HSCARG Inhibits NADPH Oxidase Activity through Regulation of the Expression of p47phox

Weichun Xiao, Yanyan Peng, Yong Liu, Zhi Li, Senlin Li, Xiaofeng Zheng

Research output: Contribution to journalArticlepeer-review

10 Scopus citations


Nicotinamide adenine dinucleotide phosphate (NADPH) oxidase catalyzes the transfer of electrons from NADPH to O2, which is the main source of reactive oxygen species (ROS) in nonphagocytic cells. Excess ROS are toxic; therefore, keeping ROS in homeostasis in cells can protect cells from oxidative damage. It is meaningful to further understand the molecular mechanism by which ROS homeostasis is mediated. Human protein HSCARG is a newly identified oxidative sensor and a negative regulator of NF-κB. Here, we find that HSCARG represses the cellular ROS generation through inhibiting mRNA and protein expression of p47phox, a subunit of NADPH oxidase. In contrast, shRNA-mediated HSCARG knockdown increases endogenous p47phox expression level. And HSCARG has no obvious effect on ROS production in p47phox-depleted cells. Furthermore, HSCARG regulates p47phox through inhibition of NF-κB activity. Our findings identify HSCARG as a novel regulator in regulation of the activity of NADPH oxidase and ROS homeostasis.

Original languageEnglish (US)
Article numbere59301
JournalPloS one
Issue number3
StatePublished - Mar 19 2013

ASJC Scopus subject areas

  • General


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