Component
Retinoid X receptor family
RXR alpha, beta and gamma; distinct from RAR family.
3 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
An RXR-selective agonist alone failed to induce mucin transcripts but enhanced a suboptimal RAR agonist response.
Experimental context and source evidence
- evidence_locator
- Abstract
- experimental_model
- Normal human tracheobronchial epithelial cultures with receptor-selective agonists/antagonists.
- exposure
- Selective receptor agonists
- limitations
- No inference that 9-cis RA improves airway disease.
- nutrient_topic
- Vitamin A research collection; topical membership is not evidence of a direct dietary effect. · Vitamin A
- organism
- Homo sapiens
- plain_language
- Both partners can cooperate, with RAR activation required in this assay.
- primary_references
- [va-koo-1999] Role of retinoid receptors in the regulation of mucin gene expression by retinoic acid in human tracheobronchial epithelial cells (1999). https://pubmed.ncbi.nlm.nih.gov/10024510/ DOI: 10.1042/bj3380351
- tissue_or_cell_type
- Normal tracheobronchial epithelial cells
Vitamin A: forms, mechanisms, deficiency and excess (2026-09-17) · lines 1370–1381
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Normal human tracheobronchial epithelial cultures with receptor-selective agonists/antagonists. · source_derived_draft · unverified_draft
### va-sig-rxr-airway-cooperation An RXR-selective agonist alone failed to induce mucin transcripts but enhanced a suboptimal RAR agonist response. Condition category: normal nutrient_topic: Vitamin A research collection; topical membership is not evidence of a direct dietary effect. plain_language: Both partners can cooperate, with RAR activation required in this assay. organism: Homo sapiens tissue_or_cell_type: Normal tracheobronchial epithelial cells experimental_model: Normal human tracheobronchial epithelial cultures with receptor-selective agonists/antagonists. limitations: No inference that 9-cis RA improves airway disease. evidence_locator: Abstract exposure: Selective receptor agonists [va-koo-1999] Role of retinoid receptors in the regulation of mucin gene expression by retinoic acid in human tracheobronchial epithelial cells (1999). https://pubmed.ncbi.nlm.nih.gov/10024510/ DOI: 10.1042/bj3380351
Complete structured claim and evidence
What acts on it
9-cis RA bound the tested RXR preparation with high affinity and activated RXR-dependent reporter responses.
Experimental context and source evidence
- evidence_locator
- Abstract
- experimental_model
- Receptor binding and cell transfection assays.
- exposure
- 9-cis RA exposure
- limitations
- Its biochemical activity does not establish a universal physiological RXR ligand pool.
- nutrient_topic
- Vitamin A research collection; topical membership is not evidence of a direct dietary effect. · Vitamin A
- organism
- Recombinant/cultured-cell system
- plain_language
- The 9-cis isomer supplies a direct experimental RXR ligand.
- primary_references
- [va-heyman-1992] 9-cis retinoic acid is a high affinity ligand for the retinoid X receptor (1992). https://pubmed.ncbi.nlm.nih.gov/1310260/ DOI: 10.1016/0092-8674(92)90479-v
- tissue_or_cell_type
- Receptor-binding preparations
Vitamin A: forms, mechanisms, deficiency and excess (2026-09-17) · lines 1069–1080
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Receptor binding and cell transfection assays. · source_derived_draft · unverified_draft
### va-sig-9cis-rxr-binding 9-cis RA bound the tested RXR preparation with high affinity and activated RXR-dependent reporter responses. Condition category: normal nutrient_topic: Vitamin A research collection; topical membership is not evidence of a direct dietary effect. plain_language: The 9-cis isomer supplies a direct experimental RXR ligand. organism: Recombinant/cultured-cell system tissue_or_cell_type: Receptor-binding preparations experimental_model: Receptor binding and cell transfection assays. limitations: Its biochemical activity does not establish a universal physiological RXR ligand pool. evidence_locator: Abstract exposure: 9-cis RA exposure [va-heyman-1992] 9-cis retinoic acid is a high affinity ligand for the retinoid X receptor (1992). https://pubmed.ncbi.nlm.nih.gov/1310260/ DOI: 10.1016/0092-8674(92)90479-v
Complete structured claim and evidenceAll-trans RA did not effectively compete for RXR binding in the tested isomer assay.
Experimental context and source evidence
- evidence_locator
- Abstract
- experimental_model
- Transfected COS-1 nucleosol; ligand competition and chimeric receptor reporters.
- exposure
- Isomer competition
- limitations
- Cell metabolism can alter apparent reporter responses.
- nutrient_topic
- Vitamin A research collection; topical membership is not evidence of a direct dietary effect. · Vitamin A
- organism
- Recombinant receptors in COS-1 cells
- plain_language
- RAR and RXR cannot be treated as interchangeable RA receptors.
- primary_references
- [va-allenby-1993] Retinoic acid receptors and retinoid X receptors: interactions with endogenous retinoic acids (1993). https://pubmed.ncbi.nlm.nih.gov/8380496/ DOI: 10.1073/pnas.90.1.30
- tissue_or_cell_type
- Nuclear extracts
Vitamin A: forms, mechanisms, deficiency and excess (2026-09-17) · lines 1056–1067
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Transfected COS-1 nucleosol; ligand competition and chimeric receptor reporters. · source_derived_draft · unverified_draft
### va-sig-atra-rxr-selectivity All-trans RA did not effectively compete for RXR binding in the tested isomer assay. Condition category: normal nutrient_topic: Vitamin A research collection; topical membership is not evidence of a direct dietary effect. plain_language: RAR and RXR cannot be treated as interchangeable RA receptors. organism: Recombinant receptors in COS-1 cells tissue_or_cell_type: Nuclear extracts experimental_model: Transfected COS-1 nucleosol; ligand competition and chimeric receptor reporters. limitations: Cell metabolism can alter apparent reporter responses. evidence_locator: Abstract exposure: Isomer competition [va-allenby-1993] Retinoic acid receptors and retinoid X receptors: interactions with endogenous retinoic acids (1993). https://pubmed.ncbi.nlm.nih.gov/8380496/ DOI: 10.1073/pnas.90.1.30
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.