Component

TAL claudin junctional localization

Accumulation of claudin proteins at thick-ascending-limb epithelial tight junctions.

1 recorded relationships. Experimental role, claim status and evidence remain attached to each record.

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 acts on it

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

    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

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