scholarly journals Antiviral gene expression in rheumatoid arthritis: Role of IKKε and interferon regulatory factor 3

2007 ◽  
Vol 56 (3) ◽  
pp. 743-752 ◽  
Author(s):  
Susan E. Sweeney ◽  
Ling Mo ◽  
Gary S. Firestein
Keyword(s):  
Rheumatoid Arthritis ◽  
Gene Expression ◽  
Interferon Regulatory Factor ◽  
Regulatory Factor ◽  
Interferon Regulatory Factor 3 ◽  
Antiviral Gene

scholarly journals Regulation of Type I Interferon Gene Expression by Interferon Regulatory Factor-3

1998 ◽  
Vol 273 (5) ◽  
pp. 2714-2720 ◽  
Author(s):  
Susan L. Schafer ◽  
Rongtuan Lin ◽  
Paul A. Moore ◽  
John Hiscott ◽  
Paula M. Pitha
Keyword(s):  
Gene Expression ◽  
Type I Interferon ◽  
Interferon Regulatory Factor ◽  
Type I ◽  
Regulatory Factor ◽  
Interferon Regulatory Factor 3 ◽  
Interferon Gene

scholarly journals Interleukin-1? repressesMRP2 gene expression through inactivation of interferon regulatory factor 3 in HepG2 cells

Hepatology ◽  
2004 ◽  
Vol 39 (6) ◽  
pp. 1574-1582 ◽  
Author(s):  
Keiji Hisaeda ◽  
Akihiko Inokuchi ◽  
Takanori Nakamura ◽  
Yukihide Iwamoto ◽  
Kimitoshi Kohno ◽  
...  
Keyword(s):  
Gene Expression ◽  
Hepg2 Cells ◽  
Interleukin 1 ◽  
Interferon Regulatory Factor ◽  
Regulatory Factor ◽  
Interferon Regulatory Factor 3

scholarly journals Classical Swine Fever Virus Can Remain Virulent after Specific Elimination of the Interferon Regulatory Factor 3-Degrading Function of Npro

2008 ◽  
Vol 83 (2) ◽  
pp. 817-829 ◽  
Author(s):  
Nicolas Ruggli ◽  
Artur Summerfield ◽  
Ana R. Fiebach ◽  
Laurence Guzylack-Piriou ◽  
Oliver Bauhofer ◽  
...  
Keyword(s):  
Classical Swine Fever Virus ◽  
Nonstructural Protein ◽  
Classical Swine Fever ◽  
Interferon Regulatory Factor ◽  
Fever Virus ◽  
Regulatory Factor ◽  
Interferon Regulatory Factor 3 ◽  
Amino Terminal ◽  
Alpha Beta

ABSTRACT Pestiviruses prevent alpha/beta interferon (IFN-α/β) production by promoting proteasomal degradation of interferon regulatory factor 3 (IRF3) by means of the viral Npro nonstructural protein. Npro is also an autoprotease, and its amino-terminal coding sequence is involved in translation initiation. We previously showed with classical swine fever virus (CSFV) that deletion of the entire Npro gene resulted in attenuation in pigs. In order to elaborate on the role of the Npro-mediated IRF3 degradation in classical swine fever pathogenesis, we searched for minimal amino acid substitutions in Npro that would specifically abrogate this function. Our mutational analyses showed that degradation of IRF3 and autoprotease activity are two independent but structurally overlapping functions of Npro. We describe two mutations in Npro that eliminate Npro-mediated IRF3 degradation without affecting the autoprotease activity. We also show that the conserved standard sequence at these particular positions is essential for Npro to interact with IRF3. Surprisingly, when these two mutations are introduced independently in the backbones of highly and moderately virulent CSFV, the resulting viruses are not attenuated, or are only partially attenuated, in 8- to 10-week-old pigs. This contrasts with the fact that these mutant viruses have lost the capacity to degrade IRF3 and to prevent IFN-α/β induction in porcine cell lines and monocyte-derived dendritic cells. Taken together, these results demonstrate that contrary to previous assumptions and to the case for other viral systems, impairment of IRF3-dependent IFN-α/β induction is not a prerequisite for CSFV virulence.

scholarly journals Distinct Functions of the Mitogen-activated Protein Kinase-activated Protein (MAPKAP) Kinases MK2 and MK3

2011 ◽  
Vol 286 (27) ◽  
pp. 24113-24124 ◽  
Author(s):  
Christian Ehlting ◽  
Natalia Ronkina ◽  
Oliver Böhmer ◽  
Ute Albrecht ◽  
Konrad A. Bode ◽  
...  
Keyword(s):  
Gene Expression ◽  
Protein Kinase ◽  
Nuclear Translocation ◽  
Interferon Regulatory Factor ◽  
Mitogen Activated Protein Kinase ◽  
Regulatory Factor ◽  
Interferon Regulatory Factor 3 ◽  
Downstream Signaling ◽  
Enhanced Expression ◽  
Regulatory Effects

In LPS-treated macrophages, activation of STAT3 is considered to be crucial for terminating the production of inflammatory cytokines. By analyzing the role of MAPK-activated protein kinase (MK) 2 and MK3 for LPS-induced STAT3 activation in macrophages, the present study provides evidence that MK2 is crucial for STAT3 activation in response to LPS because it prevents MK3 from impeding IFNβ gene expression. Accordingly, LPS-induced IFNβ gene expression is down-regulated in MK2-deficient macrophages and can be reconstituted by additional ablation of the MK3 gene in MK2/3−/− macrophages. This is in contrast to LPS-induced IL-10 expression, which essentially requires the presence of MK2. Further analysis of downstream signaling events involved in the transcriptional regulation of IFNβ gene expression suggests that, in the absence of MK2, MK3 impairs interferon regulatory factor 3 protein expression and activation and inhibits nuclear translocation of p65. This inhibition of p65 nuclear translocation coincides with enhanced expression and delayed degradation of IκBβ, whereas expression of IκBα mRNA and protein is impaired in the absence of MK2. The observation that siRNA directed against IκBβ is able to reconstitute IκBα expression in MK2−/− macrophages suggests that enhanced expression and delayed degradation of IκBβ and impaired NFκB-dependent IκBα expression are functionally linked. In summary, evidence is provided that MK2 regulates LPS-induced IFNβ expression and downstream STAT3 activation as it restrains MK3 from mediating negative regulatory effects on NFκB- and interferon regulatory factor 3-dependent LPS signaling.

scholarly journals Protective Role of Interferon Regulatory Factor 3-Mediated Signaling against Prion Infection

2012 ◽  
Vol 86 (9) ◽  
pp. 4947-4955 ◽  
Author(s):  
D. Ishibashi ◽  
R. Atarashi ◽  
T. Fuse ◽  
T. Nakagaki ◽  
N. Yamaguchi ◽  
...  
Keyword(s):  
Interferon Regulatory Factor ◽  
Protective Role ◽  
Regulatory Factor ◽  
Interferon Regulatory Factor 3 ◽  
Prion Infection
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