{"id":"7c2aec2e-85e7-5486-aa7b-55eb4280938a","stable_key":"0ad8610d-d575-5870-b7cd-763a9f750783:copper-cp-iron-mobilization","predicate":"loss_impairs","statement":"Cp-null mice had impaired iron release from hepatocytes and reticuloendothelial cells, while measured iron absorption and plasma turnover were comparable to controls.","claim_class":"mechanistic","status":"source_derived_draft","evidence_grade":"ungraded","direction":"context_dependent","is_public":true,"mechanism_event_id":"27de6841-29f2-521c-8c23-dac455e45564","mechanism_event_label":"The main defect was moving stored iron out of cells.","subject":{"id":"34665f8c-8d15-577c-9244-75a3c6ca61f8","slug":"mouse-cp","display_name":"Mouse ceruloplasmin Cp","entity_type_key":"protein"},"object":{"id":"4e029a0e-8b9c-5e32-b41e-f98ca84ea6e6","slug":"mouse-tissue-iron-mobilization","display_name":"Mouse release of stored iron from hepatocytes and reticuloendothelial cells","entity_type_key":"cellular_process"},"evidence_count":1,"mechanism_event":{"id":"27de6841-29f2-521c-8c23-dac455e45564","stable_key":"0ad8610d-d575-5870-b7cd-763a9f750783:copper-cp-iron-mobilization-event","event_type":"biochemical_relationship","label":"The main defect was moving stored iron out of cells.","description":"Cp-null mice had impaired iron release from hepatocytes and reticuloendothelial cells, while measured iron absorption and plasma turnover were comparable to controls.","status":"provisional","compartment":null,"participants":[{"entity":{"id":"89bcaf42-b4ab-5760-8c2e-44eace10cee0","slug":"iron","display_name":"Iron","entity_type_key":"nutrient_element"},"role":"retained nutrient","stoichiometry":null,"state_label":"","sequence_order":0,"notes":""},{"entity":{"id":"34665f8c-8d15-577c-9244-75a3c6ca61f8","slug":"mouse-cp","display_name":"Mouse ceruloplasmin Cp","entity_type_key":"protein"},"role":"subject","stoichiometry":null,"state_label":"","sequence_order":1,"notes":""},{"entity":{"id":"4e029a0e-8b9c-5e32-b41e-f98ca84ea6e6","slug":"mouse-tissue-iron-mobilization","display_name":"Mouse release of stored iron from hepatocytes and reticuloendothelial cells","entity_type_key":"cellular_process"},"role":"target","stoichiometry":null,"state_label":"","sequence_order":2,"notes":""}]},"contexts":[{"dimension":"availability_state","value_text":"machinery_impairment","comparator":null,"unit":null,"notes":"Imported condition classification; unverified.","entity":null},{"dimension":"evidence_span","value_text":"{\"source_cache\": \"artifacts/copper-research/10485908.abstract.txt\", \"locator\": \"Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets\", \"file_sha256\": \"2feaccc19bf8f4480643a918de9300a6c224935b47c24e251d96050599e3b067\", \"start_char\": 0, \"end_char\": 1368, \"text_sha256\": \"2feaccc19bf8f4480643a918de9300a6c224935b47c24e251d96050599e3b067\"}","comparator":null,"unit":null,"notes":"","entity":null},{"dimension":"experimental_model","value_text":"Ceruloplasmin gene disruption and ferrokinetics","comparator":null,"unit":null,"notes":"","entity":null},{"dimension":"exposure","value_text":"Cp knockout followed through one year","comparator":null,"unit":null,"notes":"","entity":null},{"dimension":"limitations","value_text":"Genetic ceruloplasmin absence differs from dietary copper shortage; normal intestinal absorption in this experiment does not imply all copper-deficient states absorb iron normally.","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":"Mouse","comparator":null,"unit":null,"notes":"","entity":null},{"dimension":"plain_language","value_text":"The main defect was moving stored iron out of cells.","comparator":null,"unit":null,"notes":"","entity":null},{"dimension":"primary_references","value_text":"[copper-p10485908] Targeted gene disruption reveals an essential role for ceruloplasmin in cellular iron efflux. (1999). https://pubmed.ncbi.nlm.nih.gov/10485908/ DOI: 10.1073/pnas.96.19.10812","comparator":null,"unit":null,"notes":"","entity":null},{"dimension":"tissue_or_cell_type","value_text":"Liver, spleen and reticuloendothelial cells","comparator":null,"unit":null,"notes":"","entity":null},{"dimension":"trigger_kind","value_text":"machinery_impairment","comparator":null,"unit":null,"notes":"Imported condition classification; unverified.","entity":null}],"evidence":[{"id":"306deb59-5654-5b16-8028-aab1d2334a52","evidence_kind":"source_excerpt","locator":"Lines 793-804","start_line":793,"end_line":804,"excerpt":"### copper-cp-iron-mobilization\nCp-null mice had impaired iron release from hepatocytes and reticuloendothelial cells, while measured iron absorption and plasma turnover were comparable to controls.\nCondition category: machinery_impairment\nnutrient_topic: Copper research collection; topical membership is not evidence of a direct dietary effect.\nplain_language: The main defect was moving stored iron out of cells.\norganism: Mouse\ntissue_or_cell_type: Liver, spleen and reticuloendothelial cells\nexperimental_model: Ceruloplasmin gene disruption and ferrokinetics\nlimitations: Genetic ceruloplasmin absence differs from dietary copper shortage; normal intestinal absorption in this experiment does not imply all copper-deficient states absorb iron normally.\nexposure: Cp knockout followed through one year\nevidence_span: {\"source_cache\": \"artifacts/copper-research/10485908.abstract.txt\", \"locator\": \"Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets\", \"file_sha256\": \"2feaccc19bf8f4480643a918de9300a6c224935b47c24e251d96050599e3b067\", \"start_char\": 0, \"end_char\": 1368, \"text_sha256\": \"2feaccc19bf8f4480643a918de9300a6c224935b47c24e251d96050599e3b067\"}\n[copper-p10485908] Targeted gene disruption reveals an essential role for ceruloplasmin in cellular iron efflux. 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