Component
Aldehyde dehydrogenase 1A2 / ALDH1A2
Independent protein identity; organism and experimental state are specified on individual claims.
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
Human ALDH1A2 oxidized all-trans-retinaldehyde to retinoic acid in comparative enzyme assays.
Experimental context and source evidence
- evidence_location
- Abstract
- experimental_model
- Side-by-side recombinant human ALDH1A1, ALDH1A2 and ALDH1A3 kinetic assays.
- exposure
- Side-by-side retinaldehyde kinetic measurements by HPLC.
- limitations
- In vitro catalytic efficiency does not specify its contribution in a particular tissue.
- nutrient_topic
- Vitamin A research collection; topical membership is not evidence of a direct dietary effect. · Vitamin A
- organism
- Homo sapiens recombinant protein
- outcome
- Human ALDH1A2 oxidized all-trans-retinaldehyde to retinoic acid in comparative enzyme assays.
- plain_language
- This independently identified enzyme supplies the acid form used for signaling.
- primary_references
- [va-pequerul-2020] Structural and kinetic features of aldehyde dehydrogenase 1A (ALDH1A) subfamily members, cancer stem cell markers active in retinoic acid biosynthesis (2020). https://pubmed.ncbi.nlm.nih.gov/31923393/ DOI: 10.1016/j.abb.2020.108256
- tissue_or_cell_type
- Cell-free enzyme
Vitamin A: forms, mechanisms, deficiency and excess (2026-09-17) · lines 573–585
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Side-by-side recombinant human ALDH1A1, ALDH1A2 and ALDH1A3 kinetic assays. · source_derived_draft · unverified_draft
### va-aldh1a2-retinal-oxidation Human ALDH1A2 oxidized all-trans-retinaldehyde to retinoic acid in comparative enzyme assays. Condition category: normal nutrient_topic: Vitamin A research collection; topical membership is not evidence of a direct dietary effect. plain_language: This independently identified enzyme supplies the acid form used for signaling. organism: Homo sapiens recombinant protein tissue_or_cell_type: Cell-free enzyme experimental_model: Side-by-side recombinant human ALDH1A1, ALDH1A2 and ALDH1A3 kinetic assays. limitations: In vitro catalytic efficiency does not specify its contribution in a particular tissue. exposure: Side-by-side retinaldehyde kinetic measurements by HPLC. outcome: Human ALDH1A2 oxidized all-trans-retinaldehyde to retinoic acid in comparative enzyme assays. evidence_location: Abstract [va-pequerul-2020] Structural and kinetic features of aldehyde dehydrogenase 1A (ALDH1A) subfamily members, cancer stem cell markers active in retinoic acid biosynthesis (2020). https://pubmed.ncbi.nlm.nih.gov/31923393/ DOI: 10.1016/j.abb.2020.108256
Complete structured claim and evidence
What acts on it
Acetate promoted B-cell IgA class switching and IgA production in vitro in the presence of wild-type but not GPR43 knockout dendritic cells, and mechanistically acetate induced dendritic-cell expression of Aldh1a2, which converts vitamin A into retinoic acid, with blockade of retinoic acid signalling inhibiting the acetate-induced IgA production.
Experimental context and source evidence
- evidence_span
- {"source_cache": "artifacts/acetate-research/27966553.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "25ef476e62dd28f354099501d2919c3f765aaddd89d1a05739e3e0dc703d11ac", "start_char": 0, "end_char": 1363, "text_sha256": "25ef476e62dd28f354099501d2919c3f765aaddd89d1a05739e3e0dc703d11ac"}
- experimental_model
- GPR43 knockout mice with B-cell and dendritic-cell coculture and retinoic acid signalling blockade
- exposure
- Dietary acetate or butyrate in wild-type and GPR43 knockout mice, with in vitro IgA class switching assays
- limitations
- A clean set of controls: butyrate did not substitute for acetate, the effect was independent of T cells, and blocking the downstream vitamin A metabolite removed it.
- nutrient_topic
- Acetic acid research collection; topical membership is not evidence of a direct clinical effect, and the ingested acid is recorded separately from the circulating acetate anion. · Acetic acid
- organism
- Mouse
- plain_language
- Acetate works by switching on the enzyme that turns vitamin A into its active form; block that and the effect is gone.
- primary_references
- [acetate-p27966553] Microbiota metabolite short-chain fatty acid acetate promotes intestinal IgA response to microbiota which is mediated by GPR43. (2017). https://pubmed.ncbi.nlm.nih.gov/27966553/ DOI: 10.1038/mi.2016.114
- tissue_or_cell_type
- Intestinal mucosa
Acetic acid: the ingested acid, the receptors acetate binds, the acetyl-CoA it becomes, and the acetyl groups that reach histones (2026-09-21) · lines 394–405
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · GPR43 knockout mice with B-cell and dendritic-cell coculture and retinoic acid signalling blockade · source_derived_draft · unverified_draft
### acetate-acetate-vitamin-a-route Acetate promoted B-cell IgA class switching and IgA production in vitro in the presence of wild-type but not GPR43 knockout dendritic cells, and mechanistically acetate induced dendritic-cell expression of Aldh1a2, which converts vitamin A into retinoic acid, with blockade of retinoic acid signalling inhibiting the acetate-induced IgA production. Condition category: normal nutrient_topic: Acetic acid research collection; topical membership is not evidence of a direct clinical effect, and the ingested acid is recorded separately from the circulating acetate anion. plain_language: Acetate works by switching on the enzyme that turns vitamin A into its active form; block that and the effect is gone. organism: Mouse tissue_or_cell_type: Intestinal mucosa experimental_model: GPR43 knockout mice with B-cell and dendritic-cell coculture and retinoic acid signalling blockade limitations: A clean set of controls: butyrate did not substitute for acetate, the effect was independent of T cells, and blocking the downstream vitamin A metabolite removed it. exposure: Dietary acetate or butyrate in wild-type and GPR43 knockout mice, with in vitro IgA class switching assays evidence_span: {"source_cache": "artifacts/acetate-research/27966553.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "25ef476e62dd28f354099501d2919c3f765aaddd89d1a05739e3e0dc703d11ac", "start_char": 0, "end_char": 1363, "text_sha256": "25ef476e62dd28f354099501d2919c3f765aaddd89d1a05739e3e0dc703d11ac"} [acetate-p27966553] Microbiota metabolite short-chain fatty acid acetate promotes intestinal IgA response to microbiota which is mediated by GPR43. (2017). https://pubmed.ncbi.nlm.nih.gov/27966553/ DOI: 10.1038/mi.2016.114
Complete structured claim and evidence
Where it participates (unsigned role)
Conditional deletion of Aldh1a1, Aldh1a2 and Aldh1a3 did not prevent fetal ovarian meiotic progression despite strongly reduced RA.
Experimental context and source evidence
- availability_state
- machinery_impairment Imported condition classification; unverified.
- cross_nutrient
- false
- experimental_model
- Three conditional deletion strategies
- exposure
- Somatic or ubiquitous Aldh1a1-3 ablation; ovarian analyses around E13.5-E16.5.
- limitations
- Minor Stra8 delay occurred; analytically zero RA from every source was not demonstrated.
- nutrient_topic
- Vitamin A expansion research collection; topical membership is not evidence of a direct dietary effect. · Vitamin A
- organism
- Mus musculus
- plain_language
- Removing the main RA-synthesis enzymes did not stop fetal ovarian meiosis.
- primary_references
- [chassot2020] Retinoic acid synthesis by ALDH1A proteins is dispensable for meiosis initiation in the mouse fetal ovary. (2020). https://pubmed.ncbi.nlm.nih.gov/32494737/ DOI: 10.1126/sciadv.aaz1261
- tissue_or_cell_type
- fetal ovary
- trigger_kind
- machinery_impairment Imported condition classification; unverified.
Vitamin A expansion: reproduction, light-driven vision and shared mechanisms (2026-09-17) · lines 291–302
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Three conditional deletion strategies · source_derived_draft · unverified_draft
### va-repro-aldh-loss-ovarian-meiosis Conditional deletion of Aldh1a1, Aldh1a2 and Aldh1a3 did not prevent fetal ovarian meiotic progression despite strongly reduced RA. Condition category: machinery_impairment nutrient_topic: Vitamin A expansion research collection; topical membership is not evidence of a direct dietary effect. plain_language: Removing the main RA-synthesis enzymes did not stop fetal ovarian meiosis. organism: Mus musculus tissue_or_cell_type: fetal ovary experimental_model: Three conditional deletion strategies limitations: Minor Stra8 delay occurred; analytically zero RA from every source was not demonstrated. exposure: Somatic or ubiquitous Aldh1a1-3 ablation; ovarian analyses around E13.5-E16.5. cross_nutrient: false [chassot2020] Retinoic acid synthesis by ALDH1A proteins is dispensable for meiosis initiation in the mouse fetal ovary. (2020). https://pubmed.ncbi.nlm.nih.gov/32494737/ DOI: 10.1126/sciadv.aaz1261
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.