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

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 hormo...

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Bibliographic Details
Main Authors: Masaki Saito, Ayano Chiba, Takeya Sato, Takahiro Moriya, Jun Sukegawa, Norimichi Nakahata
Format: Article
Language:English
Published: Elsevier 2021-01-01
Series:Journal of Pharmacological Sciences
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Online Access:http://www.sciencedirect.com/science/article/pii/S1347861320301171
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Summary: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 Gs/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/Gs signaling regulated by Tctex-1.
ISSN:1347-8613