IPS-1, an adaptor triggering RIG-I- and Mda5-mediated type I interferon induction

@article{Kawai2005IPS1AA,
  title={IPS-1, an adaptor triggering RIG-I- and Mda5-mediated type I interferon induction},
  author={Taro Kawai and Ken Takahashi and Shintaro Sato and Cevayir Coban and Himanshu Kumar and Hiroki Kato and Ken J. Ishii and Osamu Takeuchi and Shizuo Akira},
  journal={Nature Immunology},
  year={2005},
  volume={6},
  pages={981-988}
}
Type I interferons are central mediators for antiviral responses. Using high-throughput functional screening of interferon inducers, we have identified here a molecule we call interferon-β promoter stimulator 1 (IPS-1). Overexpression of IPS-1 induced type I interferon and interferon-inducible genes through activation of IRF3, IRF7 and NF-κB transcription factors. TBK1 and IKKi protein kinases were required for the IPS-1-mediated interferon induction. IPS-1 contained an N-terminal CARD-like… 
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IPS-1 is the sole adapter in both RIG-I and Mda5 signaling that mediates effective responses against a variety of RNA viruses, and is the critical role of IPS-1 in antiviral responses in vivo.
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The RNA-activated Protein Kinase Enhances the Induction of Interferon-β and Apoptosis Mediated by Cytoplasmic RNA Sensors*
TLDR
This work investigated the ability of short interfering RNAs, including T7 phage polymerase-synthesized RNA (PRNA), to selectively silence gene expression and to cause induction of IFN-β and apoptosis and found that PRNA-mediated gene silencing and associated nonspecific pro-apoptotic and IFn-inducing effects were dependent on the cell line and RNA length.
Viral and therapeutic control of IFN-beta promoter stimulator 1 during hepatitis C virus infection.
  • Y. Loo, D. Owen, +15 authors M. Gale
  • Biology, Medicine
    Proceedings of the National Academy of Sciences of the United States of America
  • 2006
TLDR
A dynamic model in which early activation of IRF-3 and induction of antiviral genes are reversed by IPS-1 proteolysis and abrogation of RIG-I signaling as NS3/4A accumulates in newly infected cells is suggested.
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