Component

Human copper-transporting ATPase ATP7B

Human copper-transporting ATPase ATP7B. Species, exposure and limitations are retained in each linked claim.

7 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. ATP7B interaction with dynactin p62 supported movement of copper-containing lysosomes toward the hepatocyte canalicular pole.

    Human copper-transporting ATPase ATP7B → Human dynactin subunit 4 / DCTN4 / dynactin p62 source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/copper-research/24909901.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "abfdc86e4b47b489037af635672033532c905d291127030d9dbcfc02e998c20b", "start_char": 0, "end_char": 1036, "text_sha256": "abfdc86e4b47b489037af635672033532c905d291127030d9dbcfc02e998c20b"}
    experimental_model
    Copper perturbation, imaging and trafficking assays in hepatocyte systems
    exposure
    Copper challenge and lysosomal exocytosis perturbation
    limitations
    The main cellular trafficking observations are mechanistic; experimental copper exposures and mutant rescue do not establish a clinical treatment. Dynactin p62 is DCTN4, not autophagy SQSTM1/p62.
    nutrient_topic
    Copper research collection; topical membership is not evidence of a direct dietary effect. · Copper
    organism
    Human HepG2 cells with complementary hepatic models
    plain_language
    Transporter placement helps route copper toward bile.
    primary_references
    [copper-p24909901] Wilson disease protein ATP7B utilizes lysosomal exocytosis to maintain copper homeostasis. (2014). https://pubmed.ncbi.nlm.nih.gov/24909901/ DOI: 10.1016/j.devcel.2014.04.033
    tissue_or_cell_type
    Golgi, lysosomes and canalicular pole

    Copper: transport, cuproenzymes, deficiency, excess and nutrient interactions (2026-09-17) · lines 442–453

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Copper perturbation, imaging and trafficking assays in hepatocyte systems · source_derived_draft · unverified_draft

    ### copper-atp7b-dynactin ATP7B interaction with dynactin p62 supported movement of copper-containing lysosomes toward the hepatocyte canalicular pole. Condition category: normal nutrient_topic: Copper research collection; topical membership is not evidence of a direct dietary effect. plain_language: Transporter placement helps route copper toward bile. organism: Human HepG2 cells with complementary hepatic models tissue_or_cell_type: Golgi, lysosomes and canalicular pole experimental_model: Copper perturbation, imaging and trafficking assays in hepatocyte systems limitations: The main cellular trafficking observations are mechanistic; experimental copper exposures and mutant rescue do not establish a clinical treatment. Dynactin p62 is DCTN4, not autophagy SQSTM1/p62. exposure: Copper challenge and lysosomal exocytosis perturbation evidence_span: {"source_cache": "artifacts/copper-research/24909901.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "abfdc86e4b47b489037af635672033532c905d291127030d9dbcfc02e998c20b", "start_char": 0, "end_char": 1036, "text_sha256": "abfdc86e4b47b489037af635672033532c905d291127030d9dbcfc02e998c20b"} [copper-p24909901] Wilson disease protein ATP7B utilizes lysosomal exocytosis to maintain copper homeostasis. (2014). https://pubmed.ncbi.nlm.nih.gov/24909901/ DOI: 10.1016/j.devcel.2014.04.033
    Complete structured claim and evidence

  2. Lysosomal ATP7B transported copper into the lysosomal lumen.

    Human copper-transporting ATPase ATP7B → Copper accumulation in the lysosomal lumen source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/copper-research/24909901.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "abfdc86e4b47b489037af635672033532c905d291127030d9dbcfc02e998c20b", "start_char": 0, "end_char": 1036, "text_sha256": "abfdc86e4b47b489037af635672033532c905d291127030d9dbcfc02e998c20b"}
    experimental_model
    Copper perturbation, imaging and trafficking assays in hepatocyte systems
    exposure
    Copper challenge and lysosomal exocytosis perturbation
    limitations
    The main cellular trafficking observations are mechanistic; experimental copper exposures and mutant rescue do not establish a clinical treatment. Dynactin p62 is DCTN4, not autophagy SQSTM1/p62.
    nutrient_topic
    Copper research collection; topical membership is not evidence of a direct dietary effect. · Copper
    organism
    Human HepG2 cells with complementary hepatic models
    plain_language
    A temporary storage compartment helps prepare copper for removal.
    primary_references
    [copper-p24909901] Wilson disease protein ATP7B utilizes lysosomal exocytosis to maintain copper homeostasis. (2014). https://pubmed.ncbi.nlm.nih.gov/24909901/ DOI: 10.1016/j.devcel.2014.04.033
    tissue_or_cell_type
    Golgi, lysosomes and canalicular pole

    Copper: transport, cuproenzymes, deficiency, excess and nutrient interactions (2026-09-17) · lines 429–440

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Copper perturbation, imaging and trafficking assays in hepatocyte systems · source_derived_draft · unverified_draft

    ### copper-atp7b-lysosomal-loading Lysosomal ATP7B transported copper into the lysosomal lumen. Condition category: normal nutrient_topic: Copper research collection; topical membership is not evidence of a direct dietary effect. plain_language: A temporary storage compartment helps prepare copper for removal. organism: Human HepG2 cells with complementary hepatic models tissue_or_cell_type: Golgi, lysosomes and canalicular pole experimental_model: Copper perturbation, imaging and trafficking assays in hepatocyte systems limitations: The main cellular trafficking observations are mechanistic; experimental copper exposures and mutant rescue do not establish a clinical treatment. Dynactin p62 is DCTN4, not autophagy SQSTM1/p62. exposure: Copper challenge and lysosomal exocytosis perturbation evidence_span: {"source_cache": "artifacts/copper-research/24909901.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "abfdc86e4b47b489037af635672033532c905d291127030d9dbcfc02e998c20b", "start_char": 0, "end_char": 1036, "text_sha256": "abfdc86e4b47b489037af635672033532c905d291127030d9dbcfc02e998c20b"} [copper-p24909901] Wilson disease protein ATP7B utilizes lysosomal exocytosis to maintain copper homeostasis. (2014). https://pubmed.ncbi.nlm.nih.gov/24909901/ DOI: 10.1016/j.devcel.2014.04.033
    Complete structured claim and evidence

  3. Elevated copper redirected ATP7B from the trans-Golgi network to a subset of lysosomes.

    Human copper-transporting ATPase ATP7B → ATP7B trafficking from Golgi to lysosomes source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/copper-research/24909901.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "abfdc86e4b47b489037af635672033532c905d291127030d9dbcfc02e998c20b", "start_char": 0, "end_char": 1036, "text_sha256": "abfdc86e4b47b489037af635672033532c905d291127030d9dbcfc02e998c20b"}
    experimental_model
    Copper perturbation, imaging and trafficking assays in hepatocyte systems
    exposure
    Copper challenge and lysosomal exocytosis perturbation
    limitations
    The main cellular trafficking observations are mechanistic; experimental copper exposures and mutant rescue do not establish a clinical treatment. Dynactin p62 is DCTN4, not autophagy SQSTM1/p62.
    nutrient_topic
    Copper research collection; topical membership is not evidence of a direct dietary effect. · Copper
    organism
    Human HepG2 cells with complementary hepatic models
    plain_language
    The liver-cell copper pump changes location when copper rises.
    primary_references
    [copper-p24909901] Wilson disease protein ATP7B utilizes lysosomal exocytosis to maintain copper homeostasis. (2014). https://pubmed.ncbi.nlm.nih.gov/24909901/ DOI: 10.1016/j.devcel.2014.04.033
    tissue_or_cell_type
    Golgi, lysosomes and canalicular pole

    Copper: transport, cuproenzymes, deficiency, excess and nutrient interactions (2026-09-17) · lines 416–427

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Copper perturbation, imaging and trafficking assays in hepatocyte systems · source_derived_draft · unverified_draft

    ### copper-atp7b-lysosomes Elevated copper redirected ATP7B from the trans-Golgi network to a subset of lysosomes. Condition category: normal nutrient_topic: Copper research collection; topical membership is not evidence of a direct dietary effect. plain_language: The liver-cell copper pump changes location when copper rises. organism: Human HepG2 cells with complementary hepatic models tissue_or_cell_type: Golgi, lysosomes and canalicular pole experimental_model: Copper perturbation, imaging and trafficking assays in hepatocyte systems limitations: The main cellular trafficking observations are mechanistic; experimental copper exposures and mutant rescue do not establish a clinical treatment. Dynactin p62 is DCTN4, not autophagy SQSTM1/p62. exposure: Copper challenge and lysosomal exocytosis perturbation evidence_span: {"source_cache": "artifacts/copper-research/24909901.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "abfdc86e4b47b489037af635672033532c905d291127030d9dbcfc02e998c20b", "start_char": 0, "end_char": 1036, "text_sha256": "abfdc86e4b47b489037af635672033532c905d291127030d9dbcfc02e998c20b"} [copper-p24909901] Wilson disease protein ATP7B utilizes lysosomal exocytosis to maintain copper homeostasis. (2014). https://pubmed.ncbi.nlm.nih.gov/24909901/ DOI: 10.1016/j.devcel.2014.04.033
    Complete structured claim and evidence

Where it participates (unsigned role)

  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.

    Human copper chaperone ATOX1 → ATP7B N-terminal metal-binding domain mobility 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
    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. Stimulating lysosomal exocytosis increased ATP7B delivery toward the canalicular membrane and copper release into the biliary space.

    Lysosomal exocytosis at the hepatocyte canalicular pole → Copper excretion toward bile source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/copper-research/24909901.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "abfdc86e4b47b489037af635672033532c905d291127030d9dbcfc02e998c20b", "start_char": 0, "end_char": 1036, "text_sha256": "abfdc86e4b47b489037af635672033532c905d291127030d9dbcfc02e998c20b"}
    experimental_model
    Copper perturbation, imaging and trafficking assays in hepatocyte systems
    exposure
    Copper challenge and lysosomal exocytosis perturbation
    limitations
    The main cellular trafficking observations are mechanistic; experimental copper exposures and mutant rescue do not establish a clinical treatment. Dynactin p62 is DCTN4, not autophagy SQSTM1/p62.
    nutrient_topic
    Copper research collection; topical membership is not evidence of a direct dietary effect. · Copper
    organism
    Human HepG2 cells with complementary hepatic models
    plain_language
    Lysosome fusion provides a route out of the liver cell for excess copper.
    primary_references
    [copper-p24909901] Wilson disease protein ATP7B utilizes lysosomal exocytosis to maintain copper homeostasis. (2014). https://pubmed.ncbi.nlm.nih.gov/24909901/ DOI: 10.1016/j.devcel.2014.04.033
    tissue_or_cell_type
    Golgi, lysosomes and canalicular pole

    Copper: transport, cuproenzymes, deficiency, excess and nutrient interactions (2026-09-17) · lines 455–466

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Copper perturbation, imaging and trafficking assays in hepatocyte systems · source_derived_draft · unverified_draft

    ### copper-lysosome-bile-export Stimulating lysosomal exocytosis increased ATP7B delivery toward the canalicular membrane and copper release into the biliary space. Condition category: normal nutrient_topic: Copper research collection; topical membership is not evidence of a direct dietary effect. plain_language: Lysosome fusion provides a route out of the liver cell for excess copper. organism: Human HepG2 cells with complementary hepatic models tissue_or_cell_type: Golgi, lysosomes and canalicular pole experimental_model: Copper perturbation, imaging and trafficking assays in hepatocyte systems limitations: The main cellular trafficking observations are mechanistic; experimental copper exposures and mutant rescue do not establish a clinical treatment. Dynactin p62 is DCTN4, not autophagy SQSTM1/p62. exposure: Copper challenge and lysosomal exocytosis perturbation evidence_span: {"source_cache": "artifacts/copper-research/24909901.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "abfdc86e4b47b489037af635672033532c905d291127030d9dbcfc02e998c20b", "start_char": 0, "end_char": 1036, "text_sha256": "abfdc86e4b47b489037af635672033532c905d291127030d9dbcfc02e998c20b"} [copper-p24909901] Wilson disease protein ATP7B utilizes lysosomal exocytosis to maintain copper homeostasis. (2014). https://pubmed.ncbi.nlm.nih.gov/24909901/ DOI: 10.1016/j.devcel.2014.04.033
    Complete structured claim and evidence

  4. Trientine tetrahydrochloride was noninferior to penicillamine for the specified non-ceruloplasmin copper endpoint at 24 weeks in stable adults with Wilson disease.

    Trientine tetrahydrochloride → Copper control during maintenance treatment of Wilson disease source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_span
    {"source_cache": "artifacts/copper-research/36183738.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "6235ee4003a7016b645aca9e0df7ea34076b266ebecb33bb878ce75e2c052166", "start_char": 0, "end_char": 4337, "text_sha256": "6235ee4003a7016b645aca9e0df7ea34076b266ebecb33bb878ce75e2c052166"}
    experimental_model
    Randomized open-label CHELATE maintenance noninferiority trial
    exposure
    Fifty-three adults previously stable on penicillamine for at least a year; trientine tetrahydrochloride versus penicillamine
    limitations
    Maintenance trial in stable adults, not initial treatment of severe disease. Noninferiority is not superiority and does not validate general detoxification.
    nutrient_topic
    Copper research collection; topical membership is not evidence of a direct dietary effect. · Copper
    organism
    Human adults with stable Wilson disease
    plain_language
    A copper-binding treatment maintained control in this defined patient group.
    primary_references
    [copper-p36183738] Trientine tetrahydrochloride versus penicillamine for maintenance therapy in Wilson disease (CHELATE): a randomised, open-label, non-inferiority, phase 3 trial. (2022). https://pubmed.ncbi.nlm.nih.gov/36183738/ DOI: 10.1016/s2468-1253(22)00270-9
    tissue_or_cell_type
    Circulating non-ceruloplasmin copper and clinical stability
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Copper: transport, cuproenzymes, deficiency, excess and nutrient interactions (2026-09-17) · lines 1469–1480

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Randomized open-label CHELATE maintenance noninferiority trial · source_derived_draft · unverified_draft

    ### copper-wilson-trientine-maintenance Trientine tetrahydrochloride was noninferior to penicillamine for the specified non-ceruloplasmin copper endpoint at 24 weeks in stable adults with Wilson disease. Condition category: machinery_impairment nutrient_topic: Copper research collection; topical membership is not evidence of a direct dietary effect. plain_language: A copper-binding treatment maintained control in this defined patient group. organism: Human adults with stable Wilson disease tissue_or_cell_type: Circulating non-ceruloplasmin copper and clinical stability experimental_model: Randomized open-label CHELATE maintenance noninferiority trial limitations: Maintenance trial in stable adults, not initial treatment of severe disease. Noninferiority is not superiority and does not validate general detoxification. exposure: Fifty-three adults previously stable on penicillamine for at least a year; trientine tetrahydrochloride versus penicillamine evidence_span: {"source_cache": "artifacts/copper-research/36183738.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "6235ee4003a7016b645aca9e0df7ea34076b266ebecb33bb878ce75e2c052166", "start_char": 0, "end_char": 4337, "text_sha256": "6235ee4003a7016b645aca9e0df7ea34076b266ebecb33bb878ce75e2c052166"} [copper-p36183738] Trientine tetrahydrochloride versus penicillamine for maintenance therapy in Wilson disease (CHELATE): a randomised, open-label, non-inferiority, phase 3 trial. (2022). https://pubmed.ncbi.nlm.nih.gov/36183738/ DOI: 10.1016/s2468-1253(22)00270-9
    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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