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Interferon (show IFNA ELISA Kits) regulatory factor (IRF (show TRIM63 ELISA Kits))10 inhibits the expression of IFN1 and IFN3 to avoid an excessive immune response, a unique regulation mechanism of the IFN responses in lower vertebrates.
Hepatitis A virus protein 2B suppresses beta interferon (show IFNA ELISA Kits) (IFN) gene transcription by interfering with IFN regulatory factor 3 activation.
MyD88 (show MYD88 ELISA Kits) interacts with interferon (show IFNA ELISA Kits) regulatory factor (IRF) 3 and IRF7 (show IRF7 ELISA Kits) in Atlantic salmon (Salmo salar)
TBK1 (show TBK1 ELISA Kits) complexes required for the phosphorylation of IRF3 and the production of interferon-beta (show IFNB1 ELISA Kits) have been identified.
RIG-I (show DDX58 ELISA Kits)-like receptor-induced IRF3 mediated pathway of apoptosis (RIPA): a new antiviral pathway
cGAs recognizes bacterial/viral DNA, and is a strong activator of STING that can further activate IRF3 and subsequent type I interferon (show IFNA ELISA Kits) production. (Review)
IRF3 overexpression in Acute myeloid leukemia (show BCL11A ELISA Kits) (AML (show RUNX1 ELISA Kits)) promotes cell growth and survival, and miR (show MLXIP ELISA Kits)-155 is involved, indicating that IRF3 may be a potential new biomarker and therapeutic target for AML (show RUNX1 ELISA Kits).
down-regulation of IRF3 inhibited the proliferation and extracellular matrix expression in keloid fibroblasts.
rotavirus NSP1 (nonstructural protein 1) employs a pLxIS motif to target IRF-3 for degradation, but phosphorylation of NSP1 is not required for its activity. These results suggest a concerted mechanism for the recruitment and activation of IRF-3 that can be subverted by viral proteins to evade innate immune responses.
Highly pathogenic Porcine reproductive and respiratory syndrome virus modulates Interferon-beta (show IFNB1 ELISA Kits) expression mainly through attenuating IRF-3 phosphorylation.
Data suggest that molecular chaperone (show HSP90AA1 ELISA Kits) GRP78 (show HSPA5 ELISA Kits) contributes to toll-like receptor-3 (TLR3 (show TLR3 ELISA Kits))-mediated, interferon regulatory factor 3 protein (IRF3)-dependent innate immune response to hepatitis C virus (HCV) in hepatocytes.
Findings suggest a common and conserved mechanism through which highly pathogenic MERS-CoV and SARS (show SARS ELISA Kits)-CoV harness their M proteins to suppress type I IFN expression at the level of TBK1 (show TBK1 ELISA Kits)-dependent phosphorylation and activation of IRF3 resulting in evasion of the host innate antiviral response.
observations suggest IRF3 may function as a novel regulator to modulate TGF-beta1 (show TGFB1 ELISA Kits)-induced LX-2 proliferation, at least in part, via AKT (show AKT1 ELISA Kits) signaling pathway
The authors used recombinant classical swine fever virus N(pro) and swine IRF3 proteins and show that N(pro) interacts with IRF3 directly without additional proteins and forms a soluble 1:1 complex.
Amino acid residues in the N-terminal domain of Npro are involved in the stability of Npro, in interaction of Npro with IRF-3 and subsequent degradation of IRF-3, leading to downregulation of IFN-alpha (show IFNA ELISA Kits)/beta production.
The obtained results showed that PRRSV nsp1 could inhibit Poly(I:C)-induced IFN-beta (show IFNB1 ELISA Kits) promoter activity in MARC (show CCL7 ELISA Kits)-145 cells by down-regulating the protein level of IRF-3 and inhibiting the phosphorylation of IRF-3.
proteasomal degradation of IRF3 is induced by a direct or indirect interaction with N(pro).
this study shows that IRF3 in antigen-presenting cells and T cells is required for optimal T-cell effector function and the ability of T cells to influence innate immune function of antigen-presenting cells
The mitochondrial damage-cGAS-STING-IRF3 pathway is critically involved in metabolic stress-induced endothelial inflammation.
this study shows that lipopolysaccharide priming of dendritic cells stabilizes their tolerogenicity through reduction of NF-kappaB (show NFKB1 ELISA Kits) and IRF3 signaling
this study shows that regulation of the IRF3 pathway can affect multiple cell types and contribute to ameliorate pathogenesis of infection-triggered exacerbation of chronic obstructive pulmonary disease
Data show that the formation of a tripartite ribosomal protein S6 kinase 1 (S6K1 (show RPS6KB1 ELISA Kits))-STING membrane protein-TANK-binding kinase 1 (TBK1 (show TBK1 ELISA Kits)) complex was necessary for the activation of interferon regulatory factor-3 (IRF3).
characterizes SREBP cleavage-activating protein as an essential adaptor in the STING signaling pathway
Study identifies crosstalk between PTEN and IRF3 in tumor suppression and innate immunity.
results revealed a new paradigm in which the antiviral host factor, IRF3, plays a cell-intrinsic pro-parasitic role.
Irf3/IFN activation in hematopoietic stem and progenitor cells expands multipotent progenitors fractions but inhibits HSC (show FUT1 ELISA Kits) mobilization
The authors demonstrate that bovine herpesvirus 1 bICP0 effectively inhibits bovine IFN-beta (show IFNB1 ELISA Kits) promoter activity and induces IRF3 degradation.
cpBVDV infection causes a marked loss of interferon regulatory factor 3 (IRF-3), a cellular transcription factor that controls interferon (show IFNA ELISA Kits) synthesis.
This gene encodes a member of the interferon regulatory transcription factor (IRF) family. The encoded protein is found in an inactive cytoplasmic form that upon serine/threonine phosphorylation forms a complex with CREBBP. This complex translocates to the nucleus and activates the transcription of interferons alpha and beta, as well as other interferon-induced genes. Alternatively spliced transcript variants encoding multiple isoforms have been observed for this gene.
interferon regulatory factor 3
, interferon regulatory factor 3-like