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1 ensitivity C-reactive protein and asymmetric dimethylarginine).
2 characteristic of symmetric omega-N(G),N(G')-dimethylarginine.
3 ethylarginine and symmetric omega-N(G),N(G')-dimethylarginine.
4 ogenous inhibitors, asymmetric and symmetric dimethylarginine.
5 y enzyme capable of metabolizing both of the dimethylarginines.
6 ns contain both symmetrical and asymmetrical dimethylarginines.
8 nitric oxide synthase inhibitor asymmetrical dimethylarginine (-28% versus +0.2%) in treatment versus
9 c arginines in these domains are modified to dimethylarginines, a common modification of unknown func
13 The endogenous methylarginines, asymmetric dimethylarginine (ADMA) and N (G)-monomethyl- l-arginine
14 thylated arginines (MA) including asymmetric dimethylarginine (ADMA) and N(G)-methyl-l-arginine (NMA)
15 The endogenous methylarginines asymmetric dimethylarginine (ADMA) and N(G)-monomethyl-L-arginine (
17 ylated arginines (MAs), including asymmetric dimethylarginine (ADMA) and NG-methyl-L-arginine (L-NMMA
18 inine intravenous infusion and on asymmetric dimethylarginine (ADMA) and symmetric dimethylarginine (
19 cells: monomethylarginine (MMA), asymmetric dimethylarginine (ADMA) and symmetric dimethylarginine (
21 ast growth factor 23 (FGF-23) and asymmetric dimethylarginine (ADMA) are associated with progression
22 endogenous NO synthase inhibitor asymmetric dimethylarginine (ADMA) circulates in plasma, and its co
24 ht to determine if a reduction in asymmetric dimethylarginine (ADMA) enhances endothelial regeneratio
25 s of the endogenous NOS inhibitor asymmetric dimethylarginine (ADMA) in the hypoxia-induced pulmonary
26 e have recently demonstrated that asymmetric dimethylarginine (ADMA) induces the translocation of end
27 We sought to determine whether asymmetric dimethylarginine (ADMA) inhibits nitric oxide (NO) elabo
35 mpact of statin therapy on plasma asymmetric dimethylarginine (ADMA) levels has not been conclusively
37 endogenous NO synthase inhibitor asymmetric dimethylarginine (ADMA) were measured with liquid chroma
38 ting the endogenous NOS inhibitor asymmetric dimethylarginine (ADMA), a cardiotoxic hormone whose eff
39 DAH1 is a key catabolic enzyme of asymmetric dimethylarginine (ADMA), a major endogenous nitric-oxide
40 Elevated blood concentrations of asymmetric dimethylarginine (ADMA), an endogenous inhibitor of nitr
41 art by elevating plasma levels of asymmetric dimethylarginine (ADMA), an endogenous inhibitor of nitr
44 late the metabolism or release of asymmetric dimethylarginine (ADMA), an endogenous inhibitor of NO s
45 or to endothelial pathobiology is asymmetric dimethylarginine (ADMA), an endogenous nitric oxide synt
48 ively determined plasma levels of asymmetric dimethylarginine (ADMA), an endogenous nitric oxide synt
49 or to endothelial pathobiology is asymmetric dimethylarginine (ADMA), an endogenous NO synthase inhib
51 morning for soluble CD40 ligand, asymmetric dimethylarginine (ADMA), and nitrotyrosine levels, as we
52 generates monomethylarginine and asymmetric dimethylarginine (ADMA), but not symmetric dimethylargin
53 rs, total homocysteine (tHcy) and asymmetric dimethylarginine (ADMA), correlate with decreased levels
54 assayed for endothelin 1 (ET-1), asymmetric dimethylarginine (ADMA), intercellular adhesion molecule
55 hibitor of nitric oxide synthase, asymmetric dimethylarginine (ADMA), is elevated in patients with ty
56 arginine, citrulline, ornithine, asymmetric dimethylarginine (ADMA), symmetric dimethylarginine (SDM
57 d raised plasma concentrations of asymmetric dimethylarginine (ADMA), the endogenous inhibitor of end
65 CS patients had higher levels of asymmetric dimethylarginine (ADMA; P<0.0001), symmetric dimethylarg
67 vels of circulating asymmetric and symmetric dimethylarginines (ADMA and SDMA) predict and potentiall
68 s nitric oxide synthase inhibitor asymmetric dimethylarginine [ADMA, via inhibition of dimethylargini
69 omplex), endothelial dysfunction (asymmetric dimethylarginine [ADMA]), and platelet-derived inflammat
70 ginine, citrulline, asymmetric and symmetric dimethylarginine, alongside decreases in sphingolipids,
72 lipoprotein AI and high levels of asymmetric dimethylarginine, an endogenous inhibitor of nitric oxid
73 C-reactive protein), or levels of asymmetric dimethylarginine, an endogenous inhibitor of nitric oxid
75 he methylated proteins showed that symmetric dimethylarginine and relatively small amounts of monomet
77 2 and subsequent impairment in metabolism of dimethylarginines and BAIB caused by HNF4alpha deficienc
78 entalized hemoglobin, arginase 1, asymmetric dimethylarginine, and adenine nucleotides are all produc
79 midine, xanthine, uracil, betaine, symmetric dimethylarginine, and asymmetric-dimethylarginine), were
84 othelial cell adhesion molecule, symmetrical dimethylarginine, asymmetrical dimethylarginine, high-se
86 showed a significant increase of asymmetric dimethylarginine concentration in plasma (1.41 micromol/
87 (PZN), a polyheterocyclic, N(alpha),N(alpha)-dimethylarginine-containing antibiotic, harbors remarkab
88 ethylarginine and asymmetric omega-N(G),N(G)-dimethylarginine derivatives on the recombinant glycine-
92 both decreased breakdown (decreased hepatic dimethylarginine-dimethylamino-hydrolase) and/or increas
93 inhibitor, undergoes hepatic metabolism via dimethylarginine-dimethylamino-hydrolase, and is derived
94 ic dimethylarginine [ADMA, via inhibition of dimethylarginine dimethylaminohydrolase (DDAH) activity]
95 minated largely through active metabolism by dimethylarginine dimethylaminohydrolase (DDAH) and thus
96 termine whether overexpression of the enzyme dimethylarginine dimethylaminohydrolase (DDAH) could enh
100 hesized that lowering ADMA concentrations by dimethylarginine dimethylaminohydrolase (DDAH) overexpre
103 The activity, but not the expression, of dimethylarginine dimethylaminohydrolase (DDAH) was reduc
104 a corresponding increase in the activity of dimethylarginine dimethylaminohydrolase (DDAH), an enzym
105 ntitumor therapeutics, as have inhibitors of dimethylarginine dimethylaminohydrolase (DDAH), an enzym
106 bstituted arginine-modifying enzymes such as dimethylarginine dimethylaminohydrolase (DDAH), arginine
107 sed to inhibit the catabolic enzyme of ADMA, dimethylarginine dimethylaminohydrolase (DDAH), but the
109 lled by two isoforms of its catabolic enzyme dimethylarginine dimethylaminohydrolase (DDAH), the dysr
110 was associated with the reduced activity of dimethylarginine dimethylaminohydrolase (DDAH), the enzy
111 vely metabolized by the intracellular enzyme dimethylarginine dimethylaminohydrolase (DDAH), which ca
112 endothelial cells (ECV304) and on the enzyme dimethylarginine dimethylaminohydrolase (DDAH), which de
113 inine is eliminated largely by the action of dimethylarginine dimethylaminohydrolase (DDAH), which ex
118 sociated with a reduction in the activity of dimethylarginine dimethylaminohydrolase (DDAH, the enzym
119 ne deiminase (PaAgDI), and N(omega),N(omega)-dimethylarginine dimethylaminohydrolase (PaDDAH) indicat
121 treatment led to proteolytic degradation of dimethylarginine dimethylaminohydrolase 2, which catabol
122 itric oxide synthase [eNOS], Rho-kinase, and dimethylarginine dimethylaminohydrolase [DDAH]) were ana
124 ysregulation of the ADMA-metabolizing enzyme dimethylarginine dimethylaminohydrolase I (DDAH I) plays
125 The enzyme dimethylargininase (also known as dimethylarginine dimethylaminohydrolase or DDAH; EC 3.5.
126 crease ADMA because they bind to and inhibit dimethylarginine dimethylaminohydrolase, the enzyme that
127 co-workers to operate in the related enzyme dimethylarginine dimethylaminohydrolase, was further exp
128 ed higher amounts of ADMA-degradation enzyme dimethylarginine dimethylaminohydrolase-1 (but similar a
129 h the FXR agonist GW4064, we have identified dimethylarginine dimethylaminohydrolase-1 (DDAH1) as an
131 verexpression of the ADMA-hydrolyzing enzyme dimethylarginine dimethylaminohydrolase-1 (DDAH1), we te
133 We further observed myocardial levels of dimethylarginine dimethylaminohydrolase-1 were increased
135 le of ADMA, and the enzymes metabolizing it, dimethylarginine dimethylaminohydrolases (DDAH) in the r
138 , symmetrical dimethylarginine, asymmetrical dimethylarginine, high-sensitivity troponin T, and cysta
142 me functions to modify specific arginines to dimethylarginines in the arginine- and glycine-rich doma
147 nt competitive interaction between symmetric dimethylarginine level and c-terminal FGF-23 level for t
148 tients with normal renal function, symmetric dimethylarginine levels inversely correlated with mean a
153 nts revealed the presence of the symmetrical dimethylarginine modification catalyzed by PRMT5 associa
154 ansferase (PRMT)-1, and nuclear asymmetrical dimethylarginine modification was increased with LRP6-VK
155 enzyme responsible for generating symmetric dimethylarginine modifications on the carboxyl-terminal
159 We show that SMN binds preferentially to the dimethylarginine-modified RG domains of SmD1 and SmD3.
160 thylarginine, not asymmetric omega-N(G),N(G)-dimethylarginine or symmetric omega-N(G),N(G')-dimethyla
161 dimethylarginine (ADMA; P<0.0001), symmetric dimethylarginine (P<0.0001), monomethylarginine (P=0.000
172 hat can result in the formation of symmetric dimethylarginine residues as observed previously in myel
173 the formation of asymmetric omega-N(G),N(G)-dimethylarginine residues by transferring methyl groups
174 rupted is viable, but the level of NG,NG-[3H]dimethylarginine residues detected in intact cells incub
175 MA and their combined sum, which we termed a dimethylarginine score, were better predictors of outcom
176 RMTs, PRMT5, affects the levels of symmetric dimethylarginine (SDMA) at Arg-3 on histone H4, leading
177 levels of L-arginine, ADMA, and symmetrical dimethylarginine (SDMA) by high-performance liquid chrom
178 metric dimethylarginine (ADMA) and symmetric dimethylarginine (SDMA) concentrations in conditions rep
183 ranslationally modified to contain symmetric dimethylarginine (sDMA) residues within their C-terminal
184 symmetric dimethylarginine (ADMA), symmetric dimethylarginine (SDMA), and N-monomethylarginine (MMA)
185 hether ADMA, and its stereo-isomer symmetric dimethylarginine (SDMA), are increased in alcoholic hepa
186 inase, cell-free hemoglobin, ADMA, symmetric-dimethylarginine (SDMA), histidine-rich protein-2, and a
187 that catalyzes the formation of symmetrical dimethylarginine (sDMA), is a nucleolin-associated prote
188 ntly generate either asymmetric or symmetric dimethylarginine (SDMA), PRMT7 is unique in producing so
189 eferentially and directly to the symmetrical dimethylarginine (sDMA)-modified arginine- and glycine-r
195 ine (asymmetric) but little or no N(G),N'(G)-dimethylarginine (symmetric) and no form of methyllysine
197 the level of p-cresol sulfate or asymmetric dimethylarginine to significant reductions in the levels
198 landin F(1alpha), endothelin-1, asymmetrical dimethylarginine, tumor necrosis factor-alpha, monocyte
201 ieu contains increased amounts of asymmetric dimethylarginine, we speculate that such accumulation of
202 ric oxide oxidation products, and asymmetric dimethylarginine were abnormal in patients with PAH and
203 ls of l-arginine, arginase-1, and asymmetric dimethylarginine were measured at serial time-points.
205 ansferase activity and asymmetric N(G), N(G)-dimethylarginine were reduced by 85 and 54%, respectivel
206 , symmetric dimethylarginine, and asymmetric-dimethylarginine), were also increased in urine from tum
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