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Cited by 418Receptor Mechanisms and SignalingProtein Kinase Regulation and GTPase SignalingNeuroscience and Neuropharmacology Research

Emerging paradigms of β-arrestin-dependent seven transmembrane receptor signaling

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Shukla, Arun K., Xiao, Kunhong, Lefkowitz, Robert J.·2011·Trends in Biochemical Sciences
DOI 10.1016/j.tibs.2011.06.003PMC PMC3168679
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Abstract

β-Arrestins, originally discovered to desensitize activated seven transmembrane receptors (7TMRs; also known as G-protein-coupled receptors, GPCRs), are now well established mediators of receptor endocytosis, ubiquitylation and G protein-independent signaling. Recent global analyses of β-arrestin interactions and β-arrestin-dependent phosphorylation events have uncovered several previously unanticipated roles of β-arrestins in a range of cellular signaling events. These findings strongly suggest that the functional roles of β-arrestins are much broader than currently understood. Biophysical studies aimed at understanding multiple active conformations of the 7TMRs and the β-arrestins have begun to unravel the mechanistic basis for the diverse functional capabilities of β-arrestins in cellular signaling.

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  • Certain biased agonists of the GLP-1 receptor may more strongly facilitate G-protein activation than recruitment of beta-arrestins.

    “Certain biased agonists of the GLP-1 receptor may more strongly facilitate G-protein activation than recruitment of beta-arrestins [22].”

    From New Developments in Pharmacological Treatment of Obesity and Type 2 Diabetes—Beyond and within GLP-1 Receptor Agonists (2024) · cites this paper as [22]

    In “Zooming in: the concept of biased agonism” (page unavailable), the review says that ligands can selectively trigger G-protein rather than β-arrestin signaling. Its example concerns the GPR109A receptor, however; the passages do not establish this preference for GLP-1 receptor agonists. (LLM, conf=0.85)

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Authors
Shukla, A. K., Xiao, K., & Lefkowitz, R. J.
Affiliations
  • Howard Hughes Medical Institute (US)
  • Duke Medical Center (US)
Corresponding author
  • Shukla, Arun K.
  • Lefkowitz, Robert J.
ORCID
Venue
Trends in Biochemical Sciences
Publisher
Elsevier BV
Published
2011-09
Volume
36
Issue
9
Pages
457-469
ISSN
0968-0004 (ISSN-L)
DOI
10.1016/j.tibs.2011.06.003
PMC
PMC3168679
OpenAlex
W2059258112
Cited by
418
References
0
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FWCI
3.37
Type
journal article
Language
en
Open access
Licence
www.elsevier.com/tdm/userlicense/1.0/ (tdm)
Locations
  • Trends in Biochemical Sciences (publishedVersion)
  • PubMed (publishedVersion)
  • Europe PMC (PubMed Central) (acceptedVersion)
  • PubMed Central (acceptedVersion)
Funders
  • Howard Hughes Medical Institute
  • National Heart, Lung, and Blood Institute (HL 16037, R01HL070631, HL-70631, R01HL016037)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Receptor Mechanisms and Signaling
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Protein Kinase Regulation and GTPase Signaling
  • Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
Keywords
beta-arrestin, G protein-coupled receptors, receptor desensitization, receptor internalization, ubiquitination, G protein-independent signaling, receptor conformation, signaling mechanisms
MeSH terms
beta-Arrestins, Angiotensin II, Animals, Endocytosis, Humans, Membrane Proteins, Phosphoproteins, Phosphorylation, Protein Conformation, Species Specificity, Signal Transduction, Arrestins, Protein Transport, Receptors, G-Protein-Coupled, Extracellular Signal-Regulated MAP Kinases, Ubiquitination

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