Source:http://linkedlifedata.com/resource/pubmed/id/17112792
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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
4
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pubmed:dateCreated |
2007-3-12
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pubmed:abstractText |
Base excision repair (BER) is the major pathway responsible for averting the mutagenic and cytotoxic effects of spontaneous hydrolytic, oxidative, and non-enzymatic alkylation DNA damage. In particular, this pathway recognizes and repairs base modifications, such as uracil and 8-hydroxyguanine, as well as abasic sites and DNA single-strand breaks. In this review, we outline the basic mechanics of the BER process, and describe the potential association of this pathway with aging and age-related disease, namely cancer and neurodegeneration.
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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 |
Apr
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pubmed:issn |
1568-7864
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:day |
1
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pubmed:volume |
6
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
544-59
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pubmed:meshHeading | |
pubmed:year |
2007
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pubmed:articleTitle |
The mechanics of base excision repair, and its relationship to aging and disease.
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pubmed:affiliation |
Laboratory of Molecular Gerontology, National Institute on Aging/NIH, Baltimore, MD 21224, USA.
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pubmed:publicationType |
Journal Article,
Review,
Research Support, N.I.H., Intramural
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