Component

Influenza-induced RIG-I and interferon gene set

The 368 genes activated by infection in RIG-I signalling, inflammatory response and interferon alpha/beta signalling.

1 recorded relationships. Experimental role, claim status and evidence remain attached to each record.

How nutrients influence it

Every nutrient with a recorded effect on this component, credited to the nutrient that acted rather than the chapter that recorded it. Open a nutrient to see the findings and the conditions they were measured under.

How nutrients reach it in more than one step

Chains of two or more recorded steps that end here, grouped by the nutrient they start from. Each step is a separate finding, so a chain is a route a mechanism could take, not proof that it does.

Tracing routes…

What it does

Every recorded relationship this component is part of, grouped by its role. Plain wording comes first; the technical statement follows.

Recorded relationships

What acts on it

  1. 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.

    Experimental context and source evidence
    duration
    Not stated here
    evidence_access
    Primary PubMed abstract and indexed metadata reviewed. Full-text method details not stated here remain unresolved.
    experimental_model
    A549 lung epithelial cells infected with influenza A virus
    exposure
    Lariciresinol-4-β-D-glucopyranoside
    limitations
    A transcriptomic null across a gene set rather than a functional interferon assay.
    organism
    A549 lung epithelial cells infected with influenza A virus
    plain_language
    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.
    primary_references
    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
    route
    In vitro
    tissue
    Transcriptome by high-throughput RNA sequencing

    Lariciresinol: five molecules under one name, and the mechanisms each one carries (2026-09-22) · lines 121–130

    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. · supports · · source_derived_draft · unverified_draft

    ## glucoside-leaves-the-interferon-block-unchanged 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. Model/species: A549 lung epithelial cells infected with influenza A virus Tissue/system: Transcriptome by high-throughput RNA sequencing Exposure: Lariciresinol-4-β-D-glucopyranoside Route: In vitro Duration: Not stated here Limits: A transcriptomic null across a gene set rather than a functional interferon assay. Primary 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 Access: Primary PubMed abstract and indexed metadata reviewed. Full-text method details not stated here remain unresolved.
    Complete structured claim and evidence

In the sources

Preserved passages that mention this component, quoted exactly. Open one to read it in context.

    This is a research prototype built from draft material. It is not medical advice, and its statements still await verification against the original studies.

    Evidence, AI assistance and curation standards