Component
Human mitogen-activated protein kinase kinase 1 / MEK1 / MAP2K1
Human mitogen-activated protein kinase kinase 1 / MEK1 / MAP2K1. Species, exposure and limitations are retained in each linked claim.
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 it acts on
MEK1 mutations disrupting copper binding reduced BRAF V600E-driven signaling in the tested human and mouse systems.
Experimental context and source evidence
- evidence_span
- {"source_cache": "artifacts/copper-research/24717435.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "4eee319f693bd307d3930073167395e5ef454f07d976ca834539b637ec4406ef", "start_char": 0, "end_char": 1471, "text_sha256": "4eee319f693bd307d3930073167395e5ef454f07d976ca834539b637ec4406ef"}
- experimental_model
- Copper-binding MEK1 mutants, CTR1 perturbation and tumor models
- exposure
- CTR1 reduction, MEK1 copper-binding disruption and chelation
- limitations
- Preclinical mechanism; does not establish dietary copper as a cancer cause or copper restriction as a treatment.
- nutrient_topic
- Copper research collection; topical membership is not evidence of a direct dietary effect. · Copper
- organism
- Human and mouse experimental systems
- plain_language
- Copper binding influenced an enzyme in a growth-signaling chain.
- primary_references
- [copper-p24717435] Copper is required for oncogenic BRAF signalling and tumorigenesis. (2014). https://pubmed.ncbi.nlm.nih.gov/24717435/ DOI: 10.1038/nature13180
- tissue_or_cell_type
- BRAF V600E-driven signaling and tumor models
Copper: transport, cuproenzymes, deficiency, excess and nutrient interactions (2026-09-17) · lines 1222–1233
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Copper-binding MEK1 mutants, CTR1 perturbation and tumor models · source_derived_draft · unverified_draft
### copper-cu-mek1-signaling MEK1 mutations disrupting copper binding reduced BRAF V600E-driven signaling in the tested human and mouse systems. Condition category: normal nutrient_topic: Copper research collection; topical membership is not evidence of a direct dietary effect. plain_language: Copper binding influenced an enzyme in a growth-signaling chain. organism: Human and mouse experimental systems tissue_or_cell_type: BRAF V600E-driven signaling and tumor models experimental_model: Copper-binding MEK1 mutants, CTR1 perturbation and tumor models limitations: Preclinical mechanism; does not establish dietary copper as a cancer cause or copper restriction as a treatment. exposure: CTR1 reduction, MEK1 copper-binding disruption and chelation evidence_span: {"source_cache": "artifacts/copper-research/24717435.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "4eee319f693bd307d3930073167395e5ef454f07d976ca834539b637ec4406ef", "start_char": 0, "end_char": 1471, "text_sha256": "4eee319f693bd307d3930073167395e5ef454f07d976ca834539b637ec4406ef"} [copper-p24717435] Copper is required for oncogenic BRAF signalling and tumorigenesis. (2014). https://pubmed.ncbi.nlm.nih.gov/24717435/ DOI: 10.1038/nature13180
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.