ReviewPharmacological reviews2010
Beyond desensitization: physiological relevance of arrestin-dependent signaling.
Review in Pharmacological reviews, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 187 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
187 citing papers in PubMed, 359 citations in OpenAlex.
- Herbacetin as a natural GPR35 agonist for allergic asthma relief via dual regulation of PI3K/Akt/mTOR and MAPK signaling.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Mice lacking β-arrestin-2 in melanocortin 4 receptor-expressing neurons show marked metabolic deficits.JCI insight · 2026Article
- Modulation of Chemokine Activity for Enhanced Angiogenesis and Tissue Regeneration in Chronic Wounds.International journal of molecular sciences · 2026Review
- The C-terminal regions of the GLP-1 and GIP receptors are not the key determinants of their differential arrestin recruitment but modulate the rate of receptor endocytosis.Frontiers in pharmacology · 2025Article
- Neuroprotective actions of norepinephrine in neurological diseases.Pflugers Archiv : European journal of physiology · 2024Review
- Adrenoceptor Desensitization: Current Understanding of Mechanisms.Pharmacological reviews · 2024Review
- CXC chemokine receptor 4 (CXCR4) blockade in cancer treatment.Journal of cancer research and clinical oncology · 2023Review
- Cellular Assay to Study β-Arrestin Recruitment by the Cannabinoid Receptors 1 and 2.Methods in molecular biology (Clifton, N.J.) · 2023Article
- Carvedilol Selectively Stimulates βArrestin2-Dependent SERCA2a Activity in Cardiomyocytes to Augment Contractility.International journal of molecular sciences · 2022Article
- Chimeric GPCRs mimic distinct signaling pathways and modulate microglia responses.Nature communications · 2022Article
- α-Arrestins and Their Functions: From Yeast to Human Health.International journal of molecular sciences · 2022Review
- Human CD4International journal of molecular sciences · 2022Article
- Molecular targets in acromegaly.Frontiers in endocrinology · 2022Review
- GPCRs in the regulation of the functional activity of multipotent mesenchymal stromal cells.Frontiers in cell and developmental biology · 2022Review
- Multifaceted Roles of Chemokine C-X-C Motif Ligand 7 in Inflammatory Diseases and Cancer.Frontiers in pharmacology · 2022Review
- Receptor-Loaded Virion Endangers GPCR Signaling: Mechanistic Exploration of SARS-CoV-2 Infections and Pharmacological Implications.International journal of molecular sciences · 2021Review
- Chemogenetic approaches to identify metabolically important GPCR signaling pathways: Therapeutic implications.Journal of neurochemistry · 2021Review
- Review
- Quantifying the Kinetics of Signaling and Arrestin Recruitment by Nervous System G-Protein Coupled Receptors.Frontiers in cellular neuroscience · 2021Article
- Activation of βArchives of pharmacal research · 2021Review
127 more citing papers are in PubMed but not listed here.
Corrections and comments
- Erratum issued
Authors and funding
2 authors at 2 institutions in 1 country.
Funding
Abstract
Heptahelical G protein-coupled receptors are the most diverse and therapeutically important family of receptors in the human genome. Ligand binding activates heterotrimeric G proteins that transmit intracellular signals by regulating effector enzymes or ion channels. G protein signaling is terminated, in large part, by arrestin binding, which uncouples the receptor and G protein and targets the receptor for internalization. It is clear, however, that heptahelical receptor signaling does not end with desensitization. Arrestins bind a host of catalytically active proteins and serve as ligand-regulated scaffolds that recruit protein and lipid kinase, phosphatase, phosphodiesterase, and ubiquitin ligase activity into the receptor-arrestin complex. Although many of these arrestin-bound effectors serve to modulate G protein signaling, degrading second messengers and regulating endocytosis and trafficking, other signals seem to extend beyond the receptor-arrestin complex to regulate such processes as protein translation and gene transcription. Although these findings have led to a re-envisioning of heptahelical receptor signaling, little is known about the physiological roles of arrestin-dependent signaling. In vivo, the duality of arrestin function makes it difficult to dissociate the consequences of arrestin-dependent desensitization from those that might be ascribed to arrestin-mediated signaling. Nonetheless, recent evidence generated using arrestin knockouts, G protein-uncoupled receptor mutants, and arrestin pathway-selective "biased agonists" is beginning to reveal that arrestin signaling plays important roles in the retina, central nervous system, cardiovascular system, bone remodeling, immune system, and cancer. Understanding the signaling roles of arrestins may foster the development of pathway-selective drugs that exploit these pathways for therapeutic benefit.
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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.