2011 | Yong Son, Yong-Kwan Cheong, Nam-Ho Kim, Hun-Taeg Chung, Dae Gill Kang and Hyun-Ock Pae
This review article explores the relationship between mitogen-activated protein kinases (MAPKs) and reactive oxygen species (ROS). MAPKs, including extracellular signal-regulated kinases (ERKs), c-jun N-terminal kinases (JNKs), and p38 MAPKs, play crucial roles in signal transduction from the cell surface to the nucleus. ROS, such as superoxide anion radical (·O2−), hydroxyl radicals (·OH), and hydrogen peroxide (H2O2), can activate these MAPKs under oxidative stress conditions. The mechanisms by which ROS activate MAPKs are not fully understood but may involve oxidative modifications of signaling proteins and the inactivation or degradation of MAPK phosphatases (MKPs). The article discusses the activation of ERKs, JNKs, and p38 MAPKs by ROS, highlighting the role of specific MAP3Ks and MAP2Ks. It also reviews the regulatory role of MKPs in controlling MAPK activity and the potential mechanisms by which ROS can inactivate or degrade MKPs. The conclusion emphasizes the importance of ROS in activating MAPK pathways and suggests that the site of ROS production, concentration, and cellular redox state are key factors in determining the effects of ROS on MAPK activation.This review article explores the relationship between mitogen-activated protein kinases (MAPKs) and reactive oxygen species (ROS). MAPKs, including extracellular signal-regulated kinases (ERKs), c-jun N-terminal kinases (JNKs), and p38 MAPKs, play crucial roles in signal transduction from the cell surface to the nucleus. ROS, such as superoxide anion radical (·O2−), hydroxyl radicals (·OH), and hydrogen peroxide (H2O2), can activate these MAPKs under oxidative stress conditions. The mechanisms by which ROS activate MAPKs are not fully understood but may involve oxidative modifications of signaling proteins and the inactivation or degradation of MAPK phosphatases (MKPs). The article discusses the activation of ERKs, JNKs, and p38 MAPKs by ROS, highlighting the role of specific MAP3Ks and MAP2Ks. It also reviews the regulatory role of MKPs in controlling MAPK activity and the potential mechanisms by which ROS can inactivate or degrade MKPs. The conclusion emphasizes the importance of ROS in activating MAPK pathways and suggests that the site of ROS production, concentration, and cellular redox state are key factors in determining the effects of ROS on MAPK activation.