ArticleBritish journal of pharmacology2018
GPR35 mediates lodoxamide-induced migration inhibitory response but not CXCL17-induced migration stimulatory response in THP-1 cells; is GPR35 a receptor for CXCL17?
Article in British journal of pharmacology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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Who cites it
37 citing papers in PubMed, 84 citations in OpenAlex.
- International Union of Basic and Clinical Pharmacology. CXXII. Applying an objective evaluation to the status of class A orphan G protein-coupled receptors.Pharmacological reviews · 2026Review
- Identification and functional characterization of two CXCL17 paralogs from zebrafish.The Biochemical journal · 2026Article
- Role of mucosal chemokines in the development of tissue-resident CD4Frontiers in immunology · 2026Review
- Nano-Luciferase complementation assay of human herpesvirus 8 chemo/cytokine-receptor interactions.Scientific reports · 2025Article
- G protein-coupled receptor 35 stimulation reduces osteoclast activity in primary human bone cells.JBMR plus · 2025Article
- Increased GPR35 expression is correlated with poor prognosis in prostate cancer.World journal of surgical oncology · 2025Article
- Gpr35 Expression Mitigates Neuroinflammation and Enriches GutResearch (Washington, D.C.) · 2025Article
- Article
- From orphan to oncogene: The role of GPR35 in cancer and immune modulation.Cytokine & growth factor reviews · 2024Review
- CXCL17 is an allosteric inhibitor of CXCR4 through a mechanism of action involving glycosaminoglycans.Science signaling · 2024Article
- The origin, evolution, and molecular diversity of the chemokine system.Life science alliance · 2024Article
- The cryptic role of CXCL17/CXCR8 axis in the pathogenesis of cancers: a review of the latest evidence.Journal of cell communication and signaling · 2023Review
- GPR35 and mediators from platelets and mast cells in neutrophil migration and inflammation.Immunological reviews · 2023Review
- Targeting Members of the Chemokine Family as a Novel Approach to Treating Neuropathic Pain.Molecules (Basel, Switzerland) · 2023Review
- Recent advances in GPR35 pharmacology; 5-HIAA serotonin metabolite becomes a ligand.Archives of pharmacal research · 2023Review
- Development and Characterization of Fluorescent Probes for the G Protein-Coupled Receptor 35.ACS medicinal chemistry letters · 2023Article
- Neuroglobin plays as tumor suppressor by disrupting the stability of GPR35 in colorectal cancer.Clinical epigenetics · 2023Article
- CXCL17 binds efficaciously to glycosaminoglycans with the potential to modulate chemokine signaling.Frontiers in immunology · 2023Article
- GPR35 acts a dual role and therapeutic target in inflammation.Frontiers in immunology · 2023Review
- Activation of the IL-17 signalling pathway by the CXCL17-GPR35 axis affects drug resistance and colorectal cancer tumorigenesis.American journal of cancer research · 2023Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
background and purposeGPR35 has long been considered an orphan GPCR, because no endogenous ligand of GPR35 has been discovered. CXCL17 (a chemokine) has been reported to be an endogenous ligand of GPR35, and it has even been suggested that it be called CXCR8. However, at present there is no supporting evidence that CXCL17 does interact with GPR35. EXPERIMENTAL APPROACH: We applied two assay systems to explore the relationship between CXCL17 and GPR35. An AP-TGF-α shedding assay in GPR35 over-expressing HEK293 cells was used as a gain-of-function assay. GPR35 knock-down by siRNA transfection was performed in endogenously GPR35-expressing THP-1 cells. KEY
resultsIn the AP-TGF-α shedding assay, lodoxamide, a well-known synthetic GPR35 agonist, was confirmed to be the most potent agonist among other reported agonists. However, neither human nor mouse CXCL17 had an effect on GPR35. Consistent with previous findings, G proteins Gα CONCLUSIONS AND IMPLICATIONS: The present findings suggest that GPR35 functions as a migration inhibitory receptor, but CXCL17-stimulated migration of THP-1 cells is not dependent on GPR35.
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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.