Component

Cellular magnesium influx

Experimentally measured magnesium entry across the plasma membrane.

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 acts on it

  1. Neither CNNM2 isoform 1 nor isoform 2 produced detectable extra Mg influx or efflux in the reported HEK293 assays.

    CNNM2 → Cellular magnesium influx source_derived_draftungraded
    Experimental context and source evidence
    evidence-system
    Inducible expression, electrophysiology and mag-fura-2 measurements
    experimental_model
    Inducible expression, electrophysiology and mag-fura-2 measurements
    limitations
    A negative expression-system result cannot exclude context-dependent transport or interaction with other machinery.
    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
    In this experiment, expressing CNNM2 did not behave like adding an independent magnesium transporter.
    primary_references
    [sponder-2016-cnnm2] Human CNNM2 is not a Mg2+ transporter per se (2016). https://pubmed.ncbi.nlm.nih.gov/27068403/ DOI: 10.1007/s00424-016-1816-7
    tissue
    HEK293 culture
    tissue_or_cell_type
    HEK293 culture

    Magnesium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 1138–1149

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Inducible expression, electrophysiology and mag-fura-2 measurements · source_derived_draft · unverified_draft

    ### cnnm2-isoforms-no-extra-mg-flux Neither CNNM2 isoform 1 nor isoform 2 produced detectable extra Mg influx or efflux in the reported HEK293 assays. Condition category: normal nutrient_topic: Magnesium research collection; topical membership is not evidence of a direct dietary effect. plain_language: In this experiment, expressing CNNM2 did not behave like adding an independent magnesium transporter. organism: Human proteins and human-derived cells tissue_or_cell_type: HEK293 culture experimental_model: Inducible expression, electrophysiology and mag-fura-2 measurements limitations: A negative expression-system result cannot exclude context-dependent transport or interaction with other machinery. evidence-system: Inducible expression, electrophysiology and mag-fura-2 measurements tissue: HEK293 culture [sponder-2016-cnnm2] Human CNNM2 is not a Mg2+ transporter per se (2016). https://pubmed.ncbi.nlm.nih.gov/27068403/ DOI: 10.1007/s00424-016-1816-7
    Complete structured claim and evidence

  2. Recombinant TRPM6 expression generated Mg2+-permeable currents, supporting its participation in apical epithelial Mg entry.

    TRPM6 → Cellular magnesium influx source_derived_draftungraded
    Experimental context and source evidence
    evidence-system
    Recombinant channel recordings and tissue localization
    experimental_model
    Recombinant channel recordings and tissue localization
    limitations
    Expression-system currents do not establish the stoichiometry of native channels; TRPM7 can contribute.
    nutrient_topic
    Magnesium research collection; topical membership is not evidence of a direct dietary effect. · Magnesium
    organism
    Human protein; mouse tissues
    plain_language
    TRPM6 is part of the route by which magnesium crosses an epithelial cell membrane.
    primary_references
    [voets-2004-trpm6] TRPM6 forms the Mg2+ influx channel involved in intestinal and renal Mg2+ absorption. (2004). https://pubmed.ncbi.nlm.nih.gov/14576148/ DOI: 10.1074/jbc.M311201200
    tissue
    HEK expression cells; intestine and distal renal tubule
    tissue_or_cell_type
    HEK expression cells; intestine and distal renal tubule
    transport_direction
    Extracellular or luminal compartment toward cytosol.

    Magnesium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 869–881

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Recombinant channel recordings and tissue localization · source_derived_draft · unverified_draft

    ### trpm6-mg-entry Recombinant TRPM6 expression generated Mg2+-permeable currents, supporting its participation in apical epithelial Mg entry. Condition category: normal nutrient_topic: Magnesium research collection; topical membership is not evidence of a direct dietary effect. plain_language: TRPM6 is part of the route by which magnesium crosses an epithelial cell membrane. organism: Human protein; mouse tissues tissue_or_cell_type: HEK expression cells; intestine and distal renal tubule experimental_model: Recombinant channel recordings and tissue localization limitations: Expression-system currents do not establish the stoichiometry of native channels; TRPM7 can contribute. transport_direction: Extracellular or luminal compartment toward cytosol. evidence-system: Recombinant channel recordings and tissue localization tissue: HEK expression cells; intestine and distal renal tubule [voets-2004-trpm6] TRPM6 forms the Mg2+ influx channel involved in intestinal and renal Mg2+ absorption. (2004). https://pubmed.ncbi.nlm.nih.gov/14576148/ DOI: 10.1074/jbc.M311201200
    Complete structured claim and evidence

  3. Potassium-depleted MDCT cells showed reduced Mg2+ uptake in a magnesium-recovery assay.

    Intracellular potassium content → Cellular magnesium influx source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    nutrient_deficiency Imported condition classification; unverified.
    cross_nutrient
    Cellular K depletion decreases magnesium entry in this DCT model.
    evidence_location
    Primary abstract; potassium-depleted-cell Mg uptake comparison.
    experimental_model
    Cultured MDCT potassium depletion; fluorescence Mg-recovery assay
    limitations
    Intracellular depletion is distinct from low extracellular K alone; TRPM6 was not identified.
    nutrient_topic
    Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium
    organism
    Mus musculus cell line
    plain_language
    Depleting cellular potassium made it harder for these kidney cells to take up magnesium.
    primary_references
    [dai-1997-k-mg] Cellular mechanisms of chlorothiazide and cellular potassium depletion on Mg2+ uptake in mouse distal convoluted tubule cells (1997). https://pubmed.ncbi.nlm.nih.gov/9083264/ DOI: 10.1038/ki.1997.141
    tissue_or_cell_type
    Distal convoluted tubule cell model
    trigger_kind
    nutrient_deficiency Imported condition classification; unverified.

    Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 484–495

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Cultured MDCT potassium depletion; fluorescence Mg-recovery assay · source_derived_draft · unverified_draft

    ### renal-cellular-k-depletion-lowers-mg-influx Potassium-depleted MDCT cells showed reduced Mg2+ uptake in a magnesium-recovery assay. Condition category: nutrient_deficiency nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Depleting cellular potassium made it harder for these kidney cells to take up magnesium. organism: Mus musculus cell line tissue_or_cell_type: Distal convoluted tubule cell model experimental_model: Cultured MDCT potassium depletion; fluorescence Mg-recovery assay limitations: Intracellular depletion is distinct from low extracellular K alone; TRPM6 was not identified. cross_nutrient: Cellular K depletion decreases magnesium entry in this DCT model. evidence_location: Primary abstract; potassium-depleted-cell Mg uptake comparison. [dai-1997-k-mg] Cellular mechanisms of chlorothiazide and cellular potassium depletion on Mg2+ uptake in mouse distal convoluted tubule cells (1997). https://pubmed.ncbi.nlm.nih.gov/9083264/ DOI: 10.1038/ki.1997.141
    Complete structured claim and evidence

  4. Thiocyanate-induced hyperpolarization restored Mg2+ uptake in potassium-depleted MDCT cells.

    DCT membrane potential → Cellular magnesium influx source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    nutrient_deficiency Imported condition classification; unverified.
    cross_nutrient
    The K-depletion effect on Mg entry is partly recoverable by membrane polarization.
    evidence_location
    Primary abstract; SCN- rescue experiment.
    experimental_model
    SCN- voltage manipulation after cell K depletion
    limitations
    Supports partial voltage mediation; does not establish an in vivo repletion strategy.
    nutrient_topic
    Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium
    organism
    Mus musculus cell line
    plain_language
    Restoring the electrical driving force helped magnesium enter despite prior potassium depletion.
    primary_references
    [dai-1997-k-mg] Cellular mechanisms of chlorothiazide and cellular potassium depletion on Mg2+ uptake in mouse distal convoluted tubule cells (1997). https://pubmed.ncbi.nlm.nih.gov/9083264/ DOI: 10.1038/ki.1997.141
    tissue_or_cell_type
    Distal convoluted tubule cell model
    trigger_kind
    nutrient_deficiency Imported condition classification; unverified.

    Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 497–508

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · SCN- voltage manipulation after cell K depletion · source_derived_draft · unverified_draft

    ### renal-hyperpolarization-rescues-mg-after-k-depletion Thiocyanate-induced hyperpolarization restored Mg2+ uptake in potassium-depleted MDCT cells. Condition category: nutrient_deficiency nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Restoring the electrical driving force helped magnesium enter despite prior potassium depletion. organism: Mus musculus cell line tissue_or_cell_type: Distal convoluted tubule cell model experimental_model: SCN- voltage manipulation after cell K depletion limitations: Supports partial voltage mediation; does not establish an in vivo repletion strategy. cross_nutrient: The K-depletion effect on Mg entry is partly recoverable by membrane polarization. evidence_location: Primary abstract; SCN- rescue experiment. [dai-1997-k-mg] Cellular mechanisms of chlorothiazide and cellular potassium depletion on Mg2+ uptake in mouse distal convoluted tubule cells (1997). https://pubmed.ncbi.nlm.nih.gov/9083264/ DOI: 10.1038/ki.1997.141
    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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