Selected article for: "antiviral state and IFN activation"

Author: Homma, Takujiro; Ishibashi, Daisuke; Nakagaki, Takehiro; Fuse, Takayuki; Sano, Kazunori; Satoh, Katsuya; Atarashi, Ryuichiro; Nishida, Noriyuki
Title: Persistent prion infection disturbs the function of Oct-1, resulting in the down-regulation of murine interferon regulatory factor-3
  • Document date: 2014_8_8
  • ID: jspxlk1a_1
    Snippet: I RF-3 is a key transcriptional factor involved in the signaling the pathway responsible for keeping the antiviral state of host cells. Viral infection triggers phosphorylation of the IRF-3 carboxyl-terminal region 1 , and the phosphorylated IRF-3 migrates to the nucleus, leading to the transcriptional activation of the type I interferon (IFN-I) genes. Interestingly, it has also been reported that infection by some viruses enhances the degradatio.....
    Document: I RF-3 is a key transcriptional factor involved in the signaling the pathway responsible for keeping the antiviral state of host cells. Viral infection triggers phosphorylation of the IRF-3 carboxyl-terminal region 1 , and the phosphorylated IRF-3 migrates to the nucleus, leading to the transcriptional activation of the type I interferon (IFN-I) genes. Interestingly, it has also been reported that infection by some viruses enhances the degradation of IRF-3 and/or inhibits its phosphorylation, resulting in the reduced response of IFN-I production and persistent infection by the virus [2] [3] [4] [5] [6] [7] .

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