Triggering the Interferon Antiviral Response Through an IKK-Related Pathway

By Sonia Sharma, B. tenOever, N. Grandvaux, Guo-Ping Zhou, R. Lin, J. Hiscott. Science, 2003

1,811 citations recorded by the source corpus.

View Paper: https://www.semanticscholar.org/paper/502bc520c6c95ce36ca1de4048a437ec476f7c31

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Citations in the corpus

VSV strains with defects in their ability to shutdown innate immunity are potent systemic anti-cancer agents. (2003, background): “Upon viral entry into the host cell, the transcription tent with the idea that the rapid and robust local stimulation of interferon by AV strains in mice successfully attenuates virus factors c-JUN and IRF-3 are phosphorylated by JNK and a recently identified virally activated kinase (Sharma et al.,”
TRAM is specifically involved in the Toll-like receptor 4–mediated MyD88-independent signaling pathway (2003, background): “Furthermore, two noncanonical IκB kinases (IKKs), IKK- i (also called IKKe) and TBK1 (also called T2K), interact with TRIF, activate IRF-3 and, finally, lead to IFN-β inductio”
TLR3: interferon induction by double-stranded RNA including poly(I:C). (2008, background): “TICAM-1 activates the transcription factors IRF-3, NF-κB and AP-1, leading to the induction of type I IFN, cytokine/chemokine production and DC maturation.”
Innate immune recognition of viral infection (2006, background): “In response to the stimulation, IRF3 is phosphorylated by noncanonical IKKs, TBK1 (also called NAK or T2K) and IKKi (also called IKKe) and then translocates into the nucleu”
RIP1 is an essential mediator of Toll-like receptor 3–induced NF-κB activation (2004, background): “Trif overexpression strongly activates IFN-β reporter genes, which correlates with the capacity of Trif to physically interact not only with interferon-regulatory factor 3 (IRF-3) but also with the IRF-3-activating kinase TBK-1 (refs”
Interferons and viruses: an interplay between induction, signalling, antiviral responses and virus countermeasures. (2008, background): “TBK-1 and the related IKKe (also known as IKKi) are the kinases that interact with and phosphorylate IRF-3 (Fitzgerald et al., 2003; Sharma et al., 2003).”
The interferon response circuit: Induction and suppression by pathogenic viruses (2005, neutral): “Two InB kinase (IKK)-related kinases, IKK( and TANK-binding kinase-1 (TBK-1), are known to phosphorylate the transcription factor IRF-3 (Fitzgerald et al., 2003; Sharma et al., 2003) .”
IPS-1, an adaptor triggering RIG-I- and Mda5-mediated type I interferon induction (2005, background): “Trif then recruits the protein kinase TBK1 (also called NAK or T2K) and its relative IKKi (also called IKKe), which catalyze transcription factors IRF3 and IRF7 and allow them to translocate into the nucleu”