|
rdf:type |
|
|
lifeskim:mentions |
|
|
pubmed:issue |
7
|
|
pubmed:dateCreated |
2007-7-5
|
|
pubmed:abstractText |
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.
|
|
pubmed:language |
eng
|
|
pubmed:journal |
|
|
pubmed:citationSubset |
IM
|
|
pubmed:chemical |
|
|
pubmed:status |
MEDLINE
|
|
pubmed:month |
Jul
|
|
pubmed:issn |
1545-9993
|
|
pubmed:author |
|
|
pubmed:issnType |
Print
|
|
pubmed:volume |
14
|
|
pubmed:owner |
NLM
|
|
pubmed:authorsComplete |
Y
|
|
pubmed:pagination |
677-9
|
|
pubmed:dateRevised |
2009-11-19
|
|
pubmed:meshHeading |
|
|
pubmed:year |
2007
|
|
pubmed:articleTitle |
Role for BLM in replication-fork restart and suppression of origin firing after replicative stress.
|
|
pubmed:affiliation |
Cancer Research UK Laboratories, Weatherall Institute of Molecular Medicine, University of Oxford, John Radcliffe Hospital, Oxford OX3 9DS, UK.
|
|
pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
|
