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NOS2 — TLR2

Pathways - manually collected, often from reviews:

• KEGG Leishmaniasis: TLR2/TLR4 → NOS2 (protein-protein, activation)

Text-mined interactions from Literome

Brightbill et al., Science 1999 : Several lipoproteins stimulated TLR dependent transcription of inducible nitric oxide synthase and the production of nitric oxide, a powerful microbicidal pathway
Suliman et al., FASEB J 2005 : In wild-type ( Wt ) mice injected with heat inactivated E. coli, hepatic TLR4 and TLR2 proteins were up-regulated with TLR dependent increases in transcript levels for tumor necrosis factor ( TNF-alpha ), interleukin 6, nitric oxide synthase-II ( iNOS ), and NADPH oxidase 2 (Nox2)
Yang et al., Kidney Int 2006 (Leptospirosis) : In conclusion, these findings indicate that the stimulation of iNOS and CCL2/MCP-1 caused by pathogenic leptospiral OMPs, in particular LipL32, in proximal tubule cells requires TLR2 for the early inflammatory response
Uno et al., Am J Physiol Gastrointest Liver Physiol 2007 (Helicobacter Infections) : The induction of iNOS and the associated nitric oxide production in response to H. pylori-LPS stimulation were inhibited by declines in not only TLR4 but also TLR2
Tsukamoto et al., J Immunol 2008 : Previous pharmacologic studies have suggested that a PI3K-Akt pathway negatively regulates TLR induced inducible NO synthase expression and cytokine production
Masamune et al., J Gastroenterol 2008 : TLR ligands induced expression of monocyte chemoattractant protein 1, cytokine induced neutrophil chemoattractant 1 ( a rat homolog of interleukin-8 ), and inducible nitric oxide synthase , but not proliferation or type I collagen production
Sosroseno et al., Oral Microbiol Immunol 2009 : Methods : Cells were stimulated directly with A. actinomycetemcomitans lipopolysaccharide or pretreated with the following l-NIL ( an iNOS inhibitor ), anti-CD14, Toll-like receptor 2 (TLR2), or TLR4 antibody before stimulation with A. actinomycetemcomitans lipopolysaccharide
Lin et al., Mol Immunol 2010 : Nevertheless TLR mediated JNK activation as well as the increased protein expression of iNOS and COX-2 remained unchanged when Syk protein was knockdown by siRNA approach