Singh N, Poirier G, Cerutti P
EMBO J. 1985 Jun;4(6):1491-4. doi: 10.1002/j.1460-2075.1985.tb03807.x.
The tumor promoter phorbol-12-myristate-13-acetate (PMA) causes an increase in pol(ADP)-ribosylation in mouse and human fibroblasts via the intermediate formation of active oxygen. In contrast to poly(ADP)-ribosylation induced by the methylating agent N-methyl-N'-nitro-N-nitrosoguanidine, de novo RNA and protein synthesis are required and the accumulation of the polymer occurs in the absence of detectable DNA strand breakage. Our results suggest a mechanism for PMA-induced modulation of chromatin structure and gene expression.
肿瘤促进剂佛波醇-12-肉豆蔻酸酯-13-乙酸酯(PMA)通过活性氧的中间形成,导致小鼠和人成纤维细胞中聚(ADP)-核糖基化增加。与甲基化剂N-甲基-N'-硝基-N-亚硝基胍诱导的聚(ADP)-核糖基化相反,需要从头合成RNA和蛋白质,并且聚合物的积累发生在没有可检测到的DNA链断裂的情况下。我们的结果提示了一种PMA诱导的染色质结构和基因表达调节机制。