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IRF1 — NFKB1
Pathways - manually collected, often from reviews:
Protein-Protein interactions - manually collected from original source literature:
Studies that report less than 10 interactions are marked with *
Text-mined interactions from Literome
Mizutani et al., J Nutr Sci Vitaminol (Tokyo) 1999
:
The inductive mechanism of ascorbate on the iNOS gene was studied by examining the degradation of I kappa B alpha by Western blotting,
activation of the
nuclear factor kappa B (NF-kappa B) by gel shift assays, and protein levels of
interferon regulatory factor 1 (IRF-1) in LPS- and IFN-gamma activated cells
Liu et al., Br J Pharmacol 2001
:
7. These studies show that
NFkappaB plays an important role in the regulation of
IRF-1 induction in HUVECs
Ochi et al., Eur J Immunol 2002
:
Transcriptional up-regulation of the VCAM-1 gene, induced by proinflammatory cytokines such as IL-1beta and TNF-alpha, requires activation of not only
NF-kappaB , but also
involves interferon regulatory factor (IRF)-1
Ackermann et al., Immunology 2004
:
Under identical conditions,
NF-kappaB inhibitors
had no effect on cytokine dependent increases in expression of the transcription factor
interferon regulatory factor-1
Sgarbanti et al., Ann N Y Acad Sci 2004
:
These results suggest that in early phases of HIV-1 infection, before detectable cytokine production,
NF-kappaB seems
responsible for HIV-1 induced
IRF-1 expression
Stangl et al., J Nutr 2005
:
Phloretin did not affect TNF-alpha stimulated activation of
nuclear factor kappaB (NF-kappaB) but
inhibited activation of
interferon regulatory factor 1 , a transcription factor involved in the regulation of endothelial cell adhesion molecule expression
Choi et al., J Neurosci Res 2005
(Alcohol-Induced Disorders, Nervous System...) :
Lipopolysaccharide (LPS), gangliosides, and interferon (IFN)-gamma induced the inflammatory activation of glia, which was differentially influenced by ethanol : 1 ) ethanol inhibited LPS- or gangliosides induced, but not IFNgamma induced, glial activation as demonstrated by the production of nitric oxide and the expression of inflammatory genes such as interleukin-1beta, tumor necrosis factor-alpha, IP-10, and CD86 ; 2 )
nuclear factor (NF)-kappaB or JAK/STAT1 pathway was necessary for LPS- or IFNgamma induced glial activation, respectively ; 3 ) ethanol inhibited LPS induced NF-kappaB activation ; and 4 ) ethanol did not significantly
affect IFNgamma induced
STAT1/IRF-1 activation
Kokkinakis et al., Cancer Lett 2006
(Neoplasms) :
The response of tumors to MET-stress depends on their mutational status, however, it always involves inhibition of CDK1 and in most cases the upregulation of p21, p27, GADDs and 14-3-3sigma in
response to upregulation of TGF-beta,
IRF-1 , TNF-alpha, Rb and/or MDA-7 and the downregulation of PI3K, RAS and
NF-kappaB
Sgarbanti et al., J Virol 2008
:
IRF-1 is
required for full
NF-kappaB transcriptional activity at the human immunodeficiency virus type 1 long terminal repeat enhancer ... In this work we demonstrate that
IRF-1 is also
required for full
NF-kappaB transcriptional activity
Jayakumar et al., Infect Immun 2008
:
The inhibition of
NF-kappaB activation by the pretreatment of DC with caffeic acid phenethyl ester
blocks L. major induced
IRF-1 and IRF-8 activation and IL-12 expression
Moschonas et al., Mol Cell Biol 2008
(Neoplasms) :
We show that unlike interferon signaling, which triggers the STAT1 mediated transcriptional activation of IRF-1, the ligation of CD40 in carcinomas induces the rapid upregulation of
IRF-1 in a STAT1 independent but
NF-kappaB dependent manner
Koetzler et al., J Allergy Clin Immunol 2009
(Picornaviridae Infections) :
In addition, the ability of HRV-16 to induce epithelial expression of
IRF-1 is
dependent , at least in part, on viral activation of
NF-kappaB
Wan et al., Nucleosides Nucleotides Nucleic Acids 2010
:
Exposure to IFN-gamma mainly affects nuclear
IRF-1 and STAT1 in EMT6, but
inhibits NF-kappaB p65 activity, indicating that the cooperative stimulation was the result of the independent activation of NF-kappaB, STAT1 and IRF-1 transcriptional factors through binding to their unique sites in the UPase promoter
Lin et al., J Biol Chem 1995
:
Transcriptional analysis in vitro demonstrated that 1 ) various dimeric complexes of NF-kappa B differentially stimulated transcription through the human immunodeficiency virus enhancer or PRDII up to 20-fold ; 2 ) recombinant I kappa B alpha specifically
inhibited NF-kappa B-dependent transcription in vitro ; and 3 ) different NF-kappa B complexes and
interferon regulatory factor 1 cooperated to stimulate transcription in vitro through the PRDIII-PRDI-PRDII virus-inducible regulatory domains of the IFN-beta promoter
Drew et al., J Interferon Cytokine Res 1995
:
We demonstrated here that TNF-alpha induced binding of
NF kappa B p50 and p65 to the NF kappa B-like element of the MHC class I promoter termed region I and IFN-gamma
induced binding of
IRF-1 to the adjacent interferon consensus sequence ( ICS )
Kinugawa et al., Circ Res 1997
:
These data suggest that ( 1 ) iNOS induction simultaneously requires both
NF-kappa B activation and
IRF-1 induction , and ( 2 ) the heterodimer between C/EBP and CREB has synergistic effects on the iNOS induction via the CAAT box
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