Component
Human TNF receptor 1 / TNFRSF1A
Context-specific entity; species, compartment and exposure are stated on each claim.
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.
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
Adding a TNF-alpha-converting-enzyme inhibitor suppressed cucurbitacin B-associated TNFR1 down-regulation in human A549 cells.
Experimental context and source evidence
- availability_state
- machinery_impairment Imported condition classification; unverified.
- evidence_access
- Primary abstract
- experimental_model
- Human A549 pharmacological perturbation.
- limitations
- Supports involvement of ADAM17-related processing; does not prove cucurbitacin binds or directly activates ADAM17.
- nutrient_topic
- Cucurbitacins collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · Cucurbitacins
- plain_language
- A receptor-processing enzyme was implicated by an inhibitor experiment.
- primary_references
- Cucurbitacin B Down-Regulates TNF Receptor 1 Expression and Inhibits the TNF-α-Dependent Nuclear Factor κB Signaling Pathway in Human Lung Adenocarcinoma A549 Cells. · 2022 · https://pubmed.ncbi.nlm.nih.gov/35806134/ · DOI 10.3390/ijms23137130
- trigger_kind
- machinery_impairment Imported condition classification; unverified.
Cucurbitacins: thiol chemistry, cytoskeleton, metabolic dependencies and signaling (2026-09-20) · lines 196–202
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Human A549 pharmacological perturbation. · source_derived_draft · unverified_draft
## cucurbitacin-b-adam17-gate A receptor-processing enzyme was implicated by an inhibitor experiment. Adding a TNF-alpha-converting-enzyme inhibitor suppressed cucurbitacin B-associated TNFR1 down-regulation in human A549 cells. Model: Human A549 pharmacological perturbation. Limitations: Supports involvement of ADAM17-related processing; does not prove cucurbitacin binds or directly activates ADAM17. Evidence access: Primary abstract Cucurbitacin B Down-Regulates TNF Receptor 1 Expression and Inhibits the TNF-α-Dependent Nuclear Factor κB Signaling Pathway in Human Lung Adenocarcinoma A549 Cells. · 2022 · https://pubmed.ncbi.nlm.nih.gov/35806134/ · DOI 10.3390/ijms23137130
Complete structured claim and evidenceCucurbitacin B lowered TNF receptor 1 expression in human A549 cells without reducing the measured TRADD, RIPK1 and TRAF2 adaptor proteins.
Experimental context and source evidence
- evidence_access
- Primary abstract
- experimental_model
- TNF-alpha-stimulated human A549 cells; dose/time not resolved in accessed abstract.
- limitations
- Protein abundance result, not demonstrated direct binding to TNFR1.
- nutrient_topic
- Cucurbitacins collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · Cucurbitacins
- plain_language
- The receptor changed before treating all downstream proteins as depleted.
- primary_references
- Cucurbitacin B Down-Regulates TNF Receptor 1 Expression and Inhibits the TNF-α-Dependent Nuclear Factor κB Signaling Pathway in Human Lung Adenocarcinoma A549 Cells. · 2022 · https://pubmed.ncbi.nlm.nih.gov/35806134/ · DOI 10.3390/ijms23137130
Cucurbitacins: thiol chemistry, cytoskeleton, metabolic dependencies and signaling (2026-09-20) · lines 188–194
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · TNF-alpha-stimulated human A549 cells; dose/time not resolved in accessed abstract. · source_derived_draft · unverified_draft
## cucurbitacin-b-tnfr1 The receptor changed before treating all downstream proteins as depleted. Cucurbitacin B lowered TNF receptor 1 expression in human A549 cells without reducing the measured TRADD, RIPK1 and TRAF2 adaptor proteins. Model: TNF-alpha-stimulated human A549 cells; dose/time not resolved in accessed abstract. Limitations: Protein abundance result, not demonstrated direct binding to TNFR1. Evidence access: Primary abstract Cucurbitacin B Down-Regulates TNF Receptor 1 Expression and Inhibits the TNF-α-Dependent Nuclear Factor κB Signaling Pathway in Human Lung Adenocarcinoma A549 Cells. · 2022 · https://pubmed.ncbi.nlm.nih.gov/35806134/ · DOI 10.3390/ijms23137130
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.