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Sci Rep. 2018 Aug 14;8(1):12117. doi: 10.1038/s41598-018-30625-0.

Dual action of the Gαq-PLCβ-PI(4,5)P2 pathway on TRPC1/4 and TRPC1/5 heterotetramers.

Author information

1
Department of Physiology, Seoul National University College of Medicine, Seoul, 03080, Republic of Korea.
2
Department of Physiology and Biophysics, University of Washington School of Medicine, Seattle, WA, 98195, USA.
3
Department of Physiology, Chosun University School of Medicine, Kwangju, 61452, Republic of Korea.
4
Department of Physiology, Gachon University College of Medicine, Incheon, 21936, Republic of Korea.
5
Department of Physiology, Sungkyunkwan University School of Medicine, Suwon, 16419, Republic of Korea. kimhyunjin@skku.edu.
6
Department of Physiology, Seoul National University College of Medicine, Seoul, 03080, Republic of Korea. insuk@snu.ac.kr.

Abstract

The transient receptor potential canonical (TRPC) 1 channel is widely distributed in mammalian cells and is involved in many physiological processes. TRPC1 is primarily considered a regulatory subunit that forms heterotetrameric channels with either TRPC4 or TRPC5 subunits. Here, we suggest that the regulation of TRPC1/4 and TRPC1/5 heterotetrameric channels by the Gαq-PLCβ pathway is self-limited and dynamically mediated by Gαq and PI(4,5)P2. We provide evidence indicating that Gαq protein directly interacts with either TRPC4 or TRPC5 of the heterotetrameric channels to permit activation. Simultaneously, Gαq-coupled PLCβ activation leads to the breakdown of PI(4,5)P2, which inhibits activity of TRPC1/4 and 1/5 channels.

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