{"id":"2f0bb518-7e7a-5561-a6d8-96c30275c1df","stable_key":"3ad23a58-d6a8-5554-81d6-9c83abd33087:akt2-null-sod3","predicate":"reported_comparison","statement":"Akt2-null vessels or vascular smooth-muscle cells had lower SOD3 activity, rescued by ATP7A overexpression.","claim_class":"mechanistic","status":"source_derived_draft","evidence_grade":"ungraded","direction":"context_dependent","is_public":true,"mechanism_event_id":"2185b1f1-2e4e-5436-81f5-358d47d9f6cd","mechanism_event_label":"Akt2-null vessels or vascular smooth-muscle cells had lower SOD3 activity, rescued by ATP7A overexpression.","subject":{"id":"274e6147-68f0-5bad-bf64-543cdfc675dc","slug":"mouse-akt2-null","display_name":"Mouse Akt2-null genotype","entity_type_key":"gene"},"object":{"id":"d0d2556c-5006-5e20-8ad1-ac84e66677fd","slug":"mouse-sod3","display_name":"Mouse extracellular superoxide dismutase Sod3","entity_type_key":"protein"},"evidence_count":1,"mechanism_event":{"id":"2185b1f1-2e4e-5436-81f5-358d47d9f6cd","stable_key":"3ad23a58-d6a8-5554-81d6-9c83abd33087:akt2-null-sod3","event_type":"reported_comparison","label":"Akt2-null vessels or vascular smooth-muscle cells had lower SOD3 activity, rescued by ATP7A overexpression.","description":"","status":"provisional","compartment":null,"participants":[{"entity":{"id":"274e6147-68f0-5bad-bf64-543cdfc675dc","slug":"mouse-akt2-null","display_name":"Mouse Akt2-null genotype","entity_type_key":"gene"},"role":"experimental_actor","stoichiometry":null,"state_label":"","sequence_order":0,"notes":""},{"entity":{"id":"d0d2556c-5006-5e20-8ad1-ac84e66677fd","slug":"mouse-sod3","display_name":"Mouse extracellular superoxide dismutase Sod3","entity_type_key":"protein"},"role":"measured_endpoint","stoichiometry":null,"state_label":"","sequence_order":1,"notes":""},{"entity":{"id":"4bd9efee-f043-5284-9e7a-13ef3c1128f0","slug":"mouse-akt2","display_name":"Mouse protein kinase Akt2","entity_type_key":"protein"},"role":"context_participant","stoichiometry":null,"state_label":"","sequence_order":2,"notes":""},{"entity":{"id":"4402b6dd-887c-52c1-befa-789a47b8dc38","slug":"mouse-atp7a","display_name":"Mouse copper-transporting ATPase Atp7a","entity_type_key":"protein"},"role":"context_participant","stoichiometry":null,"state_label":"","sequence_order":3,"notes":""},{"entity":{"id":"9f0afdde-1ec1-5c8a-bb5e-f3b2b75f67f6","slug":"copper","display_name":"Copper","entity_type_key":"nutrient_element"},"role":"context_participant","stoichiometry":null,"state_label":"","sequence_order":4,"notes":""}]},"contexts":[{"dimension":"availability_state","value_text":"machinery_impairment","comparator":null,"unit":null,"notes":"Imported condition classification; unverified.","entity":null},{"dimension":"curation_topic","value_text":"copper","comparator":null,"unit":null,"notes":"","entity":{"slug":"copper","display_name":"Copper","entity_type_key":"nutrient_element"}},{"dimension":"experimental_condition","value_text":"Akt2 loss","comparator":"Control; ATP7A overexpression tested as rescue","unit":null,"notes":"Condition belongs to the full experimental contrast; do not separate a joint intervention.","entity":{"slug":"mouse-akt2-null","display_name":"Mouse Akt2-null genotype","entity_type_key":"gene"}},{"dimension":"experimental_contrast","value_text":"{\"intervention\": \"Akt2 loss\", \"comparator\": \"Control; ATP7A overexpression tested as rescue\", \"endpoint\": \"SOD3 activity\", \"effect_direction\": \"decrease\", \"combination\": \"single\", \"conditions\": [{\"entity_slug\": \"mouse-akt2-null\", \"state\": \"Akt2 loss\"}]}","comparator":null,"unit":null,"notes":"Explicit extracted experimental comparison; source-derived draft.","entity":null},{"dimension":"experimental_model","value_text":"Mouse Akt2-null vascular experiments; primary abstract reviewed","comparator":null,"unit":null,"notes":"","entity":null},{"dimension":"limitations","value_text":"Genetic signaling defect, not dietary copper deficiency. Mechanistic phosphorylation experiments are not substituted for human causal evidence.","comparator":null,"unit":null,"notes":"","entity":null},{"dimension":"primary_references","value_text":"Sudhahar et al. 2018; DOI:10.1161/ATVBAHA.117.309819; PMID:29301787; https://pubmed.ncbi.nlm.nih.gov/29301787/","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":"631fbb67-62c7-5d49-bad1-b2d1b4b72ad2","evidence_kind":"source_excerpt","locator":"Lines 42-42","start_line":42,"end_line":42,"excerpt":"Akt2-null vessels or vascular smooth-muscle cells had lower SOD3 activity, rescued by ATP7A overexpression. Model: Mouse Akt2-null vascular experiments; primary abstract reviewed. Limits: Genetic signaling defect, not dietary copper deficiency. Mechanistic phosphorylation experiments are not substituted for human causal evidence. 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