Component

Human ZnT2 S296L

Human SLC30A2 protein carrying the S296L amino-acid substitution; not a gene or wild-type protein. Residue numbering refers to long isoform NP_001004434.

2 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. Human ZnT2 S296L retained zinc transport and dimer-forming capacity in the DT40 characterization but had markedly reduced protein stability.

    Human ZnT2 S296L → ZnT2 protein stability source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    cross_nutrient
    false
    experimental_model
    Human ZnT2 variants in zinc-sensitive DT40 cells; sequence reference NP_001004434
    exposure
    S296L variant compared with wild type.
    limitations
    Intrinsic activity and protein abundance must be separated; the variant is not described as completely transport-inactive.
    nutrient_topic
    Zinc research collection; topical membership is not evidence of a direct dietary effect. · Zinc
    organism
    Human protein in Gallus gallus cells
    plain_language
    Another ZnT2 variant could work when present, but was unstable.
    primary_references
    [zinc-trans-23741301] Compound heterozygous mutations in SLC30A2/ZnT2 results in low milk zinc concentrations: a novel mechanism for zinc deficiency in a breast-fed infant. (2013). https://pubmed.ncbi.nlm.nih.gov/23741301/ DOI: 10.1371/journal.pone.0064045
    tissue_or_cell_type
    Engineered DT40 cells
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Zinc: transport, enzyme loading, deficiency and nutrient interactions (2026-09-17) · lines 349–360

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human ZnT2 variants in zinc-sensitive DT40 cells; sequence reference NP_001004434 · source_derived_draft · unverified_draft

    ### zinc-trans-znt2-s296l-stability Human ZnT2 S296L retained zinc transport and dimer-forming capacity in the DT40 characterization but had markedly reduced protein stability. Condition category: machinery_impairment nutrient_topic: Zinc research collection; topical membership is not evidence of a direct dietary effect. plain_language: Another ZnT2 variant could work when present, but was unstable. organism: Human protein in Gallus gallus cells tissue_or_cell_type: Engineered DT40 cells experimental_model: Human ZnT2 variants in zinc-sensitive DT40 cells; sequence reference NP_001004434 limitations: Intrinsic activity and protein abundance must be separated; the variant is not described as completely transport-inactive. exposure: S296L variant compared with wild type. cross_nutrient: false [zinc-trans-23741301] Compound heterozygous mutations in SLC30A2/ZnT2 results in low milk zinc concentrations: a novel mechanism for zinc deficiency in a breast-fed infant. (2013). https://pubmed.ncbi.nlm.nih.gov/23741301/ DOI: 10.1371/journal.pone.0064045
    Complete structured claim and evidence

Where it participates (unsigned role)

  1. A mother carrying W152R and S296L on different SLC30A2 alleles had a reported greater-than-90% reduction in milk zinc; her breastfed infant developed severe zinc deficiency.

    Human ZnT2 (SLC30A2) → Breast-milk zinc concentration source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    cross_nutrient
    Maternal zinc secretion determines a source of infant zinc supply.
    evidence_span
    {"source_cache": "artifacts/zinc-transport-sources/23741301-abstract.txt", "locator": "Primary indexed abstract; case results", "file_sha256": "b422d27e8731293ae1597e65a72d9a6f6c1a161b7adaff3f114ee23f0e95408a"}
    experimental_model
    Human mother–infant clinical genetic observations
    exposure
    Naturally occurring maternal SLC30A2 variants; exclusive breastfeeding in the reported case setting.
    limitations
    Small family/case evidence does not establish population frequency or penetrance. Molecular cell assays are separate linked claims; maternal supplementation response is not inferred for these individuals from introductory background.
    nutrient_topic
    Zinc research collection; topical membership is not evidence of a direct dietary effect. · Zinc
    organism
    Homo sapiens
    plain_language
    Two different maternal variants were linked to profoundly low milk zinc.
    primary_references
    [zinc-trans-23741301] Compound heterozygous mutations in SLC30A2/ZnT2 results in low milk zinc concentrations: a novel mechanism for zinc deficiency in a breast-fed infant. (2013). https://pubmed.ncbi.nlm.nih.gov/23741301/ DOI: 10.1371/journal.pone.0064045
    tissue_or_cell_type
    Maternal milk and breastfed infant
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Zinc: transport, enzyme loading, deficiency and nutrient interactions (2026-09-17) · lines 571–583

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human mother–infant clinical genetic observations · source_derived_draft · unverified_draft

    ### zinc-trans-milk-compound-variants A mother carrying W152R and S296L on different SLC30A2 alleles had a reported greater-than-90% reduction in milk zinc; her breastfed infant developed severe zinc deficiency. Condition category: machinery_impairment nutrient_topic: Zinc research collection; topical membership is not evidence of a direct dietary effect. plain_language: Two different maternal variants were linked to profoundly low milk zinc. organism: Homo sapiens tissue_or_cell_type: Maternal milk and breastfed infant experimental_model: Human mother–infant clinical genetic observations limitations: Small family/case evidence does not establish population frequency or penetrance. Molecular cell assays are separate linked claims; maternal supplementation response is not inferred for these individuals from introductory background. exposure: Naturally occurring maternal SLC30A2 variants; exclusive breastfeeding in the reported case setting. cross_nutrient: Maternal zinc secretion determines a source of infant zinc supply. evidence_span: {"source_cache": "artifacts/zinc-transport-sources/23741301-abstract.txt", "locator": "Primary indexed abstract; case results", "file_sha256": "b422d27e8731293ae1597e65a72d9a6f6c1a161b7adaff3f114ee23f0e95408a"} [zinc-trans-23741301] Compound heterozygous mutations in SLC30A2/ZnT2 results in low milk zinc concentrations: a novel mechanism for zinc deficiency in a breast-fed infant. (2013). https://pubmed.ncbi.nlm.nih.gov/23741301/ DOI: 10.1371/journal.pone.0064045
    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