Component
MYPT1 Thr696 phosphorylation
Study-scoped entity; inspect species, exposure, model and limitations 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
EGCG dephosphorylated MYPT1 Thr696 through 67LR and eEF1A.
Experimental context and source evidence
- experimental_model
- Genetic screen, cell signaling and experimental tumor-growth models.
- limitations
- Pathway dependency in these models does not establish human cancer treatment or a dietary threshold.
- nutrient_topic
- EGCG collection; comparator and shared-pathway records retain their actual intervention. · Epigallocatechin-3-gallate (EGCG)
- plain_language
- EGCG removed an inhibitory phosphorylation mark in this pathway.
- primary_references
- Green tea polyphenol epigallocatechin-3-gallate signaling pathway through 67-kDa laminin receptor. · 2008 · https://pubmed.ncbi.nlm.nih.gov/18079119/ · DOI 10.1074/jbc.m707892200
EGCG: receptor signaling, metabolism, nutrient interactions and discovery questions (2026-09-18) · lines 36–42
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Genetic screen, cell signaling and experimental tumor-growth models. · source_derived_draft · unverified_draft
## egcg-mypt EGCG removed an inhibitory phosphorylation mark in this pathway. EGCG dephosphorylated MYPT1 Thr696 through 67LR and eEF1A. Model: Genetic screen, cell signaling and experimental tumor-growth models. Limitations: Pathway dependency in these models does not establish human cancer treatment or a dietary threshold. Evidence access: primary abstract. Green tea polyphenol epigallocatechin-3-gallate signaling pathway through 67-kDa laminin receptor. · 2008 · https://pubmed.ncbi.nlm.nih.gov/18079119/ · DOI 10.1074/jbc.m707892200
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.