| RBRC No. | RBRC01348 |
||||||||||||||||
|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|
| Type | Targeted Mutation |
 |
|||||||||||||||
| Species | Mus musculus | ||||||||||||||||
| Strain name | ICR.Cg-Trp53<tm1Sia>/Rbrc | ||||||||||||||||
| Former Common name | ICR-p53+/- | ||||||||||||||||
| H-2 Haplotype | No Data | ||||||||||||||||
| ES cell line | TT2 [(C57BL/6NCrlj x CBA/JNCrlj)F1] | ||||||||||||||||
| Donor strain | (C57BL/6 x CBA)F1 via TT2 ES cell line | ||||||||||||||||
| Background strain | No Data | ||||||||||||||||
| Appearance | |||||||||||||||||
| 1 | Appearance | albino | |||||||||||||||
| Genotype | c/c | ||||||||||||||||
| Strain development | Developed by Shinichi Aizawa, RIKEN Tsukuba Institute. The TT2 ES cells derived from B6CBAF1 were used to disrupt the p53 gene by homologous recombination. The mutant mice were backcrossed to C57BL/6, ICR and C3H, respectively by Ohtura Niwa, Radiation Biology Center, Kyoto University, to DBA/2 by Takeshi Yagi, Graduate School of Frontier Biosciences, Osaka University, to MSM by Ryo Kominami, Niigata University Graduate School of Medical and Dental Sciences. | ||||||||||||||||
| Strain description | Trp53 gene knockout mice. 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. Several congenic strains were generated. C57BL/6 background (RBRC01361), ICR background (RBRC01348), C3H background (RBRC00107), DBA/2 background (RBRC01518), and MSM background (RBRC00815). In C57BL/6 background most of the female homozygotes die in utero (probably, also in MSM background). | ||||||||||||||||
| Colony maintenance | Heterozygote x Wild-type [or Crossing to Slc:ICR] | ||||||||||||||||
| Health Report |
BRC facility Health Report in the last year and a half
|
||||||||||||||||
| Gene Details | |||||||||||||||||
| Promoter | No Data | ||||||||||||||||
| 1 | Symbol | Trp53 | |||||||||||||||
| Symbol name | transformation-related protein 53 | ||||||||||||||||
| Chromosome | 11 | ||||||||||||||||
| Common name | p53 | ||||||||||||||||
| Symbol description | No Data | ||||||||||||||||
| Promoter | herpes simplex virus thymidine kinase promoter (HSV tk promoter) | ||||||||||||||||
| 2 | Symbol | neo | |||||||||||||||
| Symbol name | neomycin resistance gene (E. coli) | ||||||||||||||||
| Chromosome | 11 | ||||||||||||||||
| Common name | neo; neomycin; | ||||||||||||||||
| Symbol description | No Data | ||||||||||||||||
| References | Oncogene. 1993 Dec;8(12):3313-22.
Enhanced proliferative potential in culture of cells from p53-deficient mice.
|
||||||||||||||||
| Research applications | Cancer Research, Cell Biology Research, Immunology and Inflammation Research, Mouse Models for Human Disease |
||||||||||||||||
| Specific Term and Conditions | The following terms and conditions will be requested by the DEPOSITOR. In publishing the research results obtained by use of the BIOLOGICAL RESOURCE, a citation of the following literature(s) designated by the DEPOSITOR is requested. Oncogene, 8, 3313-3322 (1993). Please inform Laboratory for Animal Resources and Genetic Engineering, CDB (e mail: mutant@cdb.riken.jp) about the paper when published. |
||||||||||||||||
| Additional information | |||||||||||||||||
| 1 | Mouse of the Month Jun 2005 Breeding characters |
||||||||||||||||
| 2 | Genotyping protocol <PCR> | ||||||||||||||||
| Depositor | Niwa, Ohtsura (Radiation Biology Center, Kyoto University)  |
||||||||||||||||
| Strain Status / Availability (Expected delivery) |
|
||||||||||||||||
| Title | Journal (PMID) |
|---|---|
| Author | |
| p53 is a Host Cell Regulator during Herpes Simplex Encephalitis. | J. Virol. (2016).(27170756) |
| Maruzuru Y, Koyanagi N, Takemura N, Uematsu S, Matsubara D, Suzuki Y, Arii J, Kato A, Kawaguchi Y. | |
| Poly(ADP-ribose) polymerase inhibitors activate the p53 signaling pathway in neural stem/progenitor cells. | BMC Neurosci18(1): 14 (2017).(28095779) |
| Okuda A, Kurokawa S, Takehashi M, Maeda A, Fukuda K, Kubo Y, Nogusa H, Takatani-Nakase T, Okuda S, Ueda K, Tanaka S. |