Component
Calcium response of human-TRPV1-expressing HEK293 cells
Species, assay, exposure and limitations are retained on linked claims.
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.
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 acts on it
Capsazepine inhibited the gamma-nonalactone-evoked TRPV1 calcium response.
Experimental context and source evidence
- dose
- Gamma-nonalactone 2 mM; capsazepine 1 micromolar or A-967079 1 micromolar
- 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
- Pharmacological specificity controls support channel involvement; they do not establish a binding pocket or oral therapeutic exposure.
- 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
- Capsazepine inhibited the gamma-nonalactone-evoked TRPV1 calcium response.
- 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 co-exposure
- tissue
- Receptor antagonist controls
Gamma-nonalactone: mechanisms, molecular forms and cross-actor connections (2026-09-20) · lines 70–79
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-capsazepine-control Capsazepine inhibited the gamma-nonalactone-evoked TRPV1 calcium response. Model/species: Human TRPV1 or TRPA1 expressed in HEK293 cells Tissue: Receptor antagonist controls Exposure: Gamma-nonalactone 2 mM; capsazepine 1 micromolar or A-967079 1 micromolar Route: In vitro co-exposure Duration: Acute fluorescence assay Limits: Pharmacological specificity controls support channel involvement; they do not establish a binding pocket or oral therapeutic exposure. 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
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.