{"id":"2f42d773-4d10-5a38-ad04-063ac42f08d8","stable_key":"0ad8610d-d575-5870-b7cd-763a9f750783:copper-atp7b-lysosomal-loading","predicate":"loads","statement":"Lysosomal ATP7B transported copper into the lysosomal lumen.","claim_class":"mechanistic","status":"source_derived_draft","evidence_grade":"ungraded","direction":"context_dependent","is_public":true,"mechanism_event_id":"b2f65387-c659-53cb-ac57-e2147b9d8de3","mechanism_event_label":"A temporary storage compartment helps prepare copper for removal.","subject":{"id":"05dae672-bbd9-585d-8713-ccfe9e14d26a","slug":"atp7b","display_name":"Human copper-transporting ATPase ATP7B","entity_type_key":"protein"},"object":{"id":"762003e8-a271-5e85-b2d9-7b60ba3f6ef4","slug":"lysosomal-copper-storage","display_name":"Copper accumulation in the lysosomal lumen","entity_type_key":"cellular_process"},"evidence_count":1,"mechanism_event":{"id":"b2f65387-c659-53cb-ac57-e2147b9d8de3","stable_key":"0ad8610d-d575-5870-b7cd-763a9f750783:copper-atp7b-lysosomal-loading-event","event_type":"biochemical_relationship","label":"A temporary storage compartment helps prepare copper for removal.","description":"Lysosomal ATP7B transported copper into the lysosomal lumen.","status":"provisional","compartment":null,"participants":[{"entity":{"id":"9f0afdde-1ec1-5c8a-bb5e-f3b2b75f67f6","slug":"copper","display_name":"Copper","entity_type_key":"nutrient_element"},"role":"transported metal","stoichiometry":null,"state_label":"","sequence_order":0,"notes":""},{"entity":{"id":"05dae672-bbd9-585d-8713-ccfe9e14d26a","slug":"atp7b","display_name":"Human copper-transporting ATPase ATP7B","entity_type_key":"protein"},"role":"subject","stoichiometry":null,"state_label":"","sequence_order":1,"notes":""},{"entity":{"id":"762003e8-a271-5e85-b2d9-7b60ba3f6ef4","slug":"lysosomal-copper-storage","display_name":"Copper accumulation in the lysosomal lumen","entity_type_key":"cellular_process"},"role":"target","stoichiometry":null,"state_label":"","sequence_order":2,"notes":""}]},"contexts":[{"dimension":"evidence_span","value_text":"{\"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\"}","comparator":null,"unit":null,"notes":"","entity":null},{"dimension":"experimental_model","value_text":"Copper perturbation, imaging and trafficking assays in hepatocyte systems","comparator":null,"unit":null,"notes":"","entity":null},{"dimension":"exposure","value_text":"Copper challenge and lysosomal exocytosis perturbation","comparator":null,"unit":null,"notes":"","entity":null},{"dimension":"limitations","value_text":"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.","comparator":null,"unit":null,"notes":"","entity":null},{"dimension":"nutrient_topic","value_text":"Copper research collection; topical membership is not evidence of a direct dietary effect.","comparator":null,"unit":null,"notes":"","entity":{"slug":"copper","display_name":"Copper","entity_type_key":"nutrient_element"}},{"dimension":"organism","value_text":"Human HepG2 cells with complementary hepatic models","comparator":null,"unit":null,"notes":"","entity":null},{"dimension":"plain_language","value_text":"A temporary storage compartment helps prepare copper for removal.","comparator":null,"unit":null,"notes":"","entity":null},{"dimension":"primary_references","value_text":"[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","comparator":null,"unit":null,"notes":"","entity":null},{"dimension":"tissue_or_cell_type","value_text":"Golgi, lysosomes and canalicular pole","comparator":null,"unit":null,"notes":"","entity":null}],"evidence":[{"id":"7c4e78e2-1e16-59b5-8f98-c7688dd720c5","evidence_kind":"source_excerpt","locator":"Lines 429-440","start_line":429,"end_line":440,"excerpt":"### copper-atp7b-lysosomal-loading\nLysosomal ATP7B transported copper into the lysosomal lumen.\nCondition category: normal\nnutrient_topic: Copper research collection; topical membership is not evidence of a direct dietary effect.\nplain_language: A temporary storage compartment helps prepare copper for removal.\norganism: Human HepG2 cells with complementary hepatic models\ntissue_or_cell_type: Golgi, lysosomes and canalicular pole\nexperimental_model: Copper perturbation, imaging and trafficking assays in hepatocyte systems\nlimitations: 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.\nexposure: Copper challenge and lysosomal exocytosis perturbation\nevidence_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\"}\n[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","model_system":"Copper perturbation, imaging and trafficking assays in hepatocyte systems","directness":"author_interpretation","verification_status":"source_derived_draft","notes":"Exact curation-document quotation, not publisher quotation. Study 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","relationship":"supports","weight":1.0,"link_notes":"","source":{"id":"9afba495-cbdc-51aa-998e-70a930dba3be","stable_key":"import-0ad8610d-d575-5870-b7cd-763a9f750783","title":"Copper: transport, cuproenzymes, deficiency, excess and nutrient interactions (2026-09-17)","document_type":"imported_text","citation_label":"AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text.","file_path":"","sha256":"84b0f62b2dae6835fa26902be87625c003c6c707492d3007e8f9d15420669008","revision_id":"d7e35b8b-3f77-56d9-90b5-5f542c63f321","review_status":"unverified_draft","notes":""}}],"relations":[],"conflicts":[],"corrections":[],"research":null}