Component

TRPM6-associated channel current

Ion current measured after expression or regulation of TRPM6; native composition can include TRPM7.

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.

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 acts on it

  1. EGF increased TRPM6-associated current in transfected HEK293 cells through EGFR-dependent signaling.

    Experimental context and source evidence
    evidence-system
    EGF exposure and receptor-blocking patch-clamp experiments
    experimental_model
    EGF exposure and receptor-blocking patch-clamp experiments
    exposure
    10 nM EGF for 30 minutes in the main stimulation experiment; a concentration-response series and EGFR blockade were also tested.
    limitations
    Channel-current regulation was directly tested in expression cells, not native human DCT recordings.
    nutrient_topic
    Magnesium research collection; topical membership is not evidence of a direct dietary effect. · Magnesium
    organism
    Human proteins and human-derived cells
    plain_language
    The growth factor EGF signals through its receptor to increase magnesium-channel activity.
    primary_references
    [groenestege-2007-egf] Impaired basolateral sorting of pro-EGF causes isolated recessive renal hypomagnesemia (2007). https://www.jci.org/articles/view/31680 DOI: 10.1172/JCI31680
    tissue
    HEK293 cells
    tissue_or_cell_type
    HEK293 cells

    Magnesium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 1016–1028

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · EGF exposure and receptor-blocking patch-clamp experiments · source_derived_draft · unverified_draft

    ### egf-increases-trpm6-current EGF increased TRPM6-associated current in transfected HEK293 cells through EGFR-dependent signaling. Condition category: normal nutrient_topic: Magnesium research collection; topical membership is not evidence of a direct dietary effect. plain_language: The growth factor EGF signals through its receptor to increase magnesium-channel activity. organism: Human proteins and human-derived cells tissue_or_cell_type: HEK293 cells experimental_model: EGF exposure and receptor-blocking patch-clamp experiments limitations: Channel-current regulation was directly tested in expression cells, not native human DCT recordings. exposure: 10 nM EGF for 30 minutes in the main stimulation experiment; a concentration-response series and EGFR blockade were also tested. evidence-system: EGF exposure and receptor-blocking patch-clamp experiments tissue: HEK293 cells [groenestege-2007-egf] Impaired basolateral sorting of pro-EGF causes isolated recessive renal hypomagnesemia (2007). https://www.jci.org/articles/view/31680 DOI: 10.1172/JCI31680
    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