The ubiquitous role of ubiquitin in the DNA damage response

被引：181

作者：

Al-Hakim, Abdallah ^{[1
]}

Escribano-Diaz, Cristina ^{[1
]}

Landry, Marie-Claude ^{[1
]}

O'Donnell, Lara ^{[1
]}

Panier, Stephanie ^{[1
,2
]}

Szilard, Rachel K. ^{[1
]}

Durocher, Daniel ^{[1
,2
]}

机构：

[1] Mt Sinai Hosp, Samuel Lunenfeld Res Inst, Toronto, ON M5G 1X5, Canada

[2] Univ Toronto, Dept Mol Genet, Toronto, ON, Canada

来源：

DNA REPAIR | 2010年 / 9卷 / 12期

关键词：

DOUBLE-STRAND BREAKS; FANCONI-ANEMIA PATHWAY; CLASS-SWITCH RECOMBINATION; REPLICATION CHECKPOINT RESPONSE; LINEAR POLYUBIQUITIN CHAINS; ANAPHASE-PROMOTING COMPLEX; CELL-CYCLE CHECKPOINTS; S-PHASE CHECKPOINT; CROSS-LINK REPAIR; BETA-TRCP;

D O I：

10.1016/j.dnarep.2010.09.011

中图分类号：

Q3 [遗传学];

学科分类号：

071007 ; 090102 ;

摘要：

Protein ubiquitylation has emerged as an important regulatory mechanism that impacts almost every aspect of the DNA damage response. In this review, we discuss how DNA repair and checkpoint pathways utilize the diversity offered by the ubiquitin conjugation system to modulate the response to genotoxic lesions in space and time. In particular, we will highlight recent work done on the regulation of DNA double-strand breaks signalling and repair by the RNF8/RNF168 E3 ubiquitin ligases, the Fanconi anemia pathway and the role of protein degradation in the enforcement and termination of checkpoint signalling. We also discuss the various functions of deubiquitylating enzymes in these processes along with potential avenues for exploiting the ubiquitin conjugation/deconjugation system for therapeutic purposes. (C) 2010 Elsevier B.V. All rights reserved.

引用

页码：1229 / 1240

页数：12

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