Search Criteria: Research Area is "Research Tools"
Strains from the Research Colonies of Jackson Laboratory Scientists
New Strains Under Development
| Stock Number |
Strain Name Phenotype |
Standard Supply |
| 001026 | BALB/cByJ | Level 1 |
| BALB/c mice are particularly well known for the production of plasmacytomas following injection with mineral oil, forming the basis for the production of monoclonal antibodies. Although not all BALB/c substrains have been examined for plasmacytoma induction, substrains derived from the Andervont (An) lineage (which includes BALB/cByJ) typically are susceptible, while those descended from BALB/cJ are resistant (see: Potter M ,1985). Mammary tumor incidence is normally low, but infection with mammary tumor virus by fostering to MMTV+ C3H mice dramatically increases tumor number and age of onset. BALB/c mice develop other cancers later in life including reticular neoplasms, primary lung tumors, and renal tumors. Rare spontaneous myoepitheliomas arising from myoepithelial cells of various exocrine glands have been observed in both BALB/cJ and BALB/cByJ substrains. BALB/cByJ has a deletion in the Qa2 subregion of the murine MHC. | ||
| 000651 | BALB/cJ | Level 1 |
| BALB/c mice are particularly well known for the production of plasmacytomas following injection with mineral oil forming the basis for the production of monoclonal antibodies. Although not all BALB/c substrains have been examined for plasmacytoma induction, substrains derived from the Andervont (An) lineage (which includes BALB/cByJ) typically are susceptible, while those descended from BALB/cJ are resistant (see: Potter M ,1985). Mammary tumor incidence is normally low but infection with mammary tumor virus by fostering to MMTV+ C3H mice dramatically increases tumor number and age of onset. BALB/c mice develop other cancers later in life including reticular neoplasms, primary lung tumors, and renal tumors. Rare spontaneous myoepitheliomas arising from myoepithelial cells of various exocrine glands have been observed in both BALB/cJ and BALB/cByJ substrains.
White et al. reported a variation in thioglycolate medium-induced peritoneal leukocyte recruitment in 4 analyzed s
..... | ||
| 000659 | C3H/HeJ | Level 1 |
| C3H/HeJ mice are used as a general purpose strain in a wide variety of research areas including cancer, immunology and inflammation, sensorineural, and cardiovascular biology. C3H/HeJ mice and all other Jackson substrains are homozygous for the retinal degeneration 1 mutation (Pde6brd1), which causes blindness by weaning age. There is also a high incidence of hepatomas in C3H mice (reportedly 72-91% in males at 14 months, 59% in virgin females, 30-38% in breeding females). Despite the lack of exogenous mouse mammary tumor virus (MMTV), virgin and breeding females may still develop some mammary tumors later in life. C3H/HeJ mice, fed an atherogenic diet (1.25% cholesterol, 0.5% cholic acid and 15% fat), fail to develop atherosclerotic aortic lesions in contrast to several highly susceptible strains of mice (e.g. C57BL/6J, Stock No. 000664; C57L/J, Stock No. 00066
..... For more information please see the full phenotype on the strain data sheet | ||
| 000664 | C57BL/6J | Level 1 |
| C57BL/6 is the most widely used inbred strain. It is commonly used as a general purpose strain and background strain for the generation of congenics carrying both spontaneous and induced mutations. Although this strain is refractory to many tumors, it is a permissive background for maximal expression of most mutations. C57BL/6J mice are used in a wide variety of research areas including cardiovascular biology, developmental biology, diabetes and obesity, genetics, immunology, neurobiology, and sensorineural research. C57BL/6J mice are also commonly used in the production of transgenic mice. Overall, C57BL/6 mice breed well, are long-lived, and have a low susceptibility to tumors. Primitive hematopoietic stem cells from C57BL/6J mice show greatly delayed senescence relative to BALB/c and DBA/2J. This is a dominant trait. Other characteristics include: 1) a high susceptibility to diet-induced obesity, type 2 diabetes, and atherosclerosis; 2) a high incidence of microphthalmia and other a
..... For more information please see the full phenotype on the strain data sheet | ||
| 000656 | CBA/J | Level 1 |
| CBA/J inbred mice are widely used as a general purpose strain. CBA/J strain is the only CBA substrain that carries the Pde6brd1 mutation, which causes blindness by wean age. CBA/J mice are not histocompatible with the CBA/CaJ (Stock No. 000654) substrain (Green and Kaufer, 1965). The CBA/J inbred mouse strain is used to study granulomatous experimental autoimmune thyroiditis (G-EAT), are relatively resistant to diet-induced atherosclerosis (Paigen et al., 1990), and develop a mild hearing loss late in life, with most of the hearing loss occurring in the higher frequencies (Sweet et al., 1988). Renal tubulointerstitial lesions have been observed in this strain at a high frequency (Rudofsky, 1978). Some CBA/J mice spontaneously develop exocrine pancreatic insufficiency syndrome (Eppig and Leiter, 1977, Leiter et al., 1977). | ||
| 000671 | DBA/2J | Level 1 |
| DBA/2J is a widely used inbred strain that is valuable in a large number of research areas, including cardiovascular biology, neurobiology, and sensorineural research. Its characteristics are often contrasted with those of the C57BL/6J inbred strain (Stock No. 000664). DBA/2J mice show a low susceptibility to developing atherosclerotic aortic lesions (20 to 350 um2 atherosclerotic aortic lesions /aortic cross-section) following 14 weeks on an atherogenic diet (1.25% cholesterol, 0.5% cholic acid and 15% fat). They also exhibit high-frequency hearing loss beginning roughly at the time of weaning/adolescence (between 3-4 weeks of age) and becoming severe by 2-3 months of age. This strain possesses three recessive alleles that cause progressive cochlear pathology initially affecting the organ of Corti. Decreasing anteroventral cochlear nucleus volume decreases and neuron loss parallel the progression of peripheral hearing loss. Young
..... For more information please see the full phenotype on the strain data sheet | ||
| 001800 | FVB/NJ | Level 1 |
| FVB/NJ was inbred for the Fv1b allele which confers sensitivity to the Friend leukemia virus B strain. Due to the prominent pronuclei in their fertilized eggs and the large litter size, FVB/NJ mice are commonly used for transgenic injection. Compared to many other inbred strains, FVB/NJ is highly susceptible to asthma-like airway responsiveness with significant generation of antigen-specific IgE. Despite having the H2q MHC haplotype, FVB/NJ are resistant to collagen-induced arthritis. This resistance stems from coding polymorphisms in Tcra-V11.1 and a genomic deletion of some Tcrb-V genes that includes Tcrb-V8.2. FVB/NJ have higher than average activity, anxiety, and basal body temperature, low stress-induced hyperthermia, and are homozygous for the Pde6brd1 allele, which results in early onset retinal degeneration. Although FVB/N typically do not develop spontaneous tumors, they are highly susceptible to chemic
..... For more information please see the full phenotype on the strain data sheet | ||
| 001303 | NOD.CB17-Prkdcscid/J | Level 1 |
| Mice homozygous for the severe combined immune deficiency spontaneous mutation (Prkdcscid, commonly referred to as scid) are characterized by an absence of functional T cells and B cells, lymphopenia, hypogammaglobulinemia, and a normal hematopoietic microenvironment. Normal antigen-presenting cell, myeloid, and NK cell functions are strain dependent. scid mice carry a DNA repair defect and a defect in the rearrangement of genes that code for antigen-specific receptors on lymphocytes. Most homozygotes have no detectable IgM, IgG1, IgG2a, IgG2b, IgG3, or IgA. Thymus, lymph nodes, and splenic follicles are virtually devoid of lymphocytes. scid mice accept allogeneic and xenogeneic grafts making them an ideal model for cell transfer experiments. Some scid mice will spontaneously develop partial immune reactivity. scid mice that have serum Ig levels greater than 1 ug/ml are considered "leaky." scid leakiness is highly strain depen
..... For more information please see the full phenotype on the strain data sheet | ||
| 001976 | NOD/ShiLtJ | Level 1 |
| Diabetes in NOD/ShiLtJ mice is characterized by insulitis, a leukocytic infiltrate of the pancreatic islets. Marked decreases in pancreatic insulin content occur in females at about 12 weeks of age and several weeks later in males. Onset of diabetes is marked by moderate glycosuria and by a non-fasting plasma glucose higher than 250 mg/dl. Diabetic mice are hypoinsulinemic and hyperglucagonemic, indicating a selective destruction of pancreatic islet beta cells. Susceptibility to IDDM in NOD/ShiLtJ mice is polygenic, and environment, including housing conditions, health status, and diet, exerts a strong effect on penetrance. NOD/ShiLtJ females are more widely used than males because the onset of IDDM symptoms occurs earlier and with a higher incidence (90-100% by 30 weeks of age). NOD/ShiLtJ males develop IDDM at a frequency of between 40-60% by 30-40 weeks of age. Male mice are useful for certain applications, including pharmaceutical studies, "accelerated transfer" of IDDM, and some <
>
..... For more information please see the full phenotype on the strain data sheet | ||
| 002448 | 129S1/SvImJ | Level 2 |
| Historically, the 129 inbred mice are known for the high incidence of spontaneous testicular teratomas, though the incidence differs between substrains.(1-3% in 129 parental substrains; 30% in teratoma substrains.) More recently, 129 mice are widely used in the production of targeted mutations due to the availability of multiple embryonic stem cell lines derived from them. There is major genetic variation within the 129 "family", which has led to an update of the nomenclature and a division of the substrains into three major groups: parental substrains (129P), steel substrains (129S) and "teratoma" substrains (129T). Investigators using 129 substrains for targeted mutagenesis should be careful in the selection of the appropriate 129 substrain to match the embryonic stem cell line. For a complete history of the numerous 129 substrains, see Simpson, et al., 1997.
| ||
| 000691 | 129X1/SvJ | Level 2 |
| Historically, the 129 inbred mice are known for the high incidence of spontaneous testicular teratomas, though the incidence differs between substrains. (1-3% in 129 parental substrains; 30% in teratoma substrains.) More recently 129 mice are widely used in the production of targeted mutations due to the availability of multiple embryonic stem cell lines derived from them. There is major genetic variation within the 129 "family", which has led to an update of the nomenclature and a division of the substrains into three major groups: parental substrains (129P), steel substrains (129S) and "teratoma" substrains (129T). Investigators using 129 substrains for targeted mutagenesis should be careful in the selection of the appropriate 129 substrain to match the embryonic stem cell line. For a complete history of the numerous 129 substrains, see Simpson, et al., 1997.
In response to challenge, 129S1/SvImJ mice develop immune-mediated nephritis characterized by proteinuria, glome
..... | ||
| 000646 | A/J | Level 2 |
| Developed by LC Strong in 1921 from a cross between a Cold Spring Harbor albino and a Bagg albino, the A inbred strain is used widely used in cancer and immunology research. It is highly susceptible to cortisone-induced congenital cleft palate. It has a high incidence of spontaneous lung adenomas, and lung tumors readily develop in response to carcinogens. A high percentage of mammary adenocarcinomas (a large proportion of acinar-type) develop in multiparous females. Rare spontaneous myoepitheliomas arising from myoepithelial cells of various exocrine glands have been observed in The Jackson Laboratory substrains. A/J mice fed an atherogenic diet (1.25% cholesterol, 0.5% cholic acid, and 15% fat) fail to develop atherosclerotic aortic lesions in contrast to several highly susceptible strains of mice (e.g. C57BL/6J, Stock No. 000664; C57L/J, Stock No. 000668, C57BR/cdJ, Sto
..... | ||
| 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. | ||
| 000463 | B10.D2-Hc1 H2d H2-T18c/nSnJ | Level 2 |
| 000406 | B6.PL-Thy1a/CyJ | Level 2 |
| This C57BL/6J congenic strain is useful because it carries the T lymphocyte specific Thy1a (Thy1.1) allele. Donor T cells can be easily distinguished from recipient T cells by both flow cytometric and histological analysis using appropriate antibodies. | ||
| 002014 | B6.SJL-Ptprca Pepcb/BoyJ | Level 2 |
| This is a congenic strain used in transplant studies because it carries the differential B cell antigen originally designated Ly5.1 and CD45.1 The current use of the Ptprc designation for Cd45 and Ly5 was based on work in humans following the report of Charbonneau and colleagues who first showed that a protein-tyrosine phosphatase (human placental protein-tyrosine phosphatase 1B) was homologous to the CD45 protein. Ptprc is one of a family of protein-tyrosine phosphatase genes involved in the regulation of cell growth. The b allele is normally present in the BALB and C57BL inbred strains. | ||
| 100010 | B6C3F1/J | Level 2 |
| 100012 | B6SJLF1/J | Level 2 |
| 000635 | C3H/HeOuJ | Level 2 |
| C3H/HeOuJ mice are used as a general purpose strain in a wide variety of research areas including cancer and sensorineural, research. C3H/HeOuJ mice and all other C3H substrains at The Jackson Laboratory are homozygous for the retinal degeneration 1 mutation (Pde6brd1), causing blindness by weaning age. There is also a high incidence of hepatomas in C3H mice (reportedly 72-91% in males at 14 months, 59% in virgin females, 30-38% in breeding females). Despite the lack of exogenous mouse mammary tumor virus (MMTV), virgin and breeding females may still develop some mammary tumors later in life. | ||
| 000658 | C3HeB/FeJ | Level 2 |
| 000665 | C57BL/10J | Level 2 |
| C57BL/10J is a substrain of C57BL, and shares a common origin with C57BL/6J (Stock No. 000664), which is one of the most widely used inbred strains. Coat color is black (non-agouti), a/a. The C57BL/10J substrain is similar to the C57BL/6J substrain, but allelic variants have been described at the H9, Igh2 and Lv loci. C57BL/10J mice have a long life-span (826 +/-29 days in males, 693 +/- 31 days in females). Overall tumor incidence is 33% in males and 31% in females, most of which is due to lymphoma. C57BL/10J mice are prone to dermatitis, which is a common problem in the C57BL strain. C57BL/10J mice are a valuable immunological research tool. They have a high lymphocyte phytohaemagglutinin response, a good immune response to ovalbumin, a poor response to DNP-keyhole limpet haemocyanin and are resistant to induction of passive cutaneous anaphylaxis (IgG1- and IgE- mediated). They are susceptible
..... For more information please see the full phenotype on the strain data sheet | ||
| 001011 | CBA/CaHN-Btkxid/J | Level 2 |
| CBA/CaHN-Btkxid/J mice have a mutation in the Bruton's tyrosine kinase gene (Btk), and are a model of human X-linked immunodeficiency. They have a B-lymphocyte-specific defect that results in an inability to launch an antibody response to thymus-independent type II antigens, although they do produce normal amounts of antibody in response to some protein antigens. They have low serum IgM and IgG3 and a reduced number of B-cells. Moreover, the B-cells that are present have a reduced surface IgM to IgD ratio, which suggests a disorder in B-cell maturation. | ||
| 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
..... | ||
| 001803 | CBySmn.CB17-Prkdcscid/J | Level 2 |
| Mice homozygous for the severe combined immune deficiency spontaneous mutation (Prkdcscid, commonly referred to as scid) are characterized by an absence of functional T cells and B cells, lymphopenia, hypogammaglobulinemia, and a normal hematopoietic microenvironment. Normal antigen-presenting cell, myeloid, and NK cell functions are strain dependent. scid mice carry a DNA repair defect and a defect in the rearrangement of genes that code for antigen-specific receptors on lymphocytes. Most homozygotes have no detectable IgM, IgG1, IgG2a, IgG2b, IgG3, or IgA. Thymus, lymph nodes, and splenic follicles are virtually devoid of lymphocytes. scid mice accept allogeneic and xenogeneic grafts making them an ideal model for cell transfer experiments. Some scid mice will spontaneously develop partial immune reactivity. scid mice that have serum Ig levels greater than 1 ug/ml are considered "leaky." scid leakiness is highly strain depen
..... For more information please see the full phenotype on the strain data sheet | ||
| 000670 | DBA/1J | Level 2 |
| DBA/1J mice are widely used as a model for rheumatoid arthritis: immunization with type II collagen leads to the development of severe polyarthritis mediated by an autoimmune response. The incidence of collagen induced arthritis varies by experimental protocol, but is less than 100%. Similar to the human condition, mice with collagen-induced arthritis display synovitis and erosions of cartilage and bone. In addition, susceptibility in both humans and mice is linked to the expression of specific MHC class II molecules. DBA/1J mice show an intermediate susceptibility to developing atherosclerotic aortic lesions on an atherogenic diet. In response to challenge, DBA/1J mice develop immune-mediated nephritis characterized by proteinuria, glomerulonephritis and tubulointerstitial disease (Xie et al., 2004). | ||
| 001140 | DBA/1LacJ | Level 2 |
| Historical reports indicate DBA/1J and DBA/1LacJ mice immunized with type II collagen develop a severe polyarthritis mediated by an autoimmune response. Recent in-house studies suggest that the response to collagen induction in the DBA/1LacJ strain is not as robust as indicated by earlier studies. Arthritis models such as B10.RIII-H2r H2-T18b/(71NS)SnJ (Stock No. 000457) and BUB/BnJ (Stock No. 000653) can be used as alternatives to DBA/1LacJ. Similar to the human condition, mice with collagen-induced arthritis display synovitis and erosions of cartilage and bone. In addition, susceptibility in both humans and mice is linked to the expression of specific MHC class II molecules. DBA/1 mice show a low susceptibility to developing atherosclerotic aortic lesions (20 to 350 um2 atherosclerotic aortic lesions/aortic cross-section) following 14 weeks on a
..... For more information please see the full phenotype on the strain data sheet | ||
| 002468 | KK.Cg-Ay/J | Level 2 |
| Ay and other mutations at the a locus conferring a completely yellow coat color are dominant to all a alleles that produce a darker coat. Hair pigment of Ay heterozygotes is yellow, but eyes are black. Heterozygotes usually become obese and infertile within a few months after birth. Increased adipose tissue mass is due to fat cell hypertrophy, and it has been hypothesized that the obesity results from the observed reduction in hypothalamic norepinephrine and dopamine. Heterozygotes are more susceptible to several kinds of tumors than are normal mice, possibly due, at least in part, to a general increase in cell proliferation that also manifests as a slight increase in lean body mass and skeletal length. Further spleen cells from heterozygotes cause a significantly lower graft vs. host reaction. Mice homozygous for the yellow spontaneous mutation (Ay) die before implantation, or shortly thereafter. The time of de
..... For more information please see the full phenotype 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 Dysfim allele has been shown to result in decreased levels of dysferlin protein in SJL/J mice and makes this strain a good model for limb girdle muscular dystrophy 2B. This spontaneous myopathy is characterized by a progressive loss of muscle mass and strength corresponding with an increase in muscle pathology incl
..... For more information please see the full phenotype on the strain data sheet | ||
| 100410 | WBB6F1/J-KitW/KitW-v/J | Level 2 |
| Kit mutant mice possess pleiotropic defects in pigment-forming cells, germ cells, RBC's and mast cells. In addition, they exhibit impaired resistance to parasitic infection and an intrinsic progenitor cell defect. KitW-v homozygotes resemble KitW homozygotes in color, anemia, and germ cells, but many of them survive to maturity. The lack of germ cells in mutant mice leads to the development of some ovarian tumors (mesotheliomas and granulosa cell), associated with an overproduction of pituitary gonadotropic hormone. KitW/KitW-v double heterozygotes are viable but sterile because of germ cell deficiency. They are also mast cell deficient. KitW/KitW-v double heterozygotes lack intermediate cells, derived from melanoblasts, in the stria vascularis resulting in endocochlear degeneration, loss of endocochlear potential, and hearing impairment. | ||
| 000461 | B10.D2-Hc0 H2d H2-T18c/oSnJ | Level 3 |
| This congenic strain carries the H2d haplotype from DBA/2J following six generations of backcrossing to C57BL/10Sn. This strain still carries the Hc0 allele from DBA/2J, making them serum C5 deficient. Mice have increased susceptibility to certain pathogens and impaired chemotactic responses of neutrophils. Allograft rejection is prolonged. The following inbred strains are also homozygous for the Hc0 allele: A/HeJ (Stock No. 000645), AKR/J (Stock No. 000648), DBA/2J (Stock No. 000671), NOD/LtJ (Stock No. 001976), NZB/BlNJ (Stock No. 000684), and SWR/J (Stock No. 000689). | ||
| 002288 | B6.129S2-Igh-6tm1Cgn/J | Level 3 |
| Mice homozygous for the Igh-6tm1Cgn targeted mutation are viable and fertile. Homozygous mutant mice lack mature B-cells. There is no expression of membrane-bound IgM, although some B-cells may be produced using a C gene other than mu. It may be useful as a model for B-cell immunodeficiency found in humans. Also known as muMT. | ||
| 002650 | B6.129S2-Il6tm1Kopf/J | Level 3 |
| Mice homozygous for the targeted mutation are viable and fertile. No gene product (mRNA) is detected by RT-PCR analysis of lipopolysaccharide (LPS) challenged macrophages. Bioassay and enzyme-linked immunosorbent assay (ELISA) analysis of serum from LPS-challenged homozygotes reveals no detectable protein activity. These interleukin 6 (IL6) mutant mice show defects in responses to various viruses and in inflammatory responses to tissue damage or infection. Of note, IL6-mutant mice may be available on different genetic backgrounds including mixed B6;129S2 (Stock No. 002254), C57BL/6J (Stock No. 002650), and BALB/cByJ (Stock No. 007078). | ||
| 002365 | B6.129S6-Cybbtm1Din/J | Level 3 |
| Chronic granulomatous disease (CGD) is a recessive disorder characterized by a defective phagocyte respiratory burst oxidase, life-threatening pyogenic infections and inflammatory granulomas. Gene targeting was used to generate mice with a null allele of the gene involved in X-linked CGD, which encodes the 91 kD subunit of the oxidase cytochrome b. Affected hemizygous male mice lack phagocyte superoxide production, manifest an increased susceptibility to infection with Staphylococcus aureus and Aspergillus fumigatus and have an altered inflammatory response in thioglycollate peritonitis. This animal model should aid in developing new treatments for CGD and in evaluating the role of phagocyte-derived oxidants in inflammation. | ||
| 002216 | B6.129S7-Rag1tm1Mom/J | Level 3 |
| Mice homozygous for the Rag1tm1Mom mutation produce no mature T cells or B cells. Their phenotype can be described as a "non-leaky" severe combined immune deficiency (Prkdcscid/Prkdcscid) (Prkdcscid mice produce some B cells and IgM). They have no CD3+ or T cell receptor (TCR) alpha-beta positive cells. The thymus of the mutant mice contains 15 to 130 times fewer cells than heterozygous or wildtype siblings. The thymocytes are CD8-CD4- and most are IL2 receptor-positive. Neither the spleen nor the bone marrow contain any IgM or IgD staining cells, indicating an absence of mature B cells. These and other data suggest that B cell and T cell development has been arrested at an early stage. Macroscopically, the mutants are indistinguishable from heterozygotes or normal wildtype siblings. | ||
| 001913 | B6.CB17-Prkdcscid/SzJ | Level 3 |
| Mice homozygous for the severe combined immune deficiency spontaneous mutation (Prkdcscid, commonly referred to as scid) are characterized by an absence of functional T cells and B cells, lymphopenia, hypogammaglobulinemia, and a normal hematopoietic microenvironment. Normal antigen-presenting cell, myeloid, and NK cell functions are strain dependent. scid mice carry a DNA repair defect and a defect in the rearrangement of genes that code for antigen-specific receptors on lymphocytes. Most homozygotes have no detectable IgM, IgG1, IgG2a, IgG2b, IgG3, or IgA. Thymus, lymph nodes, and splenic follicles are virtually devoid of lymphocytes. scid mice accept allogeneic and xenogeneic grafts making them an ideal model for cell transfer experiments. Some scid mice will spontaneously develop partial immune reactivity. scid mice that have serum Ig levels greater than 1 ug/ml are considered "leaky." scid leakiness is highly strain depen
..... For more information please see the full phenotype on the strain data sheet | ||
| 003303 | C.Cg-Tg(DO11.10)10Dlo/J | Level 3 |
| Mice carrying the MHC class II restricted rearranged T cell receptor transgene, Tg(DO11.10)10Dlo, react to ovalbumin (OVA) peptide antigen. Intraperitoneal administration of OVA to transgenic mice results in a rapid deletion of the immature CD4+ CD8+ TCRlo thymocytes with progression to mature thymocytes. Apoptosis of cortical thymocytes within 20 hours of treatment indicates that apoptosis in important in the development of antigen-induced tolerance. Use of this rearranged T cell receptor transgene requires H2d background. | ||
| 000666 | C57BL/10SnJ | Level 3 |
| C57BL/10SnJ is a substrain of C57BL, which is one of the most widely used inbred strains. Coat color is black (non-agouti) a/a. C57BL/10SnJ are similar to other C57BL substrains. | ||
| 000662 | C57BLKS/J | Level 3 |
| Although C57BLKS/J is estimated to have more than 70% of its genome derived from C57BL/6J, these strains are phenotypically distinct. Diet-induced atherosclerotic lesions are much more severe in C57BLKS/J than in C57BL/6J or many other inbred strains. Compared with a panel of inbred strains, C57BLKS/J was found to have low total cholesterol and low HDL cholesterol when fed a normal diet and high total cholesterol and HDL cholesterol in an atherogenic diet. Paigen et al. found high levels of plasma bile salts in C57BLKS/J females after 8 weeks on an atherogenic diet. The mutations diabetes (Leprdb) and obese (Lepob) each express a much more severe phenotype on the C57BLKS/J background than on the C57BL/6J background. The Cpefat mutation causes severe obesity, hyperinsulinemia, and hyperglycemia on the C57BLKS/J background rather than the hyperinsulinemia, and mild obesity without hyperglycemia found on the HRS/J background. In
..... For more information please see the full phenotype on the strain data sheet | ||
| 000928 | CAST/EiJ | Level 3 |
| 005557 | NOD.Cg-Prkdcscid Il2rgtm1Wjl/SzJ | Level 3 |
| The NOD.Cg-Prkdcscid Il2rgtm1Wjl/SzJ mice, commonly known as NOD scid gamma (NSG), do not express the Prkdc gene nor the X-linked Il2rg gene. NSG mice are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Histological examination of lymphoid tissues reveals absence of lymphoid cells and some cystic structures in the thymus, an absence of follicles in the spleen and markedly diminished celluarity of lymph nodes. NSG mice are deficient in mature lymphocytes, serum Ig is not detectable and natural killer (NK) cell cytotoxic activity is extremely low. These mice are resistant to lymphoma development even after sublethal irradiation treatment. These mutant mice have been shown to readily support engraftment of human CD34+ hematopoietic stem cells and represent a superior, long-lived model suitable for studies employing xenotransplantation strategies. Please note that the NSG carries the tr
..... For more information please see the full phenotype on the strain data sheet | ||
| 002019 | NU/J | Level 3 |
| The two main defects of mice homozygous for the nude spontaneous mutation (Foxn1nu, formerly Hfh11nu) are abnormal hair growth and defective development of the thymic epithelium. Although the mice appear hairless, they are born with functional but faulty hair growth follicles. Hair growth cycles and patterns are evident especially in pigmented mice but the faulty follicles do not allow the hair to properly erupt. Homozygous pups can be identified as young as 24 hours by their lack of whiskers or poorly developed, crinkled whiskers. Nude mice are also athymic caused by a developmental failure of the thymic anlage. Consequently, homozygous nude mice lack T cells and suffer from a lack of cell-mediated immunity. However there is not a defect in T-cell precursors, and under the right conditions some functional mature T cells can be found especially in adult mice. Because of a defect in helper T-cell activity, responses to thymus-dependent antigens when d
..... For more information please see the full phenotype on the strain data sheet | ||
| 000689 | SWR/J | Level 3 |
| SWR/J mice are used widely in research as a general purpose strain. Aging mice exhibit a high incidence of lung and mammary gland tumors. They also develop extreme polydipsia and polyuria (nephrogenic diabetes insipidus) with increasing age. SWR/J mice are highly susceptible to experimental allergic encephalomyelitis (EAE). Germline deletion of about 50% of T-cell receptor V beta-chain gene segments and a T-cell receptor V alpha polymorphism are responsible for the resistance of SWR/J mice to collagen type II-induced arthritis. SWR/J mice show an intermediate susceptibility to developing atherosclerotic aortic lesions (1670 to 1690 um2 atherosclerotic aortic lesions/aortic cross-section) following 14 weeks on an atherogenic diet (1.25% cholesterol, 0.5% cholic acid and 15% fat). SWR/J mice have been recommended for generation and propogation of transgenic mice because they are high responders to exogenous hormones, have large and prominant pronuclei with good resistance to l
..... For more information please see the full phenotype on the strain data sheet | ||
| 000690 | 129P3/J | Level 4 |
| Historically, the 129 inbred mice are known for the high incidence of spontaneous testicular teratomas, though the incidence differs between substrains. (1-3% in 129 parental substrains; 30% in teratoma substrains.) More recently, 129 mice are widely used in the production of targeted mutations due to the availability of multiple embryonic stem cell lines derived from them. There is major genetic variation within the 129 "family", which has led to an update of the nomenclature and a division of the substrains into three major groups: parental substrains (129P), steel substrains (129S) and "teratoma" substrains (129T). Investigators using 129 substrains for targeted mutagenesis should be careful in the selection of the appropriate 129 substrain to match the embryonic stem cell line. For a complete history of the numerous 129 substrains, see Simpson, et al., 1997. | ||
| 002065 | 129T2/SvEmsJ | Level 4 |
| Historically, the 129 inbred mice are known for the high incidence of spontaneous testicular teratomas, though the incidence differs between substrains. (1-3% in 129 parental substrains; 30% in teratoma substrains.) More recently 129 mice are widely used in the production of targeted mutations due to the availability of multiple embryonic stem cell lines derived from them. There is major genetic variation within the 129 "family", which has led to an update of the nomenclature and a division of the substrains into three major groups: parental substrains (129P), steel substrains (129S) and "teratoma" substrains (129T). Investigators using 129 substrains for targeted mutagenesis should be careful in the selection of the appropriate 129 substrain to match the embryonic stem cell line. For a complete history of the numerous 129 substrains, see Simpson, et al., 1997. | ||
| 000645 | A/HeJ | Level 4 |
| Developed by LC Strong in 1921 from a cross between a Cold Spring Harbor albino and a Bagg albino, the A inbred strain is used widely used in cancer and immunology research. It is highly susceptible to induction of congenital cleft palate by cortisone. It has a high incidence of spontaneous lung adenomas and lung tumors readily develop in response to carcinogens. High percentage of mammary adenocarcinomas (a large proportion acinar type) develop in multiparous females. Rare spontaneous myoepitheliomas arising from myoepithelial cells of various exocrine glands have been observed in The Jackson Laboratory substrains. A small percent (4%) of nonproductive males are hermaphrodites. An additional 17% of nonproductive males have abnormally small testes containing no sperm. | ||
| 002087 | B6.129P2-B2mtm1Unc/J | Level 4 |
| Mice homozygous for the B2mtm1Unc targeted mutation have little if any MHC class I protein expression on the cell surface. There are few CD8+ cytotoxic T-cells and under some circumstances a compensatory increase in CD4+ cytotoxic T-cells. Immune responses involving CD8+ T-cells are severely deficient providing a model to assess the role of CD8+ cells and class I MHC in various experimental systems. Hemachromatosis has been noted in certain genetic backgrounds (Rothenberg BE, Voland JR, Proc Natl Acad Sci USA 93:1529-34, 1996). 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
..... For more information please see the full phenotype on the strain data sheet | ||
| 002118 | B6.129P2-Tcrbtm1Mom/J | Level 4 |
| Mice homozygous for the Tcrbtm1Mom targeted mutation are viable and fertile. Mice are deficient in alpha beta T-cell receptor. The total number of cells in the thymus is ~8% that of wildtype; CD4+CD8+ cells ~6% of wildtype. The proportion of CD4-CD8- (IL2 receptor positive) cells increases to about 50% of the total cell number. Alpha beta thymocyte differentiation is blocked at an earlier stage than the Tcratm1Mom strain. There is normal differentiation of gamma delta thymocytes. Mice may develop inflammatory bowel disease beginning at ~4-6 months of age. | ||
| 002120 | B6.129P2-Tcrdtm1Mom/J | Level 4 |
| Mice homozygous for the Tcrdtm1Mom targeted mutation are viable and fertile. Gamma delta T-cell receptor expression is deficient in all adult lymphoid and epithelial organs. There is normal development of the alpha beta T-cell lineage. Patterns of CD4+CD8- and CD4-CD8+ alpha beta T-cells are apparently normal. Mice do not develop inflammatory bowel disease. | ||
| 002663 | B6.129S2-Cd4tm1Mak/J | Level 4 |
| Mice homozygous for the Cd4tm1Mak targeted mutation have a significant block in CD4+ T-cell development; 90% of their circulating T-cells are CD8+. Cell surface expression of CD4 protein is not detected on thymocytes and lymph node cells from homozygous mice. Homozygous mutant mice also show a Class II restricted deficit in helper T-cell activity and other T-cell responses. This mutant mouse strain may be useful in studies of T cell development, susceptibility to viral infection and inflammation. | ||
| 002116 | B6.129S2-Tcratm1Mom/J | Level 4 |
| Mice homozygous mice for the Tcratm1Mom targeted mutation are viable and fertile. They are deficient in the alpha beta T-cell receptor. The thymus is devoid of CD4+CD8- and CD4-CD8+ cells. Normal numbers of CD4+CD8+ cells are retained without the IL2 receptor. There are normal numbers of CD4-CD8- cells. ~1% of the thymocytes express the gamma delta TCR. Mice may develop inflammatory bowel disease beginning at ~4-6 months of age. | ||
| 002101 | B6.129S2-Trp53tm1Tyj/J | Level 4 |
| Mice homozygous for the Trp53tm1Tyj mutation show no visible phenotype but most develop tumors (principally lymphomas and osteosarcoma) at 3-6 months of age. Heterozygous mice develop tumors at about 10 months of age. These mice model some of the features of human Li-Fraumeni syndrome, a form of familial breast cancer with mutations in TRP53. Homozygous mice may produce a litter before succumbing to tumors. | ||
| 003474 | B6.129S4-Gt(ROSA)26Sortm1Sor/J | Level 4 |
| Homozygous mice are viable and fertile, with a loxP-flanked DNA STOP sequence preventing expression of the downstream lacZ gene. When crossed with a cre transgenic strain, the STOP sequence is removed and lacZ is expressed in cells/tissues where cre is expressed. These mutant mice may be used as a Cre-reporter strain; to test the tissue/cellular expression pattern of cre transgenic mice. | ||
| 000819 | B6.Cg-Foxn1nu/J | Level 4 |
| The two main defects of mice homozygous for the nude spontaneous mutation (Foxn1nu, formerly Hfh11nu) are abnormal hair growth and defective development of the thymic epithelium. Although the mice appear hairless, they are born with functional but faulty hair growth follicles. Hair growth cycles and patterns are evident especially in pigmented mice but the faulty follicles do not allow the hair to properly erupt. Homozygous pups can be identified as young as 24 hours by their lack of whiskers or poorly developed, crinkled whiskers. Nude mice are also athymic caused by a developmental failure of the thymic anlage. Consequently, homozygous nude mice lack T cells and suffer from a lack of cell-mediated immunity. However there is not a defect in T-cell precursors, and under the right conditions some functional mature T cells can be found especially in adult mice. Because of a defect in helper T-cell activity, responses to thymus-dependent antigens when
..... For more information please see the full phenotype on the strain data sheet | ||
| 003145 | C.129S7(B6)-Rag1tm1Mom/J | Level 4 |
| Mice homozygous for the Rag1tm1Mom mutation produce no mature T cells or B cells. Their phenotype can be described as a "non-leaky" severe combined immune deficiency (Prkdcscid/Prkdcscid) (Prkdcscid mice produce some B cells and IgM). They have no CD3+ or T cell receptor (TCR) alpha-beta positive cells. The thymus of the mutant mice contains 15 to 130 times fewer cells than heterozygous or wildtype siblings. The thymocytes are CD8-CD4- and most are IL-2 receptor positive. Neither the spleen nor bone marrow contain any IgM or IgD staining cells, indicating an absence of mature B cells. These and other data suggest that B cell and T cell development has been arrested at an early stage. Macroscopically, the mutants are indistinguishable from heterozygotes or wildtype siblings. | ||
| 000661 | C3H/HeSnJ | Level 4 |
| 001131 | C3SnSmn.CB17-Prkdcscid/J | Level 4 |
| Mice homozygous for the severe combined immune deficiency spontaneous mutation (Prkdcscid, commonly referred to as scid) are characterized by an absence of functional T cells and B cells, lymphopenia, hypogammaglobulinemia, and a normal hematopoietic microenvironment. Normal antigen-presenting cell, myeloid, and NK cell functions are strain dependent. scid mice carry a DNA repair defect and a defect in the rearrangement of genes that code for antigen-specific receptors on lymphocytes. Most homozygotes have no detectable IgM, IgG1, IgG2a, IgG2b, IgG3, or IgA. Thymus, lymph nodes, and splenic follicles are virtually devoid of lymphocytes. scid mice accept allogeneic and xenogeneic grafts making them an ideal model for cell transfer experiments. Some scid mice will spontaneously develop partial immune reactivity. scid mice that have serum Ig levels greater than 1 ug/ml are considered "leaky." scid leakiness is highly strain depe
..... For more information please see the full phenotype on the strain data sheet | ||
| 003291 | C57BL/6-Tg(CAG-EGFP)1Osb/J | Level 4 |
| This transgenic mouse line with an "enhanced" GFP (EGFP) cDNA under the control of a chicken beta-actin promoter and cytomegalovirus enhancer makes all of the tissues, with the exception of erythrocytes and hair, appear green under excitation light. Note that mice homozygous for this transgene die within the first two weeks following birth. | ||
| 003831 | C57BL/6-Tg(TcraTcrb)1100Mjb/J | Level 4 |
| These mice contain transgenic inserts for mouse Tcra-V2 and Tcrb-V5 genes. The transgenic T cell receptor was designed to recognize ovalbumin residues 257-264 in the context of H2Kb and used to study the role of peptides in positive selection and the response of CD8+ T cells to antigen. Like most TCR transgenics, these mice are somewhat immunodeficient. | ||
| 004194 | C57BL/6-Tg(TcraTcrb)425Cbn/J | Level 4 |
| These transgenic mice express the mouse alpha-chain and beta-chain T-cell receptor that pairs with the CD4 coreceptor and is specific for chicken ovalbumin 323-339 in the context of I-A b. Homozygous mice are viable and fertile. In these mice there is a four-fold increase in the CD4 to CD8 peripheral T-cell ratio, and lymph node T-cells demonstrate a dose-dependent proliferative response to the specific ovalbumin ligand. These transgenic mice are useful for studying in vivo T-cell biology such as TCR-ligand interactions, T-cell activation, thymic selection, cross-presentation of antigens, process of thymic selection and central and peripheral T-cell tolerance and induction. | ||
| 004353 | C57BL/6-Tg(UBC-GFP)30Scha/J | Level 4 |
| These transgenic mice express Green Fluorescent Protein (GFP) under the direction of the human ubiqutin C promoter. Mice homozygous for the transgene are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. These mice express GFP in all tissues examined. Certain hematapoetic cell types display distinct expression levels of GFP, allowing identification of different cells types by FACS analysis. GFP expression is uniform within a cell type lineage and remains constant throughout development. T cells have a 2-fold higher GFP expression than CD19+B220+ B cells or peripheral blood cells. Leukocytes and red blood cells from homozygous mice fluoresce at approximately twice the level of cells from hemizygous mice. This mutant mouse strain represents a useful tool in studies related to hematopoetic cell differentiation and in vivo tracking of leukocytes. | ||
| 000049 | C57BL/6J-KitW-v/J | Level 4 |
| Kit mice possess pleiotropic defects in pigment-forming cells, germ cells, RBC's and mast cells. In addition, they exhibit impaired resistance to parasitic infection and an intrinsic progenitor cell defect. KitW-v homozygotes resemble KitW homozygotes in color, anemia, and germ cells, but many of them survive to maturity. The lack of germ cells in mutant mice leads to the development of some ovarian tumors (mesotheliomas and granulosa cell), associated with an overproduction of pituitary gonadotropic hormone. | ||
| 000629 | C57BL/6J-Lystbg-J/J | Level 4 |
| Mice homozygous for the beige-J spontaneous mutation (Lystbg-J) are identical to the original beige mutation (Lystbg). The phenotype closely resembles Chediak-Higashi disease in man and similar conditions in mink and cattle. Abnormal giant lysosomal granules occur in all tissues with granule-containing cells, including granulocytes, lymphocytes, cells of the liver, kidney, central nervous system, pancreas, and thyroid, and the ducts of most glands; in type II pneumocytes; in mast cells; and in retinal pigment epithelium. Granulocytes from beige homozygous mutant mice mice show defective chemotaxis and reduced bactericidal activity. Beige mice are more susceptible than controls to pneumonitis and to various viral, bacterial, and parasitic infections. Natural killer (NK) cells from beige mice exhibit decreased endogenous cytotoxic activity. Beige mice also have a defective cytotoxic T-cell and cytotoxic antibody response to allogeneic tumor cells. Syn
..... For more information please see the full phenotype on the strain data sheet | ||
| 000711 | CByJ.Cg-Foxn1nu/J | Level 4 |
| The two main defects of mice homozygous for the nude spontaneous mutation (Foxn1nu, formerly Hfh11nu) are abnormal hair growth and defective development of the thymic epithelium. Although the mice appear hairless, they are born with functional but faulty hair growth follicles. Hair growth cycles and patterns are evident especially in pigmented mice but the faulty follicles do not allow the hair to properly erupt. Homozygous pups can be identified as young as 24 hours by their lack of whiskers or poorly developed, crinkled whiskers. Nude mice are also athymic caused by a developmental failure of the thymic anlage. Consequently, homozygous nude mice lack T cells and suffer from a lack of cell-mediated immunity. However there is not a defect in T-cell precursors, and under the right conditions some functional mature T cells can be found especially in adult mice. Because of a defect in helper T-cell activity, responses to thymus-dependent antigens when d
..... For more information please see the full phenotype on the strain data sheet | ||
| 002570 | NOD.Cg-Prkdcscid B2mtm1Unc/J | Level 4 |
| Mice homozygous for both the B2mtm1Unc and Prkdcscid (commonly referred to as scid) mutations on the NOD/ShiLtSz background are class I deficient, B and T cell deficient, C-5 deficient (Hc0), and have low NK cells. This strain is an ideal model for xenograft transplantation studies and is an excellent source for insulitis-free, MHC class I-negative islets for transplantation studies. | ||
| 000684 | NZB/BlNJ | Level 4 |
| NZB/BlNJ mice display a number of autoimmune abnormalities including hemolytic anemia, elevated levels of immunoglobulin, anti-DNA antibodies, anti-thymocyte antibodies, and circulating immune complexes causing glomerulonephritis. F1 hybrids of NZB/BlNJ and NZW/LacJ (NZBWF1/J, Stock No. 100008) are widely used as a model for autoimmune disease resembling human systemic lupus erythematosus. NZB/BlNJ mice, fed an atherogenic diet (1.25% cholesterol, 0.5% cholic acid and 15% fat), fail to develop atherosclerotic aortic lesions in contrast to several highly susceptible strains of mice (e.g. C57BL/6J, Stock No. 000664; C57L/J, Stock No. 000668, C57BR/cdJ, Stock No. 000667, and SM/J, Stock No. 000687). | ||
| 000726 | RBF/DnJ | Level 4 |
| The RBF inbred strain arose from crosses with wild mice, originally known as "tobacco mouse", captured in Valle di Poschiavo in S.E. Switzerland. The wild mice originally known as 'tobacco mouse' because of the coat colour. The strain was transferred to Dr. M. Davisson (Dn) in 1981 and subsequently to the production colony of The Jackson Laborotory (J). Mice are homozygous for Robertsonian translocation Rb(1.3)1Bnr, Rb(8.12)5Bnr and Rb(9.14)6Bnr. This strain is useful for production of antibody producing hybridomas. | ||
| 003658 | STOCK Tg(TIE2GFP)287Sato/J | Level 4 |
| This strain expresses Green Fluorescent Protein (GFP) under the direction of the endothelial-specific receptor tyrosine kinase (Tek, formerly, Tie2) promoter. Endothelial cells expressing GFP can be visualized via fluorescent microscopy or purified by FACS. | ||
| 000692 | WB/ReJ KitW/J | Level 4 |
| Kit mice possess pleiotropic defects in pigment-forming cells, germ cells, RBC's and mast cells. In addition, they exhibit impaired resistance to parasitic infection and an intrinsic progenitor cell defect. The lack of germ cells in homozygous mutant mice leads to the development of some ovarian tumors (mesotheliomas and granulosa cell), associated with an overproduction of pituitary gonadotropic hormone. | ||
| 008215 | (C57BL/6-Tg(TRAMP)8247Ng/J X FVB/NJ)F1/J | Repository- Live |
| Mice carrying the TRAMP (Transgenic Adenocarcinoma of Mouse Prostate) transgene develop progressive forms of prostate cancer with distant site metastasis, primarily to the lymph nodes and lungs. These transgenic mice express the simian virus 40 (SV40) large tumor T antigen (Tag) under the control of the rat probasin promoter. Expression of the transgene is specific to the prostate epithelium. Transgenic mice exhibit various forms of disease from mild intraepithelial hyperplasia to large multinodular malignant neoplasia. The median survival time for these F1 transgenic mice is 19 weeks, very few mice survive past 33 weeks of age, which is significantly shorter than the lifespan of transgenic mice on the C57BL/6 background. Comparative histological analysis of tumors from these F1 transgenic mice and from transgenic mice on the C57BL/6 background reveals that the tumors found in these F1 mutants arise from the dorsolateral and ventral lobes of the prostate and are more spherical, hig
..... For more information please see the full phenotype on the strain data sheet | ||
| 004337 | 129(Cg)-Foxg1tm1(cre)Skm/J | Repository- Live |
| This strain expresses Cre recombinase from the endogenous Foxg1 locus. Forkhead box G1 is required for telencephalon development and is expressed specifically in the telencephalon and discrete head structures. When crossed with a strain containing loxP site flanked sequence of interest, Cre-mediated recombination results in tissue-specific deletion of the target. Recombination occurs in the telencephalon, anterior optic vesicle (developing lens and retina), otic vesicle, facial and head ectoderm, olfactory epithelium, mid-hindbrain junction and pharyngeal pouches. Mice that are homozygous for the targeted mutation die perinatally. Heterozygous mutant mice are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. This mutant mouse strain represents a model that may be useful in studies of telencephalic development. | ||
| 006373 | 129-Braftm1Sva/J | Repository- Live |
| Homozygous "floxed B-raf" (B-raff/f) mice are viable and fertile with normal B-raf protein expression. When bred to mice expressing Cre recombinase under the control of a promoter of interest, exon 12 of the targeted gene is deleted in the tissue of interest. These mutant mice may be useful in neurological studies such as Ras/Raf and MEK/ERK signaling, synaptic (neural) plasticity, learning and memory. For example, when crossed to a strain expressing Cre recombinase in nervous tissue (see Stock No. 003771), this mutant mouse strain may be useful in studies of neuron development. For example, when crossed to a strain expressing interferon inducible Cre recombinase (see Stock No. 003755), this mutant mouse strain may be useful in studies of extraembryonic mammmalian development. | ||
| 006835 | 129-Dag1tm2Kcam/J | Repository- Live |
| Mice that are homozygous for this floxed allele are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. When these mutant mice are bred to mice that express cre recombinase, resulting offspring can have exon 2 of the targeted gene deleted in the cre-expressing tissue(s). As the targeted gene has three loxP sites, other genotypes may also result. These mutant mice may be useful in studying muscle disease and regeneration. When bred to a strain expressing Cre recombinase under the control of the human glial fibrillary acidic protein promoter (GFAP) (see Stock No. 004600 for example), this mutant mouse strain may be useful in studies of brain abnormalities observed in congenital muscular dystrophies. | ||
| 002292 | 129-Gt(ROSA)26Sor/J | Repository- Live |
| Mice heterozygous or homozygous for the ROSA26 retroviral insertion display no distinguishing phenotype. lacZ is expressed in all tissues of the developing embryo and in most tissues of the adult mouse. Formerly named TgR(ROSA26)26Sor. | ||
| 006053 | 129-Gt(ROSA)26Sortm1Luo/J | Repository- Live |
| MADM-GG mice are viable with no gross behavioral or observable abnormalities. Regardless of Cre-recombination, these mice express EGFP as their N- and C-terminal coding sequences are interrupted by the beta-actin intron in-frame. High EGFP expression in every cell can be visualized in vivo and in fixed samples. These mutant mice are a control EGFP-expressing strain for use with MADM (mosaic analysis with double markers) mice (see Stock No. 006041 [MADM-GR (EGFP/Dsred2)] and Stock No. 006067 [MADM-RG (Dsred2/EGFP)]). Using the MADM system, a researcher can generate genetic mosaics in which an individual organism contains somatic cells of different genotypes. This allows the researcher to ascertain lineal relationships and pleiotropic gene function in multicellular organisms. These mice may also be useful in studies of cell differentiation and mitosis.
Mice harbor
..... | ||
| 006067 | 129-Gt(ROSA)26Sortm2Luo/J | Repository- Live |
| MADM-RG mice are viable with no gross behavioral or observable abnormalities. Homozygous females produce less pups to weaning age compared to heterozygotes. These mutants are designed for MADM (mosaic analysis with double markers), and must be crossed to mice harboring a reciprocal mutation at the same locus (see Stock No. 006041 or Stock No. 006075, MADM-GR (EGFP/Dsred2)). The resulting offspring have one copy of each reciprocal mutation on homologous chromosomes ("trans-heterozygous") and must next be bred to a Cre-expressing strain for fluorescent protein expression. Prior to Cre-recombination, double mutant mice do not have colored cells: the chimeric genes do not produce functional proteins because their coding sequences are interrupted by the beta-actin intron in different reading frames. After DNA replication (G2 phase) in double mutant mice, Cre-recombinase introducti
..... For more information please see the full phenotype on the strain data sheet | ||
| 006041 | 129-Gt(ROSA)26Sortm3Luo/J | Repository- Live |
| MADM-GR mice are viable with no gross behavioral or observable abnormalities. Homozygous mice have low fertility, while heterozygous mice have no reported fertility defects. These mutants are designed for MADM (mosaic analysis with double markers), and must be crossed to mice harboring a reciprocal mutation at the same locus (see Stock No. 006067 or Stock No. 006080, MADM-RG (Dsred2/EGFP)). The resulting offspring have one copy of each reciprocal mutation on homologous chromosomes ("trans-heterozygous") and must next be bred to a Cre-expressing strain for fluorescent protein expression. Prior to Cre-recombination, double mutant mice do not have colored cells: the chimeric genes do not produce functional proteins because their coding sequences are interrupted by the beta-actin intron in different reading frames. After DNA replication (G2 phase) in double mutant mice, Cre-recom
..... For more information please see the full phenotype on the strain data sheet | ||
| 004293 | 129-Shhtm2Amc/J | Repository- Live |
| Mice that are homozygous for the Shhtm2Amc targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. This conditional mutant contains two loxP sites flanking exon 2 of the targeted allele. Cre-mediated recombination excises exon 2 and some surrounding intronic sequence, generating a null allele. When the conditional mutant is crossed with a ubiquitously-expressing Cre recombinase carrier to remove Shh activity in the early embryo, the resulting phenotype resembles the Shh null mutation. These conditional mutant mice may be mated to strains expressing Cre recombinase to study the effects of temporal and tissue-specific ablation of the targeted allele. This mutant mouse strain represents a model that may be useful in studies of developmental defects resulting from disruption of Shh-dependent pathways.
When bred to a strain expressing Cre recombinase under the control of a tet
..... | ||
| 006050 | 129-Sirt6tm1Fwa/J | Repository- Live |
| Homozygous neonates are smaller than their wildtype and heterozygous littermates. They develop normally until approximately 21 days of age, when they develop an acute and rapid, aging-like degenerative pathology resulting in death by postnatal day 24. Homozygous mutant mice exhibit subcutaneous fat loss, lordokyphosis (hunchbacked spine) with osteopenia (30% loss of bone mineral density), colitis, and severe lymphopenia due to increased lymphocyte apoptosis. At day 12, mice have reduced insulin-like growth factor I (IGF-1) levels in serum, and develop severe hypoglycemia. Mouse embryonic fibroblasts (MEFs) prepared from homozygous embryos exhibit reduced proliferation, defective base excision repair function, as indicated by increased sensitivity to alkylating agents and ionizing radiation, and increased chromosomal aberrations. The donating investigators report that no gene product (mRNA or protein) is detected by RT-PCR or immuoblot analysis of tissues, MEFs or embryonic stem cells f
..... For more information please see the full phenotype on the strain data sheet | ||
| 003328 | 129-Tg(Prm-cre)58Og/J | Repository- Live |
| Mice homozygous for this PrmCre transgene are viable and fertile. Embryonic stem cells containing recombinase transgenes that are expressed in the male germ line, but not in other tissues or in the embryonic stem cells themselves, substantially simplify the production of subtle or conditional mutations in mice. This strain shows that transgenes comprised of the mouse protamine 1 promoter and the Cre recombinase coding sequence mediate the efficient recombination of a cre target transgene in the male germ line, but not in other tissues. This system can be used for reducing the time, effort, and resources required to produce homologously recombined alleles in mice that have been secondarily rearranged by site-specific recombinase. | ||
| 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. | ||
| 007175 | 129S-Cyp4a14tm1Jhc/J | Repository- Live |
| Mice homozygous for this "Cyp 4a14" mutant allele are viable and fertile. Homozygous deficiency of the targeted gene leads to spontaneous hypertension (more severe in males) that is androgen-sensitive. Homozygotes also exhibit other interrelated metabolic and regulatory effects; increased renal vascular resistance, impaired renal hemodynamics, elevated plasma androgens (5a-dihydrotestosterone (DHT) and testosterone), upregulated Cyp4a12 gene expression, and increased formation of prohypertensive 20-HETE. These "Cyp 4a14" mutant mice may be useful studying kidney function and metabolism, cardiovascular physiology, hypertension, and the relationships between blood pressure, sex hormones, and p450 w-hydroxylases. | ||
| 007664 | 129S-Efnb1tm1Sor/J | Repository- Live |
| These mice possess loxP sites flanking exons 2 through 5 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 these mutant mice are bred to mice that express Cre recombinase, resulting offspring will have exons 2 through 5 deleted in the cre-expressing tissue(s). These Efnb1 conditional mutant mice may be useful in studying cellular signaling in embryonic development and adult mice; specifically receptor tyrosine kinases. For example, when crossed to a strain expressing Cre recombinase in epiblast-derived tissues (see Stock No. 003755), this mutant mouse strain may be useful in embryogenesis research. | ||
| 004545 | 129S-Npytm1Rpa/J | Repository- Live |
| Mice that are homozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. No gene product (mRNA or protein) is detected by Northern or Western blot analysis of brain or adrenal gland tissue. Beta-galactosidase activity assays and in situ hybridization demonstrate similar expression patterns for the lacZ gene and the endogenous wildtype gene. Spontaneous seizures are exhibited by some mice at age 6 to 8 weeks. Homozygous mice are susceptible to seizures induced by GABA antagonist treatment. Mutant mice have an increased sensitivity to leptin treatment which results in a greater initial reduction of food intake and weight loss when compared to wildtype mice. This mutant mouse strain may be useful in studies related to the role of neuropeptide Y in obesity. | ||
| 008002 | 129S-Pafah1b1tm2Awb/J | Repository- Live |
| These mice possess loxP sites flanking exons 3 through 6 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. Histological analysis of brains from homozygotes reveals slightly wider CA1 and CA3 regions and a split in CA2 region in the hippocampus. When these mutant mice are bred to mice that express Cre recombinase, resulting offspring will have exons 3 through 6 deleted in the cre-expressing tissue(s). | ||
| 007005 | 129S-Scg5tm1Led/J | Repository- Live |
| The following text reflects the phenotype reported by the donating investigator on a "129Sv" genetic background (probably "Taconic Sv129" (129S6/SvEvJ)). While heterozygotes are viable and fertile, mice homozygous for this mutation (7B2-null) die in prepubertal or pubertal ages (5 weeks) with severe cardio-respiratory failure, convulsions, and hypothermia. No transcripts are detected in brain tissue from the targeted gene. 7B2 null mice are unable to make an active form of prohormone convertase 2 (PC2) and have high circulating corticosterone. Homozygotes on the 129S genetic background exhibit Cushing's-like disease pathologies of liver, pancreas, and pituitary; including pituitary-dependent hyperadrenocorticosteronism, severe hypoglycemia, hyperproinsulinemia, adrenal hypertrophy, pituitary hypotrophy, and altered islet cell morphology. 7B2-null mice develop the disease from intermediate lobe ACTH hypersecretion (rather than from pituitary adenomas). Other abnormalities include thinni
..... For more information please see the full phenotype on the strain data sheet | ||
| 007199 | 129S-Sgpl1Gt(ROSA)78Sor/J | Repository- Live |
| Mice homozygous for this mutant allele have reduced size and weight gains after birth and do not survive past 8 weeks of age. Homozygotes occur at a lower than Mendelian ratio (19%) from heterozygote X heterozygote crosses. No gene product is detected in homozygous embryos aged ED9.5-12.5 or in adult gonad. Beta-galactosidase staining pattern mimics the endogenous gene expression pattern in adult intestinal epithelial cells. Homozygous embryos E11.5 to E18.5 exhibit hemorrhages and microaneurisms. Vascular defects persist into adulthood. At 6 weeks of age, mutant mice are anemic (low hemoglobin concentration, reduced red blood cell count, low hematocrit). Mutants exhibit polychromasia (abnormally high number of immature blood cells), kidney defects (blood urea nitrogen level abnormally high, kidney size smaller than wildtype, swollen blood filled glomeruli, reduced number of vascular smooth muscle cells) and abnormalities in palate bone fusion. Homozygotes are infertile. Heterozygote
..... For more information please see the full phenotype on the strain data sheet | ||
| 006661 | 129S.B6-Tg(KRT14-RAF1/ESR1)1Pkha/J | Repository- Live |
| Mice hemizygous for this "K14-Raf:ER" transgene are viable and fertile. Inducible expression of the human Raf1(Raf-1 [DD]):estrogen receptor (ER) fusion protein is observed in the epidermis following topical application of 4-hydroxytamoxifen (4OHT). Prolonged (4 weeks) induction of human Raf-1[DD] activity promotes the undifferentiated, proliferative phenotypic characteristics observed in epidermal cancer; including hyperplasia, increased mitotic index, decreased expression of differentiation markers and increased expression of beta-1 and beta-4 integrin subunits. Raf-1[DD]-induced skin abnormalities are entirely reversed within one month after 4OHT cessation. These mice have a similar 4OHT-inducible skin phenotype as the transgenic mice expressing human H-RasG12V (Stock No. 006403) or human Mek1R4F (Stock No. 006822), and may be useful in studies of the
..... For more information please see the full phenotype on the strain data sheet | ||
| 006409 | 129S1.Cg-Tg(APPSw)40Btla/J | Repository- Live |
| These transgenic mice express all mRNA and protein isoforms of the human amyloid beta (A4) precursor protein APP containing the Familial Alzheimer's Disease (FAD) Swedish mutation K670N/M671L. Transgene expression (mRNA and full-length protein) is 2 to 3 fold the wild-type mouse App expression level in the hemizygous state in brain tissue as revealed by RT-PCR and Western Blot analysis. Transgene expression pattern mimics wild-type mouse gene expression patterns. This mutant mouse strain represents a model that may be useful in studies of the pathogenesis of Familial Alzheimer's Disease and possible therapeutic treatments.
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. A publication (Lehman et al. 2003 Hum Mol Genet 12:2949) compar
..... | ||
| 003946 | 129S4/SvJaeSor-Gt(ROSA)26Sortm1(FLP1)Dym/J | Repository- Live |
| This knock-in strain expresses a variant of the Saccharomyces cerevisiae FLP1 recombinase gene under the direction of the Gt(ROSA)26Sor promoter. The FLPe recombinase variant exhibits enhanced thermostability with recombination activity being four-fold and ten-fold that of wild type FLP at 37C and 40C, respectively. Homozygous mice for the knock-in allele are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. The Gt(ROSA)26Sor promoter drives expression in a constitutive fashion from preimplantation onward. Extensive target gene recombination can be achieved in most tissue types, including cells of the developing germ line. This mutant strain is suitable for use as a deleter strain and serves as a source of FLP1-expressing primary cell lines. | ||
| 007689 | 129S4/SvJaeSor-Gt(ROSA)26Sortm4(attB/attP)Sor/J | Repository- Live |
| These mutant mice contain a beta-galactosidase gene, lacZ, inserted into the Gt(ROSA)26Sor locus. Expression of the lacZ gene is blocked by a attB and attP site flanked STOP fragment placed between the lacZ sequence and the Gt(ROSA)26Sor promoter. This strain serves as a reporter strain, with successful PhiC31o recombination being indicated by beta-galactosidase expression in PhiC31o-expressing tissues. Mice that are homozygous for the transgenic insert are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. | ||
| 002655 | Mus pahari/EiJ | Repository- Live |
| 006555 | A.129(B6)-Tg(APPSw)40Btla/J | Repository- Live |
| These transgenic mice express all mRNA and protein isoforms of the human amyloid beta (A4) precursor protein APP containing the Familial Alzheimer's Disease (FAD) Swedish mutation K670N/M671L. Transgene expression (mRNA and full-length protein) is 2 to 3 fold the endogenous mouse App expression level in the hemizygous state in brain tissue as revealed by RT-PCR and Western Blot analysis. Transgene expression pattern mimics endogenous mouse gene expression patterns. The donating investigator reports increased mortality in young homozygous animals (higher incidence in females). This mutant mouse strain represents a model that may be useful in studies of the pathogenesis of Familial Alzheimer's Disease and possible therapeutic treatments.
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 p
..... | ||
| 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). | ||
| 003070 | ALR/LtJ | Repository- Live |
| ALS/LtJ (Stock No. 003072) and ALR/LtJ inbred strains are of interest to investigators across a wide range of scientific disciplines including type 1 and type 2 diabetes, obesity, metabolism and toxicology research. Treatment of alloxan or streptozotocin causing pancreatic beta cell destruction, leads to severe hyperglycemia and hypoinsulinemia in ALS/LtJ mice. ALR/LtJ mice are resistant to these toxins. ALR/LtJ mice are of particular interest to investigators studying the immunogenetics of NOD/LtJ mice in that the ALR/LtJ MHC haplotype (H2gx) is a variant of the diabetogenic NOD H2g7 haplotype. The (H2gx) haplotype is identical to the H2g7 haplotype from the H2-K end of the complex through the class II and class III region distal to Hsp70. However, at the distal H2-D end of the complex, ALR/LtJ mice have a rare H2-Dgx allele. Despite the similarities to the NOD/ShiLtJ mice, ALR/LtJ mice do not develop
..... For more information please see the full phenotype on the strain data sheet | ||
| 003072 | ALS/LtJ | Repository- Live |
| ALS/LtJ and ALR/LtJ (Stock No. 003070) inbred strains are of interest to investigators across a wide range of scientific disciplines including type 1 and type 2 diabetes, obesity, metabolism and toxicology research. Treatment of alloxan or streptozotocin causing pancreatic beta cell destruction, leads to severe hyperglycemia and hypoinsulinemia in ALS/LtJ mice. ALR/LtJ mice are resistant to these toxins. By 34 wk of age, both untreated ALS/Lt and ALR/Lt males fed a 6% fat-containing chow diet attain a mean body weight of around 50 grams. Genome wide scan comparison shows that ALS/LtJ mice are more closely related to NON/ShiLtJ mice (they share the H2nb1 haplotype) than to NOD/ShiLtJ. Like two other ICR-derived inbred strains selected in Japan (NON and NSY), alloxan-untreated ALS/Lt males exhibit impaired glucose tolerance when tested by intraperitoneal administration of glucose. However, unlike NON/ShiLt males, which exhibit impaired glucose tolerance in the presence
..... For more information please see the full phenotype on the strain data sheet | ||
| 001673 | AXB1/PgnJ | Repository- Live |
| The AXB and BXA set of RI strains are useful in the genetic analysis of several complex diseases including cardiovascular disease, diabetes, cancer, cleft palate, and hydrocephalus. The individual strains within the RI set also differ in their susceptibility to infectious diseases and in their responses to alcohol, stress, and endotoxin. The strain distribution pattern (SDP) for both the AXB and BXA RI strains is available through the Mouse Genome Informatics Recombinant Inbred Strain Distribution Patterns Query Form | ||
| 001681 | AXB10/PgnJ | Repository- Live |
| The AXB and BXA set of RI strains are useful in the genetic analysis of several complex diseases including cardiovascular disease, diabetes, cancer, cleft palate, and hydrocephalus. The individual strains within the RI set also differ in their susceptibility to infectious diseases and in their responses to alcohol, stress, and endotoxin. The strain distribution pattern (SDP) for both the AXB and BXA RI strains is available through the Mouse Genome Informatics Recombinant Inbred Strain Distribution Patterns Query Form | ||
| 001683 | AXB12/PgnJ | Repository- Live |
| The AXB and BXA set of RI strains are useful in the genetic analysis of several complex diseases including cardiovascular disease, diabetes, cancer, cleft palate, and hydrocephalus. The individual strains within the RI set also differ in their susceptibility to infectious diseases and in their responses to alcohol, stress, and endotoxin. The strain distribution pattern (SDP) for both the AXB and BXA RI strains is available through the Mouse Genome Informatics Recombinant Inbred Strain Distribution Patterns Query Form | ||
| 001826 | AXB13/PgnJ | Repository- Live |
| Through high density SNP analysis, some AXB and BXA recombinant inbred strains were shown to be the same or nearly the same genetically. AXB13/PgnJ and AXB14/PgnJ are considered ?sister strains? being identical throughout much of the genome but differing in large regions of Chromosomes 11, 12, 13, and in small regions of a few other Chromosomes. Because these two strains are "near congenics" a nomenclature change has been made to update AXB14/PgnJ to AXB13a/PgnJ. In general, 'sister" strains (those with suffixes of a or b) should not be used for primary screening/QTL mapping. However, if a QTL is located in a region of difference in a sister recombinant inbred then this strain can serve as a ?near congenic? for additional analysis. The AXB and BXA set of RI strains are useful in the genetic analysis of several complex diseases including cardiovascular disease, diabetes, cancer, cleft palate, and hydrocephalus. The individual strains within the RI set also differ in their suscepti
..... | ||
| 001685 | AXB15/PgnJ | Repository- Live |
| The AXB and BXA set of RI strains are useful in the genetic analysis of several complex diseases including cardiovascular disease, diabetes, cancer, cleft palate, and hydrocephalus. The individual strains within the RI set also differ in their susceptibility to infectious diseases and in their responses to alcohol, stress, and endotoxin. The strain distribution pattern (SDP) for both the AXB and BXA RI strains is available through the Mouse Genome Informatics Recombinant Inbred Strain Distribution Patterns Query Form | ||
| 001687 | AXB19/PgnJ | Repository- Live |
| Through high density SNP analysis, some AXB and BXA recombinant inbred strains were shown to be the same or nearly the same genetically. AXB18/Pgn, AXB19/Pgn, and AXB20/Pgn were found to be highly similar in their overall genomes, but with particular Chromosomes differing between them. Two of these "sister" strains were renamed. AXB19/Pgn was designated the primary strain since it has the best traceable history, and therefore its name remained unchanged. AXB18/Pgn was renamed AXB19a/Pgn and AXB20/Pgn was renamed AXB19b/Pgn. In general, the "sister" strains (those with suffixes of a or b) should not be used for primary screening/QTL mapping. However, if a QTL is located in a region of difference in a sister recombinant inbred then this strain can serve as a "near congenic" for additional analysis. The AXB and BXA set of RI strains are useful in the genetic analysis of several complex diseases including cardiovascular disease, diabetes, cancer, cleft palate, and hydrocephalu ..... For more information please see the full phenotype on the strain data sheet | ||
| 001686 | AXB19a/PgnJ | Repository- Live |
| Through high density SNP analysis, some AXB and BXA recombinant inbred strains were shown to be the same or nearly the same genetically. AXB18/Pgn, AXB19/Pgn, and AXB20/Pgn were found to be highly similar in their overall genomes, but with particular Chromosomes differing between them. Two of these "sister" strains were renamed. AXB19/Pgn was designated the primary strain since it has the best traceable history, and therefore its name remained unchanged. AXB18/Pgn was renamed AXB19a/Pgn and AXB20/Pgn was renamed AXB19b/Pgn. In general, the "sister" strains (those with suffixes of a or b) should not be used for primary screening/QTL mapping. However, if a QTL is located in a region of difference in a sister recombinant inbred then this strain can serve as a "near congenic" for additional analysis. The AXB and BXA set of RI strains are useful in the genetic analysis of several complex diseases including cardiovascular disease, diabetes, cancer, cleft palate, and hydrocephalu ..... For more information please see the full phenotype on the strain data sheet | ||
| 001688 | AXB19b/PgnJ | Repository- Live |
| Through high density SNP analysis, some AXB and BXA recombinant inbred strains were shown to be the same or nearly the same genetically. AXB18/Pgn, AXB19/Pgn, and AXB20/Pgn were found to be highly similar in their overall genomes, but with particular Chromosomes differing between them. Two of these "sister" strains were renamed. AXB19/Pgn was designated the primary strain since it has the best traceable history, and therefore its name remained unchanged. AXB18/Pgn was renamed AXB19a/Pgn and AXB20/Pgn was renamed AXB19b/Pgn. In general, the "sister" strains (those with suffixes of a or b) should not be used for primary screening/QTL mapping. However, if a QTL is located in a region of difference in a sister recombinant inbred then this strain can serve as a "near congenic" for additional analysis. The AXB and BXA set of RI strains are useful in the genetic analysis of several complex diseases including cardiovascular disease, diabetes, cancer, cleft palate, and hydrocephalu ..... For more information please see the full phenotype on the strain data sheet | ||
| 001674 | AXB2/PgnJ | Repository- Live |
| The AXB and BXA set of RI strains are useful in the genetic analysis of several complex diseases including cardiovascular disease, diabetes, cancer, cleft palate, and hydrocephalus. The individual strains within the RI set also differ in their susceptibility to infectious diseases and in their responses to alcohol, stress, and endotoxin. The strain distribution pattern (SDP) for both the AXB and BXA RI strains is available through the Mouse Genome Informatics Recombinant Inbred Strain Distribution Patterns Query Form | ||
| 001690 | AXB23/PgnJ | Repository- Live |
| The AXB and BXA set of RI strains are useful in the genetic analysis of several complex diseases including cardiovascular disease, diabetes, cancer, cleft palate, and hydrocephalus. The individual strains within the RI set also differ in their susceptibility to infectious diseases and in their responses to alcohol, stress, and endotoxin. The strain distribution pattern (SDP) for both the AXB and BXA RI strains is available through the Mouse Genome Informatics Recombinant Inbred Strain Distribution Patterns Query Form. | ||
| 001691 | AXB24/PgnJ | Repository- Live |
| The AXB and BXA set of RI strains are useful in the genetic analysis of several complex diseases including cardiovascular disease, diabetes, cancer, cleft palate, and hydrocephalus. The individual strains within the RI set also differ in their susceptibility to infectious diseases and in their responses to alcohol, stress, and endotoxin. The strain distribution pattern (SDP) for both the AXB and BXA RI strains is available through the Mouse Genome Informatics Recombinant Inbred Strain Distribution Patterns Query Form. | ||
| 001676 | AXB4/PgnJ | Repository- Live |
| The AXB and BXA set of RI strains are useful in the genetic analysis of several complex diseases including cardiovascular disease, diabetes, cancer, cleft palate, and hydrocephalus. The individual strains within the RI set also differ in their susceptibility to infectious diseases and in their responses to alcohol, stress, and endotoxin. The strain distribution pattern (SDP) for both the AXB and BXA RI strains is available through the Mouse Genome Informatics Recombinant Inbred Strain Distribution Patterns Query Form | ||
| 001677 | AXB5/PgnJ | Repository- Live |
| The AXB and BXA set of RI strains are useful in the genetic analysis of several complex diseases including cardiovascular disease, diabetes, cancer, cleft palate, and hydrocephalus. The individual strains within the RI set also differ in their susceptibility to infectious diseases and in their responses to alcohol, stress, and endotoxin. The strain distribution pattern (SDP) for both the AXB and BXA RI strains is available through the Mouse Genome Informatics Recombinant Inbred Strain Distribution Patterns Query Form | ||
| 001678 | AXB6/PgnJ | Repository- Live |
| The AXB and BXA set of RI strains are useful in the genetic analysis of several complex diseases including cardiovascular disease, diabetes, cancer, cleft palate, and hydrocephalus. The individual strains within the RI set also differ in their susceptibility to infectious diseases and in their responses to alcohol, stress, and endotoxin. The strain distribution pattern (SDP) for both the AXB and BXA RI strains is available through the Mouse Genome Informatics Recombinant Inbred Strain Distribution Patterns Query Form | ||
| 001679 | AXB8/PgnJ | Repository- Live |
| The AXB and BXA set of RI strains are useful in the genetic analysis of several complex diseases including cardiovascular disease, diabetes, cancer, cleft palate, and hydrocephalus. The individual strains within the RI set also differ in their susceptibility to infectious diseases and in their responses to alcohol, stress, and endotoxin. The strain distribution pattern (SDP) for both the AXB and BXA RI strains is available through the Mouse Genome Informatics Recombinant Inbred Strain Distribution Patterns Query Form | ||
| 002249 | B10.129S2(B6)-Igh-6tm1Cgn/J | Repository- Live |
| Mice homozygous for the Igh-6tm1Cgn targeted mutation are viable and fertile. Homozygous mutant mice lack mature B-cells. There is no expression of membrane-bound IgM, although some B-cells may be produced using a C gene other than mu. It may be useful as a model for B-cell immunodeficiency found in humans. Also know as muMT. | ||
| 006102 | B10.Cg-H2k Tg(Il2/NFAT-luc)83Rinc/J | Repository- Live |
| Hemizygous transgenic mice are viable, fertile, normal in size, and do not display any gross physical or behavioral abnormalities. The donating investigator reports that homozygous females in their colony are subfertile. These transgenic mice express luciferase under the regulation of the Il2 minimal promoter and 3 binding sites for the NFAT inducible nuclear factor involved in the regulation of interleukin-2 and other cytokine expression. Luciferase activity in these transgenic mice identifies NFAT-mediated transcription. These NFAT-luc transgenic mice may be useful be useful as reporters for NFAT-mediated expression during thymocyte development and selection and in studies related to signal transduction, apoptosis, and transcriptional regulation. | ||
| 006100 | B10.Cg-H2k Tg(NFkB/Fos-luc)26Rinc/J | Repository- Live |
| Hemizygous mice are viable, fertile, normal in size, and do not display any gross physical or behavioral abnormalities. Mutant mice have the luciferase gene driven by two copies of the NF-kappaB (NF-kB or NFkB) regulatory element. The presence of nuclear NF-kB DNA binding activity (as detected by electrophoretic mobility shift assay [EMSA]) is consistent with luciferase reporter activity; these reporter mice identify NF-kB transcriptional activity in any tissue. These transgenic mice may be useful in studies of immunology, cellular signaling, signal transduction, apoptosis, and transcription factor function. | ||
| 005895 | B10.Cg-Thy1a H2d Tg(TcraCl1,TcrbCl1)1Shrm/J | Repository- Live |
| Male mice that are hemizygous for the Clone-1 TCR (also called Clone 1 Thy1.1 TCR or Cl.1 TCR) transgene are viable, fertile, and normal in size. Females are very weak and have low fecundity. The donating investigator reports that all transgenic mice are prone to tumor development by 5-6 months of age. The transgene encodes a rearranged low avidity T cell receptor that recognizes an influenza virus hemagglutinin epitope (HA518-526) restricted by MHC class I H-2Kd. Flow cytometric analysis shows appropriate skewing towards the CD8+ T cell compartment in thymocytes and peripheral lymphocytes. Both naive and activated clone 1 T cells exhibit decreased responsiveness when presented with their cognate antigen in vitro and when transferred into mice expressing HA on pancreatic beta cells. CD8+ T cells can be induced to exhibit both effector function and antitumor activity. This mouse is further modified with the Thy1.1 allele, rather than th
..... For more information please see the full phenotype on the strain data sheet | ||
| 002761 | B10.Cg-Tg(TcrAND)53Hed/J | Repository- Live |
| Mice carrying the (TcrAND)53Hed transgene express a rearranged T-cell receptor (V alpha 11.1 / V beta 3) specific for the carboxy-terminal fragment of pigeon cytochrome c and the Ek molecule, resulting in a major subpopulation of T cells restricted to class II MHC proteins. There are an abnormally high percentage of mature CD4+CD8- cells. The peripheral T-cell population is almost exclusively CD4+. The original C57BL/6 and SJL mixed background strain (Stock number 002408) was backcrossed to C57BL/10 to create this strain. Both strains are fixed for H2b. Because C57BL/10 mice do not express I-E, this mouse must be crossed to a strain that expresses I-Ek to study the interaction of the transgenic T-cell receptor with the pigeon cytochrome c antigen. The lack of I-Ek expression in the transgenic line allows it to serve as a universal donor for crossing the transgene onto other strains expressing I-Ek<
>
..... For more information please see the full phenotype on the strain data sheet | ||
| 005379 | B6(A)-Rpe65rd12/J | Repository- Live |
| 008149 | B6(Cg)-Snord116tm1.1Uta/J | Repository- Live |
| Mice homozygous for this Snord116del (1-loxP or knockout) allele are viable and fertile. As the Snord116 gene cluster is imprinted and expressed only from the paternal allele, mice with paternal inheritance of the deletion lack expression of the targeted Snord116 small nucleolar RNAs (snoRNAs) gene cluster in brain tissues. Similarly, paternal transmission of the mutant allele is required to obtain the mutant phenotype in offspring. Affected heterozygotes (paternal deleted/maternal wildtype) recapitulate a subset of Prader-Willi syndrome (PWS) characteristics, including early-onset postnatal growth retardation, delayed sexual maturation, increased anxiety, motor learning deficit and hyperphagia (but not obesity). Other reported abnormalities include altered metabolic fuel usage, prolonged meal time, and increased levels of circulating ghrelin. These Snord116del mice may be useful in studying growth and feeding regulation, mechanisms of obesity, and pa
..... For more information please see the full phenotype on the strain data sheet | ||
| 008118 | B6(Cg)-Snord116tm1Uta/J | Repository- Live |
| Mice homozygous for this 2-loxP (floxed) allele are viable and fertile, with loxP sites flanking the Snord116 small nucleolar RNAs (snoRNAs) gene cluster. When bred to mice that express Cre recombinase, the resulting offspring will have this gene cluster deleted in the cre-expressing tissue(s). Because the Snord116 gene cluster is imprinted and only expressed from the paternal allele, breeding 2-loxP males with cre-expressing females may be required to generate deleted offspring with the knockout phenotype. The donating investigator reports that the distance between the two loxP sites (~140 kb) may reduce the recombination efficiency in somatic cells. As deletions of the Snord116 cluster are associated with Prader-Willi syndrome (PWS), mice carrying the 2-loxP (floxed) allele may be useful in generating conditional mutations for studying the role of Snord116 in growth and feeding regulation, mechanisms of obesity, and patho
..... For more information please see the full phenotype on the strain data sheet | ||
| 007212 | B6(Cg)-Tnfrsf13ctm1Mass/J | Repository- Live |
| Mice that are homozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. No gene product (mRNA or protein) is detected by RT-PCR or FACS analysis of spleen tissue and cells, respectively. Homozygotes have reduced numbers of mature recirculating bone marrow and splenic B cells. B cell development is arrested between the transitional IgM+ (T1 + T2) and IgMlow (T3) stages. Homozygotes exhibit diminished antigen-specific antibody responses with decreased levels of IgM, IgG1, IgG2, IgG2b and IgG3. This mutant mouse strain may be useful in studies of B cell development and differentiation. | ||
| 005999 | B6(SJL)-Tg(SBE/Tk-luc)7Twc/J | Repository- Live |
| Mice hemizygous for the transgenic insert are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. These transgenic mice express luciferase in response to activation of the Smad2/3-dependent signaling pathway. Cultured primary astrocytes isolated from transgenic mice exhibited luciferase activity when stimulated with TGF-beta. Higher treatment levels of activin and nodal elicited similar luciferase activity. Lipopolysaccharide (LPS) challenge results in strong bioluminescence emissions from the intestinal region and brain. Mechanical injury to the neocortex results in an increase of bioluminescence in 2 hours, which peaks at 4 hours and returns to baseline approximately 48 hours after the injury. Biochemical assays for luciferase activity correlated with noninvasive bioluminescence imaging analysis. The strain was backcrossed to the albino C57BL/6J-Tyrc-2J/J strain for 2 generations to facilitate bioluminescence imaging.
..... For more information please see the full phenotype on the strain data sheet | ||
| 004178 | B6.129(Cg)-Tg(CAG-Bgeo/GFP)21Lbe/J | Repository- Live |
| These Z/EG transgenic mice constitutively express lacZ under the control of the CMV enhancer/chicken actin promoter. Expression is widespread with notable exceptions being liver and lung tissue. Expression is observed throughout all embryonic and adult stages. When crossed with a Cre recombinase-expressing strain, lacZ expression is replaced with enhanced GFP expression in tissues expressing Cre. This double reporter system makes it possible to distinguish a lack of reporter expression from a lack of Cre recombinase expression while providing a means to assess Cre excision activity in live animals and cells.
As an example, when crossed to a strain expressing Cre recombinase in olfactory sensory neurons (see Stock No. 006668), this mutant mouse strain may be useful in lineage tracing. In an attempt to offer alleles on well-characterized or multiple genetic backgrounds, alleles are frequently moved t
..... | ||
| 004218 | B6.129(ICR)-Tg(CAG-ECFP)CK6Nagy/J | Repository- Live |
| Mice that are hemizygous for the transgenic insert are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. All tissues from hemizygous animals display fluorescence in all cell types under appropriate lighting conditions. Notable exceptions to this phenotype are erythrocytes and adipocytes in which fluorescence is negligible or absent. 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. | ||
| 006257 | B6.129-Aldh5a1tm1Kmg/J | Repository- Live |
| Homozygous mutation of this gene results in reduced body weight, ataxia, seizures, gliosis of the hippocampus, and eventual status epilepticus. From 19-26 days of age, repetitive tonic-clonic seizures results in more than 95% mortality. Biochemical assays shows complete ablation of the endogenous enzymatic activity in the brains, livers, hearts, and kidneys of homozygous mutant mice. Homozygotes have increased levels of GHB and GABA in liver and brain tissues, as well as in urine. Phenotype can be rescued to varying degrees utilizing a number of both pharmacotherapeutic and gene therapeutic approaches. Although heterozygous mice have approximately 50% of the endogenous enzyme activity compared to wildtype mice, they are viable and fertile. Mice with this targeted mutation may be useful in studying succinate semialdehyde dehydrogenase (SSADH) deficiency and to explore the effect of GABA and GHB accumulation on central nervous system development and function. | ||
| 003173 | B6.129-Cd47tm1Fpl/J | Repository- Live |
| Mice homozygous for the targeted mutation are viable, fertile, and display no obvious phenotypic abnormalities. Homozygous mutant mice display normal blood counts except for a reduction in the CD3+ fraction of peripheral lymphocytes. Integrin-associated protein (IAP; CD47) expression in heterozygous mice was approximately 40% of wildtype. Intraperitoneal injection of virulent Escherichia coli kills IAP-deficient mice, indicating a defect in the host defense pathway. This response appears to be secondary to both delayed polymorphonuclear leukocyte (PMN) migration to the site of infection and to defective activation at the site. | ||
| 005319 | B6.129-Cdh1tm2Kem/J | Repository- Live |
| These mice possess loxP sites flanking exons 6 to 10 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 used in conjunction with a Cre recombinase-expressing strain, this strain is useful in generating tissue-specific mutants of the floxed allele. | ||
| 006910 | B6.129-Crkltm1Hkp/J | Repository- Live |
| While heterozygous mice are viable and fertile, mice homozygous for this targeted allele die in utero. Immunoblots from homozygous tissues show no protein expression from the targeted gene. The prenatal lethality exhibited by homozygotes on this C57BL/6J congenic background (and also on a 129Sv genetic background) likely results from heart, liver, and placental defects. Please note that homozygous mutants on a mixed/outbred genetic background (129/Sv X Black Swiss) are viable and fertile. These mutant mice may be useful in studying the role of Crkl tyrosine-phosphorylation in Bcr/Abl (Philadelphia chromosome) chronic myelogenous leukemia (CML), acute lym | ||