◀ Back to NOS2
NOS2 — STAT1
Pathways - manually collected, often from reviews:
-
KEGG Tuberculosis:
STAT1
→
NOS2
(gene expression, expression)
Text-mined interactions from Literome
Sekine et al., J Cell Physiol 2000
:
These effects of IFN-gamma and TNF-alpha seem physiologically relevant, because either inhibition of
STAT1 by the tyrosine kinase inhibitor herbimycin A or that of NF-kappaB by sulfasalazine
resulted in the reduction of
iNOS mRNA expression
Samardzic et al., Cytokine 2001
:
STAT1 is
required for
iNOS activation, but not IL-6 production in murine fibroblasts ... These results indicate that
STAT1 activation and subsequent IRF-1 transcription are
required for induction of
iNOS , but not IL-6 in murine fibroblasts
Ganster et al., Proc Natl Acad Sci U S A 2001
:
Complex
regulation of human inducible
nitric oxide synthase gene transcription by
Stat 1 and NF-kappa B
Dell'Albani et al., J Neurosci Res 2001
(Central Nervous System Diseases) :
Inhibition experiments showed that JAK2 and
STAT1 alpha/beta tyrosine phosphorylation were
necessary for IFN gamma mediated
iNOS induction in astroglial cells
Teng et al., Am J Physiol Cell Physiol 2002
:
We conclude that in RASMC, NF-kappa B and C/EBP mediate the IL-1 beta induced iNOS expression, whereas IRF-1 and
STAT1 mediate the IFN-gamma enhanced
iNOS induction
Sur et al., Biochem Pharmacol 2002
:
Transient transfection assays using wild-type and mutant NOS2 promoter/luciferase reporter constructs showed that DNA binding of the transcription factors
Stat1 and NF-kappaB was
essential for optimal expression of the
NOS2 gene
Hadjur et al., Blood 2003
:
Suggesting a plausible mechanism for the increased expression of iNOS, IFNgamma stimulated Fancc ( -/- ) macrophages generated higher levels of
phospho-Stat1 , a positive
regulator of
inos ( nos2 ) gene expression
Blanchette et al., Immunology 2003
(Translocation, Genetic) :
In addition, electrophoretic mobility shift assay ( EMSA ) analysis revealed that
STAT1alpha is
essential for IFN-gamma-inducible
iNOS expression and NO production, whereas the contribution of NF-kappaB to this cellular regulation seems to be minimal
Kreiselmeier et al., Am J Physiol Lung Cell Mol Physiol 2003
(Adenocarcinoma, Bronchiolo-Alveolar...) :
Mouse embryonic fibroblasts null for p190B Rho GTPase activating protein exhibit increased RhoA protein content and activation, similar to what is observed in CF models, and also exhibit CF-like alterations in STAT1 regulation, including decreased
STAT1 activation, increased PIAS1 protein expression, and reduced
NOS2 induction , implicating RhoA mediated signaling in CF-related STAT1 alterations
Chen et al., Eur J Pharmacol 2005
:
Inhibition of
iNOS gene expression by quercetin is
mediated by the inhibition of IkappaB kinase, nuclear factor-kappa B and
STAT1 , and depends on heme oxygenase-1 induction in mouse BV-2 microglia
Ganster et al., J Interferon Cytokine Res 2005
(Inflammation) :
Further, ChIP analysis was applied to detect cytokine induced in vivo binding and transcriptional
regulation of the human
inducible nitric oxide synthase (iNOS) gene by NF-kappaB and
Stat1
Gao et al., J Immunol 2007
:
In this current study, using a system of LPS treated RAW264.7 macrophages, we go on to demonstrate that OPN increases
STAT1 ubiquitination and subsequent 26s proteasome mediated degradation to
inhibit STAT1 dependent
iNOS promoter activity, transcription, and protein expression
Stempelj et al., J Biol Chem 2007
:
Silencing of
STAT1 , a major transcription factor involved in signaling by IFNgamma, or pharmacological inhibition of JAKs, kinases that phosphorylate STATs,
prevented the induction of
iNOS and the production of NO in response to stimulation of cells with LPS/IFNgamma or TNF/IFNgamma, underscoring the importance of the intact JAK/STAT signaling in the regulation of iNOS expression in intestinal epithelial cells
Lee et al., J Mol Biol 2007
:
Additionally, the synergistic effects of TNF-alpha/IFN-gamma on
iNOS/NO induction, ROS production, and apoptosis were significantly
inhibited by overexpression of dominant negative
STAT1 in contrast to overexpression of wild-type STAT1
Paukkeri et al., Br J Pharmacol 2007
:
However, PPARalpha agonists did not alter LPS induced
iNOS mRNA expression or
activation of NF-kappaB or
STAT1 which are important transcription factors for iNOS
Kim et al., Free Radic Biol Med 2008
:
The inhibition of
STAT1 and STAT3 by EP prevented their translocation to the nucleus and consequently
inhibited expression of
iNOS and COX-2 by inhibiting STAT1- and STAT3 mediated transcriptional activity, followed by changes in chromatin conformation via deacetylation of histones H3 and H4 in both gene promoters
Tsoyi et al., Cell Signal 2008
:
However, AG490, a specific
JAK-2/STAT-1 inhibitor, efficiently
prevented LPS mediated
iNOS induction but not the induction of COX-2, and CKD712 completely blocked STAT-1 phosphorylation by LPS, suggesting that the NF-kappaB and JAK-2/STAT-1 pathways but not the JNK pathway are important for CKD712 action
Guo et al., Surgery 2008
(Sepsis) :
Osteopontin mediates
Stat1 degradation to
inhibit iNOS transcription in a cecal ligation and puncture model of sepsis
Dai et al., J Immunol 2009
(Inflammation) :
In this study, we report that activation of both
STAT-1 and NF-kappaB signaling is
essential for Con A-induced
inducible NO synthase (iNOS) and NO in murine splenocytes
Howard et al., Thorax 2010
:
Recovery of
STAT1 activation and recovery of
iNOS synthesis occurred within 12 h after SPR activation ( p=0.02 )
Kou et al., Int Immunopharmacol 2011
:
The inhibitions of
STAT1 and STAT 3 by arctigenin prevented their translocation to the nucleus and consequently
inhibited expression of
iNOS , thereby suppressing the expression of inflammation associated genes, such as IL-1ß, IL-6 and MCP-1, whose promoters contain STAT binding elements
Qi et al., Inflamm Res 2013
:
Baicalein suppressed the nuclear translocation of
STAT1 and STAT3 and
inhibited production of
iNOS upon LPS-stimulation, resulting in the inhibition of releases of NO and pro-inflammatory cytokines such as IL-1ß, IL-6, and TNF-a, in a dose dependent manner
Nishiya et al., FEBS Lett 1997
(Glioma) :
Thus, we examined the role of the Ras-MAPK pathway in
Stat1 activation and subsequent
iNOS induction in C6 glioma cells ... Further experiments showed that neither Asn-17 Ras expression nor concentrations of PD98059, which completely abrogated IFN-gamma induced ERK1 and ERK2 activation, affected
Stat1 DNA binding activity or
iNOS induction , indicating that the Ras-MAPK pathway does not appear to be involved in the activation of Stat1 and subsequent iNOS induction in C6 glioma cells
Gao et al., J Immunol 1998
:
Autocrine/paracrine IFN-alphabeta
mediates the lipopolysaccharide induced activation of transcription factor
Stat1alpha in mouse macrophages : pivotal role of Stat1alpha in induction of the inducible
nitric oxide synthase gene ... We have examined the
role of
Stat1alpha in the induction by LPS of the mouse inducible
nitric oxide synthase ( EC 1.14.13.39 ) gene