Component

Claudin-2

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. Claudin-2 manipulation changes calcium permeability across Caco-2 epithelial monolayers.

    Claudin-2 → Paracellular calcium permeability source_derived_draftungraded
    Experimental context and source evidence
    experimental_model
    Caco-2 knockdown/overexpression and mouse VDR-null intestinal expression
    limitations
    Cell-line permeability; not an obligatory route in every intestinal segment.
    nutrient_topic
    Calcium research collection; topical membership is not evidence of a direct dietary effect. · Calcium
    organism
    Homo sapiens cell line
    plain_language
    Claudin-2 supports calcium movement between cells.
    primary_references
    [fujita2008] Tight junction proteins claudin-2 and -12 are critical for vitamin D-dependent Ca2+ absorption between enterocytes (2008). https://pmc.ncbi.nlm.nih.gov/articles/PMC2366872/ DOI: 10.1091/mbc.E07-09-0973
    tissue_or_cell_type
    Caco-2 epithelial tight junctions

    Calcium: mechanism-first literature curation (2026-09-17) · lines 192–201

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Caco-2 knockdown/overexpression and mouse VDR-null intestinal expression · source_derived_draft · unverified_draft

    ### cldn2-calcium-permeability Claudin-2 manipulation changes calcium permeability across Caco-2 epithelial monolayers. Condition category: normal nutrient_topic: Calcium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Claudin-2 supports calcium movement between cells. organism: Homo sapiens cell line tissue_or_cell_type: Caco-2 epithelial tight junctions experimental_model: Caco-2 knockdown/overexpression and mouse VDR-null intestinal expression limitations: Cell-line permeability; not an obligatory route in every intestinal segment. [fujita2008] Tight junction proteins claudin-2 and -12 are critical for vitamin D-dependent Ca2+ absorption between enterocytes (2008). https://pmc.ncbi.nlm.nih.gov/articles/PMC2366872/ DOI: 10.1091/mbc.E07-09-0973
    Complete structured claim and evidence

What acts on it

  1. Calcitriol increased Claudin-2 expression in human Caco-2 intestinal epithelial cells.

    Calcitriol → Claudin-2 source_derived_draftungraded
    Experimental context and source evidence
    cross_nutrient
    Vitamin D–calcium–phosphate regulation.
    evidence_locator
    Primary abstract and Results/Discussion on calcitriol-induced claudin expression; cached web-primary-excerpts.json
    evidence_scope
    D3 active metabolite or VDR machinery experiment; not a direct D2-versus-D3 comparison.
    experimental_model
    Human Caco-2 cells; RT-PCR, immunoblotting and junctional localization
    exposure
    Calcitriol-treated versus vehicle Caco-2 cultures; exact hormone dose/time not recovered in the primary passages used.
    limitations
    Cell-line expression response; the separately reused permeability experiments support function, but neither establishes a universal fraction of human dietary calcium absorption.
    nutrient
    Vitamin D2 and D3 · Vitamin D2 and D3
    nutrient_topic
    Vitamin D2 and D3 research collection; topical membership is not evidence of a direct dietary effect. · Vitamin D2 and D3
    organism
    Homo sapiens
    plain_language
    Active vitamin D can increase a tight-junction protein involved in calcium movement between intestinal cells.
    primary_references
    [vdm-fujita2008] Tight junction proteins claudin-2 and -12 are critical for vitamin D-dependent Ca2+ absorption between enterocytes. (2008). https://pubmed.ncbi.nlm.nih.gov/18287530/ DOI: 10.1091/mbc.e07-09-0973
    tissue_or_cell_type
    Intestinal epithelial cell model

    Vitamin D2 and D3: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 617–631

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human Caco-2 cells; RT-PCR, immunoblotting and junctional localization · source_derived_draft · unverified_draft

    ### vdm-calcitriol-induces-cldn2 Calcitriol increased Claudin-2 expression in human Caco-2 intestinal epithelial cells. Condition category: normal nutrient_topic: Vitamin D2 and D3 research collection; topical membership is not evidence of a direct dietary effect. plain_language: Active vitamin D can increase a tight-junction protein involved in calcium movement between intestinal cells. organism: Homo sapiens tissue_or_cell_type: Intestinal epithelial cell model experimental_model: Human Caco-2 cells; RT-PCR, immunoblotting and junctional localization limitations: Cell-line expression response; the separately reused permeability experiments support function, but neither establishes a universal fraction of human dietary calcium absorption. exposure: Calcitriol-treated versus vehicle Caco-2 cultures; exact hormone dose/time not recovered in the primary passages used. cross_nutrient: Vitamin D–calcium–phosphate regulation. evidence_locator: Primary abstract and Results/Discussion on calcitriol-induced claudin expression; cached web-primary-excerpts.json nutrient: Vitamin D2 and D3 evidence_scope: D3 active metabolite or VDR machinery experiment; not a direct D2-versus-D3 comparison. [vdm-fujita2008] Tight junction proteins claudin-2 and -12 are critical for vitamin D-dependent Ca2+ absorption between enterocytes. (2008). https://pubmed.ncbi.nlm.nih.gov/18287530/ DOI: 10.1091/mbc.e07-09-0973
    Complete structured claim and evidence

Where it participates (unsigned role)

  1. Cldn2/Cldn12 double-null mice lose more urinary calcium than Cldn2-null mice.

    Claudin-2 and claudin-12 → Urinary calcium excretion source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    experimental_model
    Cldn2/Cldn12 single/double knockout mice, ex vivo epithelia and cell models
    limitations
    Global deletion also affects intestinal handling.
    nutrient_topic
    Calcium research collection; topical membership is not evidence of a direct dietary effect. · Calcium
    organism
    Mus musculus
    plain_language
    The two claudins provide complementary renal retention.
    primary_references
    [beggs2021] Claudin-2 and claudin-12 form independent, complementary pores required to maintain calcium homeostasis (2021). https://pmc.ncbi.nlm.nih.gov/articles/PMC8694054/ DOI: 10.1073/pnas.2111247118
    tissue_or_cell_type
    Kidney; proximal-tubule localization
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Calcium: mechanism-first literature curation (2026-09-17) · lines 225–234

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Cldn2/Cldn12 single/double knockout mice, ex vivo epithelia and cell models · source_derived_draft · unverified_draft

    ### cldn2-cldn12-double-loss-calciuria Cldn2/Cldn12 double-null mice lose more urinary calcium than Cldn2-null mice. Condition category: machinery_impairment nutrient_topic: Calcium research collection; topical membership is not evidence of a direct dietary effect. plain_language: The two claudins provide complementary renal retention. organism: Mus musculus tissue_or_cell_type: Kidney; proximal-tubule localization experimental_model: Cldn2/Cldn12 single/double knockout mice, ex vivo epithelia and cell models limitations: Global deletion also affects intestinal handling. [beggs2021] Claudin-2 and claudin-12 form independent, complementary pores required to maintain calcium homeostasis (2021). https://pmc.ncbi.nlm.nih.gov/articles/PMC8694054/ DOI: 10.1073/pnas.2111247118
    Complete structured claim and evidence

  2. Cldn2/Cldn12 double deletion lowers colonic calcium permeability; small-intestinal permeability was unchanged.

    Claudin-2 and claudin-12 → Colonic paracellular calcium permeability source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    experimental_model
    Cldn2/Cldn12 single/double knockout mice, ex vivo epithelia and cell models
    limitations
    Global double knockout; single proteins are partly redundant.
    nutrient_topic
    Calcium research collection; topical membership is not evidence of a direct dietary effect. · Calcium
    organism
    Mus musculus
    plain_language
    The measured defect was segment specific.
    primary_references
    [beggs2021] Claudin-2 and claudin-12 form independent, complementary pores required to maintain calcium homeostasis (2021). https://pmc.ncbi.nlm.nih.gov/articles/PMC8694054/ DOI: 10.1073/pnas.2111247118
    tissue_or_cell_type
    Colon
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Calcium: mechanism-first literature curation (2026-09-17) · lines 214–223

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Cldn2/Cldn12 single/double knockout mice, ex vivo epithelia and cell models · source_derived_draft · unverified_draft

    ### cldn2-cldn12-double-loss-colon Cldn2/Cldn12 double deletion lowers colonic calcium permeability; small-intestinal permeability was unchanged. Condition category: machinery_impairment nutrient_topic: Calcium research collection; topical membership is not evidence of a direct dietary effect. plain_language: The measured defect was segment specific. organism: Mus musculus tissue_or_cell_type: Colon experimental_model: Cldn2/Cldn12 single/double knockout mice, ex vivo epithelia and cell models limitations: Global double knockout; single proteins are partly redundant. [beggs2021] Claudin-2 and claudin-12 form independent, complementary pores required to maintain calcium homeostasis (2021). https://pmc.ncbi.nlm.nih.gov/articles/PMC8694054/ DOI: 10.1073/pnas.2111247118
    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