Search Criteria: Research Area is "Mouse/Human Gene Homologs: Li-Fraumeni syndrome"
| Stock Number |
Strain Name Strain Description |
Standard Supply |
| 002101 | B6.129S2-Trp53tm1Tyj/J | Repository- Live |
| Mice homozygous for the Trp53tm1Tyj mutation show no visible phenotype but most develop tumors (principally lymphomas and osteosarcoma) at three to six months of age. Heterozygous mice develop tumors at about 10 months of age. These mice model some of the features of human Li-Fraumeni syndrome, a form of familial breast cancer with mutations in TRP53. Homozygous mice may produce a litter before succumbing to tumors. | ||
| 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. | ||
| 008045 | B6;129-Trp53tm2Holl/J | Repository- Live |
| In this mutant strain, exons 4-9 of the endogenous mouse Trp53 gene have been replaced with the homologous human TRP53 region. Transcription of the human sequence is under the control of the endogenous mouse promoter. The inserted human sequence segment encodes the DNA binding domain and the TRP53 polyproline domain. This latter domain contains a polymorphism at codon 72 that encodes either arginine or proline in human populations. This mutant strain expresses the proline variant at codon 72 and the related strain, 129-Trp53tm1Holl/J (Stock No. 004301) expresses the arginine variant. Mice that are homozygous for this mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Immortalized cell lines derived from primary embryonic fibroblasts harvested from these mice frequently harbor a TRP53 (p53) mutation in the DNA binding domain t
..... For more information please see the full descriiption on the strain data sheet | ||
| 006980 | B6;129-Trp53tm2Xu/J | Repository- Live |
| Mice homozygous for this targeted mutation are viable and fertile. They carry two phosphorylation site disruptions: Ser18 to Ala (S18A), and Ser23 to Ala (S23A). Trp53-dependent apoptosis is essentially abolished in thymocytes. These mice develop spontaneous tumors at approximately 1.5 years of age and a range of malignancies that are distinct from those found in animals carrying either a single S23A mutation or a complete knockout of the gene. This mutant mouse strain may be useful in studies of phosphorylation events in cancer development and apoptosis. | ||
| 004301 | 129-Trp53tm1Holl/J | Repository-Cryopreserved |
| In this mutant mouse strain, the endogenous murine sequence for exons 4-9 of the targeted gene, which encode the DNA binding domain of the tumor suppressor protein, have been replaced with the homologous normal human sequence. Transcription is under the control of the endogenous mouse promoter. Mice that are homozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Homozygous mutant mice exhibit normal expression and functional activity of the chimeric gene. Homozygous mutant mice have normal immunodetectable levels of p53 protein accumulation in nuclei in response to UV-induced DNA damage. Thymocytes from mutant mice are as susceptible to gamma-irradiation-induced and dexamethaxone-induced apoptosis as wildtype thymocytes. This mutant mouse strain may be useful in studies related to in vivo spontaneous and induced mutation of the human TRP53 gene sequence, and pharmacological agents for alt
..... For more information please see the full descriiption on the strain data sheet | ||
| 002080 | 129-Trp53tm1Tyj/J | Repository-Cryopreserved |
| 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. | ||
| 008183 | B6.129S4(Cg)-Trp53tm2.1Tyj/J | Repository-Cryopreserved |
| Mice carrying this Trp53 (p53) R172H point mutation mimic human Li-Fraumeni Syndrome, both genotypically and phenotypically. Heterozygotes develop a broad spectrum of tumors with a mean survival time of 16 months. Prominent tumor types include osteosarcomas (often metastatic), hemangiosarcomas, B-cell lymphomas and a variety of carcinomas. Homozygous mice also develop a broad spectrum of tumors, particularly T-cell lymphomas, hemangiosarcomas, soft-tissue sarcomas, osteosarcomas, primitive tumors (particularly male teratocarcinomas), and a variety of epithelial carcinomas. Mutant protein is expressed at high levels in mouse embryonic fibroblasts, as determined by Western blotting. | ||
| 008182 | B6.129S4-Trp53tm3.1Tyj/J | Repository-Cryopreserved |
| These targeted mutant mice carry a R270H missense mutation in exon 8 of the gene. Heterozygous mice develop a broad spectrum of tumors with a mean survival time of 16 months. Prominent tumor types include osteosarcomas (often metastatic), hemangiosarcomas, B-cell lymphomas and a variety of carcinomas. Homozygous mice also develop an array of tumor types including a variety of hematological tumors (particularly T-cell lymphomas), hemangiosarcomas, soft-tissue sarcomas, ostersarcomas, primitive tumors (particularly male teratocarcinomas), and a variety of epithelial carcinomas. Homozygotes have a mean survival time of 4.5 months. Mutant protein is expressed in all of the places that wildtype protein is expressed in normal tissues. Irradiation or DNA damage leads to substantially increased protein levels. Expression is also upregulated in some tumor types. This strain may be useful in studies of cancer and Li-Fraumeni Syndrome. | ||
| 008191 | B6;129S2-Trp53tm1Tyj Nf1tm1Tyj/J | Repository-Cryopreserved |
| These mice carry Trp53 and Nf1 targeted mutations on the same chromosome (cis). Double homozygotes are embryonic lethal. Double heterozygotes survive an average of five months and exhibit a significant increase in the percentage of soft tissue sarcomas compared with mice of other genotypes (Nf1 +/-, 5%; p53, 57%; Nf1/Trp53 trans, 36%; Nf1/Trp53 cis, 81%). Furthermore, although Nf1/Trp53 trans mice exclusively develop osteo-, fibro-, rhabdomyo-, and hemangiosarcomas, about 30% of tumors from the Nf1/Trp53 cis animals stain positively for S100 (consistent with glial cell origin) and exhibit classic histological features of malignant peripheral nerve sheath tumors (MPNSTs). This strain may be useful in studies of astrocytomas/glioblastomas and tumor suppressor genes. | ||
| 002103 | B6;129S2-Trp53tm1Tyj/J | Repository-Cryopreserved |
| 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. | ||
| 008181 | B6;129S4-Trp53tm4Tyj/J | Repository-Cryopreserved |
| Mice homozygous for this S23A point mutation are viable and fertile. Cells from the mice, including thymocytes and neurons in the cerebellum, exhibit defective apoptosis in response to DNA damage and exhibit partially impaired TRP53 (p53) stabilization. Mice develop increased lymphomas (especially B-cell lineage) and other tumors between one and two years of age. | ||
| 002526 | C.129S2(B6)-Trp53tm1Tyj/J | Repository-Cryopreserved |
| 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. 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. | ||
| 002547 | C3Ou.129S2(B6)-Trp53tm1Tyj/J | Repository-Cryopreserved |
| 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. | ||
| 002899 | FVB.129S2(B6)-Trp53tm1Tyj/J | Repository-Cryopreserved |
| 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. | ||
| 002659 | FVB/N-Tg(Trp53R172H)8512Jmr/J | Repository-Cryopreserved |
| The FVB/NTgN(Trp53R172H)8512Jmr express TRP53 with both dominant-negative and a gain-of function properties, i.e. this mutant is capable of inducing multiple drug resistance(MDR) promoter-driven reporter gene expression in transfection studies performed in p53 null cells. Transgene expression alone exerts no apparent effect on normal mammary gland development. Mice treated with the chemical carcinogen, dimethylbenz(a)anthracine (DMBA) or crossed with mice overexpressing erb-B2 develop tumors with significantly shorter latencies than controls. These tumors are characterized by large pleiomorphic nuclei and genomic instability. Spontaneous tumors are rarely observed in multiply bred animals in the first year of life. | ||
| 002660 | FVB/N-Tg(Trp53R172L)4491Jmr/J | Repository-Cryopreserved |
| The FVB/N-TgN(Trp53R172L)4491Jmr express TRP53 with pseudo-wildtype properties capable of inducing p21 and mdm-2 expression. Lobuloalveolar development is altered and apoptosis is increased during late pregnancy. The few normal lobules observed during early lactation did not express the Trp53 transgene suggesting that they arose by clonal expansion of cells not expressing the transgene during mid-pregnancy. Transgenic mice fail to lactate. There is no apparent alteration in ductal development. Mice expressing a dominant negative 172Arg-His mutation do not exhibit any detectable alterations in mammary gland development and have a very low incidence of spontaneous mammary tumors. Mice bearing the 172Arg-Leu transgene and a pituitary isograft displayed a marked increase in apoptosis and a significant delay in DMBA-induced tumorigenesis, while those bearing the 172Arg-His dominant negative p53 transgene were more susceptible to DMBA-induced tumorigenesis. | ||
| 003262 | STOCK Tg(Trp53A135V)L3Ber/J | Repository-Cryopreserved |
| Mice homozygous for the (Trp53A135V)2Ber transgene are viable and fertile, but show a high incidence of tumors, particularly lung adenocarcinomas, osteosarcomas, and lymphomas. This strain may serve as a model for Li-Fraumeni syndrome. | ||
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