Tctex-1 通过激活腺苷酸环化酶增强 G 蛋白偶联受体介导的 G 信号转导。
Tctex-1 augments G protein-coupled receptor-mediated G signaling by activating adenylyl cyclase.
机构信息
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.
Department of Cellular Signaling, Graduate School of Pharmaceutical Sciences, Tohoku University, Sendai, 980-8578, Japan.
出版信息
J Pharmacol Sci. 2021 Jan;145(1):150-154. doi: 10.1016/j.jphs.2020.11.011. Epub 2020 Nov 27.
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/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 signaling regulated by Tctex-1.
与 G 蛋白偶联受体 (GPCR) 相互作用的蛋白质可以调节这些受体的信号转导。然而，相互作用蛋白质的调节机制多种多样，在很大程度上尚不清楚。我们之前已经表明 Tctex-1（或 DYNLT1）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 来增强 PTHR 介导的 G/腺苷酸环化酶 (AC) 途径，而不依赖于与 PTHR 的结合。此外，Tctex-1 直接与 AC 类型 6 结合。这些数据表明 Tctex-1 调节 GPCR/G 信号的一种新机制。
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