Component

Mouse intestinal apical Ctr1 protein abundance

Mouse intestinal apical Ctr1 protein abundance. Species, exposure and limitations are retained in each linked claim.

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. Dietary copper limitation increased total and apically localized Ctr1 protein in mouse intestine.

    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/copper-research/20699218.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "c638594d4e707bb39a8f2e8c1fed15a42982e1dc4d525fda112d28281a853012", "start_char": 0, "end_char": 1749, "text_sha256": "c638594d4e707bb39a8f2e8c1fed15a42982e1dc4d525fda112d28281a853012"}
    experimental_model
    Intestinal immunolocalization and dietary copper limitation
    exposure
    Copper limitation in mice
    limitations
    Apical Ctr1 was observed in the examined mammalian preparations; membrane localization is model dependent and cannot be assigned universally to every human intestinal condition.
    nutrient_topic
    Copper research collection; topical membership is not evidence of a direct dietary effect. · Copper
    organism
    Mouse, rat and pig; human HEK293T cells for separate processing experiments
    plain_language
    The intestine increased an entry route when copper supply fell.
    primary_references
    [copper-p20699218] Ctr1 is an apical copper transporter in mammalian intestinal epithelial cells in vivo that is controlled at the level of protein stability. (2010). https://pubmed.ncbi.nlm.nih.gov/20699218/ DOI: 10.1074/jbc.m110.143826
    tissue_or_cell_type
    Intestinal epithelium

    Copper: transport, cuproenzymes, deficiency, excess and nutrient interactions (2026-09-17) · lines 351–362

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Intestinal immunolocalization and dietary copper limitation · source_derived_draft · unverified_draft

    ### copper-ctr1-intestinal-adaptation Dietary copper limitation increased total and apically localized Ctr1 protein in mouse intestine. Condition category: normal nutrient_topic: Copper research collection; topical membership is not evidence of a direct dietary effect. plain_language: The intestine increased an entry route when copper supply fell. organism: Mouse, rat and pig; human HEK293T cells for separate processing experiments tissue_or_cell_type: Intestinal epithelium experimental_model: Intestinal immunolocalization and dietary copper limitation limitations: Apical Ctr1 was observed in the examined mammalian preparations; membrane localization is model dependent and cannot be assigned universally to every human intestinal condition. exposure: Copper limitation in mice evidence_span: {"source_cache": "artifacts/copper-research/20699218.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "c638594d4e707bb39a8f2e8c1fed15a42982e1dc4d525fda112d28281a853012", "start_char": 0, "end_char": 1749, "text_sha256": "c638594d4e707bb39a8f2e8c1fed15a42982e1dc4d525fda112d28281a853012"} [copper-p20699218] Ctr1 is an apical copper transporter in mammalian intestinal epithelial cells in vivo that is controlled at the level of protein stability. (2010). https://pubmed.ncbi.nlm.nih.gov/20699218/ DOI: 10.1074/jbc.m110.143826
    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