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• W4225133075 abstract "Clathrin-mediated endocytosis (CME) is the main mechanism by which mammalian cells control their cell surface proteome. Proper operation of the pivotal CME cargo adaptor AP2 requires membrane-localized Fer/Cip4 homology domain-only proteins (FCHO). Here, live-cell enhanced total internal reflection fluorescence–structured illumination microscopy shows that FCHO marks sites of clathrin-coated pit (CCP) initiation, which mature into uniform-sized CCPs comprising a central patch of AP2 and clathrin corralled by an FCHO/Epidermal growth factor potential receptor substrate number 15 (Eps15) ring. We dissect the network of interactions between the FCHO interdomain linker and AP2, which concentrates, orients, tethers, and partially destabilizes closed AP2 at the plasma membrane. AP2’s subsequent membrane deposition drives its opening, which triggers FCHO displacement through steric competition with phosphatidylinositol 4,5-bisphosphate, clathrin, cargo, and CME accessory factors. FCHO can now relocate toward a CCP’s outer edge to engage and activate further AP2s to drive CCP growth/maturation." @default.
• W4225133075 created "2022-05-01" @default.
• W4225133075 creator A5005955851 @default.
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• W4225133075 creator A5076814516 @default.
• W4225133075 creator A5079022054 @default.
• W4225133075 creator A5081228886 @default.
• W4225133075 date "2022-04-29" @default.
• W4225133075 modified "2023-09-30" @default.
• W4225133075 title "FCHO controls AP2’s initiating role in endocytosis through a PtdIns(4,5)P ₂ -dependent switch" @default.
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