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NOS3 — PRDX2
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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