Apurinic/Apyrimindinic Endonuclease in Redox Regulation and Oxidative Stress: Implications for Regulation of DNA Repair and Therapeutic Development

Research output: Chapter in Book/Report/Conference proceedingChapter


This chapter focuses on the role of apurinic/apyrimidinic endonuclease (APE1) in redox regulation and response to oxidative stress and recent therapeutic developments targeting APE1's redox function. A key enzyme in BER, APE1,6 recognizes a basic sites produced either spontaneously or through removal of an oxidized base by a DNA glycosylase. Knock-out of APE1 in mice is embryonic lethal establishing APE1 as an essential enzyme; 7 APE1 functions in base excision repair by cleaving the phosphodiester backbone 5' of a basic site resulting in a 3'OH and 5' deoxyribose phosphate. Further processing by DNA polymerase beta and DNA ligase completes the DNA repair. APE1 is also a nuclear redox factor that recognizes oxidized transcription factors and reduces them, significantly stimulating their DNA-binding properties. In this regard, APE1 plays a unique role in that it repairs both oxidized DNA and a number of transcription factors, which in turn regulate expression of DNA repair genes.

Original languageEnglish (US)
Title of host publicationDNA Repair in Cancer Therapy
PublisherElsevier Inc.
Number of pages21
ISBN (Print)9780123849991
StatePublished - Dec 1 2012


ASJC Scopus subject areas

  • Dentistry(all)
  • Medicine(all)

Cite this