POLY(ADP-RIBOSE) CATABOLISM IN MAMMALIAN-CELLS EXPOSED TO DNA-DAMAGING AGENTS
POLY(ADP-RIBOSE) CATABOLISM IN MAMMALIAN-CELLS EXPOSED TO DNA-DAMAGING AGENTS
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DOI：
10.1016/0921-8777(89)90012-8
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发表时间：
1989-09-01
期刊：
影响因子：
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通讯作者：
ALTHAUS, FR
中科院分区：
文献类型：
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作者：
ALVAREZGONZALEZ, R;ALTHAUS, FR
用烷化剂N-甲基-N“-硝基-N-亚硝基胍或紫外线254 nm对培养的肝细胞的DNA造成损伤，刺激染色质中蛋白结合的聚（ADP-核糖）的催化。在最大剂量的DNA损伤处理中刺激最高。因此，ADP-核糖基聚合物的半衰期可降至小于41秒。这种快速周转与聚合物组成部分的缓慢催化形成对比，其半衰期为7.7小时。我们的数据表明，在DNA切除修复的多聚（ADP-核糖）的生物合成的切口后刺激耦合在哺乳动物细胞中的多聚（ADP-核糖）催化剂的适应。
DNA damage inflicted by the alkylating agent N-methyl-N''-nitro-N-nitrosoguanidine, or by UV254nm, stimulated the catabolism of protein-bound poly(ADP-ribose) in the chromatin of cultured hepatocytes. The stimulation was highest at the largest doses of DNA-damaging treatment. As a consequence, the half-life of ADP-ribosyl polymers may drop to less than 41 s. This rapid turnover contrasts with the slow catabolism of a constitutive fraction of polymers exhibiting a half-life of 7.7 h. Our data suggest that post-incisional stimulation of poly(ADP-ribose) biosynthesis in DNA-excision repair is coupled with an adaptation of poly(ADP-ribose) catabolism in mammalian cells.