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Mol. Cells 2011; 32(6): 491-509

Published online December 22, 2011

https://doi.org/10.1007/s10059-011-0276-3

© The Korean Society for Molecular and Cellular Biology

Regulation of Reactive Oxygen Species Generation in Cell Signaling

Yun Soo Bae1,*, Hyunjin Oh1, Sue Goo Rhee1,*, and Young Do Yoo2,*

1Department of Life Science, Division of Life and Pharmaceutical Sciences, Ewha Womans University, Seoul 120-750, Korea, 2Laboratory of Molecular Cell Biology, Graduate School of Medicine, Korea University College of Medicine, Korea University, Seoul 136-705, Korea

Correspondence to : *Correspondence: baeys@ewha.ac.kr (YSB); rheesg@ewha.ac.kr (SGR); ydy1130@korea.ac.kr (YDY)

Received: December 6, 2011; Accepted: December 12, 2011

Abstract

Reactive oxygen species (ROS) including superoxide anion and hydrogen peroxide (H2O2) are thought to be by-products of aerobic respiration with damaging effects on DNA, protein, and lipid. A growing body of evidence indicates, however, that ROS are involved in the maintenance of redox homeostasis and various cellular signaling pathways. ROS are generated from diverse sources including mitochondrial respiratory chain, enzymatic activation of cytochrome p450, and NADPH oxidases further suggesting involvement in a complex array of cellular processes. This review summarizes the production and function of ROS. In particular, how cytosolic and membrane proteins regulate ROS generation for intracellular redox signaling will be detailed.

Keywords apoptosis, cell signaling, cytochrome p450, mitochondria, NADPH oxidase, reactive oxygen species

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Mol. Cells 2011; 32(6): 491-509

Published online December 31, 2011 https://doi.org/10.1007/s10059-011-0276-3

Copyright © The Korean Society for Molecular and Cellular Biology.

Regulation of Reactive Oxygen Species Generation in Cell Signaling

Yun Soo Bae1,*, Hyunjin Oh1, Sue Goo Rhee1,*, and Young Do Yoo2,*

1Department of Life Science, Division of Life and Pharmaceutical Sciences, Ewha Womans University, Seoul 120-750, Korea, 2Laboratory of Molecular Cell Biology, Graduate School of Medicine, Korea University College of Medicine, Korea University, Seoul 136-705, Korea

Correspondence to:*Correspondence: baeys@ewha.ac.kr (YSB); rheesg@ewha.ac.kr (SGR); ydy1130@korea.ac.kr (YDY)

Received: December 6, 2011; Accepted: December 12, 2011

Abstract

Reactive oxygen species (ROS) including superoxide anion and hydrogen peroxide (H2O2) are thought to be by-products of aerobic respiration with damaging effects on DNA, protein, and lipid. A growing body of evidence indicates, however, that ROS are involved in the maintenance of redox homeostasis and various cellular signaling pathways. ROS are generated from diverse sources including mitochondrial respiratory chain, enzymatic activation of cytochrome p450, and NADPH oxidases further suggesting involvement in a complex array of cellular processes. This review summarizes the production and function of ROS. In particular, how cytosolic and membrane proteins regulate ROS generation for intracellular redox signaling will be detailed.

Keywords: apoptosis, cell signaling, cytochrome p450, mitochondria, NADPH oxidase, reactive oxygen species

Mol. Cells
Feb 28, 2023 Vol.46 No.2, pp. 69~129
COVER PICTURE
The bulk tissue is a heterogeneous mixture of various cell types, which is depicted as a skein of intertwined threads with diverse colors each of which represents a unique cell type. Single-cell omics analysis untangles efficiently the skein according to the color by providing information of molecules at individual cells and interpretation of such information based on different cell types. The molecules that can be profiled at the individual cell by single-cell omics analysis includes DNA (bottom middle), RNA (bottom right), and protein (bottom left). This special issue reviews single-cell technologies and computational methods that have been developed for the single-cell omics analysis and how they have been applied to improve our understanding of the underlying mechanisms of biological and pathological phenomena at the single-cell level.

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