Endocytosis mediates the uptake of extracellular proteins, micronutrients and transmembrane cell surface proteins. Importantly, many viruses, toxins and bacteria hijack endocytosis to infect cells. The canonical pathway is clathrin-mediated endocytosis (CME) and is active in all eukaryotic cells to support critical house-keeping functions. Unconventional mechanisms of endocytosis exit in parallel of CME, to internalize specific cargoes and support various cellular functions. These clathrin-independent endocytic (CIE) routes use three distinct mechanisms: acute signaling-induced membrane remodeling drives macropinocytosis, activity-dependent bulk endocytosis (ADBE), massive endocytosis (MEND) and EGFR non-clathrin endocytosis (EGFR-NCE). Cargo capture and local membrane deformation by cytosolic proteins is used by fast endophilin-mediated endocytosis (FEME), IL-2Rβ endocytosis and ultrafast endocytosis at synapses. Finally, the formation of endocytic pits by clustering of extracellular lipids or cargoes according to the Glycolipid-Lectin (GL-Lect) hypothesis mediates the uptake of SV40 virus, Shiga and cholera toxins, and galectin-clustered receptors by the CLIC/GEEC and the endophilin-A3-mediated CIE.

胞吞作用介导细胞外蛋白质、微量营养素和跨膜细胞表面蛋白质的摄取。重要的是，许多病毒、毒素和细菌会劫持内吞作用来感染细胞。经典途径是网格蛋白介导的内吞作用 (CME)，在所有真核细胞中都很活跃，以支持关键的看家功能。内吞作用的非常规机制与 CME 并行退出，以内化特定的货物并支持各种细胞功能。这些不依赖网格蛋白的内吞 (CIE) 途径使用三种不同的机制：急性信号传导诱导的膜重塑驱动巨胞饮作用、活性依赖的大量内吞作用 (ADBE)、大量内吞作用 (MEND) 和 EGFR 非网格蛋白内吞作用 (EGFR-NCE)。细胞质蛋白的货物捕获和局部膜变形用于快速内皮素介导的内吞作用 (FEME)、IL-2Rβ 内吞作用和突触处的超快内吞作用。最后，根据糖脂-凝集素 (GL-Lect) 假说，通过细胞外脂质或货物聚集形成的内吞凹坑介导了 CLIC/GEEC 和内皮素-A3 介导的 CIE。