Ferguson S S, Caron M G
John P. Robarts Research Institute, London, Ontario, Canada.
Semin Cell Dev Biol. 1998 Apr;9(2):119-27. doi: 10.1006/scdb.1997.0216.
G protein-coupled receptors (GPCRs) transduce extracellular signals that modulate the activity of a wide variety of biological processes, such as neurotransmission, chemoattraction, cardiac function, olfaction, and vision. However, GPCR signalling desensitizes rapidly as the consequence of receptor phosphorylation. G protein-coupled receptor kinase-mediated receptor phosphorylation promotes the binding of beta-arrestin proteins, which not only uncouple GPCRs from their cognate heterotrimeric G protein, but also target them for endocytosis. The sequestration (endocytosis) of desensitized GPCRs to endosomes is required for their dephosphorylation and subsequent resensitization to their pre-ligand exposed state. This review concentrates on the mechanisms underlying GPCR desensitization and resensitization.
G蛋白偶联受体（GPCRs）转导细胞外信号，调节多种生物过程的活性，如神经传递、化学吸引、心脏功能、嗅觉和视觉。然而，由于受体磷酸化，GPCR信号会迅速脱敏。G蛋白偶联受体激酶介导的受体磷酸化促进β-抑制蛋白的结合，β-抑制蛋白不仅使GPCRs与其同源异源三聚体G蛋白解偶联，还将它们靶向内吞作用。脱敏的GPCRs被隔离（内吞）到内体中，这是它们去磷酸化并随后重新敏感到配体暴露前状态所必需的。本综述集中于GPCR脱敏和重新敏感化的潜在机制。
