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

Abstract

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.
Pages235-255
Number of pages21
ISBN (Print)9780123849991
DOIs
StatePublished - Dec 1 2012

ASJC Scopus subject areas

  • Dentistry(all)
  • Medicine(all)

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