Component

Mouse ZIP4 (Slc39a4)

Mus musculus ZIP4 zinc uptake protein; distinct from human SLC39A4.

5 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. Expression of mouse ZIP4 increased zinc influx into transfected cells.

    Mouse ZIP4 (Slc39a4) → Cellular zinc influx source_derived_draftungraded
    Experimental context and source evidence
    cross_nutrient
    false
    experimental_model
    Transfected mammalian cells
    exposure
    ZIP4 expression versus controls; abstract does not specify zinc concentration.
    limitations
    Transport in engineered cells establishes capacity, not the fraction of human dietary zinc absorption.
    nutrient_topic
    Zinc research collection; topical membership is not evidence of a direct dietary effect. · Zinc
    organism
    Mouse protein in cultured mammalian cells
    plain_language
    Mouse ZIP4 can bring zinc into cells.
    primary_references
    [zinc-trans-12801924] The acrodermatitis enteropathica gene ZIP4 encodes a tissue-specific, zinc-regulated zinc transporter in mice. (2003). https://pubmed.ncbi.nlm.nih.gov/12801924/ DOI: 10.1074/jbc.m305000200
    tissue_or_cell_type
    Cell plasma membrane

    Zinc: transport, enzyme loading, deficiency and nutrient interactions (2026-09-17) · lines 219–230

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Transfected mammalian cells · source_derived_draft · unverified_draft

    ### zinc-trans-zip4-influx Expression of mouse ZIP4 increased zinc influx into transfected cells. Condition category: normal nutrient_topic: Zinc research collection; topical membership is not evidence of a direct dietary effect. plain_language: Mouse ZIP4 can bring zinc into cells. organism: Mouse protein in cultured mammalian cells tissue_or_cell_type: Cell plasma membrane experimental_model: Transfected mammalian cells limitations: Transport in engineered cells establishes capacity, not the fraction of human dietary zinc absorption. exposure: ZIP4 expression versus controls; abstract does not specify zinc concentration. cross_nutrient: false [zinc-trans-12801924] The acrodermatitis enteropathica gene ZIP4 encodes a tissue-specific, zinc-regulated zinc transporter in mice. (2003). https://pubmed.ncbi.nlm.nih.gov/12801924/ DOI: 10.1074/jbc.m305000200
    Complete structured claim and evidence

Where it participates (unsigned role)

  1. Enterocyte-specific Slc39a4 deletion rapidly lowered total zinc in mouse small intestine, liver and pancreas.

    Mouse enterocyte-specific Slc39a4 knockout genotype → Tissue total zinc content source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    cross_nutrient
    false
    experimental_model
    Tamoxifen-inducible enterocyte-specific knockout and tissue elemental analysis
    exposure
    Conditional gene deletion compared with intact controls.
    limitations
    A genetic transport defect is not interchangeable with low intake. Total tissue zinc does not resolve labile versus protein-bound zinc.
    nutrient_topic
    Zinc research collection; topical membership is not evidence of a direct dietary effect. · Zinc
    organism
    Mus musculus
    plain_language
    Disabling intestinal ZIP4 depleted zinc beyond the intestine.
    primary_references
    [zinc-trans-22737083] A mouse model of acrodermatitis enteropathica: loss of intestine zinc transporter ZIP4 (Slc39a4) disrupts the stem cell niche and intestine integrity. (2012). https://pubmed.ncbi.nlm.nih.gov/22737083/ DOI: 10.1371/journal.pgen.1002766
    tissue_or_cell_type
    Small intestine, liver, pancreas
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Zinc: transport, enzyme loading, deficiency and nutrient interactions (2026-09-17) · lines 271–282

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Tamoxifen-inducible enterocyte-specific knockout and tissue elemental analysis · source_derived_draft · unverified_draft

    ### zinc-trans-zip4-knockout-tissue-zinc Enterocyte-specific Slc39a4 deletion rapidly lowered total zinc in mouse small intestine, liver and pancreas. Condition category: machinery_impairment nutrient_topic: Zinc research collection; topical membership is not evidence of a direct dietary effect. plain_language: Disabling intestinal ZIP4 depleted zinc beyond the intestine. organism: Mus musculus tissue_or_cell_type: Small intestine, liver, pancreas experimental_model: Tamoxifen-inducible enterocyte-specific knockout and tissue elemental analysis limitations: A genetic transport defect is not interchangeable with low intake. Total tissue zinc does not resolve labile versus protein-bound zinc. exposure: Conditional gene deletion compared with intact controls. cross_nutrient: false [zinc-trans-22737083] A mouse model of acrodermatitis enteropathica: loss of intestine zinc transporter ZIP4 (Slc39a4) disrupts the stem cell niche and intestine integrity. (2012). https://pubmed.ncbi.nlm.nih.gov/22737083/ DOI: 10.1371/journal.pgen.1002766
    Complete structured claim and evidence

  2. Dietary zinc deficiency increased mouse Zip4 mRNA by greater transcript stability rather than an increased relative transcription rate.

    Zinc → Mouse Slc39a4 messenger RNA source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    nutrient_deficiency Imported condition classification; unverified.
    cross_nutrient
    false
    experimental_model
    Mouse intestine with nuclear run-on assays; supporting Hepa-cell analyses
    exposure
    Defined zinc-deficient versus adequate diets; transcription assessed after 24 hours from gestational day 8.
    limitations
    Transcript stabilization in mice is not a serum-zinc threshold or proof that all zinc deficiency responses are post-transcriptional.
    nutrient_topic
    Zinc research collection; topical membership is not evidence of a direct dietary effect. · Zinc
    organism
    Mus musculus
    plain_language
    With little dietary zinc, mice preserve the message used to make ZIP4.
    primary_references
    [zinc-trans-18020946] Novel zinc-responsive post-transcriptional mechanisms reciprocally regulate expression of the mouse Slc39a4 and Slc39a5 zinc transporters (Zip4 and Zip5). (2007). https://pubmed.ncbi.nlm.nih.gov/18020946/ DOI: 10.1515/bc.2007.149
    tissue_or_cell_type
    Small intestine; supporting cultured hepatic cells
    trigger_kind
    nutrient_deficiency Imported condition classification; unverified.

    Zinc: transport, enzyme loading, deficiency and nutrient interactions (2026-09-17) · lines 232–243

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Mouse intestine with nuclear run-on assays; supporting Hepa-cell analyses · source_derived_draft · unverified_draft

    ### zinc-trans-zip4-mrna-stability Dietary zinc deficiency increased mouse Zip4 mRNA by greater transcript stability rather than an increased relative transcription rate. Condition category: nutrient_deficiency nutrient_topic: Zinc research collection; topical membership is not evidence of a direct dietary effect. plain_language: With little dietary zinc, mice preserve the message used to make ZIP4. organism: Mus musculus tissue_or_cell_type: Small intestine; supporting cultured hepatic cells experimental_model: Mouse intestine with nuclear run-on assays; supporting Hepa-cell analyses limitations: Transcript stabilization in mice is not a serum-zinc threshold or proof that all zinc deficiency responses are post-transcriptional. exposure: Defined zinc-deficient versus adequate diets; transcription assessed after 24 hours from gestational day 8. cross_nutrient: false [zinc-trans-18020946] Novel zinc-responsive post-transcriptional mechanisms reciprocally regulate expression of the mouse Slc39a4 and Slc39a5 zinc transporters (Zip4 and Zip5). (2007). https://pubmed.ncbi.nlm.nih.gov/18020946/ DOI: 10.1515/bc.2007.149
    Complete structured claim and evidence

  3. After enterocyte Zip4 deletion in mice, liver iron, manganese and copper gradually accumulated as the zinc-depletion disease progressed.

    Mouse enterocyte-specific Slc39a4 knockout genotype → Hepatic iron, manganese and copper accumulation source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    cross_nutrient
    false
    evidence_span
    {"source_cache": "artifacts/zinc-transport-sources/22737083-abstract.txt", "locator": "Primary indexed abstract; tissue elemental analysis", "file_sha256": "4643d3986c556a001c45365febbb07095bcdc8bc604e30488d3fb98a23511a4b"}
    experimental_model
    Tamoxifen-inducible enterocyte-specific knockout and tissue elemental analysis
    exposure
    Conditional gene deletion compared with intact controls.
    limitations
    A genetic transport defect is not interchangeable with low intake. Total tissue zinc does not resolve labile versus protein-bound zinc. Tissue accumulation is not proof of systemic nutritional adequacy of the other metals.
    nutrient_topic
    Zinc research collection; topical membership is not evidence of a direct dietary effect. · Zinc
    organism
    Mus musculus
    plain_language
    Loss of zinc uptake disrupted the distribution of several other metals.
    primary_references
    [zinc-trans-22737083] A mouse model of acrodermatitis enteropathica: loss of intestine zinc transporter ZIP4 (Slc39a4) disrupts the stem cell niche and intestine integrity. (2012). https://pubmed.ncbi.nlm.nih.gov/22737083/ DOI: 10.1371/journal.pgen.1002766
    tissue_or_cell_type
    Small intestine, liver, pancreas
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Zinc: transport, enzyme loading, deficiency and nutrient interactions (2026-09-17) · lines 585–597

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Tamoxifen-inducible enterocyte-specific knockout and tissue elemental analysis · source_derived_draft · unverified_draft

    ### zinc-trans-zip4-other-metals After enterocyte Zip4 deletion in mice, liver iron, manganese and copper gradually accumulated as the zinc-depletion disease progressed. Condition category: machinery_impairment nutrient_topic: Zinc research collection; topical membership is not evidence of a direct dietary effect. plain_language: Loss of zinc uptake disrupted the distribution of several other metals. organism: Mus musculus tissue_or_cell_type: Small intestine, liver, pancreas experimental_model: Tamoxifen-inducible enterocyte-specific knockout and tissue elemental analysis limitations: A genetic transport defect is not interchangeable with low intake. Total tissue zinc does not resolve labile versus protein-bound zinc. Tissue accumulation is not proof of systemic nutritional adequacy of the other metals. exposure: Conditional gene deletion compared with intact controls. cross_nutrient: false evidence_span: {"source_cache": "artifacts/zinc-transport-sources/22737083-abstract.txt", "locator": "Primary indexed abstract; tissue elemental analysis", "file_sha256": "4643d3986c556a001c45365febbb07095bcdc8bc604e30488d3fb98a23511a4b"} [zinc-trans-22737083] A mouse model of acrodermatitis enteropathica: loss of intestine zinc transporter ZIP4 (Slc39a4) disrupts the stem cell niche and intestine integrity. (2012). https://pubmed.ncbi.nlm.nih.gov/22737083/ DOI: 10.1371/journal.pgen.1002766
    Complete structured claim and evidence

  4. Oral zinc repletion caused mouse ZIP4 internalization from enterocyte apical membranes after dietary zinc deficiency.

    Zinc(II) ion → ZIP4 endocytosis source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    nutrient_deficiency Imported condition classification; unverified.
    cross_nutrient
    false
    experimental_model
    Dietary depletion followed by oral gavage and immunolocalization
    exposure
    Zinc-deficient weanlings for 10 days; 100 micromol ZnCl2/kg oral gavage with time-course localization.
    limitations
    Acute experimental repletion; the gavage is not a recommended human dose and internalization is distinct from later degradation.
    nutrient_topic
    Zinc research collection; topical membership is not evidence of a direct dietary effect. · Zinc
    organism
    Mus musculus
    plain_language
    After zinc becomes available again, intestinal cells pull ZIP4 away from their surface.
    primary_references
    [zinc-trans-18020946] Novel zinc-responsive post-transcriptional mechanisms reciprocally regulate expression of the mouse Slc39a4 and Slc39a5 zinc transporters (Zip4 and Zip5). (2007). https://pubmed.ncbi.nlm.nih.gov/18020946/ DOI: 10.1515/bc.2007.149
    tissue_or_cell_type
    Duodenal enterocytes
    trigger_kind
    nutrient_deficiency Imported condition classification; unverified.

    Zinc: transport, enzyme loading, deficiency and nutrient interactions (2026-09-17) · lines 245–256

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Dietary depletion followed by oral gavage and immunolocalization · source_derived_draft · unverified_draft

    ### zinc-trans-zip4-repletion-endocytosis Oral zinc repletion caused mouse ZIP4 internalization from enterocyte apical membranes after dietary zinc deficiency. Condition category: nutrient_deficiency nutrient_topic: Zinc research collection; topical membership is not evidence of a direct dietary effect. plain_language: After zinc becomes available again, intestinal cells pull ZIP4 away from their surface. organism: Mus musculus tissue_or_cell_type: Duodenal enterocytes experimental_model: Dietary depletion followed by oral gavage and immunolocalization limitations: Acute experimental repletion; the gavage is not a recommended human dose and internalization is distinct from later degradation. exposure: Zinc-deficient weanlings for 10 days; 100 micromol ZnCl2/kg oral gavage with time-course localization. cross_nutrient: false [zinc-trans-18020946] Novel zinc-responsive post-transcriptional mechanisms reciprocally regulate expression of the mouse Slc39a4 and Slc39a5 zinc transporters (Zip4 and Zip5). (2007). https://pubmed.ncbi.nlm.nih.gov/18020946/ DOI: 10.1515/bc.2007.149
    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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