RESPONSE OF ATAXIA TELANGIECTASIA CELLS TO BLEOMYCIN

被引:79
作者
LEHMANN, AR
STEVENS, S
机构
[1] MRC Cell Mutation Unit, University of Sussex, Falmer
关键词
D O I
10.1093/nar/6.5.1953
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
The autosomal recessive disorder, ataxia telangiectasia (AT) is characterised by cellular sensitivity to ionizing radiation. The molecular basis of this radiosensitivity is the subject of controversy. We report here that cultured fibroblasts from AT patients are also sensitive to the lethal effects of bleomycin. As with ionizing radiation, no defect has been observed the overall rejoining of single or double-strand breaks produced by bleomycin. Since, however, only apyrimidinic (and to a lesser extent apurinic) sites arid strand breaks are known to be produced by bleomycin, we tentatively suggest that AT cells are unable to rejoin a very small fraction of the total strand breaks. We attribute our inability to detect such unrejoined strand breaks to the relative insensitivity of the sucrose gradient procedures normally used to detect strand breaks. © 1979 Information Retrieval Limited.
引用
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页码:1953 / 1960
页数:8
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