Selected article for: "NF κB activation and viral infection"
Author: Heaton, Steven M.; Borg, Natalie A.; Dixit, Vishva M.
Title: Ubiquitin in the activation and attenuation of innate antiviral immunity
  • Document date: 2016_1_11
    • ID: 42d77vxf_45
    Snippet: JEM Vol. 213, No. 1 Several additional E3s regulate IRF abundance. The Skp-Cullin-F-box (SCF)-containing complex, of which cullin1 (Cul1) is a core component, catalyzes IRF3 degradation as well as IκB degradation, promoting NF-κB activation ( Fig. 3 ; Bibeau-Poirier et al., 2006) . RanBP-type and C3HC4-type zinc finger-containing protein 1 (RBCK1) catalyzes K48-linked polyubiquitination and degradation of IRF3 during viral infection ( Fig. 3 ; .....
    Document: JEM Vol. 213, No. 1 Several additional E3s regulate IRF abundance. The Skp-Cullin-F-box (SCF)-containing complex, of which cullin1 (Cul1) is a core component, catalyzes IRF3 degradation as well as IκB degradation, promoting NF-κB activation ( Fig. 3 ; Bibeau-Poirier et al., 2006) . RanBP-type and C3HC4-type zinc finger-containing protein 1 (RBCK1) catalyzes K48-linked polyubiquitination and degradation of IRF3 during viral infection ( Fig. 3 ; Zhang et al., 2008) . Finally, the forkhead box protein O1 (FoxO1), a regulator of insulin signaling, binds IRF3 and promotes its degradation by recruiting an unknown E3. FoxO1 also negatively regulates IRF7 transcription (Lei et al., 2013) , altogether implying a link between metabolism and innate immune induction. Expression of Cul1 and the E3s RBCK1, TRIM21, TRIM26, and HERC5 is IFN-I inducible (Henig et al., 2013) , constituting a multiply redundant negative feedback web in which IFN-I expression is self-restraining.

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