Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2009-7-27
pubmed:abstractText
Abstract Double-strand breaks (DSBs) can be generated in the DNA of mammalian cells when heat-labile sites induced by ionizing radiation within a clustered DNA damage site are thermally transformed to single-strand breaks (SSBs) and combine with other SSBs or heat-labile sites in the opposite DNA strand. When this thermal transformation of heat-labile sites to SSBs occurs during DNA preparation using high-temperature lysis, the DSB yield is overestimated by including DSBs not present in the tested cell. Low-temperature lysis avoids this artifact but shows slower repair kinetics for prompt DSBs than high-temperature lysis. The apparent slowdown of DSB repair after low-temperature lysis is particularly pronounced in mutants defective in the DNA-PK-dependent pathway of NHEJ (D-NHEJ) and has led to the postulate that these cells may actually be entirely deficient in DSB repair. Since our work as well as that of others provides strong evidence for DSB repair in D-NHEJ-deficient cells by alternative repair pathways operating as a backup (B-NHEJ), we re-examine here DSB repair in several D-NHEJ-deficient mutants using low-temperature lysis. The results demonstrate extensive but slow repair of DSBs after low-temperature lysis indicative of a robust function of B-NHEJ. At the same time, the results demonstrate a pronounced sensitivity of heat-labile sites to lysis at 37 degrees C, which indicates that DSBs generated by transformation of heat-labile sites may be in part a reality that the irradiated cell faces at all times.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Aug
pubmed:issn
0033-7587
pubmed:author
pubmed:issnType
Print
pubmed:volume
172
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
152-64
pubmed:meshHeading
pubmed:year
2009
pubmed:articleTitle
Extensive repair of DNA double-strand breaks in cells deficient in the DNA-PK-dependent pathway of NHEJ after exclusion of heat-labile sites.
pubmed:affiliation
Institute of Medical Radiation Biology, University of Duisburg-Essen Medical School, Essen, Germany.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't