Component

Human zinc transporter ZIP6 / SLC39A6

Human zinc transporter ZIP6 / SLC39A6; model and exposure are recorded in linked claims.

4 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 it acts on

  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. Higher extracellular zinc sustained the cytoplasmic calcium signal after T-cell activation; initial calcium rises were similar, then the signals diverged.

    Zinc(II) ion → T-cell cytoplasmic calcium signal source_derived_draftungraded
    Experimental context and source evidence
    cross_nutrient
    calcium ion (signaling_ion); Human zinc transporter ZIP6 / SLC39A6 (upstream_transporter)
    evidence_span
    {"source_cache": "artifacts/zinc-signaling-sources/21422171.txt", "locator": "Results: zinc availability and TCR signaling; Figure 4e calcium time course", "file_sha256": "4d36b4fdeeff83b602b0532796814981ee45409241fe40fcd8f7bc1da8beff19"}
    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
    Zinc availability affected how long the calcium signal lasted.
    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 1055–1067

    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-zinc-calcium-signal Higher extracellular zinc sustained the cytoplasmic calcium signal after T-cell activation; initial calcium rises were similar, then the signals diverged. Condition category: normal nutrient_topic: Zinc research collection; topical membership is not evidence of a direct dietary effect. plain_language: Zinc availability affected how long the calcium signal lasted. 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: calcium ion (signaling_ion); Human zinc transporter ZIP6 / SLC39A6 (upstream_transporter) evidence_span: {"source_cache": "artifacts/zinc-signaling-sources/21422171.txt", "locator": "Results: zinc availability and TCR signaling; Figure 4e calcium time course", "file_sha256": "4d36b4fdeeff83b602b0532796814981ee45409241fe40fcd8f7bc1da8beff19"} [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

  2. Increased zinc influx reduced recruitment of SHP-1 to the T-cell receptor activation complex.

    Zinc(II) ion → SHP-1 recruitment to the T-cell receptor complex source_derived_draftungraded
    Experimental context and source evidence
    cross_nutrient
    Human SHP-1 / PTPN6 (affected_protein); Human zinc transporter ZIP6 / SLC39A6 (upstream_transporter)
    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
    The zinc signal reduced recruitment of an inhibitory phosphatase.
    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 1027–1039

    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-zinc-shp1 Increased zinc influx reduced recruitment of SHP-1 to the T-cell receptor activation complex. Condition category: normal nutrient_topic: Zinc research collection; topical membership is not evidence of a direct dietary effect. plain_language: The zinc signal reduced recruitment of an inhibitory phosphatase. 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: Human SHP-1 / PTPN6 (affected_protein); Human zinc transporter ZIP6 / SLC39A6 (upstream_transporter) 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

  3. Greater activation-associated zinc influx augmented ZAP70 phosphorylation in the human T-cell study.

    Zinc(II) ion → ZAP70 phosphorylation source_derived_draftungraded
    Experimental context and source evidence
    cross_nutrient
    Human ZAP70 (affected_kinase); Human zinc transporter ZIP6 / SLC39A6 (upstream_transporter)
    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
    A local zinc signal strengthened this receptor-associated kinase response.
    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 1041–1053

    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-zinc-zap70 Greater activation-associated zinc influx augmented ZAP70 phosphorylation in the human T-cell study. Condition category: normal nutrient_topic: Zinc research collection; topical membership is not evidence of a direct dietary effect. plain_language: A local zinc signal strengthened this receptor-associated kinase response. 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: Human ZAP70 (affected_kinase); Human zinc transporter ZIP6 / SLC39A6 (upstream_transporter) 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

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.

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