alkaline phosphatase (ALPP or PLAP) to proceed in the Cre recombinase expressing cells. While pan expression of AML1-ETO leads to embryonic lethality (E7.5), hematopoietic and endothelial expression leads to malignancy in B- and T- lymphoid cells and secondary mutations that closely resemble the association of AML1-ETO with acute myeloid leukemia in humans. These transgenic mice may ..... For more information please see the full descriiption on the strain data sheet
006876	STOCK Tg(CAG-Bgeo,-TEL/AML1,-EGFP)A6Lbe/J	Repository- Live
	Mice hemizygous for this Cre-conditional TEL-AML1 (or iZ/EG-TEL-AML1) transgene are viable and fertile. Homozygotes die in utero, presumably due to high lacZ expression. Prior to Cre-mediated excision of the "floxed" STOP sequence, high expression of lacZ is observed in cells and tissues. When bred to Cre recombinase transgenic mice, the STOP sequence (and beta-geo) is removed in the resulting offspring, allowing transcription/co-expression of both the human TEL-AML1 fusion protein and EGFP in all cre-expressing cells. TEL-AML1 transcripts are not observed in adult organ tissues prior to excision of the floxed sequences. Following Cre-mediated deletion of the STOP sequence (by B6.Cg-Tg(Tek-cre)12Flv/J, Stock No. 004128), Western blot analysis reveals that EGFP levels are well correlated with TEL-AML1 transcript levels. While global expression of TEL-AML1 leads to embryonic lethality (E7.5), hematopoieti ..... For more information please see the full descriiption on the strain data sheet
006613	STOCK Tg(CAG-Bgeo,-Tle1,-ALPP)1Lbe/J	Repository- Live
	Hemizygous transgenic mice are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. These transgenic mice express the mouse transducin-like enhancer of split 1, homolog of Drosophila E(spl) gene, Tle1 (also known as Groucho-related gene 1; Grg1) under the regulation of the chicken beta actin promoter (ACTB) and the cytomegalovirus (CMV) intermediate-early enhancer. An internal ribosome entry sequence (IRES) followed by the human alkaline phosphatase (ALPP) reporter gene inserted downstream of the Tle1 gene directs co-expression of ALPP and TLE1. TLE1 and ALPP co-expression is blocked, however, by the presence of a loxP-flanked Bgeo (beta-galactosidase/neomycin resistance fusion protein) cassette inserted between the ACTB/CMV promoter and the Tle1 coding sequence. In the absence of Cre recombinase, beta-galactosidase activity is detected in all tissues tested including pancreas, lung, kidney, cerebellum, heart, m ..... For more information please see the full descriiption on the strain data sheet
006619	STOCK Tg(Cga-LHB/CGB)94Jhn/J	Repository- Live
	Hemizygous females are not fertile and hemizygous males are sub-fertile. Hemizygotes hypersecrete luteinizing hormone (LH) from pituitary gonadotropes under hypothalamic control. Inclusion of a bovine luteinizing hormone beta (LHB) sequence in the transgene results in a longer hormone half-life. Transgenic females display a range of reproductive and endocrine anomalies, while males are largely phenotypically normal. Transgenic males do not have elevated serum LH or testosterone when compared to wildtype animals, although their testes are significantly smaller. Transgenic females display elevated serum LH, androgens, and estrogens, with subsequent phenotypes including infertility with chronic anovulation and ovarian pathologies ranging from ovarian cysts to strain-dependent granulosa and theca-interstitial cell tumors. Tumors have been noted in mice from age 4 to 9 months. Other major phenotypes include hyperandrogenemia and precocious puberty, defects in uterine receptivity and mid-ges ..... For more information please see the full descriiption on the strain data sheet
000693	WC/ReJ Kitl^Sl/J	Repository- Live
	The multiple steel mutations (Kitl^Sl) behave in a semidominant fashion and cause deficiencies in pigment cells, germ cells, and blood cells paralleling those caused by the Kit locus mutations (dominant spotting alleles). Most of the alleles at steel locus cause severe anemia in utero and death by 15 to 16 days of gestation in homozygous mutant mice. However, compounds of two steel mutants (e.g. Kitl^Sl/Kitl^Sl-d) are viable, black-eyed white, are usually sterile in one or both sexes, and have severe macrocytic anemia. Heterozygous steel mice have a diluted coat color with a small amount of white spotting, are viable and fertile, and may have a slight macrocytic anemia. Primordial germ cells are absent in the nonviable steel homozygotes and severely reduced in steel heterozygotes. Mast cells are virtually absent in skin and other tissues of steel mutant mice. Tumors tend to develop in germ-cell-deficient ovaries with advancing ..... For more information please see the full descriiption on the strain data sheet
100401	WCB6F1/J Kitl^Sl Kitl^Sl-d	Repository- Live
	The multiple steel mutations (Kitl^Sl) behave in a semidominant fashion and cause deficiencies in pigment cells, germ cells, and blood cells paralleling those caused by the Kit locus mutations (dominant spotting alleles). Many steel alleles cause severe anemia resulting in death in utero of homozygous mutant mice. However, mice homozygous for some steel mutations and compound heterozygotes for two steel alleles (e.g., Kitl^Sl/Kitl^Sl-d) are viable and have black eyes and a white coat; they have severe macrocytic anemia, and both sexes are usually sterile due to failure of germ cells to migrate correctly during development. Mice heterozygous for a single steel mutation have diluted coat color with a small amount of white spotting, are viable and fertile, and may have a slight macrocytic anemia. Primordial germ cells are absent in the nonviable steel homozygotes and severely reduced in steel heterozygotes. Mast cells are virtuall ..... For more information please see the full descriiption on the strain data sheet
002674	129-Kras^tm1Tyj/J	Repository-Cryopreserved
	Homozygous mice die at about embryonic day 12-13. They have a hypocellular fetal liver which also displays extensive cell death. They also appear to have a defect in both the hematopoietic cells and their microenvironment.
003451	129-Smad3^tm1Par/J	Repository-Cryopreserved
	Mice homozygous for the targeted mutation are viable. Although fertile, they produce litters at reduced efficacy compared to wild type or heterozygous mice. Null mutants are approximately 20%-30% smaller than heterozygous or wildtype litter mates, with males exhibiting a more pronounced size reduction. Reporter lacZ expression is observed in many developing embryonic tissues with highest levels in mesenchymal derivatives. Expression in adult mutant mice is observed in the colon, with highest levels in the muscularis propria and submucosa with lower levels in the epithelium. At approximately 4-6 months of age, they develop gastric tumors. The donating investigator originally described spontaneous, deeply invasive colorectal adenocarcinomas that penetrate through all layers of the intestinal wall and metastasize to lymph nodes. Colorectal adenocarcinomas are not a component of the phenotype observed in this strain at The Jackson Laboratory. However, the gastric epithelium was fo ..... For more information please see the full descriiption on the strain data sheet
004301	129-Trp53^tm1Holl/J	Repository-Cryopreserved
	In this mutant mouse strain, the endogenous murine sequence for exons 4-9 of the targeted gene, which encode the DNA binding domain of the tumor suppressor protein, have been replaced with the homologous normal human sequence. Transcription is under the control of the endogenous mouse promoter. Mice that are homozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Homozygous mutant mice exhibit normal expression and functional activity of the chimeric gene. Homozygous mutant mice have normal immunodetectable levels of p53 protein accumulation in nuclei in response to UV-induced DNA damage. Thymocytes from mutant mice are as susceptible to gamma-irradiation-induced and dexamethaxone-induced apoptosis as wildtype thymocytes. This mutant mouse strain may be useful in studies related to in vivo spontaneous and induced mutation of the human TRP53 gene sequence, and pharmacological agents for alt ..... For more information please see the full descriiption on the strain data sheet
002080	129-Trp53^tm1Tyj/J	Repository-Cryopreserved
	Mice homozygous for the Trp53^tm1Tyj mutation show no visible phenotype but most develop tumors (principally lymphomas and osteosarcoma) at 3-6 months of age. Heterozygous mice develop tumors at about 10 months of age. These mice model some of the features of human Li-Fraumeni syndrome, a form of familial breast cancer with mutations in TRP53. Homozygous mice may produce a litter before succumbing to tumors.
002357	129P3/JEmsJ	Repository-Cryopreserved

001198	129P4/RrRkJ	Repository-Cryopreserved
	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.
005109	129S(FVB)-Men1^tm1.2Ctre/J	Repository-Cryopreserved
	These mice possess loxP sites flanking exons 3 to 8 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 a strain expressing Cre recombinase in pancreatic beta cells (see Stock No. 003573 for example), this mutant mouse strain may be useful in studies of pancreatic islet adenomas.
002082	129S-Rb1^tm1Tyj/J	Repository-Cryopreserved
	Mice homozygous for this targeted mutation die in utero, apparently from a failure to produce erythrocytes in the liver, demonstrating that the endogenous gene is essential for normal development. Heterozygous mice, which are analogous to human carrier individuals, do not develop retinal tumors, but do develop pituitary tumors by 8 months of age.
006403	129S.B6-Tg(KRT14-Esr1/HRAS)1Pkha/J	Repository-Cryopreserved
	Mice hemizygous for this "K14-ER:Ras" transgene are viable and fertile. Inducible expression of the ER:Ras fusion protein is observed in the epidermis following topical application of 4-hydroxytamoxifen (4OHT). Prolonged (4 weeks) induction of human H-Ras^G12V 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. H-Ras^G12V-induced skin abnormalities were entirely reversed within one month after 4OHT cessation. These mice have a similar 4OHT-inducible skin phenotype as the transgenic mice expressing human Raf-1[DD] (Stock No. 006661) or human Mek1^R4F (Stock No. 006822), and may be useful in studies of the Ras/Raf/MEK/ERK cell proli ..... For more information please see the full descriiption on the strain data sheet
000090	129S1/Sv-Oca2⁺ Tyr⁺ Kitl^Sl-J/J	Repository-Cryopreserved
	The multiple steel mutations (Kitl^Sl) behave in a semidominant fashion and cause deficiencies in pigment cells, germ cells, and blood cells paralleling those caused by the Kit locus mutations (dominant spotting alleles). Most of the alleles at steel locus cause severe anemia in utero and death by 15 to 16 days of gestation in homozygous mutant mice. However, compounds of two steel mutants (e.g. Kitl^Sl/Kitl^Sl-d) are viable, black-eyed white, are usually sterile in one or both sexes, and have severe macrocytic anemia. Heterozygous steel mice have a diluted coat color with a small amount of white spotting, are viable and fertile, and may have a slight macrocytic anemia. Primordial germ cells are absent in the nonviable steel homozygotes and severely reduced in steel heterozygotes. Mast cells are virtually absent in skin and other tissues of steel mutant mice. Tumors tend to develop in germ-cell-deficient ovaries with advancing a ..... For more information please see the full descriiption on the strain data sheet
000091	129T1/Sv-Oca2⁺ Tyr^c-ch Dnd1^Ter/J	Repository-Cryopreserved

002064	129T2/SvEms	Repository-Cryopreserved

001263	129XAM/SvJ	Repository-Cryopreserved
	Leroy Stevens reported that 96% (81 or 84) of 9XAM male genital ridges grafted to the testes of adults develop into testes with teratomas. Spontaneous teratomas were found in 1 of 187.
003382	B10.D2-Tg(C3-1-TAg)cJeg/J	Repository-Cryopreserved
	This transgenic strain is a model for the study of multistage oncogenesis in the prostate and mammary glands. Male transgenic mice develop prostatic hyperplasia in early life that progresses to adenoma or adenocarcinoma in about half of the animals which survive longer 7 months of age. Female animals generally develop mammary intraepithelial neoplasia with similarities to DCIS by 3 months of age with subsequent development of mammary adenocarcinoma by 6 months of age in 100% of the animals. About 10 - 15% of female mice develop lung metastases, although lung metastases from prostate cancer is extremely rare. Bone metastases have not been observed. Please note that the phenotype description above was developed for this allele on an FVB background (stock number 3381). The mammary and prostate tumor phenotypes may be different on the C57BL/10 background in this strain.
000599	B6 x B6CBCa A^w-J/A-T(5;13)264Ca Kit^W-v/J	Repository-Cryopreserved

006564	B6(C)-Kit^W-41J Gusb^mps/BrkJ	Repository-Cryopreserved
	Mice homozygous for the "mps" (mucopolysaccharidosis type VII or MPS VII) mutation are devoid of expression of the lysosomal enzyme beta glucuronidase. Homozygous animals are viable, but females have a deficiency in lactation. Skeletal and connective tissue anomalies in both males and females are believed to prevent successful breeding. As this mutation is recessive, heterozygous mice are phenotypically similar to wildtype. Homozygotes exhibit short and thickened long bones (smaller than heterozygous or wildtype littermates), "pug type" appearance of the nose, hepatomegaly, splenomegaly, corneal clouding, and deafness. In appearance, homozygous Kit^W-41J mice are mostly white with black eyes and brown or grey spots. MPS VII mice are a model of the beta glucuronidase enzyme deficiency in humans called Sly Disease. They may be useful in developing new therapies (enzyme replacement, cell transplantation, gene therapy) broadly applicable to other lysosomal storage disease ..... For more information please see the full descriiption on the strain data sheet
003509	B6.129-Blmh^tm1Geh/J	Repository-Cryopreserved
	Bleomycin (BLM) is a clinically used glycopeptide anticancer agent. It is deaminated in vitro by BLMH. Blmh null mice have decreased viability and fertitility. Only about 65% of the expected number survive the neonatal period. Mice lacking Blmh exhibit variably penetrant tail dermatitis that resembles rodent ringtail. This resembles skin lesions in humans with pellagra, necrolytic migratory erythema, and acrodermatitis enteropathica. Null mice also are more sensitive to acute BLM lethality and develop pulmonary fibrosis following BLM treatment.
005709	B6.129-Ski^tm1Cco/J	Repository-Cryopreserved
	This mutant was created on a mixed (129 x C57BL/6J) background. Greater than 80% of mice on this mixed background had severe neural tube closure defects (such as exencephaly) while less than 16% exhibited facial clefting. The penetrance of these phenotypes has segregated with further backcross to C57BL/6J. The congenic mutant described here was backcrossed 12-14 times to wildtype C57BL/6J. Mice homozygous for the targeted mutation die before or shortly after birth due to developmental defects. Null mice are distinguishable from wildtype and heterozygous littermates at embryonic day 8.5 (E8.5) with delayed, but complete, cranial neural tube closure (incomplete at the normal E9.5). Ninety percent of null mice alive at E18.5 exhibit facial clefting. Other highly penetrant phenotypes include flattened snout, depressed nasal bridge, excessive orbital separation, elongated subventricular zones, vestigial polydactyly, and malformations of the olfactory bulb, iris, and ventral septum. Heterozy ..... For more information please see the full descriiption on the strain data sheet
003180	B6.129S-Cdh3^tm1Hyn/J	Repository-Cryopreserved
	Mice homozygous for the Cdh3^tm1Hyn targeted mutation (P-cadherin deficient) are viable and fertile with females able to nurse and maintain their litters. Virgin homozygous mutant females display precocious differentiation of the mammary gland. Aging mice develop hyperplasia and dysplasia of the mammary epithelium. In addition, mammary glands from P-cadherin deficient mice show abnormal lymphocyte infiltration.
004372	B6.129S2-Mad2l1^tm1Sorg/J	Repository-Cryopreserved
	Mice that are heterozygous for the Mad2l1^tm1Sorg targeted allele are viable, fertile, normal in size, and do not display any gross physical or behavioral abnormalities. Homozygous null mice are embryonic lethal; they fail to develop past embryonic days 6-7 due to catastrophic chromosome missegregation and apoptosis. Histological analysis of heterozygous mutant mice reveal increased germinal center formation in spleen and a higher incidence of lung carcinomas when compared to the wildtype. This mutant mouse strain represents a model that may be useful in studies of the role cell-division checkpoints in tumorogenesis.
008192	B6.129S2-Nf1^tm1Tyj/J	Repository-Cryopreserved
	Heterozygous animals do not exhibit the classical symptoms of Human neurofibromatosis type 1, but are highly predisposed to the formation of various tumor types, notably phaeochromocytoma, a tumor of the neural crest-derived adrenal medulla, and myeloid leukemia. Homozygosity leads to abnormal cardiac development and mid-gestational embryonic lethality. This strain may be useful in studies of cancer and developmental biology.
002102	B6.129S2-Rb1^tm1Tyj/J	Repository-Cryopreserved
	Mice homozygous for this targeted mutation die in utero, apparently from a failure to produce erythrocytes in the liver, demonstrating that the endogenous gene is essential for normal development. Heterozygous mice, which are analogous to human carrier individuals, do not develop retinal tumors, but do develop pituitary tumors by 8 months of age. In an attempt to offer alleles on well-characterized or multiple genetic backgrounds, alleles are frequently moved to a genetic background different from that on which an allele was first characterized. This is the case for this strain. It should be noted that the phenotype could vary from that originally described. We will modify the strain description if necessary as published results become available.
008183	B6.129S4(Cg)-Trp53^tm2.1Tyj/J	Repository-Cryopreserved
	Mice carrying this Trp53 (p53) R172H point mutation mimic human Li-Fraumeni Syndrome, both genotypically and phenotypically. Heterozygotes develop a broad spectrum of tumors with a mean survival time of 16 months. Prominent tumor types include osteosarcomas (often metastatic), hemangiosarcomas, B-cell lymphomas and a variety of carcinomas. Homozygous mice also develop a broad spectrum of tumors, particularly T-cell lymphomas, hemangiosarcomas, soft-tissue sarcomas, osteosarcomas, primitive tumors (particularly male teratocarcinomas), and a variety of epithelial carcinomas. Mutant protein is expressed at high levels in mouse embryonic fibroblasts, as determined by Western blotting.
008182	B6.129S4-Trp53^tm3.1Tyj/J	Repository-Cryopreserved
	These targeted mutant mice carry a R270H missense mutation in exon 8 of the gene. Heterozygous mice develop a broad spectrum of tumors with a mean survival time of 16 months. Prominent tumor types include osteosarcomas (often metastatic), hemangiosarcomas, B-cell lymphomas and a variety of carcinomas. Homozygous mice also develop an array of tumor types including a variety of hematological tumors (particularly T-cell lymphomas), hemangiosarcomas, soft-tissue sarcomas, ostersarcomas, primitive tumors (particularly male teratocarcinomas), and a variety of epithelial carcinomas. Homozygotes have a mean survival time of 4.5 months. Mutant protein is expressed in all of the places that wildtype protein is expressed in normal tissues. Irradiation or DNA damage leads to substantially increased protein levels. Expression is also upregulated in some tumor types. This strain may be useful in studies of cancer and Li-Fraumeni Syndrome.
002646	B6.129S6-Nf1^tm1Fcr/J	Repository-Cryopreserved
	Mice homozygous for the Nf1^tm1Fcr targeted mutation die during embryonic development due to severe heart malformation (~E13). They also show hyperplasia of neural crest-derived sympathetic ganglia. Heterozygotes do not exhibit any overt disease symptoms. However, as noted in a another targeted mutation deleting the same exon of the Nf1 gene (Jacks, et al., Nat Genetics 7:353-361, 1994), they do show a predisposition to many types of tumors and were recently shown to have deficits in learning and memory (Silva, et al., Nat Genetics 15:281-284, 1997).
002188	B6.129S7-Amh^tm1Bhr/J	Repository-Cryopreserved
	Male mice homozygous for the Amh^tm1Bhr mutation have testes that are fully descended and produce functional sperm. They also develop a uterus which interferes with sperm transfer rendering most infertile. The testes develop Leydig cell hyperplasia. Homozygous females are fertile.
001737	B6.A-H2-T18^a.HRS-Hr^hr/J	Repository-Cryopreserved
	Mice homozygous for the hr mutation have a higher incidence and earlier onset of leukemia, reducible by virus-specific antibody. Deficiency of splenic T helper cells (Ly-1+) may account for low cellular immune response of homozygous mutant mice. The coat is normal on hr/hr mice up to 10 days but then hair is lost from the follicle. Waves of hair growth with few thin fuzzy hairs ocur at monthly intervals for some time but homozygotes eventually become continuously hairless. Vibrissae are repeatedly regrown and shed, becoming more abnormal with age. Toenails are long and curved. There is hyperkeratosis of statified epithelium and the upper part of hair canals beginning at 14 days. Hair club formation is abnormal. Cysts form from the hyperkeratotic upper part of hair canals and sheaths of abnormal follicles stranded in dermis. Some cysts also form from sebaceous glands. All cysts undergo sebaceous transformation and later keratinization. In an attempt to offer alleles on ..... For more information please see the full descriiption on the strain data sheet
000495	B6.C-H38^c/By-Kit^W-56J/J	Repository-Cryopreserved

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

000122	B6.C3-Kit^W-44J/J	Repository-Cryopreserved
	Kit^W-44J heterozygotes have white-tipped feet and a white tail tip although the belly spot standardly found in Kit^W* mutations is very small in this mutant, sometimes restricted to only a few hairs. Homozygotes have a flecked pelt that is predominantly white, especially ventrally, with pigmented patches particularly at the lateral borders. The pigmentation fades with age yielding black-eyed white mice by approximately 9 months of age. While many Kit^W-44J homozygotes are viable, fertility is diminished. Homozygous females have greatly reduced fertility and gonads that are smaller in size with reduced activity. Homozygous males are sterile although spermatogenesis occurs. The Kit^W-44J allele does not produce anemia in either its heterozygous or homozygous state. The red blood cell count, white blood cell count, hematocrit, and mean cell volume are normal. However, bone marrow transplantation experiments reveal that t ..... For more information please see the full descriiption on the strain data sheet
004853	B6.C3-Tg(KRT14-Birc5)19Gros/J	Repository-Cryopreserved
	These transgenic mice express the mouse baculoviral IAP repeat-containing 5, Birc5 (survivin), gene under the direction of the human keratin 14 promoter. Transgene expression is specific to epidermal and follicular keratinocytes. Mice hemizygous for the transgenic insert are resistant to chemical (DMBA)- and UVB-induced keratinocyte apoptosis in vivo. Although hemizygotes were less susceptible to DMBA-induced papilloma formation, spontaneous papilloma regression was not observed and there was enhanced conversion of papillomas to carcinomas. This mutant mouse strain represents a model that may be useful in studies of keratinocyte apoptosis and skin cancer development.
000991	B6.C58-Kit^W-57J/J	Repository-Cryopreserved

000133	B6.Cg-Kit^W-24J/J	Repository-Cryopreserved

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

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

000124	B6.Cg-Kitl^Sl Krt71^Ca/J	Repository-Cryopreserved
	The multiple steel mutations (Kitl^Sl) behave in a semidominant fashion and cause deficiencies in pigment cells, germ cells, and blood cells paralleling those caused by the Kit locus mutations (dominant spotting alleles). Most of the alleles at steel locus cause severe anemia in utero and death by 15 to 16 days of gestation in homozygous mutant mice. However, compounds of two steel mutants (e.g. Kitl^Sl/Kitl^Sl-d are viable, black-eyed white, are usually sterile in one or both sexes, and have severe macrocytic anemia. Heterozygous steel mice have a diluted coat color with a small amount of white spotting, are viable and fertile, and may have a slight macrocytic anemia. Primordial germ cells are absent in the nonviable steel homozygotes and severely reduced in steel heterozygotes. Mast cells are virtually absent in skin and other tissues of steel mutant mice. Tumors tend to develop in germ-cell-deficient ovaries with adva ..... For more information please see the full descriiption on the strain data sheet
000194	B6.Cg-Lx Kit^W-v/J	Repository-Cryopreserved
	Kit mice possess pleiotropic defects in pigment-forming cells, germ cells, RBC's and mast cells. In addition, they exhibit impaired resistance to parasitic infection and an intrinsic progenitor cell defect. Kit^W-v homozygotes resemble Kit^W homozygotes in color, anemia, and germ cells, but many of them survive to maturity. The lack of germ cells in mutant mice leads to the development of some ovarian tumors (mesotheliomas and granulosa cell), associated with an overproduction of pituitary gonadotropic hormone. Heterozygous lx mice show preaxial polydactyly (including hyperphalangy of the first digit) of the hindfeet. Homozygotes show preaxial polydactyly or oligodactyly of the hindfeet, reduction of the tibia, loss of part of the femur and pubis, decrease in number of presacral vertebrae, and anomalies of the urogenital system including horseshoe kidney, hydronephrosis, and hydroureter. Although homozygous Kit^W-v/ ..... For more information please see the full descriiption on the strain data sheet
002306	B6.Cg-an/BrkJ	Repository-Cryopreserved

002319	B6.Cg-Tg(BCL2)22Wehi/J	Repository-Cryopreserved
	Expression of the human BCL2 transgene is restricted to B cell lineage (no T cell expression) in which it enhances cell survival. Hemizygotes show increased numbers of B lymphocytes, Ig-secreting cells and serum Ig, as well as a heightened and prolonged antibody response to immunization. This phenotype is somewhat greater on the BALB/c than on the C57BL/6 background. Hemizygotes on a mixed B6,SJL background (but not on the BALB/c background) develop autoimmune disease characterized by immune complex glomerulonephritis, anti-nuclear antibodies, lymphadenopathy and myocardial infarction. These mice serve as a robust source for the production of B cells and antibodies. Although mice bearing this allele exhibit a mild increase in spontaneous lymphoma and plasmacytoma occurrence (<10% to 18 months) on a (C57BL/6 x SJL)F2 background, on the BALB/c and C57BL/6 backgrounds tumor incidence is insignificant. When this transgene is crossed with an Emu-myc transgene bearing strain (Stock ..... For more information please see the full descriiption on the strain data sheet
000171	B6.D2-Kit^W-45J/J	Repository-Cryopreserved

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

003380	B6.FVB-Tg(C3-1-TAg)cJeg/J	Repository-Cryopreserved
	TgN(C3-1-TAg)cJeg mice are transgenic for the SV-40 Large tumor antigen (TAg) driven by the rat prostatic steroid binding protein (C3(1))promoter. Male mice survive up to 11 months of age. They develop hyperplastic changes in the prostate epithelium which progress to prostate adenocarcinoma in the majority of mice after 8 months of age. Carcinogenic changes in female mice begin with development of hyperplasia of the mammary gland ducts and acini by 3 months of age and progress to multifocal mammary adenocarcinoma with death by 6 month of age. Homozygous mothers can bear offspring but pregnancy appears to accelerate tumor development and foster mothers are required for pups due to lactation difficulties. Evidence of pulmonary metastases has been seen in both male and female mice. These C3-1-TAg transgenic mice provide a model to study TAg-induced progression of hormone responsive tumors. Please note that the phenotype description above was developed for this allele on an FVB backgrou ..... For more information please see the full descriiption on the strain data sheet
001177	B6.LP-Kit^W-49J/J	Repository-Cryopreserved

004338	B6;129-E2f2^tm1Zubi/J	Repository-Cryopreserved
	Mice that are homozygous for the targeted mutation are viable and normal in size. No gene product, mRNA or protein, was detected. At age 15 months mutant mice have a 27% survival rate due to diffuse autoimmune disease that resembles systemic lupus erythematosus (SLE). The phenotype includes splenomegaly by 8-12 weeks of age, glomerulonephritis, accumulated inflammatory infiltrates in the lung, liver, and skin abnormalities such as hair loss, skin wounds, erythema. Anti-dsDNA antibodies are detected in the serum. There are an increased number of mature CD8+ thymocytes and an abnormal accumulation of CD8+ Cd44high Cd69- T effector/memory cells that are autoreactive in peripheral lymphoid organs. E2F2 deficient mice appear to have normal negative selection of thymocytes but demonstrate defects in peripheral tolerance of T lymphoctes (especially Cd8+ T cells) leading to progressive autoimmune disease. This mutant mouse strain may be useful in studies of autoimmunity and may serve as model ..... For more information please see the full descriiption on the strain data sheet
006099	B6;129-Sfpi1^tm1.2Dgt/J	Repository-Cryopreserved
	Mice that are homozygous for the targeted mutation are viable, normal in size, and do not display any gross physical or behavioral abnormalities. Endogenous protein expression is unaffected by the loxP sequences flanking an upstream regulatory region (URE). When bred to mice with a cre recombinase gene under the control of a promoter of interest, the URE of the targeted gene is deleted in the tissue of interest. Deletion of this "floxed" URE may be useful in studying T cell lymphoma, AML and other cancers, as well as transcription factors, hematopoiesis, and development of multiple cell lineages.
008191	B6;129S2-Trp53^tm1Tyj Nf1^tm1Tyj/J	Repository-Cryopreserved
	These mice carry Trp53 and Nf1 targeted mutations on the same chromosome (cis). Double homozygotes are embryonic lethal. Double heterozygotes survive an average of five months and exhibit a significant increase in the percentage of soft tissue sarcomas compared with mice of other genotypes (Nf1 +/-, 5%; p53, 57%; Nf1/Trp53 trans, 36%; Nf1/Trp53 cis, 81%). Furthermore, although Nf1/Trp53 trans mice exclusively develop osteo-, fibro-, rhabdomyo-, and hemangiosarcomas, about 30% of tumors from the Nf1/Trp53 cis animals stain positively for S100 (consistent with glial cell origin) and exhibit classic histological features of malignant peripheral nerve sheath tumors (MPNSTs). This strain may be useful in studies of astrocytomas/glioblastomas and tumor suppressor genes.
002103	B6;129S2-Trp53^tm1Tyj/J	Repository-Cryopreserved
	Mice homozygous for the Trp53^tm1Tyj mutation show no visible phenotype but most develop tumors (principally lymphomas and osteosarcoma) at 3-6 months of age. Heterozygous mice develop tumors at about 10 months of age. These mice model some of the features of human Li-Fraumeni syndrome, a form of familial breast cancer with mutations in TRP53. Homozygous mice may produce a litter before succumbing to tumors.
008181	B6;129S4-Trp53^tm4Tyj/J	Repository-Cryopreserved
	Mice homozygous for this S23A point mutation are viable and fertile. Cells from the mice, including thymocytes and neurons in the cerebellum, exhibit defective apoptosis in response to DNA damage and exhibit partially impaired TRP53 (p53) stabilization. Mice develop increased lymphomas (especially B-cell lineage) and other tumors between one and two years of age.
004686	B6;129S4-Tsc2^tm1Djk/J	Repository-Cryopreserved
	Mice that are heterozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Homozygous null mice have an embryonic lethal phenotype, failing to develop past embryonic days 9.5 to 12.5 due to hepatic hypoplasia. Cultured neuroepithelial progenitor cells isolated from embryonic day 10.5 embryos display abnormal growth and differentiation. All heterozygotes develop multiple bilateral renal cystadenomas by 12-15 months of age. By 15 months, about half develop liver hemangiomas (more common in females than in males). Less than 10% develop extremity angiosarcomas or renal carcinoma. Little or no gene product (protein) is detected by Western blot in renal cystadenomas. PCR analysis reveals loss of the wildtype allele in about 30% of lesions. Phenotype variability is dependent on genetic background. This mutant mouse strain may be useful in studies of tuberous sclerosis (TSC).
002187	B6;129S7-Amh^tm1Bhr/J	Repository-Cryopreserved
	Male mice homozygous for the Amh^tm1Bhr mutation have testes that are fully descended and produce functional sperm. They also develop a uterus which interferes with sperm transfer rendering most infertile. The testes develop Leydig cell hyperplasia.
005514	B6;129X1-Mmp8^tm1Lotn/J	Repository-Cryopreserved
	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 (protein) is detected by Western blot analysis of peripheral blood cells. Male mice homozygous for the mutation are more susceptible to experimentally induced invasive papillomas and fibrosarcomas. Latency of papilloma tumor formation is shorter. Female homozygotes exhibit increased skin cancer incidence when treated with tamoxifen or ovarectomy. Carcinogen administration causes persistent inflammatory response with neutrophil accumulation at the site of injection. Lipopolysaccharide (LPS) challenge causes a two-fold increase in polymorphonuclear cell accumulation in affected lung tissue of male homozygotes. This mutant mouse strain may be useful in studies of carcinogenesis, metastasis, and inflammation.
004187	B6;SJL-Tg(MCL1)8Caig/J	Repository-Cryopreserved
	These transgenic mice express the human MCL1 under the direction of the human MCL1 promoter. Expression of the human MCL1 protein was immunodetectable. Mice hemizygous for the transgene exhibited human MCL1 in bone marrow, lymph node, thymus and spleen (both B- and T-cell populations). Low levels of transgene expression was found in kidney, small intestine, uterus, lung and liver. The majority of the transgenic mice had enlarged spleens, with an increased total splenocyte number (both B- and T-cell). Transgenic mice displayed an increase of myeloid cells relative to lymphoid cells in bone marrow, and an enhanced viability of hematopoietic and lymphoid cells (B, T and myeloid) at immature and mature stages of development. In transgenic mice from 6 to 11 months of age, 27% displayed lymph node enlargement. Transgenic mice had an 88% probability of developing pathologic lymph node disease, and a 60% probability of developing disseminated disease from 6 months to 2 years of a ..... For more information please see the full descriiption on the strain data sheet
002409	B6;SJL-Tg(Wap-HRAS)69Lln Chr Y^SJL/J	Repository-Cryopreserved
	The transgene integrated into the Y chromosome. These transgenics serve as models for male mammary cancer and ras-mediated solid tumors. The transgene also can be used as a Y-chromosome marker. On the B6,SJL background males develop multiple mammary tumors and salivary gland tumors by one year of age. The salivary tumors are adenocarcinomas arising from serous areas of the submandibular gland. The mammary gland tumors are adenosquamous carcinomas. Microscopic lung metastases were present in 14% of tumor bearing animals. On the FVB background males develop multiple mammary tumors at 6-8 weeks. The tumors are adenosquamous carcinomas with multiple foci of squamous differentiation or adenocarcinomas containing glandular tissue. There is no metastasis observed.
000350	B6By.Cg-Kit^W-v Mitf^Mi-wh T/J	Repository-Cryopreserved
	Kit mice possess pleiotropic defects in pigment-forming cells, germ cells, RBC's and mast cells. In addition, they exhibit impaired resistance to parasitic infection and an intrinsic progenitor cell defect. Kit^W-v homozygotes resemble Kit^W homozygotes in color, anemia, and germ cells, but many of them survive to maturity. The lack of germ cells in mutant mice leads to the development of some ovarian tumors (mesotheliomas and granulosa cell), associated with an overproduction of pituitary gonadotropic hormone. Mutations at the Mitf locus affect eye size, pigmentation, and the capacity for secondary bone resorption. Mice homozygous for the white allele (Mitf^Mi-wh) display an overall absence of pigment cells with the exception of the retina which expresses a few giving the eye a small amount of pigment. Homozygotes show slight microphthalmia but a normal skeleton. Heterozygotes (Mitf^Mi-wh/+) have a dilut ..... For more information please see the full descriiption on the strain data sheet
002459	B6D2-Tg(MMTVTGFA)254Rjc/J	Repository-Cryopreserved
	The phenotype of TgN(MMTVTGFA)254Rjc transgenic mice is very similar to that of B6D2-TgN(MMTVTGFA)29Rjc (Stock No. 002373). Mice are viable and fertile, but lactate insufficiently to support the litter. Virgin transgenic mice show no mammary gland abnormalities prepubertally, but adult virgin mice have considerable alveolar gland hyperplasia. Pregnant transgenic mice show marked proliferation of the stromal cells, and alveolar secretion is markedly increased compared to nontransgenic mice. After multiple pregnancies, isolated adenocarcinomas develop. There is no apparent phenotypic effect in males. In females transgene expression was localized to the small ducts and alveoli in both virgin and pregnant mice as evidenced by in situ hybridization and by immunohistochemistry. Immunostaining also revealed some stromal staining in the hyperplastic areas. Egfr mRNA expression was also increased in mammary tissues expressing high levels of the transgene. Crosses between TGFA transgenic ..... For more information please see the full descriiption on the strain data sheet
002373	B6D2-Tg(MMTVTGFA)29Rjc/J	Repository-Cryopreserved
	Mice are viable and fertile, although mice of the most extensively studied line lactate insufficiently to support the litter. Virgin transgenic mice show no mammary gland abnormalities prepubertally, but adult virgin mice have considerable alveolar gland hyperplasia. Pregnant transgenic mice show marked proliferation of the stromal cells, and alveolar secretion is markedly increased compared to nontransgnic mice. After multiple pregnancies, isolated adenocarcinomas develop. There is no apparent phenotypic effect in males. In females, transgene expression is localized to the small ducts and alveoli in both virgin and pregnant mice as evidenced by in situ hybridization and by immunohistochemistry. Immunostaining also reveals some stromal staining in the hyperplastic areas. Egfr mRNA expression is also increased in mammary tissues expressing high levels of the transgene. Crosses between TGFA transgenic mice and TGFB1 transgenic mice demonstrate that these growth factors oppose each other' ..... For more information please see the full descriiption on the strain data sheet
002870	B6SJL-Tg(Wnt1)1Hev/J	Repository-Cryopreserved
	Mammary glands from virgin hemizygous females carrying the (Wnt1)1Hev transgene resemble hormonally-stimulated glands from pregnant mice. There was a marked increase in numbers of terminal branches and alveoli, producing a diffuse lobular hyperplasia. Parous transgenic females were unable to lactate. Hemizygous transgenic male glands, while less developed, also were hyperplastic. Adenocarcinomas developed between 3 and 7 months in females and more rarely in males. Occasional metastatic lesions were observed in females. Salivary adenocarcinomas were also occasionally observed in both males and females. Tumors arose stochastically, indicating additional events are required for neoplasia. Subsequent work with Wnt1 transgenic mice includes infection with MMTV to identify contributing oncogenes and mating to transgenic mice bearing other oncogenes.
002526	C.129S2(B6)-Trp53^tm1Tyj/J	Repository-Cryopreserved
	Mice homozygous for the Trp53^tm1Tyj mutation show no visible phenotype but most develop tumors (principally lymphomas and osteosarcoma) at 3-6 months of age. Heterozygous mice develop tumors at about 10 months of age. These mice model some of the features of human Li-Fraumeni syndrome, a form of familial breast cancer with mutations in TRP53. Homozygous mice may produce a litter before succumbing to tumors. In an attempt to offer alleles on well-characterized or multiple genetic backgrounds, alleles are frequently moved to a genetic background different from that on which an allele was first characterized. This is the case for the strain above. It should be noted that the phenotype could vary from that originally described. We will modify the strain description if necessary as published results become available.
002662	C.Cg-Fech^m1Pas/J	Repository-Cryopreserved
	Homozygous mutants are recognizable by the intense yellow color of their sera, gross bilirubinemia, and, especially in albino mice, jaundice. Photosensitivity is evidenced by the appearance of inflammatory skin lesions, often becoming ulcerous, under standard mouseroom conditions (fluorescent light). Mutants do not differ from their normal littermates in body size or weight, nor are they retarded in growth. They exhibit hepatomegaly and splenomegaly, leading to enlarged abdomens after several months of age. Although mutants are not anemic at one month old, normocytic anemia develops with age.
002318	C.Cg-Tg(BCL2)22Wehi/J

JAX® Mice Strains

JAX^® Mice Strains