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首页> 外文期刊>Life sciences >Novel roles for arrestins in the post-endocytic trafficking of G protein-coupled receptors.
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Novel roles for arrestins in the post-endocytic trafficking of G protein-coupled receptors.

机译：抑制蛋白在G蛋白偶联受体的内吞后运输中的新作用。

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摘要

G protein-coupled receptors (GPCRs) represent the largest family of transmembrane signaling molecules in the human genome. As such, they interact with numerous intracellular molecules, which can act either to propagate or curtail signaling from the receptor. Their primary mode of cellular activation occurs through heterotrimeric G proteins, which in turn can activate a wide spectrum of effector molecules, including phosphodiesterases, phospholipases, adenylyl cyclases and ion channels. Active GPCRs are also the target of G protein-coupled receptor kinases, which phosphorylate the receptors culminating in the binding of the protein arrestin. This results in rapid desensitization through inhibition of G protein binding, as well as novel mechanisms of cellular activation that involve the scaffolding of cellular kinases to GPCR-arrestin complexes. Arrestins can also serve to mediate the internalization of certain GPCRs, a process which plays an important role in regulating cellular activity both by mediating long-term desensitization through down regulation (degradation) of receptors and by recycling desensitized receptors back to the cell surface to initiate additional rounds of signaling. The mechanisms that regulate the subsequent intracellular trafficking of GPCRs following internalization are largely unknown. Recently however, it has become clear that the pattern of receptor phosphorylation and subsequent binding of arrestin play a critical role in the intracellular trafficking of internalized receptors, thereby dictating the ultimate fate of the receptor. In addition, arrestins have now been shown to be required for the recycling of GPCRs that are capable of internalizing through arrestin-independent mechanisms. This review will summarize recent advances in our understanding of the roles of arrestins in post-endocytic GPCR trafficking.
机译：G蛋白偶联受体（GPCR）代表了人类基因组中最大的跨膜信号分子家族。因此，它们与众多细胞内分子相互作用，这些分子可以起到传播或减少来自受体的信号传导的作用。它们的细胞激活的主要模式是通过异源三聚体G蛋白发生的，后者可以激活多种效应分子，包括磷酸二酯酶，磷脂酶，腺苷酸环化酶和离子通道。活性GPCR也是G蛋白偶联受体激酶的靶标，该受体激酶使受体磷酸化，最终使蛋白抑制素结合。这会通过抑制G蛋白结合而导致快速脱敏，以及涉及细胞激酶与GPCR-arrestin复合物的支架作用的新型细胞活化机制。抑制蛋白还可以用于介导某些GPCR的内在化，这一过程在调节细胞活性中起着重要作用，通过介导受体的下调（降解）介导长期的脱敏作用，以及通过将脱敏的受体循环回细胞表面以启动该过程额外的信号回合。内在化后调节随后的GPCR的细胞内运输的机制很大程度上未知。然而，最近，已经清楚的是，受体磷酸化的模式和随后的抑制蛋白结合在内化受体的细胞内运输中起关键作用，从而决定了受体的最终命运。此外，现已显示，抑制蛋白必须回收能够通过不依赖抑制蛋白的机制进行内在化的GPCR。这篇综述将总结我们对抑制蛋白在内吞后GPCR交易中的作用的最新进展。

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