Table of Contents
Journal of Signal Transduction
Volume 2011 (2011), Article ID 792639, 6 pages
Review Article

Mitogen-Activated Protein Kinases and Reactive Oxygen Species: How Can ROS Activate MAPK Pathways?

1Department of Anesthesiology and Pain Medicine, Wonkwang University School of Medicine, Iksan 570-749, Republic of Korea
2Department of Cardiovascular Medicine, Wonkwang University Hospital, Iksan 570-711, Republic of Korea
3Department of Biological Science, University of Ulsan, Ulsan 680-749, Republic of Korea
4Professional Graduate School of Oriental Medicine and Hanbang Body-Fluid Research Center, Wonkwang University, Iksan 570-749, Republic of Korea
5Department of Microbiology and Immunology, Wonkwang University School of Medicine, 344-2 Shinyong-dong, Iksan, Chonbuk 570-749, Republic of Korea

Received 16 August 2010; Revised 25 December 2010; Accepted 11 January 2011

Academic Editor: Zhilin Qu

Copyright © 2011 Yong Son et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Mitogen-activated protein kinases (MAPKs) are serine-threonine protein kinases that play the major role in signal transduction from the cell surface to the nucleus. MAPKs, which consist of growth factor-regulated extracellular signal-related kinases (ERKs), and the stress-activated MAPKs, c-jun NH2-terminal kinases (JNKs) and p38 MAPKs, are part of a three-kinase signaling module composed of the MAPK, an MAPK kinase (MAP2K) and an MAPK kinase (MAP3K). MAP3Ks phosphorylate MAP2Ks, which in turn activate MAPKs. MAPK phosphatases (MKPs), which recognize the TXY amino acid motif present in MAPKs, dephosphorylate and deactivate MAPKs. MAPK pathways are known to be influenced not only by receptor ligand interactions, but also by different stressors placed on the cell. One type of stress that induces potential activation of MAPK pathways is the oxidative stress caused by reactive oxygen species (ROS). Generally, increased ROS production in a cell leads to the activation of ERKs, JNKs, or p38 MAPKs, but the mechanisms by which ROS can activate these kinases are unclear. Oxidative modifications of MAPK signaling proteins and inactivation and/or degradation of MKPs may provide the plausible mechanisms for activation of MAPK pathways by ROS, which will be reviewed in this paper.