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Letter
Nature Cell Biology 9, 1311–1318 (1 November 2007) | doi:10.1038/ncb1651
Rapid activation of ATM on DNA flanking double-strand breaks
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Abstract
The tumour-suppressor gene ATM, mutations in which cause the human genetic disease ataxia telangiectasia (A-T), encodes a key protein kinase that controls the cellular response to DNA double-strand breaks (DSBs). DNA DSBs caused by ionizing radiation or chemicals result in rapid ATM autophosphorylation, leading to checkpoint activation and phosphorylation of substrates that regulate cell-cycle progression, DNA repair, transcription and cell death.
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