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IRF3 — NFKB1

Text-mined interactions from Literome

Kim et al., J Biol Chem 2000 : Taken together with previous observations, these results implicate that, for the assembly of an IFN-beta enhanceosome, MEKK1 can induce IRF3 and ATF2/c-JUN through the JNK pathway, whereas it can induce NF-kappaB through the IKK pathway
Jiang et al., Proc Natl Acad Sci U S A 2004 : In support of this finding, we showed that DN-TRAF6 and DN-TAK1 blocked poly ( I.C ) -induced NF-kappaB but not IRF3 activation
Harii et al., Mol Endocrinol 2005 (Thyroiditis, Autoimmune...) : In this report, we demonstrate TLR3 mRNA and protein are expressed on Fisher rat thyroid cell line-5 ( FRTL-5 ) thyroid cells and are functional because incubating cells with polyinosine-polycytidylic acid causes 1 ) transcriptional activation of both the nuclear factor kappaB (NF-kappaB)/Elk1 and interferon (IFN) regulatory factor-3/IFN-beta signal paths, 2 ) posttranscriptional activation of NF-kappaB and ERK1/2, and 3 ) increased IFN-beta mRNA
Ock et al., J Neurosci Res 2007 (Inflammation) : Hypoxia, however, differentially regulated MyD88 dependent and -independent pathways of TLR4 signaling : Hypoxia enhanced lipopolysaccharide (LPS) induced interferon regulatory factor-3 (IRF-3) activation and the subsequent expression of IFNbeta ( MyD88 independent pathway ), whereas it suppressed LPS induced NF-kappaB activation ( MyD88 dependent pathway )
Lee et al., Mol Cells 2008 : Acrolein inhibited NF-kappaB and IRF3 activation by LPS, but it did not inhibit NF-kappaB or IRF3 activation by MyD88, inhibitor kappaB kinase (IKK)beta, TRIF, or TNF-receptor associated factor family member associated NF-kappaB activator ( TANK) binding kinase 1 (TBK1 )
Alff et al., J Virol 2008 : The formation of TBK1-TRAF3 complexes directs IRF-3 phosphorylation, and both IRF-3 and NF-kappaB activation are required for transcription from the IFN-beta promoter
Koarai et al., Am J Respir Cell Mol Biol 2010 : One hundred micromoles of H ( 2 ) O ( 2 ) enhanced the translocation of nuclear factor (NF)-kappaB p65, but not that of interferon regulatory factor-3 (IRF-3), into the nucleus and the NF-kappaB DNA binding activity after poly ( I:C ) stimulation, which effect was inhibited not by the silencing of IRF-3 but by MG132, a proteasome inhibitor, or dexamethasone
Samanta et al., Cancer Sci 2010 (Burkitt Lymphoma) : In BL cells, EBERs activate RIG-I signaling and induce the expression of type-I IFNs and interferon stimulated genes ( ISGs ) through the activation of RIG-I substrates, nuclear factor-kappa B (NF-kappaB), and IFN regulatory factor 3 (IRF-3) , and anti-inflamatory cytokine IL-10 through IRF-3 but not NF-kappaB signaling
Cheng et al., J Interferon Cytokine Res 1998 : Therefore, effective ISRE activity of IP-10 VRE may require an IRF-like protein binding, which is enhanced by an NF-kappaB heterodimer binding to an adjacent KB site