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).
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.
Recognizes the CHK2 protein
Western blot CHK2 from human and mouse cells
CHK2 from other species may also be detectable.
Host / Isotype / Clone#:
Mouse, IgG1, 7F9
Human full length recombinant CHK1
Store at 4oC (add 0.1% NaN3) for several months, and at -20oC for longer periods. For optimal storage, aliquot target into smaller quantities after centrifugation and store at recommended temperature. For optimal performance, avoid repeated handling and multiple freeze/thaw cycles.
Representative western blot (1:1000) with Anti-CHK2 using 20 ng of GST-tagged human full length recombinant CHK1 and CHK2.
Representative western blot (1:1000) with Anti-CHK2 using 3 µg, 10 µg, 30µg of 293T cell lysate.
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Cell Cycle, Ser/Thr Kinases