Component

Cellular copper efflux

Cellular copper efflux. Species, exposure and limitations are retained in each linked claim.

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 acts on it

  1. Atox1-deficient fibroblasts accumulated copper because cellular copper efflux was reduced.

    Mouse copper chaperone Atox1 → Cellular copper efflux source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_span
    {"source_cache": "artifacts/copper-research/12538877.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "480f54240ace7abfb1e0a00ae4f113de3bb518ae356fc523354ced9619428283", "start_char": 0, "end_char": 1579, "text_sha256": "480f54240ace7abfb1e0a00ae4f113de3bb518ae356fc523354ced9619428283"}
    experimental_model
    Atox1-null and control immortalized embryonic fibroblasts
    exposure
    Atox1 deletion and copper challenge
    limitations
    Trafficking and efflux are related but distinguishable; this is a cell knockout study, not human dietary depletion.
    nutrient_topic
    Copper research collection; topical membership is not evidence of a direct dietary effect. · Copper
    organism
    Mouse
    plain_language
    Copper can build up while its delivery and removal machinery works poorly.
    primary_references
    [copper-p12538877] Essential role for Atox1 in the copper-mediated intracellular trafficking of the Menkes ATPase. (2003). https://pubmed.ncbi.nlm.nih.gov/12538877/ DOI: 10.1073/pnas.0336230100
    tissue_or_cell_type
    Fibroblast Golgi and cellular copper pools
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Copper: transport, cuproenzymes, deficiency, excess and nutrient interactions (2026-09-17) · lines 364–375

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Atox1-null and control immortalized embryonic fibroblasts · source_derived_draft · unverified_draft

    ### copper-atox1-efflux Atox1-deficient fibroblasts accumulated copper because cellular copper efflux was reduced. Condition category: machinery_impairment nutrient_topic: Copper research collection; topical membership is not evidence of a direct dietary effect. plain_language: Copper can build up while its delivery and removal machinery works poorly. organism: Mouse tissue_or_cell_type: Fibroblast Golgi and cellular copper pools experimental_model: Atox1-null and control immortalized embryonic fibroblasts limitations: Trafficking and efflux are related but distinguishable; this is a cell knockout study, not human dietary depletion. exposure: Atox1 deletion and copper challenge evidence_span: {"source_cache": "artifacts/copper-research/12538877.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "480f54240ace7abfb1e0a00ae4f113de3bb518ae356fc523354ced9619428283", "start_char": 0, "end_char": 1579, "text_sha256": "480f54240ace7abfb1e0a00ae4f113de3bb518ae356fc523354ced9619428283"} [copper-p12538877] Essential role for Atox1 in the copper-mediated intracellular trafficking of the Menkes ATPase. (2003). https://pubmed.ncbi.nlm.nih.gov/12538877/ DOI: 10.1073/pnas.0336230100
    Complete structured claim and evidence

  2. SCO1-associated cellular copper deficiency reflected increased copper efflux rather than reduced high-affinity uptake in the studied patient-cell models.

    Human cytochrome c oxidase assembly protein SCO1 → Cellular copper efflux source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_span
    {"source_cache": "artifacts/copper-research/17189203.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "7653227df0fe557c484a72eafed6a7a96dc06f5d4f63f7eea4a5b9568949a698", "start_char": 0, "end_char": 950, "text_sha256": "7653227df0fe557c484a72eafed6a7a96dc06f5d4f63f7eea4a5b9568949a698"}
    experimental_model
    SCO1/SCO2 patient-cell analysis and genetic complementation
    exposure
    Pathogenic SCO variants; transporter and rescue assays
    limitations
    Copper effects varied with allele and tissue. A genetic assembly defect does not prove inadequate intake or universal response to copper supplementation.
    nutrient_topic
    Copper research collection; topical membership is not evidence of a direct dietary effect. · Copper
    organism
    Human
    plain_language
    The problem was copper leaving the cell too quickly.
    primary_references
    [copper-p17189203] The human cytochrome c oxidase assembly factors SCO1 and SCO2 have regulatory roles in the maintenance of cellular copper homeostasis. (2007). https://pubmed.ncbi.nlm.nih.gov/17189203/ DOI: 10.1016/j.cmet.2006.12.001
    tissue_or_cell_type
    Patient-derived cellular systems
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Copper: transport, cuproenzymes, deficiency, excess and nutrient interactions (2026-09-17) · lines 702–713

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · SCO1/SCO2 patient-cell analysis and genetic complementation · source_derived_draft · unverified_draft

    ### copper-sco1-copper-efflux SCO1-associated cellular copper deficiency reflected increased copper efflux rather than reduced high-affinity uptake in the studied patient-cell models. Condition category: machinery_impairment nutrient_topic: Copper research collection; topical membership is not evidence of a direct dietary effect. plain_language: The problem was copper leaving the cell too quickly. organism: Human tissue_or_cell_type: Patient-derived cellular systems experimental_model: SCO1/SCO2 patient-cell analysis and genetic complementation limitations: Copper effects varied with allele and tissue. A genetic assembly defect does not prove inadequate intake or universal response to copper supplementation. exposure: Pathogenic SCO variants; transporter and rescue assays evidence_span: {"source_cache": "artifacts/copper-research/17189203.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "7653227df0fe557c484a72eafed6a7a96dc06f5d4f63f7eea4a5b9568949a698", "start_char": 0, "end_char": 950, "text_sha256": "7653227df0fe557c484a72eafed6a7a96dc06f5d4f63f7eea4a5b9568949a698"} [copper-p17189203] The human cytochrome c oxidase assembly factors SCO1 and SCO2 have regulatory roles in the maintenance of cellular copper homeostasis. (2007). https://pubmed.ncbi.nlm.nih.gov/17189203/ DOI: 10.1016/j.cmet.2006.12.001
    Complete structured claim and evidence

  3. SCO2 variants also produced tissue- and allele-specific cellular copper deficiency through increased efflux.

    Human cytochrome c oxidase assembly protein SCO2 → Cellular copper efflux source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_span
    {"source_cache": "artifacts/copper-research/17189203.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "7653227df0fe557c484a72eafed6a7a96dc06f5d4f63f7eea4a5b9568949a698", "start_char": 0, "end_char": 950, "text_sha256": "7653227df0fe557c484a72eafed6a7a96dc06f5d4f63f7eea4a5b9568949a698"}
    experimental_model
    SCO1/SCO2 patient-cell analysis and genetic complementation
    exposure
    Pathogenic SCO variants; transporter and rescue assays
    limitations
    Copper effects varied with allele and tissue. A genetic assembly defect does not prove inadequate intake or universal response to copper supplementation.
    nutrient_topic
    Copper research collection; topical membership is not evidence of a direct dietary effect. · Copper
    organism
    Human
    plain_language
    A second mitochondrial assembly protein also influences whole-cell copper balance.
    primary_references
    [copper-p17189203] The human cytochrome c oxidase assembly factors SCO1 and SCO2 have regulatory roles in the maintenance of cellular copper homeostasis. (2007). https://pubmed.ncbi.nlm.nih.gov/17189203/ DOI: 10.1016/j.cmet.2006.12.001
    tissue_or_cell_type
    Patient-derived cellular systems
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Copper: transport, cuproenzymes, deficiency, excess and nutrient interactions (2026-09-17) · lines 715–726

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · SCO1/SCO2 patient-cell analysis and genetic complementation · source_derived_draft · unverified_draft

    ### copper-sco2-copper-homeostasis SCO2 variants also produced tissue- and allele-specific cellular copper deficiency through increased efflux. Condition category: machinery_impairment nutrient_topic: Copper research collection; topical membership is not evidence of a direct dietary effect. plain_language: A second mitochondrial assembly protein also influences whole-cell copper balance. organism: Human tissue_or_cell_type: Patient-derived cellular systems experimental_model: SCO1/SCO2 patient-cell analysis and genetic complementation limitations: Copper effects varied with allele and tissue. A genetic assembly defect does not prove inadequate intake or universal response to copper supplementation. exposure: Pathogenic SCO variants; transporter and rescue assays evidence_span: {"source_cache": "artifacts/copper-research/17189203.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "7653227df0fe557c484a72eafed6a7a96dc06f5d4f63f7eea4a5b9568949a698", "start_char": 0, "end_char": 950, "text_sha256": "7653227df0fe557c484a72eafed6a7a96dc06f5d4f63f7eea4a5b9568949a698"} [copper-p17189203] The human cytochrome c oxidase assembly factors SCO1 and SCO2 have regulatory roles in the maintenance of cellular copper homeostasis. (2007). https://pubmed.ncbi.nlm.nih.gov/17189203/ DOI: 10.1016/j.cmet.2006.12.001
    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