DIFFERENTIAL INDUCTION OF TRANSCRIPTIONALLY ACTIVE P53 FOLLOWING UV OR IONIZING-RADIATION - DEFECTS IN CHROMOSOME INSTABILITY SYNDROMES
DIFFERENTIAL INDUCTION OF TRANSCRIPTIONALLY ACTIVE P53 FOLLOWING UV OR IONIZING-RADIATION - DEFECTS IN CHROMOSOME INSTABILITY SYNDROMES
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DOI：
10.1016/0092-8674(93)90496-d
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发表时间：
1993-11-19
期刊：
影响因子：
64.5
通讯作者：
LANE, DP
中科院分区：
文献类型：
--
作者：
LU, X;LANE, DP
p53蛋白的积累被认为是在哺乳动物细胞的细胞核中的DNA损伤引起的紫外线辐射（UV），X射线，或限制性内切酶。含有p53结合位点的启动子对DNA损伤表现出显著的转录反应。p53对X射线的反应是迅速的，在辐射后2小时达到峰值，但与对UV的反应相比，p53的反应是非常短暂的，并且在幅度上有所降低。我们发现共济失调毛细血管扩张症或着色性干皮病互补组A患者的细胞p53反应没有实质性缺陷。相比之下，11例Bloom患者的原代培养物中有2例显示在UV照射或SV 40感染后完全不存在p53积累，并且在X射线后出现严重延迟和异常反应。
Accumulation of p53 protein was seen in the nuclei of mammalian cells following DNA damage caused by ultraviolet radiation (UV), X-ray, or a restriction enzyme. Promoters containing p53-binding sites show a dramatic transcriptional response to DNA damage. The p53 response to X-ray is rapid, reaching a peak at 2 hr after radiation, but is very transitory and reduced in magnitude compared with that seen in response to UV. We find no substantive defect in the p53 response of cells from ataxia telangiectasia or xeroderma pigmentosum complementation group A patients. In contrast, 2 out of 11 primary cultures from Bloom's patients showed a complete absence of p53 accumulation following UV irradiation or SV40 infection and a grossly delayed and aberrant response following X-ray.