Component
Mouse retinoic-acid-receptor signaling in butyrate/DC experiments; receptor subtype unresolved
Context-specific entity; species, compartment and exposure are stated on each claim.
1 recorded relationships. Experimental role, claim status and evidence remain attached to each record.
How nutrients influence it
Every nutrient with a recorded effect on this component, credited to the nutrient that acted rather than the chapter that recorded it. Open a nutrient to see the findings and the conditions they were measured under.
Other things that act on it
Enzymes, hormones, genes, and other components with a recorded effect. These are not nutrients, so they do not count toward the arrows above. Each finding names the chapter that recorded it.
How nutrients reach it in more than one step
Chains of two or more recorded steps that end here, grouped by the nutrient they start from. Each step is a separate finding, so a chain is a route a mechanism could take, not proof that it does.
Tracing routes…
What it does
Every recorded relationship this component is part of, grouped by its role. Plain wording comes first; the technical statement follows.
What it acts on
The retinoic-acid-receptor antagonist LE135 abolished the increased Treg conversion induced by butyrate- or niacin-treated wild-type mouse dendritic cells.
Experimental context and source evidence
- availability_state
- machinery_impairment Imported condition classification; unverified.
- evidence_access
- Primary full text, Figure S2I and methods
- experimental_model
- Mouse dendritic/T-cell coculture; LE135 1 micromolar.
- limitations
- Antagonist exposure is not a vitamin A withdrawal experiment; extra vitamin A was not demonstrated to improve a replete response.
- nutrient_topic
- Butyrate collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Butyrate
- plain_language
- Blocking vitamin A–related receptor signaling removed this immune-cell response.
- primary_references
- Activation of Gpr109a, receptor for niacin and the commensal metabolite butyrate, suppresses colonic inflammation and carcinogenesis. · 2014 · https://pubmed.ncbi.nlm.nih.gov/24412617/ · DOI 10.1016/j.immuni.2013.12.007
- trigger_kind
- machinery_impairment Imported condition classification; unverified.
Butyrate: microbial production, fuel use, signaling and nutrient interactions (2026-09-19) · lines 374–380
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Mouse dendritic/T-cell coculture; LE135 1 micromolar. · source_derived_draft · unverified_draft
## butyrate-retinoid-block Blocking vitamin A–related receptor signaling removed this immune-cell response. The retinoic-acid-receptor antagonist LE135 abolished the increased Treg conversion induced by butyrate- or niacin-treated wild-type mouse dendritic cells. Model: Mouse dendritic/T-cell coculture; LE135 1 micromolar. Limitations: Antagonist exposure is not a vitamin A withdrawal experiment; extra vitamin A was not demonstrated to improve a replete response. Evidence access: Primary full text, Figure S2I and methods Activation of Gpr109a, receptor for niacin and the commensal metabolite butyrate, suppresses colonic inflammation and carcinogenesis. · 2014 · https://pubmed.ncbi.nlm.nih.gov/24412617/ · DOI 10.1016/j.immuni.2013.12.007
Complete structured claim and evidence
The events it takes part in
A mechanism often involves more than two components. These are the full events, with every participant and its role.
Situations it appears in
Low-supply and faulty-machinery situations recorded in the chapters where this component plays a part.
In the sources
Preserved passages that mention this component, quoted exactly. Open one to read it in context.
Open hypotheses
Proposed ideas that involve this component. They are labeled as hypotheses and do not change any recorded statement.
This is a research prototype built from draft material. It is not medical advice, and its statements still await verification against the original studies.