摘要
In order to investigate ATM in mediating DNA damage signal to p53 in the cellular response to IR, kinase activities of ATM and c-Abl immunoprecipitates and its activation by IR and damaged DNA have been analyzed. Results demonstrate that deficient ATM caused failure to activate phosphorylation of many proteins in response to radiation . ATM
In order to investigate ATM in mediating DNA damage signal to p53 in the cellular response to IR, kinase activities of ATM and c-AbI immunoprecipitates and its activation by IR and damaged DNA have been analyzed. Results demonstrate that deficient ATM caused failure to activate phosphorylation of many proteins in response to radiation. ATM coimmunoprecipitates with c-AbI and can catalyze phosphorylation of many proteins including p53 in response to radiation. Kinase activity of ATM / c-AbI immunoprecipitate stimulated by damaged DNAin vitro phosphorylation demonstrates that ATM can detect damaged DNA and initiate DNA damage signals. ATM can be phosphorylatedin vitro and inhibited by wortmannin, a specific inhibitor of PI3K family. These results confirm that ATM acts in DNA damage detection and signal transduction.
