Linked Life Data

19772495

Source:http://linkedlifedata.com/resource/pubmed/id/19772495

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2009-9-23
pubmed:abstractText
DNA chromosomal DSBs (double-strand breaks) are potentially hazardous DNA lesions, and their accurate repair is essential for the successful maintenance and propagation of genetic information. Two major pathways have evolved to repair DSBs: HR (homologous recombination) and NHEJ (non-homologous end-joining). Depending on the context in which the break is encountered, HR and NHEJ may either compete or co-operate to fix DSBs in eukaryotic cells. Defects in either pathway are strongly associated with human disease, including immunodeficiency and cancer predisposition. Here we review the current knowledge of how NHEJ and HR are controlled in somatic mammalian cells, and discuss the role of the chromatin context in regulating each pathway. We also review evidence for both co-operation and competition between the two pathways.
pubmed:grant
pubmed:commentsCorrections
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:status
MEDLINE
pubmed:month
Oct
pubmed:issn
1470-8728
pubmed:author
pubmed:issnType
Electronic
pubmed:day
15
pubmed:volume
423
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
157-68
pubmed:dateRevised
2011-5-18
pubmed:meshHeading
pubmed:year
2009
pubmed:articleTitle
Mechanisms of double-strand break repair in somatic mammalian cells.
pubmed:affiliation
Department of Medicine, Harvard Medical School and Beth Israel Deaconess Medical Center, Boston, MA 02215, USA.
pubmed:publicationType
Journal Article, Review, Research Support, Non-U.S. Gov't, Research Support, N.I.H., Extramural