◀ 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