Your browser version may not work well with NCBI's Web applications. More information here...
1: Nat Struct Mol Biol. 2007 Jul;14(7):677-9. Epub 2007 Jun 24.
Related Articles, Links
Click here to read Click here to read
Role for BLM in replication-fork restart and suppression of origin firing after replicative stress.

Davies SL, North PS, Hickson ID.

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

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.

Publication Types:
PMID: 17603497 [PubMed - indexed for MEDLINE]