Component

CaV1.2 alpha1C / CACNA1C

Pore-forming alpha1C subunit of L-type voltage-gated calcium channels.

3 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

Where it participates (unsigned role)

  1. CaV1.2 EF-hand substitutions shifted Mg inhibition, with D1546K eliminating sensitivity across the tested range.

    CaV1.2 EF-hand mutants tested by Brunet et al. → CaV1.2-mediated ionic current source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    cross_nutrient
    The regulatory protein site connects intracellular magnesium with calcium-channel current.
    evidence-system
    EF-hand mutagenesis and patch clamp; rabbit cardiac CaV1.2 with beta1b and alpha2delta auxiliary subunits
    experimental_model
    EF-hand mutagenesis and patch clamp; rabbit cardiac CaV1.2 with beta1b and alpha2delta auxiliary subunits
    exposure
    Calculated intracellular free Mg was varied over 0.1-7.2 mM, with a 0.8 mM control; pipette MgATP was held at 5 mM. Ca2+ or Ba2+ served as the permeant ion in separate recordings.
    limitations
    Supports an EF-hand-associated regulatory mechanism; not direct structural observation of bound Mg.
    nutrient_topic
    Magnesium research collection; topical membership is not evidence of a direct dietary effect. · Magnesium
    organism
    Rabbit cardiac CaV1.2 protein expressed in human-derived tsA-201 cells
    plain_language
    Changing the channel regulatory site changed its response to intracellular magnesium.
    primary_references
    [brunet-2005-cav12] Modulation of CaV1.2 channels by Mg2+ acting at an EF-hand motif in the COOH-terminal domain (2005). https://pmc.ncbi.nlm.nih.gov/articles/PMC2266622/ DOI: 10.1085/jgp.200509333
    tissue
    tsA-201 cells
    tissue_or_cell_type
    tsA-201 cells
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Magnesium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 1303–1316

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · EF-hand mutagenesis and patch clamp; rabbit cardiac CaV1.2 with beta1b and alpha2delta auxiliary subunits · source_derived_draft · unverified_draft

    ### cav12-ef-hand-magnesium-sensitivity CaV1.2 EF-hand substitutions shifted Mg inhibition, with D1546K eliminating sensitivity across the tested range. Condition category: machinery_impairment nutrient_topic: Magnesium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Changing the channel regulatory site changed its response to intracellular magnesium. organism: Rabbit cardiac CaV1.2 protein expressed in human-derived tsA-201 cells tissue_or_cell_type: tsA-201 cells experimental_model: EF-hand mutagenesis and patch clamp; rabbit cardiac CaV1.2 with beta1b and alpha2delta auxiliary subunits limitations: Supports an EF-hand-associated regulatory mechanism; not direct structural observation of bound Mg. cross_nutrient: The regulatory protein site connects intracellular magnesium with calcium-channel current. exposure: Calculated intracellular free Mg was varied over 0.1-7.2 mM, with a 0.8 mM control; pipette MgATP was held at 5 mM. Ca2+ or Ba2+ served as the permeant ion in separate recordings. evidence-system: EF-hand mutagenesis and patch clamp; rabbit cardiac CaV1.2 with beta1b and alpha2delta auxiliary subunits tissue: tsA-201 cells [brunet-2005-cav12] Modulation of CaV1.2 channels by Mg2+ acting at an EF-hand motif in the COOH-terminal domain (2005). https://pmc.ncbi.nlm.nih.gov/articles/PMC2266622/ DOI: 10.1085/jgp.200509333
    Complete structured claim and evidence

  2. Increasing intracellular free Mg reduced Ca2+ and Ba2+ currents through recombinant CaV1.2.

    Mg2+ → CaV1.2-mediated ionic current source_derived_draftungraded
    Experimental context and source evidence
    cross_nutrient
    Mg availability directly modulated Ca-channel function in an expression assay, not intestinal calcium absorption.
    evidence-system
    Whole-cell recordings with intracellular free-Mg control; rabbit cardiac CaV1.2 with beta1b and alpha2delta auxiliary subunits
    experimental_model
    Whole-cell recordings with intracellular free-Mg control; rabbit cardiac CaV1.2 with beta1b and alpha2delta auxiliary subunits
    exposure
    Calculated intracellular free Mg was varied over 0.1-7.2 mM, with a 0.8 mM control; pipette MgATP was held at 5 mM. Ca2+ or Ba2+ served as the permeant ion in separate recordings.
    limitations
    Free Mg was experimentally controlled; no dietary intake, serum threshold or cardiac event was measured.
    nutrient_topic
    Magnesium research collection; topical membership is not evidence of a direct dietary effect. · Magnesium
    organism
    Rabbit cardiac CaV1.2 protein expressed in human-derived tsA-201 cells
    plain_language
    Free magnesium inside the cell can restrain current through a calcium-entry channel.
    primary_references
    [brunet-2005-cav12] Modulation of CaV1.2 channels by Mg2+ acting at an EF-hand motif in the COOH-terminal domain (2005). https://pmc.ncbi.nlm.nih.gov/articles/PMC2266622/ DOI: 10.1085/jgp.200509333
    tissue
    tsA-201 cells
    tissue_or_cell_type
    tsA-201 cells

    Magnesium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 1288–1301

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Whole-cell recordings with intracellular free-Mg control; rabbit cardiac CaV1.2 with beta1b and alpha2delta auxiliary subunits · source_derived_draft · unverified_draft

    ### intracellular-magnesium-reduces-cav12-current Increasing intracellular free Mg reduced Ca2+ and Ba2+ currents through recombinant CaV1.2. Condition category: normal nutrient_topic: Magnesium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Free magnesium inside the cell can restrain current through a calcium-entry channel. organism: Rabbit cardiac CaV1.2 protein expressed in human-derived tsA-201 cells tissue_or_cell_type: tsA-201 cells experimental_model: Whole-cell recordings with intracellular free-Mg control; rabbit cardiac CaV1.2 with beta1b and alpha2delta auxiliary subunits limitations: Free Mg was experimentally controlled; no dietary intake, serum threshold or cardiac event was measured. cross_nutrient: Mg availability directly modulated Ca-channel function in an expression assay, not intestinal calcium absorption. exposure: Calculated intracellular free Mg was varied over 0.1-7.2 mM, with a 0.8 mM control; pipette MgATP was held at 5 mM. Ca2+ or Ba2+ served as the permeant ion in separate recordings. evidence-system: Whole-cell recordings with intracellular free-Mg control; rabbit cardiac CaV1.2 with beta1b and alpha2delta auxiliary subunits tissue: tsA-201 cells [brunet-2005-cav12] Modulation of CaV1.2 channels by Mg2+ acting at an EF-hand motif in the COOH-terminal domain (2005). https://pmc.ncbi.nlm.nih.gov/articles/PMC2266622/ DOI: 10.1085/jgp.200509333
    Complete structured claim and evidence

  3. GS-967 suppressed hypokalemic early afterdepolarizations; simulations implicated CaMKII-enhanced late sodium current in a sodium/calcium feedback loop.

    Cardiac late sodium current → Cardiac early afterdepolarizations source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    nutrient_deficiency Imported condition classification; unverified.
    cross_nutrient
    Sodium entry and calcium loading interact during low extracellular potassium.
    experimental_model
    Low-K cardiac inhibition experiments and computational model.
    limitations
    The complete feedback sequence is model-supported, not every step directly measured.
    nutrient_topic
    Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium
    organism
    Rabbit/rat and mathematical model
    plain_language
    Persistent sodium entry helped sustain low-potassium electrical instability.
    primary_references
    [pezhouman-2015-camkii] Molecular Basis of Hypokalemia-Induced Ventricular Fibrillation (2015). https://pubmed.ncbi.nlm.nih.gov/26269574/ DOI: 10.1161/CIRCULATIONAHA.115.016217
    tissue_or_cell_type
    Ventricular myocardium
    trigger_kind
    nutrient_deficiency Imported condition classification; unverified.

    Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 657–667

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Low-K cardiac inhibition experiments and computational model. · source_derived_draft · unverified_draft

    ### k-low-late-sodium-feedback GS-967 suppressed hypokalemic early afterdepolarizations; simulations implicated CaMKII-enhanced late sodium current in a sodium/calcium feedback loop. Condition category: nutrient_deficiency nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Persistent sodium entry helped sustain low-potassium electrical instability. organism: Rabbit/rat and mathematical model tissue_or_cell_type: Ventricular myocardium experimental_model: Low-K cardiac inhibition experiments and computational model. limitations: The complete feedback sequence is model-supported, not every step directly measured. cross_nutrient: Sodium entry and calcium loading interact during low extracellular potassium. [pezhouman-2015-camkii] Molecular Basis of Hypokalemia-Induced Ventricular Fibrillation (2015). https://pubmed.ncbi.nlm.nih.gov/26269574/ DOI: 10.1161/CIRCULATIONAHA.115.016217
    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