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NOS2 — PRDX2

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Yu et al., J Am Soc Nephrol 2002 : TSA inhibited induction of endogenous NO production and iNOS as well as NF-kappa B element promoter activity in response to interleukin-1 beta (IL-1 beta) or lipopolysaccharide (LPS) + interferon-gamma (IFN-gamma) in both cell types without altering NF-kappa B DNA binding activity
Suuronen et al., J Neurochem 2003 (Inflammation) : TSA clearly potentiated the LPS induced expression of interleukin (IL)-6 and inducible nitric oxide synthase mRNAs, as well as the secretion of cytokines IL-6, tumour necrosis factor-alpha and macrophage inflammatory protein (MIP)-2, and nitric oxide ( NO )
Yu et al., American journal of physiology. Renal physiology 2006 : Thus TSA diminishes IL-1beta induced iNOS transcription through phosphoinositide 3-kinase- and p70s6 kinase dependent pathways that increase site-specific histone H4 acetylation at the -978 to -710 region of the iNOS promoter
Susick et al., J Cell Mol Med 2008 : Trichostatin A (TSA) , a known inhibitor of HDACs, markedly reduced IL-1beta mediated iNOS expression and NO release from these cells in a concentration dependent manner
Chabane et al., Osteoarthritis Cartilage 2008 : In the present study, we determined the effect of trichostatin A (TSA) and butyric acid ( BA ), two histone deacetylase (HDAC) inhibitors, on NO and PGE ( 2 ) synthesis, inducible NO synthase (iNOS) and cyclooxygenase (COX)-2 expression, and nuclear factor (NF)-kappaB DNA binding activity, in interleukin-1beta (IL-1) stimulated human OA chondrocytes, and on IL-1 induced proteoglycan degradation in cartilage explants
Lu et al., Am J Physiol Cell Physiol 2009 : This article reports on a study of the effect of trichostatin A (TSA) , an inhibitor of histone deacetylase, on lipopolysaccharide (LPS) induced expression of inducible nitric oxide synthase (iNOS) in RAW 264.7 macrophages and its underlying mechanisms ... This study demonstrates that TSA diminishes iNOS expression in LPS treated macrophages by inhibiting Oct-2 expression and thus reducing the production of NO