Dong Chunmin, Filipeanu Catalin M, Duvernay Matthew T, Wu Guangyu
Department of Pharmacology and Experimental Therapeutics, Louisiana State University Health Sciences Center, New Orleans, LA 70112, USA.
Biochim Biophys Acta. 2007 Apr;1768(4):853-70. doi: 10.1016/j.bbamem.2006.09.008. Epub 2006 Sep 23.
G protein-coupled receptors (GPCRs) constitute a superfamily of cell-surface receptors which share a common topology of seven transmembrane domains and modulate a variety of cell functions through coupling to heterotrimeric G proteins by responding to a vast array of stimuli. The magnitude of cellular response elicited by a given signal is dictated by the level of GPCR expression at the plasma membrane, which is the balance of elaborately regulated endocytic and exocytic trafficking. This review will cover recent advances in understanding the molecular mechanism underlying anterograde transport of the newly synthesized GPCRs from the endoplasmic reticulum (ER) through the Golgi to the plasma membrane. We will focus on recently identified motifs involved in GPCR exit from the ER and the Golgi, GPCR folding in the ER and the rescue of misfolded receptors from within, GPCR-interacting proteins that modulate receptor cell-surface targeting, pathways that mediate GPCR traffic, and the functional role of export in controlling GPCR signaling.
G蛋白偶联受体（GPCRs）构成了一个细胞表面受体超家族，它们具有共同的七跨膜结构域拓扑结构，并通过与异源三聚体G蛋白偶联，对大量刺激作出反应，从而调节多种细胞功能。给定信号引发的细胞反应强度取决于质膜上GPCR的表达水平，而这是精细调控的内吞和外排运输平衡的结果。本综述将涵盖在理解新合成的GPCR从内质网（ER）通过高尔基体向前运输到质膜的分子机制方面的最新进展。我们将重点关注最近确定的参与GPCR从ER和高尔基体输出的基序、ER中GPCR的折叠以及从内部挽救错误折叠的受体、调节受体细胞表面靶向的GPCR相互作用蛋白、介导GPCR运输的途径，以及输出在控制GPCR信号传导中的功能作用。
