Component
NIMA-related kinase 7 / NEK7
NIMA-related kinase 7 / NEK7; interpretation depends on linked experimental context.
2 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 it acts on
NEK7 loss blocked inflammasome assembly downstream of preserved K efflux; 50 mM KCl prevented the induced NEK7-NLRP3 interaction.
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
Where it participates (unsigned role)
Imiquimod and CL097 activated NLRP3 without requiring potassium efflux in the studied myeloid-cell experiments.
Experimental context and source evidence
- experimental_model
- Myeloid-cell inflammasome experiments using imiquimod and CL097, potassium-efflux tests and mitochondrial target analysis.
- limitations
- Stimulus-specific boundary, not opposing evidence for the toxin/particle experiments.
- nutrient_topic
- Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium
- organism
- Mouse experimental systems
- plain_language
- Some drug-triggered inflammasome routes bypass potassium loss.
- primary_references
- [gross-2016-independent] K+ Efflux-Independent NLRP3 Inflammasome Activation by Small Molecules Targeting Mitochondria (2016). https://pubmed.ncbi.nlm.nih.gov/27692612/ DOI: 10.1016/j.immuni.2016.08.010
- tissue_or_cell_type
- Myeloid cells
Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 891–900
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Myeloid-cell inflammasome experiments using imiquimod and CL097, potassium-efflux tests and mitochondrial target analysis. · source_derived_draft · unverified_draft
### k-independent-drug-nlrp3 Imiquimod and CL097 activated NLRP3 without requiring potassium efflux in the studied myeloid-cell experiments. Condition category: normal nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Some drug-triggered inflammasome routes bypass potassium loss. organism: Mouse experimental systems tissue_or_cell_type: Myeloid cells experimental_model: Myeloid-cell inflammasome experiments using imiquimod and CL097, potassium-efflux tests and mitochondrial target analysis. limitations: Stimulus-specific boundary, not opposing evidence for the toxin/particle experiments. [gross-2016-independent] K+ Efflux-Independent NLRP3 Inflammasome Activation by Small Molecules Targeting Mitochondria (2016). https://pubmed.ncbi.nlm.nih.gov/27692612/ DOI: 10.1016/j.immuni.2016.08.010
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.