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
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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收藏
页码:293 / 296
页数:4
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