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DDAH2 — NOS1

Text-mined interactions from Literome

Dayoub et al., Circulation 2003 : The overexpression of DDAH in cultured endothelial cells in vitro induced a 2-fold increase in NOS activity and NO production
Loyaga-Rendon et al., Atherosclerosis 2005 (Hyperplasia) : The intimal hyperplasia was associated with the impaired cyclic GMP production without change in endothelial NOS activity per se, accumulation of endogenous NOS inhibitors in endothelial cells, attenuated DDAH activity in endothelial cells and enhanced arginase activity in endothelial cells and smooth muscle layer ... These findings suggest that the impaired cyclic GMP production as a marker of NO production is possibly due to the accumulated endogenous NOS inhibitors and enhanced arginase activity, which, in turn, closely relates to the occurrence of intimal hyperplasia, and that the impaired DDAH activity would result in the accumulation of endogenous NOS inhibitors in endothelial cells
Chen et al., Am J Physiol Heart Circ Physiol 2005 (Heart Failure) : Decreased DDAH activity and DDAH-2 protein expression may cause accumulation of endogenous inhibitors of endothelial NOS , thereby contributing to endothelial dysfunction in the failing heart
Frey et al., Structure 2006 : Dimethylarginine dimethylaminohydrolase ( DDAH ) is involved in the regulation of nitric oxide synthase (NOS) by metabolizing the free endogenous arginine derivatives N ( omega ) -methyl-L-arginine ( MMA ) and N ( omega ), N ( omega ) -dimethyl-L-arginine ( ADMA ), which are competitive inhibitors of NOS
Imamura et al., Am J Physiol Regul Integr Comp Physiol 2007 : The impaired DDAH activity due to decreased expression of DDAH I protein would result in an accumulation of endogenous NOS inhibitors with CSE
Mizuno et al., Vascul Pharmacol 2008 (Lung Diseases...) : The accumulated endogenous NOS inhibitors at least partly result from the decreased DDAH activity
Feng et al., Eur J Pharmacol 2008 : DDAH2 gene transfer not only prevented the suppression of DDAH activity and the elevation of endogenous ADMA, but also attenuated the inhibition of NOS activity and the reduction of NO level induced by LPC in endothelial cells
Wu et al., Nan Fang Yi Ke Da Xue Xue Bao 2011 (Acute Lung Injury...) : Exogenous DDAH obviously decreased the levels of ADMA in the BALF and blood flowing into the lungs, increased NO concentration and NOS activity, and down-regulated MLCK and PKC mRNA and protein expressions in lung tissues of rats with cerebral I/R injury ( P < 0.05 )