Mechanisms of the anterograde trafficking of GPCRs: Regulation of AT1R transport by interacting proteins and motifs
Mechanisms of the anterograde trafficking of GPCRs: Regulation of AT1R transport by interacting proteins and motifs
复制标题
GPCR 顺行运输的机制：通过相互作用的蛋白质和基序调节 AT1R 运输
作者：
Zhang Maoxiang;Wu Guangyu
新生G蛋白偶联受体（GPCR）在从内质网（ER）通过高尔基体的途中的顺行细胞表面转运代表了控制功能目的地的受体量和受体活化引起的细胞反应的强度的关键检查点。然而，与广泛研究的内化和再循环过程相比，GPCR的细胞表面运输的分子机制相对较少定义。在这里，我们将回顾目前的进展，了解ER-高尔基体细胞表面转运的GPCR和使用血管紧张素II 1型受体作为代表GPCR讨论受体相互作用蛋白和特定的基序嵌入在控制GPCR的前向交通沿着生物合成途径的受体中的新兴作用。
Anterograde cell surface transport of nascent G protein‐coupled receptors (GPCRs) en route from the endoplasmic reticulum (ER) through the Golgi apparatus represents a crucial checkpoint to control the amount of the receptors at the functional destination and the strength of receptor activation‐elicited cellular responses. However, as compared with extensively studied internalization and recycling processes, the molecular mechanisms of cell surface trafficking of GPCRs are relatively less defined. Here, we will review the current advances in understanding the ER‐Golgi‐cell surface transport of GPCRs and use angiotensin II type 1 receptor as a representative GPCR to discuss emerging roles of receptor‐interacting proteins and specific motifs embedded within the receptors in controlling the forward traffic of GPCRs along the biosynthetic pathway.