Figure - PMC

Skip to main content

An official website of the United States government

Here's how you know

Here's how you know

Official websites use .gov
A .gov website belongs to an official government organization in the United States.

Secure .gov websites use HTTPS
A lock ( ) or https:// means you've safely connected to the .gov website. Share sensitive information only on official, secure websites.

View full-text article in PMC

. 2019 Jan 29;8(2):100. doi: 10.3390/cells8020100

Search in PMC
Search in PubMed
View in NLM Catalog
Add to search

© 2019 by the authors.

Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/).

PMC Copyright notice

Base Excision Repair (BER) in mitochondria. Generation of free radicals induces DNA lesions in the form of oxidized bases, affecting base-pairing properties. Oxidative lesions are repaired via the BER pathway. BER is initiated by the activity of DNA glycosylases such as monofunctional glycosylases which recognize and cleave the N-glycosidic bond between the modified base and sugar, creating an abasic site and bifunctional glycosylases which have an additional intrinsic Apurinic/Apyrimidinic (AP)lyase activity. The incision of the AP site occurs via β elimination or β-δ elimination which is further processed by APE1 or PNKP, followed by gap-filling by DNA pol gamma (PolG). Once the AP site has been processed and the correct nucleotide recruited by PolG, the free DNA ends are ligated by DNA ligase III (LIG3).