Feedback regulation of G protein-coupled receptor signaling by GRKs and arrestins.
Feedback regulation of G protein-coupled receptor signaling by GRKs and arrestins.
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DOI：
10.1016/j.semcdb.2015.12.015
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发表时间：
2016-02
影响因子：
7.3
通讯作者：
Daaka Y
中科院分区：
文献类型：
--
作者：
Black JB;Premont RT;Daaka Y
GPCR在哺乳动物细胞中普遍存在，并为细胞信号和通讯提供复杂的机制。从机制上讲，GPCR信号是通过受GRK和arrestin效应器负调控的异三聚体G蛋白在载体上发生的。新出现的证据突出了GRK和arrestin合作伙伴的其他作用，并确立了共同定义GPCR信号的相互关联的反馈途径的存在。GPCR影响细胞动力学，并可介导肿瘤和心血管重塑等病理发展。因此，更好地了解它们的整体信号调节具有很大的翻译兴趣，研究继续开发调节它们活动的药理学潜力。
GPCR are ubiquitous in mammalian cells and present intricate mechanisms for cellular signaling and communication. Mechanistically, GPCR signaling was identified to occur vectorially through heterotrimeric G proteins that are negatively regulated by GRK and arrestin effectors. Emerging evidence highlights additional roles for GRK and Arrestin partners, and establishes the existence of interconnected feedback pathways that collectively define GPCR signaling. GPCR influence cellular dynamics and can mediate pathologic development, such as cancer and cardiovascular remolding. Hence, a better understanding of their overall signal regulation is of great translational interest and research continues to exploit the pharmacologic potential for modulating their activity.