. Author manuscript; available in PMC: 2008 Jun 1.

Published in final edited form as: DNA Repair (Amst). 2007 Mar 6;6(6):695–711. doi: 10.1016/j.dnarep.2007.01.009

Table I.

Possible entry mechanisms of a unified base excision repair model

Substrate Recognized	Enzyme/Event Creating the Break	DNA Ends Flanking the Gap	Gap Tailoring Protein Required	Current Sub-Pathway
Alkylation Damage (e.g. 3Me-adenine)	Monofunctional Glycosylase	3’-OH 5’-dRP	pol ß	BER
Spontaneous Base Loss (e.g. AP Site)	APE1	3’-OH 5’-dRP	pol ß	BER
Oxidative Damage (e.g. 8-oxo-guanine)	Bifunctional Glycosylase	3’-α,ß unsaturated aldehyde 5’- PO₄	APE1	BER
Oxidative Damage (e.g. 5-OH-cytosine)	APE1	3’-OH 5’-OH cytosine residue	FEN1	NIR or LP BER
Oxidative Damage (e.g. 5-OH-uracil)	NEIL1/NEIL2	3’-PO₄ 5’- PO₄	PNKP	NEIL-directed BER
Supercoiled DNA	Topoisomerase I malfunction	3’-tyrosyl residue 5’-PO₄	Tdp1	SSBR
DNA	Radiation	5’phosphate, 3’phosphate, 3’phosphoglycolate (and others)[138]	APE1 FEN1 PNKP	SSBR