| pubmed-article:2821021 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:2821021 | lifeskim:mentions | umls-concept:C0004135 | lld:lifeskim |
| pubmed-article:2821021 | lifeskim:mentions | umls-concept:C0374711 | lld:lifeskim |
| pubmed-article:2821021 | lifeskim:mentions | umls-concept:C0043240 | lld:lifeskim |
| pubmed-article:2821021 | lifeskim:mentions | umls-concept:C0178539 | lld:lifeskim |
| pubmed-article:2821021 | lifeskim:mentions | umls-concept:C1521991 | lld:lifeskim |
| pubmed-article:2821021 | lifeskim:mentions | umls-concept:C1457869 | lld:lifeskim |
| pubmed-article:2821021 | lifeskim:mentions | umls-concept:C0034558 | lld:lifeskim |
| pubmed-article:2821021 | lifeskim:mentions | umls-concept:C1705181 | lld:lifeskim |
| pubmed-article:2821021 | lifeskim:mentions | umls-concept:C2603343 | lld:lifeskim |
| pubmed-article:2821021 | lifeskim:mentions | umls-concept:C0349590 | lld:lifeskim |
| pubmed-article:2821021 | pubmed:dateCreated | 1987-11-20 | lld:pubmed |
| pubmed-article:2821021 | 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. | lld:pubmed |
| pubmed-article:2821021 | pubmed:language | eng | lld:pubmed |
| pubmed-article:2821021 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:2821021 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:2821021 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:2821021 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:2821021 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:2821021 | pubmed:issn | 0269-3518 | lld:pubmed |
| pubmed-article:2821021 | pubmed:author | pubmed-author:CoxRR | lld:pubmed |
| pubmed-article:2821021 | pubmed:author | pubmed-author:DebenhamP GPG | lld:pubmed |
| pubmed-article:2821021 | pubmed:author | pubmed-author:JonesN JNJ | lld:pubmed |
| pubmed-article:2821021 | pubmed:author | pubmed-author:WebbM BMB | lld:pubmed |
| pubmed-article:2821021 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:2821021 | pubmed:volume | 6 | lld:pubmed |
| pubmed-article:2821021 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:2821021 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:2821021 | pubmed:pagination | 177-89 | lld:pubmed |
| pubmed-article:2821021 | pubmed:dateRevised | 2007-7-23 | lld:pubmed |
| pubmed-article:2821021 | pubmed:meshHeading | pubmed-meshheading:2821021-... | lld:pubmed |
| pubmed-article:2821021 | pubmed:meshHeading | pubmed-meshheading:2821021-... | lld:pubmed |
| pubmed-article:2821021 | pubmed:meshHeading | pubmed-meshheading:2821021-... | lld:pubmed |
| pubmed-article:2821021 | pubmed:meshHeading | pubmed-meshheading:2821021-... | lld:pubmed |
| pubmed-article:2821021 | pubmed:meshHeading | pubmed-meshheading:2821021-... | lld:pubmed |
| pubmed-article:2821021 | pubmed:meshHeading | pubmed-meshheading:2821021-... | lld:pubmed |
| pubmed-article:2821021 | pubmed:meshHeading | pubmed-meshheading:2821021-... | lld:pubmed |
| pubmed-article:2821021 | pubmed:meshHeading | pubmed-meshheading:2821021-... | lld:pubmed |
| pubmed-article:2821021 | pubmed:meshHeading | pubmed-meshheading:2821021-... | lld:pubmed |
| pubmed-article:2821021 | pubmed:year | 1987 | lld:pubmed |
| pubmed-article:2821021 | pubmed:articleTitle | Molecular studies on the nature of the repair defect in ataxia-telangiectasia and their implications for cellular radiobiology. | lld:pubmed |
| pubmed-article:2821021 | pubmed:affiliation | Division of Cell and Molecular Biology, MRC Radiobiology Unit, Chilton, Oxon, UK. | lld:pubmed |
| pubmed-article:2821021 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:2821021 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
| http://linkedlifedata.com/r... | pubmed:referesTo | pubmed-article:2821021 | lld:pubmed |
| http://linkedlifedata.com/r... | pubmed:referesTo | pubmed-article:2821021 | lld:pubmed |
