Component

Claudin-19

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. Biallelic CLDN19 variants were identified in families with renal magnesium wasting, hypercalciuria and nephrocalcinosis.

    Claudin-19 → Urinary calcium excretion source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    experimental_model
    Human affected families; linkage, sequencing and claudin trafficking/assembly assays
    limitations
    Multimineral genetic disorder; ocular and renal manifestations vary.
    nutrient_topic
    Calcium research collection; topical membership is not evidence of a direct dietary effect. · Calcium
    organism
    Homo sapiens
    plain_language
    Inherited junction defects can waste calcium.
    primary_references
    [konrad2006] Mutations in the tight-junction gene claudin 19 (CLDN19) are associated with renal magnesium wasting, renal failure, and severe ocular involvement (2006). https://pmc.ncbi.nlm.nih.gov/articles/PMC1698561/ DOI: 10.1086/508617
    tissue_or_cell_type
    Kidney tubules
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Calcium: mechanism-first literature curation (2026-09-17) · lines 269–278

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human affected families; linkage, sequencing and claudin trafficking/assembly assays · source_derived_draft · unverified_draft

    ### cldn19-variants-renal-calcium-wasting Biallelic CLDN19 variants were identified in families with renal magnesium wasting, hypercalciuria and nephrocalcinosis. Condition category: machinery_impairment nutrient_topic: Calcium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Inherited junction defects can waste calcium. organism: Homo sapiens tissue_or_cell_type: Kidney tubules experimental_model: Human affected families; linkage, sequencing and claudin trafficking/assembly assays limitations: Multimineral genetic disorder; ocular and renal manifestations vary. [konrad2006] Mutations in the tight-junction gene claudin 19 (CLDN19) are associated with renal magnesium wasting, renal failure, and severe ocular involvement (2006). https://pmc.ncbi.nlm.nih.gov/articles/PMC1698561/ DOI: 10.1086/508617
    Complete structured claim and evidence

What acts on it

  1. Claudin-16/19 coexpression increases paracellular cation selectivity in LLC-PK1 epithelial monolayers.

    Claudin-16 → Claudin-19 source_derived_draftungraded
    Experimental context and source evidence
    experimental_model
    Claudin expression in LLC-PK1/MDCK epithelia; interaction and permeability assays
    limitations
    Effects differ in MDCK cells; cation selectivity does not prove a calcium-specific pore.
    nutrient_topic
    Calcium research collection; topical membership is not evidence of a direct dietary effect. · Calcium
    organism
    Heterologous renal epithelial systems
    plain_language
    These renal junction proteins work together.
    primary_references
    [hou2008] Claudin-16 and claudin-19 interact and form a cation-selective tight junction complex (2008). https://pmc.ncbi.nlm.nih.gov/articles/PMC2176193/ DOI: 10.1172/JCI33970
    tissue_or_cell_type
    Renal tight-junction model

    Calcium: mechanism-first literature curation (2026-09-17) · lines 258–267

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Claudin expression in LLC-PK1/MDCK epithelia; interaction and permeability assays · source_derived_draft · unverified_draft

    ### cldn16-cldn19-cation-selectivity Claudin-16/19 coexpression increases paracellular cation selectivity in LLC-PK1 epithelial monolayers. Condition category: normal nutrient_topic: Calcium research collection; topical membership is not evidence of a direct dietary effect. plain_language: These renal junction proteins work together. organism: Heterologous renal epithelial systems tissue_or_cell_type: Renal tight-junction model experimental_model: Claudin expression in LLC-PK1/MDCK epithelia; interaction and permeability assays limitations: Effects differ in MDCK cells; cation selectivity does not prove a calcium-specific pore. [hou2008] Claudin-16 and claudin-19 interact and form a cation-selective tight junction complex (2008). https://pmc.ncbi.nlm.nih.gov/articles/PMC2176193/ DOI: 10.1172/JCI33970
    Complete structured claim and evidence

Where it participates (unsigned role)

  1. In the cited RNAi mice, depletion of either claudin-16 or claudin-19 displaced the other from TAL tight junctions.

    Claudin-16/claudin-19 complex → TAL claudin junctional localization source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence-system
    Reciprocal claudin RNAi mouse models and immunolocalization
    experimental_model
    Reciprocal claudin RNAi mouse models and immunolocalization
    limitations
    RNAi-model result; do not universalize junctional interdependence across all knockout backgrounds or human tissue.
    nutrient_topic
    Magnesium research collection; topical membership is not evidence of a direct dietary effect. · Magnesium
    organism
    Mouse
    plain_language
    The two proteins depended on each other for normal junction placement in these knockdown mice.
    primary_references
    [hou-2009-claudin-assembly] Claudin-16 and claudin-19 interaction is required for their assembly into tight junctions and for renal reabsorption of magnesium (2009). https://pmc.ncbi.nlm.nih.gov/articles/PMC2741254/ DOI: 10.1073/pnas.0907724106
    tissue
    Renal thick ascending limb
    tissue_or_cell_type
    Renal thick ascending limb
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Magnesium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 1084–1095

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Reciprocal claudin RNAi mouse models and immunolocalization · source_derived_draft · unverified_draft

    ### claudin-depletion-displaces-partner In the cited RNAi mice, depletion of either claudin-16 or claudin-19 displaced the other from TAL tight junctions. Condition category: machinery_impairment nutrient_topic: Magnesium research collection; topical membership is not evidence of a direct dietary effect. plain_language: The two proteins depended on each other for normal junction placement in these knockdown mice. organism: Mouse tissue_or_cell_type: Renal thick ascending limb experimental_model: Reciprocal claudin RNAi mouse models and immunolocalization limitations: RNAi-model result; do not universalize junctional interdependence across all knockout backgrounds or human tissue. evidence-system: Reciprocal claudin RNAi mouse models and immunolocalization tissue: Renal thick ascending limb [hou-2009-claudin-assembly] Claudin-16 and claudin-19 interaction is required for their assembly into tight junctions and for renal reabsorption of magnesium (2009). https://pmc.ncbi.nlm.nih.gov/articles/PMC2741254/ DOI: 10.1073/pnas.0907724106
    Complete structured claim and evidence

  2. Pathogenic CLDN19 variants were identified in families with renal magnesium loss and hypomagnesemia.

    CLDN19 loss-of-function genotype → Urinary magnesium excretion source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    cross_nutrient
    The disorder also includes abnormal calcium handling; shared renal machinery is implicated rather than competition for dietary absorption.
    curation_notes
    Existing catalog claim fb9278a2-5be5-5e4b-92f3-e02f00f3cfc7 covers the same families with urinary-calcium-excretion endpoint. This magnesium endpoint is deliberately separate.
    evidence-system
    Human family genetics with trafficking and assembly support
    experimental_model
    Human family genetics with trafficking and assembly support
    limitations
    Associated retinal abnormalities are not assigned solely to low Mg.
    nutrient_topic
    Magnesium research collection; topical membership is not evidence of a direct dietary effect. · Magnesium
    organism
    Human
    plain_language
    Claudin-19 failure can make the kidneys lose magnesium.
    primary_references
    [konrad-2006-cldn19] Mutations in the tight-junction gene claudin 19 (CLDN19) are associated with renal magnesium wasting, renal failure, and severe ocular involvement (2006). https://pubmed.ncbi.nlm.nih.gov/17033971/ DOI: 10.1086/508617
    tissue
    Renal tubules
    tissue_or_cell_type
    Renal tubules
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Magnesium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 1069–1082

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human family genetics with trafficking and assembly support · source_derived_draft · unverified_draft

    ### human-cldn19-magnesium-wasting Pathogenic CLDN19 variants were identified in families with renal magnesium loss and hypomagnesemia. Condition category: machinery_impairment nutrient_topic: Magnesium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Claudin-19 failure can make the kidneys lose magnesium. organism: Human tissue_or_cell_type: Renal tubules experimental_model: Human family genetics with trafficking and assembly support limitations: Associated retinal abnormalities are not assigned solely to low Mg. cross_nutrient: The disorder also includes abnormal calcium handling; shared renal machinery is implicated rather than competition for dietary absorption. curation_notes: Existing catalog claim fb9278a2-5be5-5e4b-92f3-e02f00f3cfc7 covers the same families with urinary-calcium-excretion endpoint. This magnesium endpoint is deliberately separate. evidence-system: Human family genetics with trafficking and assembly support tissue: Renal tubules [konrad-2006-cldn19] Mutations in the tight-junction gene claudin 19 (CLDN19) are associated with renal magnesium wasting, renal failure, and severe ocular involvement (2006). https://pubmed.ncbi.nlm.nih.gov/17033971/ DOI: 10.1086/508617
    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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