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. 2014 Jul 18;46(7):e106. doi: 10.1038/emm.2014.42

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Copyright © 2014 KSBMB.

This work is licensed under a Creative Commons Attribution-NonCommercial-ShareAlike 3.0 Unported License. The images or other third party material in this article are included in the article's Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by-nc-sa/3.0/

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A schematic representation of the mechanism of the short-patch (SN-BER) and long-patch (LP-BER) sub-pathways of base excision repair (BER) in mammalian cells. apurinic/apyrimidinic endonuclease 1 (APE1)/redox effector factor-1 (Ref-1) functions as an AP endonuclease in SN-BER, initiated by monofunctional DNA glycosylase (DG), and as a 3′phosphodiesterase in LP-BER, initiated by bifunctional DG. Pol β, X-ray repair cross-complementing protein 1 (XRCC1) and ligase III are required for SN-BER to conduct SN repair, whereas proliferating cell nuclear antigen (PCNA), Pol δ/ɛ, flap endonuclease 1 (FEN-1) and ligase I are required for LP-BER to conduct multinucleotide repair in mammalian cells.