Transcription profiling of mouse Nbs1a??B/a??B Chk2-/- and Mre11ATLD1/ATLD1 Chk2-/- animals reveals Chk2 suppresses the oncogenic potential of DNA replication-associated DNA damage

ABSTRACT: The Mre11 complex (Mre11, Rad50, and Nbs1) and Chk2 have been implicated in the DNA damage response, an inducible process required for the suppression of malignancy. The Mre11 complex is predominantly required for repair and checkpoint activation in S phase, while Chk2 governs apoptosis. We examined the relationship between the Mre11 complex and Chk2 in the DNA damage response via the establishment of Nbs1∆B/∆B Chk2-/- and Mre11ATLD1/ATLD1 Chk2-/- mice. Chk2 deficiency did not modify the checkpoint defects or chromosomal instability of Mre11 complex mutants; however, the double mutant mice exhibited synergistic defects in DNA damage-induced p53 regulation and apoptosis. Nbs1∆B/∆B Chk2-/- and Mre11ATLD1/ATLD1 Chk2-/- mice were also predisposed to tumors. In contrast, DNA-PKcs d

ORGANISM(S): Homo sapiens

SUBMITTER: Agnes Viale 

PROVIDER: E-GEOD-11436 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress