© 1987 Oxford University Press
research-article |
DNA alkylation repair and the induction of cell death and sister chromatid exchange in human cells
Charles A.Dana Laboratoiy of Toxicology, Harvard School of Public Health Boston, MA 02115
1Department of Biochemistiy, University of California Berkeley, CA 94720, USA
Mer human cells, which lack O6-methylguanine DNA methyltransferase activity, are extremely sensitive to alkylation induced killing, mutation and sister chromalid exchange. We have analyzed a Mer+ , a Mer, and a Mer revertant HeLa cell line and found that the methyltransferase deficiency correlates with increased levels of mutation and sister chromatid exchange, but does not correlate with increased killing of Mer HeLa cells by alkylating agents. Furthermore, we show that HeLa Mer cells repair N-3-methylguanine and N-3-methyladenine just as efficiently as HeLa Mer+ cells.
![]()
CiteULike
Connotea
Del.icio.us What's this?
This article has been cited by other articles:
![]() |
B. P. Engelward, G. Weeda, M. D. Wyatt, J. L. M. Broekhof, J. de Wit, I. Donker, J. M. Allan, B. Gold, J. H. J. Hoeijmakers, and L. D. Samson Base excision repair deficient mice lacking the Aag alkyladenine DNA glycosylase PNAS, November 25, 1997; 94(24): 13087 - 13092. [Abstract] [Full Text] [PDF] |
||||
