Component

Intracellular potassium concentration

Intracellular potassium concentration; interpretation depends on linked experimental context.

4 recorded relationships. Experimental role, claim status and evidence remain attached to each record.

Read recorded mechanisms Open recursive mind map

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.

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.

Recorded relationships

What it acts on

  1. 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.

    Intracellular potassium concentration → TCR-driven Akt-mTOR phosphorylation source_derived_draftungraded
    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

    GABA: a ligand with no sign of its own, the cofactor that limits its synthesis, the barrier that keeps it out of the brain, and the immune settings where the same molecule protects and harms (2026-09-22) · lines 612–623

    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

  2. K-free medium triggered NLRP3-dependent IL-1beta release in primed macrophages, accompanying intracellular K loss.

    Intracellular potassium concentration → NLRP3 inflammasome source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    nutrient_deficiency Imported condition classification; unverified.
    experimental_model
    LPS-primed mouse macrophages, 0 versus 5 mM K; response by 30 minutes.
    limitations
    Artificial cellular depletion; not a blood threshold or dietary inflammation experiment.
    nutrient_topic
    Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium
    organism
    Mouse
    plain_language
    Experimentally losing cellular potassium could trigger this immune sensor.
    primary_references
    [munoz-2013-nlrp3] K+ efflux is the Common Trigger of NLRP3 inflammasome Activation by Bacterial Toxins and Particulate Matter (2013). https://pmc.ncbi.nlm.nih.gov/articles/PMC3730833/ DOI: 10.1016/j.immuni.2013.05.016
    tissue_or_cell_type
    Bone-marrow macrophages
    trigger_kind
    nutrient_deficiency Imported condition classification; unverified.

    Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 857–866

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · LPS-primed mouse macrophages, 0 versus 5 mM K; response by 30 minutes. · source_derived_draft · unverified_draft

    ### k-macrophage-loss-nlrp3 K-free medium triggered NLRP3-dependent IL-1beta release in primed macrophages, accompanying intracellular K loss. Condition category: nutrient_deficiency nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Experimentally losing cellular potassium could trigger this immune sensor. organism: Mouse tissue_or_cell_type: Bone-marrow macrophages experimental_model: LPS-primed mouse macrophages, 0 versus 5 mM K; response by 30 minutes. limitations: Artificial cellular depletion; not a blood threshold or dietary inflammation experiment. [munoz-2013-nlrp3] K+ efflux is the Common Trigger of NLRP3 inflammasome Activation by Bacterial Toxins and Particulate Matter (2013). https://pmc.ncbi.nlm.nih.gov/articles/PMC3730833/ DOI: 10.1016/j.immuni.2013.05.016
    Complete structured claim and evidence

  3. Elevated intracellular K suppressed TCR-driven AKT-mTOR signaling through a PP2A-dependent process.

    Intracellular potassium concentration → T-cell AKT-mTOR signaling source_derived_draftungraded
    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

Where it participates (unsigned role)

  1. Kv1.3 overexpression lowered intracellular K and improved antitumor T-cell function; engineered cells improved melanoma control in mice.

    Kv1.3 / KCNA3 → T-cell effector function source_derived_draftungraded
    Experimental context and source evidence
    experimental_model
    Engineered T cells, culture and adoptive transfer.
    limitations
    Genetic cell intervention cannot be translated into a dietary potassium claim.
    nutrient_topic
    Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium
    organism
    Mouse with human-cell complementary assays
    plain_language
    Increasing potassium exit rescued cells in this tumor model.
    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
    Tumor-infiltrating T cells

    Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 913–922

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Engineered T cells, culture and adoptive transfer. · source_derived_draft · unverified_draft

    ### k-tcell-kv13-efflux Kv1.3 overexpression lowered intracellular K and improved antitumor T-cell function; engineered cells improved melanoma control in mice. Condition category: normal nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Increasing potassium exit rescued cells in this tumor model. organism: Mouse with human-cell complementary assays tissue_or_cell_type: Tumor-infiltrating T cells experimental_model: Engineered T cells, culture and adoptive transfer. limitations: Genetic cell intervention cannot be translated into a dietary potassium claim. [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

In the sources

Preserved passages that mention this component, quoted exactly. Open one to read it in context.

    This is a research prototype built from draft material. It is not medical advice, and its statements still await verification against the original studies.

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