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Open AccessReview

Post-Translational Modification and Natural Mutation of TRPC Channels

by Xianji Liu 1, Xiaoqiang Yao 2 and Suk Ying Tsang 1,3,4,5,*
1
School of Life Sciences, The Chinese University of Hong Kong, Hong Kong, China
2
School of Biomedical Sciences, The Chinese University of Hong Kong, Hong Kong, China
3
State Key Laboratory of Agrobiotechnology, The Chinese University of Hong Kong, Hong Kong, China
4
Key Laboratory for Regenerative Medicine, Ministry of Education, The Chinese University of Hong Kong, Hong Kong, China
5
The Institute for Tissue Engineering and Regenerative Medicine (iTERM), The Chinese University of Hong Kong, Hong Kong, China
*
Author to whom correspondence should be addressed.
Cells 2020, 9(1), 135; https://doi.org/10.3390/cells9010135 (registering DOI)
Received: 30 November 2019 / Revised: 3 January 2020 / Accepted: 3 January 2020 / Published: 7 January 2020
(This article belongs to the Special Issue TRPC Channels)
Transient Receptor Potential Canonical (TRPC) channels are homologues of Drosophila TRP channel first cloned in mammalian cells. TRPC family consists of seven members which are nonselective cation channels with a high Ca2+ permeability and are activated by a wide spectrum of stimuli. These channels are ubiquitously expressed in different tissues and organs in mammals and exert a variety of physiological functions. Post-translational modifications (PTMs) including phosphorylation, N-glycosylation, disulfide bond formation, ubiquitination, S-nitrosylation, S-glutathionylation, and acetylation play important roles in the modulation of channel gating, subcellular trafficking, protein-protein interaction, recycling, and protein architecture. PTMs also contribute to the polymodal activation of TRPCs and their subtle regulation in diverse physiological contexts and in pathological situations. Owing to their roles in the motor coordination and regulation of kidney podocyte structure, mutations of TRPCs have been implicated in diseases like cerebellar ataxia (moonwalker mice) and focal and segmental glomerulosclerosis (FSGS). The aim of this review is to comprehensively integrate all reported PTMs of TRPCs, to discuss their physiological/pathophysiological roles if available, and to summarize diseases linked to the natural mutations of TRPCs. View Full-Text
Keywords: transient receptor potential canonical channel; post-translational modification; natural mutation transient receptor potential canonical channel; post-translational modification; natural mutation
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Liu, X.; Yao, X.; Tsang, S.Y. Post-Translational Modification and Natural Mutation of TRPC Channels. Cells 2020, 9, 135.

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