ArticleNature communications2017
A new inhibitor of the β-arrestin/AP2 endocytic complex reveals interplay between GPCR internalization and signalling.
Article in Nature communications, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 89 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
89 citing papers in PubMed, 215 citations in OpenAlex.
- Mechanisms of XCR1 Membrane Trafficking and Constitutive Endocytosis.Basic & clinical pharmacology & toxicology · 2026Article
- Targeting β2-Adrenergic Receptor Stability With Lycorine Reveals a Host-Directed Pathway for Antiviral Defense Against Poxviruses.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Small-molecule modulation of β-arrestins.Nature · 2026Article
- Development and Biological Characterization of Fluorescent Dynorphins for the Visualization of Kappa Opioid Receptors.Journal of medicinal chemistry · 2026Article
- Roflumilast Enhances Liraglutide's Atrial Natriuretic Peptide-Dependent Suppression of Adrenal Aldosterone Secretion.International journal of molecular sciences · 2026Article
- Article
- Multi-faceted roles of β-arrestins in G protein-coupled receptor endocytosis.Nature communications · 2025Article
- Discovery of a β-arrestin-biased CCKBR agonist that blocks CCKBR-dependent long-term potentiation.Nature communications · 2025Article
- Development of ketobenzothiazole-based peptidomimetic TMPRSS13 inhibitors with low nanomolar potency.Journal of enzyme inhibition and medicinal chemistry · 2025Article
- Article
- A Novel Class of Complement 3a Receptor Agonists and Antagonists Derived from the TLQP-21 Peptide.Journal of medicinal chemistry · 2025Article
- Arrestins as Possible Drug Targets.Biomolecules & therapeutics · 2025Review
- FMRP-dependent translational control negatively regulates adapter protein complex 2-mediated endocytosis.iScience · 2025Article
- Chemical biology approaches to resolve the subcellular GPCR signaling landscape.Nature chemical biology · 2025Review
- Multiple intramolecular triggers converge to preferential G protein coupling in the CBNature communications · 2025Article
- Succinate receptor 1 signaling mutually depends on subcellular localization and cellular metabolism.The FEBS journal · 2025Article
- From metabolic regulation to kidney protection: β-arrestin 2 as a dual-function therapeutic target.World journal of diabetes · 2025Article
- G protein-coupled receptor 107 deficiency promotes development of diabetic nephropathy.Molecular biomedicine · 2025Article
- GRK6 palmitoylation dictates triple-negative breast cancer metastasis via recruiting the β-Arrestin 2/MAPKs/NF-κB signaling axis.Breast cancer research : BCR · 2024Article
- Does Incretin Agonism Have Sustainable Efficacy?Cells · 2024Review
29 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
16 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In addition to G protein-coupled receptor (GPCR) desensitization and endocytosis, β-arrestin recruitment to ligand-stimulated GPCRs promotes non-canonical signalling cascades. Distinguishing the respective contributions of β-arrestin recruitment to the receptor and β-arrestin-promoted endocytosis in propagating receptor signalling has been limited by the lack of selective analytical tools. Here, using a combination of virtual screening and cell-based assays, we have identified a small molecule that selectively inhibits the interaction between β-arrestin and the β2-adaptin subunit of the clathrin adaptor protein AP2 without interfering with the formation of receptor/β-arrestin complexes. This selective β-arrestin/β2-adaptin inhibitor (Barbadin) blocks agonist-promoted endocytosis of the prototypical β2-adrenergic (β2AR), V2-vasopressin (V2R) and angiotensin-II type-1 (AT1R) receptors, but does not affect β-arrestin-independent (transferrin) or AP2-independent (endothelin-A) receptor internalization. Interestingly, Barbadin fully blocks V2R-stimulated ERK1/2 activation and blunts cAMP accumulation promoted by both V2R and β2AR, supporting the concept of β-arrestin/AP2-dependent signalling for both G protein-dependent and -independent pathways.
Indexed as
Identifiers
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.