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Author Yano, Masato
Source United States Department of Energy Office of Scientific and Technical Information
Content type Text
Language English
Subject Keyword APPLIED LIFE SCIENCES ♦ ATP ♦ DAMAGE ♦ EXPORTS ♦ MITOCHONDRIA ♦ SIGNALS
Abstract Mitochondria have many functions, including ATP generation. The electron transport chain (ETC) and the coupled ATP synthase generate ATP by consuming oxygen. Reactive oxygen species (ROS) are also produced by ETC, and ROS damage deoxyribonucleic acids, membrane lipids and proteins. Recent analysis indicate that mitochondrial unfolded protein response (UPR{sup mt}), which enhances expression of mitochondrial chaperones and proteases to remove damaged proteins, is activated when damaged proteins accumulate in the mitochondria. In Caenorhabditis elegans, HAF-1, a putative ortholog of human ABCB10, plays an essential role in signal transduction from mitochondria to nuclei to enhance UPR{sup mt}. Therefore, it is possible that ABCB10 has a role similar to that of HAF-1. However, it has not been reported whether ABCB10 is a factor in the signal transduction pathway to enhance UPR{sup mt}. In this study, ABCB10 was depleted in HepG2 cells using small interfering RNA (siRNA), and the effect was examined. ABCB10 depletion upregulated ROS and the expression of ROS-detoxifying enzymes (SOD2, GSTA1, and GSTA2), and SESN3, a protein induced by ROS to protect the cell from oxidative stress. In addition, ABCB10 depletion significantly decreased expression of UPR{sup mt}-related mitochondrial chaperones (HSPD1 and DNAJA3), and a mitochondrial protease (LONP1). However, the putative activity of ABCB10 to export peptides from mitochondria was not lost by ABCB10 depletion. Altogether, these data suggest that ABCB10 is involved in UPR{sup mt} signaling pathway similar to that of HAF-1, although ABCB10 probably does not participate in peptide export from mitochondria. - Highlights: • ABCB10-KD upregulated ROS and the expression of ROS-detoxifying enzymes and SESN3. • ABCB10 is involved in UPR{sup mt} signaling pathway. • ABCB10 probably does not participate in peptide export from mitochondria.
ISSN 0006291X
Educational Use Research
Learning Resource Type Article
Publisher Date 2017-04-29
Publisher Place United States
Journal Biochemical and Biophysical Research Communications
Volume Number 486
Issue Number 2


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