{"id":"bbb34386-8ed0-52a7-9f80-85006643defc","stable_key":"0ad8610d-d575-5870-b7cd-763a9f750783:copper-cp-liver-iron","predicate":"loss_increases","statement":"By one year, Cp-null mice had three- to sixfold higher liver and spleen iron with increased serum ferritin.","claim_class":"mechanistic","status":"source_derived_draft","evidence_grade":"ungraded","direction":"context_dependent","is_public":true,"mechanism_event_id":"46eaf03e-3b32-5995-8696-a96a417f2bee","mechanism_event_label":"High storage markers can coexist with an iron-distribution problem.","subject":{"id":"34665f8c-8d15-577c-9244-75a3c6ca61f8","slug":"mouse-cp","display_name":"Mouse ceruloplasmin Cp","entity_type_key":"protein"},"object":{"id":"836f4b32-4d8b-5b4a-b308-8645c7a7ea9d","slug":"mouse-hepatic-iron-loading","display_name":"Mouse hepatic iron accumulation","entity_type_key":"cellular_process"},"evidence_count":1,"mechanism_event":{"id":"46eaf03e-3b32-5995-8696-a96a417f2bee","stable_key":"0ad8610d-d575-5870-b7cd-763a9f750783:copper-cp-liver-iron-event","event_type":"biochemical_relationship","label":"High storage markers can coexist with an iron-distribution problem.","description":"By one year, Cp-null mice had three- to sixfold higher liver and spleen iron with increased serum ferritin.","status":"provisional","compartment":null,"participants":[{"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":0,"notes":""},{"entity":{"id":"836f4b32-4d8b-5b4a-b308-8645c7a7ea9d","slug":"mouse-hepatic-iron-loading","display_name":"Mouse hepatic iron accumulation","entity_type_key":"cellular_process"},"role":"target","stoichiometry":null,"state_label":"","sequence_order":1,"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":"High storage markers can coexist with an iron-distribution problem.","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":"d3285e7f-adef-5447-a4e6-b55190effe14","evidence_kind":"source_excerpt","locator":"Lines 806-817","start_line":806,"end_line":817,"excerpt":"### copper-cp-liver-iron\nBy one year, Cp-null mice had three- to sixfold higher liver and spleen iron with increased serum ferritin.\nCondition category: machinery_impairment\nnutrient_topic: Copper research collection; topical membership is not evidence of a direct dietary effect.\nplain_language: High storage markers can coexist with an iron-distribution problem.\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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