Noncanonical scaffolding of G αi and β-arrestin by G protein-coupled receptors

Heterotrimeric guanine nucleotide-binding protein (G protein)-coupled receptors (GPCRs) are common drug targets and canonically couple to specific G protein subtypes and β-arrestin adaptor proteins. G protein-mediated signaling and β-arrestin-mediated signaling have been considered separable. We sho...

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Veröffentlicht in:	Science (American Association for the Advancement of Science) 2021-03, Vol.371 (6534)
Hauptverfasser:	Smith, Jeffrey S, Pack, Thomas F, Inoue, Asuka, Lee, Claudia, Zheng, Kevin, Choi, Issac, Eiger, Dylan S, Warman, Anmol, Xiong, Xinyu, Ma, Zhiyuan, Viswanathan, Gayathri, Levitan, Ian M, Rochelle, Lauren K, Staus, Dean P, Snyder, Joshua C, Kahsai, Alem W, Caron, Marc G, Rajagopal, Sudarshan
Format:	Artikel
Sprache:	eng
Schlagworte:	Arrestin beta-Arrestins - metabolism Bioluminescence Resonance Energy Transfer Techniques Calcium Cell adhesion & migration Cell Movement Coordination Energy transfer Extracellular Signal-Regulated MAP Kinases - metabolism Fatty acids GTP-Binding Protein alpha Subunits, Gi-Go - metabolism HEK293 Cells Humans Kinases Ligands Migration Narcotics Peptides Protein kinase Proteins Receptors, G-Protein-Coupled - metabolism Resonance Scaffolding Side effects Signal Transduction Therapeutic targets
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container_issue	6534
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container_title	Science (American Association for the Advancement of Science)
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creator	Smith, Jeffrey S Pack, Thomas F Inoue, Asuka Lee, Claudia Zheng, Kevin Choi, Issac Eiger, Dylan S Warman, Anmol Xiong, Xinyu Ma, Zhiyuan Viswanathan, Gayathri Levitan, Ian M Rochelle, Lauren K Staus, Dean P Snyder, Joshua C Kahsai, Alem W Caron, Marc G Rajagopal, Sudarshan
description	Heterotrimeric guanine nucleotide-binding protein (G protein)-coupled receptors (GPCRs) are common drug targets and canonically couple to specific G protein subtypes and β-arrestin adaptor proteins. G protein-mediated signaling and β-arrestin-mediated signaling have been considered separable. We show here that GPCRs promote a direct interaction between G protein subtype family members and β-arrestins regardless of their canonical G protein subtype coupling. G :β-arrestin complexes bound extracellular signal-regulated kinase (ERK), and their disruption impaired both ERK activation and cell migration, which is consistent with β-arrestins requiring a functional interaction with G for certain signaling events. These results introduce a GPCR signaling mechanism distinct from canonical G protein activation in which GPCRs cause the formation of G :β-arrestin signaling complexes.
doi_str_mv	10.1126/science.aay1833
format	Article
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subjects	Arrestin beta-Arrestins - metabolism Bioluminescence Resonance Energy Transfer Techniques Calcium Cell adhesion & migration Cell Movement Coordination Energy transfer Extracellular Signal-Regulated MAP Kinases - metabolism Fatty acids GTP-Binding Protein alpha Subunits, Gi-Go - metabolism HEK293 Cells Humans Kinases Ligands Migration Narcotics Peptides Protein kinase Proteins Receptors, G-Protein-Coupled - metabolism Resonance Scaffolding Side effects Signal Transduction Therapeutic targets
title	Noncanonical scaffolding of G αi and β-arrestin by G protein-coupled receptors
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