Component
Epidermal growth factor receptor
Receptor tyrosine kinase activated by EGF.
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 acts on it
Cucurbitacin D interfered with EGF–EGFR binding in a solid-phase binding assay and reduced EGFR phosphorylation in the NSCLC study.
Experimental context and source evidence
- evidence_access
- Primary abstract
- experimental_model
- Binding assay and gefitinib-resistant human NSCLC cell models.
- limitations
- This does not establish a clinically effective replacement for an EGFR inhibitor.
- nutrient_topic
- Cucurbitacins collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · Cucurbitacins
- plain_language
- A growth-factor interaction was tested upstream of signaling.
- primary_references
- Cucurbitacin D Overcomes Gefitinib Resistance by Blocking EGF Binding to EGFR and Inducing Cell Death in NSCLCs. · 2020 · https://pubmed.ncbi.nlm.nih.gov/32133284/ · DOI 10.3389/fonc.2020.00062
Cucurbitacins: thiol chemistry, cytoskeleton, metabolic dependencies and signaling (2026-09-20) · lines 332–338
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Binding assay and gefitinib-resistant human NSCLC cell models. · source_derived_draft · unverified_draft
## cucurbitacin-d-egf-binding A growth-factor interaction was tested upstream of signaling. Cucurbitacin D interfered with EGF–EGFR binding in a solid-phase binding assay and reduced EGFR phosphorylation in the NSCLC study. Model: Binding assay and gefitinib-resistant human NSCLC cell models. Limitations: This does not establish a clinically effective replacement for an EGFR inhibitor. Evidence access: Primary abstract Cucurbitacin D Overcomes Gefitinib Resistance by Blocking EGF Binding to EGFR and Inducing Cell Death in NSCLCs. · 2020 · https://pubmed.ncbi.nlm.nih.gov/32133284/ · DOI 10.3389/fonc.2020.00062
Complete structured claim and evidence
Where it participates (unsigned role)
EGF increased TRPM6-associated current in transfected HEK293 cells through EGFR-dependent signaling.
Experimental context and source evidence
- evidence-system
- EGF exposure and receptor-blocking patch-clamp experiments
- experimental_model
- EGF exposure and receptor-blocking patch-clamp experiments
- exposure
- 10 nM EGF for 30 minutes in the main stimulation experiment; a concentration-response series and EGFR blockade were also tested.
- limitations
- Channel-current regulation was directly tested in expression cells, not native human DCT recordings.
- nutrient_topic
- Magnesium research collection; topical membership is not evidence of a direct dietary effect. · Magnesium
- organism
- Human proteins and human-derived cells
- plain_language
- The growth factor EGF signals through its receptor to increase magnesium-channel activity.
- primary_references
- [groenestege-2007-egf] Impaired basolateral sorting of pro-EGF causes isolated recessive renal hypomagnesemia (2007). https://www.jci.org/articles/view/31680 DOI: 10.1172/JCI31680
- tissue
- HEK293 cells
- tissue_or_cell_type
- HEK293 cells
Magnesium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 1016–1028
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · EGF exposure and receptor-blocking patch-clamp experiments · source_derived_draft · unverified_draft
### egf-increases-trpm6-current EGF increased TRPM6-associated current in transfected HEK293 cells through EGFR-dependent signaling. Condition category: normal nutrient_topic: Magnesium research collection; topical membership is not evidence of a direct dietary effect. plain_language: The growth factor EGF signals through its receptor to increase magnesium-channel activity. organism: Human proteins and human-derived cells tissue_or_cell_type: HEK293 cells experimental_model: EGF exposure and receptor-blocking patch-clamp experiments limitations: Channel-current regulation was directly tested in expression cells, not native human DCT recordings. exposure: 10 nM EGF for 30 minutes in the main stimulation experiment; a concentration-response series and EGFR blockade were also tested. evidence-system: EGF exposure and receptor-blocking patch-clamp experiments tissue: HEK293 cells [groenestege-2007-egf] Impaired basolateral sorting of pro-EGF causes isolated recessive renal hypomagnesemia (2007). https://www.jci.org/articles/view/31680 DOI: 10.1172/JCI31680
Complete structured claim and evidencePro-EGF P1070L impaired basolateral delivery of TRPM6-stimulating EGF activity in polarized MDCK experiments.
Experimental context and source evidence
- availability_state
- machinery_impairment Imported condition classification; unverified.
- evidence-system
- Polarized MDCK conditioned-medium assays applied to TRPM6-expressing HEK293 cells
- experimental_model
- Polarized MDCK conditioned-medium assays applied to TRPM6-expressing HEK293 cells
- limitations
- Functional conditioned-medium evidence; no quantitative human DCT ligand measurement.
- nutrient_topic
- Magnesium research collection; topical membership is not evidence of a direct dietary effect. · Magnesium
- organism
- Human protein; canine and human-derived cells
- plain_language
- The mutation sends insufficient active signal to the epithelial side containing the relevant receptor.
- primary_references
- [groenestege-2007-egf] Impaired basolateral sorting of pro-EGF causes isolated recessive renal hypomagnesemia (2007). https://www.jci.org/articles/view/31680 DOI: 10.1172/JCI31680
- tissue
- Polarized epithelial model
- tissue_or_cell_type
- Polarized epithelial model
- trigger_kind
- machinery_impairment Imported condition classification; unverified.
Magnesium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 1030–1041
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Polarized MDCK conditioned-medium assays applied to TRPM6-expressing HEK293 cells · source_derived_draft · unverified_draft
### pro-egf-variant-loses-basolateral-signal Pro-EGF P1070L impaired basolateral delivery of TRPM6-stimulating EGF activity in polarized MDCK experiments. Condition category: machinery_impairment nutrient_topic: Magnesium research collection; topical membership is not evidence of a direct dietary effect. plain_language: The mutation sends insufficient active signal to the epithelial side containing the relevant receptor. organism: Human protein; canine and human-derived cells tissue_or_cell_type: Polarized epithelial model experimental_model: Polarized MDCK conditioned-medium assays applied to TRPM6-expressing HEK293 cells limitations: Functional conditioned-medium evidence; no quantitative human DCT ligand measurement. evidence-system: Polarized MDCK conditioned-medium assays applied to TRPM6-expressing HEK293 cells tissue: Polarized epithelial model [groenestege-2007-egf] Impaired basolateral sorting of pro-EGF causes isolated recessive renal hypomagnesemia (2007). https://www.jci.org/articles/view/31680 DOI: 10.1172/JCI31680
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.