Component

TRPM7

Divalent-cation-permeable channel-kinase; protein and catalytic kinase function are not interchangeable.

9 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. TRPM6 coassembled with TRPM7 to form functional surface channel complexes in the tested expression systems.

    TRPM6 → TRPM7 source_derived_draftungraded
    Experimental context and source evidence
    evidence-system
    HEK293 and Xenopus heterologous coexpression
    experimental_model
    HEK293 and Xenopus heterologous coexpression
    limitations
    TRPM6 isoforms and cellular background affect results; not proof every native complex has identical composition.
    nutrient_topic
    Magnesium research collection; topical membership is not evidence of a direct dietary effect. · Magnesium
    organism
    Human proteins; human-derived and Xenopus cells
    plain_language
    A TRPM7 partner enabled TRPM6-containing channels to reach and function at the cell surface.
    primary_references
    [chubanov-2004-trpm6-trpm7] Disruption of TRPM6/TRPM7 complex formation by a mutation in the TRPM6 gene causes hypomagnesemia with secondary hypocalcemia. (2004). https://pubmed.ncbi.nlm.nih.gov/14976260/ DOI: 10.1073/pnas.0305252101
    tissue
    Expression systems
    tissue_or_cell_type
    Expression systems

    Magnesium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 883–894

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · HEK293 and Xenopus heterologous coexpression · source_derived_draft · unverified_draft

    ### trpm6-trpm7-coassembly TRPM6 coassembled with TRPM7 to form functional surface channel complexes in the tested expression systems. Condition category: normal nutrient_topic: Magnesium research collection; topical membership is not evidence of a direct dietary effect. plain_language: A TRPM7 partner enabled TRPM6-containing channels to reach and function at the cell surface. organism: Human proteins; human-derived and Xenopus cells tissue_or_cell_type: Expression systems experimental_model: HEK293 and Xenopus heterologous coexpression limitations: TRPM6 isoforms and cellular background affect results; not proof every native complex has identical composition. evidence-system: HEK293 and Xenopus heterologous coexpression tissue: Expression systems [chubanov-2004-trpm6-trpm7] Disruption of TRPM6/TRPM7 complex formation by a mutation in the TRPM6 gene causes hypomagnesemia with secondary hypocalcemia. (2004). https://pubmed.ncbi.nlm.nih.gov/14976260/ DOI: 10.1073/pnas.0305252101
    Complete structured claim and evidence

  2. TRPM7 currents depended on PI(4,5)P2 in the reported experiments, and PLC-mediated PIP2 hydrolysis inhibited the current.

    Phosphatidylinositol 4,5-bisphosphate → TRPM7 source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/inositol-research/11941371.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "5b6343b08188b699a19591013fdcd2d9d604f8ae15adc5771b4bc677369d10b0", "start_char": 0, "end_char": 729, "text_sha256": "5b6343b08188b699a19591013fdcd2d9d604f8ae15adc5771b4bc677369d10b0"}
    experimental_model
    Electrophysiology and phosphoinositide manipulation
    exposure
    PLC activation and PIP2 depletion
    limitations
    PIP2 regulation is conditional; the 2007 study shows intracellular Mg and patch configuration can reverse the PLC response.
    nutrient_topic
    Inositol research collection; topical membership is not evidence of a direct dietary effect. · Inositol (stereoisomer family)
    organism
    Mammalian heterologous cells and cardiac preparations
    plain_language
    A membrane inositol lipid helps regulate a channel that carries mineral ions; the response depends on the recording conditions.
    primary_references
    [ino-p11941371] The TRPM7 channel is inactivated by PIP(2) hydrolysis. (2002). https://pubmed.ncbi.nlm.nih.gov/11941371/ DOI: 10.1038/ncb781
    tissue_or_cell_type
    TRPM7-associated membrane currents

    Inositol: synthesis, signaling, mineral interactions and conditional deficiency (2026-09-17) · lines 951–962

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Electrophysiology and phosphoinositide manipulation · source_derived_draft · unverified_draft

    ### ino-pip2-trpm7 TRPM7 currents depended on PI(4,5)P2 in the reported experiments, and PLC-mediated PIP2 hydrolysis inhibited the current. Condition category: normal nutrient_topic: Inositol research collection; topical membership is not evidence of a direct dietary effect. plain_language: A membrane inositol lipid helps regulate a channel that carries mineral ions; the response depends on the recording conditions. organism: Mammalian heterologous cells and cardiac preparations tissue_or_cell_type: TRPM7-associated membrane currents experimental_model: Electrophysiology and phosphoinositide manipulation limitations: PIP2 regulation is conditional; the 2007 study shows intracellular Mg and patch configuration can reverse the PLC response. exposure: PLC activation and PIP2 depletion evidence_span: {"source_cache": "artifacts/inositol-research/11941371.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "5b6343b08188b699a19591013fdcd2d9d604f8ae15adc5771b4bc677369d10b0", "start_char": 0, "end_char": 729, "text_sha256": "5b6343b08188b699a19591013fdcd2d9d604f8ae15adc5771b4bc677369d10b0"} [ino-p11941371] The TRPM7 channel is inactivated by PIP(2) hydrolysis. (2002). https://pubmed.ncbi.nlm.nih.gov/11941371/ DOI: 10.1038/ncb781
    Complete structured claim and evidence

Where it participates (unsigned role)

  1. CNNM2 coexpression increased TRPM7-dependent zinc influx, and the TRPM7 E1047K pore mutant prevented this increase.

    CNNM2 → Cellular zinc influx source_derived_draftungraded
    Experimental context and source evidence
    cross_nutrient
    A protein associated with Mg homeostasis regulates a Zn-permeable channel in culture; nutritional co-dependence was not tested.
    evidence-system
    Coexpression, TRPM7 knockout and pore-inactivation tests
    experimental_model
    Coexpression, TRPM7 knockout and pore-inactivation tests
    limitations
    Zinc is a divalent-flux reporter here; this does not establish CNNM2 as a magnesium pore or dietary Mg-to-Zn dependence.
    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
    CNNM2 can regulate entry through a separate channel whose pore carries the ion.
    primary_references
    [bai-2021-cnnm-trpm7] CNNM proteins selectively bind to the TRPM7 channel to stimulate divalent cation entry into cells (2021). https://pmc.ncbi.nlm.nih.gov/articles/PMC8726484/ DOI: 10.1371/journal.pbio.3001496
    tissue
    HEK293-family cells; supporting HAP1 cells
    tissue_or_cell_type
    HEK293-family cells; supporting HAP1 cells

    Magnesium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 1151–1163

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Coexpression, TRPM7 knockout and pore-inactivation tests · source_derived_draft · unverified_draft

    ### cnnm2-stimulates-trpm7-zinc-influx CNNM2 coexpression increased TRPM7-dependent zinc influx, and the TRPM7 E1047K pore mutant prevented this increase. Condition category: normal nutrient_topic: Magnesium research collection; topical membership is not evidence of a direct dietary effect. plain_language: CNNM2 can regulate entry through a separate channel whose pore carries the ion. organism: Human proteins and human-derived cells tissue_or_cell_type: HEK293-family cells; supporting HAP1 cells experimental_model: Coexpression, TRPM7 knockout and pore-inactivation tests limitations: Zinc is a divalent-flux reporter here; this does not establish CNNM2 as a magnesium pore or dietary Mg-to-Zn dependence. cross_nutrient: A protein associated with Mg homeostasis regulates a Zn-permeable channel in culture; nutritional co-dependence was not tested. evidence-system: Coexpression, TRPM7 knockout and pore-inactivation tests tissue: HEK293-family cells; supporting HAP1 cells [bai-2021-cnnm-trpm7] CNNM proteins selectively bind to the TRPM7 channel to stimulate divalent cation entry into cells (2021). https://pmc.ncbi.nlm.nih.gov/articles/PMC8726484/ DOI: 10.1371/journal.pbio.3001496
    Complete structured claim and evidence

  2. Intestinal Trpm7 deletion reduced serum and bone calcium in suckling mice.

    Intestine-specific Trpm7-null mouse genotype → Serum calcium concentration source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    cross_nutrient
    TRPM7 is shared machinery for magnesium and calcium handling in this developmental model; causal Mg-to-Ca nutritional dependence was not isolated.
    evidence-system
    Conditional knockout; postnatal mineral phenotyping
    experimental_model
    Conditional knockout; postnatal mineral phenotyping
    limitations
    Shared channel loss; does not prove low Mg intake causes calcium malabsorption.
    nutrient_topic
    Magnesium research collection; topical membership is not evidence of a direct dietary effect. · Magnesium
    organism
    Mouse
    plain_language
    The same epithelial channel machinery supports calcium as well as magnesium supply.
    primary_references
    [mittermeier-2019-trpm7] TRPM7 is the central gatekeeper of intestinal mineral absorption essential for postnatal survival (2019). https://pubmed.ncbi.nlm.nih.gov/30770447/ DOI: 10.1073/pnas.1810633116
    tissue
    Intestine; serum and bone
    tissue_or_cell_type
    Intestine; serum and bone
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Magnesium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 988–1000

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Conditional knockout; postnatal mineral phenotyping · source_derived_draft · unverified_draft

    ### intestinal-trpm7-loss-calcium Intestinal Trpm7 deletion reduced serum and bone calcium in suckling mice. Condition category: machinery_impairment nutrient_topic: Magnesium research collection; topical membership is not evidence of a direct dietary effect. plain_language: The same epithelial channel machinery supports calcium as well as magnesium supply. organism: Mouse tissue_or_cell_type: Intestine; serum and bone experimental_model: Conditional knockout; postnatal mineral phenotyping limitations: Shared channel loss; does not prove low Mg intake causes calcium malabsorption. cross_nutrient: TRPM7 is shared machinery for magnesium and calcium handling in this developmental model; causal Mg-to-Ca nutritional dependence was not isolated. evidence-system: Conditional knockout; postnatal mineral phenotyping tissue: Intestine; serum and bone [mittermeier-2019-trpm7] TRPM7 is the central gatekeeper of intestinal mineral absorption essential for postnatal survival (2019). https://pubmed.ncbi.nlm.nih.gov/30770447/ DOI: 10.1073/pnas.1810633116
    Complete structured claim and evidence

  3. Intestinal Trpm7 deletion lowered magnesium availability in early postnatal mice.

    Intestine-specific Trpm7-null mouse genotype → Serum magnesium concentration source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence-system
    Villin1-Cre conditional deletion and mineral phenotyping
    experimental_model
    Villin1-Cre conditional deletion and mineral phenotyping
    limitations
    Early developmental model; not a test of dietary Mg restriction.
    nutrient_topic
    Magnesium research collection; topical membership is not evidence of a direct dietary effect. · Magnesium
    organism
    Mouse
    plain_language
    Suckling mice required intestinal TRPM7 to maintain their magnesium supply.
    primary_references
    [mittermeier-2019-trpm7] TRPM7 is the central gatekeeper of intestinal mineral absorption essential for postnatal survival (2019). https://pubmed.ncbi.nlm.nih.gov/30770447/ DOI: 10.1073/pnas.1810633116
    tissue
    Intestinal enterocytes; serum
    tissue_or_cell_type
    Intestinal enterocytes; serum
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Magnesium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 975–986

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Villin1-Cre conditional deletion and mineral phenotyping · source_derived_draft · unverified_draft

    ### intestinal-trpm7-loss-magnesium Intestinal Trpm7 deletion lowered magnesium availability in early postnatal mice. Condition category: machinery_impairment nutrient_topic: Magnesium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Suckling mice required intestinal TRPM7 to maintain their magnesium supply. organism: Mouse tissue_or_cell_type: Intestinal enterocytes; serum experimental_model: Villin1-Cre conditional deletion and mineral phenotyping limitations: Early developmental model; not a test of dietary Mg restriction. evidence-system: Villin1-Cre conditional deletion and mineral phenotyping tissue: Intestinal enterocytes; serum [mittermeier-2019-trpm7] TRPM7 is the central gatekeeper of intestinal mineral absorption essential for postnatal survival (2019). https://pubmed.ncbi.nlm.nih.gov/30770447/ DOI: 10.1073/pnas.1810633116
    Complete structured claim and evidence

  4. Intestinal Trpm7 deletion reduced circulating zinc in early postnatal mice.

    Intestine-specific Trpm7-null mouse genotype → Serum zinc concentration source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    cross_nutrient
    Shared intestinal TRPM7 machinery links zinc and magnesium availability; Mg deficiency as the cause of Zn deficiency was not demonstrated.
    evidence-system
    Conditional intestinal knockout and mineral phenotyping
    experimental_model
    Conditional intestinal knockout and mineral phenotyping
    limitations
    Not evidence that magnesium supplementation universally increases zinc absorption.
    nutrient_topic
    Magnesium research collection; topical membership is not evidence of a direct dietary effect. · Magnesium
    organism
    Mouse
    plain_language
    A single epithelial machinery defect depleted zinc along with magnesium.
    primary_references
    [mittermeier-2019-trpm7] TRPM7 is the central gatekeeper of intestinal mineral absorption essential for postnatal survival (2019). https://pubmed.ncbi.nlm.nih.gov/30770447/ DOI: 10.1073/pnas.1810633116
    tissue
    Intestine; serum
    tissue_or_cell_type
    Intestine; serum
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Magnesium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 1002–1014

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Conditional intestinal knockout and mineral phenotyping · source_derived_draft · unverified_draft

    ### intestinal-trpm7-loss-zinc Intestinal Trpm7 deletion reduced circulating zinc in early postnatal mice. Condition category: machinery_impairment nutrient_topic: Magnesium research collection; topical membership is not evidence of a direct dietary effect. plain_language: A single epithelial machinery defect depleted zinc along with magnesium. organism: Mouse tissue_or_cell_type: Intestine; serum experimental_model: Conditional intestinal knockout and mineral phenotyping limitations: Not evidence that magnesium supplementation universally increases zinc absorption. cross_nutrient: Shared intestinal TRPM7 machinery links zinc and magnesium availability; Mg deficiency as the cause of Zn deficiency was not demonstrated. evidence-system: Conditional intestinal knockout and mineral phenotyping tissue: Intestine; serum [mittermeier-2019-trpm7] TRPM7 is the central gatekeeper of intestinal mineral absorption essential for postnatal survival (2019). https://pubmed.ncbi.nlm.nih.gov/30770447/ DOI: 10.1073/pnas.1810633116
    Complete structured claim and evidence

  5. 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

  6. TRPM6 S141L disrupted oligomeric assembly and functional TRPM6/TRPM7 complex formation.

    TRPM6 S141L → TRPM6/TRPM7 heteromeric channel complex source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence-system
    Mutant coexpression and channel assembly assays
    experimental_model
    Mutant coexpression and channel assembly assays
    limitations
    A particular variant mechanism; not all TRPM6 variants act by defective trafficking.
    nutrient_topic
    Magnesium research collection; topical membership is not evidence of a direct dietary effect. · Magnesium
    organism
    Human proteins
    plain_language
    This disease-associated substitution damages assembly of the magnesium-entry machinery.
    primary_references
    [chubanov-2004-trpm6-trpm7] Disruption of TRPM6/TRPM7 complex formation by a mutation in the TRPM6 gene causes hypomagnesemia with secondary hypocalcemia. (2004). https://pubmed.ncbi.nlm.nih.gov/14976260/ DOI: 10.1073/pnas.0305252101
    tissue
    HEK293 and Xenopus expression systems
    tissue_or_cell_type
    HEK293 and Xenopus expression systems
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Magnesium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 896–907

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Mutant coexpression and channel assembly assays · source_derived_draft · unverified_draft

    ### trpm6-s141l-assembly-defect TRPM6 S141L disrupted oligomeric assembly and functional TRPM6/TRPM7 complex formation. Condition category: machinery_impairment nutrient_topic: Magnesium research collection; topical membership is not evidence of a direct dietary effect. plain_language: This disease-associated substitution damages assembly of the magnesium-entry machinery. organism: Human proteins tissue_or_cell_type: HEK293 and Xenopus expression systems experimental_model: Mutant coexpression and channel assembly assays limitations: A particular variant mechanism; not all TRPM6 variants act by defective trafficking. evidence-system: Mutant coexpression and channel assembly assays tissue: HEK293 and Xenopus expression systems [chubanov-2004-trpm6-trpm7] Disruption of TRPM6/TRPM7 complex formation by a mutation in the TRPM6 gene causes hypomagnesemia with secondary hypocalcemia. (2004). https://pubmed.ncbi.nlm.nih.gov/14976260/ DOI: 10.1073/pnas.0305252101
    Complete structured claim and evidence

  7. TRPM7-deficient DT40 cells became magnesium depleted.

    TRPM7 loss-of-function genotype → Cellular magnesium content source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence-system
    Targeted gene disruption and Mg measurements in DT40 cells
    experimental_model
    Targeted gene disruption and Mg measurements in DT40 cells
    limitations
    Cell-line dependence does not establish universal necessity in every mammalian cell.
    nutrient_topic
    Magnesium research collection; topical membership is not evidence of a direct dietary effect. · Magnesium
    organism
    Chicken
    plain_language
    Loss of this entry channel reduced the cells magnesium supply.
    primary_references
    [schmitz-2003-trpm7] Regulation of vertebrate cellular Mg2+ homeostasis by TRPM7 (2003). https://pubmed.ncbi.nlm.nih.gov/12887921/ DOI: 10.1016/S0092-8674(03)00556-7
    tissue
    B-cell line
    tissue_or_cell_type
    B-cell line
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Magnesium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 949–960

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Targeted gene disruption and Mg measurements in DT40 cells · source_derived_draft · unverified_draft

    ### trpm7-loss-cellular-magnesium TRPM7-deficient DT40 cells became magnesium depleted. Condition category: machinery_impairment nutrient_topic: Magnesium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Loss of this entry channel reduced the cells magnesium supply. organism: Chicken tissue_or_cell_type: B-cell line experimental_model: Targeted gene disruption and Mg measurements in DT40 cells limitations: Cell-line dependence does not establish universal necessity in every mammalian cell. evidence-system: Targeted gene disruption and Mg measurements in DT40 cells tissue: B-cell line [schmitz-2003-trpm7] Regulation of vertebrate cellular Mg2+ homeostasis by TRPM7 (2003). https://pubmed.ncbi.nlm.nih.gov/12887921/ DOI: 10.1016/S0092-8674(03)00556-7
    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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