ReviewFrontiers in immunology2021
GPR35 in Intestinal Diseases: From Risk Gene to Function.
Review in Frontiers in immunology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 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
23 citing papers in PubMed, 43 citations in OpenAlex.
- Dietary anthocyanidin pelargonidin activates G protein-coupled receptor 35.The FEBS journal · 2026Article
- G Protein-Coupled Receptors in Irritable Bowel Syndrome: Mechanisms and Therapeutic Opportunities.International journal of molecular sciences · 2026Review
- Tryptophan metabolic gatekeeping in epithelial repair: GPR35-KLF5 circuitry decodes mucosal damage signals for repair programming.Cell death & disease · 2026Article
- Immune remodeling and metabolic reprogramming in chronic fatigue: insights into GPCR signaling and epigenetic regulation.Frontiers in immunology · 2026Review
- Intestinal amino acid metabolic response and its roles in inflammatory bowel disease.Cell communication and signaling : CCS · 2025Review
- Utilization of AhR and GPR35 Receptor Ligands as Superfoods in Cancer Prevention for Individuals with IBD.International journal of molecular sciences · 2025Review
- Review
- Herbal Amara extract induces gastric fundus relaxation via inhibition of the M2 muscarinic receptor.Neurogastroenterology and motility · 2025Article
- Gpr35 Expression Mitigates Neuroinflammation and Enriches GutResearch (Washington, D.C.) · 2025Article
- Gene expression profiling reveals host defense strategies for restrictingInfection and immunity · 2024Article
- The tryptophan metabolic pathway of the microbiome and host cells in health and disease.International immunology · 2024Review
- Genetic overlap between inflammatory bowel disease and iridocyclitis: insights from a genome-wide association study in a European population.BMC genomic data · 2024Article
- Kynurenine Pathway after Kidney Transplantation: Friend or Foe?International journal of molecular sciences · 2024Review
- The Effects of Kynurenic Acid in Zebrafish Embryos and Adult Rainbow Trout.Biomolecules · 2024Article
- Ethanol Extract ofMarine drugs · 2024Article
- DNA methylation in necrotizing enterocolitis.Expert reviews in molecular medicine · 2024Review
- GPR35-mediated kynurenic acid sensing contributes to maintenance of gut microbiota homeostasis in ulcerative colitis.FEBS open bio · 2023Article
- The Tryptophan and Kynurenine Pathway Involved in the Development of Immune-Related Diseases.International journal of molecular sciences · 2023Review
- Valorization of leftover green tea residues through conversion to bioactive peptides using probiotics-aided anaerobic digestion.Microbial biotechnology · 2023Article
- GPR35 antagonist CID-2745687 attenuates anchorage-independent cell growth by inhibiting YAP/TAZ activity in colorectal cancer cells.Frontiers in pharmacology · 2023Article
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
No grant is acknowledged in the PubMed record.
Abstract
Diet and gut microbial metabolites mediate host immune responses and are central to the maintenance of intestinal health. The metabolite-sensing G-protein coupled receptors (GPCRs) bind metabolites and trigger signals that are important for the host cell function, survival, proliferation and expansion. On the contrary, inadequate signaling of these metabolite-sensing GPCRs most likely participate to the development of diseases including inflammatory bowel diseases (IBD). In the intestine, metabolite-sensing GPCRs are highly expressed by epithelial cells and by specific subsets of immune cells. Such receptors provide an important link between immune system, gut microbiota and metabolic system. Member of these receptors, GPR35, a class A rhodopsin-like GPCR, has been shown to be activated by the metabolites tryptophan-derived kynurenic acid (KYNA), the chemokine CXCL17 and phospholipid derivate lysophosphatidic acid (LPA) species. There have been studies on GPR35 in the context of intestinal diseases since its identification as a risk gene for IBD. In this review, we discuss the pharmacology of GPR35 including its proposed endogenous and synthetic ligands as well as its antagonists. We elaborate on the risk variants of GPR35 implicated in gut-related diseases and the mechanisms by which GPR35 contribute to intestinal homeostasis.
Indexed as
Identifiers
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.