Clathrin and AP2 Sites in the CTail

Clathrin and AP2 binding sites in the arrestin C-tail were localized with high precision (Kim and Benovic 2002). Over-expressed arrestin C-tail binds clathrin and AP2, effectively functioning as a competitive suppressor of arrestin-dependent GPCR internalization (Orsini and Benovic 1998), suggesting that small molecule mimics of these two sites can be quite effective. However, pharmacological disruption of these interactions would unavoidably affect the internalization of all GPCRs in the cell, which reduces their appeal as possible therapeutic targets.

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