Gene interactions and pathways from curated databases and text-mining

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NFKB1 — STAT3

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

Zhang et al., Blood 2000 : Exposing primary rat hepatocytes to IL-1beta had no effect on IL-6 mediated STAT3 activation ; instead, IL-1beta activated NF-kappaB associated with 2 IL-6 responsive elements ( STAT3 binding site ) on the rat gamma fibrinogen promoter and blocked STAT3 binding to these regions
Yang et al., J Biol Chem 2001 : NF-kappaB activation requires the IFN dependent association of STAT3 with the IFNAR1 chain of the IFN receptor
Vancurova et al., J Virol 2002 (Laryngeal Neoplasms...) : Increased NF-kappaB activity and cytoplasmic accumulation of p21 ( CIP1/WAF1 ) might counteract death promoting effects elicited by overexpressed PTEN and reduced activation of Akt and STAT3 previously noted in these tissues
Xie et al., Blood 2003 : Thus, our study demonstrates that beta ( 2 ) M at high concentrations retards the generation of MoDCs, which may involve down-regulation of major histocompatibility complex class I molecules, inactivation of Raf/MEK/ERK cascade and NF-kappaB , and activation of STAT3 , and it merits further study to elucidate the underlying mechanisms
Kanauchi et al., J Gastroenterol 2003 (Colitis) : GBF has the potential to reduce the epithelial inflammatory response by depressing STAT-3 expression and inhibiting NFkB binding activity
Hoentjen et al., Blood 2005 : STAT3 regulates NF-kappaB recruitment to the IL-12p40 promoter in dendritic cells ... Chromatin immunoprecipitation demonstrated enhanced NF-kappaB ( cRel, RelA ) binding to the IL-12p40 promoter in IL-10 ( -/- ) but not WT BMDCs. Interestingly, LPS induced STAT3 phosphorylation in WT but not IL-10 ( -/- ) BMDCs, a process blocked by IL-10 receptor blocking antibody
Debidda et al., J Biol Chem 2005 (Inflammation) : STAT3 was required for the RhoA induced NF-kappaB and cyclin D1 transcription and was involved in NF-kappaB nuclear translocation
Nefedova et al., J Immunol 2005 : Inhibition of Jak2/STAT3 signaling resulted in activation of the transcription factor NF-kappaB
Fritzenwanger et al., Cytokine 2006 : STAT3 phosphorylation, the activation of JAK2 and NF-kappaB are involved in this pathway
Rigby et al., Oncogene 2007 (Colonic Neoplasms...) : In vitro, SOCS3 overexpression reduced proliferation, IL-6 mediated STAT3 activation and tumor necrosis factor (TNF) alpha mediated NF-kappaB activation
Nishinakamura et al., Int Immunol 2007 : An RNA binding protein alphaCP-1 is involved in the STAT3 mediated suppression of NF-kappaB transcriptional activity ... In this study, we investigated the effect of constitutively activated STAT3 ( STAT3C ) on LPS induced nuclear factor-kappaB (NF-kappaB) activation ... The forced expression of STAT3C in HEK293/TLR4 cells, but neither wild-type STAT3 nor dominant negative form of STAT3, suppressed LPS-TLR4 mediated NF-kappaB reporter activation ... Thus, STAT3C could suppress the transcriptional and/or translational activity of NF-kappaB ... These data suggest that alphaCP-1 is involved in the STAT3 mediated suppression of NF-kappaB activity
Lu et al., Cell Physiol Biochem 2008 : Direct activation of NF-kappaB also enhanced STAT3 expression, an effect abrogated by NF-kappaB inhibitor
Kanda et al., Endocrinology 2008 : IL-1beta enhanced the transcriptional activity of NF-kappaB , whereas leptin enhanced STAT1 and STAT3 activity
Di Paola et al., Intensive Care Med 2009 (Hypertension...) : Administration of glycyrrhizin, significantly reduced the ( a ) fall of mean arterial blood pressure, ( b ) mortality rate, ( c ) myeloperoxidase (MPO) activity, ( d ) production of pro-inflammatory cytokines [tumor necrosis factor-alpha ( TNF-alpha ) and interleukin-1beta (IL-1beta) ], ( e ) histological evidence of gut injury, ( f ) immunoreactivity of nitrotyrosine, ( g ) poly ADP-ribose ( PAR ) formation, ( h ) the expression of ICAM-1 and P-selectin, ( i ) activation of nuclear factor-kappaB (NF-kappaB) and ( j ) signal transducer and activator transcription-3 ( STAT-3 ) induced by splanchnic artery occlusion-reperfusion shock
Aggarwal et al., Clin Cancer Res 2009 (Anoxia...) : Linkage between cancer and inflammation is indicated by numerous lines of evidence ; first, transcription factors nuclear factor-kappaB (NF-kappaB) and signal transducers and activators of transcription 3 ( STAT3 ), two major pathways for inflammation, are activated by most cancer risk factors ; second, an inflammatory condition precedes most cancers ; third, NF-kappaB and STAT3 are constitutively active in most cancers ; fourth, hypoxia and acidic conditions found in solid tumors activate NF-kappaB ; fifth, chemotherapeutic agents and gamma-irradiation activate NF-kappaB and lead to chemoresistance and radioresistance ; sixth, most gene products linked to inflammation, survival, proliferation, invasion, angiogenesis, and metastasis are regulated by NF-kappaB and STAT3 ; seventh, suppression of NF-kappaB and STAT3 inhibits the proliferation and invasion of tumors ; and eighth, most chemopreventive agents mediate their effects through inhibition of NF-kappaB and STAT3 activation pathways
Hasegawa et al., J Immunol 2009 : The ASC mediated AP-1 activation was NF-kappaB independent and primarily cell-autonomous response, whereas the STAT3 activation required NF-kappaB activation and was mediated by a factor that can act in a paracrine manner
Correa-de-Santana et al., J Endocrinol 2009 : Furthermore, silencing STAT3 inhibited basal, LPS and MDP stimulated NFKB protein expression and overexpression of protein inhibitor of activated STAT3 ( Pias3 ) markedly decreased basal NFKB activity ... Furthermore, silencing STAT3 inhibited basal, LPS and MDP stimulated NFKB protein expression and overexpression of protein inhibitor of activated STAT3 ( Pias3 ) markedly decreased basal NFKB activity
Iliopoulos et al., Cell 2009 (Inflammation) : IL6 mediated activation of the STAT3 transcription factor is necessary for transformation, and IL6 activates NF-kappaB , thereby completing a positive feedback loop
Grivennikov et al., Cytokine Growth Factor Rev 2010 (Colitis...) : Other interactions and forms of crosstalk between NF-kappaB and STAT3 include physical interaction between the two, cooperation of these factors at gene promoters/enhancers, the NF-kappaB dependent expression of inhibitors of STAT3 activation and the participation of STAT3 in inflammatory cells in the negative regulation NF-kappaB
Han et al., Molecular cancer 2010 (Disease Models, Animal...) : Co-treatment with NF-kappaB , STAT3 or/and PI3K inhibitors led to additive inhibition of iMyc E mu-1 cell proliferation, suggesting that these signaling pathways converge
Xie et al., PloS one 2010 (Breast Neoplasms...) : NF-kappaB inhibition attenuated STAT3 and Smad3 activities whereas PGN-SA stimulated cell culture supernatants reversed these inhibitory effects
Knorr et al., Neurosci Lett 2010 (Fever...) : Local MALP-2-treatment induced a moderate STAT3 activation and a small but significant increase in COX-2 IR while no NFkappaB-activation could be observed in the brains of these animals
Liu et al., Mol Cancer Res 2011 (Leukemia, Lymphocytic, Chronic, B-Cell) : STAT-3 activates NF-kappaB in chronic lymphocytic leukemia cells
Guo et al., Zhongguo Zhong Xi Yi Jie He Za Zhi 2013 : Compared with the vehicle control group, the NF-kappaB p65 activity, the expressions of STAT3 and VEGF mRNA increased significantly in RSC-364 induced by IL-17 +TNF-alpha ( P < 0.01, P < 0.05 ). Compared with the model group, the NF-kappaB p65 activity, the expressions of STAT3 and VEGF mRNA decreased significantly in the DT containing serum group and the positive control group ( P < 0.01, P < 0.05 ). There was no statistical difference between the two groups ( P > 0.05 )
Yang et al., Proc Natl Acad Sci U S A 1998 : A human cell line that is resistant to the antiviral and antiproliferative activities of IFN but is still IFN-responsive by virtue of STAT1 and STAT2 activation was found to be defective in STAT3 activation and in induction of NF-kappaB DNA binding activity ... Because STAT3 is involved in the induction of NF-kappaB DNA binding activity and in the induction of antiviral and antiproliferative activity, our results place STAT3 as an important upstream element in type I IFN signal transduction and in the induction of biological activities