The process by which clathrin-coated vesicles are produced involves interactions of multifunctional adaptor proteins with the plasma membrane, as well as with clathrin and several accessory proteins and phosphoinositides. Here we review recent findings highlighting new insights into mechanisms underlying clathrin-dependent endocytosis.

Abbreviations used: ANTH, AP180 N-terminal homology; AP, adaptor (or assembly) protein; CALM, clathrin assembly lymphoid myeloid leukaemia; CIN85, Cbl-interacting protein of 85 kDa; Dab2, Disabled protein 2; E1, ubiquitin-activating enzyme; E2, ubiquitin-conjugating enzyme; E3, ubiquitin ligase; EGF, epidermal growth factor; EH, Eps15 homology; ENTH, Epsin N-terminal homology; Epsin, Eps15-interacting protein; GED, GTPase effector domain; GH, growth hormone; GPCR, G-protein-coupled receptor; HIP1, huntingtin-interacting protein; JAK, Janus kinase; LDL, low-density lipoprotein; LPA, lysophosphatidic acid; PA, phosphatidic acid; PH, pleckstrin homology; PRD, proline-rich domain; PTB domain, phosphotyrosine-binding domain; RTK, receptor tyrosine kinase; SH2, Src homology 2; SH3, Src homology 3; Tf, transferrin; TGN, trans-Golgi network; UIM, ubiquitin-interacting motif.

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