Component

Human ZnT2 H54R

Human SLC30A2 protein carrying the H54R amino-acid substitution; not a gene or wild-type protein.

3 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. Coexpressing human ZnT2 H54R with wild-type ZnT2 did not abolish the increased zinc secretion produced by wild-type ZnT2 overexpression alone.

    Human ZnT2 H54R → Cellular zinc secretion source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    cross_nutrient
    false
    experimental_model
    Wild-type/mutant coexpression in HEK293 cells
    exposure
    H54R plus wild type compared with wild type alone.
    limitations
    Negative result in an overexpression assay; it does not establish complete compensation in lactating women or the penetrance of the variant.
    nutrient_topic
    Zinc research collection; topical membership is not evidence of a direct dietary effect. · Zinc
    organism
    Homo sapiens
    plain_language
    In this assay, the H54R variant did not block the working ZnT2 protein.
    primary_references
    [zinc-trans-17065149] Identification of a mutation in SLC30A2 (ZnT-2) in women with low milk zinc concentration that results in transient neonatal zinc deficiency. (2006). https://pubmed.ncbi.nlm.nih.gov/17065149/ DOI: 10.1074/jbc.m605821200
    tissue_or_cell_type
    HEK293 cells
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Zinc: transport, enzyme loading, deficiency and nutrient interactions (2026-09-17) · lines 323–334

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Wild-type/mutant coexpression in HEK293 cells · source_derived_draft · unverified_draft

    ### zinc-trans-znt2-h54r-coexpression Coexpressing human ZnT2 H54R with wild-type ZnT2 did not abolish the increased zinc secretion produced by wild-type ZnT2 overexpression alone. Condition category: machinery_impairment nutrient_topic: Zinc research collection; topical membership is not evidence of a direct dietary effect. plain_language: In this assay, the H54R variant did not block the working ZnT2 protein. organism: Homo sapiens tissue_or_cell_type: HEK293 cells experimental_model: Wild-type/mutant coexpression in HEK293 cells limitations: Negative result in an overexpression assay; it does not establish complete compensation in lactating women or the penetrance of the variant. exposure: H54R plus wild type compared with wild type alone. cross_nutrient: false [zinc-trans-17065149] Identification of a mutation in SLC30A2 (ZnT-2) in women with low milk zinc concentration that results in transient neonatal zinc deficiency. (2006). https://pubmed.ncbi.nlm.nih.gov/17065149/ DOI: 10.1074/jbc.m605821200
    Complete structured claim and evidence

  2. Human ZnT2 H54R expressed in HEK293 cells accumulated in perinuclear aggresomal structures and showed reduced zinc secretion.

    Human ZnT2 H54R → Cellular zinc secretion source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    cross_nutrient
    false
    experimental_model
    H54R expression and localization assays in HEK293 cells
    exposure
    H54R compared with wild-type ZnT2.
    limitations
    Cultured kidney-derived cells do not reproduce all lactating mammary processes; a specific variant cannot represent all maternal low-zinc milk.
    nutrient_topic
    Zinc research collection; topical membership is not evidence of a direct dietary effect. · Zinc
    organism
    Homo sapiens
    plain_language
    A milk-zinc-associated ZnT2 variant was misplaced inside cells and exported less zinc.
    primary_references
    [zinc-trans-17065149] Identification of a mutation in SLC30A2 (ZnT-2) in women with low milk zinc concentration that results in transient neonatal zinc deficiency. (2006). https://pubmed.ncbi.nlm.nih.gov/17065149/ DOI: 10.1074/jbc.m605821200
    tissue_or_cell_type
    HEK293 cells; variant identified in mothers with low milk zinc
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Zinc: transport, enzyme loading, deficiency and nutrient interactions (2026-09-17) · lines 310–321

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · H54R expression and localization assays in HEK293 cells · source_derived_draft · unverified_draft

    ### zinc-trans-znt2-h54r-export Human ZnT2 H54R expressed in HEK293 cells accumulated in perinuclear aggresomal structures and showed reduced zinc secretion. Condition category: machinery_impairment nutrient_topic: Zinc research collection; topical membership is not evidence of a direct dietary effect. plain_language: A milk-zinc-associated ZnT2 variant was misplaced inside cells and exported less zinc. organism: Homo sapiens tissue_or_cell_type: HEK293 cells; variant identified in mothers with low milk zinc experimental_model: H54R expression and localization assays in HEK293 cells limitations: Cultured kidney-derived cells do not reproduce all lactating mammary processes; a specific variant cannot represent all maternal low-zinc milk. exposure: H54R compared with wild-type ZnT2. cross_nutrient: false [zinc-trans-17065149] Identification of a mutation in SLC30A2 (ZnT-2) in women with low milk zinc concentration that results in transient neonatal zinc deficiency. (2006). https://pubmed.ncbi.nlm.nih.gov/17065149/ DOI: 10.1074/jbc.m605821200
    Complete structured claim and evidence

Where it participates (unsigned role)

  1. In the reported family, two exclusively breastfed infants developed zinc deficiency associated with low maternal milk zinc; affected mothers carried SLC30A2 H54R.

    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/17065149-abstract.txt", "locator": "Primary indexed abstract; case results", "file_sha256": "a10d24cc13794e7cda0ab3553fa7b351c4f2faa583c78331b96f96edfacbe9d1"}
    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
    A maternal transport variant was linked to low milk zinc and infant deficiency.
    primary_references
    [zinc-trans-17065149] Identification of a mutation in SLC30A2 (ZnT-2) in women with low milk zinc concentration that results in transient neonatal zinc deficiency. (2006). https://pubmed.ncbi.nlm.nih.gov/17065149/ DOI: 10.1074/jbc.m605821200
    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 557–569

    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-h54r-family In the reported family, two exclusively breastfed infants developed zinc deficiency associated with low maternal milk zinc; affected mothers carried SLC30A2 H54R. Condition category: machinery_impairment nutrient_topic: Zinc research collection; topical membership is not evidence of a direct dietary effect. plain_language: A maternal transport variant was linked to low milk zinc and infant deficiency. 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/17065149-abstract.txt", "locator": "Primary indexed abstract; case results", "file_sha256": "a10d24cc13794e7cda0ab3553fa7b351c4f2faa583c78331b96f96edfacbe9d1"} [zinc-trans-17065149] Identification of a mutation in SLC30A2 (ZnT-2) in women with low milk zinc concentration that results in transient neonatal zinc deficiency. (2006). https://pubmed.ncbi.nlm.nih.gov/17065149/ DOI: 10.1074/jbc.m605821200
    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