Tctex-1 augments G protein-coupled receptor-mediated Gs signaling by activating adenylyl cyclase
Tctex-1 augments G protein-coupled receptor-mediated Gs signaling by activating adenylyl cyclase
复制标题
Tctex-1 通过激活腺苷酸环化酶增强 G 蛋白偶联受体介导的 Gs 信号传导
DOI：
10.1016/j.jphs.2020.11.011
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发表时间：
2021
影响因子：
3.5
通讯作者：
Nakahata Norimichi
中科院分区：
文献类型：
--
作者：
Saito Masaki;Chiba Ayano;Sato Takeya;Moriya Takahiro;Sukegawa Jun;Nakahata Norimichi
与G蛋白偶联受体（GPCRs）相互作用的蛋白质可以调节这些受体的信号转导。然而，相互作用的蛋白质的调节机制是多种多样的，在很大程度上是未知的。我们以前已经表明，Tctex-1（或DYNLT 1）可以与甲状旁腺激素受体（PTHR）相互作用。在本研究中，我们研究了Tctex-1在PTHR信号转导中的作用，发现Tctex-1通过激活AC而增强PTHR介导的Gs/腺苷酸环化酶（AC）通路，而不管与PTHR的结合如何。此外，Tctex-1直接与AC 6型结合。这些数据证明了Tctex-1调控GPCR/GS信号转导的一种新机制。
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/Gssignaling regulated by Tctex-1.