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Overview
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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. 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.
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Overview