ATM signaling and genornic stability in response to DNA damage

被引:160
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
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
收藏
页码:123 / 132
页数:10
相关论文
共 102 条
  • [1] Cell cycle checkpoint signaling through the ATM and ATR kinases
    Abraham, RT
    [J]. GENES & DEVELOPMENT, 2001, 15 (17) : 2177 - 2196
  • [2] Althaus F R, 1987, Mol Biol Biochem Biophys, V37, P1
  • [3] Structure of the Rad50-Mre11 DNA repair complex from Saccharomyces cerevisiae by electron microscopy
    Anderson, DE
    Trujillo, KM
    Sung, P
    Erickson, HP
    [J]. JOURNAL OF BIOLOGICAL CHEMISTRY, 2001, 276 (40) : 37027 - 37033
  • [4] [Anonymous], 1982, ATAXIA TELANGIECTASI
  • [5] DNA damage activates ATM through intermolecular autophosphorylation and dimer dissociation
    Bakkenist, CJ
    Kastan, MB
    [J]. NATURE, 2003, 421 (6922) : 499 - 506
  • [6] Atm haploinsufficiency results in increased sensitivity to sublethal doses of ionizing radiation in mice
    Barlow, C
    Eckhaus, MA
    Schäffer, AA
    Wynshaw-Boris, A
    [J]. NATURE GENETICS, 1999, 21 (04) : 359 - 360
  • [7] Non-homologous end joining as a mechanism of DNA repair
    Barnes, DE
    [J]. CURRENT BIOLOGY, 2001, 11 (12) : R455 - R457
  • [8] Functional link between BLM defective in Bloom's syndrome and the ataxia-telangiectasia-mutated protein, ATM
    Beamish, H
    Kedar, P
    Kaneko, H
    Chen, P
    Fukao, T
    Peng, C
    Beresten, S
    Gueven, N
    Purdie, D
    Lees-Miller, S
    Ellis, N
    Kondo, N
    Lavin, MF
    [J]. JOURNAL OF BIOLOGICAL CHEMISTRY, 2002, 277 (34) : 30515 - 30523
  • [9] BLOK J, 1973, CURR TOP RADIAT RES, V9, P162
  • [10] FAT: a novel domain in PIK-related kinases
    Bosotti, R
    Isacchi, A
    Sonnhammer, ELL
    [J]. TRENDS IN BIOCHEMICAL SCIENCES, 2000, 25 (05) : 225 - 227