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• W2012486985 abstract "DNA double strand breaks represent the most threatening lesion to the integrity of the genome in cells exposed to ionizing radiation and radiomimetic chemicals. Those breaks are recognized, signaled to cell cycle checkpoints and repaired by protein complexes. The product of the gene (ATM) mutated in the human genetic disorder ataxia–telangiectasia (A–T) plays a central role in the recognition and signaling of DNA damage. ATM is one of an ever growing number of proteins which when mutated compromise the stability of the genome and predispose to tumour development. Mechanisms for recognising double strand breaks in DNA, maintaining genome stability and minimizing risk of cancer are discussed." @default.
• W2012486985 created "2016-06-24" @default.
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• W2012486985 date "2005-01-01" @default.
• W2012486985 modified "2023-10-14" @default.
• W2012486985 title "ATM signaling and genomic stability in response to DNA damage" @default.
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• W2012486985 doi "https://doi.org/10.1016/j.mrfmmm.2004.04.020" @default.
• W2012486985 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/15603757" @default.
• W2012486985 hasPublicationYear "2005" @default.
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