◀ Back to STAT3
NFKB1 — STAT3
Pathways - manually collected, often from reviews:
-
NCI Pathway Database IL23-mediated signaling events:
STAT3 (dimer ) complex (STAT3)
→
NF kappa B1 p50/RelA/I kappa B alpha complex (NFKB1-NFKBIA-RELA)
(transcription, activates)
Aggarwal et al., J Biol Chem 2003*, Langrish et al., J Exp Med 2005, Park et al., Nat Immunol 2005*, Harrington et al., Nat Immunol 2005, Cho et al., J Immunol 2006
Evidence: mutant phenotype, other species
Protein-Protein interactions - manually collected from original source literature:
Studies that report less than 10 interactions are marked with *
-
IRef Biogrid Interaction:
STAT3
—
NFKB1
(physical association, affinity chromatography technology)
Yu et al., Biochem J 2002*
-
IRef Biogrid Interaction:
STAT3
—
NFKB1
(direct interaction, pull down)
Yu et al., Biochem J 2002*
-
IRef Hprd Interaction:
STAT3
—
NFKB1
(in vivo)
Yu et al., Biochem J 2002*
-
IRef Hprd Interaction:
STAT3
—
NFKB1
(in vitro)
Yu et al., Biochem J 2002*
-
IRef Ophid Interaction:
NFKB1
—
STAT3
(aggregation, interologs mapping)
Brown et al., Bioinformatics 2005
-
IRef Ophid Interaction:
NFKB1
—
STAT3
(aggregation, confirmational text mining)
Yu et al., Biochem J 2002*
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