Linked Life Data

17213818

Source:http://linkedlifedata.com/resource/pubmed/id/17213818

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
27
pubmed:dateCreated
2007-6-7
pubmed:abstractText
The Cockayne syndrome B protein (CSB) has long been known to be involved in the repair of DNA modifications that block the RNA polymerase in transcribed DNA sequences (transcription-coupled repair). Recent evidence suggests that it also has a more general role in the repair of oxidative DNA base modifications such as 7,8-dihydro-8-oxo-2'-deoxyguanosine (8-oxoG). In mammalian cells, 8-oxoG is a substrate of the repair glycosylase OGG1. Mice without this enzyme accumulate 8-oxoG in the genome and have elevated spontaneous mutation rates. To elucidate the role of CSB in the prevention of mutations by oxidative DNA base damage, we have generated mice that are deficient in Csb or Ogg1 or both genes and carry a non-transcribed bacterial lacI gene for mutation analysis (Big Blue mice). Our results indicate that the overall spontaneous mutation frequencies in the livers of Csb(m/m)/Ogg1-/- -mice are elevated not only compared with heterozygous control mice (factor 3.3), but also with Ogg1-/- -animals (factor 1.6). Sequence analysis revealed that the additional mutations caused by CSB deficiency in an Ogg1-/- background are mostly G:C to T:A transversions and small deletions. For all mouse strains, the background levels of oxidative purine modifications in the livers correlate linearly with the numbers of G:C to T:A transversions observed. The data indicate that CSB is involved in the inhibition of mutations caused by spontaneous oxidative DNA base damage in a non-transcribed gene.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jun
pubmed:issn
0950-9232
pubmed:author
pubmed:issnType
Print
pubmed:day
7
pubmed:volume
26
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
4044-8
pubmed:dateRevised
2009-11-19
pubmed:meshHeading
pubmed-meshheading:17213818-Animals, pubmed-meshheading:17213818-Bacterial Proteins, pubmed-meshheading:17213818-DNA Damage, pubmed-meshheading:17213818-DNA Glycosylases, pubmed-meshheading:17213818-DNA Repair Enzymes, pubmed-meshheading:17213818-Female, pubmed-meshheading:17213818-Genomic Instability, pubmed-meshheading:17213818-Lac Repressors, pubmed-meshheading:17213818-Liver, pubmed-meshheading:17213818-Male, pubmed-meshheading:17213818-Mice, pubmed-meshheading:17213818-Mice, Inbred Strains, pubmed-meshheading:17213818-Mice, Knockout, pubmed-meshheading:17213818-Mice, Transgenic, pubmed-meshheading:17213818-Mutagenesis, Insertional, pubmed-meshheading:17213818-Mutation, pubmed-meshheading:17213818-Oxidative Stress, pubmed-meshheading:17213818-Point Mutation, pubmed-meshheading:17213818-Repressor Proteins, pubmed-meshheading:17213818-Sequence Deletion
pubmed:year
2007
pubmed:articleTitle
Deficiency of the Cockayne syndrome B (CSB) gene aggravates the genomic instability caused by endogenous oxidative DNA base damage in mice.
pubmed:affiliation
Institute of Pharmacy, University of Mainz, Mainz, Germany.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't