期刊
TOXICOLOGY
卷 177, 期 2-3, 页码 123-130出版社
ELSEVIER SCI IRELAND LTD
DOI: 10.1016/S0300-483X(02)00220-2
关键词
DNA double-strand breaks; neocarzinostatin; phosphorylation; nuclear focus formation; cell cycle
DNA double-strand breaks, if unrepaired, may lead to the accumulation of chromosomal aberrations and eventually cancer cell formation. Components of the Rad50/NBS/Mre11 nuclease complex are essential for the effective repair of DNA double-stranded breaks. Here, we show that neocarzinostatin, a radiomimetic enediyne antibiotic, induces phosphorylation and nuclear focus formation of Mre11 and NBS1 through a cell cycle-independent mechanism. Furthermore, neocarzinostatin-induced Mre11 phosphorylation and nuclear focus formation are defective in AT and NBS cells, but not wild type cells. Our results suggest that ATM and NBS1 are required for the effective repair of neocarzinostatin-induced DNA double-strand breaks by both non-homologous end joining and homologous recombinational repair pathways. (C) 2002 Elsevier Science Ireland Ltd. All rights reserved.
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