Component
Lysosomal exocytosis at the hepatocyte canalicular pole
Lysosomal exocytosis at the hepatocyte canalicular pole. Species, exposure and limitations are retained in each linked claim.
2 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.
Other things that act on it
Enzymes, hormones, genes, and other components with a recorded effect. These are not nutrients, so they do not count toward the arrows above. Each finding names the chapter that recorded it.
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.
What it acts on
Stimulating lysosomal exocytosis increased ATP7B delivery toward the canalicular membrane and copper release into the biliary space.
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
Where it participates (unsigned role)
ATP7B interaction with dynactin p62 supported movement of copper-containing lysosomes toward the hepatocyte canalicular pole.
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
The events it takes part in
A mechanism often involves more than two components. These are the full events, with every participant and its role.
Situations it appears in
Low-supply and faulty-machinery situations recorded in the chapters where this component plays a part.
In the sources
Preserved passages that mention this component, quoted exactly. Open one to read it in context.
Open hypotheses
Proposed ideas that involve this component. They are labeled as hypotheses and do not change any recorded statement.
This is a research prototype built from draft material. It is not medical advice, and its statements still await verification against the original studies.