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ATM signaling and genomic stability in response to DNA damage

Citation

Lavin, MF and Birrell, G and Chen, P and Kozlov, S and Scott, S and Gueven, N, ATM signaling and genomic stability in response to DNA damage, Mutation Research - D N Aging, 569, (1-2) pp. 123-32. ISSN 0921-8734 (2005) [Substantial Review]


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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.

Item Details

Item Type:Substantial Review
Keywords:ATM, DNA damage, genome instability
Research Division:Biological Sciences
Research Group:Biochemistry and Cell Biology
Research Field:Biochemistry and Cell Biology not elsewhere classified
Objective Division:Expanding Knowledge
Objective Group:Expanding Knowledge
Objective Field:Expanding Knowledge in the Biological Sciences
Author:Gueven, N (Dr Nuri Guven)
ID Code:79295
Year Published:2005
Deposited By:Pharmacy
Deposited On:2012-08-29
Last Modified:2014-10-24
Downloads:0

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