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rdf:type | |
lifeskim:mentions | |
pubmed:dateCreated |
1987-11-20
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pubmed:abstractText |
We have utilized DNA transfer and recombinant DNA techniques to probe DNA double-strand break repair in the human ionizing radiation-sensitive genetic syndrome ataxia-telangiectasia (A-T). Using restriction enzyme-generated double-strand breaks in the coding sequence of a selectable gene we have detected a significantly greater frequency of mis-repair of such breaks in a permanent A-T cell line compared with cell lines of normal radiosensitivity. This mis-repair in A-T can plausibly explain many of the clinical features of the disease but was insufficiently detailed to address the broad problem of DNA repair mechanisms relevant to ionizing radiation-induced damage. To extend these observations of DNA double-strand break mis-repair we have now applied this type of repair assay to novel, de novo induced mammalian X-ray-sensitive cell lines and to appropriate Escherichia coli mutants. In both cellular systems we have now found some equivalence to the A-T repair defect. In particular, studies on one E. coli mutant have provided evidence suggesting an involvement of a topoisomerase activity in DNA double-strand break mis-repair, which may be relevant to the biochemical defect in A-T.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical | |
pubmed:status |
MEDLINE
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pubmed:issn |
0269-3518
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
6
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
177-89
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pubmed:dateRevised |
2007-7-23
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pubmed:meshHeading |
pubmed-meshheading:2821021-Ataxia Telangiectasia,
pubmed-meshheading:2821021-Cell Line,
pubmed-meshheading:2821021-DNA,
pubmed-meshheading:2821021-DNA Repair,
pubmed-meshheading:2821021-DNA Topoisomerases, Type II,
pubmed-meshheading:2821021-Humans,
pubmed-meshheading:2821021-Phenotype,
pubmed-meshheading:2821021-Radiation Tolerance,
pubmed-meshheading:2821021-X-Rays
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pubmed:year |
1987
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pubmed:articleTitle |
Molecular studies on the nature of the repair defect in ataxia-telangiectasia and their implications for cellular radiobiology.
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pubmed:affiliation |
Division of Cell and Molecular Biology, MRC Radiobiology Unit, Chilton, Oxon, UK.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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