Component

Iron uptake and efflux in cultured intestinal epithelia

Iron uptake and efflux in cultured intestinal epithelia. Species, exposure and limitations are retained in each linked claim.

2 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 acts on it

  1. ATP7A silencing impaired iron uptake and efflux in differentiated human Caco-2 cells.

    Human copper-transporting ATPase ATP7A → Iron uptake and efflux in cultured intestinal epithelia source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/copper-research/27714044.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "5e8791edb75475ba74e95cddc330c06512ef3b9c02a0c5a6b203327c047dff37", "start_char": 0, "end_char": 1780, "text_sha256": "5e8791edb75475ba74e95cddc330c06512ef3b9c02a0c5a6b203327c047dff37"}
    experimental_model
    ATP7A knockdown in differentiated intestinal cell cultures
    exposure
    ATP7A knockdown and radiolabeled iron transport
    limitations
    Reductionist cell models; increased enzyme activity did not guarantee increased net iron flux. Molecular expression details were measured in the rat line.
    nutrient_topic
    Copper research collection; topical membership is not evidence of a direct dietary effect. · Copper
    organism
    Human
    plain_language
    A copper transporter also helps the intestinal iron-handling system function.
    primary_references
    [copper-p27714044] Knockdown of copper-transporting ATPase 1 (Atp7a) impairs iron flux in fully-differentiated rat (IEC-6) and human (Caco-2) intestinal epithelial cells. (2016). https://pubmed.ncbi.nlm.nih.gov/27714044/ DOI: 10.1039/c6mt00126b
    tissue_or_cell_type
    Caco-2 cells

    Copper: transport, cuproenzymes, deficiency, excess and nutrient interactions (2026-09-17) · lines 897–908

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · ATP7A knockdown in differentiated intestinal cell cultures · source_derived_draft · unverified_draft

    ### copper-human-atp7a-iron ATP7A silencing impaired iron uptake and efflux in differentiated human Caco-2 cells. Condition category: normal nutrient_topic: Copper research collection; topical membership is not evidence of a direct dietary effect. plain_language: A copper transporter also helps the intestinal iron-handling system function. organism: Human tissue_or_cell_type: Caco-2 cells experimental_model: ATP7A knockdown in differentiated intestinal cell cultures limitations: Reductionist cell models; increased enzyme activity did not guarantee increased net iron flux. Molecular expression details were measured in the rat line. exposure: ATP7A knockdown and radiolabeled iron transport evidence_span: {"source_cache": "artifacts/copper-research/27714044.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "5e8791edb75475ba74e95cddc330c06512ef3b9c02a0c5a6b203327c047dff37", "start_char": 0, "end_char": 1780, "text_sha256": "5e8791edb75475ba74e95cddc330c06512ef3b9c02a0c5a6b203327c047dff37"} [copper-p27714044] Knockdown of copper-transporting ATPase 1 (Atp7a) impairs iron flux in fully-differentiated rat (IEC-6) and human (Caco-2) intestinal epithelial cells. (2016). https://pubmed.ncbi.nlm.nih.gov/27714044/ DOI: 10.1039/c6mt00126b
    Complete structured claim and evidence

Where it participates (unsigned role)

  1. Rat Atp7a knockdown increased hephaestin expression more than tenfold and increased ferroxidase activity, even though net iron uptake and efflux fell.

    Rat copper-transporting ATPase Atp7a → Rat hephaestin Heph source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/copper-research/27714044.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "5e8791edb75475ba74e95cddc330c06512ef3b9c02a0c5a6b203327c047dff37", "start_char": 0, "end_char": 1780, "text_sha256": "5e8791edb75475ba74e95cddc330c06512ef3b9c02a0c5a6b203327c047dff37"}
    experimental_model
    ATP7A knockdown in differentiated intestinal cell cultures
    exposure
    ATP7A knockdown and radiolabeled iron transport
    limitations
    Reductionist cell models; increased enzyme activity did not guarantee increased net iron flux. Molecular expression details were measured in the rat line.
    nutrient_topic
    Copper research collection; topical membership is not evidence of a direct dietary effect. · Copper
    organism
    Rat
    plain_language
    Compensatory enzyme increases did not repair the overall transport chain.
    primary_references
    [copper-p27714044] Knockdown of copper-transporting ATPase 1 (Atp7a) impairs iron flux in fully-differentiated rat (IEC-6) and human (Caco-2) intestinal epithelial cells. (2016). https://pubmed.ncbi.nlm.nih.gov/27714044/ DOI: 10.1039/c6mt00126b
    tissue_or_cell_type
    IEC-6 cells

    Copper: transport, cuproenzymes, deficiency, excess and nutrient interactions (2026-09-17) · lines 910–921

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · ATP7A knockdown in differentiated intestinal cell cultures · source_derived_draft · unverified_draft

    ### copper-rat-atp7a-heph-compensation Rat Atp7a knockdown increased hephaestin expression more than tenfold and increased ferroxidase activity, even though net iron uptake and efflux fell. Condition category: normal nutrient_topic: Copper research collection; topical membership is not evidence of a direct dietary effect. plain_language: Compensatory enzyme increases did not repair the overall transport chain. organism: Rat tissue_or_cell_type: IEC-6 cells experimental_model: ATP7A knockdown in differentiated intestinal cell cultures limitations: Reductionist cell models; increased enzyme activity did not guarantee increased net iron flux. Molecular expression details were measured in the rat line. exposure: ATP7A knockdown and radiolabeled iron transport evidence_span: {"source_cache": "artifacts/copper-research/27714044.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "5e8791edb75475ba74e95cddc330c06512ef3b9c02a0c5a6b203327c047dff37", "start_char": 0, "end_char": 1780, "text_sha256": "5e8791edb75475ba74e95cddc330c06512ef3b9c02a0c5a6b203327c047dff37"} [copper-p27714044] Knockdown of copper-transporting ATPase 1 (Atp7a) impairs iron flux in fully-differentiated rat (IEC-6) and human (Caco-2) intestinal epithelial cells. (2016). https://pubmed.ncbi.nlm.nih.gov/27714044/ DOI: 10.1039/c6mt00126b
    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