Department of Cellular and Molecular Medicine, Howard Hughes Medical Institute, University of California at San Diego, La Jolla, CA 92093, USA.
Cold Spring Harb Perspect Biol. 2013 Feb 1;5(2):a013367. doi: 10.1101/cshperspect.a013367.
Protein egress from the endoplasmic reticulum (ER) is driven by a conserved cytoplasmic coat complex called the COPII coat. The COPII coat complex contains an inner shell (Sec23/Sec24) that sorts cargo into ER-derived vesicles and an outer cage (Sec13/Sec31) that leads to coat polymerization. Once released from the ER, vesicles must tether to and fuse with the target membrane to deliver their protein and lipid contents. This delivery step also depends on the COPII coat, with coat proteins binding directly to tethering and regulatory factors. Recent findings have yielded new insight into how COPII-mediated vesicle traffic is regulated. Here we discuss the molecular basis of COPII-mediated ER-Golgi traffic, focusing on the surprising complexity of how ER-derived vesicles form, package diverse cargoes, and correctly target these cargoes to their destination.
蛋白质从内质网（ER）中排出是由一种称为 COPII 衣被的保守细胞质衣被复合物驱动的。COPII 衣被复合物包含一个将货物分拣到 ER 衍生小泡中的内壳（Sec23/Sec24）和一个导致衣被聚合的外壳（Sec13/Sec31）。从小泡从 ER 释放出来后，小泡必须与靶膜结合并融合以输送其蛋白质和脂质内容物。这个输送步骤也依赖于 COPII 衣被，衣被蛋白直接与停泊和调节因子结合。最近的发现为 COPII 介导的小泡运输如何被调节提供了新的见解。在这里，我们讨论了 COPII 介导的 ER-Golgi 运输的分子基础，重点讨论了 ER 衍生小泡形成、包装不同货物以及将这些货物正确靶向其目的地的惊人复杂性。
