Component

Mouse manganese exporter Slc30a10

Mouse manganese exporter Slc30a10

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

Where it participates (unsigned role)

  1. Combined liver and small-intestine Slc30a10 deficiency caused manganese excess that was less severe than in whole-body deficient mice.

    Mouse liver-and-small-intestine Slc30a10 double-knockout genotype → Systemic manganese accumulation source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    cross_nutrient
    false
    experimental_model
    Whole-body and tissue-specific Slc30a10 knockout mice
    exposure
    Liver-and-small-intestine Slc30a10 deficiency compared with controls and whole-body deficiency.
    limitations
    The residual difference suggests other sites or adaptation; it does not identify a specific untested tissue.
    nutrient_topic
    Manganese research collection; topical membership is not evidence of a direct dietary effect. · Manganese
    organism
    Mus musculus
    plain_language
    Deleting the liver and gut exporter did not reproduce the full severity of deleting it everywhere.
    primary_references
    [mn-trans-31527311] Manganese transporter Slc30a10 controls physiological manganese excretion and toxicity. (2019). https://pubmed.ncbi.nlm.nih.gov/31527311/ DOI: 10.1172/jci129710
    tissue_or_cell_type
    Hepatocytes and small-intestinal enterocytes
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Manganese: enzyme cofactors, glycosylation, transport and nutrient interactions (2026-09-17) · lines 279–290

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Whole-body and tissue-specific Slc30a10 knockout mice · source_derived_draft · unverified_draft

    ### mn-trans-slc30a10-double-versus-global Combined liver and small-intestine Slc30a10 deficiency caused manganese excess that was less severe than in whole-body deficient mice. Condition category: machinery_impairment nutrient_topic: Manganese research collection; topical membership is not evidence of a direct dietary effect. plain_language: Deleting the liver and gut exporter did not reproduce the full severity of deleting it everywhere. organism: Mus musculus tissue_or_cell_type: Hepatocytes and small-intestinal enterocytes experimental_model: Whole-body and tissue-specific Slc30a10 knockout mice limitations: The residual difference suggests other sites or adaptation; it does not identify a specific untested tissue. exposure: Liver-and-small-intestine Slc30a10 deficiency compared with controls and whole-body deficiency. cross_nutrient: false [mn-trans-31527311] Manganese transporter Slc30a10 controls physiological manganese excretion and toxicity. (2019). https://pubmed.ncbi.nlm.nih.gov/31527311/ DOI: 10.1172/jci129710
    Complete structured claim and evidence

  2. Whole-body Slc30a10 deficiency impaired systemic manganese excretion in mice.

    Mouse whole-body Slc30a10 knockout genotype → Systemic manganese excretion source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    cross_nutrient
    false
    experimental_model
    Whole-body and tissue-specific Slc30a10 knockout mice
    exposure
    Whole-body Slc30a10-deficient mice versus controls.
    limitations
    Genetic manganese retention is manganese excess, not nutrient deficiency.
    nutrient_topic
    Manganese research collection; topical membership is not evidence of a direct dietary effect. · Manganese
    organism
    Mus musculus
    plain_language
    Loss of Slc30a10 throughout the body reduced manganese clearance.
    primary_references
    [mn-trans-31527311] Manganese transporter Slc30a10 controls physiological manganese excretion and toxicity. (2019). https://pubmed.ncbi.nlm.nih.gov/31527311/ DOI: 10.1172/jci129710
    tissue_or_cell_type
    Hepatocytes and small-intestinal enterocytes
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Manganese: enzyme cofactors, glycosylation, transport and nutrient interactions (2026-09-17) · lines 240–251

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Whole-body and tissue-specific Slc30a10 knockout mice · source_derived_draft · unverified_draft

    ### mn-trans-slc30a10-global-excretion Whole-body Slc30a10 deficiency impaired systemic manganese excretion in mice. Condition category: machinery_impairment nutrient_topic: Manganese research collection; topical membership is not evidence of a direct dietary effect. plain_language: Loss of Slc30a10 throughout the body reduced manganese clearance. organism: Mus musculus tissue_or_cell_type: Hepatocytes and small-intestinal enterocytes experimental_model: Whole-body and tissue-specific Slc30a10 knockout mice limitations: Genetic manganese retention is manganese excess, not nutrient deficiency. exposure: Whole-body Slc30a10-deficient mice versus controls. cross_nutrient: false [mn-trans-31527311] Manganese transporter Slc30a10 controls physiological manganese excretion and toxicity. (2019). https://pubmed.ncbi.nlm.nih.gov/31527311/ DOI: 10.1172/jci129710
    Complete structured claim and evidence

  3. Hepatic Slc30a10 deficiency impaired biliary manganese excretion in mice despite only minimal manganese excess.

    Mouse hepatocyte-specific Slc30a10 knockout genotype → Biliary manganese excretion source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    cross_nutrient
    false
    experimental_model
    Whole-body and tissue-specific Slc30a10 knockout mice
    exposure
    Liver-specific Slc30a10 deficiency versus controls.
    limitations
    Minimal systemic excess does not negate the measured biliary transport defect.
    nutrient_topic
    Manganese research collection; topical membership is not evidence of a direct dietary effect. · Manganese
    organism
    Mus musculus
    plain_language
    The liver exporter supplied biliary clearance, while other routes limited whole-body accumulation.
    primary_references
    [mn-trans-31527311] Manganese transporter Slc30a10 controls physiological manganese excretion and toxicity. (2019). https://pubmed.ncbi.nlm.nih.gov/31527311/ DOI: 10.1172/jci129710
    tissue_or_cell_type
    Liver canalicular membrane and bile
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Manganese: enzyme cofactors, glycosylation, transport and nutrient interactions (2026-09-17) · lines 253–264

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Whole-body and tissue-specific Slc30a10 knockout mice · source_derived_draft · unverified_draft

    ### mn-trans-slc30a10-hepatic-excretion Hepatic Slc30a10 deficiency impaired biliary manganese excretion in mice despite only minimal manganese excess. Condition category: machinery_impairment nutrient_topic: Manganese research collection; topical membership is not evidence of a direct dietary effect. plain_language: The liver exporter supplied biliary clearance, while other routes limited whole-body accumulation. organism: Mus musculus tissue_or_cell_type: Liver canalicular membrane and bile experimental_model: Whole-body and tissue-specific Slc30a10 knockout mice limitations: Minimal systemic excess does not negate the measured biliary transport defect. exposure: Liver-specific Slc30a10 deficiency versus controls. cross_nutrient: false [mn-trans-31527311] Manganese transporter Slc30a10 controls physiological manganese excretion and toxicity. (2019). https://pubmed.ncbi.nlm.nih.gov/31527311/ DOI: 10.1172/jci129710
    Complete structured claim and evidence

  4. Small-intestinal Slc30a10 deficiency impaired manganese export into the intestinal lumen in mice despite minimal manganese excess.

    Mouse small-intestine Slc30a10 knockout genotype → Manganese export into the intestinal lumen source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    cross_nutrient
    false
    experimental_model
    Whole-body and tissue-specific Slc30a10 knockout mice
    exposure
    Small-intestine-specific Slc30a10 deficiency versus controls.
    limitations
    The cell-surface location is apical; net dietary absorption is a different measurement.
    nutrient_topic
    Manganese research collection; topical membership is not evidence of a direct dietary effect. · Manganese
    organism
    Mus musculus
    plain_language
    Enterocyte Slc30a10 helps secrete manganese directly into the intestine.
    primary_references
    [mn-trans-31527311] Manganese transporter Slc30a10 controls physiological manganese excretion and toxicity. (2019). https://pubmed.ncbi.nlm.nih.gov/31527311/ DOI: 10.1172/jci129710
    tissue_or_cell_type
    Small-intestinal enterocyte apical membrane and lumen
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Manganese: enzyme cofactors, glycosylation, transport and nutrient interactions (2026-09-17) · lines 266–277

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Whole-body and tissue-specific Slc30a10 knockout mice · source_derived_draft · unverified_draft

    ### mn-trans-slc30a10-intestinal-excretion Small-intestinal Slc30a10 deficiency impaired manganese export into the intestinal lumen in mice despite minimal manganese excess. Condition category: machinery_impairment nutrient_topic: Manganese research collection; topical membership is not evidence of a direct dietary effect. plain_language: Enterocyte Slc30a10 helps secrete manganese directly into the intestine. organism: Mus musculus tissue_or_cell_type: Small-intestinal enterocyte apical membrane and lumen experimental_model: Whole-body and tissue-specific Slc30a10 knockout mice limitations: The cell-surface location is apical; net dietary absorption is a different measurement. exposure: Small-intestine-specific Slc30a10 deficiency versus controls. cross_nutrient: false [mn-trans-31527311] Manganese transporter Slc30a10 controls physiological manganese excretion and toxicity. (2019). https://pubmed.ncbi.nlm.nih.gov/31527311/ DOI: 10.1172/jci129710
    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