Overview:

CHK2 is rapidly phosphorylated and activated in response to replication blocks and DNA damage; the response to DNA damage occurs in an ataxia telangiectasia mutated (ATM)-dependent manner (1). Expression of wild-type Chk2 leads to increased p53 stabilization after DNA damage, whereas expression of a dominant-negative Chk2 mutant abrogated both phosphorylation of p53 on Ser-20 and p53 stabilization (2).

Genbank Number:

NM_007194

References:

1. Matsuoka, S. et al: Linkage of ATM to cell cycle regulation by the Chk2 protein kinase. Science. 1998 Dec 4;282(5395):1893-7.

2. Chehab NH. et al: Chk2/hCds1 functions as a DNA damage checkpoint in G(1) by stabilizing p53. Genes Dev. 2000 Feb 1;14(3):278-88.