Component

ZIP4 endocytosis

ZIP4 endocytosis

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. Oral zinc repletion caused mouse ZIP4 internalization from enterocyte apical membranes after dietary zinc deficiency.

    Zinc(II) ion → ZIP4 endocytosis source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    nutrient_deficiency Imported condition classification; unverified.
    cross_nutrient
    false
    experimental_model
    Dietary depletion followed by oral gavage and immunolocalization
    exposure
    Zinc-deficient weanlings for 10 days; 100 micromol ZnCl2/kg oral gavage with time-course localization.
    limitations
    Acute experimental repletion; the gavage is not a recommended human dose and internalization is distinct from later degradation.
    nutrient_topic
    Zinc research collection; topical membership is not evidence of a direct dietary effect. · Zinc
    organism
    Mus musculus
    plain_language
    After zinc becomes available again, intestinal cells pull ZIP4 away from their surface.
    primary_references
    [zinc-trans-18020946] Novel zinc-responsive post-transcriptional mechanisms reciprocally regulate expression of the mouse Slc39a4 and Slc39a5 zinc transporters (Zip4 and Zip5). (2007). https://pubmed.ncbi.nlm.nih.gov/18020946/ DOI: 10.1515/bc.2007.149
    tissue_or_cell_type
    Duodenal enterocytes
    trigger_kind
    nutrient_deficiency Imported condition classification; unverified.

    Zinc: transport, enzyme loading, deficiency and nutrient interactions (2026-09-17) · lines 245–256

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Dietary depletion followed by oral gavage and immunolocalization · source_derived_draft · unverified_draft

    ### zinc-trans-zip4-repletion-endocytosis Oral zinc repletion caused mouse ZIP4 internalization from enterocyte apical membranes after dietary zinc deficiency. Condition category: nutrient_deficiency nutrient_topic: Zinc research collection; topical membership is not evidence of a direct dietary effect. plain_language: After zinc becomes available again, intestinal cells pull ZIP4 away from their surface. organism: Mus musculus tissue_or_cell_type: Duodenal enterocytes experimental_model: Dietary depletion followed by oral gavage and immunolocalization limitations: Acute experimental repletion; the gavage is not a recommended human dose and internalization is distinct from later degradation. exposure: Zinc-deficient weanlings for 10 days; 100 micromol ZnCl2/kg oral gavage with time-course localization. cross_nutrient: false [zinc-trans-18020946] Novel zinc-responsive post-transcriptional mechanisms reciprocally regulate expression of the mouse Slc39a4 and Slc39a5 zinc transporters (Zip4 and Zip5). (2007). https://pubmed.ncbi.nlm.nih.gov/18020946/ DOI: 10.1515/bc.2007.149
    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