Search Criteria: Research Area is "Apoptosis Research: Extracellular Modulators"
Strains from the Research Colonies of Jackson Laboratory Scientists
New Strains Under Development
| Stock Number |
Strain Name Phenotype |
Standard Supply |
| 003008 | B6;129S-Tnftm1Gkl/J | Level 4 |
| Mice homozygous for the Tnftm1Gkl targeted mutation are viable and fertile. Development of both lymph nodes and Peyer's patches is normal, and homozygous mutant mice show no apparent phenotypic abnormalities. Homozygous mice completely lack splenic primary B cell follicles and cannot form organized follicular dendritic cell networks and germinal centers. TNF-deficient mice treated to induce skin carcinogenesis develop significantly less benign and malignant tumors than treated wildtype mice. Nonobese homozygous mutant mice show modest decreases in body weight, epididymal fat depot weight, and percent body fat (statistically significant in males at 28 weeks of age). Further characterization indicates that 28 week old male mutant mice display lower insulin, triglyceride, and leptin levels compared to wildtype controls. Characterization of TNF deficient homozygotes injected with gold-thioglucose (GTG) to induce hyperphagic obesity indicates that the presence of TNF does
..... For more information please see the full phenotype on the strain data sheet | ||
| 001021 | B6Smn.C3-Faslgld/J | Level 4 |
| Mice homozygous for the Faslgld mutation display lymphadenopathy and systemic autoimmunity similar to that in Fasllpr homozygous mice. There is significant enlargement of all lymph nodes to 50 times the control weight by 20 weeks of age. Homozygotes also have an enlarged spleen, greatly increased numbers of T, B, and null lymphocytes and develop immune complex glomerulonephrosis. Onset of symptoms is dependent on genetic background with the C3H/HeJ strain having the earliest onset exhibiting glomerulonephritis by 22 weeks. In an attempt to offer alleles on well-characterized or multiple genetic backgrounds, alleles are frequently moved to a genetic background different from that on which an allele was first characterized. This is the case for the strain above. It should be noted that the phenotype could vary from that originally described. We will modify the strain description if necessary as published results become available. The Cryaa
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| 002407 | C57BL/6-Prf1tm1Sdz/J | Level 4 |
| Mice homozygous for the targeted mutation are viable and fertile. Homozygous mutant mice have normal numbers of CD8+ T cells and NK cells. CTL and NK cells are unable to lyse virus-infected or allogeneic fibroblasts in vitro. Homozygotes fail to clear lymphocytic choriomeningitis virus. Fibrosarcoma tumor cells are eliminated with reduced efficiency. Also known as perforin. | ||
| 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 | ||
| 005530 | B6.129S-Ddit3tm1Dron/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 toxin challenged mouse embryonic fibroblasts (MEFs). MEFs and renal proximal tubular epithelial cells have decreased apoptosis in response to endoplasmic reticulum stress induced by the toxin, tunicamycin. Pancreatic islets cells are more resistant to nitric oxide induced apoptosis. MEFs exhibit a delayed onset of unfolded protein response (UPR) target gene expression when treated with tunicamycin. This mutant mouse strain may be useful in studies of apoptosis and pathogenesis due to endoplasmic reticulum stress. | ||
| 005540 | B6.129S-Tnftm1Gkl/J | Repository- Live |
| Mice homozygous for the targeted mutation are viable and fertile. Development of both lymph nodes and Peyer's patches is normal, and homozygous mutant mice show no apparent phenotypic abnormalities. Homozygous mice completely lack splenic primary B cell follicles and cannot form organized follicular dendritic cell networks and germinal centers. TNF-deficient mice treated to induce skin carcinogenesis develop significantly less benign and malignant tumors than treated wildtype mice. Nonobese homozygous mutant mice show modest decreases in body weight, epididymal fat depot weight, and percent body fat (statistically significant in males at 28 weeks of age). Further characterization indicates that 28 week old male mutant mice display lower insulin, triglyceride, and leptin levels compared to wildtype controls. Characterization of TNF deficient homozygotes injected with gold-thioglucose (GTG) to induce hyperphagic obesity indicates that the presence of TNF does not affect the degree of obe
..... For more information please see the full phenotype on the strain data sheet | ||
| 006141 | B6.129S2-Thbs1tm1Hyn/J | Repository- Live |
| Mice homozygous for this targeted mutation are viable and fertile, with an approximate 20% decrease in embryo/neonate viability and a mild and variable lordotic curvature of the spine apparent from birth. Homozygous mice have an abnormal, but no full length transcript in multiple tissues. Western analysis confirmed the absence of the protein in platelets. Homozygotes exhibit an increase in the number of circulating white blood cells. During the first four to ten weeks of life, homozygotes exhibit patches of acute and organizing pneumonia. At later time points, there is considerable hyperplasia of the various epithelial cell lineages. Mutant mice also have an increased number of retinal endothelial cells and inappropriate remodeling and maturation of retinal vasculature following injury. On the FVB/N background, spontaneous tumor growth and vasculature are significantly increased compared to wildtype. Mutant mice may be useful in studies of inflammatory responses in the lungs, eye, and
..... For more information please see the full phenotype on the strain data sheet | ||
| 002266 | B6.129S4-Bdnftm1Jae/J | Repository- Live |
| Mice heterozygous for the Bdnftm1Jae mutation show about half normal levels of Bdnf mRNA, but appear normal. Mice homozygous for the Bdnftm1Jae mutation are smaller than normal siblings and most die within the second postnatal week. They have defective coordination of movements and balance. They also exhibit head bobbing and spinning during periods of hyperactivity. There are rare survivors to adulthood. There is excessive degeneration in all sensory ganglia examined, including the vestibular ganglion. Motor neurons are not affected. BDNF can prevent death of central motor neurons and other neurons in vitro, but does not affect these in vivo. | ||
| 003135 | C57BL/6-Tg(TRAMP)8247Ng/J | Repository- Live |
| Mice carrying the (TRAMP) transgene develop progressive forms of prostate cancer with distant site metastasis. Transgenic mice exhibit various forms of disease from mild intraepithelial hyperplasia to large multinodular malignant neoplasia. Tumors have been detected in the prostate as early as 10 weeks of age. The tumors have elevated levels of nuclear TRP53 and decreased androgen receptor expression. | ||
| 006481 | C57BL/6J-Tg(ACTB-NOTCH1)1Shn/J | Repository- Live |
| Transgenic mice are viable, fertile and behaviorally normal. These "CALSL-NICD (H)" mice (or simply CALSL-NICD) reportedly carry 10-20 copies of the transgene inserted into a single genomic locus. Expression of the transgene-derived intracellular domain of human NOTCH1 is prevented by a "Lox-STOP-Lox" cassette. When transgenic mice are bred to a strain expressing Cre recombinase, the "floxed stop" cassette is excised in the resulting offspring, and human NOTCH1 expression is observed in the cre-expressing tissue(s). These transgenic mice may be useful in studying early neural progenitor cell development and apoptosis, and responses to tissue-specific Notch activation. For example, when crossed to a strain expressing Cre recombinase in the nervous system (see Stock No. 003771), this transgenic mouse strain may be useful in studies of notch signaling during apoptotic cell death. | ||
| 002932 | CPt.C3-Faslgld/J | Repository- Live |
| Mice homozygous for the Faslgld mutation display lymphadenopathy and systemic autoimmunity similar to that in Faslpr homozygous mice. There is significant enlargement of all lymph nodes to 50 times the control weight by 20 weeks of age. Homozygotes also have an enlarged spleen, greatly increased numbers of T, B, and null lymphocytes and develop immune complex glomerulonephrosis. Onset of symptoms is dependent on genetic background with the C3H/HeJ strain having the earliest onset exhibiting glomerulonephritis by 22 weeks. In an attempt to offer alleles on well-characterized or multiple genetic backgrounds, alleles are frequently moved to a genetic background different from that on which an allele was first characterized. This is the case for the strain above. It should be noted that the phenotype could vary from that originally described. We will modify the strain description if necessary as published results become available. | ||
| 005564 | FVB(Cg)-Tg(Ins2-CALM1)26Ove Tg(Cryaa-TAg)1Ove/PneJ | Repository- Live |
| Transgenic mice are viable, display small eyes with cataracts and are hyperglycemic within 24 hours of age. S1 Nuclease protection assays indicate expression of calmodulin in the pancreas of 40-60 day old transgenic mice. Immunofluorescence analysis of the pancreas indicates increased levels of camodulin in B-cells of the pancreas. Camodulin fluorescing cells were not detected in the pancreatic acinar cells or any other tissue. Digital image scanning indicates the concentration of camodulin in transgenic B-cells is 5-fold higher than in wild type controls. Pancreatic insulin is 28% of control levels by 15 days of age. Insulin mRNA levels were also reduced in the transgenic animals. Transgenic mice experience hypoalbuminemia, elevated blood pressure, impaired cardiomyocytes and late stage diabetic nephropathy. Although transgenic mice are hyperglycemic within 24 hours of age, they are able to survive over a year without insulin treatment. This stock is useful for studying systemic c
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| 008223 | NOD.C3(B6)-Faslgld /LwnJ | Repository- Live |
| Mice homozygous for the Faslgld spontaneous mutation are viable and fertile. Homozygous males and females develop lymphadenopathy and systemic autoimmunity beginning at 8 weeks of age, but do not develop diabetes. The Lupus phenotype is accelerated in this strain when compared to the B6-Faslgldstrain. This mutant strain may be useful in the studies of apoptosis of lymphocytes, particularly T cells, and in studies of Lupus. 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. | ||
| 004848 | NOD.Cg-Rag1tm1Mom Prf1tm1Sdz/SzJ | Repository- Live |
| Mice that are homozygous for both targeted mutations are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities when housed under specific pathogen free conditions. These double homozygote mutant mice have no mature T or B lymphocytes, no detectable NK cell cytotoxic activity, and lack serum immunoglobulin. The number of nucleated spleen cells is significantly reduced in double mutant mice, when compared to the single homozygote, NOD.129S7(B6)-Rag1tm1Mom/J (Stock No. 003729). Although an increased number of DX5+CD122+ NK cells are found in the spleens of double mutants, these NK cells have impaired cytotoxic activity. The disruption of Prf1 ablates NK cell cytotoxic activity resulting in increased engraftment levels over that observed with Stock No. 003729. All mutant mice develop thymic lymphomas. This double mutant mouse strain may be useful in studies involving engraftment of human hematolympho
..... For more information please see the full phenotype on the strain data sheet | ||
| 004339 | STOCK Bdnftm3Jae/J | Repository- Live |
| These mice possess loxP sites on either side of exon 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 bred to a strain expressing Cre recombinase under the control of a tetracycline-responsive promoter element (see Stock No. 006224, 006234, 006244) and a strain expressing a tetracycline-controlled activator protein in brain tissues (see Stock No. 003763), this mutant mouse strain may be useful in studies of hippocampal-dependent learning and long-term potentiation. When bred to a strain expressing Cre recombinase in neuronal cells (see Stock No. 003966 for example), this
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| 002497 | 129-Ntf5tm1Jae/J | Repository-Cryopreserved |
| Mice homozygous for the targeted mutation are viable and fertile. Homozygous mutant mice lose sensory neurons in the nodose-petrosal and geniculate ganglia. However, they do not show loss of facial nucleus motor neurons, sympathetic neurons of the superior cervical ganglion, or dopaminergic neurons in the substantia nigra. | ||
| 003382 | B10.D2-Tg(C3-1-TAg)cJeg/J | Repository-Cryopreserved |
| This transgenic strain is a model for the study of multistage oncogenesis in the prostate and mammary glands. Male transgenic mice develop prostatic hyperplasia in early life that progresses to adenoma or adenocarcinoma in about half of the animals which survive longer 7 months of age. Female animals generally develop mammary intraepithelial neoplasia with similarities to DCIS by 3 months of age with subsequent development of mammary adenocarcinoma by 6 months of age in 100% of the animals. About 10 - 15% of female mice develop lung metastases, although lung metastases from prostate cancer is extremely rare. Bone metastases have not been observed. Please note that the phenotype description above was developed for this allele on an FVB background (stock number 3381). The mammary and prostate tumor phenotypes may be different on the C57BL/10 background in this strain. | ||
| 002248 | B6.129S2-Gzmbtm1Ley/J | Repository-Cryopreserved |
| Mice homozygous for the Gzmbtm1Ley mutation are viable and fertile. Lymphopoiesis and peripheral lymphoid tissue development is normal. T cell responses to mitogenic (Con A and IL2) and allogeneic (mixed lymphocyte culture) stimulation are unaffected. There is a 10-fold reduction in condensation of chromatin resulting in nuclear crescents and pyknosis when Gzmbtm1Ley CTL are used as effectors. Thus, activated CTL from homozygous mice are deficient in the early induction of DNA fragmentation and apoptosis in allogeneic target cells. Formerly called Ctla1. | ||
| 002275 | B6.129S4-Ntf3tm1Jae/J | Repository-Cryopreserved |
| Mice homozygous for the Ntf3tm1Jae targeted mutation are smaller than their normal littermates and most die shortly after birth. Survivors die prior to weaning. They display limb ataxia, an inability to position the limbs properly when attempting to move, and there is a tendency for all four limbs to intermittently stiffen in an extensor posture. Autopsy showed all peripheral ganglia markedly smaller in the mutant. Spinal proprioceptive afferents and their peripheral sense organs are completely absent. Heterozygous mice appear normal; however, the number of muscle spindles in heterozygotes is half that of normal wildtype siblings. There is approximately a 50% reduction in the sympathetic superior cervical ganglion (SCG) neurons caused by excessive apoptosis of sympathetic neuroblasts during neurogenesis. | ||
| 003541 | B6.129S4-Ntf3tm2Jae/J | Repository-Cryopreserved |
| This strain has loxP sites located on either side of the Ntf3 exon 2. Mice homozygous for this allele are viable, fertile and without behavioral abnormalities. If this strain is crossed with a transgenic strain bearing Cre recombinase, expression of the Ntf3 gene in offspring can be blocked in a tissue-specific manner depending on the promoter controlling the recombinase. Strains under the control of the rat nestin promoter block expression in the central nervous system; see strains 002275 and 002276. | ||
| 004197 | B6.129S6-Rac2tm1Mddw/J | Repository-Cryopreserved |
| Mice that are homozygous for the targeted mutation are viable, fertile, and normal in size but exhibit phagocytic immunodeficiency. No endogenous gene product (mRNA or protein) was detected by Northern blot analysis, RT-PCR or Western blot analysis. The Rac proteins are a subclass of the Rho family of GTPases, and are involved in actin cytoskeletal organization in cell movement, cell proliferation, kinase signaling pathways, and in superoxide production in phagocytic cells. Neutrophils and mast cells derived from homozygous mice display abnormal actin-based functions: cytoskeleton remodeling ability, adhesion, migration, degranulation, and phagocytosis. Diminished superoxide production in response to some agonists, and reduced total number of leukocytes and neutrophils in peritoneal exudate is observed. As result of functional deficiencies in neutrophil and mast cell populations, these mutant mice are more vulnerable to invasive infection. Slowed growth of mast cells, accompanying redu
..... For more information please see the full phenotype on the strain data sheet | ||
| 004853 | B6.C3-Tg(KRT14-Birc5)19Gros/J | Repository-Cryopreserved |
| These transgenic mice express the mouse baculoviral IAP repeat-containing 5, Birc5 (survivin), gene under the direction of the human keratin 14 promoter. Transgene expression is specific to epidermal and follicular keratinocytes. Mice hemizygous for the transgenic insert are resistant to chemical (DMBA)- and UVB-induced keratinocyte apoptosis in vivo. Although hemizygotes were less susceptible to DMBA-induced papilloma formation, spontaneous papilloma regression was not observed and there was enhanced conversion of papillomas to carcinomas. This mutant mouse strain represents a model that may be useful in studies of keratinocyte apoptosis and skin cancer development. | ||
| 003380 | B6.FVB-Tg(C3-1-TAg)cJeg/J | Repository-Cryopreserved |
| TgN(C3-1-TAg)cJeg mice are transgenic for the SV-40 Large tumor antigen (TAg) driven by the rat prostatic steroid binding protein (C3(1))promoter. Male mice survive up to 11 months of age. They develop hyperplastic changes in the prostate epithelium which progress to prostate adenocarcinoma in the majority of mice after 8 months of age. Carcinogenic changes in female mice begin with development of hyperplasia of the mammary gland ducts and acini by 3 months of age and progress to multifocal mammary adenocarcinoma with death by 6 month of age. Homozygous mothers can bear offspring but pregnancy appears to accelerate tumor development and foster mothers are required for pups due to lactation difficulties. Evidence of pulmonary metastases has been seen in both male and female mice. These C3-1-TAg transgenic mice provide a model to study TAg-induced progression of hormone responsive tumors. Please note that the phenotype description above was developed for this allele on an FVB backgrou
..... For more information please see the full phenotype on the strain data sheet | ||
| 004264 | B6;129-Cycstm1Wlm/J | Repository-Cryopreserved |
| Mice homozygous for the Cycstm1Wlm targeted-mutant allele die in utero by embryonic day 10.5, but cell lines established from early Cycs-null embryos are viable under conditions that compensate for defective oxidative phosphorylation. Cells lacking cytochrome c show reduced caspase 3 activation, and are resistant to the proapoptotic effects of UV irradiation, serum withdrawal, and staurosporine. Cells lacking cytochrome c, however, do demonstrate an increased sensitivity to cell death signals triggered by tumor necrosis factor, alpha. Heterozygous mice are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. | ||
| 002247 | B6;129S2-Gzmbtm1Ley/J | Repository-Cryopreserved |
| Mice homozygous for the Gzmbtm1Ley mutation are viable and fertile. Lymphopoiesis and peripheral lymphoid tissue development is normal. T cell responses to mitogenic (Con A and IL2) and allogeneic (mixed lymphocyte culture) stimulation are unaffected. There is a 10-fold reduction in condensation of chromatin resulting in nuclear crescents and pyknosis when Gzmbtm1Ley CTL are used as effectors. Thus, activated CTL from homozygous mice are deficient in the early induction of DNA fragmentation and apoptosis in allogeneic target cells. Formerly called Ctla1. | ||
| 000784 | C3H/HeJ-Faslgld/J | Repository-Cryopreserved |
| Mice homozygous for the Faslgld mutation display lymphadenopathy and systemic autoimmunity similar to that in Fasllpr homozygous mice. There is significant enlargement of all lymph nodes to 50 times the control weight by 20 weeks of age. Homozygotes also have an enlarged spleen, greatly increased numbers of T, B, and null lymphocytes and develop immune complex glomerulonephrosis. Onset of symptoms is dependent on genetic background with the C3H/HeJ strain having the earliest onset exhibiting glomerulonephritis by 22 weeks. | ||
| 003445 | C57BL/6J-Tg(Amy1TAg)354Knw/J | Repository-Cryopreserved |
| C57BL/6-TgN(Amy1TAg)354Knw mice are viable and fertile. They express the SV40 tumor antigen under control of the liver promoter of the mouse alpha-amylase gene (Amy-1a). This transgenic strain develops malignant tumors of the brown adipose tissue at about 18 months of age. The tumors have high metastatic potential, with metastases commonly occurring in liver, lung, spleen, heart and adrenal glands. Note: This line, '354', contains the same trangene construct as line '501' (Stock No. 003446). Divergent tumor development between these lines is reported to be a result of different transgene integration sites. | ||
| 003446 | C57BL/6J-Tg(Amy1TAg)501Knw/J | Repository-Cryopreserved |
| C57BL/6-TgN(Amy1TAg)501Knw mice are viable and fertile. They express the SV40 tumor antigen under control of the liver promoter of the mouse alpha-amylase gene (Amy1a). This transgenic strain develops metastatic osteosarcomas at about 13 months of age. Note: This line, '501', contains the same trangene constuct as line '354' (Stock No. 003445). Divergent tumor development between these lines is reported to be a result of different transgene integration sites. | ||
| 002233 | C57BL/6J-Tg(SV)7Bri/J | Repository-Cryopreserved |
| Transgenic mice overexpressing the SV40 enhancer and large-T antigen develop brain tumors in the choroid plexus beginning at three to four months of age. | ||
| 003189 | C57BL/6J-Tg(WAPTAg)3Knw/J | Repository-Cryopreserved |
| Multiparous females of the WapTag3 lineage have hyperplastic mammary glands and occasionally develop mammary adenocarcinomas by 6 months of age. At this age, both males and females of this lineage develop osteosarcomas arising from the ospetrosium and renal adenocarcinomas. WAPTag3 females do not suckle their pups. | ||
| 003381 | FVB-Tg(C3-1-TAg)cJeg/J | Repository-Cryopreserved |
| This transgenic strain is a model for the study of multistage oncogenesis in the prostate and mammary glands. Male transgenic mice develop prostatic hyperplasia in early life that progresses to adenoma or adenocarcinoma in about half of the animals which survive longer 7 months of age. Female animals generally develop mammary intraepithelial neoplasia with similarities to DCIS by 3 months of age with subsequent development of mammary adenocarcinoma by 6 months of age in 100% of the animals. About 10 - 15% of female mice develop lung metastases, although lung metastases from prostate cancer is extremely rare. Bone metastases have not been observed. The phenotype for this transgene has been most extensively studied in the FVB/N background. | ||
| 003505 | NOD.B6-Prf1tm1Sdz/J | Repository-Cryopreserved |
| Mice homozygous for the Prf1tm1Sdz targeted mutation are viable and fertile. Homozygous mutant mice on an autoimmune type 1 diabetes prone NOD background have normal numbers of CD4- CD8+ T cells in the spleen. CD4- CD8- expressing T lymphocytes were also normal. NOD mice show a progressive infilitatraion of mononuclear cells into pancreatic islets beginning around 5 weeks of age. NOD wildtype and PRF1 deficient mice show similar development of insulititis. However, disease incidence was decreased from 77% in wildtype females to 16% in homozygotes. The onset of disease was also delayed from a median of 19 weeks to 39.5 weeks of age. These results show the importance of perforin-mediated cytotoxic T cells in development of autoimmune diabetes. (Kagi et al., 1994; Kagi et al., 1997.) | ||
| 002380 | NOD.Cg-Tg(Ins2-TAg)1Lt Prkdcscid/DvsJ | Repository-Cryopreserved |
| Homozygous NOD/Lt-TgN(RipTag)1Lt-Prkdcscid mice develop pancreatic beta cell adenomas. They are able to produce 2-3 litters before the insulin secreted from the adenoma makes them too hypoglycemic. Because Prkdcscid mice lack T-cells the adenomas from this strain are free of the autoimmune T-cells found in the adenomas of NOD/Lt-TgN(RipTag)1Lt mice. | ||
| 002033 | NOD/ShiLt-Tg(RipTAg)1Lt/J | Repository-Cryopreserved |
| Homozygous NOD/Lt-Tg(RipTag)1Lt mice develop pancreatic beta cell adenomas. They are able to produce 2-3 litters before the insulin secreted from the adenoma makes them too hypoglycemic. | ||
| 002267 | STOCK Bdnftm1Jae/J | Repository-Cryopreserved |
| Mice heterozygous for the Bdnftm1Jae mutation show about 1/2 normal levels of Bdnf mRNA, but appear normal. Mice homozygous for the Bdnftm1Jae mutation are smaller than normal siblings and most die within the second postnatal week. They have defective coordination of movements and balance. They also exhibit head bobbing and spinning during periods of hyperactivity. There are rare survivors to adulthood. There is excessive degeneration in all sensory ganglia examined, including the vestibular ganglion. Motor neurons are not affected. BDNF can prevent death of central motor neurons and other neurons in vitro, but does not affect these in vivo. | ||
| 002276 | STOCK Ntf3tm1Jae/J | Repository-Cryopreserved |
| Mice homozygous for the Ntf3tm1Jae targeted mutation are smaller than their normal littermates and most die shortly after birth. Survivors die prior to weaning. They display limb ataxia, an inability to position the limbs properly when attempting to move, and there is a tendency for all four limbs to intermittently stiffen in an extensor posture. Autopsy showed all peripheral ganglia markedly smaller in the mutant. Spinal proprioceptive afferents and their peripheral sense organs are completely absent. Heterozygous mice appear normal; however, the number of muscle spindles in heterozygotes is half that of normal wildtype siblings. There is approximately a 50% reduction in the sympathetic superior cervical ganglion (SCG) neurons caused by excessive apoptosis of sympathetic neuroblasts during neurogenesis. | ||
(36 stocks) Back to Top
IMPORTANT NOTE: Price information is on the strain data sheet which can be viewed by clicking on the strain name.
| Stock Number |
Strain Name Phenotype |
Standard Supply |
| 003188 | C57BL/6J-Tg(WapTAg)1Knw | Research Strain |
| Multiparous female mice of the WapTag1 lineage develop mammary adenocarcinomas with an average latency of 13 months. The histopathological phenotype is heterogeneous; papillary, ductal, tubular, and sometimes solid phenotypes are observed. Those tumors with a papillary morphology closely resemble human papillary carcinomas. Tumors arise adjacent to morphologically normal mammary epithelium or hyperplastic lesions. Mammary carcinomas are extremely rare in virgin female mice. Male mice, and those female mice that do not develop mammary carcinoma develop undifferentiated soft tissue sarcomas. Multiparous females of the WapTag3 lineage have hyperplastic mammary glands and occasionally develop mammary adenocarcinomas by 6 months of age. At this age, both males and females of this lineage develop osteosarcomas arising from the os petrosum and renal adenocarcinomas. | ||
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How to Register Interest
Please indicate your interest in purchasing any of the strains listed below when they become available for distribution by checking the box next to the strain(s) of interest and then selecting the "Continue" button which leads to an Interest Form.View a Data sheet for New Strains Under Development
Select the strain name to link to the strain data sheet.
New Strains Under DevelopmentThe Jackson Laboratory serves as a worldwide distributor and national repository for common and rare strains of inbred mice and mice carrying spontaneous mutations or induced mutations (i.e., transgenic, targeted/"knockout", or chemically induced mutations). At any one time, we have over 100 strains at various stages of development and colony expansion. Strains "Under Development" fall into two categories depending on the anticipated demand from the scientific community.
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It is VERY IMPORTANT that you register interest in strains Under Development. The anticipated demand for a strain enables us to determine effectively the distribution plan for each strain Under Development. Registering interest also provides benefits to you (including advance notification of pending availability). Whether a strain is made available from a live colony OR from our cryopreservation repository, you may want to consider the option of Dedicated Supply. To learn more about Dedicated Supply, go to Services.
- Strains that will be made available from a live distribution colony at The Jackson Laboratory.
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