{"id":"47e047f7-ec93-5dbe-8f7c-a2f2d146f9b9","stable_key":"96d9034a-2550-5f3c-b767-1767c982533c:glucoside-leaves-the-interferon-block-unchanged","predicate":"no_detected_effect_on","statement":"Influenza A infection activated 368 genes in RIG-I signalling, inflammatory response and interferon alpha/beta signalling, and this block was reported as unaffected by lariciresinol-4-β-D-glucopyranoside treatment.","claim_class":"mechanistic","status":"source_derived_draft","evidence_grade":"ungraded","direction":"neutral","is_public":true,"mechanism_event_id":"2e7b413f-ea0a-54c1-8c4d-16e0e7e13152","mechanism_event_label":"Influenza A infection activated 368 genes in RIG-I signalling, inflammatory response and interferon alpha/beta signalling, and this block was reported as unaffected by lariciresinol-4-β-D-glucopyranoside treatment.","subject":{"id":"6f5b3b44-5ea8-5441-8653-89a548721566","slug":"lariciresinol-4-o-glucoside","display_name":"Lariciresinol-4-O-beta-D-glucopyranoside","entity_type_key":"small_molecule"},"object":{"id":"2847c261-0ce3-5551-873e-01044ab59592","slug":"influenza-rig-i-interferon-gene-block","display_name":"Influenza-induced RIG-I and interferon gene set","entity_type_key":"cellular_process"},"evidence_count":1,"mechanism_event":{"id":"2e7b413f-ea0a-54c1-8c4d-16e0e7e13152","stable_key":"96d9034a-2550-5f3c-b767-1767c982533c:glucoside-leaves-the-interferon-block-unchanged-event","event_type":"observed_relationship","label":"Influenza A infection activated 368 genes in RIG-I signalling, inflammatory response and interferon alpha/beta signalling, and this block was reported as unaffected by lariciresinol-4-β-D-glucopyranoside treatment.","description":"Influenza A infection activated 368 genes in RIG-I signalling, inflammatory response and interferon alpha/beta signalling, and this block was reported as unaffected by lariciresinol-4-β-D-glucopyranoside treatment.","status":"provisional","compartment":null,"participants":[{"entity":{"id":"6f5b3b44-5ea8-5441-8653-89a548721566","slug":"lariciresinol-4-o-glucoside","display_name":"Lariciresinol-4-O-beta-D-glucopyranoside","entity_type_key":"small_molecule"},"role":"subject","stoichiometry":null,"state_label":"","sequence_order":0,"notes":""},{"entity":{"id":"2847c261-0ce3-5551-873e-01044ab59592","slug":"influenza-rig-i-interferon-gene-block","display_name":"Influenza-induced RIG-I and interferon gene set","entity_type_key":"cellular_process"},"role":"target","stoichiometry":null,"state_label":"","sequence_order":1,"notes":""}]},"contexts":[{"dimension":"duration","value_text":"Not stated here","comparator":null,"unit":null,"notes":"","entity":null},{"dimension":"evidence_access","value_text":"Primary PubMed abstract and indexed metadata reviewed. Full-text method details not stated here remain unresolved.","comparator":null,"unit":null,"notes":"","entity":null},{"dimension":"experimental_model","value_text":"A549 lung epithelial cells infected with influenza A virus","comparator":null,"unit":null,"notes":"","entity":null},{"dimension":"exposure","value_text":"Lariciresinol-4-β-D-glucopyranoside","comparator":null,"unit":null,"notes":"","entity":null},{"dimension":"limitations","value_text":"A transcriptomic null across a gene set rather than a functional interferon assay.","comparator":null,"unit":null,"notes":"","entity":null},{"dimension":"organism","value_text":"A549 lung epithelial cells infected with influenza A virus","comparator":null,"unit":null,"notes":"","entity":null},{"dimension":"plain_language","value_text":"Influenza A infection activated 368 genes in RIG-I signalling, inflammatory response and interferon alpha/beta signalling, and this block was reported as unaffected by lariciresinol-4-β-D-glucopyranoside treatment.","comparator":null,"unit":null,"notes":"","entity":null},{"dimension":"primary_references","value_text":"Transcriptomic Analysis of Human Lung Epithelial Cells Infected with Influenza A Virus and Treated with Lariciresinol-4-β-D-glucopyranoside. (2017). https://pubmed.ncbi.nlm.nih.gov/28273165/ DOI: 10.1371/journal.pone.0173058","comparator":null,"unit":null,"notes":"","entity":null},{"dimension":"route","value_text":"In vitro","comparator":null,"unit":null,"notes":"","entity":null},{"dimension":"tissue","value_text":"Transcriptome by high-throughput RNA sequencing","comparator":null,"unit":null,"notes":"","entity":null}],"evidence":[{"id":"3b91a28c-9fe2-5d53-94da-f517affc5b1b","evidence_kind":"source_excerpt","locator":"Lines 121-130","start_line":121,"end_line":130,"excerpt":"## glucoside-leaves-the-interferon-block-unchanged\nInfluenza A infection activated 368 genes in RIG-I signalling, inflammatory response and interferon alpha/beta signalling, and this block was reported as unaffected by lariciresinol-4-β-D-glucopyranoside treatment.\nModel/species: A549 lung epithelial cells infected with influenza A virus\nTissue/system: Transcriptome by high-throughput RNA sequencing\nExposure: Lariciresinol-4-β-D-glucopyranoside\nRoute: In vitro\nDuration: Not stated here\nLimits: A transcriptomic null across a gene set rather than a functional interferon assay.\nPrimary reference: Transcriptomic Analysis of Human Lung Epithelial Cells Infected with Influenza A Virus and Treated with Lariciresinol-4-β-D-glucopyranoside. (2017). https://pubmed.ncbi.nlm.nih.gov/28273165/ DOI: 10.1371/journal.pone.0173058\nAccess: Primary PubMed abstract and indexed metadata reviewed. Full-text method details not stated here remain unresolved.","model_system":"","directness":"reported_statement","verification_status":"source_derived_draft","notes":"","relationship":"supports","weight":1.0,"link_notes":"","source":{"id":"48c58761-0291-5bad-a926-75e904b2d802","stable_key":"import-96d9034a-2550-5f3c-b767-1767c982533c","title":"Lariciresinol: five molecules under one name, and the mechanisms each one carries (2026-09-22)","document_type":"imported_text","citation_label":"Original AI-assisted curation of twelve primary studies, every abstract read and all DOIs cross-checked against live PubMed metadata. Mechanism edges only, with no conclusion or claim of benefit recorded. Three author clusters account for eight of the twelve and carry shared laboratory keys. Study-specific concentrations, negative findings and limitations retained. Not publisher full text.","file_path":"","sha256":"6bf0015b7ff727b7a80d693dd18ffdd227d0e16ae45d9e85a5f81fa733edd3a4","revision_id":"219d9b0c-1a71-5e27-8d6c-7b3e77a594c6","review_status":"unverified_draft","notes":""}}],"relations":[],"conflicts":[],"corrections":[],"research":null}