Component

Claudin-16

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

5 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. 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. Claudin-16 RNAi reduced paracellular cation selectivity in isolated mouse thick ascending limbs.

    Claudin-16 RNAi mouse genotype → TAL paracellular cation selectivity source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    cross_nutrient
    TAL electrical selectivity participates in magnesium and calcium conservation; no dietary synergy is implied.
    evidence-system
    Renal RNAi and isolated TAL electrophysiology
    experimental_model
    Renal RNAi and isolated TAL electrophysiology
    limitations
    Selectivity evidence is not proof claudin-16 alone forms a specifically magnesium-selective pore.
    nutrient_topic
    Magnesium research collection; topical membership is not evidence of a direct dietary effect. · Magnesium
    organism
    Mouse
    plain_language
    The junction lost part of its preference for positively charged ions, changing the conditions that support mineral recovery.
    primary_references
    [hou-2007-cldn16] Transgenic RNAi depletion of claudin-16 and the renal handling of magnesium. (2007). https://pubmed.ncbi.nlm.nih.gov/17442678/ DOI: 10.1074/jbc.M700632200
    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 1097–1109

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Renal RNAi and isolated TAL electrophysiology · source_derived_draft · unverified_draft

    ### cldn16-depletion-selectivity Claudin-16 RNAi reduced paracellular cation selectivity in isolated mouse thick ascending limbs. Condition category: machinery_impairment nutrient_topic: Magnesium research collection; topical membership is not evidence of a direct dietary effect. plain_language: The junction lost part of its preference for positively charged ions, changing the conditions that support mineral recovery. organism: Mouse tissue_or_cell_type: Renal thick ascending limb experimental_model: Renal RNAi and isolated TAL electrophysiology limitations: Selectivity evidence is not proof claudin-16 alone forms a specifically magnesium-selective pore. cross_nutrient: TAL electrical selectivity participates in magnesium and calcium conservation; no dietary synergy is implied. evidence-system: Renal RNAi and isolated TAL electrophysiology tissue: Renal thick ascending limb [hou-2007-cldn16] Transgenic RNAi depletion of claudin-16 and the renal handling of magnesium. (2007). https://pubmed.ncbi.nlm.nih.gov/17442678/ DOI: 10.1074/jbc.M700632200
    Complete structured claim and evidence

  3. Claudin-16 RNAi mice developed renal magnesium wasting.

    Claudin-16 RNAi mouse genotype → Urinary magnesium excretion source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    cross_nutrient
    Calcium wasting accompanied magnesium loss after shared tight-junction impairment.
    evidence-system
    Transgenic Cldn16 RNAi with renal mineral phenotyping
    experimental_model
    Transgenic Cldn16 RNAi with renal mineral phenotyping
    limitations
    This organismal endpoint accompanies selectivity changes; the experiment does not isolate every intervening transport step.
    nutrient_topic
    Magnesium research collection; topical membership is not evidence of a direct dietary effect. · Magnesium
    organism
    Mouse
    plain_language
    Reducing this tight-junction component made the kidneys lose magnesium.
    primary_references
    [hou-2007-cldn16] Transgenic RNAi depletion of claudin-16 and the renal handling of magnesium. (2007). https://pubmed.ncbi.nlm.nih.gov/17442678/ DOI: 10.1074/jbc.M700632200
    tissue
    Kidney; urine
    tissue_or_cell_type
    Kidney; urine
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Magnesium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 1111–1123

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Transgenic Cldn16 RNAi with renal mineral phenotyping · source_derived_draft · unverified_draft

    ### cldn16-rnai-magnesium-loss Claudin-16 RNAi mice developed renal magnesium wasting. Condition category: machinery_impairment nutrient_topic: Magnesium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Reducing this tight-junction component made the kidneys lose magnesium. organism: Mouse tissue_or_cell_type: Kidney; urine experimental_model: Transgenic Cldn16 RNAi with renal mineral phenotyping limitations: This organismal endpoint accompanies selectivity changes; the experiment does not isolate every intervening transport step. cross_nutrient: Calcium wasting accompanied magnesium loss after shared tight-junction impairment. evidence-system: Transgenic Cldn16 RNAi with renal mineral phenotyping tissue: Kidney; urine [hou-2007-cldn16] Transgenic RNAi depletion of claudin-16 and the renal handling of magnesium. (2007). https://pubmed.ncbi.nlm.nih.gov/17442678/ DOI: 10.1074/jbc.M700632200
    Complete structured claim and evidence

  4. Human CLDN16 mutations were linked to renal magnesium wasting in the positional-cloning study.

    CLDN16 loss-of-function genotype → Urinary magnesium excretion source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence-system
    Human familial positional genetics and kidney localization
    experimental_model
    Human familial positional genetics and kidney localization
    limitations
    Establishes essential machinery; does not by itself identify a Mg-selective pore.
    nutrient_topic
    Magnesium research collection; topical membership is not evidence of a direct dietary effect. · Magnesium
    organism
    Human
    plain_language
    A renal tight-junction protein is necessary for the kidney to retain magnesium normally.
    primary_references
    [simon-1999-cldn16] Paracellin-1, a renal tight junction protein required for paracellular Mg2+ resorption (1999). https://pubmed.ncbi.nlm.nih.gov/10390358/ DOI: 10.1126/science.285.5424.103
    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 1056–1067

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

    ### human-cldn16-magnesium-wasting Human CLDN16 mutations were linked to renal magnesium wasting in the positional-cloning study. Condition category: machinery_impairment nutrient_topic: Magnesium research collection; topical membership is not evidence of a direct dietary effect. plain_language: A renal tight-junction protein is necessary for the kidney to retain magnesium normally. organism: Human tissue_or_cell_type: Renal thick ascending limb experimental_model: Human familial positional genetics and kidney localization limitations: Establishes essential machinery; does not by itself identify a Mg-selective pore. evidence-system: Human familial positional genetics and kidney localization tissue: Renal thick ascending limb [simon-1999-cldn16] Paracellin-1, a renal tight junction protein required for paracellular Mg2+ resorption (1999). https://pubmed.ncbi.nlm.nih.gov/10390358/ DOI: 10.1126/science.285.5424.103
    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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