Component

Cytosolic labile zinc availability

Cytosolic labile zinc availability; model and exposure are recorded in linked claims.

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. T-cell receptor activation raised cytoplasmic zinc within one minute, especially near the receptor-contact region; the rise depended on extracellular zinc and was attenuated by ZIP6 suppression.

    Human zinc transporter ZIP6 / SLC39A6 → Cytosolic labile zinc availability source_derived_draftungraded
    Experimental context and source evidence
    cross_nutrient
    Zinc(II) ion (transported_ion)
    evidence_span
    {"source_cache": "artifacts/zinc-signaling-sources/21422171-abstract.txt", "locator": "Primary indexed abstract", "file_sha256": "e3b0e519eb5c44185655c0195cb81c713f2b005d70a982466e3e041e997fae59"}
    experimental_model
    Primary human T-cell receptor signaling study
    exposure
    Receptor activation, extracellular zinc availability and ZIP6 suppression comparisons.
    limitations
    Culture zinc availability and local signals cannot be mapped directly to oral doses or plasma thresholds. Calcium fluorescence tracks the signal rather than proving one specific calcium channel mechanism.
    nutrient_topic
    Zinc research collection; topical membership is not evidence of a direct dietary effect. · Zinc
    organism
    Homo sapiens
    plain_language
    ZIP6 helped generate a rapid local zinc signal after receptor activation.
    primary_references
    [zn-sig-21422171] Regulation of T cell receptor signaling by activation-induced zinc influx. (2011). https://pubmed.ncbi.nlm.nih.gov/21422171/ DOI: 10.1084/jem.20100031
    tissue_or_cell_type
    CD4 T cells at the receptor-contact region

    Zinc: transport, enzyme loading, deficiency and nutrient interactions (2026-09-17) · lines 1013–1025

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Primary human T-cell receptor signaling study · source_derived_draft · unverified_draft

    ### zn-sig-zip6-influx T-cell receptor activation raised cytoplasmic zinc within one minute, especially near the receptor-contact region; the rise depended on extracellular zinc and was attenuated by ZIP6 suppression. Condition category: normal nutrient_topic: Zinc research collection; topical membership is not evidence of a direct dietary effect. plain_language: ZIP6 helped generate a rapid local zinc signal after receptor activation. organism: Homo sapiens tissue_or_cell_type: CD4 T cells at the receptor-contact region experimental_model: Primary human T-cell receptor signaling study limitations: Culture zinc availability and local signals cannot be mapped directly to oral doses or plasma thresholds. Calcium fluorescence tracks the signal rather than proving one specific calcium channel mechanism. exposure: Receptor activation, extracellular zinc availability and ZIP6 suppression comparisons. cross_nutrient: Zinc(II) ion (transported_ion) evidence_span: {"source_cache": "artifacts/zinc-signaling-sources/21422171-abstract.txt", "locator": "Primary indexed abstract", "file_sha256": "e3b0e519eb5c44185655c0195cb81c713f2b005d70a982466e3e041e997fae59"} [zn-sig-21422171] Regulation of T cell receptor signaling by activation-induced zinc influx. (2011). https://pubmed.ncbi.nlm.nih.gov/21422171/ DOI: 10.1084/jem.20100031
    Complete structured claim and evidence

Where it participates (unsigned role)

  1. ZIP7 phosphorylation was linked to release of stored zinc and downstream AKT and ERK1/2 phosphorylation in the studied human cells.

    Human zinc transporter ZIP7 / SLC39A7 → Endoplasmic-reticulum zinc release source_derived_draftungraded
    Experimental context and source evidence
    cross_nutrient
    Human protein kinase CK2 complex (upstream_kinase); AKT serine/threonine kinase family (downstream_kinase_family); Human ERK2 / MAPK1 (downstream_kinase); Human ERK1 / MAPK3 (downstream_kinase); Cytosolic labile zinc availability (increased_pool)
    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
    Zinc redistribution connected a storage compartment to kinase signaling.
    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 999–1011

    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-zip7-release ZIP7 phosphorylation was linked to release of stored zinc and downstream AKT and ERK1/2 phosphorylation in the studied human cells. Condition category: normal nutrient_topic: Zinc research collection; topical membership is not evidence of a direct dietary effect. plain_language: Zinc redistribution connected a storage compartment to kinase signaling. 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: Human protein kinase CK2 complex (upstream_kinase); AKT serine/threonine kinase family (downstream_kinase_family); Human ERK2 / MAPK1 (downstream_kinase); Human ERK1 / MAPK3 (downstream_kinase); Cytosolic labile zinc availability (increased_pool) 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