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1 ethyltransferases (PRMTs) and is degraded by dimethylarginine dimethylaminohydrolase.
3 ed higher amounts of ADMA-degradation enzyme dimethylarginine dimethylaminohydrolase-1 (but similar a
4 h the FXR agonist GW4064, we have identified dimethylarginine dimethylaminohydrolase-1 (DDAH1) as an
6 verexpression of the ADMA-hydrolyzing enzyme dimethylarginine dimethylaminohydrolase-1 (DDAH1), we te
9 treatment led to proteolytic degradation of dimethylarginine dimethylaminohydrolase 2, which catabol
11 ic dimethylarginine [ADMA, via inhibition of dimethylarginine dimethylaminohydrolase (DDAH) activity]
12 minated largely through active metabolism by dimethylarginine dimethylaminohydrolase (DDAH) and thus
13 termine whether overexpression of the enzyme dimethylarginine dimethylaminohydrolase (DDAH) could enh
17 hesized that lowering ADMA concentrations by dimethylarginine dimethylaminohydrolase (DDAH) overexpre
20 The activity, but not the expression, of dimethylarginine dimethylaminohydrolase (DDAH) was reduc
21 ntitumor therapeutics, as have inhibitors of dimethylarginine dimethylaminohydrolase (DDAH), an enzym
22 a corresponding increase in the activity of dimethylarginine dimethylaminohydrolase (DDAH), an enzym
23 bstituted arginine-modifying enzymes such as dimethylarginine dimethylaminohydrolase (DDAH), arginine
24 sed to inhibit the catabolic enzyme of ADMA, dimethylarginine dimethylaminohydrolase (DDAH), but the
26 lled by two isoforms of its catabolic enzyme dimethylarginine dimethylaminohydrolase (DDAH), the dysr
27 was associated with the reduced activity of dimethylarginine dimethylaminohydrolase (DDAH), the enzy
28 vely metabolized by the intracellular enzyme dimethylarginine dimethylaminohydrolase (DDAH), which ca
29 endothelial cells (ECV304) and on the enzyme dimethylarginine dimethylaminohydrolase (DDAH), which de
30 inine is eliminated largely by the action of dimethylarginine dimethylaminohydrolase (DDAH), which ex
35 sociated with a reduction in the activity of dimethylarginine dimethylaminohydrolase (DDAH, the enzym
36 le of ADMA, and the enzymes metabolizing it, dimethylarginine dimethylaminohydrolases (DDAH) in the r
37 itric oxide synthase [eNOS], Rho-kinase, and dimethylarginine dimethylaminohydrolase [DDAH]) were ana
39 ysregulation of the ADMA-metabolizing enzyme dimethylarginine dimethylaminohydrolase I (DDAH I) plays
40 The enzyme dimethylargininase (also known as dimethylarginine dimethylaminohydrolase or DDAH; EC 3.5.
41 ne deiminase (PaAgDI), and N(omega),N(omega)-dimethylarginine dimethylaminohydrolase (PaDDAH) indicat
42 crease ADMA because they bind to and inhibit dimethylarginine dimethylaminohydrolase, the enzyme that
43 co-workers to operate in the related enzyme dimethylarginine dimethylaminohydrolase, was further exp
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