期刊
JOURNAL OF VIROLOGY
卷 86, 期 18, 页码 10211-10217出版社
AMER SOC MICROBIOLOGY
DOI: 10.1128/JVI.00323-12
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资金
- Deutsche Forschungsgemeinschaft (DFG) [Lu477/16-1]
- BMBF zoonosis network FluResearchNet,
- IZKF from the University of Muenster Medical School [Lud2/032/06]
Influenza A virus (IAV) infection of epithelial cells activates NF-kappa B transcription factors via the canonical NF-kappa B signaling pathway, which modulates both the antiviral immune response and viral replication. Since almost nothing is known so far about a function of noncanonical NF-kappa B signaling after IAV infection, we tested infected cells for activation of p52 and RelB. We show that the viral NS1 protein strongly inhibits RIG-I-mediated noncanonical NF-kappa B activation and expression of the noncanonical target gene CCL19.
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