Component

EGTA

Ethylene glycol-bis(2-aminoethylether)-N,N,N-prime,N-prime-tetraacetic acid; experimental calcium chelator, not the microbial EgtA 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. EGTA treatment suppressed the gamma-nonalactone-evoked TRPA1 calcium signal.

    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    dose
    Gamma-nonalactone 2 mM and EGTA 5 mM
    duration
    Acute fluorescence assay
    evidence_access
    Primary full-text methods/results inspected; PubMed metadata where indexed.
    evidence_scope
    literature_reviewed; model-specific source-derived curation
    experimental_model
    Human TRPV1 or TRPA1 expressed in HEK293 cells
    limitations
    Experimental extracellular calcium removal is not dietary calcium deficiency. A calcium-flux readout cannot establish every downstream cellular consequence.
    nutrient_topic
    Gamma-nonalactone flavor-compound chapter; nutrient and drug interactions retain their experimental settings. · Gamma-nonalactone
    organism
    Human TRPV1 or TRPA1 expressed in HEK293 cells
    plain_language
    EGTA treatment suppressed the gamma-nonalactone-evoked TRPA1 calcium signal.
    primary_references
    Agonistic/antagonistic properties of lactones in food flavors on the sensory ion channels TRPV1 and TRPA1. (2022). https://pubmed.ncbi.nlm.nih.gov/36374622/ DOI: 10.1093/chemse/bjac023
    route
    In vitro calcium chelation
    tissue
    Extracellular calcium-chelation control
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Gamma-nonalactone: mechanisms, molecular forms and cross-actor connections (2026-09-20) · lines 92–101

    Original AI-assisted curation of eight primary studies. Study-specific citations, negative findings and limitations retained. Not publisher full text. · supports · Human TRPV1 or TRPA1 expressed in HEK293 cells · source_derived_draft · unverified_draft

    ## gamma-nonalactone-egta-trpa1 EGTA treatment suppressed the gamma-nonalactone-evoked TRPA1 calcium signal. Model/species: Human TRPV1 or TRPA1 expressed in HEK293 cells Tissue: Extracellular calcium-chelation control Exposure: Gamma-nonalactone 2 mM and EGTA 5 mM Route: In vitro calcium chelation Duration: Acute fluorescence assay Limits: Experimental extracellular calcium removal is not dietary calcium deficiency. A calcium-flux readout cannot establish every downstream cellular consequence. Primary reference: Agonistic/antagonistic properties of lactones in food flavors on the sensory ion channels TRPV1 and TRPA1. (2022). https://pubmed.ncbi.nlm.nih.gov/36374622/ DOI: 10.1093/chemse/bjac023 Access: Primary full-text methods/results inspected; PubMed metadata where indexed.
    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