June 2005 Mouse of the Month |
A Model for Tumor Biology: p53 KO mouse
Trp53 regulates cell cycle and apoptosis |
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Targeted mutation, Trp53tm1Sia, Chr 11
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Research Application: Apoptosis; Cell Cycle; Cancer; Immunology and Inflammation; Aging; DNA repair Mechanism; Toxicology The Trp53tm1Sia mutant allele was created by Dr. Shinichi Aizawa in the Molecular Oncology Laboratory of the RIKEN, Tsukuba. The TT2 ES cells originated from an F1 embryo between C57BL/6 and CBA mice were used to disrupt the Trp53 gene by homologous recombination. A neomycin selection cassette was inserted into the second exon of the Trp53 gene. Homozygous deficient mice can grow after birth, but often suffered from development of tumors in various region of the body. In C57BL/6 background most of the female homozygotes die in utero. A series of congenic p53 KO mice have been deposited to the RIKEN BRC. |
BRC No.00107, | C3H/HeN- p53 KO / C3.Cg-Trp53tm1Sia (available) |
BRC No.01348, | ICR-p53+/- / ICR.Cg-Trp53tm1Sia (available) |
BRC No.00815, | MSM- p53 KO / MSM.Cg-Trp53tm1Sia (available, depositor: Dr. Ryo Kominami) |
DEPOSITOR: | Dr. Ohtsura Niwa |
Reference: | Tsukada T, Tomooka Y, Takai S, Ueda Y, Nishikawa S, Yagi T, Tokunaga T, Takeda N, Suda Y, Abe S, et al. Enhanced proliferative potential in culture of cells from p53-deficient mice. Oncogene 8, 3313-3322 (1993). |