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Cagdas Devrim Son

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A small molecule enhances arrestin-3 binding to the β2-adrenergic receptor - Communications Chemistry

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By Han Kurt, Ali Akyol, Chen Zheng, Massimiliano Meli, Erica Elisa Ferrandi, Vsevolod V. Gurevich, Giulia Morra, Cagdas Devrim Son, Irene Gado, Aylin Nebol
| Nature
Abstract Excessive signaling by various GPCRs underlies a variety of human disorders. Suppression of GPCRs by “enhanced” arrestin mutants was proposed as therapy. We hypothesized that GPCR binding of endogenous arrestins can be increased by small molecules stabilizing pre-activated conformation. Using molecular dynamics, we identified potentially druggable pockets in pre-activated conformation of arrestin-3 and discovered a compound targeting one of these pockets.
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