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EC Number Application Commentary Reference
Display the word mapDisplay the reaction diagram Show all sequences 3.5.3.18medicine seven days after coronary artery ligation, L-Arg and methylated arginine content, as well as DDAH activity are determined in homogenates of left ventricular infarct and border. In healthy hearts, DDAHI is absent, and DDAHII is localized to endothelium and endocardium with a similar distribution to that of eNOS. Following myocardial infarction, left ventricular DDAH activity is increased to 210% of control. Both DDAHI and DDAHII proteins are detected in peri-infarct cardiomyocytes, while DDAHII immunoreactivity is additionally localized to infiltrating inflammatory cells and blood vessels in the healing infarct. Both plasma and left ventricular concentrations of the DDAH substrate, ADMA, are increased post-myocardial infarction, although the ratio of Arg:ADMA is retained in the left ventricular post-myocardial infarction relative to sham operated controls 710771
Display the word mapDisplay the reaction diagram Show all sequences 3.5.3.18medicine structure-based development of specific DDAH-1 inhibitors that might be useful in the therapeutic treatment of NOS dysfunction-related diseases 670913
Display the word mapDisplay the reaction diagram Show all sequences 3.5.3.18analysis use of inhibitor N-(but-3-yn-1-yl)-2-chloroethanimidamide as a broad-specificity probe for labeling endogenous DDAH isoforms and enzymes with similar pharmacophores. Inhibitor labels the active fraction of DDAH-1 in intact mammalian cells and can be blocked by the presence of competitive reversible and irreversible inhibitors. Incorporation of the alkyne tag allows to derivatize with a variety of reagents after in vivo tagging 712238
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