ArticleInternational journal of molecular sciences2020
Gut Microbial Catabolites of Tryptophan Are Ligands and Agonists of the Aryl Hydrocarbon Receptor: A Detailed Characterization.
Article in International journal of molecular sciences, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 85 papers, 1 of them a synthesis that pooled it.
What it found
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Who cites it
85 citing papers in PubMed, 1 synthesis or guideline pooled it, 141 citations in OpenAlex.
- Pooled it
- Inhibition of Aryl hydrocarbon receptor Interleukin-22 signaling and worsening of intestinal inflammation byGut microbes · 2026Article
- Indole-3-acetic acid production is rare among gut bacteria and reflects OFOR-driven amino acid oxidation in acetogens.Gut microbes · 2026Article
- Multi-omics analysis of saccharomyces boulardii supplementation reveals coordinated microbiome, metabolic, and immune signaling changes accompanying tumor suppression.Gut microbes · 2026Article
- Microbiome-Derived Tryptophan Metabolites Regulate AhR Signaling to Restore Epithelial Barrier Integrity in Inflammatory Bowel Disease.MicrobiologyOpen · 2026Review
- Amino Acid Metabolism in Health and Disease.MedComm · 2026Review
- Microbiota-Derived Metabolites in the Epigenetic Regulation of Redox Homeostasis.Antioxidants (Basel, Switzerland) · 2026Review
- The Gut-Lung Microbiome Axis in Alveolar Stem Cell Regeneration and Lung Repair.Microorganisms · 2026Review
- Aryl hydrocarbon receptor pharmacology-mechanisms, ligands, and therapeutic potential.Pharmacological reviews · 2026Review
- Comparative 28-day mouse study of topically applied aryl hydrocarbon receptor ligands: microbiota-derived indoles, therapeutic tapinarof, pollutants 2,3,7,8-tetrachlorodibenzo-p-dioxin and diesel exhaust particles.Chemico-biological interactions · 2026Article
- Tryptophan Metabolism and Aryl-Hydrocarbon Receptor Agonists in the Gut Microbiome of People With Myalgic Encephalomyelitis/Chronic Fatigue Syndrome.MicrobiologyOpen · 2026Article
- Cell Signaling by Tryptophan Catabolism.Biochemistry · 2026Review
- Ultraviolet radiation reshapes the metabolome of skin commensal bacteria, influencing AhR signaling and barrier function.Applied and environmental microbiology · 2026Article
- Review
- Tryptophan metabolism alterations in neurological and psychiatric diseases: Molecular mechanisms and pharmacological targets.Metabolic brain disease · 2026Review
- ExploringBiomolecules & therapeutics · 2026Article
- Indole-3-Acetic Acid and Skatole Exert Opposing Effects on MDR1 Proteostasis in Human Colonic Epithelial Cells: A Molecular Basis for the Gut Microbial Metabolic Switch.Journal of xenobiotics · 2026Article
- Article
- Indole-3-acetic acid production is rare among gut bacteria and reflects OFOR-driven amino acid oxidation in acetogens.bioRxiv : the preprint server for biology · 2026Article
- The aryl hydrocarbon receptor: structure, signaling, physiology and pathology.Signal transduction and targeted therapy · 2026Review
25 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
12 authors at 4 institutions in 2 countries.
Funding
Abstract
We examined the effects of gut microbial catabolites of tryptophan on the aryl hydrocarbon receptor (AhR). Using a reporter gene assay, we show that all studied catabolites are low-potency agonists of human AhR. The efficacy of catabolites differed substantially, comprising agonists with no or low (i3-propionate, i3-acetate, i3-lactate, i3-aldehyde), medium (i3-ethanol, i3-acrylate, skatole, tryptamine), and high (indole, i3-acetamide, i3-pyruvate) efficacies. We displayed ligand-selective antagonist activities by i3-pyruvate, i3-aldehyde, indole, skatole, and tryptamine. Ligand binding assay identified low affinity (skatole, i3-pyruvate, and i3-acetamide) and very low affinity (i3-acrylate, i3-ethanol, indole) ligands of the murine AhR. Indole, skatole, tryptamine, i3-pyruvate, i3-acrylate, and i3-acetamide induced
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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.