阿非科林抑制短DNA片段的合成和连接，但不抑制10千碱基DNA复制中间体的结合。
Aphidicolin inhibits the synthesis and joining of short DNA fragments but not the union of 10-kilobase DNA replication intermediates.
作者信息
Lönn U, Lönn S
出版信息
Proc Natl Acad Sci U S A. 1983 Jul;80(13):3996-9. doi: 10.1073/pnas.80.13.3996.
Abstract
DNA replication intermediates in human melanoma cells have been investigated by using the drug aphidicolin, which inhibits DNA polymerase alpha. In untreated cells, Okazaki fragments and 10-kilobase (kb) DNA intermediates are formed. In aphidicolin-treated cells, the replication fork is stopped and there is no formation of DNA replication intermediates. However, 10-kb DNA intermediates formed before the drug blockade are ligated to high molecular weight DNA whereas already formed Okazaki fragments accumulate in the cell. Moreover, in cells released from aphidicolin inhibition there is preferential labeling of 10-kb DNA compared to Okazaki fragments. The 10-kb DNA and the Okazaki fragments, therefore, respond differently to aphidicolin.
摘要
通过使用抑制DNA聚合酶α的药物阿非迪霉素，对人黑色素瘤细胞中的DNA复制中间体进行了研究。在未处理的细胞中，会形成冈崎片段和10千碱基（kb）的DNA中间体。在阿非迪霉素处理的细胞中，复制叉停止，且不会形成DNA复制中间体。然而，在药物阻断之前形成的10-kb DNA中间体会连接成高分子量DNA，而已经形成的冈崎片段则在细胞中积累。此外，在从阿非迪霉素抑制中释放出来的细胞中，与冈崎片段相比，10-kb DNA有优先标记。因此，10-kb DNA和冈崎片段对阿非迪霉素的反应不同。
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