Base excision repair and design of small molecule inhibitors of human DNA polymerase β Review

Wilson, SH, Beard, WA, Shock, DD et al. (2010). Base excision repair and design of small molecule inhibitors of human DNA polymerase β . Cellular and Molecular Life Sciences, 67(21), 3633-3647. 10.1007/s00018-010-0489-1

cited authors

  • Wilson, SH; Beard, WA; Shock, DD; Batra, VK; Cavanaugh, NA; Prasad, R; Hou, EW; Liu, Y; Asagoshi, K; Horton, JK; Stefanick, DF; Kedar, PS; Carrozza, MJ; Masaoka, A; Heacock, ML

abstract

  • Base excision repair (BER) can protect a cell after endogenous or exogenous genotoxic stress, and a deficiency in BER can render a cell hypersensitive to stress-induced apoptotic and necrotic cell death, mutagenesis, and chromosomal rearrangements. However, understanding of the mammalian BER system is not yet complete as it is extraordinarily complex and has many back-up processes that complement a deficiency in any one step. Due of this lack of information, we are unable to make accurate predictions on therapeutic approaches targeting BER. A deeper understanding of BER will eventually allow us to conduct more meaningful clinical interventions. In this review, we will cover historical and recent information on mammalian BER and DNA polymerase β and discuss approaches toward development and use of small molecule inhibitors to manipulate BER. With apologies to others, we will emphasize results obtained in our laboratory and those of our collaborators. © 2010 US Government.

authors

publication date

  • November 1, 2010

published in

Digital Object Identifier (DOI)

start page

  • 3633

end page

  • 3647

volume

  • 67

issue

  • 21