共济失调毛细血管扩张症细胞提取物中的脱嘌呤和/或脱嘧啶内切酶活性。
Apurinic and/or apyrimidinic endonuclease activity in ataxia telangiectasia cell extracts.
作者信息
Sheridan R B, Huang P C
出版信息
Mutat Res. 1978 Oct;52(1):129-36. doi: 10.1016/0027-5107(78)90101-x.
PMID:215905
Abstract
The possibility that the increased sensitivity of ataxia telangiectasia towards ionizing radiation is related to a DNA-repair deficiency has been examined further. When compared to unaffected controls, 6 lines of fibroblast cells derived from ataxia patients demonstrated a slightly reduced endonucleolytic activity (165 +/- 12 units vs. 214 +/- 28 units) towards apurinic and/or apyrimidinic sites as determined in a "nicking" assay.
摘要
共济失调毛细血管扩张症对电离辐射的敏感性增加与DNA修复缺陷有关这一可能性已得到进一步研究。与未受影响的对照相比，源自共济失调患者的6株成纤维细胞系在“切口”试验中测定的对无嘌呤和/或无嘧啶位点的核酸内切酶活性略有降低（165±12单位对214±28单位）。
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