Component
The serine/threonine phosphatase PP2A
The serine/threonine phosphatase PP2A. 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.
Where it participates (unsigned role)
Necrosis releases intracellular potassium ions into the extracellular fluid of mouse and human tumours causing profound suppression of T cell effector function, elevation of the extracellular potassium concentration impairs T cell receptor-driven Akt-mTOR phosphorylation and effector programmes, potassium-mediated suppression of Akt-mTOR signalling and T cell function is dependent upon the activity of the serine/threonine phosphatase PP2A, although the suppressive effect mediated by elevated extracellular potassium is independent of changes in plasma membrane potential it requires an increase in intracellular potassium, and augmenting potassium efflux in tumour-specific T cells by overexpressing the potassium channel Kv1.3 lowers intracellular potassium and improves effector functions in vitro and in vivo.
Experimental context and source evidence
- evidence_span
- {"source_cache": "artifacts/gaba-research/27626381.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "73f83e208d8ad23be6c7ada4127b06536cdfd3156c4ac588e004e775761214f8", "start_char": 0, "end_char": 1240, "text_sha256": "73f83e208d8ad23be6c7ada4127b06536cdfd3156c4ac588e004e775761214f8"}
- experimental_model
- Measurement of potassium released by tumour necrosis with T cell signalling, phosphatase dependency and channel overexpression in melanoma-bearing mice
- exposure
- Elevated extracellular potassium from necrotic tumour areas, with Kv1.3 overexpression in tumour-specific T cells
- limitations
- Included here because it is routinely placed alongside the tumour GABA story. Its own abstract states that the suppression is independent of changes in plasma membrane potential, which is the opposite of what that pairing usually assumes.
- nutrient_topic
- GABA research collection; topical membership is not evidence of a direct clinical effect, and the sign of a GABA response depends on the chloride gradient of the cell it was measured in. · Gamma-aminobutyric acid
- organism
- Mouse and human
- plain_language
- The tumour potassium that disarms T cells does so by getting inside them and switching on a phosphatase, not by changing the voltage across the membrane.
- primary_references
- [gb-p27626381] Ionic immune suppression within the tumour microenvironment limits T cell effector function. (2016). https://pubmed.ncbi.nlm.nih.gov/27626381/ DOI: 10.1038/nature19364
- tissue_or_cell_type
- Tumour microenvironment and T cell
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Measurement of potassium released by tumour necrosis with T cell signalling, phosphatase dependency and channel overexpression in melanoma-bearing mice · source_derived_draft · unverified_draft
### gb-the-potassium-effect-is-not-electrical Necrosis releases intracellular potassium ions into the extracellular fluid of mouse and human tumours causing profound suppression of T cell effector function, elevation of the extracellular potassium concentration impairs T cell receptor-driven Akt-mTOR phosphorylation and effector programmes, potassium-mediated suppression of Akt-mTOR signalling and T cell function is dependent upon the activity of the serine/threonine phosphatase PP2A, although the suppressive effect mediated by elevated extracellular potassium is independent of changes in plasma membrane potential it requires an increase in intracellular potassium, and augmenting potassium efflux in tumour-specific T cells by overexpressing the potassium channel Kv1.3 lowers intracellular potassium and improves effector functions in vitro and in vivo. Condition category: normal nutrient_topic: GABA research collection; topical membership is not evidence of a direct clinical effect, and the sign of a GABA response depends on the chloride gradient of the cell it was measured in. plain_language: The tumour potassium that disarms T cells does so by getting inside them and switching on a phosphatase, not by changing the voltage across the membrane. organism: Mouse and human tissue_or_cell_type: Tumour microenvironment and T cell experimental_model: Measurement of potassium released by tumour necrosis with T cell signalling, phosphatase dependency and channel overexpression in melanoma-bearing mice limitations: Included here because it is routinely placed alongside the tumour GABA story. Its own abstract states that the suppression is independent of changes in plasma membrane potential, which is the opposite of what that pairing usually assumes. exposure: Elevated extracellular potassium from necrotic tumour areas, with Kv1.3 overexpression in tumour-specific T cells evidence_span: {"source_cache": "artifacts/gaba-research/27626381.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "73f83e208d8ad23be6c7ada4127b06536cdfd3156c4ac588e004e775761214f8", "start_char": 0, "end_char": 1240, "text_sha256": "73f83e208d8ad23be6c7ada4127b06536cdfd3156c4ac588e004e775761214f8"} [gb-p27626381] Ionic immune suppression within the tumour microenvironment limits T cell effector function. (2016). https://pubmed.ncbi.nlm.nih.gov/27626381/ 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.