IMPC phenotypes (gene matching)
- increased circulating sodium level / IMPC
B6.129P2-Chek2tm1Mak/Cnbc
| Status | Available to order |
| EMMA ID | EM:06380 |
| International strain name | B6.129P2-Chek2tm1Mak/Cnbc |
| Alternative name | Chk2 |
| Strain type | Targeted Mutant Strains : Knock-out |
| Allele/Transgene symbol | Chek2tm1Mak |
| Gene/Transgene symbol | Chek2 |
Information from provider
| Provider | Tak W Mak |
| Provider affiliation | Mak Lab, Campbell Family Breast Cancer reseach Institute |
| Genetic information | Exons 8 to 11 were replaced with a neomycin cassette (Neo). |
| Phenotypic information | Chk2(-/-) mice do not spontaneously develop tumors, although Chk2 does suppress 7,12-dimethylbenzanthracene-induced skin tumors. Tissues from Chk2(-/-) mice, including those from the thymus, central nervous system, fibroblasts, epidermis, and hair follicles, show significant defects in IR-induced apoptosis or impaired G(1)/S arrest. Quantitative comparison of the G(1)/S checkpoint, apoptosis, and expression of p53 proteins in Chk2(-/-) versus ATM(-/-) thymocytes suggested that Chk2 can regulate p53-dependent apoptosis in an ATM-independent manner. |
| Breeding history | Backcrossed 10 times to C57BL/6. |
| References |
|
| Homozygous fertile | yes |
| Homozygous viable | yes |
| Homozygous matings required | no |
| Immunocompromised | no |
Information from EMMA
| Archiving centre | CNB-CSIC, Centro Nacional de Biotecnologia, Madrid, Spain |
| Animals used for archiving | heterozygous C57BL/6J |
Disease and phenotype information
MGI phenotypes (gene matching)
- decreased mortality induced by ionizing radiation / MGI
- abnormal cell cycle / MGI
- decreased cellular sensitivity to gamma-irradiation / MGI
- polyploidy / MGI
- abnormal cell cycle checkpoint function / MGI
- decreased cellular sensitivity to ionizing radiation / MGI
- increased incidence of tumors by chemical induction / MGI
- abnormal cell physiology / MGI
Literature references
- Chk2 is a tumor suppressor that regulates apoptosis in both an ataxia telangiectasia mutated (ATM)-dependent and an ATM-independent manner.;Hirao Atsushi, Cheung Alison, Duncan Gordon, Girard Pierre-Marie, Elia Andrew J, Wakeham Andrew, Okada Hitoshi, Sarkissian Talin, Wong Jorge A, Sakai Takashi, De Stanchina Elisa, Bristow Robert G, Suda Toshio, Lowe Scott W, Jeggo Penny A, Elledge Stephen J, Mak Tak W, ;2002;Molecular and cellular biology;22;6521-32; 12192050
- Inactivation of chk2 and mus81 leads to impaired lymphocytes development, reduced genomic instability, and suppression of cancer.;El Ghamrasni Samah, Pamidi Ashwin, Halaby Marie Jo, Bohgaki Miyuki, Cardoso Renato, Li Li, Venkatesan Shriram, Sethu Swaminathan, Hirao Atsushi, Mak Tak W, Hande Manoor Prakash, Hakem Anne, Hakem Razqallah, ;2011;PLoS genetics;7;e1001385; 21625617
- Cross-talk between Chk1 and Chk2 in double-mutant thymocytes.;Zaugg Kathrin, Su Yu-Wen, Reilly Patrick T, Moolani Yasmin, Cheung Carol C, Hakem Razquallah, Hirao Atsushi, Liu Qinghua, Elledge Stephen J, Mak Tak W, ;2007;Proceedings of the National Academy of Sciences of the United States of America;104;3805-10; 17360434