IRF-7 is the master regulator of type-I interferon-dependent immune responses
By K. Honda, H. Yanai, Hideo Negishi, M. Asagiri, Mitsuharu Sato, T. Mizutani, Naoya Shimada, Y. Ohba, A. Takaoka, N. Yoshida and 1 more. Nature, 2005
2,448 citations recorded by the source corpus.
Subfields: Immunology
View Paper: https://www.semanticscholar.org/paper/ae1b136a899b1ba95b16ebaf401eca0c8a8415df
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In Immunology
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Citations in the corpus
- Shared and Distinct Functions of Type I and Type III Interferons (2019, neutral): “first wave of type I IFN induction (Honda et al., 2005; Lazear et al., 2013).”
- Identification and Characterization of MAVS, a Mitochondrial Antiviral Signaling Protein that Activates NF-κB and IRF3 (2005, positive): “TBK1 and IKK can also phosphorylate and activate IRF7 (tenOever et al., 2004), another IRF family member essential for the production of type-I interferons such as interferon-α ( Honda et al., 2005 ).”
- Innate Immunity to Virus Infection (2009, background): “Next, the IRF-3 ⁄ -7 homodimers and ⁄ or heterodimers translocate into the nucleus and bind to IFN-sensitive response elements (ISREs), resulting in the expression of type I IFNs and a set of IFN-inducible genes (55, 56).”
- Innate Immune Pattern Recognition: A Cell Biological Perspective (2015, neutral): “Instead, these cells initiate an alternative MyD88dependent signaling pathway that activates the transcription factor IRF7 (Figure 4) (165).”
- MDA5/RIG-I and virus recognition. (2008, background): “Phosphorylation of IRF-3 and IRF-7 by these kinases induces the formation of homodimers and/or heterodimers [38], which translocate into the nucleus and bind to IFN-stimulated response elements (ISREs), thereby resulting in the expression of type I IFN genes and a set of IFN-inducible genes.”
- Interferons and viruses: an interplay between induction, signalling, antiviral responses and virus countermeasures. (2008, methodology): “In pDCs, IFN induction requires endosomal retention of the CpG ligand (Honda et al., 2005a) and involves a MyD88-dependent signalling pathway that is identical to the TLR7-mediated activation of IRF-7 and NF-kB, as discussed above (Fig.”
- Biology of Zika Virus Infection in Human Skin Cells (2015, background): “The detection of ZIKV-expressed PAMPs also resulted in an increase in transcriptional levels of IRF7, a transcription factor that binds to the interferon-stimulated response element, located on the promoters of type I IFN genes (30).”
- DNA damage primes the type I interferon system via the cytosolic DNA sensor STING to promote anti-microbial innate immunity. (2015, background): “Similarly, transcripts for the IFN-inducible genes Irf7 and Sting (Tmem173)-signaling molecules that are essential for an amplified type I IFN response (Honda et al., 2005; Ishikawa and Barber, 2008) were elevated in Atm / splenocytes and BMDMs at steady state.”
- Structural design of engineered costimulation determines tumor rejection kinetics and persistence of CAR T cells (2015, positive): “IRF7 is one of the main transcription factors regulating the IFN-I pathway (Honda et al., 2005; Sato et al., 1998).”
- IRFs: master regulators of signalling by Toll-like receptors and cytosolic pattern-recognition receptors (2006, background): “In MEFs from Irf7 −/− mice, the induction of type I IFN genes by ssRNA viruses (VSV and EMCV) is severely impaire”
- Spatiotemporal regulation of MyD88–IRF-7 signalling for robust type-I interferon induction (2005, background): “This robust IFN induction in pDCs is absolutely dependent on the MyD88–IRF-7 signalling pathwa”