Antidepressants, β-Arrestins and GRKs: From Regulation of Signal Desensitization to Intracellular Multifunctional Adaptor Functions

Golan, Moran; Schreiber, Gabriel; Avissar, Sofia

doi:10.2174/138161209788168038

Cited by 22Receptor Mechanisms and SignalingNeuroscience and Neuropharmacology ResearchTreatment of Major Depression

Antidepressants, β-Arrestins and GRKs: From Regulation of Signal Desensitization to Intracellular Multifunctional Adaptor Functions

Golan, Moran, Schreiber, Gabriel, Avissar, Sofia·2009·Current Pharmaceutical Design

DOI 10.2174/138161209788168038

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Abstract

G protein-coupled receptors (GPCR) have generated considerable interest in the pharmaceutical industry as drug targets. Theories concerning antidepressant targets of action suggested pre-synaptic monoamine reuptake mechanisms regulating GPCR activities including delayed receptor desensitization and down-regulation. GRKs and beta-arrestins translocate to the cell membrane and bind to agonist-occupied receptors. This uncouples these receptors from G proteins and promotes their internalization, leading to desensitization and down-regulation. Thus, GRKs and beta-arrestins serve as negative regulators of GPCR signaling. Recently, GPCR have been demonstrated to elicit signals through interaction with beta-arrestin as scaffolding proteins, independent of heterotrimeric G-protein coupling. beta-arrestins function as scaffold proteins that interact with several cytoplasmic proteins and link GPCR to intracellular signaling pathways such as MAPK cascades. Recent work has also revealed that beta-arrestins translocate from the cytoplasm to the nucleus and associate with transcription cofactors such as p300 and CREB. They also interact with regulators of transcription factors. We review findings concerning effects of antidepressants on GRKs and beta-arrestins and the plethora of antidepressants effects on signal transduction elements in which GRKs and beta-arrestins serve as signaling scaffold proteins, and on transcription factors and cofactors in which beta-arrestins mediate regulation of transcription. The emergence of G-protein-independent signaling pathways, through beta-arrestins, changes the way in which GPCR signaling is evaluated, from a cell biological to a pharmaceutical perspective and raises the possibility for the development of pathway specific therapeutics e.g., antidepressant medications targeting GRKs and beta-arrestin regulatory and signaling proteins.

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The genes chosen for expression analysis have all recently been implicated in antidepressant drug action and neurogenesis.
“These genes were chosen because they have all recently been implicated in antidepressant drug action and neurogenesis.35, 36, 37, 38, 39, 12, 40, 41, 42, 43, 44, 45, 46, 47, 48, 49”
From Antidepressants increase human hippocampal neurogenesis by activating the glucocorticoid receptor (2011) · cites this paper as [41]

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Authors: Golan, M., Schreiber, G., & Avissar, S.
Affiliations: Ben-Gurion University of the Negev (IL)
ORCID: Golan, Moran
Venue: Current Pharmaceutical Design
Publisher: Bentham Science Publishers Ltd.
Published: 2009-05-01
Volume: 15
Issue: 14
Pages: 1699-1708
ISSN: 1381-6128 (ISSN-L)
DOI: 10.2174/138161209788168038
OpenAlex: W2094317231
Cited by: 22
References: 126
Citations by year: 2026: 1 · 2022: 1 · 2019: 2 · 2018: 1 · 2017: 2 · 2016: 2 · 2013: 3 · 2012: 3
FWCI: 1.34
Type: journal article
Language: en
Open access: closed
Locations: Current Pharmaceutical Design (publishedVersion)
PubMed (publishedVersion)
Topics: Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Receptor Mechanisms and Signaling
Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
Health Sciences › Medicine › Pharmacology › Treatment of Major Depression
Keywords: antidepressants, beta-arrestin, G protein-coupled receptors, G protein-coupled receptor kinases, receptor desensitization, receptor down-regulation, scaffold proteins, G protein-independent signaling, MAPK signaling, transcriptional regulation, CREB, P300, monoamine reuptake
MeSH terms: beta-Arrestins, Animals, Antidepressive Agents, Depressive Disorder, Humans, Transcription, Genetic, Signal Transduction, Drug Delivery Systems, Arrestins, Receptors, G-Protein-Coupled, G-Protein-Coupled Receptor Kinases

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Antidepressants, β-Arrestins and GRKs: From Regulation of Signal Desensitization to Intracellular Multifunctional Adaptor Functions

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