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Figure 1


Fig. 1. Basic scheme for beta-arrestin negative feedback and GPCR endocytosis. Agonist exposure stimulates activation of GPCR, which leads to the dissociation of G proteins into activated {alpha} subunit and beta{gamma} dimers and triggers the activation of various effectors, such as adenylate cyclase and phospholipase C. The agonist-occupied GPCR is phosphorylated by GRKs, leading to signal desensitization, binding of beta-arrestin to the activated, phosphorylated GPCR and subsequent endocytosis of the receptor.





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