ReviewCurrent opinion in cell biology2014
Role of β-arrestins and arrestin domain-containing proteins in G protein-coupled receptor trafficking.
Review in Current opinion in cell biology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 101 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
101 citing papers in PubMed, 188 citations in OpenAlex.
- Trial
- Structural mechanism for noncanonical GPCR signaling in the Hedgehog pathway.Nature structural & molecular biology · 2026Article
- The clinical implication of β-arrestins-mediated signaling in memory and cognition.Molecular and cellular biochemistry · 2025Review
- A genetically encoded nanobody sensor reveals conformational diversity in β-arrestins orchestrated by distinct seven transmembrane receptors.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Role of the G protein-coupled receptor kinase 2/3 N terminus in discriminating the endocytic effects of opioid agonist drugs.Molecular pharmacology · 2025Article
- Cryo-electron microscopy for GPCR research and drug discovery in endocrinology and metabolism.Nature reviews. Endocrinology · 2024Review
- CYRI-B-mediated macropinocytosis drives metastasis via lysophosphatidic acid receptor uptake.eLife · 2024Article
- Organelle proteomic profiling reveals lysosomal heterogeneity in association with longevity.eLife · 2024Article
- Molecular insights into atypical modes of β-arrestin interaction with seven transmembrane receptors.Science (New York, N.Y.) · 2024Article
- Article
- G Protein-Coupled Receptor Kinase 2 Selectively Enhances β-Arrestin Recruitment to the DBiomolecules · 2023Article
- Review
- Structural snapshots uncover a key phosphorylation motif in GPCRs driving β-arrestin activation.Molecular cell · 2023Article
- Article
- Platelet P2YBMC biology · 2023Article
- Article
- Surveying nonvisual arrestins reveals allosteric interactions between functional sites.Proteins · 2023Article
- Discrete GPCR-triggered endocytic modes enable β-arrestins to flexibly regulate cell signaling.eLife · 2022Article
- Allosteric modulation of GPCR-induced β-arrestin trafficking and signaling by a synthetic intrabody.Nature communications · 2022Article
- Agonist concentration-dependent changes in FPR1 conformation lead to biased signaling for selective activation of phagocyte functions.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
41 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
The arrestin clan can now be broadly divided into three structurally similar subgroups: the originally identified arrestins (visual and β-arrestins), the α-arrestins and a group of Vps26-related proteins. The visual and β-arrestins selectively bind to agonist-occupied phosphorylated G protein-coupled receptors (GPCRs) and inhibit GPCR coupling to heterotrimeric G proteins while the β-arrestins also function as adaptor proteins to regulate GPCR trafficking and G protein-independent signaling. The α-arrestins have also recently been implicated in regulating GPCR trafficking while Vps26 regulates retrograde trafficking. In this review, we provide an overview of the α-arrestins and β-arrestins with a focus on our current understanding of how these adaptor proteins regulate GPCR trafficking.
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What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.