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Gβγ如何将Gα偶联到GPCR的模型。

The Journal of General Physiology Pub Date : 2022-05-02 Epub Date: 2022-03-25 DOI:10.1085/jgp.202112982
William E McIntire
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引用次数: 4

摘要

g蛋白偶联受体(gpcr)占人类基因组的约5%，是药物发现的主要靶点;然而，它们如何与异三聚体G蛋白亚基偶联的分子细节尚不完全清楚。在这里，我提出了一个假设的GPCR与Gβγ相遇的初始对接模型，该模型由GPCR的细胞质表面与Gγ亚基c端的丙烯基部分和三肽基，天冬氨酸-脯氨酸-苯丙氨酸(NPF)之间的短暂相互作用定义。对A类gpcr的分析揭示了一个由TM1和H8相互作用形成的保守的NPF结合位点。利用差异戊烯基化蛋白和肽的功能研究进一步表明，GPCR的细胞内疏水核心是一个戊烯基结合位点。结合GPCR的TM1和H8后，Gγ的c端区转化为α螺旋的倾向使其能够延伸到GPCR的疏水核心，促进GPCR的活性状态。GPCR-G蛋白信号转导的一般机制是GPCR-G蛋白亚型中NPF基序的保护以及TM1和H8中相互作用残基的保护。对视紫红质二聚体的分析也表明，g - γ-视紫红质相互作用可能促进GPCR二聚体的反激活。
本文章由计算机程序翻译，如有差异，请以英文原文为准。

A model for how Gβγ couples Gα to GPCR.

A model for how Gβγ couples Gα to GPCR.

A model for how Gβγ couples Gα to GPCR.

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A model for how Gβγ couples Gα to GPCR.
The heterotrimeric G protein contains an α subunit and βγ dimer, which relay signals from G-protein-coupled receptors (GPCRs) to the intracellular milieu. McIntire proposes a model in which initial interactions between Gβγ and GPCR prime the receptor for subsequent interactions with Gα.
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The Journal of General Physiology
The Journal of General Physiology
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