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NOS3 — PRDX2

Text-mined interactions from Literome

Rössig et al., Circ Res 2002 : To address the underlying signaling mechanism, we characterized the effect of TSA on eNOS gene transcription and mRNA half-life ... Although TSA decreased both eNOS protein and mRNA levels, TSA paradoxically enhanced the activity of the eNOS promoter, and did not alter the eNOS transcription rate in nuclear run-on experiments, suggesting that TSA posttranscriptionally targets eNOS mRNA
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 )
Gan et al., J Biol Chem 2005 : Chromatin immunoprecipitation assays showed that the induction of eNOS expression by TSA was accompanied by a remarkable increase of acetylation of histone H3 associated with the eNOS 5'-flanking region in the non-endothelial cells ... Moreover, DNA methylation mediated repression of eNOS promoter activity was partially reversed by TSA treatment, and combined treatment of TSA and 5-aza-2'-deoxycytidine ( AzadC ) synergistically induced eNOS expression in non-endothelial cells ... Combined TSA and AzadC treatment increased Sp1 binding to the endogenous eNOS promoter but decreased the association between HDAC1 and Sp1 in HeLa cells
Gan et al., Biochem Biophys Res Commun 2006 : We demonstrated that at low dose ( 0.1 microg ) TSA increased the eNOS mRNA levels, which was followed by a time- and dose dependent down-regulation ... Cycloheximide, a protein synthesis inhibitor, completely abolished TSA induced decrease in eNOS expression, indicating that new protein synthesis is required for the inhibiting effect