Activity of T-type calcium channels is independent of CRMP2 in sensory neurons
Name:
Activity of T type calcium ...
Size:
1.239Mb
Format:
PDF
Description:
Final Published Version
Affiliation
Univ Arizona Hlth Sci, Coll Med, Dept PharmacolIssue Date
2019-04-26
Metadata
Show full item recordPublisher
TAYLOR & FRANCIS INCCitation
Cai, S., Shan, Z., Zhang, Z., Moutal, A., & Khanna, R. (2019). Activity of T-type calcium channels is independent of CRMP2 in sensory neurons. Channels, 13(1), 147-152.Journal
CHANNELSRights
Copyright © 2019 The Author(s). Published by Informa UK Limited, trading as Taylor & Francis Group. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0/).Collection Information
This item from the UA Faculty Publications collection is made available by the University of Arizona with support from the University of Arizona Libraries. If you have questions, please contact us at repository@u.library.arizona.edu.Abstract
Amongst the regulators of voltage-gated ion channels is the collapsin response mediator protein 2 (CRMP2). CRMP2 regulation of the activity and trafficking of NaV1.7 voltage-gated sodium channels as well as the N-type (CaV2.2) voltage-gated calcium channel (VGCC) has been reported. On the other hand, CRMP2 does not appear to regulate L- (CaV1.x), P/Q- (CaV2.1), and R- (CaV2.3) type high VGCCs. Whether CRMP2 regulates low VGCCs remains an open question. Here, we asked if CRMP2 could regulate the low voltage-gated (T-type/CaV3.x) channels in sensory neurons. Reducing CRMP2 protein levels with short interfering RNAs yielded no change in macroscopic currents carried by T-type channels. No change in biophysical properties of the T-type currents was noted. Future studies pursuing CRMP2 druggability in neuropathic pain will benefit from the findings that CRMP2 regulates only the N-type (CaV2.2) calcium channels.Note
Open access journalISSN
1933-6950PubMed ID
31025580Version
Final published versionSponsors
Guangdong Medical Research Foundation [A2017047]; National Institute of Neurological Disorders and Stroke [R01NS098772]; National Institute on Drug Abuse [R01DA042852]ae974a485f413a2113503eed53cd6c53
10.1080/19336950.2019.1608129
Scopus Count
Collections
Except where otherwise noted, this item's license is described as Copyright © 2019 The Author(s). Published by Informa UK Limited, trading as Taylor & Francis Group. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0/).
Related articles
- Inhibition of the Ubc9 E2 SUMO-conjugating enzyme-CRMP2 interaction decreases NaV1.7 currents and reverses experimental neuropathic pain.
- Authors: François-Moutal L, Dustrude ET, Wang Y, Brustovetsky T, Dorame A, Ju W, Moutal A, Perez-Miller S, Brustovetsky N, Gokhale V, Khanna M, Khanna R
- Issue date: 2018 Oct
- A membrane-delimited N-myristoylated CRMP2 peptide aptamer inhibits CaV2.2 trafficking and reverses inflammatory and postoperative pain behaviors.
- Authors: François-Moutal L, Wang Y, Moutal A, Cottier KE, Melemedjian OK, Yang X, Wang Y, Ju W, Largent-Milnes TM, Khanna M, Vanderah TW, Khanna R
- Issue date: 2015 Jul
- Regulation of N-type voltage-gated calcium channels (Cav2.2) and transmitter release by collapsin response mediator protein-2 (CRMP-2) in sensory neurons.
- Authors: Chi XX, Schmutzler BS, Brittain JM, Wang Y, Hingtgen CM, Nicol GD, Khanna R
- Issue date: 2009 Dec 1
- CRMP2 protein SUMOylation modulates NaV1.7 channel trafficking.
- Authors: Dustrude ET, Wilson SM, Ju W, Xiao Y, Khanna R
- Issue date: 2013 Aug 23
- Phosphorylated CRMP2 Regulates Spinal Nociceptive Neurotransmission.
- Authors: Yu J, Moutal A, Dorame A, Bellampalli SS, Chefdeville A, Kanazawa I, Pham NYN, Park KD, Weimer JM, Khanna R
- Issue date: 2019 Jul