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Double life: How GRK2 and β-arrestin signaling participate in diseases
Journal article   Open access   Peer reviewed

Double life: How GRK2 and β-arrestin signaling participate in diseases

Ruxu Zhai, Jonathan Snyder, Sarah Montgomery and Priscila Y Sato
Cellular signalling, v 94, pp 110333-110333
Jun 2022
PMID: 35430346
url
https://doi.org/10.1016/j.cellsig.2022.110333View
Published, Version of Record (VoR)CC BY V4.0 Open

Abstract

Arrestins - metabolism beta-Arrestin 1 - metabolism beta-Arrestin 2 - metabolism beta-Arrestins - metabolism G-Protein-Coupled Receptor Kinases - metabolism Phosphorylation Receptors, G-Protein-Coupled - metabolism Signal Transduction - physiology
G-protein coupled receptor (GPCR) kinases (GRKs) and β-arrestins play key roles in GPCR and non-GPCR cellular responses. In fact, GRKs and arrestins are involved in a plethora of pathways vital for physiological maintenance of inter- and intracellular communication. Here we review decades of research literature spanning from the discovery, identification of key structural elements, and findings supporting the diverse roles of these proteins in GPCR-mediated pathways. We then describe how GRK2 and β-arrestins partake in non-GPCR signaling and briefly summarize their involvement in various pathologies. We conclude by presenting gaps in knowledge and our prospective on the promising pharmacological potential in targeting these proteins and/or downstream signaling. Future research is warranted and paramount for untangling these novel and promising roles for GRK2 and arrestins in metabolism and disease progression.

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Web of Science research areas
Cell Biology
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