Component

Human ALDOB Arg303Trp variant

Variant numbering follows the original report; impaired fructose-1-phosphate activity is demonstrated in recombinant 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.

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. The human ALDOB Arg303Trp variant had no detectable fructose-1-phosphate activity in the reported assay.

    Human ALDOB Arg303Trp variant → D-Fructose 1-phosphate source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    dose
    Wild-type versus hereditary-fructose-intolerance-associated variants; exact substrate series not in abstract
    duration
    Assay duration not recovered
    evidence_access
    Primary abstract/metadata; unrecovered methods explicitly retained.
    evidence_scope
    literature_reviewed; source-specific curation
    experimental_model
    Recombinant wild-type and Arg303Trp human ALDOB
    exposure_scope
    Human genetic machinery / fructose component
    limitations
    A mutation-specific activity defect is not ordinary dietary intolerance or a population toxicity threshold. Full article is scanned; abstract kinetics used.
    nutrient_topic
    HFCS chapter: actual formulation studies, component biochemistry and interventions are explicitly distinguished. · High-Fructose Corn Syrup / HFCS
    organism
    Recombinant wild-type and Arg303Trp human ALDOB
    plain_language
    The human ALDOB Arg303Trp variant had no detectable fructose-1-phosphate activity in the reported assay.
    primary_references
    Functional and molecular modelling studies of two hereditary fructose intolerance-causing mutations at arginine 303 in human liver aldolase. (2000). https://pubmed.ncbi.nlm.nih.gov/10970798/
    route
    In vitro recombinant enzyme assay
    tissue
    Fructose-1-phosphate enzyme assay
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    High-Fructose Corn Syrup: mechanism of action and metabolic impact (2026-09-20) · lines 125–135

    Original AI-assisted curation of twenty primary studies and official FDA composition information, with one reused canonical glucose-transport claim. Study-specific citations, negative findings and limitations retained. Not publisher full text. · supports · Recombinant wild-type and Arg303Trp human ALDOB · source_derived_draft · unverified_draft

    ## hfcs-aldob-variant The human ALDOB Arg303Trp variant had no detectable fructose-1-phosphate activity in the reported assay. Model/species: Recombinant wild-type and Arg303Trp human ALDOB Tissue: Fructose-1-phosphate enzyme assay Exposure: Wild-type versus hereditary-fructose-intolerance-associated variants; exact substrate series not in abstract Route: In vitro recombinant enzyme assay Duration: Assay duration not recovered Exposure scope: Human genetic machinery / fructose component Limits: A mutation-specific activity defect is not ordinary dietary intolerance or a population toxicity threshold. Full article is scanned; abstract kinetics used. Reference: Functional and molecular modelling studies of two hereditary fructose intolerance-causing mutations at arginine 303 in human liver aldolase. (2000). https://pubmed.ncbi.nlm.nih.gov/10970798/ Access: Primary abstract/metadata; unrecovered methods explicitly retained.
    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