Gamma-ray induced inhibition of DNA synthesis in ataxia telangiectasia fibroblasts is a function of excision repair capacity.
Gamma-ray induced inhibition of DNA synthesis in ataxia telangiectasia fibroblasts is a function of excision repair capacity.
复制标题
伽马射线诱导的共济失调毛细血管扩张成纤维细胞 DNA 合成抑制是切除修复能力的函数。
DOI：
10.1016/0006-291x(80)91461-8
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发表时间：
1980
影响因子：
3.1
通讯作者：
Paterson,MC
中科院分区：
文献类型：
--
作者：
Smith,PJ;Paterson,MC
共济失调毛细血管扩张 (AT) 人成纤维细胞菌株中 γ 射线诱导的 DNA 修复合成的缺陷程度被发现没有显示出氧增强，这与碱基损伤修复的缺陷一致。 AT 细胞中的修复缺陷而非修复能力伴随着 γ 射线或拟放射药物博来霉素缺乏 DNA 合成（复制子起始）抑制。使用 4-硝基喹啉 1-氧化物进行的实验表明，缺乏抑制作用对于放射源性损伤具有特异性。因此，切除修复（可能是通过 DNA 链切口或染色质修饰）似乎会停止受辐射修复能力强的细胞中的复制子起始，而在修复有缺陷的 AT 菌株中，这种假定的重要生物学功能不起作用。
The extent of the deficiency in γ-ray induced DNA repair synthesis in an ataxia telangiectasia (AT) human fibroblast strain was found to show no oxygen enhancement, consistent with a defect in the repair of base damage. Repair deficiency, but not repair proficiency, in AT cells were accompanied by a lack of inhibition of DNA synthesis (replicon initiation) neither γ-rays or the radiomimetic drug bleomycin. Experiments with 4-nitroquinoline 1-oxide indicated that lack of inhibition was specific for radiogenic type damage. Thus excision repair, perhaps by DNA strand incision or chromatin modification, appears to halt replicon initiation in irradiated repair proficient cells whereas in repair defective AT strains this putatively important biological function is inoperative.