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Nat Struct Mol Biol. 2007 Jul;14(7):677-9. Epub 2007 Jun 24.

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

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1
Cancer Research UK Laboratories, Weatherall Institute of Molecular Medicine, University of Oxford, John Radcliffe Hospital, Oxford OX3 9DS, UK.

Abstract

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.

PMID:
17603497
DOI:
10.1038/nsmb1267
[Indexed for MEDLINE]
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