The Mre11 complex and ATM: collaborating to navigate S phase

被引：184

作者：

Petrini, JHJ ^{[1
]}

机构：

[1] Univ Wisconsin, Sch Med, Madison, WI 53706 USA

来源：

CURRENT OPINION IN CELL BIOLOGY | 2000年 / 12卷 / 03期

关键词：

D O I：

10.1016/S0955-0674(00)00091-0

中图分类号：

Q2 [细胞生物学];

学科分类号：

071009 ; 090102 ;

摘要：

Recently, findings regarding a group of cancer predisposition and chromosome instability syndromes, Nijmegen breakage syndrome (NBS), the ataxia-telangiectasia-like disorder (A-TLD) and ataxia telangiectasia have shed light on the unexpected role of recombinational DNA repair proteins in DNA-damage-dependent cell-cycle regulation. Mutations in the Mre11 complex cause A-TLD and NBS. In addition, functions of the Mre11 complex have been biochemically linked to ATM, the large protein kinase that is defective in ataxia-telangiectasia cells by the observation that Nbs1 is a bona fide substrate of the ATM kinase.

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页码：293 / 296

页数：4

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