Repair of and checkpoint response to topoisomerase I-mediated DNA damage

被引：243

作者：

Pommier, Y ^{[1
]}

Redon, C ^{[1
]}

Rao, VA ^{[1
]}

Seiler, JA ^{[1
]}

Sordet, O ^{[1
]}

Takemura, H ^{[1
]}

Antony, S ^{[1
]}

Meng, LH ^{[1
]}

Liao, ZY ^{[1
]}

Kohlhagen, G ^{[1
]}

Zhang, HL ^{[1
]}

Kohn, KW ^{[1
]}

机构：

[1] NCI, Mol Pharmacol Lab, Ctr Canc Res, NIH, Bethesda, MD 20892 USA

来源：

MUTATION RESEARCH-FUNDAMENTAL AND MOLECULAR MECHANISMS OF MUTAGENESIS | 2003年 / 532卷 / 1-2期

关键词：

topoisomerase; homologous recombination; camptothecin; Tdp1; Mre11; ATM; ATR; BRCA1; BRCA2; RAD52; RAD51; RPA; DNA-PK; cell cycle checkpoints;

D O I：

10.1016/j.mrfmmm.2003.08.016

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：

Topoisomerase I (Top1) catalyzes two transesterification reactions: single-strand DNA cleavage and religation that are normally coupled for the relaxation of DNA supercoiling in transcribing and replicating chromatin. A variety of endogenous DNA modifications, potent anticancer drugs and carcinogens uncouple these two reactions, resulting in the accumulation of Top I cleavage complexes. Top I cleavage complexes damage DNA and kill cells by generating replication-mediated DNA double-strand breaks (DSBs) and by stalling transcription complexes. The repair of Top1-mediated DNA lesions involves integrated pathways that are conserved from yeasts to humans. Top1-mediated DNA damage and cell cycle checkpoint responses can be studied biochemically and genetically in yeast and human cells with known genetic defects. Defects in these repair/checkpoint pathways, which promote tumor development, explain, at least in part, the selectivity of camptothecins and other Top I inhibitors for cancer cells. (C) 2003 Elsevier B.V. All rights reserved.

引用

页码：173 / 203

页数：31

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