Component

Human alpha-tocopherol transfer protein

Human alpha-TTP encoded by TTPA; distinguish protein from gene and orthologs. Alpha-tocopherol transfer protein / alpha-TTP. Read linked claims for the population, experiment and limits.

6 recorded relationships. Experimental role, claim status and evidence remain attached to each record.

Read recorded mechanisms Open recursive mind map

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. Ataxia Rating Scale scores improved modestly but significantly after one year of vitamin E in the AVED cohort; results were better with shorter disease duration.

    Vitamin E → Cerebellar ataxia severity source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    cross_nutrient
    false
    experimental_model
    Uncontrolled one-year supplementation study; 24 genetically investigated AVED patients
    exposure
    Vitamin E 800 mg/day for one year; formulation stereochemistry not specified in the retrieved abstract.
    limitations
    Small uncontrolled genetic-disease cohort; no inference of complete reversal, a general population dose or isolated dietary deficiency.
    nutrient_topic
    Vitamin E research collection; topical membership is not evidence of a direct dietary effect. · Vitamin E
    organism
    Homo sapiens
    plain_language
    Treating the inherited vitamin E shortage modestly improved coordination in this study.
    primary_references
    [e-clin-aved2001] Effect of vitamin E supplementation in patients with ataxia with vitamin E deficiency. (2001). https://pubmed.ncbi.nlm.nih.gov/11554913/ DOI: 10.1046/j.1468-1331.2001.00273.x
    tissue_or_cell_type
    Nervous system and serum
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Vitamin E: transport, membrane protection and nutrient interactions (2026-09-17) · lines 1167–1178

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Uncontrolled one-year supplementation study; 24 genetically investigated AVED patients · source_derived_draft · unverified_draft

    ### e-clin-aved-ataxia Ataxia Rating Scale scores improved modestly but significantly after one year of vitamin E in the AVED cohort; results were better with shorter disease duration. Condition category: machinery_impairment nutrient_topic: Vitamin E research collection; topical membership is not evidence of a direct dietary effect. plain_language: Treating the inherited vitamin E shortage modestly improved coordination in this study. organism: Homo sapiens tissue_or_cell_type: Nervous system and serum experimental_model: Uncontrolled one-year supplementation study; 24 genetically investigated AVED patients limitations: Small uncontrolled genetic-disease cohort; no inference of complete reversal, a general population dose or isolated dietary deficiency. exposure: Vitamin E 800 mg/day for one year; formulation stereochemistry not specified in the retrieved abstract. cross_nutrient: false [e-clin-aved2001] Effect of vitamin E supplementation in patients with ataxia with vitamin E deficiency. (2001). https://pubmed.ncbi.nlm.nih.gov/11554913/ DOI: 10.1046/j.1468-1331.2001.00273.x
    Complete structured claim and evidence

  2. Absent reflexes and posterior-column disturbances persisted despite normalization of serum vitamin E during AVED supplementation.

    Vitamin E → AVED reflex and posterior-column deficits source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    cross_nutrient
    false
    experimental_model
    Uncontrolled one-year supplementation study; 24 genetically investigated AVED patients
    exposure
    Vitamin E 800 mg/day for one year; formulation stereochemistry not specified in the retrieved abstract.
    limitations
    Small uncontrolled genetic-disease cohort; no inference of complete reversal, a general population dose or isolated dietary deficiency.
    nutrient_topic
    Vitamin E research collection; topical membership is not evidence of a direct dietary effect. · Vitamin E
    organism
    Homo sapiens
    plain_language
    Correcting the blood level did not reverse every established nerve deficit.
    primary_references
    [e-clin-aved2001] Effect of vitamin E supplementation in patients with ataxia with vitamin E deficiency. (2001). https://pubmed.ncbi.nlm.nih.gov/11554913/ DOI: 10.1046/j.1468-1331.2001.00273.x
    tissue_or_cell_type
    Nervous system and serum
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Vitamin E: transport, membrane protection and nutrient interactions (2026-09-17) · lines 1180–1191

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Uncontrolled one-year supplementation study; 24 genetically investigated AVED patients · source_derived_draft · unverified_draft

    ### e-clin-aved-residual-deficits Absent reflexes and posterior-column disturbances persisted despite normalization of serum vitamin E during AVED supplementation. Condition category: machinery_impairment nutrient_topic: Vitamin E research collection; topical membership is not evidence of a direct dietary effect. plain_language: Correcting the blood level did not reverse every established nerve deficit. organism: Homo sapiens tissue_or_cell_type: Nervous system and serum experimental_model: Uncontrolled one-year supplementation study; 24 genetically investigated AVED patients limitations: Small uncontrolled genetic-disease cohort; no inference of complete reversal, a general population dose or isolated dietary deficiency. exposure: Vitamin E 800 mg/day for one year; formulation stereochemistry not specified in the retrieved abstract. cross_nutrient: false [e-clin-aved2001] Effect of vitamin E supplementation in patients with ataxia with vitamin E deficiency. (2001). https://pubmed.ncbi.nlm.nih.gov/11554913/ DOI: 10.1046/j.1468-1331.2001.00273.x
    Complete structured claim and evidence

  3. Serum vitamin E normalized during one year of supplementation in the 24-patient AVED cohort.

    Vitamin E → Circulating alpha-tocopherol concentration source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    cross_nutrient
    false
    experimental_model
    Uncontrolled one-year supplementation study; 24 genetically investigated AVED patients
    exposure
    Vitamin E 800 mg/day for one year; formulation stereochemistry not specified in the retrieved abstract.
    limitations
    Small uncontrolled genetic-disease cohort; no inference of complete reversal, a general population dose or isolated dietary deficiency.
    nutrient_topic
    Vitamin E research collection; topical membership is not evidence of a direct dietary effect. · Vitamin E
    organism
    Homo sapiens
    plain_language
    Extra vitamin E restored the blood measurement despite the inherited transport disorder.
    primary_references
    [e-clin-aved2001] Effect of vitamin E supplementation in patients with ataxia with vitamin E deficiency. (2001). https://pubmed.ncbi.nlm.nih.gov/11554913/ DOI: 10.1046/j.1468-1331.2001.00273.x
    tissue_or_cell_type
    Nervous system and serum
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Vitamin E: transport, membrane protection and nutrient interactions (2026-09-17) · lines 1154–1165

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Uncontrolled one-year supplementation study; 24 genetically investigated AVED patients · source_derived_draft · unverified_draft

    ### e-clin-aved-serum Serum vitamin E normalized during one year of supplementation in the 24-patient AVED cohort. Condition category: machinery_impairment nutrient_topic: Vitamin E research collection; topical membership is not evidence of a direct dietary effect. plain_language: Extra vitamin E restored the blood measurement despite the inherited transport disorder. organism: Homo sapiens tissue_or_cell_type: Nervous system and serum experimental_model: Uncontrolled one-year supplementation study; 24 genetically investigated AVED patients limitations: Small uncontrolled genetic-disease cohort; no inference of complete reversal, a general population dose or isolated dietary deficiency. exposure: Vitamin E 800 mg/day for one year; formulation stereochemistry not specified in the retrieved abstract. cross_nutrient: false [e-clin-aved2001] Effect of vitamin E supplementation in patients with ataxia with vitamin E deficiency. (2001). https://pubmed.ncbi.nlm.nih.gov/11554913/ DOI: 10.1046/j.1468-1331.2001.00273.x
    Complete structured claim and evidence

  4. Adding alpha-tocopherol to vitamin E-depleted rat hepatoma cells expressing human TTP changed its punctate perinuclear distribution to a diffuse cellular pattern.

    RRR-alpha-tocopherol → Alpha-TTP intracellular redistribution source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    nutrient_deficiency Imported condition classification; unverified.
    cross_nutrient
    false
    experimental_model
    Human TTP expressed in depleted McARH7777 cells; Figure 2A
    exposure
    More than 10 passages in alpha-tocopherol-free defined serum; 35 µM serum-complexed d-alpha-tocopherol for 24 hours.
    limitations
    Depletion/repletion model with overexpressed human protein; localization is not a clinical deficiency threshold.
    nutrient_topic
    Vitamin E research collection; topical membership is not evidence of a direct dietary effect. · Vitamin E
    organism
    Rattus norvegicus cells; Homo sapiens protein
    plain_language
    Vitamin E supply changed where its transfer protein accumulated in these cells.
    primary_references
    [chung2016] Vitamin E and Phosphoinositides Regulate the Intracellular Localization of the Hepatic α-Tocopherol Transfer Protein. (2016). https://pubmed.ncbi.nlm.nih.gov/27307040/ DOI: 10.1074/jbc.m116.734210
    tissue_or_cell_type
    Hepatoma cells
    trigger_kind
    nutrient_deficiency Imported condition classification; unverified.

    Vitamin E: transport, membrane protection and nutrient interactions (2026-09-17) · lines 337–348

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human TTP expressed in depleted McARH7777 cells; Figure 2A · source_derived_draft · unverified_draft

    ### ve-transport-depletion-repletion-ttp-localization Adding alpha-tocopherol to vitamin E-depleted rat hepatoma cells expressing human TTP changed its punctate perinuclear distribution to a diffuse cellular pattern. Condition category: nutrient_deficiency nutrient_topic: Vitamin E research collection; topical membership is not evidence of a direct dietary effect. plain_language: Vitamin E supply changed where its transfer protein accumulated in these cells. organism: Rattus norvegicus cells; Homo sapiens protein tissue_or_cell_type: Hepatoma cells experimental_model: Human TTP expressed in depleted McARH7777 cells; Figure 2A limitations: Depletion/repletion model with overexpressed human protein; localization is not a clinical deficiency threshold. exposure: More than 10 passages in alpha-tocopherol-free defined serum; 35 µM serum-complexed d-alpha-tocopherol for 24 hours. cross_nutrient: false [chung2016] Vitamin E and Phosphoinositides Regulate the Intracellular Localization of the Hepatic α-Tocopherol Transfer Protein. (2016). https://pubmed.ncbi.nlm.nih.gov/27307040/ DOI: 10.1074/jbc.m116.734210
    Complete structured claim and evidence

  5. Engineered depletion of plasma-membrane PI(4,5)P2 impaired TTP-dependent NBD-alpha-tocopherol secretion in McARH7777 cells.

    Plasma membrane PI(4,5)P2 depletion → TTP-dependent NBD-alpha-tocopherol secretion source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    cross_nutrient
    false
    experimental_model
    Human TTP-expressing cells with membrane-targeted inositol phosphatase; Figure 5
    exposure
    IPP-CAAX expression; pulse loading with 10 µM serum-complexed NBD-alpha-tocopherol.
    limitations
    Phosphoinositide machinery perturbation and fluorescent analog; not dietary phosphorus or vitamin E deprivation as the causal contrast.
    nutrient_topic
    Vitamin E research collection; topical membership is not evidence of a direct dietary effect. · Vitamin E
    organism
    Rattus norvegicus cells; Homo sapiens TTP
    plain_language
    A membrane lipid signal was needed for efficient reporter export.
    primary_references
    [chung2016] Vitamin E and Phosphoinositides Regulate the Intracellular Localization of the Hepatic α-Tocopherol Transfer Protein. (2016). https://pubmed.ncbi.nlm.nih.gov/27307040/ DOI: 10.1074/jbc.m116.734210
    tissue_or_cell_type
    Hepatoma cells
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Vitamin E: transport, membrane protection and nutrient interactions (2026-09-17) · lines 363–374

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human TTP-expressing cells with membrane-targeted inositol phosphatase; Figure 5 · source_derived_draft · unverified_draft

    ### ve-transport-pip2-depletion-ttp-export Engineered depletion of plasma-membrane PI(4,5)P2 impaired TTP-dependent NBD-alpha-tocopherol secretion in McARH7777 cells. Condition category: machinery_impairment nutrient_topic: Vitamin E research collection; topical membership is not evidence of a direct dietary effect. plain_language: A membrane lipid signal was needed for efficient reporter export. organism: Rattus norvegicus cells; Homo sapiens TTP tissue_or_cell_type: Hepatoma cells experimental_model: Human TTP-expressing cells with membrane-targeted inositol phosphatase; Figure 5 limitations: Phosphoinositide machinery perturbation and fluorescent analog; not dietary phosphorus or vitamin E deprivation as the causal contrast. exposure: IPP-CAAX expression; pulse loading with 10 µM serum-complexed NBD-alpha-tocopherol. cross_nutrient: false [chung2016] Vitamin E and Phosphoinositides Regulate the Intracellular Localization of the Hepatic α-Tocopherol Transfer Protein. (2016). https://pubmed.ncbi.nlm.nih.gov/27307040/ DOI: 10.1074/jbc.m116.734210
    Complete structured claim and evidence

  6. Human TTP(R221W) remained punctate after alpha-tocopherol treatment in rat McARH7777 cells, unlike wild-type TTP.

    Human alpha-TTP R221W → Alpha-TTP intracellular redistribution source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    cross_nutrient
    false
    experimental_model
    Human wild-type versus R221W TTP expression; Figure 2B
    exposure
    35 µM serum-complexed alpha-tocopherol for 24 hours after medium depletion.
    limitations
    Mutation contrast is machinery impairment; this does not establish that supplementation cannot help AVED clinically.
    nutrient_topic
    Vitamin E research collection; topical membership is not evidence of a direct dietary effect. · Vitamin E
    organism
    Human proteins in Rattus norvegicus cells
    plain_language
    An AVED-associated variant failed to change location when vitamin E was supplied.
    primary_references
    [chung2016] Vitamin E and Phosphoinositides Regulate the Intracellular Localization of the Hepatic α-Tocopherol Transfer Protein. (2016). https://pubmed.ncbi.nlm.nih.gov/27307040/ DOI: 10.1074/jbc.m116.734210
    tissue_or_cell_type
    Hepatoma cells
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Vitamin E: transport, membrane protection and nutrient interactions (2026-09-17) · lines 350–361

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human wild-type versus R221W TTP expression; Figure 2B · source_derived_draft · unverified_draft

    ### ve-transport-r221w-localization Human TTP(R221W) remained punctate after alpha-tocopherol treatment in rat McARH7777 cells, unlike wild-type TTP. Condition category: machinery_impairment nutrient_topic: Vitamin E research collection; topical membership is not evidence of a direct dietary effect. plain_language: An AVED-associated variant failed to change location when vitamin E was supplied. organism: Human proteins in Rattus norvegicus cells tissue_or_cell_type: Hepatoma cells experimental_model: Human wild-type versus R221W TTP expression; Figure 2B limitations: Mutation contrast is machinery impairment; this does not establish that supplementation cannot help AVED clinically. exposure: 35 µM serum-complexed alpha-tocopherol for 24 hours after medium depletion. cross_nutrient: false [chung2016] Vitamin E and Phosphoinositides Regulate the Intracellular Localization of the Hepatic α-Tocopherol Transfer Protein. (2016). https://pubmed.ncbi.nlm.nih.gov/27307040/ DOI: 10.1074/jbc.m116.734210
    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.

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