Component

RDH10 silencing

Experimental siRNA-mediated reduction of RDH10 expression.

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.

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

Where it participates (unsigned role)

  1. Silencing endogenous RDH10 reduced retinoic-acid production from retinol in human cells.

    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_location
    Experimental Procedures: siRNA-mediated Knockdowns; Results: endogenous SDR silencing
    experimental_model
    Human RDH10 in Sf9 microsomes and siRNA perturbation in human cells.
    exposure
    RDH10 siRNA at 100 nanomolar, two transfections 24 hours apart; 10 micromolar retinol for 24 hours after silencing.
    limitations
    Residual activity and other enzymes prevent an exclusive RDH10 interpretation.
    nutrient_topic
    Vitamin A research collection; topical membership is not evidence of a direct dietary effect. · Vitamin A
    organism
    Homo sapiens
    outcome
    Silencing endogenous RDH10 reduced retinoic-acid production from retinol in human cells.
    plain_language
    Reducing precursor oxidation lowered downstream active retinoid production.
    primary_references
    [va-belyaeva-2008] Kinetic Analysis of Human Enzyme RDH10 Defines the Characteristics of a Physiologically Relevant Retinol Dehydrogenase (2008). https://pmc.ncbi.nlm.nih.gov/articles/PMC2459273/ DOI: 10.1074/jbc.M800019200
    tissue_or_cell_type
    HEK293 cells
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Vitamin A: forms, mechanisms, deficiency and excess (2026-09-17) · lines 502–514

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human RDH10 in Sf9 microsomes and siRNA perturbation in human cells. · source_derived_draft · unverified_draft

    ### va-rdh10-silencing-ra Silencing endogenous RDH10 reduced retinoic-acid production from retinol in human cells. Condition category: machinery_impairment nutrient_topic: Vitamin A research collection; topical membership is not evidence of a direct dietary effect. plain_language: Reducing precursor oxidation lowered downstream active retinoid production. organism: Homo sapiens tissue_or_cell_type: HEK293 cells experimental_model: Human RDH10 in Sf9 microsomes and siRNA perturbation in human cells. limitations: Residual activity and other enzymes prevent an exclusive RDH10 interpretation. exposure: RDH10 siRNA at 100 nanomolar, two transfections 24 hours apart; 10 micromolar retinol for 24 hours after silencing. outcome: Silencing endogenous RDH10 reduced retinoic-acid production from retinol in human cells. evidence_location: Experimental Procedures: siRNA-mediated Knockdowns; Results: endogenous SDR silencing [va-belyaeva-2008] Kinetic Analysis of Human Enzyme RDH10 Defines the Characteristics of a Physiologically Relevant Retinol Dehydrogenase (2008). https://pmc.ncbi.nlm.nih.gov/articles/PMC2459273/ DOI: 10.1074/jbc.M800019200
    Complete structured claim and evidence

In the sources

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    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