Component
T-cell AKT-mTOR signaling
T-cell AKT-mTOR signaling; interpretation depends on linked experimental context.
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
Elevated intracellular K suppressed TCR-driven AKT-mTOR signaling through a PP2A-dependent process.
Experimental context and source evidence
- experimental_model
- High-K mouse/human T-cell cultures; PP2A perturbations.
- limitations
- PP2A dependence does not demonstrate direct K binding; no diet manipulation.
- nutrient_topic
- Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium
- organism
- Mouse and human
- plain_language
- Local potassium accumulation dampened T-cell activation signals.
- primary_references
- [eil-2016-tcells] Ionic immune suppression within the tumour microenvironment limits T cell effector function (2016). https://pmc.ncbi.nlm.nih.gov/articles/PMC5204372/ DOI: 10.1038/nature19364
- tissue_or_cell_type
- T cells
Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 902–911
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · High-K mouse/human T-cell cultures; PP2A perturbations. · source_derived_draft · unverified_draft
### k-tcell-pp2a-suppression Elevated intracellular K suppressed TCR-driven AKT-mTOR signaling through a PP2A-dependent process. Condition category: normal nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Local potassium accumulation dampened T-cell activation signals. organism: Mouse and human tissue_or_cell_type: T cells experimental_model: High-K mouse/human T-cell cultures; PP2A perturbations. limitations: PP2A dependence does not demonstrate direct K binding; no diet manipulation. [eil-2016-tcells] Ionic immune suppression within the tumour microenvironment limits T cell effector function (2016). https://pmc.ncbi.nlm.nih.gov/articles/PMC5204372/ DOI: 10.1038/nature19364
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.