Component

Na+/Ca2+ exchanger 1 / SLC8A1

Independent biological entity. Read linked claims for experimental scope and context.

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 it acts on

  1. Human cardiac NCX1 exchanges calcium and sodium in opposing directions across the membrane.

    Na+/Ca2+ exchanger 1 / SLC8A1 → Calcium ion source_derived_draftungraded
    Experimental context and source evidence
    compartment_description
    Plasma membrane
    experimental_model
    Human cardiac NCX1; cryo-EM and functional exchange assays
    limitations
    Net direction depends on electrochemical gradients and voltage; NCX1 is not an ATP-hydrolyzing pump.
    nutrient_topic
    Calcium research collection; topical membership is not evidence of a direct dietary effect. · Calcium
    organism
    Homo sapiens
    plain_language
    NCX1 couples calcium movement to sodium moving the other way.
    primary_references
    [ca-xue2023] Structural mechanisms of the human cardiac sodium-calcium exchanger NCX1 (2023). https://pubmed.ncbi.nlm.nih.gov/37794011/ DOI: 10.1038/s41467-023-41885-4
    research_relationship_category
    transport
    tissue_or_cell_type
    Cardiac NCX1 expression system
    transport_effect
    depends Reversible exchange: forward mode extrudes calcium and reverse mode admits it, which the record states.
    transport_or_reaction_direction
    Reversible Na+/Ca2+ exchange; forward calcium extrusion or reverse calcium entry
    transport_pool
    cytosolic calcium Reversible exchange: forward mode extrudes calcium and reverse mode admits it, which the record states.

    Calcium: mechanism-first literature curation (2026-09-17) · lines 625–637

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human cardiac NCX1; cryo-EM and functional exchange assays · source_derived_draft · unverified_draft

    ### ca-ncx1-calcium-sodium-exchange Human cardiac NCX1 exchanges calcium and sodium in opposing directions across the membrane. Condition category: normal nutrient_topic: Calcium research collection; topical membership is not evidence of a direct dietary effect. plain_language: NCX1 couples calcium movement to sodium moving the other way. organism: Homo sapiens tissue_or_cell_type: Cardiac NCX1 expression system experimental_model: Human cardiac NCX1; cryo-EM and functional exchange assays limitations: Net direction depends on electrochemical gradients and voltage; NCX1 is not an ATP-hydrolyzing pump. research_relationship_category: transport transport_or_reaction_direction: Reversible Na+/Ca2+ exchange; forward calcium extrusion or reverse calcium entry compartment_description: Plasma membrane [ca-xue2023] Structural mechanisms of the human cardiac sodium-calcium exchanger NCX1 (2023). https://pubmed.ncbi.nlm.nih.gov/37794011/ DOI: 10.1038/s41467-023-41885-4
    Complete structured claim and evidence

What acts on it

  1. Calcium binding to the cytosolic CBD2 regulatory domain disrupts an inactive NCX1 assembly and permits exchange.

    Calcium ion → Na+/Ca2+ exchanger 1 / SLC8A1 source_derived_draftungraded
    Experimental context and source evidence
    compartment_description
    Cytosolic regulatory domain of plasma-membrane exchanger
    experimental_model
    Human cardiac NCX1; cryo-EM and functional exchange assays
    limitations
    Regulatory calcium binding is distinct from calcium being transported; the measured splice form and assay conditions matter.
    nutrient_topic
    Calcium research collection; topical membership is not evidence of a direct dietary effect. · Calcium
    organism
    Homo sapiens
    plain_language
    Calcium also regulates NCX1 at a site separate from the transported-ion pathway.
    primary_references
    [ca-xue2023] Structural mechanisms of the human cardiac sodium-calcium exchanger NCX1 (2023). https://pubmed.ncbi.nlm.nih.gov/37794011/ DOI: 10.1038/s41467-023-41885-4
    research_relationship_category
    regulation
    tissue_or_cell_type
    Cardiac NCX1 expression system

    Calcium: mechanism-first literature curation (2026-09-17) · lines 639–650

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human cardiac NCX1; cryo-EM and functional exchange assays · source_derived_draft · unverified_draft

    ### ca-ncx1-regulatory-calcium Calcium binding to the cytosolic CBD2 regulatory domain disrupts an inactive NCX1 assembly and permits exchange. Condition category: normal nutrient_topic: Calcium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Calcium also regulates NCX1 at a site separate from the transported-ion pathway. organism: Homo sapiens tissue_or_cell_type: Cardiac NCX1 expression system experimental_model: Human cardiac NCX1; cryo-EM and functional exchange assays limitations: Regulatory calcium binding is distinct from calcium being transported; the measured splice form and assay conditions matter. research_relationship_category: regulation compartment_description: Cytosolic regulatory domain of plasma-membrane exchanger [ca-xue2023] Structural mechanisms of the human cardiac sodium-calcium exchanger NCX1 (2023). https://pubmed.ncbi.nlm.nih.gov/37794011/ DOI: 10.1038/s41467-023-41885-4
    Complete structured claim and evidence

  2. Pump inhibition during low-K exposure increased sodium sensed by NCX and favored cellular calcium loading.

    Sodium-potassium ATPase complexes → Na+/Ca2+ exchanger 1 / SLC8A1 source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    nutrient_deficiency Imported condition classification; unverified.
    cross_nutrient
    Potassium-to-sodium-to-calcium coupling is experimentally supported; dietary effect magnitude is untested.
    experimental_model
    Rat ventricular ion assays plus modeling.
    limitations
    NCX microdomain interpretation; source ouabain units differ between methods and figure legends.
    nutrient_topic
    Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium
    organism
    Rat
    plain_language
    Potassium-dependent sodium pumping helps the exchanger remove calcium.
    primary_references
    [aronsen-2015-cardiac] Hypokalaemia induces Ca2+ overload and Ca2+ waves in ventricular myocytes by reducing Na+,K+-ATPase alpha2 activity (2015). https://pmc.ncbi.nlm.nih.gov/articles/PMC4376427/ DOI: 10.1113/jphysiol.2014.279893
    tissue_or_cell_type
    Ventricular myocytes
    trigger_kind
    nutrient_deficiency Imported condition classification; unverified.

    Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 622–632

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Rat ventricular ion assays plus modeling. · source_derived_draft · unverified_draft

    ### k-low-cardiac-ncx-calcium Pump inhibition during low-K exposure increased sodium sensed by NCX and favored cellular calcium loading. Condition category: nutrient_deficiency nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Potassium-dependent sodium pumping helps the exchanger remove calcium. organism: Rat tissue_or_cell_type: Ventricular myocytes experimental_model: Rat ventricular ion assays plus modeling. limitations: NCX microdomain interpretation; source ouabain units differ between methods and figure legends. cross_nutrient: Potassium-to-sodium-to-calcium coupling is experimentally supported; dietary effect magnitude is untested. [aronsen-2015-cardiac] Hypokalaemia induces Ca2+ overload and Ca2+ waves in ventricular myocytes by reducing Na+,K+-ATPase alpha2 activity (2015). https://pmc.ncbi.nlm.nih.gov/articles/PMC4376427/ DOI: 10.1113/jphysiol.2014.279893
    Complete structured claim and evidence

Where it participates (unsigned role)

  1. Low-K exposure increased calcium waves in ventricular and tubulated atrial cells, with a weaker response in untubulated atrial cells.

    Extracellular potassium concentration → Propagating cardiac calcium waves source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    nutrient_deficiency Imported condition classification; unverified.
    cross_nutrient
    The calcium response to potassium depends on cellular transport organization.
    experimental_model
    Rat myocytes, 5.0 to 2.7 mM K, 3 minutes.
    limitations
    Architecture-dependent findings should not be generalized to all heart cells.
    nutrient_topic
    Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium
    organism
    Rat
    plain_language
    Internal membrane architecture changed how low potassium disturbed calcium.
    primary_references
    [tazmini-2020-cardiac] Hypokalemia Promotes Arrhythmia by Distinct Mechanisms in Atrial and Ventricular Myocytes (2020). https://pmc.ncbi.nlm.nih.gov/articles/PMC7098435/ DOI: 10.1161/CIRCRESAHA.119.315641
    tissue_or_cell_type
    Atrial/ventricular myocardium
    trigger_kind
    nutrient_deficiency Imported condition classification; unverified.

    Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 669–679

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Rat myocytes, 5.0 to 2.7 mM K, 3 minutes. · source_derived_draft · unverified_draft

    ### k-low-calcium-waves-tubules Low-K exposure increased calcium waves in ventricular and tubulated atrial cells, with a weaker response in untubulated atrial cells. Condition category: nutrient_deficiency nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Internal membrane architecture changed how low potassium disturbed calcium. organism: Rat tissue_or_cell_type: Atrial/ventricular myocardium experimental_model: Rat myocytes, 5.0 to 2.7 mM K, 3 minutes. limitations: Architecture-dependent findings should not be generalized to all heart cells. cross_nutrient: The calcium response to potassium depends on cellular transport organization. [tazmini-2020-cardiac] Hypokalemia Promotes Arrhythmia by Distinct Mechanisms in Atrial and Ventricular Myocytes (2020). https://pmc.ncbi.nlm.nih.gov/articles/PMC7098435/ DOI: 10.1161/CIRCRESAHA.119.315641
    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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