Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4
pubmed:dateCreated
2004-12-20
pubmed:abstractText
The mechanisms of sister chromatid exchanges (SCEs) are not known. One hypothesis is that SCE is a manifestation of Rad51-dependent homologous recombination repair. In order to test this hypothesis, we have compared the frequencies of SCEs induced by mitomycin C (MMC) and 254nm ultraviolet radiation (UVC) in wt V79B and the Rad51C-deficient CL-V4B cells. SCEs were analysed in the first (M1) and second (M2) post-treatment mitoses. In M1 MMC induced the same frequencies of SCEs in CL-V4B and V79B cells, while the UVC-induced SCE frequencies were lower in CL-V4B than V79B cells. In CL-V4B cells, MMC-induced SCEs were higher in M2 than in M1, suggesting that interstrand cross-links (ICL) are either not removed completely or are transformed into another form of DNA damage that persists until the next cell cycle. We suggest that SCEs may represent a mechanism to bypass MMC-induced ICL without their removal.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jan
pubmed:issn
0006-291X
pubmed:author
pubmed:issnType
Print
pubmed:day
28
pubmed:volume
326
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
805-10
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
2005
pubmed:articleTitle
Rad51C-deficient CL-V4B cells exhibit normal levels of mitomycin C-induced SCEs but reduced levels of UVC-induced SCEs.
pubmed:affiliation
Institute of Nuclear Chemistry and Technology, 03-195 Warszawa, Poland. awojcik@pu.kielce.pl
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't