{"id":"b90e089c-038a-5a1b-834b-e3a588ea0dc1","stable_key":"e1af6d55-ced5-56c9-9a2d-8cc2ae6ec3ff:nasunin-ikba-preservation","predicate":"suppressed_degradation_of","statement":"Nasunin suppressed stimulus-associated I-kappa-B-alpha degradation.","claim_class":"mechanistic","status":"source_derived_draft","evidence_grade":"ungraded","direction":"context_dependent","is_public":true,"mechanism_event_id":"bd6879ae-592d-579e-b3da-700cd81c6ec8","mechanism_event_label":"The inhibitory control protein was better retained.","subject":{"id":"6553997f-f098-5507-95b4-0fdb8aac491d","slug":"nasunin","display_name":"Nasunin","entity_type_key":"small_molecule"},"object":{"id":"f9782d80-c880-5839-ab60-535bb9808f34","slug":"mouse-nfkbia","display_name":"Mouse inhibitor of NF-kappa-B alpha / Nfkbia","entity_type_key":"protein"},"evidence_count":1,"mechanism_event":{"id":"bd6879ae-592d-579e-b3da-700cd81c6ec8","stable_key":"e1af6d55-ced5-56c9-9a2d-8cc2ae6ec3ff:nasunin-ikba-preservation-event","event_type":"biochemical_relationship","label":"The inhibitory control protein was better retained.","description":"Nasunin suppressed stimulus-associated I-kappa-B-alpha degradation.","status":"provisional","compartment":null,"participants":[{"entity":{"id":"e96aad69-74fb-55c6-8378-7d5c281003eb","slug":"lipopolysaccharide","display_name":"Lipopolysaccharide","entity_type_key":"chemical_species"},"role":"challenge","stoichiometry":null,"state_label":"","sequence_order":0,"notes":""},{"entity":{"id":"6553997f-f098-5507-95b4-0fdb8aac491d","slug":"nasunin","display_name":"Nasunin","entity_type_key":"small_molecule"},"role":"subject","stoichiometry":null,"state_label":"","sequence_order":1,"notes":""},{"entity":{"id":"f9782d80-c880-5839-ab60-535bb9808f34","slug":"mouse-nfkbia","display_name":"Mouse inhibitor of NF-kappa-B alpha / Nfkbia","entity_type_key":"protein"},"role":"target","stoichiometry":null,"state_label":"","sequence_order":2,"notes":""}]},"contexts":[{"dimension":"evidence_span","value_text":"{\"source_cache\": \"artifacts/nasunin-research/28812425.abstract.txt\", \"locator\": \"Primary indexed abstract; zero-based, end-exclusive Unicode character offsets\", \"file_sha256\": \"7a697b4eb979f1e6349bc79f4d2ed0d3994de51dfed777a71fb04740819eeabf\", \"start_char\": 0, \"end_char\": 1094, \"text_sha256\": \"7a697b4eb979f1e6349bc79f4d2ed0d3994de51dfed777a71fb04740819eeabf\"}","comparator":null,"unit":null,"notes":"","entity":null},{"dimension":"experimental_model","value_text":"LPS-stimulated macrophage experiments","comparator":null,"unit":null,"notes":"","entity":null},{"dimension":"exposure","value_text":"Dose-dependent nasunin treatment; exact dose/time not reported in indexed abstract","comparator":null,"unit":null,"notes":"","entity":null},{"dimension":"limitations","value_text":"These measurements do not prove direct binding to Akt, p38, NF-kappa-B or NOS2; reduced NOS2 expression is not direct enzyme inhibition. Response is LPS/cell-context dependent.","comparator":null,"unit":null,"notes":"","entity":null},{"dimension":"nutrient_topic","value_text":"Nasunin research collection; topical membership is not evidence of a direct dietary effect.","comparator":null,"unit":null,"notes":"","entity":{"slug":"nasunin","display_name":"Nasunin","entity_type_key":"small_molecule"}},{"dimension":"organism","value_text":"Mouse RAW264 macrophages","comparator":null,"unit":null,"notes":"","entity":null},{"dimension":"plain_language","value_text":"The inhibitory control protein was better retained.","comparator":null,"unit":null,"notes":"","entity":null},{"dimension":"primary_references","value_text":"[nasunin-p28812425] Nasunin inhibits the lipopolysaccharide-induced pro-inflammatory mediator production in RAW264 mouse macrophages by suppressing ROS-mediated activation of PI3 K/Akt/NF-κB and p38 signaling pathways. (2017). https://pubmed.ncbi.nlm.nih.gov/28812425/ DOI: 10.1080/09168451.2017.1362973","comparator":null,"unit":null,"notes":"","entity":null},{"dimension":"tissue_or_cell_type","value_text":"Inflammatory mediator secretion and signaling","comparator":null,"unit":null,"notes":"","entity":null}],"evidence":[{"id":"15359ca2-a012-590b-95e4-4e24352ec287","evidence_kind":"source_excerpt","locator":"Lines 250-261","start_line":250,"end_line":261,"excerpt":"### nasunin-ikba-preservation\nNasunin suppressed stimulus-associated I-kappa-B-alpha degradation.\nCondition category: normal\nnutrient_topic: Nasunin research collection; topical membership is not evidence of a direct dietary effect.\nplain_language: The inhibitory control protein was better retained.\norganism: Mouse RAW264 macrophages\ntissue_or_cell_type: Inflammatory mediator secretion and signaling\nexperimental_model: LPS-stimulated macrophage experiments\nlimitations: These measurements do not prove direct binding to Akt, p38, NF-kappa-B or NOS2; reduced NOS2 expression is not direct enzyme inhibition. Response is LPS/cell-context dependent.\nexposure: Dose-dependent nasunin treatment; exact dose/time not reported in indexed abstract\nevidence_span: {\"source_cache\": \"artifacts/nasunin-research/28812425.abstract.txt\", \"locator\": \"Primary indexed abstract; zero-based, end-exclusive Unicode character offsets\", \"file_sha256\": \"7a697b4eb979f1e6349bc79f4d2ed0d3994de51dfed777a71fb04740819eeabf\", \"start_char\": 0, \"end_char\": 1094, \"text_sha256\": \"7a697b4eb979f1e6349bc79f4d2ed0d3994de51dfed777a71fb04740819eeabf\"}\n[nasunin-p28812425] Nasunin inhibits the lipopolysaccharide-induced pro-inflammatory mediator production in RAW264 mouse macrophages by suppressing ROS-mediated activation of PI3 K/Akt/NF-κB and p38 signaling pathways. (2017). https://pubmed.ncbi.nlm.nih.gov/28812425/ DOI: 10.1080/09168451.2017.1362973","model_system":"LPS-stimulated macrophage experiments","directness":"author_interpretation","verification_status":"source_derived_draft","notes":"Exact curation-document quotation, not publisher quotation. Study references: [nasunin-p28812425] Nasunin inhibits the lipopolysaccharide-induced pro-inflammatory mediator production in RAW264 mouse macrophages by suppressing ROS-mediated activation of PI3 K/Akt/NF-κB and p38 signaling pathways. 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