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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)
FAF1 (show FAF1 ELISA Kits) plays a novel role in negatively regulating virus-induced IFN-beta (show IFNB1 ELISA Kits) production and the antiviral response by inhibiting the translocation of active, phosphorylated IRF3 from the cytosol to the nucleus
the LxxLL motifs of IRF3 binds within the hydrophobic pocket of E6, precluding Ser (show SIGLEC1 ELISA Kits)-patch phosphorylation, necessary for IRF3 activation and interferon (show IFNA ELISA Kits) induction.
the suppression of type I IFN production by HTLV-1 Tax (show CNTN2 ELISA Kits) through interaction with and inhibition of TBK1 (show TBK1 ELISA Kits) kinase that phosphorylates IRF3
The authors found that Ca(2 (show CA2 ELISA Kits)+) signaling associated with membrane perturbation and recognition of incoming viral genomes by cytosolic nucleic acid receptors are required to activate IRF3 in response to Sendai virus and human cytomegalovirus.
Study identifies crosstalk between PTEN and IRF3 in tumor suppression and innate immunity.
Viral infection induced DAPK1 (show DAPK1 ELISA Kits)-IRF7 (show IRF7 ELISA Kits) and DAPK1 (show DAPK1 ELISA Kits)-IRF3 interactions and overexpression of DAPK1 (show DAPK1 ELISA Kits) enhanced virus-induced activation of the interferon (show IFNA ELISA Kits)-stimulated response element (ISRE) and IFN-beta (show IFNB1 ELISA Kits) promoters and the expression of the IFNB1 (show IFNB1 ELISA Kits) gene.
TEL (show ETV6 ELISA Kits)-AML1 (show RUNX1 ELISA Kits) fusion protein blocks B-cell differentiation and downregulates the IRF3-IFNalpha/beta pathway by modulating expression and phosphorylation of IRF3 in human primary hematopoietic precursor cells.
The expression levels of IRF3 were not different between CHB patients and healthy controls.
results revealed a new paradigm in which the antiviral host factor, IRF3, plays a cell-intrinsic pro-parasitic role.
The results of this study suggested that IRF3 is likely a risk gene for schizophrenia, at least in Caucasians.
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).
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
Irf3/IFN activation in hematopoietic stem and progenitor cells expands multipotent progenitors fractions but inhibits HSC (show FUT1 ELISA Kits) mobilization
find that IRF3 versus ISGF3 (show IRF9 ELISA Kits) specificity may be critical to limiting IFN-beta (show IFNB1 ELISA Kits) production and ISGF3 (show IRF9 ELISA Kits) activation, temporally and spatially, but that partial overlap in their specificity is tolerable and may enhance the effectiveness of the innate-immune response
Bipartite nuclear localization signal controls nuclear import and DNA-binding activity of IRF3.
Our findings delineate a novel mechanism for the termination of IRF3 activation in nucleus through TRIM26 (show TRIM26 ELISA Kits)-mediated IRF3 ubiquitination and degradation.
PP1 (show PPP1CC ELISA Kits) directly interacts with IRF3 and dephosphorylates IRF3 at Ser385 and Ser396, resulting in the suppression of TLR- and RLR (show DHX58 ELISA Kits)-triggered IFN-beta (show IFNB1 ELISA Kits) production.
our results identify CK2 (show CSNK2A1 ELISA Kits) as a novel regulator of TBK1 (show TBK1 ELISA Kits) and IRF3 and suggest that targeting CK2 (show CSNK2A1 ELISA Kits) by small molecular inhibitor may be a viable approach to prevent and treat viral infections.
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