Linked Life Data

15272504

Source:http://linkedlifedata.com/resource/pubmed/id/15272504

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
6
pubmed:dateCreated
2004-7-23
pubmed:abstractText
The hypothesis discussed here is that a major component of aging in metazoans is oxidative damage to nuclear DNA. Such a viewpoint would be consistent with the fact that all of the thus far identified premature aging syndromes in mammals involve mutations in nuclear proteins. Several of these nuclear proteins are enzymes that are related to DNA metabolism or DNA repair. Among the single- and double-stranded DNA damage repair pathways present in eukaryotes, only one pathway often fails to restore the full information content of the genome and typically would result in a deletion of a few base pairs. This pathway is called nonhomologous DNA end joining (NHEJ) and it is a major pathway for the repair of double-strand DNA breaks. Repetitive DNA content may determine the extent to which any organism can use this pathway, and therefore, may dictate a key factor in the balance between oxidation and organismal lifespan.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:status
MEDLINE
pubmed:month
Jun
pubmed:issn
0047-6374
pubmed:author
pubmed:issnType
Print
pubmed:volume
125
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
405-16
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
2004
pubmed:articleTitle
DNA damage and aging.
pubmed:affiliation
Department of Pathology, USC Norris Comprehensive Center, Los Angeles, CA 90033, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Review