ライフサイエンスコーパス: dimethylarginine

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 1 triple Tudor domain and histone asymmetric dimethylarginine.

5 were traceable to altered nuclear levels of dimethylarginine.

6 ogenous inhibitors, asymmetric and symmetric dimethylarginine.

7 ns contain both symmetrical and asymmetrical dimethylarginines.

8 y enzyme capable of metabolizing both of the dimethylarginines.

9 Asymmetric dimethylarginine (10 microM) or native low-density lipop

10 nitric oxide synthase inhibitor asymmetrical dimethylarginine (-28% versus +0.2%) in treatment versus

11 tissue demonstrated a decrease in symmetric dimethylarginine, a PRMT5-catalyzed modification.

12 c arginines in these domains are modified to dimethylarginines, a common modification of unknown func

13 Asymmetric dimethylarginine (ADMA) and homocysteine are mechanistic

14 etin-2, osteoprotegerin, ICAM-1), asymmetric dimethylarginine (ADMA) and impaired microvascular react

15 Asymmetric dimethylarginine (ADMA) and monomethyl arginine (L-NMMA)

16 itric oxide synthase inhibitors asymmetrical dimethylarginine (ADMA) and monomethyl-l-arginine.

17 The endogenous methylarginines, asymmetric dimethylarginine (ADMA) and N (G)-monomethyl- l-arginine

18 thylated arginines (MA) including asymmetric dimethylarginine (ADMA) and N(G)-methyl-l-arginine (NMA)

19 The endogenous methylarginines asymmetric dimethylarginine (ADMA) and N(G)-monomethyl-L-arginine (

20 ntrations of two methylarginines, asymmetric dimethylarginine (ADMA) and N(G)-monomethyl-l-arginine,

21 The NOS inhibitors asymmetric dimethylarginine (ADMA) and N-monomethylarginine are met

22 ylated arginines (MAs), including asymmetric dimethylarginine (ADMA) and NG-methyl-L-arginine (L-NMMA

23 e associations were found for the asymmetric dimethylarginine (ADMA) and symmetric dimethlyarginine (

24 rginine derivatives homoarginine, asymmetric dimethylarginine (ADMA) and symmetric dimethyarginine (S

25 inine intravenous infusion and on asymmetric dimethylarginine (ADMA) and symmetric dimethylarginine (

26 cells: monomethylarginine (MMA), asymmetric dimethylarginine (ADMA) and symmetric dimethylarginine (

27 Elevated plasma concentrations of asymmetric dimethylarginine (ADMA) are associated with an increased

28 Increased levels of asymmetric dimethylarginine (ADMA) are associated with endothelial

29 ast growth factor 23 (FGF-23) and asymmetric dimethylarginine (ADMA) are associated with progression

30 endogenous NO synthase inhibitor asymmetric dimethylarginine (ADMA) circulates in plasma, and its co

31 Elevated levels of asymmetric dimethylarginine (ADMA) correlate with risk factors for

32 ht to determine if a reduction in asymmetric dimethylarginine (ADMA) enhances endothelial regeneratio

33 bility, inflammation profile, and asymmetric dimethylarginine (ADMA) in patients undergoing HD.

34 s of the endogenous NOS inhibitor asymmetric dimethylarginine (ADMA) in the hypoxia-induced pulmonary

35 e have recently demonstrated that asymmetric dimethylarginine (ADMA) induces the translocation of end

36 We sought to determine whether asymmetric dimethylarginine (ADMA) inhibits nitric oxide (NO) elabo

37 Asymmetric dimethylarginine (ADMA) is an endogenous competitive inh

38 Asymmetric dimethylarginine (ADMA) is an endogenous inhibitor of ni

39 Asymmetrical dimethylarginine (ADMA) is an endogenous inhibitor of ni

40 Plasma asymmetrical dimethylarginine (ADMA) is an endogenous inhibitor of ni

41 Asymmetric dimethylarginine (ADMA) is an endogenous inhibitor of NO

42 Asymmetric dimethylarginine (ADMA) is an endogenous metabolite.

43 and the inhibitor of NO synthesis asymmetric dimethylarginine (ADMA) is increased.

44 mpact of statin therapy on plasma asymmetric dimethylarginine (ADMA) levels has not been conclusively

45 Asymmetric-dimethylarginine (ADMA) limits NO production by inhibiti

46 Asymmetric dimethylarginine (ADMA) plays a crucial role in endothel

47 oncentrations of the uremic toxin asymmetric dimethylarginine (ADMA) were elevated in 2KO mice.

48 endogenous NO synthase inhibitor asymmetric dimethylarginine (ADMA) were measured with liquid chroma

49 ting the endogenous NOS inhibitor asymmetric dimethylarginine (ADMA), a cardiotoxic hormone whose eff

50 DAH1 is a key catabolic enzyme of asymmetric dimethylarginine (ADMA), a major endogenous nitric-oxide

51 Asymmetric dimethylarginine (ADMA), an endogenous inhibitor and unc

52 Asymmetric dimethylarginine (ADMA), an endogenous inhibitor of nitr

53 Elevated blood concentrations of asymmetric dimethylarginine (ADMA), an endogenous inhibitor of nitr

54 art by elevating plasma levels of asymmetric dimethylarginine (ADMA), an endogenous inhibitor of nitr

55 Both asymmetric dimethylarginine (ADMA), an endogenous inhibitor of NO p

56 late the metabolism or release of asymmetric dimethylarginine (ADMA), an endogenous inhibitor of NO s

57 or to endothelial pathobiology is asymmetric dimethylarginine (ADMA), an endogenous nitric oxide synt

58 Asymmetric dimethylarginine (ADMA), an endogenous nitric oxide synt

59 Increased levels of asymmetric dimethylarginine (ADMA), an endogenous nitric oxide synt

60 ively determined plasma levels of asymmetric dimethylarginine (ADMA), an endogenous nitric oxide synt

61 or to endothelial pathobiology is asymmetric dimethylarginine (ADMA), an endogenous NO synthase inhib

62 essed associations with arginine, asymmetric dimethylarginine (ADMA), and hemolysis.

63 morning for soluble CD40 ligand, asymmetric dimethylarginine (ADMA), and nitrotyrosine levels, as we

64 generates monomethylarginine and asymmetric dimethylarginine (ADMA), but not symmetric dimethylargin

65 rs, total homocysteine (tHcy) and asymmetric dimethylarginine (ADMA), correlate with decreased levels

66 assayed for endothelin 1 (ET-1), asymmetric dimethylarginine (ADMA), intercellular adhesion molecule

67 hibitor of nitric oxide synthase, asymmetric dimethylarginine (ADMA), is elevated in patients with ty

68 arginine, citrulline, ornithine, asymmetric dimethylarginine (ADMA), symmetric dimethylarginine (SDM

69 d raised plasma concentrations of asymmetric dimethylarginine (ADMA), the endogenous inhibitor of end

70 Asymmetric dimethylarginine (ADMA), which inhibits NO synthase, is

71 s nitric-oxide synthase inhibitor asymmetric dimethylarginine (ADMA).

72 ic oxide synthase (NOS) inhibitor asymmetric dimethylarginine (ADMA).

73 synthase has been characterized: asymmetric dimethylarginine (ADMA).

74 evels of l-arginine and increased asymmetric dimethylarginine (ADMA).

75 e by metabolising the risk factor asymmetric dimethylarginine (ADMA).

76 MT7 into a type I PRMT, producing asymmetric dimethylarginine (ADMA).

77 We focused on asymmetric dimethylarginine (ADMA, the endogenous inhibitor of nitr

78 CS patients had higher levels of asymmetric dimethylarginine (ADMA; P<0.0001), symmetric dimethylarg

79 Asymmetric and symmetric dimethylarginines (ADMA and SDMA) impair nitric oxide bi

80 vels of circulating asymmetric and symmetric dimethylarginines (ADMA and SDMA) predict and potentiall

81 s nitric oxide synthase inhibitor asymmetric dimethylarginine [ADMA, via inhibition of dimethylargini

82 omplex), endothelial dysfunction (asymmetric dimethylarginine [ADMA]), and platelet-derived inflammat

83 ginine, citrulline, asymmetric and symmetric dimethylarginine, alongside decreases in sphingolipids,

84 Asymmetric dimethylarginine also stimulated MCP-1 formation by endo

85 lipoprotein AI and high levels of asymmetric dimethylarginine, an endogenous inhibitor of nitric oxid

86 C-reactive protein), or levels of asymmetric dimethylarginine, an endogenous inhibitor of nitric oxid

87 ases (DDAHs) are known to degrade asymmetric dimethylarginine, an endogenous inhibitor of NOS, and ma

88 pected to lead to accumulation of asymmetric dimethylarginine and inhibition of NOS.

89 he methylated proteins showed that symmetric dimethylarginine and relatively small amounts of monomet

90 SLC25A45 binds with dimethylarginine and trimethyllysine but has no affinity

91 f the molecules naturally contain asymmetric dimethylarginine and/or monomethylarginine.

92 2 and subsequent impairment in metabolism of dimethylarginines and BAIB caused by HNF4alpha deficienc

93 n several metabolites, including tryptophan, dimethylarginine, and a recently discovered antiviral ri

94 entalized hemoglobin, arginase 1, asymmetric dimethylarginine, and adenine nucleotides are all produc

95 midine, xanthine, uracil, betaine, symmetric dimethylarginine, and asymmetric-dimethylarginine), were

96 t increases in myeloperoxidase, asymmetrical dimethylarginine, and cardiac fibrosis.

97 Choline, dimethylarginine, arginine, valine, proline, serine, his

98 CARM1 catalyzed formation of N(G),N(G)-dimethylarginine (asymmetric) but little or no N(G),N'(G

99 substrates, to form NG-monomethyl and NG,NG-dimethylarginine (asymmetric).

100 othelial cell adhesion molecule, symmetrical dimethylarginine, asymmetrical dimethylarginine, high-se

101 elop small molecule inhibitors targeting the dimethylarginine binding pocket of the SMNDC1 Tudor doma

102 n of its tetramerized coiled-coil domain and dimethylarginine-binding Tudor domains but is independen

103 The two types of dimethylarginines can lead to distinct biological output

104 anced glycation end-products, and asymmetric dimethylarginine), can be involved.

105 showed a significant increase of asymmetric dimethylarginine concentration in plasma (1.41 micromol/

106 (PZN), a polyheterocyclic, N(alpha),N(alpha)-dimethylarginine-containing antibiotic, harbors remarkab

107 ethylarginine and asymmetric omega-N(G),N(G)-dimethylarginine derivatives on the recombinant glycine-

108 biologically inactive stereoisomer symmetric dimethylarginine did not inhibit NO release.

109 nine whose cellular levels are controlled by dimethylarginine dimethylamino-hydrolase (DDAH).

110 Dimethylarginine-dimethylamino-hydrolase protein express

111 both decreased breakdown (decreased hepatic dimethylarginine-dimethylamino-hydrolase) and/or increas

112 inhibitor, undergoes hepatic metabolism via dimethylarginine-dimethylamino-hydrolase, and is derived

113 ic dimethylarginine [ADMA, via inhibition of dimethylarginine dimethylaminohydrolase (DDAH) activity]

114 minated largely through active metabolism by dimethylarginine dimethylaminohydrolase (DDAH) and thus

115 termine whether overexpression of the enzyme dimethylarginine dimethylaminohydrolase (DDAH) could enh

116 Dimethylarginine dimethylaminohydrolase (DDAH) enzymes a

117 The enzyme dimethylarginine dimethylaminohydrolase (DDAH) hydrolyse

118 In mammals, the enzyme dimethylarginine dimethylaminohydrolase (DDAH) is implic

119 hesized that lowering ADMA concentrations by dimethylarginine dimethylaminohydrolase (DDAH) overexpre

120 Dimethylarginine dimethylaminohydrolase (DDAH) regulates

121 To clarify this issue, we crossed dimethylarginine dimethylaminohydrolase (DDAH) transgeni

122 The activity, but not the expression, of dimethylarginine dimethylaminohydrolase (DDAH) was reduc

123 ntitumor therapeutics, as have inhibitors of dimethylarginine dimethylaminohydrolase (DDAH), an enzym

124 a corresponding increase in the activity of dimethylarginine dimethylaminohydrolase (DDAH), an enzym

125 bstituted arginine-modifying enzymes such as dimethylarginine dimethylaminohydrolase (DDAH), arginine

126 sed to inhibit the catabolic enzyme of ADMA, dimethylarginine dimethylaminohydrolase (DDAH), but the

127 ADMA is metabolized by the enzyme dimethylarginine dimethylaminohydrolase (DDAH), the acti

128 lled by two isoforms of its catabolic enzyme dimethylarginine dimethylaminohydrolase (DDAH), the dysr

129 was associated with the reduced activity of dimethylarginine dimethylaminohydrolase (DDAH), the enzy

130 vely metabolized by the intracellular enzyme dimethylarginine dimethylaminohydrolase (DDAH), which ca

131 endothelial cells (ECV304) and on the enzyme dimethylarginine dimethylaminohydrolase (DDAH), which de

132 inine is eliminated largely by the action of dimethylarginine dimethylaminohydrolase (DDAH), which ex

133 its NO synthase, is inactivated by N(G),N(G)-dimethylarginine dimethylaminohydrolase (DDAH).

134 methylarginine are metabolized by the enzyme dimethylarginine dimethylaminohydrolase (DDAH).

135 abel for the nitric oxide controlling enzyme dimethylarginine dimethylaminohydrolase (DDAH).

136 The enzymes dimethylargininase [dimethylarginine dimethylaminohydrolase (DDAH); EC 3.5.3

137 sociated with a reduction in the activity of dimethylarginine dimethylaminohydrolase (DDAH, the enzym

138 ne deiminase (PaAgDI), and N(omega),N(omega)-dimethylarginine dimethylaminohydrolase (PaDDAH) indicat

139 lowering of ADMA by recombinant recombinant dimethylarginine dimethylaminohydrolase (rDDAH)-1 improv

140 Effects of recombinant dimethylarginine dimethylaminohydrolase (rDDAH)-1 on I/R

141 Dimethylarginine dimethylaminohydrolase 1 (DDAH1) degrad

142 Dimethylarginine dimethylaminohydrolase 1 (DDAH1) protec

143 Neuropilin-1 maintains dimethylarginine dimethylaminohydrolase 1 expression in

144 treatment led to proteolytic degradation of dimethylarginine dimethylaminohydrolase 2, which catabol

145 itric oxide synthase [eNOS], Rho-kinase, and dimethylarginine dimethylaminohydrolase [DDAH]) were ana

146 Reports have shown that dimethylarginine dimethylaminohydrolase activity is down

147 ysregulation of the ADMA-metabolizing enzyme dimethylarginine dimethylaminohydrolase I (DDAH I) plays

148 The enzyme dimethylargininase (also known as dimethylarginine dimethylaminohydrolase or DDAH; EC 3.5.

149 crease ADMA because they bind to and inhibit dimethylarginine dimethylaminohydrolase, the enzyme that

150 co-workers to operate in the related enzyme dimethylarginine dimethylaminohydrolase, was further exp

151 ed higher amounts of ADMA-degradation enzyme dimethylarginine dimethylaminohydrolase-1 (but similar a

152 h the FXR agonist GW4064, we have identified dimethylarginine dimethylaminohydrolase-1 (DDAH1) as an

153 Dimethylarginine dimethylaminohydrolase-1 (DDAH1) is a m

154 verexpression of the ADMA-hydrolyzing enzyme dimethylarginine dimethylaminohydrolase-1 (DDAH1), we te

155 Dimethylarginine dimethylaminohydrolase-1 transgenic (TG

156 We further observed myocardial levels of dimethylarginine dimethylaminohydrolase-1 were increased

157 ethyltransferases (PRMTs) and is degraded by dimethylarginine dimethylaminohydrolase.

158 le of ADMA, and the enzymes metabolizing it, dimethylarginine dimethylaminohydrolases (DDAH) in the r

159 ADMA can be metabolized by dimethylarginine dimethylaminohydrolases (DDAHs) and by

160 Dimethylarginine dimethylaminohydrolases (DDAHs) are kno

161 ADMA levels are controlled by dimethylarginine dimethylaminohydrolases (DDAHs), cytoso

162 at contribute to BMC formation by binding to dimethylarginine (DMA) modifications on protein ligands.

163 Binding to dimethylarginine (DMA) modified protein ligands was requ

164 Dimethylarginines (DMA) interfere with nitric oxide form

165 s showed changes in 21 metabolites including Dimethylarginine (DMAG) and activation of tryptophan met

166 RMT1) catalyzing the formation of asymmetric dimethylarginines has been implicated in cancer developm

167 , symmetrical dimethylarginine, asymmetrical dimethylarginine, high-sensitivity troponin T, and cysta

168 ethylarginine and symmetric omega-N(G),N(G')-dimethylarginine in a variety of proteins.

169 ponsible for the deposition of the symmetric dimethylarginine in mammalian cells.

170 talyzes the formation of asymmetric (type I) dimethylarginine in vitro.

171 me functions to modify specific arginines to dimethylarginines in the arginine- and glycine-rich doma

172 Asymmetric dimethylarginine increases endothelial oxidative stress

173 Asymmetric dimethylarginine-induced monocyte binding was diminished

174 Asymmetric dimethylarginine is an endogenous inhibitor of nitric ox

175 Asymmetric dimethylarginine is eliminated largely by the action of

176 nt competitive interaction between symmetric dimethylarginine level and c-terminal FGF-23 level for t

177 Elevated asymmetric and symmetric dimethylarginine levels combined with reduced arginine l

178 tients with normal renal function, symmetric dimethylarginine levels inversely correlated with mean a

179 els were lower and plasma CFH and asymmetric dimethylarginine levels were higher in patients with mal

180 Symmetric dimethylarginine levels were increased in serum and frac

181 ell adhesion molecule (VCAM), and asymmetric dimethylarginine levels were measured.

182 PRMT1, which deposits an asymmetric dimethylarginine mark on histone/non-histone proteins, i

183 Asymmetric dimethylarginine may be an endogenous proatherogenic mol

184 Elevated dimethylarginines may serve as important biological mark

185 Additionally, symmetrical dimethylarginine (mean, 1.97+/-0.61 [SD]; P=0.01) was id

186 nts revealed the presence of the symmetrical dimethylarginine modification catalyzed by PRMT5 associa

187 ansferase (PRMT)-1, and nuclear asymmetrical dimethylarginine modification was increased with LRP6-VK

188 enzyme responsible for generating symmetric dimethylarginine modifications on the carboxyl-terminal

189 the exon unique to CSR-1A contains multiple dimethylarginine modifications, which are necessary for

190 nce contexts, and identification of isomeric dimethylarginine modifications.

191 However, symmetrical dimethylarginine-modified proteins were not detected at

192 ting discrete biological roles for mono- and dimethylarginine-modified proteins.

193 We show that SMN binds preferentially to the dimethylarginine-modified RG domains of SmD1 and SmD3.

194 remarkably, the formation of monomethyl- and dimethylarginine on histone H3 and within octamers.

195 thylarginine, not asymmetric omega-N(G),N(G)-dimethylarginine or symmetric omega-N(G),N(G')-dimethyla

196 dimethylarginine (ADMA; P<0.0001), symmetric dimethylarginine (P<0.0001), monomethylarginine (P=0.000

197 Asymmetric dimethylarginine plays a role in endothelial dysfunction

198 S from SMs were asymmetrical and symmetrical dimethylarginine, pregnenolone sulfate, and adenosine.

199 In the absence of the omega-NG, NG-[3H]dimethylarginine product of the RMT1 methyltransferase,

200 dent inhibition of PRMT5-dependent symmetric dimethylarginine protein modification in MTAP-deleted tu

201 peptide (r=0.25, P=0.001), and asymmetrical dimethylarginine (r=0.32, P<0.001).

202 The arginine-to-dimethylarginine ratio is associated with severe sepsis,

203 We hypothesized that the arginine-to-dimethylarginine ratio is reduced in patients with sever

204 The arginine-to-dimethylarginine ratio may be a useful biomarker, and in

205 The arginine-to-dimethylarginine ratio was correlated with Acute Physiol

206 The arginine-to-dimethylarginine ratio was correlated with the urinary n

207 The arginine-to-dimethylarginine ratio was higher in control subjects vs

208 A declining arginine-to-dimethylarginine ratio was independently associated with

209 hat can result in the formation of symmetric dimethylarginine residues as observed previously in myel

210 the formation of asymmetric omega-N(G),N(G)-dimethylarginine residues by transferring methyl groups

211 rupted is viable, but the level of NG,NG-[3H]dimethylarginine residues detected in intact cells incub

212 apable of selectively recognizing asymmetric dimethylarginine (Rme2a).

213 ogical pathways via recognition of symmetric dimethylarginine (Rme2s) on proteins by its Tudor domain

214 MA and their combined sum, which we termed a dimethylarginine score, were better predictors of outcom

215 RMTs, PRMT5, affects the levels of symmetric dimethylarginine (SDMA) at Arg-3 on histone H4, leading

216 levels of L-arginine, ADMA, and symmetrical dimethylarginine (SDMA) by high-performance liquid chrom

217 metric dimethylarginine (ADMA) and symmetric dimethylarginine (SDMA) concentrations in conditions rep

218 Elevated symmetric dimethylarginine (SDMA) has been shown to predict cardio

219 tify proteins with PRMT5-dependent symmetric dimethylarginine (SDMA) modification induced upon RS.

220 We uncover the presence of symmetrical dimethylarginine (sDMA) on chromatoid body components an

221 mmalian enzymes capable of forming symmetric dimethylarginine (SDMA) residues as type II PRMTs.

222 spliceosomal Sm proteins contain symmetrical dimethylarginine (sDMA) residues in vivo.

223 ranslationally modified to contain symmetric dimethylarginine (sDMA) residues within their C-terminal

224 symmetric dimethylarginine (ADMA), symmetric dimethylarginine (SDMA), and N-monomethylarginine (MMA)

225 hether ADMA, and its stereo-isomer symmetric dimethylarginine (SDMA), are increased in alcoholic hepa

226 inase, cell-free hemoglobin, ADMA, symmetric-dimethylarginine (SDMA), histidine-rich protein-2, and a

227 that catalyzes the formation of symmetrical dimethylarginine (sDMA), is a nucleolin-associated prote

228 t post-translational modification, symmetric dimethylarginine (sDMA), of Aub is essential for piRNA b

229 ntly generate either asymmetric or symmetric dimethylarginine (SDMA), PRMT7 is unique in producing so

230 eferentially and directly to the symmetrical dimethylarginine (sDMA)-modified arginine- and glycine-r

231 edominantly monomethylarginine and symmetric dimethylarginine (SDMA).

232 decreased amounts of proteins with symmetric dimethylarginine (sDMA).

233 c dimethylarginine (ADMA), but not symmetric dimethylarginine (SDMA).

234 ydrolase (DDAH) activity] and with symmetric dimethylarginine (SDMA).

235 metric dimethylarginine (ADMA) and symmetric dimethylarginine (SDMA).

236 atographed with a symmetric omega-N(G),N(G')-dimethylarginine standard.

237 ine (asymmetric) but little or no N(G),N'(G)-dimethylarginine (symmetric) and no form of methyllysine

238 Coilin contains symmetrical dimethylarginines that modulate its affinity for SMN, an

239 the level of p-cresol sulfate or asymmetric dimethylarginine to significant reductions in the levels

240 landin F(1alpha), endothelin-1, asymmetrical dimethylarginine, tumor necrosis factor-alpha, monocyte

241 vity) as well as small amounts of asymmetric dimethylarginine (type I activity).

242 the resulting methylated product: asymmetric dimethylarginine (Type I PRMT), symmetric dimethylargini

243 ic dimethylarginine (Type I PRMT), symmetric dimethylarginine (Type II PRMT), or monomethylated argin

244 characterized by higher levels of asymmetric dimethylarginine, tyramine, 2-hydroxybutyric acid, phosp

245 methylarginine or symmetric omega-N(G),N(G')-dimethylarginine, under the conditions tested.

246 ieu contains increased amounts of asymmetric dimethylarginine, we speculate that such accumulation of

247 ric oxide oxidation products, and asymmetric dimethylarginine were abnormal in patients with PAH and

248 ls of l-arginine, arginase-1, and asymmetric dimethylarginine were measured at serial time-points.

249 amounts of monomethylarginine and asymmetric dimethylarginine were produced.

250 ansferase activity and asymmetric N(G), N(G)-dimethylarginine were reduced by 85 and 54%, respectivel

251 laria, hematocrit and CFH but not asymmetric dimethylarginine were significant predictors.

252 , symmetric dimethylarginine, and asymmetric-dimethylarginine), were also increased in urine from tum