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Role of Reactive Oxygen Species and Redox in Regulating the Function of Transient Receptor Potential Channels

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Title: Role of Reactive Oxygen Species and Redox in Regulating the Function of Transient Receptor Potential Channels
Author(s): Song, Michael Y.; Mainko, Ayako; Yuan, Jason X.-J.
Subject(s): Cellular redox status transient receptor potential
Abstract: Cellular redox status, regulated by production of reactive oxygen species (ROS), greatly contributes to the regulation of vascular smooth muscle cell contraction, migration, proliferation, and apoptosis by modulating the function of transient receptor potential (TRP) channels in the plasma membrane. ROS functionally interact with the channel protein via oxidizing the redox-sensitive residues, whereas nitric oxide (NO) regulates TRP channel function by cyclic GMP/protein kinase G-dependent and -independent pathways. Based on the structural differences among different TRP isoforms, the effects of ROS and NO are also different. In addition to regulating TRP channels in the plasma membrane, ROS and NO also modulate Ca2+ release channels (e.g., IP3 and ryanodine receptors) on the sarcoplasmic/endoplasmic reticulum membrane. This review aims at briefly describing (a) the role of TRP channels in receptor-operated and store-operated Ca2+ entry, and (b) the role of ROS and redox status in regulating the function and structure of TRP channels.
Issue Date: 2011-04-11
Publisher: Mary Ann Liebert
Citation Info: Song, M. Y., Makino, A., & Yuan, J. X. 2010. Role of Reactive Oxygen Species and Redox in Regulating the Function of Transient Receptor Potential Channels. Antioxidants and Redox Signaling. DOI: 10.1089/ars.2010.3648
Type: Article
Description: This is a copy of an article published in the Antioxidants and Redox Signaling © 2011 Copyright Mary Ann Liebert, Inc.]; Antioxidants and Redox Signaling is available online at: http://www.liebertonline.com. The final version is available through Mary Ann Liebert at DOI: 10.1089/ars.2010.3648
URI: http://hdl.handle.net/10027/7589
ISSN: 1557-7716
Sponsor: This work was supported in part by grants from the National Institutes of Health (HL054043 and HL066012 to J.X.-J.Y., and DK083506 to A.M.). M.Y.S. is supported by an NIH training grant (T32 DK007202).
Date Available in INDIGO: 2011-05-07
 

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