ReviewNeuropharmacology2019
Arrestin recruitment and signaling by G protein-coupled receptor heteromers.
Review in Neuropharmacology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 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
26 citing papers in PubMed, 47 citations in OpenAlex.
- Structural Modification and Development ofJournal of medicinal chemistry · 2026Article
- Local GPCR density tips the balance of μ-opioid receptor trafficking.bioRxiv : the preprint server for biology · 2026Article
- Review
- GPCR Heterodimers: Implications for Biased Signaling.Handbook of experimental pharmacology · 2026Review
- Activation of dimerized BRS3-EP3 suppresses melanoma cell migration through coupling GαFundamental research · 2025Article
- Stabilized DNature communications · 2025Article
- Exploring Pharmacokinetic interactions between SHR8554, a µ-opioid receptor biased agonist, and Itraconazole in healthy Chinese subjects.Scientific reports · 2025Article
- Somatostatin: Linking Cognition and Alzheimer Disease to Therapeutic Targeting.Pharmacological reviews · 2024Review
- Exploiting Cell-Based Assays to Accelerate Drug Development for G Protein-Coupled Receptors.International journal of molecular sciences · 2024Review
- Buprenorphine for Chronic Pain Management: a Narrative Review.Current pain and headache reports · 2023Review
- Brain Structure and Function: Insights from Chemical Neuroanatomy.Life (Basel, Switzerland) · 2023Article
- Modified Akuamma Alkaloids with Increased Potency at the Mu-opioid Receptor.Journal of medicinal chemistry · 2023Article
- Opioid signaling and design of analgesics.Progress in molecular biology and translational science · 2023Review
- The role of G protein-coupled receptor in neutrophil dysfunction during sepsis-induced acute respiratory distress syndrome.Frontiers in immunology · 2023Review
- βγ G-proteins, but not regulators of G-protein signaling 4, modulate opioid-induced respiratory rate depression.Frontiers in physiology · 2023Article
- Biased signaling due to oligomerization of the G protein-coupled platelet-activating factor receptor.Nature communications · 2022Article
- β-Arrestin 2 (ARRB2) Polymorphism is Associated With Adverse Consequences of Chronic Heroin Use.The American journal on addictions · 2021Article
- Buprenorphine: Far Beyond the "Ceiling".Biomolecules · 2021Review
- The Roles of Orphan G Protein-Coupled Receptors in Autoimmune Diseases.Clinical reviews in allergy & immunology · 2021Review
- Synthesis and Pharmacology of a Novel μ-δ Opioid Receptor Heteromer-Selective Agonist Based on the Carfentanyl Template.Journal of medicinal chemistry · 2020Article
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
G protein-coupled receptors (GPCR) have a long history of being considered a prime target for drug development to treat a plethora of diseases and disorders. In fact in 1827, the first approved therapeutic in the United States was morphine, a drug that targets a GPCR, namely the mu opioid receptor. However, with the rise in biologics over the last two decades, the market share of small molecules targeting GPCRs has declined. Still, two phenomena concerning GPCR pharmacology, specifically heteromerization and biased signaling, have bolstered new interests in this particular class of drug targets. Heteromerization, the process by which two distinct GPCRs come together to form a unique signaling complex, has been demonstrated between many different GPCRs and has spurred efforts to discover heteromer selective drugs. Additionally, the discovery of biased signaling, a concept by which a GPCR can transduce intracellular signaling by favoring a specific pathway (e.g. G-protein) over another pathway (e.g. arrestin), has led to the development of signal-biased drugs with potentially fewer side effects. Our goal for this review is to highlight studies that have investigated the interplay of these two phenomena by providing an overview of the current literature describing instances where GPCR heteromers have distinct arrestin recruitment profiles when compared to the individual GPCRs, with a focus on those GPCRs expressed in the central nervous system. This article is part of the Special Issue entitled 'Receptor heteromers and their allosteric receptor-receptor interactions'.
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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.