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• W1979989319 abstract "The phosphatidylinositol-3-kinase-like kinase ATM (ataxia-telangiectasia mutated) has a central role in coordinating DNA damage responses, including cell-cycle checkpoint control, DNA repair and apoptosis. Mutations of ATM cause a spectrum of defects ranging from neurodegeneration to cancer predisposition. However, the mechanism by which DNA damage activates ATM is poorly understood. Here we show that Cdk5 (cyclin-dependent kinase 5), activated by DNA damage, directly phosphorylates ATM at Ser 794 in post-mitotic neurons. Phosphorylation at Ser 794 precedes, and is required for, ATM autophosphorylation at Ser 1981, and activates ATM kinase activity. The Cdk5-ATM signal regulates phosphorylation and function of the ATM targets p53 and H2AX. Interruption of the Cdk5-ATM pathway attenuates DNA-damage-induced neuronal cell cycle re-entry and expression of the p53 targets PUMA and Bax, protecting neurons from death. Thus, activation of Cdk5 by DNA damage serves as a critical signal to initiate the ATM response and regulate ATM-dependent cellular processes." @default.
• W1979989319 created "2016-06-24" @default.
• W1979989319 creator A5005308572 @default.
• W1979989319 creator A5006784348 @default.
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• W1979989319 date "2009-01-18" @default.
• W1979989319 modified "2023-10-17" @default.
• W1979989319 title "Phosphorylation of ATM by Cdk5 mediates DNA damage signalling and regulates neuronal death" @default.
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• W1979989319 doi "https://doi.org/10.1038/ncb1829" @default.
• W1979989319 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/2760486" @default.
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