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. Author manuscript; available in PMC: 2020 Jul 30.
Published in final edited form as: Adv Cancer Res. 2020 Feb 5;145:139–156. doi: 10.1016/bs.acr.2020.01.001

Fig. 1.

Fig. 1

A schematic representation showing the multifaceted role of β-arrestins in GPCR signaling and regulation. Agonist-stimulation leads to a conformational change in GPCRs followed by the interaction and activation of heterotrimeric G-proteins. Subsequently, GPCRs are phosphorylated by GPCR kinases (GRKs) that facilitate the binding of β-arrestins. GPCR-β-arrestin interaction terminates further G-protein coupling via steric hindrance mechanism on one hand while on the other, it initiates receptor internalization and β-arrestin mediated signaling.