Component

Aldehyde dehydrogenase 1A3 / ALDH1A3

Independent protein identity; organism and experimental state are specified on individual claims.

2 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.

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.

Recorded relationships

What it acts on

  1. Human ALDH1A3 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 ALDH1A3 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 587–599

    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-aldh1a3-retinal-oxidation Human ALDH1A3 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 ALDH1A3 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

Where it participates (unsigned role)

  1. 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

In the sources

Preserved passages that mention this component, quoted exactly. Open one to read it in context.

    This is a research prototype built from draft material. It is not medical advice, and its statements still await verification against the original studies.

    Evidence, AI assistance and curation standards