Component

Human copper-transporting ATPase ATP7A

Human copper-transporting ATPase ATP7A. Species, exposure and limitations are retained in each linked claim.

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

What it acts on

  1. ATP7A silencing impaired iron uptake and efflux in differentiated human Caco-2 cells.

    Human copper-transporting ATPase ATP7A → Iron uptake and efflux in cultured intestinal epithelia source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/copper-research/27714044.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "5e8791edb75475ba74e95cddc330c06512ef3b9c02a0c5a6b203327c047dff37", "start_char": 0, "end_char": 1780, "text_sha256": "5e8791edb75475ba74e95cddc330c06512ef3b9c02a0c5a6b203327c047dff37"}
    experimental_model
    ATP7A knockdown in differentiated intestinal cell cultures
    exposure
    ATP7A knockdown and radiolabeled iron transport
    limitations
    Reductionist cell models; increased enzyme activity did not guarantee increased net iron flux. Molecular expression details were measured in the rat line.
    nutrient_topic
    Copper research collection; topical membership is not evidence of a direct dietary effect. · Copper
    organism
    Human
    plain_language
    A copper transporter also helps the intestinal iron-handling system function.
    primary_references
    [copper-p27714044] Knockdown of copper-transporting ATPase 1 (Atp7a) impairs iron flux in fully-differentiated rat (IEC-6) and human (Caco-2) intestinal epithelial cells. (2016). https://pubmed.ncbi.nlm.nih.gov/27714044/ DOI: 10.1039/c6mt00126b
    tissue_or_cell_type
    Caco-2 cells

    Copper: transport, cuproenzymes, deficiency, excess and nutrient interactions (2026-09-17) · lines 897–908

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · ATP7A knockdown in differentiated intestinal cell cultures · source_derived_draft · unverified_draft

    ### copper-human-atp7a-iron ATP7A silencing impaired iron uptake and efflux in differentiated human Caco-2 cells. Condition category: normal nutrient_topic: Copper research collection; topical membership is not evidence of a direct dietary effect. plain_language: A copper transporter also helps the intestinal iron-handling system function. organism: Human tissue_or_cell_type: Caco-2 cells experimental_model: ATP7A knockdown in differentiated intestinal cell cultures limitations: Reductionist cell models; increased enzyme activity did not guarantee increased net iron flux. Molecular expression details were measured in the rat line. exposure: ATP7A knockdown and radiolabeled iron transport evidence_span: {"source_cache": "artifacts/copper-research/27714044.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "5e8791edb75475ba74e95cddc330c06512ef3b9c02a0c5a6b203327c047dff37", "start_char": 0, "end_char": 1780, "text_sha256": "5e8791edb75475ba74e95cddc330c06512ef3b9c02a0c5a6b203327c047dff37"} [copper-p27714044] Knockdown of copper-transporting ATPase 1 (Atp7a) impairs iron flux in fully-differentiated rat (IEC-6) and human (Caco-2) intestinal epithelial cells. (2016). https://pubmed.ncbi.nlm.nih.gov/27714044/ DOI: 10.1039/c6mt00126b
    Complete structured claim and evidence

  2. The two early-treated children with normal neurodevelopment and myelination had variants permitting residual ATP7A activity or some correctly spliced transcript.

    Human copper-transporting ATPase ATP7A → Neurodevelopment following early copper treatment in Menkes disease source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_span
    {"source_cache": "artifacts/copper-research/18256395.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "e855a0286cb633432b654005d756aa1e887ddace4f2a4dc5fee6cca518d895ce", "start_char": 0, "end_char": 2319, "text_sha256": "e855a0286cb633432b654005d756aa1e887ddace4f2a4dc5fee6cca518d895ce"}
    experimental_model
    Early-treatment Menkes cohort with historical comparison and functional genotyping
    exposure
    Copper injections begun by 22 days in twelve infants; comparison with fifteen later-treated historical patients
    limitations
    Not randomized; survival follow-up differed between cohorts. Genotype and residual function influenced outcome, so results cannot be generalized to every ATP7A variant.
    nutrient_topic
    Copper research collection; topical membership is not evidence of a direct dietary effect. · Copper
    organism
    Human infants
    plain_language
    Delivering copper early worked best when some transport machinery still functioned.
    primary_references
    [copper-p18256395] Neonatal diagnosis and treatment of Menkes disease. (2008). https://pubmed.ncbi.nlm.nih.gov/18256395/ DOI: 10.1056/nejmoa070613
    tissue_or_cell_type
    Survival and neurodevelopment
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Copper: transport, cuproenzymes, deficiency, excess and nutrient interactions (2026-09-17) · lines 1456–1467

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Early-treatment Menkes cohort with historical comparison and functional genotyping · source_derived_draft · unverified_draft

    ### copper-menkes-residual-function The two early-treated children with normal neurodevelopment and myelination had variants permitting residual ATP7A activity or some correctly spliced transcript. Condition category: machinery_impairment nutrient_topic: Copper research collection; topical membership is not evidence of a direct dietary effect. plain_language: Delivering copper early worked best when some transport machinery still functioned. organism: Human infants tissue_or_cell_type: Survival and neurodevelopment experimental_model: Early-treatment Menkes cohort with historical comparison and functional genotyping limitations: Not randomized; survival follow-up differed between cohorts. Genotype and residual function influenced outcome, so results cannot be generalized to every ATP7A variant. exposure: Copper injections begun by 22 days in twelve infants; comparison with fifteen later-treated historical patients evidence_span: {"source_cache": "artifacts/copper-research/18256395.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "e855a0286cb633432b654005d756aa1e887ddace4f2a4dc5fee6cca518d895ce", "start_char": 0, "end_char": 2319, "text_sha256": "e855a0286cb633432b654005d756aa1e887ddace4f2a4dc5fee6cca518d895ce"} [copper-p18256395] Neonatal diagnosis and treatment of Menkes disease. (2008). https://pubmed.ncbi.nlm.nih.gov/18256395/ DOI: 10.1056/nejmoa070613
    Complete structured claim and evidence

What acts on it

  1. Vascular specimens from patients with type 2 diabetes showed lower ATP7A protein.

    Human vascular specimens from patients with type 2 diabetes → Human copper-transporting ATPase ATP7A source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    biomarker_context Imported condition classification; unverified.
    curation_topic
    copper · Copper
    experimental_condition
    Control vascular specimens Type 2 diabetes vascular specimens · Human vascular specimens from patients with type 2 diabetes Condition belongs to the full experimental contrast; do not separate a joint intervention.
    experimental_contrast
    {"intervention": "Type 2 diabetes vascular specimens", "comparator": "Control vascular specimens", "endpoint": "ATP7A protein abundance", "effect_direction": "decrease", "combination": "single", "conditions": [{"entity_slug": "human-t2d-vessel-state", "state": "Type 2 diabetes vascular specimens"}]} Explicit extracted experimental comparison; source-derived draft.
    experimental_model
    Human vascular specimens; primary abstract reviewed
    limitations
    Observational human finding; detailed sampling and covariate analysis require full-methods review.
    primary_references
    Sudhahar et al. 2018; DOI:10.1161/ATVBAHA.117.309819; PMID:29301787; https://pubmed.ncbi.nlm.nih.gov/29301787/
    trigger_kind
    biomarker_context Imported condition classification; unverified.

    Diabetes cascade: targeted primary-source supplement · lines 39–39

    See claim-local references; curated paraphrases reviewed 2026-09-20. · supports · Human vascular specimens; primary abstract reviewed · source_derived_draft · unverified_draft

    Vascular specimens from patients with type 2 diabetes showed lower ATP7A protein. Model: Human vascular specimens; primary abstract reviewed. Limits: Observational human finding; detailed sampling and covariate analysis require full-methods review. Primary reference: Sudhahar et al. 2018; DOI:10.1161/ATVBAHA.117.309819; PMID:29301787; https://pubmed.ncbi.nlm.nih.gov/29301787/
    Complete structured claim and evidence

Where it participates (unsigned role)

  1. Survival was 92% in the twelve early-treated infants at median 4.6-year follow-up versus 13% in the historical late-treatment group at median 1.8 years.

    Copper → Survival following early copper treatment in Menkes disease source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_span
    {"source_cache": "artifacts/copper-research/18256395.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "e855a0286cb633432b654005d756aa1e887ddace4f2a4dc5fee6cca518d895ce", "start_char": 0, "end_char": 2319, "text_sha256": "e855a0286cb633432b654005d756aa1e887ddace4f2a4dc5fee6cca518d895ce"}
    experimental_model
    Early-treatment Menkes cohort with historical comparison and functional genotyping
    exposure
    Copper injections begun by 22 days in twelve infants; comparison with fifteen later-treated historical patients
    limitations
    Not randomized; survival follow-up differed between cohorts. Genotype and residual function influenced outcome, so results cannot be generalized to every ATP7A variant.
    nutrient_topic
    Copper research collection; topical membership is not evidence of a direct dietary effect. · Copper
    organism
    Human infants
    plain_language
    Early treatment was associated with much better survival in this cohort, with important comparison limits.
    primary_references
    [copper-p18256395] Neonatal diagnosis and treatment of Menkes disease. (2008). https://pubmed.ncbi.nlm.nih.gov/18256395/ DOI: 10.1056/nejmoa070613
    tissue_or_cell_type
    Survival and neurodevelopment
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Copper: transport, cuproenzymes, deficiency, excess and nutrient interactions (2026-09-17) · lines 1443–1454

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Early-treatment Menkes cohort with historical comparison and functional genotyping · source_derived_draft · unverified_draft

    ### copper-menkes-early-survival Survival was 92% in the twelve early-treated infants at median 4.6-year follow-up versus 13% in the historical late-treatment group at median 1.8 years. Condition category: machinery_impairment nutrient_topic: Copper research collection; topical membership is not evidence of a direct dietary effect. plain_language: Early treatment was associated with much better survival in this cohort, with important comparison limits. organism: Human infants tissue_or_cell_type: Survival and neurodevelopment experimental_model: Early-treatment Menkes cohort with historical comparison and functional genotyping limitations: Not randomized; survival follow-up differed between cohorts. Genotype and residual function influenced outcome, so results cannot be generalized to every ATP7A variant. exposure: Copper injections begun by 22 days in twelve infants; comparison with fifteen later-treated historical patients evidence_span: {"source_cache": "artifacts/copper-research/18256395.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "e855a0286cb633432b654005d756aa1e887ddace4f2a4dc5fee6cca518d895ce", "start_char": 0, "end_char": 2319, "text_sha256": "e855a0286cb633432b654005d756aa1e887ddace4f2a4dc5fee6cca518d895ce"} [copper-p18256395] Neonatal diagnosis and treatment of Menkes disease. (2008). https://pubmed.ncbi.nlm.nih.gov/18256395/ DOI: 10.1056/nejmoa070613
    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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