Beta-arrestin acts as a clathrin adaptor in endocytosis of the beta2-adrenergic receptor.

摘要: The ability of a system to regulate its responsiveness in the presence continuous stimulus, often termed desensitization, has been extensively characterized for beta2-adrenergic receptor (beta2AR). beta2AR signalling is rapidly attenuated through phosphorylation and subsequent binding protein beta-arrestin. Ultimately undergoes internalization, although molecular mechanism unclear, beta-arrestin have implicated this processs. Here we report that arrestin-3, but not visual arrestin, promote internalization bind with high affinity directly stoichiometrically clathrin, major structural coated pits. Moreover, beta-arrestin/arrestin chimaeras are defective either or clathrin show reduced endocytosis. Immunofluorescence microscopy intact cells indicates an agonist-dependent colocalization clathrin. These results functions as adaptor receptor-mediated endocytosis pathway, suggest general regulating trafficking G-protein-coupled receptors.