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Molecular Mechanism of Reactive Oxygen Species-dependent ASK1 Activation in Innate Immunity  

Yamauchi, Shota (Laboratory of Cell Signaling, Graduate School of Pharmaceutical Sciences, Strategic Approach to Drug Discovery and Development in Pharmaceutical Sciences, Center of Excellence (COE) Program, and Core Research for Evolutional Science and Technology (CREST), Japan Science and Technology Corporation, The University of Tokyo)
Noguchi, Takuya (Laboratory of Cell Signaling, Graduate School of Pharmaceutical Sciences, Strategic Approach to Drug Discovery and Development in Pharmaceutical Sciences, Center of Excellence (COE) Program, and Core Research for Evolutional Science and Technology (CREST), Japan Science and Technology Corporation, The University of Tokyo)
Ichijo, Hidenori (Laboratory of Cell Signaling, Graduate School of Pharmaceutical Sciences, Strategic Approach to Drug Discovery and Development in Pharmaceutical Sciences, Center of Excellence (COE) Program, and Core Research for Evolutional Science and Technology (CREST), Japan Science and Technology Corporation, The University of Tokyo)
Publication Information
IMMUNE NETWORK / v.8, no.1, 2008 , pp. 1-6 More about this Journal
Abstract
Apoptosis signal-regulating kinase 1 (ASK1), a mitogen- activated protein kinase kinase kinase, plays pivotal roles in stress responses. In addition, ASK1 has emerged as a key regulator of immune responses elicited by pathogen-associated molecular patterns (PAMPs) and endogenous danger signals. Recent studies have demonstrated that reactive oxygen species (ROS)-dependent activation of ASK1 is required for LPS-stimulated cytokine production as well as extracellular ATP-induced apoptosis in immune cells. The mechanism of ROS-dependent regulation of ASK1 activity by thioredoxin and TRAFs has been well characterized. In this review, we focus on the molecular details of the activation of ASK1 and its involvement in innate immunity.
Keywords
ASK1; ROS; thioredoxin; TRAF; TLR4; $P2X_7$ receptor;
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