Molecular and functional characterization of interferon regulatory factor 1 (IRF1) in amphibian Xenopus tropicalis
9
Citation
48
Reference
10
Related Paper
Citation Trend
Keywords:
IRF1
Immunofluorescence
Cite
Citations (0)
Interferon regulatory factor 3 (427 aa, ~47 kDa) is encoded by the human IRF3 gene. This protein plays a role in the modulation of both antiviral activity and interferon-stimulated response element promoter activation.
IRF3
IRF1
IRF8
Cite
Citations (0)
Interferon regulatory factor 1(IRF-1)is a important multifunctional transcription factor for regulating of expression of interferon(IFN)and having cantivirus action,antineoplastic activity.Indeed,IRF-1selectively modulates different sets of genes,depending on the cell type in order to evoke appropriate responses in each.The author summarizes the structure,the transcriptional regulation and the multiple biological effects.
IRF1
IRF8
IRF4
Cite
Citations (0)
IRF1
IRF3
IRF7
Mediator
MDA5
Cite
Citations (30)
African clawed frog
Cite
Citations (2)
IRF1
IRF7
IRF3
IRF8
Cite
Citations (40)
Interferon regulatory factor 1 (IRF1) is an important transcription factor that activates the type I interferon (IFN-I) response and plays a vital role in the antiviral immune response. Although IRF1 has been identified in several mammals, little information related to its function in canines has been described.In this study, canine IRF1 (CaIRF1) was cloned. After a series of bioinformatics analyses, we found that the CaIRF1 protein structure was similar to that of other animal IRF1 proteins, including a conserved DNA-binding domain (DBD), an IRF-association domain 2 (IAD2) domain and two nuclear localization signals (NLSs). An indirect immunofluorescence assay (IFA) revealed that CaIRF1 was mainly distributed in the nucleus. Overexpression of CaIRF1 in Madin-Darby canine kidney cells (MDCK) induced high levels of interferon β (IFNβ) and IFN-stimulated response element (ISRE) promoter activation and induced interferon-stimulated gene (ISG) expression. Subsequently, we assayed the antiviral activity of CaIRF1 against vesicular stomatitis virus (VSV) and canine parvovirus type-2 (CPV-2) in MDCK cells. Overexpression of CaIRF1 effectively inhibited the viral yields of VSV and CPV-2, while knocking down of CaIRF1 expression mildly increased viral gene copies.CaIRF1 is involved in the cellular IFN-I signaling pathway and plays an important role in the antiviral response.
IRF1
IRF7
Cite
Citations (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.
IRF1
Feline calicivirus
Caliciviridae
Cite
Citations (11)
The interferon regulatory factor 1 (IRF‐1) is a positive transcriptional regulatory protein which acts in the interferon signal transduction pathway to activate the transcription of the type I interferon genes by binding to the PRDI response element. The aim of this study was to explore the role of IRF‐1 in regulating the expression of other interferon‐stimulated genes in the interferon signal transduction pathway. A transient transfection assay was used to show that IRF‐1 induced the expression of interferon‐stimulated genes. The induction was a direct result of IRF‐1 binding to the promoters of the interferon‐stimulated response element (ISRE). The levels of endogenous mRNA of two interferon‐stimulated genes, 6‐16 and 9‐27, were increased in cells containing increased levels of IRF‐1. In addition, IRF‐1 activates the expression of IRF‐2, a negative regulator of the type I interferon genes themselves. Two sequences were found in the IRF‐2 promoter which were the binding sites for IRF‐1. Mutations in the oligonucleotide sequences of these sites could abolish the binding of the IRF‐1. These data suggested that IRF‐1 not only plays an important role in the induction of type I interferon genes, but also in the activation of interferon‐stimulated genes.
IRF1
Response element
IRF8
Cite
Citations (26)
Host cell-intrinsic antiviral responses are largely mediated by pattern-recognition receptor (PRR) signaling and the interferon (IFN) system. The IFN regulatory factor (IRF) family of transcription factors takes up a central role in transcriptional regulation of antiviral innate immunity. IRF3 and IRF7 are known to be key players downstream of PRRs mediating the induction of type I and III IFNs. IFN signaling then requires IRF9 for the expression of the full array of interferon stimulated genes (ISGs) ultimately defining the antiviral state of the cell. Other members of the IRF family clearly play a role in mediating or modulating IFN responses, such as IRF1, IRF2 or IRF5, however their relative contribution to mounting a functional antiviral response is much less understood. In this study, we systematically and comparatively assessed the impact of six members of the IRF family on antiviral signaling in alveolar epithelial cells. We generated functional knockouts of IRF1, -2, -3, -5, -7, and -9 in A549 cells, and measured their impact on the expression of IFNs and further cytokines, ISGs and other IRFs, as well as on viral replication. Our results confirmed the vital importance of IRF3 and IRF9 in establishing an antiviral state, whereas IRF1, 5 and 7 were largely dispensable. The previously described inhibitory activity of IRF2 could not be observed in our experimental system.
IRF7
IRF3
IRF1
IRF5
STAT1
Cite
Citations (20)