scholarly journals Type I Inteferon Gene Induction by the Interferon Regulatory Factor Family of Transcription Factors

Immunity ◽  
2006 ◽  
Vol 25 (3) ◽  
pp. 349-360 ◽  
Author(s):  
Kenya Honda ◽  
Akinori Takaoka ◽  
Tadatsugu Taniguchi
Keyword(s):  
Transcription Factors ◽  
Gene Induction ◽  
Interferon Regulatory Factor ◽  
Type I ◽  
Regulatory Factor

Targeting IRFs by ubiquitination: regulating antiviral responses

2008 ◽  
Vol 36 (3) ◽  
pp. 453-458 ◽  
Author(s):  
Rowan Higgs ◽  
Caroline A. Jefferies
Keyword(s):  
Transcription Factors ◽  
Viral Infection ◽  
Viral Proteins ◽  
Interferon Regulatory Factor ◽  
Type I ◽  
Regulatory Factor ◽  
Ubiquitin Pathway ◽  
Cellular Processes ◽  
Antiviral Responses ◽  
Type I Ifns

The IRF [IFN (interferon) regulatory factor] family of transcription factors control many cellular processes, including induction of key antiviral cytokines, type I IFNs, following viral infection. Recent studies have revealed several endogenous and viral proteins involved in ubiquitin-mediated regulation of IRF activity and thus having an impact on type I IFN signalling. Through the ubiquitin pathway, these proteins can manipulate the antiviral response either by initiating proteasomal degradation of the IRFs or, in contrast, by promoting activation of the IRFs.

scholarly journals Identification of Feline Interferon Regulatory Factor 1 as an Efficient Antiviral Factor against the Replication of Feline Calicivirus and Other Feline Viruses

2018 ◽  
Vol 2018 ◽  
pp. 1-10 ◽  
Author(s):  
Yongxiang Liu ◽  
Xiaoxiao Liu ◽  
Hongtao Kang ◽  
Xiaoliang Hu ◽  
Jiasen Liu ◽  
...  
Keyword(s):  
Antiviral Activity ◽  
Viral Infections ◽  
Interferon Regulatory Factor ◽  
Feline Calicivirus ◽  
Type I ◽  
Norwalk Virus ◽  
Regulatory Factor ◽  
Feline Panleukopenia Virus ◽  
Protein Levels ◽  
Interferon Regulatory Factor 1

Interferons (IFNs) can inhibit most, if not all, viral infections by eliciting the transcription of hundreds of interferon-stimulated genes (ISGs). Feline calicivirus (FCV) is a highly contagious pathogen of cats and a surrogate for Norwalk virus. Interferon efficiently inhibits the replication of FCV, but the mechanism of the antiviral activity is poorly understood. Here, we evaluated the anti-FCV activity of ten ISGs, whose antiviral activities were previously reported. The results showed that interferon regulatory factor 1 (IRF1) can significantly inhibit the replication of FCV, whereas the other ISGs tested in this study failed. Further, we found that IRF1 was localized in the nucleus and efficiently activated IFN-β and the ISRE promoter. IRF1 can trigger the production of endogenous interferon and the expression of ISGs, suggesting that IRF1 can positively regulate IFN signalling. Importantly, the mRNA and protein levels of IRF1 were reduced upon FCV infection, which may be a new strategy for FCV to evade the innate immune system. Finally, the antiviral activity of IRF1 against feline panleukopenia virus, feline herpesvirus, and feline infectious peritonitis virus was demonstrated. These data indicate that feline IRF1 plays an important role in regulating the host type I IFN response and inhibiting feline viral infections.

Structure and regulation of the human interferon regulatory factor 1 (IRF-1) and IRF-2 genes: implications for a gene network in the interferon system

1994 ◽  
Vol 14 (2) ◽  
pp. 1500-1509
Author(s):  
H Harada ◽  
E Takahashi ◽  
S Itoh ◽  
K Harada ◽  
T A Hori ◽  
...  
Keyword(s):  
Gene Network ◽  
Interferon Regulatory Factor ◽  
Chromosomal Mapping ◽  
Human Interferon ◽  
Type I ◽  
Regulatory Factor ◽  
Nf Kappa B ◽  
Interferon Regulatory Factor 1 ◽  
Two Factors ◽  
Dna Binding Factors

Interferon regulatory factor 1 (IRF-1) and IRF-2 are structurally similar DNA-binding factors which were originally identified as regulators of the type I interferon (IFN) system; the former functions as a transcriptional activator, and the latter represses IRF-1 function by competing for the same cis elements. More recent studies have revealed new roles of the two factors in the regulation of cell growth; IRF-1 and IRF-2 manifest antioncogenic and oncogenic activities, respectively. In this study, we determined the structures and chromosomal locations of the human IRF-1 and IRF-2 genes and further characterized the promoters of the respective genes. Comparison of exon-intron organization of the two genes revealed a common evolutionary structure, notably within the exons encoding the N-terminal portions of the two factors. We confirmed the chromosomal mapping of the human IRF-1 gene to 5q31.1 and newly assigned the IRF-2 gene to 4q35.1, using fluorescence in situ hybridization. The 5' regulatory regions of both genes contain highly GC-rich sequences and consensus binding sequences for several known transcription factors, including NF-kappa B. Interestingly, one IRF binding site was found within the IRF-2 promoter, and expression of the IRF-2 gene was affected by both transient and stable IRF-1 expression. In addition, one potential IFN-gamma-activated sequence was found within the IRF-1 promoter. Thus, these results may shed light on the complex gene network involved in regulation of the IFN system.

scholarly journals Mutations in P63 and IRF-6 Present with Overlapping Craniofacial Defects: A study from Lebanon

2019 ◽  
pp. 1-3
Author(s):  
Mazen Kurban ◽  
Edgar Jabbour ◽  
Lamiaa Hamie ◽  
Mazen Kurban ◽  
Pamela Kassabian
Keyword(s):  
Transcription Factors ◽  
Cleft Lip ◽  
Interferon Regulatory Factor ◽  
Craniofacial Development ◽  
Regulatory Factor ◽  
Van Der Woude Syndrome ◽  
Interferon Regulatory Factor 6 ◽  
Cleft Lip Palate ◽  
Exon 9 ◽  
Craniofacial Defects

Interferon Regulatory Factor 6 (IRF-6) and p63 are two vital transcription factors implicated in normal craniofacial development. In this report, we present a family with Van Der Woude Syndrome (VWS) with a mutation in exon 9 of IRF-6 gene and a phenotypically overlapping case of Rapp-Hodgkin Syndrome (RHS) resulting from a mutation in the p63 gene. Members from both families presented with congenital lip pits and cleft lip/palate. The RHS case had additional ectodermal features that underscore the upstream nature of p63 in the complex p63-IRF-6 interactive pathway.

scholarly journals DHAV-1 Blocks the Signaling Pathway Upstream of Type I Interferon by Inhibiting the Interferon Regulatory Factor 7 Protein

2021 ◽  
Vol 12 ◽  
Author(s):  
Yalan Lai ◽  
Xiaoyan Xia ◽  
Anchun Cheng ◽  
Mingshu Wang ◽  
Xumin Ou ◽  
...  
Keyword(s):  
Immune Response ◽  
Innate Immunity ◽  
Viral Protein ◽  
Interferon Regulatory Factor ◽  
Host Cells ◽  
Luciferase Reporter ◽  
Type I ◽  
Dependent Manner ◽  
Regulatory Factor ◽  
Interferon Regulatory Factor 7

Duck hepatitis A virus (DHAV), which mainly infects 1- to 4-week-old ducklings, has a fatality rate of 95% and poses a huge economic threat to the duck industry. However, the mechanism by which DHAV-1 regulates the immune response of host cells is rarely reported. This study examined whether DHAV-1 contains a viral protein that can regulate the innate immunity of host cells and its specific regulatory mechanism, further exploring the mechanism by which DHAV-1 resists the host immune response. In the study, the dual-luciferase reporter gene system was used to screen the viral protein that regulates the host innate immunity and the target of this viral protein. The results indicate that the DHAV-1 3C protein inhibits the pathway upstream of interferon (IFN)-β by targeting the interferon regulatory factor 7 (IRF7) protein. In addition, we found that the 3C protein inhibits the nuclear translocation of the IRF7 protein. Further experiments showed that the 3C protein interacts with the IRF7 protein through its N-terminus and that the 3C protein degrades the IRF7 protein in a caspase 3-dependent manner, thereby inhibiting the IFN-β-mediated antiviral response to promote the replication of DHAV-1. The results of this study are expected to serve as a reference for elucidating the mechanisms of DHAV-1 infection and pathogenicity.

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