Component

TRPM6

Magnesium-permeable channel-kinase expressed in magnesium-absorbing epithelia.

11 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 it acts on

  1. 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

  2. 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

Where it participates (unsigned role)

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

    Epidermal growth factor → TRPM6-associated channel current source_derived_draftungraded
    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

  2. Two homozygous EGF P1070L sisters had low serum magnesium with inappropriately sustained urinary Mg loss.

    Pro-EGF P1070L → Urinary magnesium excretion source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence-system
    Human pedigree and serum/urine phenotyping
    experimental_model
    Human pedigree and serum/urine phenotyping
    limitations
    Small kindred; cellular sorting experiments support the explanation rather than directly measuring the entire cascade in vivo.
    nutrient_topic
    Magnesium research collection; topical membership is not evidence of a direct dietary effect. · Magnesium
    organism
    Human
    plain_language
    The inherited EGF defect was linked to failure of the kidneys to conserve magnesium.
    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
    Kidney; serum and urine
    tissue_or_cell_type
    Kidney; serum and urine
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Magnesium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 1043–1054

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human pedigree and serum/urine phenotyping · source_derived_draft · unverified_draft

    ### egf-variant-human-magnesium-wasting Two homozygous EGF P1070L sisters had low serum magnesium with inappropriately sustained urinary Mg loss. Condition category: machinery_impairment nutrient_topic: Magnesium research collection; topical membership is not evidence of a direct dietary effect. plain_language: The inherited EGF defect was linked to failure of the kidneys to conserve magnesium. organism: Human tissue_or_cell_type: Kidney; serum and urine experimental_model: Human pedigree and serum/urine phenotyping limitations: Small kindred; cellular sorting experiments support the explanation rather than directly measuring the entire cascade in vivo. evidence-system: Human pedigree and serum/urine phenotyping tissue: Kidney; serum and urine [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

  3. Pathogenic biallelic TRPM6 variants were identified in families with hypomagnesemia and secondary hypocalcemia.

    TRPM6 loss-of-function genotype → Serum magnesium concentration source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    cross_nutrient
    Calcium concentration also fell in the inherited Mg-handling disorder; this record does not specify the downstream endocrine mechanism.
    evidence-system
    Familial positional genetics
    experimental_model
    Familial positional genetics
    limitations
    Mapping alone does not apportion intestinal versus renal contributions or prove every downstream symptom is Mg-only.
    nutrient_topic
    Magnesium research collection; topical membership is not evidence of a direct dietary effect. · Magnesium
    organism
    Human
    plain_language
    Inherited failure of magnesium handling produced a recognizable low-magnesium disorder.
    primary_references
    [schlingmann-2002-trpm6] Hypomagnesemia with secondary hypocalcemia is caused by mutations in TRPM6, a new member of the TRPM gene family. (2002). https://pubmed.ncbi.nlm.nih.gov/12032568/ DOI: 10.1038/ng889
    tissue
    Intestine and kidney implicated; serum phenotype
    tissue_or_cell_type
    Intestine and kidney implicated; serum phenotype
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Magnesium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 909–921

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

    ### human-trpm6-loss-low-magnesium Pathogenic biallelic TRPM6 variants were identified in families with hypomagnesemia and secondary hypocalcemia. Condition category: machinery_impairment nutrient_topic: Magnesium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Inherited failure of magnesium handling produced a recognizable low-magnesium disorder. organism: Human tissue_or_cell_type: Intestine and kidney implicated; serum phenotype experimental_model: Familial positional genetics limitations: Mapping alone does not apportion intestinal versus renal contributions or prove every downstream symptom is Mg-only. cross_nutrient: Calcium concentration also fell in the inherited Mg-handling disorder; this record does not specify the downstream endocrine mechanism. evidence-system: Familial positional genetics tissue: Intestine and kidney implicated; serum phenotype [schlingmann-2002-trpm6] Hypomagnesemia with secondary hypocalcemia is caused by mutations in TRPM6, a new member of the TRPM gene family. (2002). https://pubmed.ncbi.nlm.nih.gov/12032568/ DOI: 10.1038/ng889
    Complete structured claim and evidence

  4. Intestine-restricted Trpm6 deletion reduced serum and bone magnesium in the tested adult mice.

    Intestine-specific Trpm6-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; six-month-old male mice
    experimental_model
    Villin1-Cre conditional deletion; six-month-old male mice
    limitations
    Colon expression was detected; the outcome does not quantify the contribution of each human intestinal segment.
    nutrient_topic
    Magnesium research collection; topical membership is not evidence of a direct dietary effect. · Magnesium
    organism
    Mouse
    plain_language
    Removing intestinal TRPM6 impaired systemic magnesium supply despite intact kidneys.
    primary_references
    [chubanov-2016-trpm6] Epithelial magnesium transport by TRPM6 is essential for prenatal development and adult survival (2016). https://elifesciences.org/articles/20914 DOI: 10.7554/eLife.20914
    tissue
    Intestinal epithelium; serum and bone
    tissue_or_cell_type
    Intestinal epithelium; serum and bone
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Magnesium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 923–934

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

    ### intestinal-trpm6-loss-low-magnesium Intestine-restricted Trpm6 deletion reduced serum and bone magnesium in the tested adult mice. Condition category: machinery_impairment nutrient_topic: Magnesium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Removing intestinal TRPM6 impaired systemic magnesium supply despite intact kidneys. organism: Mouse tissue_or_cell_type: Intestinal epithelium; serum and bone experimental_model: Villin1-Cre conditional deletion; six-month-old male mice limitations: Colon expression was detected; the outcome does not quantify the contribution of each human intestinal segment. evidence-system: Villin1-Cre conditional deletion; six-month-old male mice tissue: Intestinal epithelium; serum and bone [chubanov-2016-trpm6] Epithelial magnesium transport by TRPM6 is essential for prenatal development and adult survival (2016). https://elifesciences.org/articles/20914 DOI: 10.7554/eLife.20914
    Complete structured claim and evidence

  5. Insulin increased TRPM6 surface abundance and channel activity through a PI3K- and RAC1-dependent pathway.

    Insulin → TRPM6 abundance at the cell surface source_derived_draftungraded
    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

  6. Insulin failed to activate tested TRPM6 V1393I and K1584E variants.

    TRPM6 V1393I variant → Insulin source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    cross_nutrient
    Insulin/TRPM6/Mg interaction can depend on genotype.
    experimental_model
    Mutant-versus-wild-type channel assays.
    limitations
    Nearby phosphorylation-site effects are proposed; association with pregnancy glycemia does not prove nutritional causality.
    nutrient_topic
    Magnesium research collection; topical membership is not evidence of a direct dietary effect. · Magnesium
    organism
    Homo sapiens
    plain_language
    A change in the channel can interrupt the signal even when insulin is present.
    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
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Magnesium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 1539–1549

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

    ### mg-trpm6-variants-insulin-response Insulin failed to activate tested TRPM6 V1393I and K1584E variants. Condition category: machinery_impairment nutrient_topic: Magnesium research collection; topical membership is not evidence of a direct dietary effect. plain_language: A change in the channel can interrupt the signal even when insulin is present. organism: Homo sapiens tissue_or_cell_type: TRPM6-expressing cells; plasma membrane experimental_model: Mutant-versus-wild-type channel assays. limitations: Nearby phosphorylation-site effects are proposed; association with pregnancy glycemia does not prove nutritional causality. cross_nutrient: Insulin/TRPM6/Mg interaction can depend on genotype. [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

  7. Pro-EGF P1070L impaired basolateral delivery of TRPM6-stimulating EGF activity in polarized MDCK experiments.

    Pro-EGF P1070L → Basolateral EGF release source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence-system
    Polarized MDCK conditioned-medium assays applied to TRPM6-expressing HEK293 cells
    experimental_model
    Polarized MDCK conditioned-medium assays applied to TRPM6-expressing HEK293 cells
    limitations
    Functional conditioned-medium evidence; no quantitative human DCT ligand measurement.
    nutrient_topic
    Magnesium research collection; topical membership is not evidence of a direct dietary effect. · Magnesium
    organism
    Human protein; canine and human-derived cells
    plain_language
    The mutation sends insufficient active signal to the epithelial side containing the relevant receptor.
    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
    Polarized epithelial model
    tissue_or_cell_type
    Polarized epithelial model
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Magnesium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 1030–1041

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Polarized MDCK conditioned-medium assays applied to TRPM6-expressing HEK293 cells · source_derived_draft · unverified_draft

    ### pro-egf-variant-loses-basolateral-signal Pro-EGF P1070L impaired basolateral delivery of TRPM6-stimulating EGF activity in polarized MDCK experiments. Condition category: machinery_impairment nutrient_topic: Magnesium research collection; topical membership is not evidence of a direct dietary effect. plain_language: The mutation sends insufficient active signal to the epithelial side containing the relevant receptor. organism: Human protein; canine and human-derived cells tissue_or_cell_type: Polarized epithelial model experimental_model: Polarized MDCK conditioned-medium assays applied to TRPM6-expressing HEK293 cells limitations: Functional conditioned-medium evidence; no quantitative human DCT ligand measurement. evidence-system: Polarized MDCK conditioned-medium assays applied to TRPM6-expressing HEK293 cells tissue: Polarized epithelial model [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

  8. Kidney-restricted Trpm6 deletion did not lower serum Mg or raise urinary Mg in the tested mice.

    Kidney-specific Trpm6-null mouse genotype → Serum magnesium concentration source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence-system
    Ksp-Cre conditional deletion; six-month-old male mice
    experimental_model
    Ksp-Cre conditional deletion; six-month-old male mice
    limitations
    Bone Mg was slightly reduced; this is not proof renal TRPM6 is dispensable under every diet or in humans.
    nutrient_topic
    Magnesium research collection; topical membership is not evidence of a direct dietary effect. · Magnesium
    organism
    Mouse
    plain_language
    These mice maintained circulating magnesium after kidney-specific TRPM6 loss.
    primary_references
    [chubanov-2016-trpm6] Epithelial magnesium transport by TRPM6 is essential for prenatal development and adult survival (2016). https://elifesciences.org/articles/20914 DOI: 10.7554/eLife.20914
    tissue
    Kidney; serum and urine
    tissue_or_cell_type
    Kidney; serum and urine
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Magnesium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 936–947

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Ksp-Cre conditional deletion; six-month-old male mice · source_derived_draft · unverified_draft

    ### renal-trpm6-loss-serum-preserved Kidney-restricted Trpm6 deletion did not lower serum Mg or raise urinary Mg in the tested mice. Condition category: machinery_impairment nutrient_topic: Magnesium research collection; topical membership is not evidence of a direct dietary effect. plain_language: These mice maintained circulating magnesium after kidney-specific TRPM6 loss. organism: Mouse tissue_or_cell_type: Kidney; serum and urine experimental_model: Ksp-Cre conditional deletion; six-month-old male mice limitations: Bone Mg was slightly reduced; this is not proof renal TRPM6 is dispensable under every diet or in humans. evidence-system: Ksp-Cre conditional deletion; six-month-old male mice tissue: Kidney; serum and urine [chubanov-2016-trpm6] Epithelial magnesium transport by TRPM6 is essential for prenatal development and adult survival (2016). https://elifesciences.org/articles/20914 DOI: 10.7554/eLife.20914
    Complete structured claim and evidence

  9. 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

In the sources

Preserved passages that mention this component, quoted exactly. Open one to read it in context.

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