Component

Human copper chaperone ATOX1

Human copper chaperone ATOX1. Species, exposure and limitations are retained in each linked claim.

3 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 it acts on

  1. Copper-loaded ATOX1 activated ATP7B ATP hydrolysis while changing interactions among its first three metal-binding domains.

    Human copper chaperone ATOX1 → ATP7B ATP hydrolysis source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/copper-research/28900031.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "64fceb98b5bf2ca406f26799cea5832b0306883118b9ad2416ba87db47b18ce8", "start_char": 0, "end_char": 1471, "text_sha256": "64fceb98b5bf2ca406f26799cea5832b0306883118b9ad2416ba87db47b18ce8"}
    experimental_model
    Biochemistry, solution NMR and small-angle X-ray scattering
    exposure
    Apo versus copper-loaded ATOX1
    limitations
    Domain motion and ATP hydrolysis were studied directly; these assays do not establish a whole-body copper requirement.
    nutrient_topic
    Copper research collection; topical membership is not evidence of a direct dietary effect. · Copper
    organism
    Human proteins
    plain_language
    The courier also helps switch on the copper pump.
    primary_references
    [copper-p28900031] The metal chaperone Atox1 regulates the activity of the human copper transporter ATP7B by modulating domain dynamics. (2017). https://pubmed.ncbi.nlm.nih.gov/28900031/ DOI: 10.1074/jbc.m117.811752
    tissue_or_cell_type
    Purified ATOX1 and ATP7B domains

    Copper: transport, cuproenzymes, deficiency, excess and nutrient interactions (2026-09-17) · lines 390–401

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Biochemistry, solution NMR and small-angle X-ray scattering · source_derived_draft · unverified_draft

    ### copper-atox1-atp7b-activation Copper-loaded ATOX1 activated ATP7B ATP hydrolysis while changing interactions among its first three metal-binding domains. Condition category: normal nutrient_topic: Copper research collection; topical membership is not evidence of a direct dietary effect. plain_language: The courier also helps switch on the copper pump. organism: Human proteins tissue_or_cell_type: Purified ATOX1 and ATP7B domains experimental_model: Biochemistry, solution NMR and small-angle X-ray scattering limitations: Domain motion and ATP hydrolysis were studied directly; these assays do not establish a whole-body copper requirement. exposure: Apo versus copper-loaded ATOX1 evidence_span: {"source_cache": "artifacts/copper-research/28900031.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "64fceb98b5bf2ca406f26799cea5832b0306883118b9ad2416ba87db47b18ce8", "start_char": 0, "end_char": 1471, "text_sha256": "64fceb98b5bf2ca406f26799cea5832b0306883118b9ad2416ba87db47b18ce8"} [copper-p28900031] The metal chaperone Atox1 regulates the activity of the human copper transporter ATP7B by modulating domain dynamics. (2017). https://pubmed.ncbi.nlm.nih.gov/28900031/ DOI: 10.1074/jbc.m117.811752
    Complete structured claim and evidence
  2. Copper transfer from ATOX1 reduced interactions within ATP7B MBD1-3 and increased domain mobility.

    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/copper-research/28900031.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "64fceb98b5bf2ca406f26799cea5832b0306883118b9ad2416ba87db47b18ce8", "start_char": 0, "end_char": 1471, "text_sha256": "64fceb98b5bf2ca406f26799cea5832b0306883118b9ad2416ba87db47b18ce8"}
    experimental_model
    Biochemistry, solution NMR and small-angle X-ray scattering
    exposure
    Apo versus copper-loaded ATOX1
    limitations
    Domain motion and ATP hydrolysis were studied directly; these assays do not establish a whole-body copper requirement.
    nutrient_topic
    Copper research collection; topical membership is not evidence of a direct dietary effect. · Copper
    organism
    Human proteins
    plain_language
    Copper handoff changes how the pump can move.
    primary_references
    [copper-p28900031] The metal chaperone Atox1 regulates the activity of the human copper transporter ATP7B by modulating domain dynamics. (2017). https://pubmed.ncbi.nlm.nih.gov/28900031/ DOI: 10.1074/jbc.m117.811752
    tissue_or_cell_type
    Purified ATOX1 and ATP7B domains

    Copper: transport, cuproenzymes, deficiency, excess and nutrient interactions (2026-09-17) · lines 403–414

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Biochemistry, solution NMR and small-angle X-ray scattering · source_derived_draft · unverified_draft

    ### copper-atox1-atp7b-mobility Copper transfer from ATOX1 reduced interactions within ATP7B MBD1-3 and increased domain mobility. Condition category: normal nutrient_topic: Copper research collection; topical membership is not evidence of a direct dietary effect. plain_language: Copper handoff changes how the pump can move. organism: Human proteins tissue_or_cell_type: Purified ATOX1 and ATP7B domains experimental_model: Biochemistry, solution NMR and small-angle X-ray scattering limitations: Domain motion and ATP hydrolysis were studied directly; these assays do not establish a whole-body copper requirement. exposure: Apo versus copper-loaded ATOX1 evidence_span: {"source_cache": "artifacts/copper-research/28900031.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "64fceb98b5bf2ca406f26799cea5832b0306883118b9ad2416ba87db47b18ce8", "start_char": 0, "end_char": 1471, "text_sha256": "64fceb98b5bf2ca406f26799cea5832b0306883118b9ad2416ba87db47b18ce8"} [copper-p28900031] The metal chaperone Atox1 regulates the activity of the human copper transporter ATP7B by modulating domain dynamics. (2017). https://pubmed.ncbi.nlm.nih.gov/28900031/ DOI: 10.1074/jbc.m117.811752
    Complete structured claim and evidence
  3. ATOX1 knockdown also impaired copper-induced SLC7A11 expression.

    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/copper-research/40944334.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "6df1716e8998546d22a1d96116e1bc35b1f7e24c94868ec5e441ada6a2be3e89", "start_char": 0, "end_char": 1634, "text_sha256": "6df1716e8998546d22a1d96116e1bc35b1f7e24c94868ec5e441ada6a2be3e89"}
    experimental_model
    Copper and iron exposure with transcription-factor knockdown
    exposure
    CuCl2 or FeCl2 exposure; NFE2L2 or ATOX1 knockdown
    limitations
    One cancer-cell model. Expression changes do not prove increased glutathione synthesis, tumor progression, or a clinical nutrient interaction.
    nutrient_topic
    Copper research collection; topical membership is not evidence of a direct dietary effect. · Copper
    organism
    Human MDA-MB-231 breast cancer cells
    plain_language
    A copper-handling protein participated in this gene-expression response.
    primary_references
    [copper-p40944334] Copper induces cystine/glutamate antiporter SLC7A11 through the activation of Nrf2 and Atox1 pathways. (2025). https://pubmed.ncbi.nlm.nih.gov/40944334/ DOI: 10.1080/10715762.2025.2560847
    tissue_or_cell_type
    Cellular amino-acid transport machinery

    Copper: transport, cuproenzymes, deficiency, excess and nutrient interactions (2026-09-17) · lines 1313–1324

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Copper and iron exposure with transcription-factor knockdown · source_derived_draft · unverified_draft

    ### copper-atox1-slc7a11 ATOX1 knockdown also impaired copper-induced SLC7A11 expression. Condition category: normal nutrient_topic: Copper research collection; topical membership is not evidence of a direct dietary effect. plain_language: A copper-handling protein participated in this gene-expression response. organism: Human MDA-MB-231 breast cancer cells tissue_or_cell_type: Cellular amino-acid transport machinery experimental_model: Copper and iron exposure with transcription-factor knockdown limitations: One cancer-cell model. Expression changes do not prove increased glutathione synthesis, tumor progression, or a clinical nutrient interaction. exposure: CuCl2 or FeCl2 exposure; NFE2L2 or ATOX1 knockdown evidence_span: {"source_cache": "artifacts/copper-research/40944334.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "6df1716e8998546d22a1d96116e1bc35b1f7e24c94868ec5e441ada6a2be3e89", "start_char": 0, "end_char": 1634, "text_sha256": "6df1716e8998546d22a1d96116e1bc35b1f7e24c94868ec5e441ada6a2be3e89"} [copper-p40944334] Copper induces cystine/glutamate antiporter SLC7A11 through the activation of Nrf2 and Atox1 pathways. (2025). https://pubmed.ncbi.nlm.nih.gov/40944334/ DOI: 10.1080/10715762.2025.2560847
    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