Component
NBD-alpha-tocopherol
Fluorescent alpha-tocopherol analog with NBD attached to the side chain; distinct from unmodified dietary alpha-tocopherol. Fluorescent 7-nitrobenz-2-oxa-1,3-diazole-tagged alpha-tocopherol research probe; not unmodified dietary vitamin E.
3 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.
Other things that act on it
Enzymes, hormones, genes, and other components with a recorded effect. These are not nutrients, so they do not count toward the arrows above. Each finding names the chapter that recorded it.
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.
What it acts on
NBD-alpha-tocopherol bound recombinant human PKC alpha in solution: fluorescence increased at 1 µM probe, and 5 µM was used in competition assays with 0.1 µM enzyme.
Experimental context and source evidence
- cross_nutrient
- false
- experimental_model
- Fluorescence ligand binding in solution
- exposure
- 0.1 µM PKC alpha; 1–5 µM NBD-alpha-tocopherol; 30 min at room temperature; 1% ethanol buffer.
- limitations
- The fluorophore reports a hydrophobic environment. Competition controls support specific binding, but the labeled probe is distinct from native tocopherol.
- nutrient_topic
- Vitamin E research collection; topical membership is not evidence of a direct dietary effect. · Vitamin E
- organism
- Homo sapiens
- plain_language
- A fluorescently tagged vitamin E probe associated directly with purified PKC alpha.
- primary_references
- [mccary2012] Vitamin E isoforms directly bind PKCα and differentially regulate activation of PKCα. (2012). https://pubmed.ncbi.nlm.nih.gov/21933153/ DOI: 10.1042/bj20111318
- tissue_or_cell_type
- Cell-free enzyme
Vitamin E: transport, membrane protection and nutrient interactions (2026-09-17) · lines 972–983
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Fluorescence ligand binding in solution · source_derived_draft · unverified_draft
### e-sig-nbd-pkc-binding NBD-alpha-tocopherol bound recombinant human PKC alpha in solution: fluorescence increased at 1 µM probe, and 5 µM was used in competition assays with 0.1 µM enzyme. Condition category: normal nutrient_topic: Vitamin E research collection; topical membership is not evidence of a direct dietary effect. plain_language: A fluorescently tagged vitamin E probe associated directly with purified PKC alpha. organism: Homo sapiens tissue_or_cell_type: Cell-free enzyme experimental_model: Fluorescence ligand binding in solution limitations: The fluorophore reports a hydrophobic environment. Competition controls support specific binding, but the labeled probe is distinct from native tocopherol. exposure: 0.1 µM PKC alpha; 1–5 µM NBD-alpha-tocopherol; 30 min at room temperature; 1% ethanol buffer. cross_nutrient: false [mccary2012] Vitamin E isoforms directly bind PKCα and differentially regulate activation of PKCα. (2012). https://pubmed.ncbi.nlm.nih.gov/21933153/ DOI: 10.1042/bj20111318
Complete structured claim and evidence
Where it participates (unsigned role)
Retinol competed with 5 µM NBD-alpha-tocopherol for binding to 0.1 µM recombinant PKC alpha, whereas phosphatidylserine and cholesterol did not compete in the same study.
Experimental context and source evidence
- cross_nutrient
- true
- experimental_model
- Fluorescence competition assay, Figure 6G
- exposure
- 5 µM NBD-alpha-tocopherol; 0.1 µM PKC alpha; retinol concentration series; 30 min at room temperature, 1% ethanol.
- limitations
- Exact retinol axis values were not extracted; this is direct in-vitro competition, not demonstrated competition between dietary vitamins in human tissues.
- nutrient_topic
- Vitamin E research collection; topical membership is not evidence of a direct dietary effect. · Vitamin E
- organism
- Homo sapiens
- plain_language
- Vitamin A alcohol competed with the labeled vitamin E probe for association with this purified kinase.
- primary_references
- [mccary2012] Vitamin E isoforms directly bind PKCα and differentially regulate activation of PKCα. (2012). https://pubmed.ncbi.nlm.nih.gov/21933153/ DOI: 10.1042/bj20111318
- tissue_or_cell_type
- Cell-free enzyme
Vitamin E: transport, membrane protection and nutrient interactions (2026-09-17) · lines 985–996
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Fluorescence competition assay, Figure 6G · source_derived_draft · unverified_draft
### e-sig-retinol-pkc-competition Retinol competed with 5 µM NBD-alpha-tocopherol for binding to 0.1 µM recombinant PKC alpha, whereas phosphatidylserine and cholesterol did not compete in the same study. Condition category: normal nutrient_topic: Vitamin E research collection; topical membership is not evidence of a direct dietary effect. plain_language: Vitamin A alcohol competed with the labeled vitamin E probe for association with this purified kinase. organism: Homo sapiens tissue_or_cell_type: Cell-free enzyme experimental_model: Fluorescence competition assay, Figure 6G limitations: Exact retinol axis values were not extracted; this is direct in-vitro competition, not demonstrated competition between dietary vitamins in human tissues. exposure: 5 µM NBD-alpha-tocopherol; 0.1 µM PKC alpha; retinol concentration series; 30 min at room temperature, 1% ethanol. cross_nutrient: true [mccary2012] Vitamin E isoforms directly bind PKCα and differentially regulate activation of PKCα. (2012). https://pubmed.ncbi.nlm.nih.gov/21933153/ DOI: 10.1042/bj20111318
Complete structured claim and evidenceEngineered depletion of plasma-membrane PI(4,5)P2 impaired TTP-dependent NBD-alpha-tocopherol secretion in McARH7777 cells.
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
The events it takes part in
A mechanism often involves more than two components. These are the full events, with every participant and its role.
Situations it appears in
Low-supply and faulty-machinery situations recorded in the chapters where this component plays a part.
In the sources
Preserved passages that mention this component, quoted exactly. Open one to read it in context.
Open hypotheses
Proposed ideas that involve this component. They are labeled as hypotheses and do not change any recorded statement.
This is a research prototype built from draft material. It is not medical advice, and its statements still await verification against the original studies.