{"id":"c46326ae-6837-567f-b61e-35b12a06b469","stable_key":"0ad8610d-d575-5870-b7cd-763a9f750783:copper-cu-ulk2","predicate":"supports_kinase_activity_of","statement":"Direct copper interaction also supported ULK2 kinase activity.","claim_class":"mechanistic","status":"source_derived_draft","evidence_grade":"ungraded","direction":"context_dependent","is_public":true,"mechanism_event_id":"b1bfd807-7735-5a77-98b7-e8b72f6aa721","mechanism_event_label":"The related recycling enzyme has a separately recorded copper interaction.","subject":{"id":"9f0afdde-1ec1-5c8a-bb5e-f3b2b75f67f6","slug":"copper","display_name":"Copper","entity_type_key":"nutrient_element"},"object":{"id":"371e0a13-f76b-557c-b12c-1da980a9f5c1","slug":"ulk2","display_name":"Human unc-51-like autophagy activating kinase ULK2","entity_type_key":"protein"},"evidence_count":1,"mechanism_event":{"id":"b1bfd807-7735-5a77-98b7-e8b72f6aa721","stable_key":"0ad8610d-d575-5870-b7cd-763a9f750783:copper-cu-ulk2-event","event_type":"biochemical_relationship","label":"The related recycling enzyme has a separately recorded copper interaction.","description":"Direct copper interaction also supported ULK2 kinase activity.","status":"provisional","compartment":null,"participants":[{"entity":{"id":"9f0afdde-1ec1-5c8a-bb5e-f3b2b75f67f6","slug":"copper","display_name":"Copper","entity_type_key":"nutrient_element"},"role":"subject","stoichiometry":null,"state_label":"","sequence_order":0,"notes":""},{"entity":{"id":"371e0a13-f76b-557c-b12c-1da980a9f5c1","slug":"ulk2","display_name":"Human unc-51-like autophagy activating kinase ULK2","entity_type_key":"protein"},"role":"target","stoichiometry":null,"state_label":"","sequence_order":1,"notes":""}]},"contexts":[{"dimension":"evidence_span","value_text":"{\"source_cache\": \"artifacts/copper-research/32203415.abstract.txt\", \"locator\": \"Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets\", \"file_sha256\": \"f248044309434e00cd35941d0e525a9c73a07e8d78eead20f7d7b6bdcb5f2915\", \"start_char\": 0, \"end_char\": 1077, \"text_sha256\": \"f248044309434e00cd35941d0e525a9c73a07e8d78eead20f7d7b6bdcb5f2915\"}","comparator":null,"unit":null,"notes":"","entity":null},{"dimension":"experimental_model","value_text":"Recombinant kinase assays, genetic perturbations and lung tumor models","comparator":null,"unit":null,"notes":"","entity":null},{"dimension":"exposure","value_text":"Copper exposure, copper-binding mutations and Ctr1 deletion","comparator":null,"unit":null,"notes":"","entity":null},{"dimension":"limitations","value_text":"Preclinical molecular evidence; not proof that copper supplementation improves autophagy in healthy people or that chelation improves cancer survival.","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 recombinant ULK1/ULK2 with complementary mouse systems","comparator":null,"unit":null,"notes":"","entity":null},{"dimension":"plain_language","value_text":"The related recycling enzyme has a separately recorded copper interaction.","comparator":null,"unit":null,"notes":"","entity":null},{"dimension":"primary_references","value_text":"[copper-p32203415] Copper is an essential regulator of the autophagic kinases ULK1/2 to drive lung adenocarcinoma. (2020). https://pubmed.ncbi.nlm.nih.gov/32203415/ DOI: 10.1038/s41556-020-0481-4","comparator":null,"unit":null,"notes":"","entity":null},{"dimension":"tissue_or_cell_type","value_text":"Autophagy signaling","comparator":null,"unit":null,"notes":"","entity":null}],"evidence":[{"id":"11b32a46-8427-5528-b4f8-01b922f363a9","evidence_kind":"source_excerpt","locator":"Lines 1248-1259","start_line":1248,"end_line":1259,"excerpt":"### copper-cu-ulk2\nDirect copper interaction also supported ULK2 kinase activity.\nCondition category: normal\nnutrient_topic: Copper research collection; topical membership is not evidence of a direct dietary effect.\nplain_language: The related recycling enzyme has a separately recorded copper interaction.\norganism: Human recombinant ULK1/ULK2 with complementary mouse systems\ntissue_or_cell_type: Autophagy signaling\nexperimental_model: Recombinant kinase assays, genetic perturbations and lung tumor models\nlimitations: Preclinical molecular evidence; not proof that copper supplementation improves autophagy in healthy people or that chelation improves cancer survival.\nexposure: Copper exposure, copper-binding mutations and Ctr1 deletion\nevidence_span: {\"source_cache\": \"artifacts/copper-research/32203415.abstract.txt\", \"locator\": \"Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets\", \"file_sha256\": \"f248044309434e00cd35941d0e525a9c73a07e8d78eead20f7d7b6bdcb5f2915\", \"start_char\": 0, \"end_char\": 1077, \"text_sha256\": \"f248044309434e00cd35941d0e525a9c73a07e8d78eead20f7d7b6bdcb5f2915\"}\n[copper-p32203415] Copper is an essential regulator of the autophagic kinases ULK1/2 to drive lung adenocarcinoma. 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