Role for BLM in replication-fork restart and suppression of origin firing after replicative stress

被引：186

作者：

Davies, Sally L. ^{[1
]}

North, Phillip S. ^{[1
]}

Hickson, Ian D. ^{[1
]}

机构：

[1] Univ Oxford, Weatherall Inst Mol Med, Canc Res UK Labs, John Radcliffe Hosp, Oxford OX3 9DS, England

来源：

NATURE STRUCTURAL & MOLECULAR BIOLOGY | 2007年 / 14卷 / 07期

关键词：

D O I：

10.1038/nsmb1267

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

Mutations in BLM give rise to Bloom's syndrome, a genetic disorder associated with cancer predisposition and chromosomal instability. Using a dual-labeling system in isolated chromosome fibers, we show that the BLM protein is required for two aspects of the cellular response to replicative stress: efficient replication-fork restart and suppression of new origin firing. These functions require the helicase activity of BLM and the Thr99 residue targeted by stress- activated kinases.

引用

页码：677 / 679

页数：3

共 15 条

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