ReviewPharmacology & therapeutics2006
The structural basis of arrestin-mediated regulation of G-protein-coupled receptors.
Review in Pharmacology & therapeutics, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 278 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
278 citing papers in PubMed.
- Arrestins as programmable integrators of GPCR signaling: structural microstates, spatiotemporal logic, and therapeutic control.Cell discovery · 2026Review
- Intrinsic conformational equilibria position arrestin-2 for activation.Protein science : a publication of the Protein Society · 2026Article
- Membrane lipid poly-unsaturation selectively affects dopamine D2 receptor endocytosis.Nature communications · 2026Article
- Selective positive allosteric modulation of βNature communications · 2026Article
- Soft Selective Sweeps Predominate in the Yellow Fever Mosquito Aedes aegypti.Molecular biology and evolution · 2026Article
- Correlation between anti-retinal antibodies and lupus retinopathy in systemic lupus erythematosus.Scientific reports · 2026Article
- Identification of a novel nonsense variant in ARR3 in a family with early-onset high myopia.Genes & genomics · 2026Article
- IGF-1 protects against acute pancreatitis by suppressing NF-κB activation through the β-arrestin1/STAT3 pathway.Molecular and cellular biochemistry · 2026Article
- GPCR Phospho-Barcodes and Biased Signaling.Handbook of experimental pharmacology · 2026Review
- Intrinsic conformational equilibria position arrestin-2 for activation.bioRxiv : the preprint server for biology · 2025Article
- Review
- G-Protein-Coupled Receptor Kinase 2 Limits CCL21-Induced T Cell Migration via Phospholipase Cγ1.Receptors (Basel, Switzerland) · 2025Article
- Identification of Bioactive Peptides fromMicroorganisms · 2025Article
- An arginine switch drives the stepwise activation of β-arrestin by CXCR7.PLoS biology · 2025Article
- Signatures of soft selective sweeps predominate in the yellow fever mosquitobioRxiv : the preprint server for biology · 2025Article
- Tonic ubiquitination of the central body weight regulator melanocortin receptor 4 (MC4R) promotes its constitutive exit from cilia.PLoS biology · 2025Article
- An RFamide signaling system balances turning and forward locomotion to optimize global food search inJournal of biosciences · 2025Article
- Advances in the study of ARR3 in myopia.Frontiers in cell and developmental biology · 2025Review
- Disease-Associated Dopamine Receptor D2 Variants Exhibit Functional Consequences Depending on Different Heterotrimeric G-Protein Subunit Combinations.Biomedicines · 2024Article
- Receptor Determinants for β-Arrestin Functional Specificity atMolecular pharmacology · 2024Article
218 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
2 authors.
Funding
Abstract
The 4 mammalian arrestins serve as almost universal regulators of the largest known family of signaling proteins, G-protein-coupled receptors (GPCRs). Arrestins terminate receptor interactions with G proteins, redirect the signaling to a variety of alternative pathways, and orchestrate receptor internalization and subsequent intracellular trafficking. The elucidation of the structural basis and fine molecular mechanisms of the arrestin-receptor interaction paved the way to the targeted manipulation of this interaction from both sides to produce very stable or extremely transient complexes that helped to understand the regulation of many biologically important processes initiated by active GPCRs. The elucidation of the structural basis of arrestin interactions with numerous non-receptor-binding partners is long overdue. It will allow the construction of fully functional arrestins in which the ability to interact with individual partners is specifically disrupted or enhanced by targeted mutagenesis. These "custom-designed" arrestin mutants will be valuable tools in defining the role of various interactions in the intricate interplay of multiple signaling pathways in the living cell. The identification of arrestin-binding sites for various signaling molecules will also set the stage for designing molecular tools for therapeutic intervention that may prove useful in numerous disorders associated with congenital or acquired disregulation of GPCR signaling.
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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.