Component

Caspase-1 / CASP1

Caspase-1 / CASP1; interpretation depends on linked experimental context.

2 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

Where it participates (unsigned role)

  1. NEK7 loss blocked inflammasome assembly downstream of preserved K efflux; 50 mM KCl prevented the induced NEK7-NLRP3 interaction.

    NIMA-related kinase 7 / NEK7 → NLRP3 inflammasome source_derived_draftungraded
    Experimental context and source evidence
    experimental_model
    Mouse macrophages with Nek7 deletion/reconstitution; ATP, nigericin or gramicidin; high-K control, interaction assays.
    limitations
    NEK7 catalytic activity was dispensable; this is not proof of potassium binding directly to NEK7.
    nutrient_topic
    Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium
    organism
    Mouse
    plain_language
    Potassium loss signals through an assembly protein before caspase activation.
    primary_references
    [he-2016-nek7] NEK7 is an essential mediator of NLRP3 activation downstream of potassium efflux (2016). https://pmc.ncbi.nlm.nih.gov/articles/PMC4810788/ DOI: 10.1038/nature16959
    tissue_or_cell_type
    Bone-marrow macrophages

    Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 880–889

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Mouse macrophages with Nek7 deletion/reconstitution; ATP, nigericin or gramicidin; high-K control, interaction assays. · source_derived_draft · unverified_draft

    ### k-efflux-nek7-assembly NEK7 loss blocked inflammasome assembly downstream of preserved K efflux; 50 mM KCl prevented the induced NEK7-NLRP3 interaction. Condition category: normal nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Potassium loss signals through an assembly protein before caspase activation. organism: Mouse tissue_or_cell_type: Bone-marrow macrophages experimental_model: Mouse macrophages with Nek7 deletion/reconstitution; ATP, nigericin or gramicidin; high-K control, interaction assays. limitations: NEK7 catalytic activity was dispensable; this is not proof of potassium binding directly to NEK7. [he-2016-nek7] NEK7 is an essential mediator of NLRP3 activation downstream of potassium efflux (2016). https://pmc.ncbi.nlm.nih.gov/articles/PMC4810788/ DOI: 10.1038/nature16959
    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

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.

    Evidence, AI assistance and curation standards