Human AP endonuclease/redox factor APE1/ref-1 modulates mitochondrial function after oxidative stress by regulating the transcriptional activity of NRF1

Free Radical Biology & Medicine
Mengxia LiDong Wang

Abstract

Maintenance of mitochondrial functionality largely depends on nuclear transcription because most mitochondrial proteins are encoded by the nuclear genome and transported to the mitochondria. Nuclear respiration factor 1 (NRF1) plays a crucial role in regulating the expression of a broad range of mitochondrial genes in the nucleus in response to cellular oxidative stress. However, little is known about the redox regulatory mechanism of the transcriptional activity of NRF1. In this study, we show that the human apurinic/apyrimidinic endonuclease/redox factor (APE1/Ref-1) is involved in mitochondrial function regulation by modulating the DNA-binding activity of NRF1. Our results show that both APE1 expression level and its redox activity are essential for maintenance of the mitochondrial function after tert-butylhydroperoxide-induced oxidative stress. Upon knocking down or redox mutation of APE1, NRF1 DNA-binding activity was impaired and, consequently, the expression of its downstream genes, including Tfam, Cox6c, and Tomm22, was significantly reduced. NRF1 knockdown blocked the restoration of mitochondrial function by APE1 overexpression, which further suggests APE1 regulates mitochondrial function through an NRF1-dependent path...Continue Reading

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Citations

May 30, 2014·Drug Design, Development and Therapy·Chengyuan QianDong Wang
Jul 10, 2013·Antioxidants & Redox Signaling·Mengxia Li, David M Wilson
Aug 14, 2015·BMC Cancer·Maohua XieXingming Deng
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Dec 3, 2014·Free Radical Biology & Medicine·Jin-Lu ShanZhen-Zhou Yang
Jan 9, 2020·Scientific Reports·Dilara AyyildizSilvano Piazza
Oct 27, 2018·Free Radical Biology & Medicine·Daniele Maria Lopes PinheiroLucymara Fassarella Agnez-Lima
Oct 8, 2021·Frontiers in Cell and Developmental Biology·Thais Teixeira OliveiraLucymara Fassarella Agnez-Lima

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