{"id":"eb54efa0-9aee-5d4f-8fa7-d7d065e04e5f","stable_key":"0ad8610d-d575-5870-b7cd-763a9f750783:copper-intestinal-ctr1-iron","predicate":"deletion_increases","statement":"Mice lacking intestinal Ctr1 developed hepatic iron overload alongside systemic copper deficiency.","claim_class":"mechanistic","status":"source_derived_draft","evidence_grade":"ungraded","direction":"context_dependent","is_public":true,"mechanism_event_id":"a25423b5-851d-5a22-a91c-c9aa304aaa9c","mechanism_event_label":"A copper transport defect also disrupted where iron accumulated.","subject":{"id":"9b443d47-b3cc-538d-ad34-e93b5c7880c8","slug":"mouse-slc31a1","display_name":"Mouse copper transporter Ctr1 / Slc31a1","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":"a25423b5-851d-5a22-a91c-c9aa304aaa9c","stable_key":"0ad8610d-d575-5870-b7cd-763a9f750783:copper-intestinal-ctr1-iron-event","event_type":"biochemical_relationship","label":"A copper transport defect also disrupted where iron accumulated.","description":"Mice lacking intestinal Ctr1 developed hepatic iron overload alongside systemic copper deficiency.","status":"provisional","compartment":null,"participants":[{"entity":{"id":"89bcaf42-b4ab-5760-8c2e-44eace10cee0","slug":"iron","display_name":"Iron","entity_type_key":"nutrient_element"},"role":"affected nutrient","stoichiometry":null,"state_label":"","sequence_order":0,"notes":""},{"entity":{"id":"9b443d47-b3cc-538d-ad34-e93b5c7880c8","slug":"mouse-slc31a1","display_name":"Mouse copper transporter Ctr1 / Slc31a1","entity_type_key":"protein"},"role":"subject","stoichiometry":null,"state_label":"","sequence_order":1,"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":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/16950140.abstract.txt\", \"locator\": \"Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets\", \"file_sha256\": \"08532f69fd9530033f8d9afcece9249fc50dd425f57313e120f55ea81cee8f98\", \"start_char\": 0, \"end_char\": 1026, \"text_sha256\": \"08532f69fd9530033f8d9afcece9249fc50dd425f57313e120f55ea81cee8f98\"}","comparator":null,"unit":null,"notes":"","entity":null},{"dimension":"experimental_model","value_text":"Intestinal epithelial Ctr1 knockout mice","comparator":null,"unit":null,"notes":"","entity":null},{"dimension":"exposure","value_text":"Intestinal Ctr1 deletion; postnatal copper rescue","comparator":null,"unit":null,"notes":"","entity":null},{"dimension":"limitations","value_text":"Genetic intestinal transport failure differs from low dietary intake. The indexed abstract does not establish the administration route of the rescue dose.","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":"A copper transport defect also disrupted where iron accumulated.","comparator":null,"unit":null,"notes":"","entity":null},{"dimension":"primary_references","value_text":"[copper-p16950140] Ctr1 drives intestinal copper absorption and is essential for growth, iron metabolism, and neonatal cardiac function. (2006). https://pubmed.ncbi.nlm.nih.gov/16950140/ DOI: 10.1016/j.cmet.2006.08.009","comparator":null,"unit":null,"notes":"","entity":null},{"dimension":"tissue_or_cell_type","value_text":"Intestine and peripheral organs","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":"6df179d4-3877-5e07-9f02-7546cb9ccc15","evidence_kind":"source_excerpt","locator":"Lines 325-336","start_line":325,"end_line":336,"excerpt":"### copper-intestinal-ctr1-iron\nMice lacking intestinal Ctr1 developed hepatic iron overload alongside systemic copper deficiency.\nCondition category: machinery_impairment\nnutrient_topic: Copper research collection; topical membership is not evidence of a direct dietary effect.\nplain_language: A copper transport defect also disrupted where iron accumulated.\norganism: Mouse\ntissue_or_cell_type: Intestine and peripheral organs\nexperimental_model: Intestinal epithelial Ctr1 knockout mice\nlimitations: Genetic intestinal transport failure differs from low dietary intake. The indexed abstract does not establish the administration route of the rescue dose.\nexposure: Intestinal Ctr1 deletion; postnatal copper rescue\nevidence_span: {\"source_cache\": \"artifacts/copper-research/16950140.abstract.txt\", \"locator\": \"Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets\", \"file_sha256\": \"08532f69fd9530033f8d9afcece9249fc50dd425f57313e120f55ea81cee8f98\", \"start_char\": 0, \"end_char\": 1026, \"text_sha256\": \"08532f69fd9530033f8d9afcece9249fc50dd425f57313e120f55ea81cee8f98\"}\n[copper-p16950140] Ctr1 drives intestinal copper absorption and is essential for growth, iron metabolism, and neonatal cardiac function. (2006). https://pubmed.ncbi.nlm.nih.gov/16950140/ DOI: 10.1016/j.cmet.2006.08.009","model_system":"Intestinal epithelial Ctr1 knockout mice","directness":"author_interpretation","verification_status":"source_derived_draft","notes":"Exact curation-document quotation, not publisher quotation. Study references: [copper-p16950140] Ctr1 drives intestinal copper absorption and is essential for growth, iron metabolism, and neonatal cardiac function. (2006). https://pubmed.ncbi.nlm.nih.gov/16950140/ DOI: 10.1016/j.cmet.2006.08.009","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}