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Updated: Oct 31, 2025

In vivo and in vitro Studies of Adaptor-clathrin Interaction
Published on: January 26, 2011
Antagonistic regulation controls clathrin-mediated endocytosis: AP2 adaptor facilitation vs restraint from clathrin
Lisa Redlingshöfer1, Frances M Brodsky1
1Research Department of Structural and Molecular Biology, Division of Biosciences, University College London, Gower Street, London WC1E 6BT, United Kingdom; Institute for Structural and Molecular Biology, Birkbeck and University College London, London WC1E 7HX, United Kingdom.
Abstract:
Orchestration of a complex network of protein interactions drives clathrin-mediated endocytosis (CME). A central role for the AP2 adaptor complex beyond cargo recognition and clathrin recruitment has emerged in recent years. It is now apparent that AP2 serves as a pivotal hub for protein interactions to mediate clathrin coated pit maturation, and couples lattice formation to membrane deformation. As a key driver for clathrin assembly, AP2 complements the attenuating role of clathrin light chain subunits, which enable dynamic lattice rearrangement needed for budding. This review summarises recent insights into AP2 function with respect to CME dynamics and biophysics, and its relationship to the role of clathrin light chains in clathrin assembly.
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