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).
RP11-436C9.1, CDS1, CHEK2, HuCds1, LFS2, PP1425, RAD53
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.
Sample Kinase Activity Plot. For specific information on a given lot, see related technical data sheet.
Sample Purity Data. For specific information on a given lot, see related technical data sheet.
Storage, Stability and Shipping:
Store product at –70oC. For optimal storage, aliquot target into smaller quantities after centrifugation and store at recommended temperature. For most favorable performance, avoid repeated handling and multiple freeze/thaw cycles.
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Cancer, Cell Cycle, Ser/Thr Kinases