Component

Mouse ZIP5 (Slc39a5)

Mus musculus zinc uptake protein with basolateral localization in polarized epithelia.

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. Mouse ZIP5 localized to the basolateral membrane when expressed in polarized MDCK cells.

    Mouse ZIP5 (Slc39a5) → Polarized epithelial basolateral membrane source_derived_draftungraded
    Experimental context and source evidence
    cross_nutrient
    false
    experimental_model
    Polarized Madin-Darby canine kidney cells expressing mouse ZIP5
    exposure
    Polarized-cell localization assay.
    limitations
    Localization supports a directional hypothesis but does not itself measure net intestinal zinc excretion or demonstrate human renal zinc reabsorption.
    nutrient_topic
    Zinc research collection; topical membership is not evidence of a direct dietary effect. · Zinc
    organism
    Mouse protein in Canis lupus familiaris cells
    plain_language
    In polarized kidney-derived cells, ZIP5 sat on the side facing the tissue rather than the lumen.
    primary_references
    [zinc-trans-15322118] The mammalian Zip5 protein is a zinc transporter that localizes to the basolateral surface of polarized cells. (2004). https://pubmed.ncbi.nlm.nih.gov/15322118/ DOI: 10.1074/jbc.m408361200
    tissue_or_cell_type
    MDCK epithelial basolateral membrane

    Zinc: transport, enzyme loading, deficiency and nutrient interactions (2026-09-17) · lines 375–386

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Polarized Madin-Darby canine kidney cells expressing mouse ZIP5 · source_derived_draft · unverified_draft

    ### zinc-trans-zip5-basolateral Mouse ZIP5 localized to the basolateral membrane when expressed in polarized MDCK cells. Condition category: normal nutrient_topic: Zinc research collection; topical membership is not evidence of a direct dietary effect. plain_language: In polarized kidney-derived cells, ZIP5 sat on the side facing the tissue rather than the lumen. organism: Mouse protein in Canis lupus familiaris cells tissue_or_cell_type: MDCK epithelial basolateral membrane experimental_model: Polarized Madin-Darby canine kidney cells expressing mouse ZIP5 limitations: Localization supports a directional hypothesis but does not itself measure net intestinal zinc excretion or demonstrate human renal zinc reabsorption. exposure: Polarized-cell localization assay. cross_nutrient: false [zinc-trans-15322118] The mammalian Zip5 protein is a zinc transporter that localizes to the basolateral surface of polarized cells. (2004). https://pubmed.ncbi.nlm.nih.gov/15322118/ DOI: 10.1074/jbc.m408361200
    Complete structured claim and evidence

  2. Mouse ZIP5 expression increased cellular Zn(II) uptake and showed selectivity for zinc among the potential substrates tested.

    Mouse ZIP5 (Slc39a5) → Cellular zinc influx source_derived_draftungraded
    Experimental context and source evidence
    cross_nutrient
    false
    experimental_model
    Heterologous mouse ZIP5 expression
    exposure
    Expression and substrate tests; abstract does not specify concentrations.
    limitations
    Selectivity is bounded by the tested panel and assay; this cannot exclude every other substrate in other systems.
    nutrient_topic
    Zinc research collection; topical membership is not evidence of a direct dietary effect. · Zinc
    organism
    Mouse protein in cultured cells
    plain_language
    Mouse ZIP5 can move zinc into cells.
    primary_references
    [zinc-trans-15322118] The mammalian Zip5 protein is a zinc transporter that localizes to the basolateral surface of polarized cells. (2004). https://pubmed.ncbi.nlm.nih.gov/15322118/ DOI: 10.1074/jbc.m408361200
    tissue_or_cell_type
    Cultured-cell plasma membrane

    Zinc: transport, enzyme loading, deficiency and nutrient interactions (2026-09-17) · lines 362–373

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Heterologous mouse ZIP5 expression · source_derived_draft · unverified_draft

    ### zinc-trans-zip5-influx Mouse ZIP5 expression increased cellular Zn(II) uptake and showed selectivity for zinc among the potential substrates tested. Condition category: normal nutrient_topic: Zinc research collection; topical membership is not evidence of a direct dietary effect. plain_language: Mouse ZIP5 can move zinc into cells. organism: Mouse protein in cultured cells tissue_or_cell_type: Cultured-cell plasma membrane experimental_model: Heterologous mouse ZIP5 expression limitations: Selectivity is bounded by the tested panel and assay; this cannot exclude every other substrate in other systems. exposure: Expression and substrate tests; abstract does not specify concentrations. cross_nutrient: false [zinc-trans-15322118] The mammalian Zip5 protein is a zinc transporter that localizes to the basolateral surface of polarized cells. (2004). https://pubmed.ncbi.nlm.nih.gov/15322118/ DOI: 10.1074/jbc.m408361200
    Complete structured claim and evidence

Where it participates (unsigned role)

  1. Enterocyte-specific Zip5 deletion increased pancreatic zinc in mice eating a zinc-adequate diet.

    Mouse enterocyte-specific Slc39a5 knockout genotype → Pancreatic total zinc content source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    cross_nutrient
    false
    experimental_model
    Conditional intestinal knockout with tissue elemental analysis
    exposure
    Induced enterocyte deletion on zinc-adequate chow.
    limitations
    This measured redistribution supports but does not directly quantify the proposed blood-to-enterocyte-to-lumen excretion route.
    nutrient_topic
    Zinc research collection; topical membership is not evidence of a direct dietary effect. · Zinc
    organism
    Mus musculus
    plain_language
    Removing intestinal ZIP5 changed where zinc accumulated, increasing the pancreatic pool.
    primary_references
    [zinc-trans-24303081] The zinc transporter Zip5 (Slc39a5) regulates intestinal zinc excretion and protects the pancreas against zinc toxicity. (2013). https://pubmed.ncbi.nlm.nih.gov/24303081/ DOI: 10.1371/journal.pone.0082149
    tissue_or_cell_type
    Intestinal enterocytes; pancreatic zinc endpoint
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Zinc: transport, enzyme loading, deficiency and nutrient interactions (2026-09-17) · lines 388–399

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

    ### zinc-trans-intestinal-zip5-pancreas-zinc Enterocyte-specific Zip5 deletion increased pancreatic zinc in mice eating a zinc-adequate diet. Condition category: machinery_impairment nutrient_topic: Zinc research collection; topical membership is not evidence of a direct dietary effect. plain_language: Removing intestinal ZIP5 changed where zinc accumulated, increasing the pancreatic pool. organism: Mus musculus tissue_or_cell_type: Intestinal enterocytes; pancreatic zinc endpoint experimental_model: Conditional intestinal knockout with tissue elemental analysis limitations: This measured redistribution supports but does not directly quantify the proposed blood-to-enterocyte-to-lumen excretion route. exposure: Induced enterocyte deletion on zinc-adequate chow. cross_nutrient: false [zinc-trans-24303081] The zinc transporter Zip5 (Slc39a5) regulates intestinal zinc excretion and protects the pancreas against zinc toxicity. (2013). https://pubmed.ncbi.nlm.nih.gov/24303081/ DOI: 10.1371/journal.pone.0082149
    Complete structured claim and evidence

  2. Pancreatic acinar-cell Zip5 deletion impaired retention of administered 67Zn despite no detected impairment of rapid pancreatic 67Zn accumulation.

    Mouse pancreatic acinar Slc39a5 knockout genotype → Pancreatic zinc retention source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    cross_nutrient
    false
    experimental_model
    Acinar-cell-specific knockout and 67Zn tracer kinetics
    exposure
    Tracer zinc uptake and retention compared between acinar knockouts and controls.
    limitations
    The negative acute-uptake result is retained; retention differences do not identify every influx or efflux pathway.
    nutrient_topic
    Zinc research collection; topical membership is not evidence of a direct dietary effect. · Zinc
    organism
    Mus musculus
    plain_language
    Pancreatic ZIP5 helped retain zinc after uptake, rather than being required for the initial uptake measured here.
    primary_references
    [zinc-trans-24303081] The zinc transporter Zip5 (Slc39a5) regulates intestinal zinc excretion and protects the pancreas against zinc toxicity. (2013). https://pubmed.ncbi.nlm.nih.gov/24303081/ DOI: 10.1371/journal.pone.0082149
    tissue_or_cell_type
    Pancreatic acinar cells
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Zinc: transport, enzyme loading, deficiency and nutrient interactions (2026-09-17) · lines 401–412

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Acinar-cell-specific knockout and 67Zn tracer kinetics · source_derived_draft · unverified_draft

    ### zinc-trans-pancreas-zip5-retention Pancreatic acinar-cell Zip5 deletion impaired retention of administered 67Zn despite no detected impairment of rapid pancreatic 67Zn accumulation. Condition category: machinery_impairment nutrient_topic: Zinc research collection; topical membership is not evidence of a direct dietary effect. plain_language: Pancreatic ZIP5 helped retain zinc after uptake, rather than being required for the initial uptake measured here. organism: Mus musculus tissue_or_cell_type: Pancreatic acinar cells experimental_model: Acinar-cell-specific knockout and 67Zn tracer kinetics limitations: The negative acute-uptake result is retained; retention differences do not identify every influx or efflux pathway. exposure: Tracer zinc uptake and retention compared between acinar knockouts and controls. cross_nutrient: false [zinc-trans-24303081] The zinc transporter Zip5 (Slc39a5) regulates intestinal zinc excretion and protects the pancreas against zinc toxicity. (2013). https://pubmed.ncbi.nlm.nih.gov/24303081/ DOI: 10.1371/journal.pone.0082149
    Complete structured claim and evidence

  3. During dietary zinc deficiency in mice, ZIP5 protein was internalized and degraded in enterocytes, pancreatic acinar cells and visceral endoderm even though Zip5 mRNA abundance did not change.

    Zinc → ZIP5 protein abundance source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    nutrient_deficiency Imported condition classification; unverified.
    cross_nutrient
    false
    experimental_model
    Dietary depletion/repletion and protein/RNA assays
    exposure
    Defined zinc-deficient diet followed in some experiments by oral zinc repletion.
    limitations
    Protein abundance, transcription and transport flux are different endpoints; this is a mouse dietary adaptation.
    nutrient_topic
    Zinc research collection; topical membership is not evidence of a direct dietary effect. · Zinc
    organism
    Mus musculus
    plain_language
    Zinc deficiency reduced ZIP5 protein without reducing its messenger RNA.
    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
    Enterocytes, acinar cells and visceral endoderm
    trigger_kind
    nutrient_deficiency Imported condition classification; unverified.

    Zinc: transport, enzyme loading, deficiency and nutrient interactions (2026-09-17) · lines 414–425

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Dietary depletion/repletion and protein/RNA assays · source_derived_draft · unverified_draft

    ### zinc-trans-zip5-diet-deficiency During dietary zinc deficiency in mice, ZIP5 protein was internalized and degraded in enterocytes, pancreatic acinar cells and visceral endoderm even though Zip5 mRNA abundance did not change. Condition category: nutrient_deficiency nutrient_topic: Zinc research collection; topical membership is not evidence of a direct dietary effect. plain_language: Zinc deficiency reduced ZIP5 protein without reducing its messenger RNA. organism: Mus musculus tissue_or_cell_type: Enterocytes, acinar cells and visceral endoderm experimental_model: Dietary depletion/repletion and protein/RNA assays limitations: Protein abundance, transcription and transport flux are different endpoints; this is a mouse dietary adaptation. exposure: Defined zinc-deficient diet followed in some experiments by oral zinc repletion. 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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