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. Author manuscript; available in PMC: 2016 Jun 29.
Published in final edited form as: Environ Mol Mutagen. 2001;38(2-3):180–190. doi: 10.1002/em.1070

Fig. 3.

Fig. 3

A model of pathway decision for repair of an AP site. After cleavage of the AP site with APE1, either Polβ or FEN1 is recruited at the lesion site because of their interaction with APE1. Multiple factors, including relative abundance of these enzymes, location of the lesion in the genome, cell cycle phase, as well as chromatin organization, may determine which enzyme takes over from APE1 and thus decide the pathway. Polβ acts as both a dRPase and a DNA polymerase to perform a single base-filling reaction as shown on the left side. In the pathway outlined on the right side, FEN1 cooperates with PCNA/Polδ(ε) or Polβ to carry out a multibase-filling reaction. No sequential order in recruitment of these proteins in completing repair is implied. The roles of XPG, BRCA1, MMR, and other accessory proteins are not indicated in these repair pathways.