Regulation of Clathrin-Mediated Endocytosis.
Regulation of Clathrin-Mediated Endocytosis.
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DOI：
10.1146/annurev-biochem-062917-012644
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发表时间：
2018-06-20
影响因子：
16.6
通讯作者：
Schmid SL
中科院分区：
文献类型：
--
作者：
Mettlen M;Chen PH;Srinivasan S;Danuser G;Schmid SL
网格蛋白介导的内吞作用（CME）是哺乳动物细胞内吞的主要途径。它负责跨膜受体和转运蛋白的摄取，响应环境变化重塑质膜组成，以及调节细胞表面信号传导。CME通过网格蛋白包被的小凹的组装和成熟而发生，所述小凹在它们内陷和夹断以形成网格蛋白包被的囊泡时集中货物。除了主要的外壳蛋白，网格蛋白和衔接蛋白复合物，CME需要大量的内吞辅助蛋白和磷脂酰肌醇脂质。CME在多个步骤中受到调节-起始，货物选择，成熟和分裂-并且通过诱导有缺陷的坑的拆卸的内吞检查点来监测。通过翻译后修饰、变构构象变化以及CME机制（包括GT3发动蛋白）组分之间的同种型和剪接变体差异进行调节。本文综述了近年来对CME的调控和这一复杂过程的演变的研究结果。
Clathrin-mediated endocytosis (CME) is the major endocytic pathway in mammalian cells. It is responsible for the uptake of transmembrane receptors and transporters, for remodeling plasma membrane composition in response to environmental changes, and for regulating cell surface signaling. CME occurs via the assembly and maturation of clathrin-coated pits that concentrate cargo as they invaginate and pinch off to form clathrin-coated vesicles. In addition to the major coat proteins, clathrin triskelia and adaptor protein complexes, CME requires a myriad of endocytic accessory proteins and phosphatidylinositol lipids. CME is regulated at multiple steps—initiation, cargo selection, maturation, and fission—and is monitored by an endocytic checkpoint that induces disassembly of defective pits. Regulation occurs via posttranslational modifications, allosteric conformational changes, and isoform and splice-variant differences among components of the CME machinery, including the GTPase dynamin. This review summarizes recent findings on the regulation of CME and the evolution of this complex process.