摘要
The antitumor drug, m-AMSA (4′-(9-acridinylamino)-methanesulfon-m-anisidide), is known to interfere with the breakage-reunion reaction of mammalian DNA topoisomerase II by blocking the enzyme-DNA complex in its putative cleavable state. Treatment of SV40 virus infected monkey cells with m-AMSA resulted in both single- and double-stranded breaks on SV40 viral chromatin. These strand breaks are unusual because they are covalently associated with protein. Immuno-precipitation results suggest that the covalently linked protein is DNA topoisomerase II. These results are consistent with the proposal that the drug action in vivo involves the stabilization of a cleavable complex between topoisomerase II and DNA in chromatin. Mapping of these double-stranded breaks on SV40 viral DNA revealed multiple topoisomerase II cleavage sites. A major topoisomerase II cleavage site was preferentially induced during late infection and was mapped in the DNAase I hypersensitive region of SV40 chromatin.
原文 | 英語 |
---|---|
頁(從 - 到) | 127-132 |
頁數 | 6 |
期刊 | Cell |
卷 | 41 |
發行號 | 1 |
DOIs | |
出版狀態 | 已發佈 - 5月 1985 |
對外發佈 | 是 |
ASJC Scopus subject areas
- 生物化學、遺傳與分子生物學 (全部)