Component

Mouse ZIP7 / Slc39a7

Mouse ZIP7 / Slc39a7; model and exposure are recorded in linked claims.

3 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

Where it participates (unsigned role)

  1. Intestinal epithelial Zip7 deletion increased ER-stress responses in proliferative progenitor cells and was followed by substantial progenitor-cell death.

    Mouse intestinal epithelial ZIP7 loss → Intestinal crypt endoplasmic-reticulum stress source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    cross_nutrient
    Mouse ZIP7 / Slc39a7 (affected_transporter); Intestinal progenitor-cell survival (reduced_endpoint)
    evidence_span
    {"source_cache": "artifacts/zinc-signaling-sources/27736879-abstract.txt", "locator": "Primary indexed abstract", "file_sha256": "4ce8fe391aff141b5145e4122917ca1c1817273ab0dd55c7a936b687d9dacdd6"}
    experimental_model
    Conditional intestinal Zip7-deficient mice and organoids
    exposure
    Intestinal epithelial versus Lgr5-cell-specific deletion; zinc supplementation comparison.
    limitations
    Cell lineage and tissue context matter. Supplementation failing to rescue a transporter defect is not evidence that ordinary dietary zinc replacement fails.
    nutrient_topic
    Zinc research collection; topical membership is not evidence of a direct dietary effect. · Zinc
    organism
    Mus musculus
    plain_language
    Loss of zinc distribution machinery stressed the cells that renew the intestinal lining.
    primary_references
    [zn-sig-27736879] Zinc Transporter SLC39A7/ZIP7 Promotes Intestinal Epithelial Self-Renewal by Resolving ER Stress. (2016). https://pubmed.ncbi.nlm.nih.gov/27736879/ DOI: 10.1371/journal.pgen.1006349
    tissue_or_cell_type
    Intestinal crypts, progenitor cells and organoids
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Zinc: transport, enzyme loading, deficiency and nutrient interactions (2026-09-17) · lines 1125–1137

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Conditional intestinal Zip7-deficient mice and organoids · source_derived_draft · unverified_draft

    ### zn-sig-zip7-er-stress Intestinal epithelial Zip7 deletion increased ER-stress responses in proliferative progenitor cells and was followed by substantial progenitor-cell death. Condition category: machinery_impairment nutrient_topic: Zinc research collection; topical membership is not evidence of a direct dietary effect. plain_language: Loss of zinc distribution machinery stressed the cells that renew the intestinal lining. organism: Mus musculus tissue_or_cell_type: Intestinal crypts, progenitor cells and organoids experimental_model: Conditional intestinal Zip7-deficient mice and organoids limitations: Cell lineage and tissue context matter. Supplementation failing to rescue a transporter defect is not evidence that ordinary dietary zinc replacement fails. exposure: Intestinal epithelial versus Lgr5-cell-specific deletion; zinc supplementation comparison. cross_nutrient: Mouse ZIP7 / Slc39a7 (affected_transporter); Intestinal progenitor-cell survival (reduced_endpoint) evidence_span: {"source_cache": "artifacts/zinc-signaling-sources/27736879-abstract.txt", "locator": "Primary indexed abstract", "file_sha256": "4ce8fe391aff141b5145e4122917ca1c1817273ab0dd55c7a936b687d9dacdd6"} [zn-sig-27736879] Zinc Transporter SLC39A7/ZIP7 Promotes Intestinal Epithelial Self-Renewal by Resolving ER Stress. (2016). https://pubmed.ncbi.nlm.nih.gov/27736879/ DOI: 10.1371/journal.pgen.1006349
    Complete structured claim and evidence

  2. Restricting Zip7 deletion to Lgr5-positive stem cells did not impair baseline epithelial homeostasis or crypt-derived organoid formation, unlike deletion across intestinal epithelial cells.

    Mouse Lgr5-positive stem-cell ZIP7 loss → Intestinal epithelial renewal source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    cross_nutrient
    Mouse ZIP7 / Slc39a7 (affected_transporter)
    evidence_span
    {"source_cache": "artifacts/zinc-signaling-sources/27736879.txt", "locator": "Results: Lgr5-positive cell-intrinsic ZIP7; supplemental Figure S4", "file_sha256": "4771f8b4a2b4e332b10bd2a5abef6f538cc38f4c85916b44ddab9f15679ed621"}
    experimental_model
    Conditional intestinal Zip7-deficient mice and organoids
    exposure
    Intestinal epithelial versus Lgr5-cell-specific deletion; zinc supplementation comparison.
    limitations
    Cell lineage and tissue context matter. Supplementation failing to rescue a transporter defect is not evidence that ordinary dietary zinc replacement fails.
    nutrient_topic
    Zinc research collection; topical membership is not evidence of a direct dietary effect. · Zinc
    organism
    Mus musculus
    plain_language
    The affected cell population changed the outcome of the same transporter loss.
    primary_references
    [zn-sig-27736879] Zinc Transporter SLC39A7/ZIP7 Promotes Intestinal Epithelial Self-Renewal by Resolving ER Stress. (2016). https://pubmed.ncbi.nlm.nih.gov/27736879/ DOI: 10.1371/journal.pgen.1006349
    tissue_or_cell_type
    Intestinal crypts, progenitor cells and organoids
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Zinc: transport, enzyme loading, deficiency and nutrient interactions (2026-09-17) · lines 1153–1165

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Conditional intestinal Zip7-deficient mice and organoids · source_derived_draft · unverified_draft

    ### zn-sig-zip7-lineage-null Restricting Zip7 deletion to Lgr5-positive stem cells did not impair baseline epithelial homeostasis or crypt-derived organoid formation, unlike deletion across intestinal epithelial cells. Condition category: machinery_impairment nutrient_topic: Zinc research collection; topical membership is not evidence of a direct dietary effect. plain_language: The affected cell population changed the outcome of the same transporter loss. organism: Mus musculus tissue_or_cell_type: Intestinal crypts, progenitor cells and organoids experimental_model: Conditional intestinal Zip7-deficient mice and organoids limitations: Cell lineage and tissue context matter. Supplementation failing to rescue a transporter defect is not evidence that ordinary dietary zinc replacement fails. exposure: Intestinal epithelial versus Lgr5-cell-specific deletion; zinc supplementation comparison. cross_nutrient: Mouse ZIP7 / Slc39a7 (affected_transporter) evidence_span: {"source_cache": "artifacts/zinc-signaling-sources/27736879.txt", "locator": "Results: Lgr5-positive cell-intrinsic ZIP7; supplemental Figure S4", "file_sha256": "4771f8b4a2b4e332b10bd2a5abef6f538cc38f4c85916b44ddab9f15679ed621"} [zn-sig-27736879] Zinc Transporter SLC39A7/ZIP7 Promotes Intestinal Epithelial Self-Renewal by Resolving ER Stress. (2016). https://pubmed.ncbi.nlm.nih.gov/27736879/ DOI: 10.1371/journal.pgen.1006349
    Complete structured claim and evidence

  3. Adding 1 µM ZnSO4 did not suppress ER-stress gene induction in Zip7-deficient intestinal organoids assessed 48 hours after induction of deletion; the study also observed no rescue in fibroblasts, while restored ZIP7 expression rescued their stress response.

    Zinc → Intestinal crypt endoplasmic-reticulum stress source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    cross_nutrient
    Mouse ZIP7 / Slc39a7 (affected_transporter)
    evidence_span
    {"source_cache": "artifacts/zinc-signaling-sources/27736879.txt", "locator": "Results: Zip7 deletion activates ER stress; Figure 4, Figure 5 and supplemental Figure S8", "file_sha256": "4771f8b4a2b4e332b10bd2a5abef6f538cc38f4c85916b44ddab9f15679ed621"}
    experimental_model
    Conditional intestinal Zip7-deficient mice and organoids
    exposure
    Supplemental Figure S8: 1 µM ZnSO4; intestinal organoids assessed 48 hours after the study-induced Zip7 deletion. The fibroblast comparison also used 1 µM ZnSO4. This exposure did not suppress the measured ER-stress gene induction.
    limitations
    Cell lineage and tissue context matter. Supplementation failing to rescue a transporter defect is not evidence that ordinary dietary zinc replacement fails.
    nutrient_topic
    Zinc research collection; topical membership is not evidence of a direct dietary effect. · Zinc
    organism
    Mus musculus
    plain_language
    More available zinc did not substitute for the missing distribution machinery.
    primary_references
    [zn-sig-27736879] Zinc Transporter SLC39A7/ZIP7 Promotes Intestinal Epithelial Self-Renewal by Resolving ER Stress. (2016). https://pubmed.ncbi.nlm.nih.gov/27736879/ DOI: 10.1371/journal.pgen.1006349
    tissue_or_cell_type
    Intestinal crypts, progenitor cells and organoids
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Zinc: transport, enzyme loading, deficiency and nutrient interactions (2026-09-17) · lines 1139–1151

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Conditional intestinal Zip7-deficient mice and organoids · source_derived_draft · unverified_draft

    ### zn-sig-zip7-zinc-no-rescue Adding 1 µM ZnSO4 did not suppress ER-stress gene induction in Zip7-deficient intestinal organoids assessed 48 hours after induction of deletion; the study also observed no rescue in fibroblasts, while restored ZIP7 expression rescued their stress response. Condition category: machinery_impairment nutrient_topic: Zinc research collection; topical membership is not evidence of a direct dietary effect. plain_language: More available zinc did not substitute for the missing distribution machinery. organism: Mus musculus tissue_or_cell_type: Intestinal crypts, progenitor cells and organoids experimental_model: Conditional intestinal Zip7-deficient mice and organoids limitations: Cell lineage and tissue context matter. Supplementation failing to rescue a transporter defect is not evidence that ordinary dietary zinc replacement fails. exposure: Supplemental Figure S8: 1 µM ZnSO4; intestinal organoids assessed 48 hours after the study-induced Zip7 deletion. The fibroblast comparison also used 1 µM ZnSO4. This exposure did not suppress the measured ER-stress gene induction. cross_nutrient: Mouse ZIP7 / Slc39a7 (affected_transporter) evidence_span: {"source_cache": "artifacts/zinc-signaling-sources/27736879.txt", "locator": "Results: Zip7 deletion activates ER stress; Figure 4, Figure 5 and supplemental Figure S8", "file_sha256": "4771f8b4a2b4e332b10bd2a5abef6f538cc38f4c85916b44ddab9f15679ed621"} [zn-sig-27736879] Zinc Transporter SLC39A7/ZIP7 Promotes Intestinal Epithelial Self-Renewal by Resolving ER Stress. (2016). https://pubmed.ncbi.nlm.nih.gov/27736879/ DOI: 10.1371/journal.pgen.1006349
    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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