Different DNA Polymerases Are Involved in the Short- and Long-Patch Base Excision Repair in Mammalian Cells†

Biochemistry ◽  
1998 ◽  
Vol 37 (11) ◽  
pp. 3575-3580 ◽  
Author(s):  
Paola Fortini ◽  
Barbara Pascucci ◽  
Eleonora Parlanti ◽  
Robert W. Sobol ◽  
Samuel H. Wilson ◽  
...  
PLoS ONE ◽  
2010 ◽  
Vol 5 (8) ◽  
pp. e12229 ◽  
Author(s):  
Elena K. Braithwaite ◽  
Padmini S. Kedar ◽  
Deborah J. Stumpo ◽  
Barbara Bertocci ◽  
Jonathan H. Freedman ◽  
...  

1999 ◽  
Vol 181 (21) ◽  
pp. 6763-6771 ◽  
Author(s):  
Lauren M. Posnick ◽  
Leona D. Samson

ABSTRACT Inappropriate expression of 3-methyladenine (3MeA) DNA glycosylases has been shown to have harmful effects on microbial and mammalian cells. To understand the underlying reasons for this phenomenon, we have determined how DNA glycosylase activity and substrate specificity modulate glycosylase effects in Escherichia coli. We compared the effects of two 3MeA DNA glycosylases with very different substrate ranges, namely, the Saccharomyces cerevisiae Mag1 and the E. coli Tag glycosylases. Both glycosylases increased spontaneous mutation, decreased cell viability, and sensitized E. coli to killing by the alkylating agent methyl methanesulfonate. However, Tag had much less harmful effects than Mag1. The difference between the two enzymes’ effects may be accounted for by the fact that Tag almost exclusively excises 3MeA lesions, whereas Mag1 excises a broad range of alkylated and other purines. We infer that the DNA lesions responsible for changes in spontaneous mutation, viability, and alkylation sensitivity are abasic sites and secondary lesions resulting from processing abasic sites via the base excision repair pathway.


EMBO Reports ◽  
2003 ◽  
Vol 4 (4) ◽  
pp. 363-367 ◽  
Author(s):  
Ulrike Sattler ◽  
Philippe Frit ◽  
Bernard Salles ◽  
Patrick Calsou

1983 ◽  
Vol 112 (6) ◽  
pp. 345-358 ◽  
Author(s):  
Edward J. Katz ◽  
Pawan K. Gupta ◽  
Michael A. Sirover

F1000Research ◽  
2017 ◽  
Vol 6 ◽  
pp. 279 ◽  
Author(s):  
Upasna Thapar ◽  
Bruce Demple

Since the discovery of the base excision repair (BER) system for DNA more than 40 years ago, new branches of the pathway have been revealed at the biochemical level by in vitro studies. Largely for technical reasons, however, the confirmation of these subpathways in vivo has been elusive. We review methods that have been used to explore BER in mammalian cells, indicate where there are important knowledge gaps to fill, and suggest a way to address them.


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