Component

Cellular manganese efflux

Cellular manganese efflux

2 recorded relationships. Experimental role, claim status and evidence remain attached to each record.

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 acts on it

  1. Cellular expression experiments identified human SLC30A10 as a cell-surface manganese efflux transporter.

    Experimental context and source evidence
    cross_nutrient
    false
    experimental_model
    Human SLC30A10 expression in cellular assays
    exposure
    SLC30A10 expression and manganese transport assays.
    limitations
    The abstract summarizes multiple models; this claim concerns the cellular efflux function and does not infer a human treatment response.
    nutrient_topic
    Manganese research collection; topical membership is not evidence of a direct dietary effect. · Manganese
    organism
    Human transporter in cultured cells
    plain_language
    SLC30A10 moves manganese out of cells.
    primary_references
    [mn-trans-25319704] SLC30A10 is a cell surface-localized manganese efflux transporter, and parkinsonism-causing mutations block its intracellular trafficking and efflux activity. (2014). https://pubmed.ncbi.nlm.nih.gov/25319704/ DOI: 10.1523/jneurosci.2329-14.2014
    tissue_or_cell_type
    Cell surface

    Manganese: enzyme cofactors, glycosylation, transport and nutrient interactions (2026-09-17) · lines 370–381

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human SLC30A10 expression in cellular assays · source_derived_draft · unverified_draft

    ### mn-trans-slc30a10-cellular-efflux Cellular expression experiments identified human SLC30A10 as a cell-surface manganese efflux transporter. Condition category: normal nutrient_topic: Manganese research collection; topical membership is not evidence of a direct dietary effect. plain_language: SLC30A10 moves manganese out of cells. organism: Human transporter in cultured cells tissue_or_cell_type: Cell surface experimental_model: Human SLC30A10 expression in cellular assays limitations: The abstract summarizes multiple models; this claim concerns the cellular efflux function and does not infer a human treatment response. exposure: SLC30A10 expression and manganese transport assays. cross_nutrient: false [mn-trans-25319704] SLC30A10 is a cell surface-localized manganese efflux transporter, and parkinsonism-causing mutations block its intracellular trafficking and efflux activity. (2014). https://pubmed.ncbi.nlm.nih.gov/25319704/ DOI: 10.1523/jneurosci.2329-14.2014
    Complete structured claim and evidence
  2. Human SLC30A10 D40A lost manganese transport function in the HEK293T assay compared with wild-type SLC30A10.

    Human SLC30A10 D40A mutant → Cellular manganese efflux source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    cross_nutrient
    false
    experimental_model
    Site-directed SLC30A10 mutagenesis in HEK293T cells
    exposure
    D40A versus wild-type human SLC30A10 expression in HEK293T cells.
    limitations
    The functional mutant comparison does not establish treatment efficacy or a dietary manganese deficiency.
    nutrient_topic
    Manganese research collection; topical membership is not evidence of a direct dietary effect. · Manganese
    organism
    Homo sapiens
    plain_language
    Changing aspartate 40 to alanine disabled the measured manganese transport function.
    primary_references
    [mn-trans-41022720] Molecular mechanisms of SLC30A10-mediated manganese transport. (2025). https://pubmed.ncbi.nlm.nih.gov/41022720/ DOI: 10.1038/s41467-025-63616-7
    tissue_or_cell_type
    HEK293T cellular manganese handling
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Manganese: enzyme cofactors, glycosylation, transport and nutrient interactions (2026-09-17) · lines 409–420

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Site-directed SLC30A10 mutagenesis in HEK293T cells · source_derived_draft · unverified_draft

    ### mn-trans-slc30a10-d40a-transport-loss Human SLC30A10 D40A lost manganese transport function in the HEK293T assay compared with wild-type SLC30A10. Condition category: machinery_impairment nutrient_topic: Manganese research collection; topical membership is not evidence of a direct dietary effect. plain_language: Changing aspartate 40 to alanine disabled the measured manganese transport function. organism: Homo sapiens tissue_or_cell_type: HEK293T cellular manganese handling experimental_model: Site-directed SLC30A10 mutagenesis in HEK293T cells limitations: The functional mutant comparison does not establish treatment efficacy or a dietary manganese deficiency. exposure: D40A versus wild-type human SLC30A10 expression in HEK293T cells. cross_nutrient: false [mn-trans-41022720] Molecular mechanisms of SLC30A10-mediated manganese transport. (2025). https://pubmed.ncbi.nlm.nih.gov/41022720/ DOI: 10.1038/s41467-025-63616-7
    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