IMR Press / FBL / Volume 22 / Issue 9 / DOI: 10.2741/4555

Frontiers in Bioscience-Landmark (FBL) is published by IMR Press from Volume 26 Issue 5 (2021). Previous articles were published by another publisher on a subscription basis, and they are hosted by IMR Press on as a courtesy and upon agreement with Frontiers in Bioscience.


Base excision repair of oxidative DNA damage: from mechanism to disease

Show Less
1 Department of Biochemistry and Molecular Biology, University of Kansas Medical Center, Kansas City, Kansas, 66160, USA
Front. Biosci. (Landmark Ed) 2017, 22(9), 1493–1522;
Published: 1 March 2017
(This article belongs to the Special Issue DNA damage, DNA repair, and DNA damage response pathways)

Reactive oxygen species continuously assault the structure of DNA resulting in oxidation and fragmentation of the nucleobases. Both oxidative DNA damage itself and its repair mediate the progression of many prevalent human maladies. The major pathway tasked with removal of oxidative DNA damage, and hence maintaining genomic integrity, is base excision repair (BER). The aphorism that structure often dictates function has proven true, as numerous recent structural biology studies have aided in clarifying the molecular mechanisms used by key BER enzymes during the repair of damaged DNA. This review focuses on the mechanistic details of the individual BER enzymes and the association of these enzymes during the development and progression of human diseases, including cancer and neurological diseases. Expanding on these structural and biochemical studies to further clarify still elusive BER mechanisms, and focusing our efforts toward gaining an improved appreciation of how these enzymes form co-complexes to facilitate DNA repair is a crucial next step toward understanding how BER contributes to human maladies and how it can be manipulated to alter patient outcomes.

Base excision repair
Oxidative DNA damage
DNA repair
Back to top