G 蛋白偶联受体信号的亚细胞结构组织。
Subcellular Organization of GPCR Signaling.
机构信息
Program in Biochemistry and Molecular Biology, University of California, San Francisco School of Medicine, San Francisco, CA 94158, USA.
Department of Psychiatry, University of California, San Francisco School of Medicine, San Francisco, CA 94158, USA; Department of Cellular and Molecular Pharmacology, University of California, San Francisco School of Medicine, San Francisco, CA 94158, USA.
出版信息
Trends Pharmacol Sci. 2018 Feb;39(2):200-208. doi: 10.1016/j.tips.2017.11.009. Epub 2018 Jan 28.
G protein-coupled receptors (GPCRs) comprise a large and diverse class of signal-transducing receptors that undergo dynamic and isoform-specific membrane trafficking. GPCRs thus have an inherent potential to initiate or regulate signaling reactions from multiple membrane locations. This review discusses emerging insights into the subcellular organization of GPCR function in mammalian cells, focusing on signaling transduced by heterotrimeric G proteins and β-arrestins. We summarize recent evidence indicating that GPCR-mediated activation of G proteins occurs not only from the plasma membrane (PM) but also from endosomes and Golgi membranes and that β-arrestin-dependent signaling can be transduced from the PM by β-arrestin trafficking to clathrin-coated pits (CCPs) after dissociation from a ligand-activated GPCR.
G 蛋白偶联受体（GPCRs）是一大类多样化的信号转导受体，它们经历动态的、亚型特异性的膜运输。因此，GPCR 具有从多个膜位置起始或调节信号反应的固有潜力。本综述讨论了哺乳动物细胞中 GPCR 功能的亚细胞组织的新见解，重点是异三聚体 G 蛋白和β-arrestin 转导的信号。我们总结了最近的证据，表明 GPCR 介导的 G 蛋白的激活不仅发生在质膜（PM）上，也发生在内体和高尔基体膜上，并且β-arrestin 依赖性信号可以通过β-arrestin 从 PM 转导，在与配体激活的 GPCR 解离后，β-arrestin 被运送到网格蛋白包被的凹陷（CCPs）。
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