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      Call for Papers: Sex and Gender in Neurodegenerative Diseases

      Submit here before September 30, 2024

      About Neurodegenerative Diseases: 3.0 Impact Factor I 4.3 CiteScore I 0.695 Scimago Journal & Country Rank (SJR)

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      Regulation of TRP Channels by Phosphorylation

      review-article
      Author(s): , ,
      Publication date (Electronic):
      Journal: Neurosignals
      Publisher: S. Karger AG
      Keywords: Ca2+ influx, TRP channels, Phosphorylation

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          Abstract

          The transient receptor potential (TRP) channels are a group of Ca<sup>2+</sup>-permeable cation channels (except TRPM4 and TRPM5) that function as cellular sensors of various internal and external stimuli. Most of these channels are expressed in the nervous system and they play a key role in sensory physiology. They may respond to temperature, pressure, inflammatory agents, pain, osmolarity, taste and many other stimuli. Recent development indicates that the activity of these channels is regulated by protein phosphorylation and dephosphorylation of serine, threonine, and tyrosine residues. In this review, we present a comprehensive summary of the literature regarding the TRP channel regulation by different protein kinases.

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          Most cited references45

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          TRP channels as cellular sensors.

          David Clapham (2003)
          TRP channels are the vanguard of our sensory systems, responding to temperature, touch, pain, osmolarity, pheromones, taste and other stimuli. But their role is much broader than classical sensory transduction. They are an ancient sensory apparatus for the cell, not just the multicellular organism, and they have been adapted to respond to all manner of stimuli, from both within and outside the cell.
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            Store-operated calcium channels.

            Anant B. Parekh, James W. Putney (2005)
            In electrically nonexcitable cells, Ca(2+) influx is essential for regulating a host of kinetically distinct processes involving exocytosis, enzyme control, gene regulation, cell growth and proliferation, and apoptosis. The major Ca(2+) entry pathway in these cells is the store-operated one, in which the emptying of intracellular Ca(2+) stores activates Ca(2+) influx (store-operated Ca(2+) entry, or capacitative Ca(2+) entry). Several biophysically distinct store-operated currents have been reported, but the best characterized is the Ca(2+) release-activated Ca(2+) current, I(CRAC). Although it was initially considered to function only in nonexcitable cells, growing evidence now points towards a central role for I(CRAC)-like currents in excitable cells too. In spite of intense research, the signal that relays the store Ca(2+) content to CRAC channels in the plasma membrane, as well as the molecular identity of the Ca(2+) sensor within the stores, remains elusive. Resolution of these issues would be greatly helped by the identification of the CRAC channel gene. In some systems, evidence suggests that store-operated channels might be related to TRP homologs, although no consensus has yet been reached. Better understood are mechanisms that inactivate store-operated entry and hence control the overall duration of Ca(2+) entry. Recent work has revealed a central role for mitochondria in the regulation of I(CRAC), and this is particularly prominent under physiological conditions. I(CRAC) therefore represents a dynamic interplay between endoplasmic reticulum, mitochondria, and plasma membrane. In this review, we describe the key electrophysiological features of I(CRAC) and other store-operated Ca(2+) currents and how they are regulated, and we consider recent advances that have shed insight into the molecular mechanisms involved in this ubiquitous and vital Ca(2+) entry pathway.
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              Src kinases: a hub for NMDA receptor regulation.

              Michael W Salter, Lorraine Kalia (2004)
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                Author and article information

                Journal
                Journal ID (publisher-id): NSG
                Journal ID (nlm-ta): Neurosignals
                Journal ID (doi): 10.1159/issn.1424-862X
                Title: Neurosignals
                Publisher: S. Karger AG
                ISSN (Print): 1424-862X
                ISSN (Electronic): 1424-8638
                Publication date Subscription-year: 2005
                Publication date (Print): June 2006
                Publication date (Electronic): 16 June 2006
                Volume: 14
                Issue: 6
                Pages: 273-280
                Affiliations
                Department of Physiology, Faculty of Medicine, The Chinese University of Hong Kong, Hong Kong, SAR, China
                Article
                Publisher ID: 93042 Other ID: Neurosignals 2005;14:273–280
                DOI: 10.1159/000093042
                PubMed ID: 16772730
                SO-VID: 00383ef6-f8e8-4b48-8f28-23f271d6d32b
                Copyright © © 2005 S. Karger AG, Basel
                License:

                Copyright: All rights reserved. No part of this publication may be translated into other languages, reproduced or utilized in any form or by any means, electronic or mechanical, including photocopying, recording, microcopying, or by any information storage and retrieval system, without permission in writing from the publisher. Drug Dosage: The authors and the publisher have exerted every effort to ensure that drug selection and dosage set forth in this text are in accord with current recommendations and practice at the time of publication. However, in view of ongoing research, changes in government regulations, and the constant flow of information relating to drug therapy and drug reactions, the reader is urged to check the package insert for each drug for any changes in indications and dosage and for added warnings and precautions. This is particularly important when the recommended agent is a new and/or infrequently employed drug. Disclaimer: The statements, opinions and data contained in this publication are solely those of the individual authors and contributors and not of the publishers and the editor(s). The appearance of advertisements or/and product references in the publication is not a warranty, endorsement, or approval of the products or services advertised or of their effectiveness, quality or safety. The publisher and the editor(s) disclaim responsibility for any injury to persons or property resulting from any ideas, methods, instructions or products referred to in the content or advertisements.

                History
                Date received : 15 August 2005
                Date accepted : 03 October 2005
                Page count
                Figures: 1, Tables: 3, References: 62, Pages: 8
                Categories
                Subject: Review

                ScienceOpen disciplines: Geriatric medicine,Neurology,Cardiovascular Medicine,Neurosciences,Clinical Psychology & Psychiatry,Public health
                Keywords: Phosphorylation,Ca2+ influx,TRP channels
                Data availability:
                ScienceOpen disciplines: Geriatric medicine, Neurology, Cardiovascular Medicine, Neurosciences, Clinical Psychology & Psychiatry, Public health
                Keywords: Phosphorylation, Ca2+ influx, TRP channels

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