ATM signaling and genornic stability in response to DNA damage

被引：161

作者：

Lavin, MF

Birrell, G

Chen, P

Kozlov, S

Scott, S

Gueven, N

机构：

[1] Queensland Inst Med Res, Queensland Canc Fund Res Unit, Brisbane, Qld 4029, Australia

[2] Univ Queensland, Cent Clin Div, Brisbane, Qld, Australia

来源：

MUTATION RESEARCH-FUNDAMENTAL AND MOLECULAR MECHANISMS OF MUTAGENESIS | 2005年 / 569卷 / 1-2期

关键词：

ATM signaling; genomic stability; ataxia-telangiectasia;

D O I：

10.1016/j.mrfmmm.2004.04.020

中图分类号：

Q81 [生物工程学（生物技术）]; Q93 [微生物学];

学科分类号：

071005 ; 0836 ; 090102 ; 100705 ;

摘要：

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-telangietasia (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. for recognising double strand breaks in DNA, maintaining genome stability and minimizing risk of cancer are discussed. (C) 2004 Published by Elsevier B.V.

引用

页码：123 / 132

页数：10

共 102 条

[1] Cell cycle checkpoint signaling through the ATM and ATR kinases [J].