Mechanisms of G2 Phase Arrest in DNA Damage-Induced Checkpoint Response

摘要: DNA damage activates cell cycle checkpoints and inhibits progression. In G2 phase cells, the checkpoint response results in inhibition of Cdc2/cyclin B activity, which, thereby, prevents G2/M transition, and, as a result, cells accumulate at boundary. Both p53-depen-dent -independent mechanisms are involved Cdc2 kinase activity during damage-induced response. The p53-independent mechanism causes an acute but transient through posttranslational modifications Cdc2-activating phosphatase Cdc25, whereas p53-dependent delayed sustained both transactivation p21, GADD45 14-3-3 tran-srepression cyclin B. Because is often defective tumor abrogation to preferentially negate induce programmed death has become attractive adjuvant strategy cancer therapy.