Component

Human apolipoprotein A-I

Human apoA-I; lipid-poor acceptor used in cellular alpha-tocopherol efflux assays.

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

Where it participates (unsigned role)

  1. Expression of human ABCA1 in BHK cells increased alpha-tocopherol efflux to apoA-I.

    Experimental context and source evidence
    cross_nutrient
    false
    experimental_model
    Human ABCA1 gain of function in BHK cells
    exposure
    Radiolabeled alpha-tocopherol; 2-hour efflux to 5 µg/mL apoA-I with 1 mg/mL BSA.
    limitations
    Engineered cell assay; does not identify ABCA1 as the only vitamin E exporter.
    nutrient_topic
    Vitamin E research collection; topical membership is not evidence of a direct dietary effect. · Vitamin E
    organism
    Human protein in hamster cells
    plain_language
    ABCA1 helped transfer cellular vitamin E to an extracellular lipoprotein protein.
    primary_references
    [oram2001] ATP-binding cassette transporter A1 mediates cellular secretion of alpha-tocopherol. (2001). https://pubmed.ncbi.nlm.nih.gov/11546785/ DOI: 10.1074/jbc.m106984200
    tissue_or_cell_type
    BHK kidney-derived cell line

    Vitamin E: transport, membrane protection and nutrient interactions (2026-09-17) · lines 272–283

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human ABCA1 gain of function in BHK cells · source_derived_draft · unverified_draft

    ### ve-transport-abca1-apoa1-efflux Expression of human ABCA1 in BHK cells increased alpha-tocopherol efflux to apoA-I. Condition category: normal nutrient_topic: Vitamin E research collection; topical membership is not evidence of a direct dietary effect. plain_language: ABCA1 helped transfer cellular vitamin E to an extracellular lipoprotein protein. organism: Human protein in hamster cells tissue_or_cell_type: BHK kidney-derived cell line experimental_model: Human ABCA1 gain of function in BHK cells limitations: Engineered cell assay; does not identify ABCA1 as the only vitamin E exporter. exposure: Radiolabeled alpha-tocopherol; 2-hour efflux to 5 µg/mL apoA-I with 1 mg/mL BSA. cross_nutrient: false [oram2001] ATP-binding cassette transporter A1 mediates cellular secretion of alpha-tocopherol. (2001). https://pubmed.ncbi.nlm.nih.gov/11546785/ DOI: 10.1074/jbc.m106984200
    Complete structured claim and evidence
  2. ApoA-I failed to remove alpha-tocopherol from Tangier disease fibroblasts with nonfunctional ABCA1.

    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    cross_nutrient
    false
    experimental_model
    Normal versus Tangier disease fibroblasts
    exposure
    Radiolabeled alpha-tocopherol; cholesterol/8-bromo-cAMP pretreatment; 6-hour apoA-I efflux assay.
    limitations
    Patient-cell machinery defect; not dietary deprivation or a claim that all HDL-mediated efflux is absent.
    nutrient_topic
    Vitamin E research collection; topical membership is not evidence of a direct dietary effect. · Vitamin E
    organism
    Homo sapiens
    plain_language
    An inherited transporter defect blocked this vitamin E export route in patient cells.
    primary_references
    [oram2001] ATP-binding cassette transporter A1 mediates cellular secretion of alpha-tocopherol. (2001). https://pubmed.ncbi.nlm.nih.gov/11546785/ DOI: 10.1074/jbc.m106984200
    tissue_or_cell_type
    Cultured fibroblasts
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Vitamin E: transport, membrane protection and nutrient interactions (2026-09-17) · lines 285–296

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Normal versus Tangier disease fibroblasts · source_derived_draft · unverified_draft

    ### ve-transport-abca1-tangier-efflux-loss ApoA-I failed to remove alpha-tocopherol from Tangier disease fibroblasts with nonfunctional ABCA1. Condition category: machinery_impairment nutrient_topic: Vitamin E research collection; topical membership is not evidence of a direct dietary effect. plain_language: An inherited transporter defect blocked this vitamin E export route in patient cells. organism: Homo sapiens tissue_or_cell_type: Cultured fibroblasts experimental_model: Normal versus Tangier disease fibroblasts limitations: Patient-cell machinery defect; not dietary deprivation or a claim that all HDL-mediated efflux is absent. exposure: Radiolabeled alpha-tocopherol; cholesterol/8-bromo-cAMP pretreatment; 6-hour apoA-I efflux assay. cross_nutrient: false [oram2001] ATP-binding cassette transporter A1 mediates cellular secretion of alpha-tocopherol. (2001). https://pubmed.ncbi.nlm.nih.gov/11546785/ DOI: 10.1074/jbc.m106984200
    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