Clathrin-mediated endocytosis is the main entry route for most cell surface receptors and their ligands. It is regulated by clathrin-coated structures that are endowed with the ability to cluster receptors and to locally bend the plasma membrane, resulting in the formation of receptor-containing vesicles that bud into the cytoplasm. This canonical role of clathrin-coated structures has been shown to play a fundamental part in many different aspects of cell physiology. However, it has recently become clear that the ability of clathrin-coated structures to deform membranes can be perturbed. In addition to chemical or genetic alterations, numerous environmental conditions can physically prevent or slow down membrane bending and/or budding at clathrin-coated structures. The resulting 'frustrated endocytosis' is emerging as not merely a passive consequence, but one that actually fulfils some very specific and important cellular functions. In this Review, we provide an historical and defining perspective on frustrated endocytosis in the clathrin pathway of mammalian cells, before discussing its causes and highlighting the possible functional consequences in physiology and diseases.

中文翻译：

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受挫的网格蛋白介导的内吞作用 - 原因和可能的功能。

网格蛋白介导的内吞作用是大多数细胞表面受体及其配体的主要进入途径。它受网格蛋白包被结构的调节，该结构具有聚集受体和局部弯曲质膜的能力，从而导致形成含受体的囊泡，这些囊泡在细胞质中出芽。网格蛋白涂层结构的这种典型作用已被证明在细胞生理学的许多不同方面发挥着重要作用。然而，最近已经很清楚，网格蛋白涂层结构使膜变形的能力可能会受到干扰。除了化学或遗传改变之外，许多环境条件可以在物理上阻止或减缓膜弯曲和/或网格蛋白涂层结构的出芽。由此产生的“受挫的内吞作用” 正在出现的不仅仅是一种被动的结果，而是一种实际上实现了一些非常具体和重要的细胞功能的结果。在这篇综述中，在讨论其原因并强调生理学和疾病中可能的功能后果之前，我们提供了关于哺乳动物细胞网格蛋白途径中受挫的内吞作用的历史和定义观点。