Tctex-1 augments G protein-coupled receptor-mediated G s signaling by activating adenylyl cyclase.

Autor: Saito M; Department of Molecular Pharmacology, Tohoku University Graduate School of Medicine, Sendai, 980-8575, Japan; Department of Cellular Signaling, Graduate School of Pharmaceutical Sciences, Tohoku University, Sendai, 980-8578, Japan. Electronic address: saimasa@med.tohoku.ac.jp., Chiba A; Department of Cellular Signaling, Graduate School of Pharmaceutical Sciences, Tohoku University, Sendai, 980-8578, Japan., Sato T; Department of Molecular Pharmacology, Tohoku University Graduate School of Medicine, Sendai, 980-8575, Japan., Moriya T; Department of Cellular Signaling, Graduate School of Pharmaceutical Sciences, Tohoku University, Sendai, 980-8578, Japan., Sukegawa J; Department of Molecular Pharmacology, Tohoku University Graduate School of Medicine, Sendai, 980-8575, Japan; Department of Human Health and Nutrition, Shokei Gakuin University, Natori, 981-1295, Japan., Nakahata N; Department of Cellular Signaling, Graduate School of Pharmaceutical Sciences, Tohoku University, Sendai, 980-8578, Japan.
Jazyk: angličtina
Zdroj: Journal of pharmacological sciences [J Pharmacol Sci] 2021 Jan; Vol. 145 (1), pp. 150-154. Date of Electronic Publication: 2020 Nov 27.
DOI: 10.1016/j.jphs.2020.11.011
Abstrakt: Proteins interacting with G protein-coupled receptors (GPCRs) can modulate signal transduction of these receptors. However, the regulatory mechanisms of the interacting proteins are diverse and largely unknown. We have previously shown that Tctex-1 (or DYNLT1) can interact with the parathyroid hormone receptor (PTHR). In the present study, we investigated the role of Tctex-1 in the PTHR signaling and found that Tctex-1 augmented the PTHR-mediated G s /adenylyl cyclase (AC) pathway by activating AC regardless of the binding to PTHR. Furthermore, Tctex-1 directly bound to AC type 6. These data demonstrate a novel mechanism underlying GPCR/G s signaling regulated by Tctex-1.
Competing Interests: Declaration of competing interest The authors declare no conflict of interest.
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Databáze: MEDLINE
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