New Roles for β-Arrestins in Cell Signaling: Not Just for Seven-Transmembrane Receptors
Open accessAbstract
beta-arrestins, originally discovered as molecules that bind to and desensitize the activated and phosphorylated form of the G protein-coupled beta2-adrenergic receptor (beta2-AR), have recently emerged as multifunctional adaptor/scaffold proteins that dynamically assemble a wide range of multiprotein complexes in response to stimulation of most seven-transmembrane receptors (7TMRs). These complexes mediate receptor signaling, trafficking, and degradation. Moreover, beta-arrestins are increasingly found to perform analogous functions for receptors from structurally diverse classes, including atypical 7TMRs such as frizzled and smoothened, the nicotinic cholinergic receptors, receptor tyrosine kinases, and cytokine receptors, thereby regulating a growing list of cellular processes such as chemotaxis, apoptosis, and metastasis.
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Beta-arrestins contribute to a reduction in the response to receptor agonism through internalization of the specific G-protein-coupled receptor.
“Beta-arrestins contribute to a reduction in the response to receptor agonism through internalization of the specific G-protein-coupled receptor [21].”
From New Developments in Pharmacological Treatment of Obesity and Type 2 Diabetes—Beyond and within GLP-1 Receptor Agonists (2024) · cites this paper as [21]
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David, D. J., Samuels, B. A., Rainer, Q., Wang, J.-W., Marsteller, D., Mendez, I., Drew, M., Craig, D. A., Guiard, B. P., Guilloux, J.-P., et al. (2009) · Neuron · doi:10.1016/j.neuron.2009.04.017 · Cited by 1,267 · see citing works
Sztanek, F., Tóth, L. I., Pető, A., Hernyák, M., Diószegi, Á., & Harangi, M. (2024) · Biomedicines · doi:10.3390/biomedicines12061320 · Cited by 43 · see citing works
“…beta-arrestins, and other Beta-arrestins contribute to a reduction in the response to receptor agonism through internalization of the speci fi c G-protein-coupled receptor [21]. non-G-protein-regulated signaling pathways, such as mitogen-activated protein kinase phosphorylation [20] (Figure 3).”
BackgroundGRKs and β-Arrestins: “Gatekeepers” of Mitochondrial Function in the Failing Heart
Sorriento, D., Gambardella, J., Fiordelisi, A., Iaccarino, G., & Illario, M. (2019) · Frontiers in Pharmacology · doi:10.3389/fphar.2019.00064 · Cited by 16 · see citing works
- Authors
- Lefkowitz, R. J., Rajagopal, K., & Whalen, E. J.
- Affiliations
- Howard Hughes Medical Institute (US)
- Corresponding author
- Lefkowitz, Robert J.
- Venue
- Molecular Cell
- Publisher
- Elsevier BV
- Published
- 2006-12
- Volume
- 24
- Issue
- 5
- Pages
- 643-652
- ISSN
- 1097-2765 (ISSN-L)
- OpenAlex
- W2002300983
- Cited by
- 301
- References
- 0
- Citations by year
- 2026: 5 · 2025: 6 · 2024: 11 · 2023: 5 · 2022: 6 · 2021: 12 · 2020: 16 · 2019: 17 · 2018: 11 · 2017: 17 · 2016: 10 · 2015: 19 · 2014: 20 · 2013: 15 · 2012: 7
- FWCI
- 2.18
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Molecular Cell (publishedVersion)
- PubMed (publishedVersion)
- 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
- Health Sciences › Medicine › Oncology › Chemokine receptors and signaling
- Keywords
- beta-arrestin, G protein-coupled receptors, receptor desensitization, adaptor proteins, receptor trafficking, receptor degradation, nicotinic acetylcholine receptors, receptor tyrosine kinase, cytokine receptors, chemotaxis, apoptosis, metastasis
- MeSH terms
- beta-Arrestins, Animals, Humans, Models, Molecular, Protein Conformation, Signal Transduction, Arrestins, Receptors, G-Protein-Coupled
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