ArticlePharmacological research2008
Translocation of arrestin induced by human A(3) adenosine receptor ligands in an engineered cell line: comparison with G protein-dependent pathways.
Article in Pharmacological research, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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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
30 citing papers in PubMed, 47 citations in OpenAlex.
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- Nucleoside transporters and immunosuppressive adenosine signaling in the tumor microenvironment: Potential therapeutic opportunities.Pharmacology & therapeutics · 2022Review
- International Union of Basic and Clinical Pharmacology. CXII: Adenosine Receptors: A Further Update.Pharmacological reviews · 2022Review
- 2‑Cl‑IB‑MECA regulates the proliferative and drug resistance pathways, and facilitates chemosensitivity in pancreatic and liver cancer cell lines.International journal of molecular medicine · 2022Article
- Pharmacological characterization of DPTN and other selective APurinergic signalling · 2021Article
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- Assessment of biased agonism at the ABiochemical pharmacology · 2020Article
- Safety evaluation of FM101, an A3 adenosine receptor modulator, in rat, for developing as therapeutics of glaucoma and hepatitis.EXCLI journal · 2020Article
- Design, Synthesis and Evaluation of New Indolylpyrimidylpiperazines for Gastrointestinal Cancer Therapy.Molecules (Basel, Switzerland) · 2019Article
- Probing structure-activity relationship in β-arrestin2 recruitment of diversely substituted adenosine derivatives.Biochemical pharmacology · 2018Article
- New paradigms in adenosine receptor pharmacology: allostery, oligomerization and biased agonism.British journal of pharmacology · 2018Review
- Distinct Signaling Patterns of Allosteric Antagonism at the P2YMolecular pharmacology · 2017Article
- Structure-Activity Analysis of Biased Agonism at the Human Adenosine A3 Receptor.Molecular pharmacology · 2016Article
- New paradigms in GPCR drug discovery.Biochemical pharmacology · 2015Review
- Probing biased/partial agonism at the G protein-coupled A(2B) adenosine receptor.Biochemical pharmacology · 2014Article
- Effect of a toggle switch mutation in TM6 of the human adenosine A₃ receptor on Gi protein-dependent signalling and Gi-independent receptor internalization.British journal of pharmacology · 2014Article
- Structure-based approaches to ligands for G-protein-coupled adenosine and P2Y receptors, from small molecules to nanoconjugates.Journal of medicinal chemistry · 2013Review
Corrections and comments
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Authors and funding
2 authors at 2 institutions in 1 country.
Funding
Abstract
Structurally diverse ligands were studied in A(3) adenosine receptor (AR)-mediated beta-arrestin translocation in engineered CHO cells. The agonist potency and efficacy were similar, although not identical, to their G protein signaling. However, differences have also been found. MRS542, MRS1760, and other adenosine derivatives, A(3)AR antagonists in cyclic AMP assays, were partial agonists in beta-arrestin translocation, indicating possible biased agonism. The xanthine 7-riboside DBXRM, a full agonist, was only partially efficacious in beta-arrestin translocation. DBXRM was shown to induce a lesser extent of desensitization compared with IB-MECA. In kinetic studies, MRS3558, a potent and selective A(3)AR agonist, induced beta-arrestin translocation significantly faster than IB-MECA and Cl-IB-MECA. Non-nucleoside antagonists showed similar inhibitory potencies as previously reported. PTX pretreatment completely abolished ERK1/2 activation, but not arrestin translocation. Thus, lead candidates for biased agonists at the A(3)AR have been identified with this arrestin-translocation assay, which promises to be an effective tool for ligand screening.
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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.