Search Criteria: Research Area is "Cancer Research: Increased Tumor Incidence (Adenomas)"
| Stock Number |
Strain Name Strain Description |
Standard Supply |
| 007218 | B6.129S6-Trp53tm2Xu/J | Repository- Live |
| Mice homozygous for this targeted mutation are viable and fertile. They carry two phosphorylation site disruptions: Ser18 to Ala (S18A), and Ser23 to Ala (S23A). Trp53-dependent apoptosis is essentially abolished in thymocytes. These mice develop spontaneous tumors at approximately 1.5 years of age and also develop a range of malignancies that are distinct from those found in animals carrying either a single S23A mutation or a complete knockout of the gene. This mutant mouse strain may be useful in studies of phosphorylation events, cancer development and apoptosis. In an attempt to offer alleles on well-characterized or multiple genetic backgrounds, alleles are frequently moved to a genetic background different from that on which an allele was first characterized. It should be noted that the phenotype could vary from that originally described. We will modify the strain description if necessary as published results become available. | ||
| 006980 | B6;129-Trp53tm2Xu/J | Repository- Live |
| Mice homozygous for this targeted mutation are viable and fertile. They carry two phosphorylation site disruptions: Ser18 to Ala (S18A), and Ser23 to Ala (S23A). Trp53-dependent apoptosis is essentially abolished in thymocytes. These mice develop spontaneous tumors at approximately 1.5 years of age and a range of malignancies that are distinct from those found in animals carrying either a single S23A mutation or a complete knockout of the gene. This mutant mouse strain may be useful in studies of phosphorylation events in cancer development and apoptosis. | ||
| 004686 | B6;129S4-Tsc2tm1Djk/J | Repository-Cryopreserved |
| Mice that are heterozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Homozygous null mice have an embryonic lethal phenotype, failing to develop past embryonic days 9.5 to 12.5 due to hepatic hypoplasia. Cultured neuroepithelial progenitor cells isolated from embryonic day 10.5 embryos display abnormal growth and differentiation. All heterozygotes develop multiple bilateral renal cystadenomas by 12-15 months of age. By 15 months, about half develop liver hemangiomas (more common in females than in males). Less than 10% develop extremity angiosarcomas or renal carcinoma. Little or no gene product (protein) is detected by Western blot in renal cystadenomas. PCR analysis reveals loss of the wildtype allele in about 30% of lesions. Phenotype variability is dependent on genetic background. This mutant mouse strain may be useful in studies of tuberous sclerosis (TSC). | ||
| 005143 | C3.B6-Tg(Fabp1-Ccnd1)4Rdb/J | Repository-Cryopreserved |
| These transgenic mice express mouse cyclin D1 under the direction of the rat fatty acid binding protein 1 promoter (-596 to +21 fragment). Mice that are hemizygous for the transgene are viable, normal in size and do not display any gross physical or behavioral abnormalities. Hemizygous mutant mice exhibit reduced fertility after 3 months of age. Transgenic mice overexpress cyclin D1 in the liver and epithelial cells of the small intestine and colon. A lower level of expression occurs in the kidneys. Onset of progressive liver disease begins at one month of age with hepatomegaly. Male transgenic mice exhibit more severe hepatomegaly than transgenic females. By 6 months of age, all transgenic males and half of the transgenic females display hepatocellular dysplasia. Eighty-seven percent of transgenic males and 69% of transgenic females develop hepatocellular adenoma or hepatocellular carcinoma by 15 months of age. This mutant mouse strain may be useful in studies of hepatocellular carcin
..... For more information please see the full descriiption on the strain data sheet | ||
| 006863 | C3Fe.B6-Mcm4chaos3/J | Repository-Cryopreserved |
| Mice homozygous for this ENU-induced F345I hypomorphic allele (Chaos3) are viable, fertile, and overtly indistinguishable from normal littermates. Homozygous, but not heterozygous, mice have slightly reduced wildtype protein levels in mouse embryonic fibroblasts (MEFs). Whereas Chaos3 heterozygotes show mildly elevated (2- to 5-fold) micronucleus frequencies compared with wildtype, homozygotes have an approximate 20-fold increase with over 7% of erythrocytes containing micronuclei. MEFs from homozygous mice exhibit mild defects (cell proliferation, S phase and G2/M populations), and are highly susceptible to chromosome breakage following treatment with the DNA replication inhibitor aphidicolin. On a congenic C3HeB/FeJ background, greater than 80% of homozygous females exhibit mammary adenocarcinomas with a mean latency of 12 months, while males have no tumor incidence. These Chaos3 mice provide a novel, non-transgenic model of breast cancer, and may be useful for s
..... For more information please see the full descriiption on the strain data sheet | ||
| 004834 | C57BL/6-Tg(Fabp1-Ccnd1)4Rdb/J | Repository-Cryopreserved |
| These transgenic mice express the mouse cyclin D1 under the direction of the rat fatty acid binding protein 1 promoter (–596 to +21 fragment). Mice that are hemizygous for the transgene are viable, normal in size and do not display any gross physical or behavioral abnormalities. Hemizygous mutant mice exhibit reduced fertility after 3 months of age. Transgenic mice overexpress cyclin D1 in the liver and epithelial cells of the small intestine and colon. A lower level of expression occurs in the kidneys. Onset of progressive liver disease begins at one month of age with hepatomegaly. Male transgenic mice exhibit more severe hepatomegaly than transgenic females. By 6 months of age, all transgenic males and half of the transgenic females display hepatocellular dysplasia. 87% of transgenic males and 69% of transgenic females develop hepatocellular adenoma or hepatocellular carcinoma by 15 months of age. By 6 months of age, approximately half of mutant mice have lost hepatic expressio
..... For more information please see the full descriiption on the strain data sheet | ||
| 002437 | FVB/N-Tg(MMTV-Notch4)3Rnc/J | Repository-Cryopreserved |
| Male mice transgenic for the Notch4 gene (previously called Int3) are sterile, and females fail to lactate. Mammary tissue of females does not develop completely, exhibiting dramatic inhibition of alveolar-lobular development and reduced penetration of the mammary fat pad by ductal epithelium. Glandular epithelia of tissues expressing the activated form of Notch4 generally display severe ductal hyperplasia. Salivary glands fail to differentiate completely. Male transgenic mice exhibit severe epididymal hyperplasia, which is thought to be the cause of their sterility. Both male and female mice develop focal adenomas of the mammary and salivary glands. | ||
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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
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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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- Strains that will be made available from a live distribution colony at The Jackson Laboratory.
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