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Original Article

Korean J Physiol Pharmacol 2019; 23(5): 357-366

Published online September 1, 2019

Copyright © Korean J Physiol Pharmacol.

Identification of phospholipase C β downstream effect on transient receptor potential canonical 1/4, transient receptor potential canonical 1/5 channels

Juyeon Ko1,#, Jongyun Myeong1,2,#, Misun Kwak1, Ju-Hong Jeon1, and Insuk So1,*

1Department of Physiology, Seoul National University College of Medicine, Seoul 03080, Korea, 2Department of Physiology and Biophysics, University of Washington School of Medicine, Seattle, WA 98195, USA

Correspondence to:*Insuk So, E-mail:

#These authors contributed equally to this work.

Received: June 17, 2019; Revised: July 25, 2019; Accepted: July 26, 2019

This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License, which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.


q-coupled receptor stimulation was implied in the activation process of transient receptor potential canonical (TRPC)1/4 and TRPC1/5 heterotetrameric channels. The inactivation occurs due to phosphatidylinositol 4,5-biphosphate (PI(4,5)P2) depletion. When PI(4,5)P2 depletion was induced by muscarinic stimulation or inositol polyphosphate 5-phosphatase (Inp54p), however, the inactivation by muscarinic stimulation was greater compared to that by Inp54p. The aim of this study was to investigate the complete inactivation mechanism of the heteromeric channels upon Gαq-phospholipase C β (Gαq-PLCβ) activation. We evaluated the activity of heteromeric channels with electrophysiological recording in HEK293 cells expressing TRPC channels. TRPC1/4 and TRPC1/5 heteromers undergo further inhibition in PLCβ activation and calcium/protein kinase C (PKC) signaling. Nevertheless, the key factors differ. For TRPC1/4, the inactivation process was facilitated by Ca2+ release from the endoplasmic reticulum, and for TRPC1/5, activation of PKC was concerned mostly. We conclude that the subsequent increase in cytoplasmic Ca2+ due to Ca2+ release from the endoplasmic reticulum and activation of PKC resulted in a second phase of channel inhibition following PI(4,5)P2 depletion.

Keywords: Calcium, GTP-binding proteins, Protein kinase C, Transient receptor potential channels, Type C phospholipases