Component

Human ZIP4 (SLC39A4)

Human intestinal zinc uptake transporter protein; gene identity is separate.

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

Where it participates (unsigned role)

  1. Elevated zinc stimulated human ZIP4 ubiquitination and degradation; a cytoplasmic histidine-rich region was required for this degradation response but dispensable for zinc-induced endocytosis.

    Zinc(II) ion → ZIP4 protein degradation source_derived_draftungraded
    Experimental context and source evidence
    cross_nutrient
    false
    experimental_model
    Cultured cells expressing human ZIP4 with mutational analysis
    exposure
    Elevated zinc exposure; detailed concentration and cell lineage not specified in the abstract.
    limitations
    Abstract extraction; the region requirement does not mean every histidine acts as an independent sensor. This is zinc exposure, not demonstrated dietary deficiency.
    nutrient_topic
    Zinc research collection; topical membership is not evidence of a direct dietary effect. · Zinc
    organism
    Human protein in cultured cells
    plain_language
    Human ZIP4 has a zinc-triggered disposal response that is separate from removal from the surface.
    primary_references
    [zinc-trans-17202136] A histidine-rich cluster mediates the ubiquitination and degradation of the human zinc transporter, hZIP4, and protects against zinc cytotoxicity. (2007). https://pubmed.ncbi.nlm.nih.gov/17202136/ DOI: 10.1074/jbc.m610552200
    tissue_or_cell_type
    Cellular zinc-uptake machinery

    Zinc: transport, enzyme loading, deficiency and nutrient interactions (2026-09-17) · lines 258–269

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Cultured cells expressing human ZIP4 with mutational analysis · source_derived_draft · unverified_draft

    ### zinc-trans-hzip4-degradation Elevated zinc stimulated human ZIP4 ubiquitination and degradation; a cytoplasmic histidine-rich region was required for this degradation response but dispensable for zinc-induced endocytosis. Condition category: normal nutrient_topic: Zinc research collection; topical membership is not evidence of a direct dietary effect. plain_language: Human ZIP4 has a zinc-triggered disposal response that is separate from removal from the surface. organism: Human protein in cultured cells tissue_or_cell_type: Cellular zinc-uptake machinery experimental_model: Cultured cells expressing human ZIP4 with mutational analysis limitations: Abstract extraction; the region requirement does not mean every histidine acts as an independent sensor. This is zinc exposure, not demonstrated dietary deficiency. exposure: Elevated zinc exposure; detailed concentration and cell lineage not specified in the abstract. cross_nutrient: false [zinc-trans-17202136] A histidine-rich cluster mediates the ubiquitination and degradation of the human zinc transporter, hZIP4, and protects against zinc cytotoxicity. (2007). https://pubmed.ncbi.nlm.nih.gov/17202136/ DOI: 10.1074/jbc.m610552200
    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