Component
Mouse Saa3 gene
Mouse serum amyloid A3 locus; do not equate with functional human SAA3 protein.
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 acts on it
RAR beta occupied the mouse Saa3 promoter; mutation of RARE -224 abolished reporter activity.
Experimental context and source evidence
- evidence_locator
- Figure 2; Methods
- experimental_model
- Mouse MODE-K cells and intestinal epithelial Rarb deletion.
- exposure
- 100 nM retinol plus 100 ng/mL LPS for 24 h
- limitations
- Direct binding to Saa1/Saa2 was predicted, not demonstrated here.
- nutrient_topic
- Vitamin A research collection; topical membership is not evidence of a direct dietary effect. · Vitamin A
- organism
- Mus musculus
- plain_language
- Epithelial retinoid sensing directly controls this mouse immune gene.
- primary_references
- [va-gattu-2019] Epithelial retinoic acid receptor beta regulates serum amyloid A expression and vitamin A-dependent intestinal immunity (2019). https://pmc.ncbi.nlm.nih.gov/articles/PMC6561173/ DOI: 10.1073/pnas.1812069116
- tissue_or_cell_type
- MODE-K intestinal epithelial cells
Vitamin A: forms, mechanisms, deficiency and excess (2026-09-17) · lines 1318–1329
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Mouse MODE-K cells and intestinal epithelial Rarb deletion. · source_derived_draft · unverified_draft
### va-sig-rarb-saa3-promoter RAR beta occupied the mouse Saa3 promoter; mutation of RARE -224 abolished reporter activity. Condition category: normal nutrient_topic: Vitamin A research collection; topical membership is not evidence of a direct dietary effect. plain_language: Epithelial retinoid sensing directly controls this mouse immune gene. organism: Mus musculus tissue_or_cell_type: MODE-K intestinal epithelial cells experimental_model: Mouse MODE-K cells and intestinal epithelial Rarb deletion. limitations: Direct binding to Saa1/Saa2 was predicted, not demonstrated here. evidence_locator: Figure 2; Methods exposure: 100 nM retinol plus 100 ng/mL LPS for 24 h [va-gattu-2019] Epithelial retinoic acid receptor beta regulates serum amyloid A expression and vitamin A-dependent intestinal immunity (2019). https://pmc.ncbi.nlm.nih.gov/articles/PMC6561173/ DOI: 10.1073/pnas.1812069116
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.