Component
TRPM6 abundance at the cell surface
Independent biological entity. Read linked claims for experimental scope and 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
Insulin increased TRPM6 surface abundance and channel activity through a PI3K- and RAC1-dependent pathway.
Experimental context and source evidence
- cross_nutrient
- Insulin -> magnesium-channel trafficking; complements the separate Mg -> insulin-response findings.
- experimental_model
- Expression-cell electrophysiology and surface fluorescence.
- limitations
- Combined pathway perturbations; no unspecified PI3K isoform assigned and no universal clinical feedback loop proven.
- nutrient_topic
- Magnesium research collection; topical membership is not evidence of a direct dietary effect. · Magnesium
- organism
- Homo sapiens
- plain_language
- Insulin can affect the magnesium entry machinery as well as glucose metabolism.
- primary_references
- [mg-nair2012] Loss of insulin-induced activation of TRPM6 magnesium channels results in impaired glucose tolerance during pregnancy (2012). https://pubmed.ncbi.nlm.nih.gov/22733750/ DOI: 10.1073/pnas.1113811109
- tissue_or_cell_type
- TRPM6-expressing cells; plasma membrane
Magnesium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 1527–1537
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Expression-cell electrophysiology and surface fluorescence. · source_derived_draft · unverified_draft
### mg-insulin-trpm6-surface-regulation Insulin increased TRPM6 surface abundance and channel activity through a PI3K- and RAC1-dependent pathway. Condition category: normal nutrient_topic: Magnesium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Insulin can affect the magnesium entry machinery as well as glucose metabolism. organism: Homo sapiens tissue_or_cell_type: TRPM6-expressing cells; plasma membrane experimental_model: Expression-cell electrophysiology and surface fluorescence. limitations: Combined pathway perturbations; no unspecified PI3K isoform assigned and no universal clinical feedback loop proven. cross_nutrient: Insulin -> magnesium-channel trafficking; complements the separate Mg -> insulin-response findings. [mg-nair2012] Loss of insulin-induced activation of TRPM6 magnesium channels results in impaired glucose tolerance during pregnancy (2012). https://pubmed.ncbi.nlm.nih.gov/22733750/ DOI: 10.1073/pnas.1113811109
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.