Component
Mouse MEK1 / Map2k1
Context-specific entity; species, compartment and exposure are stated on each 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 acts on it
Myricetin inhibited MEK1 activity in the mouse JB6 transformation system; GST-MEK1 pull-down supported ATP-noncompetitive binding.
Experimental context and source evidence
- evidence_access
- Primary abstract
- experimental_model
- Mouse epidermal JB6 P+ cells and GST-MEK1 binding; recombinant construct species not resolved in accessed abstract.
- limitations
- Cellular node is mouse; do not assume recombinant construct species or selective human inhibition.
- nutrient_topic
- Myricetin collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Myricetin
- plain_language
- This kinase experiment differs from ATP-competitive targets.
- primary_references
- Myricetin is a novel natural inhibitor of neoplastic cell transformation and MEK1. · 2007 · https://pubmed.ncbi.nlm.nih.gov/17693661/ · DOI 10.1093/carcin/bgm110
Myricetin: metabolism, immune signaling, redox chemistry and cross-nutrient mechanisms (2026-09-19) · lines 452–458
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Mouse epidermal JB6 P+ cells and GST-MEK1 binding; recombinant construct species not resolved in accessed abstract. · source_derived_draft · unverified_draft
## myricetin-mek1 This kinase experiment differs from ATP-competitive targets. Myricetin inhibited MEK1 activity in the mouse JB6 transformation system; GST-MEK1 pull-down supported ATP-noncompetitive binding. Model: Mouse epidermal JB6 P+ cells and GST-MEK1 binding; recombinant construct species not resolved in accessed abstract. Limitations: Cellular node is mouse; do not assume recombinant construct species or selective human inhibition. Evidence access: Primary abstract Myricetin is a novel natural inhibitor of neoplastic cell transformation and MEK1. · 2007 · https://pubmed.ncbi.nlm.nih.gov/17693661/ · DOI 10.1093/carcin/bgm110
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.