ArticleBritish journal of pharmacology2011
Agonist activation of the G protein-coupled receptor GPR35 involves transmembrane domain III and is transduced via Gα₁₃ and β-arrestin-2.
Article in British journal of pharmacology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
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Who cites it
40 citing papers in PubMed, 78 citations in OpenAlex.
- Cell Signaling by Tryptophan Catabolism.Biochemistry · 2026Review
- Dietary anthocyanidin pelargonidin activates G protein-coupled receptor 35.The FEBS journal · 2026Article
- Receptor-Mitochondria Crosstalk in the Kynurenine Metabolic Pathway: Integrating Metabolomics and Clinical Mass Spectrometry.Antioxidants (Basel, Switzerland) · 2026Review
- GPR35 protects against reperfusion injury in ischemic stroke by binding with the CR2 domain of Raf1.Journal of neuroinflammation · 2026Article
- G protein-coupled receptor 35 stimulation reduces osteoclast activity in primary human bone cells.JBMR plus · 2025Article
- GPR35 prevents drug-induced liver injury via the Gαs-cAMP-PKA axis in macrophages.Cellular and molecular life sciences : CMLS · 2025Article
- GPR35-mediated metabolic reprogramming promotes tumorigenesis in digestive cancers.Frontiers in immunology · 2025Review
- The Complex World of Kynurenic Acid: Reflections on Biological Issues and Therapeutic Strategy.International journal of molecular sciences · 2024Review
- From orphan to oncogene: The role of GPR35 in cancer and immune modulation.Cytokine & growth factor reviews · 2024Review
- GPR35 and mediators from platelets and mast cells in neutrophil migration and inflammation.Immunological reviews · 2023Review
- Recent advances in GPR35 pharmacology; 5-HIAA serotonin metabolite becomes a ligand.Archives of pharmacal research · 2023Review
- GPR35 acts a dual role and therapeutic target in inflammation.Frontiers in immunology · 2023Review
- GPR35 antagonist CID-2745687 attenuates anchorage-independent cell growth by inhibiting YAP/TAZ activity in colorectal cancer cells.Frontiers in pharmacology · 2023Article
- Insights into divalent cation regulation and GCell discovery · 2022Article
- Mitochondrial remodeling and ischemic protection by G protein-coupled receptor 35 agonists.Science (New York, N.Y.) · 2022Article
- Article
- G-protein coupled receptor 35 (GPR35) regulates the colonic epithelial cell response to enterotoxigenic Bacteroides fragilis.Communications biology · 2021Article
- Article
- Activation of GPR35 protects against cerebral ischemia by recruiting monocyte-derived macrophages.Scientific reports · 2020Article
- Receptor selectivity between the G proteins GαFASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2019Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
background and purposeGPR35 is a poorly characterized G protein-coupled receptor at which kynurenic acid has been suggested to be the endogenous ligand. We wished to test this and develop assays appropriate for the study of this receptor. EXPERIMENTAL APPROACH: Human and rat orthologues of GPR35 were engineered and expressed and assays developed to assess interaction with β-arrestin-2, activation of Gα₁₃ and agonist-induced internalization. KEY
resultsGPR35-β-arrestin-2 interaction assays confirmed that both the endogenous tryptophan metabolite kynurenic acid and the synthetic ligand zaprinast had agonist action at each orthologue. Zaprinast was substantially more potent than kynurenic acid at each and both agonists displayed substantially greater potency at rat GPR35. Two novel thiazolidinediones also displayed agonism and displayed similar potency at each GPR35 orthologue. The three ligand classes acted orthosterically with respect to each other, suggesting overlapping binding sites and, consistent with this, mutation to alanine of the conserved arginine at position 3.36 or tyrosine 3.32 in transmembrane domain III abolished β-arrestin-2 recruitment in response to each ligand at each orthologue. CONCLUSIONS AND IMPLICATIONS: These studies indicate that β-arrestin-2 interaction assays are highly appropriate to explore the pharmacology of GPR35 and that Gα₁₃ activation is an alternative avenue of signal generation from GPR35. Arginine and tyrosine residues in transmembrane domain III are integral to agonist recognition and function of this receptor. The potency of kynurenic acid at human GPR35 is sufficiently low, however, to question whether it is likely to be the true endogenous ligand for this receptor.
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