Source:http://linkedlifedata.com/resource/pubmed/id/14506474
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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
9
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pubmed:dateCreated |
2003-9-24
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pubmed:abstractText |
Non-homologous DNA end-joining (NHEJ)--the main pathway for repairing double-stranded DNA breaks--functions throughout the cell cycle to repair such lesions. Defects in NHEJ result in marked sensitivity to ionizing radiation and ablation of lymphocytes, which rely on NHEJ to complete the rearrangement of antigen-receptor genes. NHEJ is typically imprecise, a characteristic that is useful for immune diversification in lymphocytes, but which might also contribute to some of the genetic changes that underlie cancer and ageing.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical | |
pubmed:status |
MEDLINE
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pubmed:month |
Sep
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pubmed:issn |
1471-0072
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
4
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
712-20
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pubmed:dateRevised |
2005-11-16
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pubmed:meshHeading | |
pubmed:year |
2003
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pubmed:articleTitle |
Mechanism and regulation of human non-homologous DNA end-joining.
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pubmed:affiliation |
Norris Comprehensive Cancer Center, Department of Pathology, University of Southern California School of Medicine, 1441 Eastlake Avenue, MS 9176, Los Angeles, California 90089, USA. lieber@usc.edu
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pubmed:publicationType |
Journal Article,
Review
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