Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
10-11
pubmed:dateCreated
2004-11-15
pubmed:abstractText
Chronic oxidative stress is generally believed to be a major etiologic factor in the aging process. In addition to modulation of signaling processes and oxidation of cellular proteins and lipids, reactive oxygen species (ROS) induce multiple damages in both nuclear and mitochondrial genomes, most of which are repaired via the DNA base excision repair pathway. 8-Oxoguanine (8-oxoG), a major ROS product in the genome, is excised by 8-oxoG-DNA glycosylase (OGG1) and the resulting abasic (AP) site is cleaved by AP-endonuclease (APE1) in the initial steps of repair. Here, we provide data showing that differences between young and aged cells' efficiency in import of OGG1 and APE1 may be responsible for age-associated increase in DNA damage in both nuclear and mitochondrial compartments. It is also evident that age-dependent changes in covalent modifications of APE1 by acetylation regulate its action as a transcriptional repressor of many Ca(2+)-responsive genes by binding to nCaRE, in addition to its endonuclease activity. Thus, ROS-induced altered signaling is responsible for age-dependent changes in post-translational modifications and import of DNA repair enzymes into nuclei and mitochondria (mt), which in turn affect repair of their genomes.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
0047-6374
pubmed:author
pubmed:issnType
Print
pubmed:volume
125
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
755-65
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed:articleTitle
Age-dependent modulation of DNA repair enzymes by covalent modification and subcellular distribution.
pubmed:affiliation
Sealy Center for Molecular Science, University of Texas Medical Branch, 6.136 Medical Research Building, Route 1079, Galveston, TX 77555, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S.