The Werner syndrome protein at the crossroads of DNA repair and apoptosis

被引：31

作者：

Comai, L ^{[1
]}

Li, BM ^{[1
]}

机构：

[1] Univ So Calif, Keck Sch Med, Dept Mol Microbiol & Immunol, Los Angeles, CA 90033 USA

来源：

MECHANISMS OF AGEING AND DEVELOPMENT | 2004年 / 125卷 / 08期

基金：

美国国家卫生研究院;

关键词：

Werner syndrome; DNA repair; apoptosis; aging; DNA strand breaks;

D O I：

10.1016/j.mad.2004.06.004

中图分类号：

Q2 [细胞生物学];

学科分类号：

071009 ; 090102 ;

摘要：

Werner syndrome (WS) is a premature aging disease characterized by genetic instability. WS is caused by mutations in a gene encoding for a 160 kDa nuclear protein, the Werner syndrome protein (WRN), which has exonuclease and helicase activities. The mechanism whereby WRN controls genome stability and life span is not known. Over the last few years, WRN has become the focus of intense investigation by a growing number of scientists. The studies carried out by many laboratories have provided a wealth of new information about the functional properties of WRN and its cellular partners. This review focuses on recent findings that demonstrate a functional interaction between WRN and two factors that bind to DNA breaks, Ku and poly(ADP-ribose) polymerase 1, and discuss how these interactions can influence fundamental cellular processes such as DNA repair, apoptosis and possibly regulate cell senescence and organismal aging. (C) 2004 Elsevier Ireland Ltd. All rights reserved.

引用

页码：521 / 528

页数：8

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