Component

ZIP7 phosphorylation

ZIP7 phosphorylation; model and exposure are recorded in linked claims.

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. The study identified CK2-dependent phosphorylation of ZIP7 as a regulatory step preceding cytosolic zinc release from intracellular stores.

    Experimental context and source evidence
    cross_nutrient
    ZIP7 phosphorylation (regulatory_event); Zinc(II) ion (transported_ion)
    evidence_span
    {"source_cache": "artifacts/zinc-signaling-sources/22317921-abstract.txt", "locator": "Primary indexed abstract", "file_sha256": "a8e31db38c22019d7ebef8ff165e2b3dc0b3a338e18514f0bf0c48cc5215944d"}
    experimental_model
    Human breast-cell model with ZIP7/CK2 perturbations
    exposure
    Signaling stimuli and ZIP7/CK2 phosphorylation comparisons.
    limitations
    Cellular signaling study; it does not establish dietary zinc supplementation as an anticancer intervention. Intracellular release is different from net dietary uptake.
    nutrient_topic
    Zinc research collection; topical membership is not evidence of a direct dietary effect. · Zinc
    organism
    Homo sapiens
    plain_language
    A kinase can open the route from stored zinc to a cytoplasmic signal.
    primary_references
    [zn-sig-22317921] Protein kinase CK2 triggers cytosolic zinc signaling pathways by phosphorylation of zinc channel ZIP7. (2012). https://pubmed.ncbi.nlm.nih.gov/22317921/ DOI: 10.1126/scisignal.2002585
    tissue_or_cell_type
    Endoplasmic reticulum and cytoplasm

    Zinc: transport, enzyme loading, deficiency and nutrient interactions (2026-09-17) · lines 985–997

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human breast-cell model with ZIP7/CK2 perturbations · source_derived_draft · unverified_draft

    ### zn-sig-ck2-zip7 The study identified CK2-dependent phosphorylation of ZIP7 as a regulatory step preceding cytosolic zinc release from intracellular stores. Condition category: normal nutrient_topic: Zinc research collection; topical membership is not evidence of a direct dietary effect. plain_language: A kinase can open the route from stored zinc to a cytoplasmic signal. organism: Homo sapiens tissue_or_cell_type: Endoplasmic reticulum and cytoplasm experimental_model: Human breast-cell model with ZIP7/CK2 perturbations limitations: Cellular signaling study; it does not establish dietary zinc supplementation as an anticancer intervention. Intracellular release is different from net dietary uptake. exposure: Signaling stimuli and ZIP7/CK2 phosphorylation comparisons. cross_nutrient: ZIP7 phosphorylation (regulatory_event); Zinc(II) ion (transported_ion) evidence_span: {"source_cache": "artifacts/zinc-signaling-sources/22317921-abstract.txt", "locator": "Primary indexed abstract", "file_sha256": "a8e31db38c22019d7ebef8ff165e2b3dc0b3a338e18514f0bf0c48cc5215944d"} [zn-sig-22317921] Protein kinase CK2 triggers cytosolic zinc signaling pathways by phosphorylation of zinc channel ZIP7. (2012). https://pubmed.ncbi.nlm.nih.gov/22317921/ DOI: 10.1126/scisignal.2002585
    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