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      GPCR signaling via β-arrestin-dependent mechanisms

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          Abstract

          β-arrestin1 (or arrestin2) and β-arrestin2 (or arrestin3) are ubiquitously expressed cytosolic adaptor proteins that were originally discovered for their inhibitory role in G protein-coupled receptor (GPCR) signaling via heterotrimeric G proteins. However, further biochemical characterization revealed that β-arrestins do not just ‘block’ the activated GPCRs, but trigger endocytosis and kinase activation leading to specific signaling pathways that can be localized on endosomes. The signaling pathways initiated by β-arrestins were also found to be independent of G protein activation by GPCRs. The discovery of ligands that blocked G protein activation but promoted β-arrestin binding, or vice-versa, suggested the exciting possibility of selectively activating intracellular signaling pathways. Additionally, it is becoming increasingly evident that β-arrestin-dependent signaling is extremely diverse and provokes distinct cellular responses through different GPCRs even when the same effector kinase is involved. In this review, we summarize various signaling pathways mediated by β-arrestins and highlight the physiologic effects of β-arrestin-dependent signaling.

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          Author and article information

          Journal
          7902492
          5285
          J Cardiovasc Pharmacol
          J. Cardiovasc. Pharmacol.
          Journal of cardiovascular pharmacology
          0160-2446
          1533-4023
          17 March 2017
          September 2017
          01 September 2018
          : 70
          : 3
          : 142-158
          Affiliations
          [1 ]Department of Medicine (Cardiology), Duke University Medical Center, Durham, North Carolina, USA
          [2 ]Department of Cell Biology, Duke University Medical Center, Durham, North Carolina, USA
          Author notes
          [** ]Correspondence: Sudha K. Shenoy, Box 103204, Duke University Medical Center, Durham NC 27710 Phone: 919-681-5061; Fax: 919-681-7851; skshenoy@ 123456dm.duke.edu
          Article
          PMC5591062 PMC5591062 5591062 nihpa857179
          10.1097/FJC.0000000000000482
          5591062
          28328745
          6175c6cc-35f8-431d-b61e-9b52b4ec6040
          History
          Categories
          Article

          biased agonist,Arrestin,endocytosis,7TMR,adaptor,GPCR,kinase
          biased agonist, Arrestin, endocytosis, 7TMR, adaptor, GPCR, kinase

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