ライフサイエンスコーパス: L-arginine

1 ic oxide synthase inhibitor (N(G)-monomethyl L-arginine).

2 itochondria isolated from rats or mice given L-arginine).

3 duct or by intraperitoneal administration of L-arginine.

4 form, indicating that the bacterium requires l-arginine.

5 , adenosine, cytosine, guanine, thymine, and l-arginine.

6 s, from physiologically abundant glucose and L-arginine.

7 ine dihydrolase pathway to generate ATP from L-arginine.

8 iated by nitric oxide-dependent depletion of l-arginine.

9 OS) and thus can catalyze NO production from L-arginine.

10 in mice after administration of cerulein or L-arginine.

11 ith the olfactory response to the amino acid L-arginine.

12 eloped sensor revealed a good selectivity to L-arginine.

13 enzymes that generate nitric oxide (NO) from L-arginine.

14 eted of DCs and challenged with caerulein or L-arginine.

15 ic hormone whose effects can be prevented by l-arginine.

16 endothelial nitric oxide synthase substrate, L-arginine.

17 rical dimethylarginine (ADMA) and monomethyl-l-arginine.

18 , an enzyme that metabolizes l-citrulline to l-arginine.

19 bition witnessed when MPhis were cultured in L-arginine.

20 -oxo mimic of the ferryl intermediate in the l-arginine 3-hydroxylase, VioC, reveals coordinated moti

21 preparation methods and on the use of dansyl-l-arginine-(3-methyl-1,5-pantanediyl)amide and a DNA apt

22 vity was measured by using Nalpha-Benzoyl-D, l-arginine 4-nitroanilide hydrochloride (BAPNA) as the s

23 le compound (N2-[(2,2-diphenylethoxy)acetyl]-l-arginine, 4), known as a weak C3aR antagonist (IC50 mu

24 Bath application of SNAP (2mM) or l-arginine (50mM) elicited similar inhibitory effects on

25 (3), L-tryptophan (4), L-phenylalanine (5), L-arginine (6) has been accomplished by employing ZnCl2

26 bition (92+/-2, 67+/-2%CVC(max), P < 0.001), L-arginine (93+/-2, 71+/-5%CVC(max), P < 0.001) and comb

27 tradermal microdialysis of l-N(G)-monomethyl-l-arginine, a nitric oxide antagonist, in response to in

28 Treatment of cells with N(G)-nitro-L-arginine, a slowly reversible competitive inhibitor th

29 c oxide synthase inhibitor l-N(G)-monomethyl-l-arginine acetate (l-NMMA) into both femoral arteries r

30 n improvement in eNOS activity and increased L-arginine/ADMA ratio and DDAH1 expression.

31 In addition, these lower L-arginine/ADMA ratios are associated with reduced lung

32 Also in this phenotype, a reduced L-arginine/ADMA was associated with less IgE, increased

33 The log of plasma L-arginine/ADMA was inversely correlated with BMI in the

34 he relationship was lost after adjusting for L-arginine/ADMA.

35 d the clinically compatible basic amino acid L-arginine against planktonic and biofilm bacteria both

36 In Escherichia coli, the l-arginine/agmatine antiporter AdiC facilitates the expo

37 ate binding and specificity of the wild-type l-arginine/agmatine antiporter AdiC.

38 r injured rats treated with either AdGDNF or l-arginine alone.

39 lin D, encoded by Ppid) by administration of L-arginine (also in rats), caerulein, bile acid, or an A

40 abeling studies reveal that N(omega)-methoxy-L-arginine, an alternative NOS substrate, produces citru

41 A series of L-arginine analogue nitric oxide synthase inhibitors wit

42 Administration of L-arginine and a beta-adrenergic receptor agonist (CL316

43 the MmMNAGS-K in the presence and absence of L-arginine and a tetramer-octamer equilibrium that shift

44 Nonetheless, many nNOS inhibitors mimic l-arginine and are poorly bioavailable.

45 consequential link between the transport of l-arginine and endothelial nitric oxide synthase uncoupl

46 omain electron transfer mechanism to oxidize l-arginine and generate NO.

47 scent strains, we studied the combination of L-arginine and gentamicin against planktonic persisters

48 in the vasculature can compete with eNOS for L-arginine and has been implicated in atherosclerosis.

49 Most nNOS inhibitors mimic l-arginine and have poor bioavailability.

50 s associated with reduced systemic levels of l-arginine and increased asymmetric dimethylarginine (AD

51 Substantial production of NH2Cl from l-arginine and l-histidine was observed at Cl/P = 1.0 an

52 as observed from UV254-irradiated samples of l-arginine and l-histidine when Cl/P = 2.0 and 3.0, as w

53 show that these proteins, which are rich in l-arginine and l-lysine amino acids, promote COM growth.

54 issociated into tetramers in the presence of l-arginine and NaCl, which was reversible upon dilution

55 , we explore the possible involvement of the L-arginine and nitric oxide (NO) pathway on RBC deformab

56 vity and neuronal NOS expression, as well as l-arginine and NO(x) production, increased along neural

57 NO is synthesized from l-arginine and oxygen (O(2)) by the enzyme nitric oxide

58 xpressing nitric oxide synthase-2 (NOS2) via l-arginine and oxygen is a key protective mechanism agai

59 creased plasma levels of ADMA and monomethyl-l-arginine and reduced endothelial nitric oxide response

60 Intrathecal injection of L-arginine and SNAP significantly increased mechanical n

61 L-arginine and SNAP significantly reduced the amplitude

62 ester (L-NAME) pretreatment blocked, whereas L-arginine and sodium nitroprusside (SNP) each enhanced,

63 , decreased bioavailability of the substrate l-arginine and/or BH(4) may contribute to decreased NO p

64 itric oxide (NO) donor (SNAP), NO substrate (l-arginine), and NO synthase inhibitor (l-NAME) on bladd

65 dation was induced by nitroguanidine itself, L-arginine, and creatinine, all being iminic compounds c

66 only the heating of a mixture of Ce(NO3 )3 , l-arginine, and preformed Pd seeds in water without addi

67 ith the interindividual variability in ADMA, l-arginine, and SDMA.

68 Treatment with gamma interferon (IFN-gamma), l-arginine, and tetrahydrobiopterin enhanced expression

69 VGSC was investigated by using substance P, l-arginine, and veratrine, respectively, as biomarkers.

70 ins (BaCl2, ouabain, L-NMMA [N(G)-monomethyl-L-arginine] and ketorolac, respectively).

71 parameters of pancreatic injury in mice with L-arginine AP.

72 method for the quantitative determination of L-arginine (Arg) has been developed.

73 Here, we show that L-arginine (Arg) uptake through the host cell's SLC7A2-e

74 OS was not affected by the concentrations of l-arginine (Arg), NADPH, FAD, FMN, tetrahydrobiopterin (

75 tive dimers by tetrahydrobiopterin (H4B) and l-arginine (Arg).

76 ry tonometry (EndoPAT), and plasma levels of l-arginine, arginase-1, and asymmetric dimethylarginine

77 L-Lysine (lysine), L-Cysteine (cysteine) and L-Arginine (arginine) as bifunctional species with (or w

78 dehydrogenase (PdhR), trehalose (TreR), and l-arginine (ArgR) repressor proteins were functionalized

79 of aminoglycoside and the non-toxic adjuvant L-arginine as catheter lock solution could constitute a

80 helial nitric-oxide synthase (eNOS) utilizes l-arginine as its principal substrate, converting it to

81 These results suggest that L-arginine availability functions as a regulatory signal

82 These data suggest that increasing L-arginine bioavailability via oral supplementation can

83 d the L-arginine to ADMA ratio (a measure of L-arginine bioavailability) were reduced in patients wit

84 re vivax malaria, is associated with reduced L-arginine bioavailability, and may contribute to microv

85 Because of deficiencies in l-arginine biosynthesis, some cancers are susceptible to

86 se (NAGS-K) catalyzes the first two steps of L-arginine biosynthesis.

87 plants, NAG is the first intermediate of the L-arginine biosynthesis; in animals, NAG is an allosteri

88 Arginase-1 (Arg1) also metabolizes l-arginine but does not require oxygen as a substrate an

89 s enhanced in cells grown in the presence of L-arginine but not L-lysine.

90 ive catalyst for the oxidation of endogenous L-arginine by hydrogen peroxide.

91 ing molecule synthesized de novo mainly from L-arginine by NO synthase (NOS) enzymes.

92 l-Citrulline is recycled to l-arginine by two enzymes, argininosuccinate synthase (A

93 L-arginine/citrulline assays suggested that Stramonita N

94 N(G)-monomethyl L-arginine completely inhibited the increase in endothel

95 iggered by mixing a reduced enzyme/N-hydroxy-l-arginine complex with an aerated buffer solution.

96 tures of SmTK complexed with taurocyamine or l-arginine compounds explain the mechanism by which an a

97 n and activity and markedly elevated cardiac l-arginine concentrations, unmasking a novel mechanism o

98 induced in CD11c.DTR mice using caerulein or L-arginine; DCs were depleted by administration of dipht

99 t therapeutic and although combining it with l-arginine decreased contusion size, it did not enhance

100 replication without immunopathology, whilst L-arginine decreased.

101 Prevention or reversal of L-arginine deficiency blunts mastocytosis in ileal villi

102 parasite-infected mice, like humans, develop L-arginine deficiency, which is associated with intestin

103 of mice with the NOS inhibitor NG-monomethyl-l-arginine delayed weight loss and death among 1918 viru

104 vity, evidenced in Pf-infected RBCs, induced L-arginine-dependent NO production.

105 OS) and nitric oxide, produced mainly via an l-arginine-dependent process, contribute to the kinase a

106 m of human arginase-1 (PEG-arg1) resulted in L-arginine depletion and significant GVHD reduction.

107 Systemic L-arginine depletion following intravenous administratio

108 L-arginine-deprived T cells upregulated system L amino a

109 In preparations from normal rats SNAP or l-arginine did not alter BAN activity.

110 The parasite Giardia lamblia utilizes the L-arginine dihydrolase pathway to generate ATP from L-ar

111 ediated L-ornithine production compared with L-arginine directly imported from the extracellular mili

112 cells in G1, and this effect is mediated by l-arginine elimination rather than metabolite generation

113 ion, and inhibition of NO by N(G)-monomethyl-L-arginine enhanced intracellular survival of Mtb.

114 ine cycle, because it provides the substrate L-arginine for subsequent NO synthesis by inducible, end

115 expressing MPhis preferred L-citrulline over L-arginine for the promotion of antimycobacterial activi

116 at shifted towards tetramers upon binding of L-arginine for the XcNAGS-K.

117 , including N-alpha-(1-deoxy-D-fructos-1-yl)-L-arginine (FruArg).

118 with single nucleotide polymorphisms in the L-arginine:glycine amidinotransferase (AGAT) gene (P<2.1

119 ep process: L-arginine (L-Arg) --> N-hydroxy-L-arginine --> citrulline + NO.

120 tion following intravenous administration of l-arginine hydrolyzing enzymes has been shown to selecti

121 injections, some animals were injected with l-arginine (i.v.).

122 n to give ethylene is promoted by binding of l-arginine in a nonoxidized conformation and of 2-oxoglu

123 by increasing cerebral blood flow (CBF) with l-arginine in conjunction with administration of AdGDNF

124 a significant decrease in the NOS substrate l-arginine in plasma from CRPS patients, suggesting redu

125 L-arginine increased thermal stability of the NAGS-K fro

126 d the clinically compatible basic amino acid L-arginine increases in vitro planktonic and biofilm sus

127 is accompanied by minimal lung injury, while L-arginine induced extremely severe pancreatic injury in

128 21 deficiency protects against caerulein- or L-arginine-induced acute pancreatitis in mice.

129 Similar results occurred in mice with L-arginine-induced AP.

130 In addition, GW eliminated L-arginine-induced enhancement of Ca(2+) oscillations, p

131 iminates ACh-induced Ca(2+) oscillations and L-arginine-induced enhancement of Ca(2+) signaling in mo

132 Similar results were obtained using an l-arginine-induced model of AP.

133 of cyclophilin D with ATP synthase mediates L-arginine-induced pancreatitis, a model of severe AP th

134 cids was between the extent of caerulein and L-arginine induction, with obvious inflammatory cells in

135 L-arginine inhibits NAGS in bacteria, fungi, and plants

136 ynthesized endogenously by the conversion of l-arginine into citrulline through nitric oxide synthase

137 L-Arginine is a critical nutrient in the metabolism of b

138 In this response, l-arginine is decarboxylated to agmatine, thereby consum

139 intra-arterial infusion of N(G) -monomethyl-L -arginine (L -NMMA) into the common femoral artery in

140 intra-arterial infusion of N(G) -monomethyl-L -arginine (L -NMMA) to inhibit nitric oxide synthase (

141 oxide (NO) synthesis via a two-step process: L-arginine (L-Arg) --> N-hydroxy-L-arginine --> citrulli

142 -Menten constant (K(M)(app)) derived from an L-arginine (L-Arg) calibration curve of 1.27 +/- 0.29 mM

143 hile also catalyzing the C5 hydroxylation of l-arginine (l-Arg) driven by the oxidative decarboxylati

144 tic depletion of the nonessential amino acid l-Arginine (l-Arg) in patients with cancer by the admini

145 c activity, as measured by the conversion of L-arginine (L-Arg) into L-citrulline, was augmented in l

146 more, the generated acidic H2 O2 can oxidize l-Arginine (l-Arg) into NO for enhanced gas therapy.

147 Increased metabolism of l-Arginine (l-Arg), through the enzymes arginase 1 and N

148 intra-arterial infusions of N(G)-monomethyl-l-arginine (L-NMMA), TEA, fluconazole, and their combina

149 a intra-arterial infusion of N(G)-monomethyl-L-arginine (L-NMMA).

150 e, sodium nitroprusside, and N(G)-monomethyl-L-arginine (L-NMMA).

151 n sites: (i) control; (ii) 10 mm N(G) -nitro-l-arginine (l-NNA), a non-specific NOS inhibitor; (iii)

152 the nitric oxide synthase inhibitor N-nitro-l-arginine (l-NNA, 200 mum) and in nNOS-knockout (KO) mo

153 e nitric oxide synthase inhibitor N(G)-nitro-l-arginine (l-NNA; 100 mum) to block purinergic and nitr

154 on (Control), 400 nm ET-1, 10 mm N(G) -nitro-l-arginine (l-NNA; a NOS inhibitor) or a combination of

155 ginase-nitric oxide pathway (N(G)-monomethyl l-arginine [l-NMMA] monoacetate) reversed the inhibitory

156 luconazole) and NO synthase (N(G)-monomethyl-l-arginine [L-NMMA]).

157 ide synthase (iNOS) inhibitor N(omega)-nitro-L-arginine(L-NNA) induced E-selectin expression at level

158 mycobacteria-infected murine MPhis supplied L-arginine, L-citrulline, or both amino acids.

159 phenylalanine, L-leucine, glycine, L-lysine, L-arginine, L-cysteine, L-alanine, and L-proline--in aqu

160 L-Arginine, L-glutamine, DL-histidine, malate, and DL-or

161 udes l-asparagine, l-glutamine, l-threonine, l-arginine, l-glycine, l-proline, l-serine, l-alanine, a

162 experiments were conducted with amino acids (l-arginine, l-histidine, and glycine) that are represent

163 In most cells, cationic amino acids such as l-arginine, l-lysine, and l-ornithine are transported by

164 ve; no evidence was found for the binding of L-arginine, L-ornithine, L-2,4-diaminobutyric acid, and

165 ade of NO synthase (NOS; via N(G)-monomethyl-L-arginine: L-NMMA) and cyclooxygenase (COX; via ketorol

166 l) and NO synthase inhibition (NG-monomethyl-L-arginine; L-NMMA) under normoxic and normocapnic hypox

167 .29-0.59], P = 0.01) and lower median plasma l-arginine (late onset, 52.3 [IQR, 43-61] compared with

168 ated infection, gentamicin supplemented with L-arginine led to complete, long-lasting eradication of

169 The L-arginine level and the L-arginine to ADMA ratio (a mea

170 aria, compared with healthy controls (median L-arginine level, 65, 66, and 98 micromol/mL, respective

171 Day0 values correlated with plasma L-arginine levels (r = 0.69; p = 0.01) and weakly with p

172 this effect correlated strongly with plasma L-arginine levels (r = 0.89; p < 0.0001).

173 tential of novel bi-ligand (transferrin-poly-l-arginine) liposomal vector for delivery of desired gen

174 nhanced NO activity, because N(G)-monomethyl-l-arginine markedly blunted the flow response to obestat

175 ase, metabolizing the nitric oxide substrate l-arginine, may result in reduced production of nitric o

176 ity (percent constriction to N(G)-monomethyl-l-arginine [mean (SEM) wild type 106% (30%); hIGFREO 48%

177 rulline (800, 1600 mum) rescued NOx when the l-arginine media concentration was 25 mum but failed to

178 Under reduced l-arginine media conditions, HBECs treated with l-citrul

179 is reliant on inducible NO synthase-mediated L-arginine metabolism in macrophages (MPhis).

180 ous studies have linked alterations in local L-arginine metabolism, principally mediated by the enzym

181 DDAH1 and MED23/Arg1 in regulating ADMA and l-arginine metabolism, respectively, and identify a nove

182 N(G)-nitro-l-arginine methyl ester (100 mumol/L) or a protease-acti

183 base material to examine the feasibility of L-Arginine methyl ester (L-AME) functionalized material

184 selective NO synthase inhibitor Nomega-nitro-L-arginine methyl ester (L-NAME) for 30 minutes, followe

185 Infusion of N(G)-nitro-L-arginine methyl ester (L-NAME) for 5 min to inhibit NO

186 Molsidomine or NG-nitro-L-arginine methyl ester (L-NAME) or saline were applied

187 We report in this article that L-N(G)-nitro-L-arginine methyl ester (L-NAME) pretreatment blocked, w

188 ocol 1 (n = 10): (1) Control, (2) N(G)-nitro-l-arginine methyl ester (l-NAME), (3) a KCa channel inhi

189 tors was reduced in the presence of NG-nitro-L-arginine methyl ester (L-NAME), a general inhibitor of

190 bolished by application of either N(G)-nitro-l-arginine methyl ester (l-NAME), an inhibitor of NO syn

191 inhibition in cancer cells using N(G)-nitro-l-arginine methyl ester (l-NAME), we demonstrate that pa

192 However, pretreatment of VEC with nitro-L-arginine methyl ester (L-NAME), while inhibiting the r

193 ated NOS small molecule inhibitor N(G)-nitro-L-arginine methyl ester (l-NAME).

194 th the constitutive NOS inhibitor N(G)-nitro-l-arginine methyl ester (L-NAME).

195 helial nitric oxide synthase with N(G)-nitro-L-arginine methyl ester (L-NAME; 300 microm) eliminated

196 xide (NO) synthase inhibitor N(omega) -nitro-l-arginine methyl ester (P > 0.05), indicating that lowe

197 ore and during NO inhibition (N(omega)-nitro-l-arginine methyl ester [L-NAME]).

198 N(omega)-Nitro-L-arginine methyl ester and 1H-[1,2,4]-oxadiazolo-[4,3-a

199 clearance, whereas infusion of Nomega-nitro-L-arginine methyl ester and a high dose of aminoguanidin

200 enic mice during coadministration of N-nitro-l-arginine methyl ester and indomethacin.

201 tion by the NO synthase inhibitor N(G)-nitro-l-arginine methyl ester and the superoxide dismutase mim

202 NOS inhibitor N(G)-nitro-L-arginine methyl ester attenuated the endothelial barri

203 reated with ceramide, whereas N(omega)-nitro-l-arginine methyl ester had no effect.

204 administration of the NOS inhibitor N-nitro-L-arginine methyl ester hydrochloride (L-NAME), includin

205 nsive challenges using either N(omega)-nitro-L-arginine methyl ester hydrochloride (L-NAME)/high salt

206 d Ringer's (control); (2) 20 mm Nomega-nitro-l-arginine methyl ester hydrochloride (non-selective NOS

207 e of DTT and the NO inhibitor N(omega)-nitro-L-arginine methyl ester hydrochloride, the ability of CO

208 The eNOS inhibitor N(G)-Nitro-l-arginine methyl ester mimicked anti-VEGF/VEGFR drugs,

209 he inhibitory effects of ADMA and N(G)-nitro-l-arginine methyl ester on inducible NOS (macrophages) a

210 Glibenclamide and N(G)-nitro-l-arginine methyl ester partially blocked the effect, in

211 N(omega)-nitro-l-arginine methyl ester reduced vasodilation to flow in

212 difluoro-2-phenyl-1H-indol-3-yl)-1-oxobutyl]-L-arginine methyl ester trifluoroacetate) in M1 ipRGCs.

213 he specific NOS inhibitor L-NAME (N(G)-nitro-l-arginine methyl ester) led to increased APP and BACE1

214 urther, the inhibition of eNOS (l-N(G)-nitro-L-arginine methyl ester), Mas (A-779), and SIRT1 (nicoti

215 with a nonselective inhibitor (Nomega-nitro-L-arginine methyl ester).

216 synthase (NOS) inhibitor L-NAME (N(D)-nitro-L-arginine methyl ester).

217 gistically amplified by co-addition of tosyl-l-arginine methyl ester, a small molecule that blocks th

218 (Ca)) channels, respectively, and N(G)-nitro-L-arginine methyl ester, an inhibitor of nitric oxide sy

219 4 expression was abrogated by N(omega)-nitro-l-arginine methyl ester, an inhibitor of NOS.

220 ind that the small-molecule inhibitor, tosyl-l-arginine methyl ester, preferentially suppresses APC/C

221 ioavailability and reduced basal and N-nitro-l-arginine methyl ester-inhibitable O(2)(.-) in internal

222 thionylation and eNOS-derived N(omega)-nitro-L-arginine methyl ester-sensitive superoxide formation i

223 c oxide synthase (eNOS) inhibitor N(G)-nitro-L-arginine methyl ester.

224 hat was abrogated by administration of nitro-l-arginine methyl ester.

225 ct was reduced by tetrodotoxin or N(G)-nitro-l-arginine methyl ester.

226 the nitric oxide synthase inhibitor NG-nitro-l-arginine methyl ester.

227 f nitric oxide synthase with N(omega) -nitro-l-arginine methyl ester.

228 L-NAME (N(omega)-nitro-L-arginine methyl ester; nitric oxide synthase inhibitor

229 with incubation of NOS inhibitor N(G)-nitro-l-arginine-methyl ester (l-NAME) in LF-SED and HF-RUN gr

230 Nomega-nitro-L-arginine-methyl-ester (L-NAME) or placebo was administ

231 Treatment with l-arginine modestly lowers blood pressure of collectrin

232 ric oxide synthase inhibitor N(G)-monomethyl-L-arginine, monoacetate salt (L-NMMA).

233 locked by the iNOS inhibitor N(G)-monomethyl-l-arginine, monoacetate salt, and 3) RA-DCs derived from

234 ne through the intermediate N(omega)-hydroxy-L-arginine (NHA), producing nitric oxide, an important m

235 , NO production increased in the presence of l-arginine (nitric-oxide synthase [NOS] substrate), and

236 N-nitro-l-arginine [NLA; a nitric oxide synthase (NOS) inhibitor

237 -selective NOS inhibitor); (3) 5 mm N-propyl-l-arginine (nNOS inhibitor); and (4) 10 mm N(5)-(1-imino

238 Naturally occurring N(omega)-hydroxy-l-arginine (NOHA, 1) is the best substrate of NO synthas

239 However, neither L-arginine nor SNAP had any effect on GABAergic IPSCs.

240 N-Hydroxy-Nor-L-arginine (Nor-NOHA) was used as an arginase inhibitor.

241 rochloride, arginase inhibitor N-hydroxy-nor-l-arginine (nor-NOHA), and blocking antibodies for IL-4R

242 the arginase inhibitor N(omega)-hydroxy-nor-l-arginine (nor-NOHA; 0.1 mg/min).

243 The inhibitory effects of L-arginine on evoked EPSCs and high voltage-activated Ca

244 ble guanylyl cyclase abolished the effect of L-arginine on glycinergic IPSCs but not on evoked monosy

245 orating affect of N-carbamylglutamate and/or l-arginine on NAGS inhibition.

246 Different effects of L-arginine on oligomerization of NAGS may have implicati

247 tion of malarial-parasite-infected mice with L-arginine or L-citrulline reduced levels of ileal trans

248 The NO precursor L-arginine or the NO donor SNAP significantly increased

249 ition of this enzyme or supplementation with L-arginine overrides immunosuppression.

250 gatively with arginase-1 and positively with l-arginine (P = .001).

251 were significantly attenuated by monomethyl-l-arginine (P<0.01 versus placebo).

252 ity, 2) the Arg-1 inhibitor N(w)-hydroxy nor-l-arginine partially reversed suppression, and 3) the su

253 Because the L-arginine pathway is essential for G. lamblia survival

254 They acted at least partly through the l-arginine pathway.

255 monstrated that rats treated with AdGDNF and l-arginine post-CCI had a significantly smaller contusio

256 tives (trehalose, glycine betaine, mannitol, L-Arginine, potassium citrate, CuCl(2), proline, xylitol

257 l-arginine prevented NO decrease in endothelial cells un

258 L-Arg reaction but also during the N-hydroxy-L-arginine reaction.

259 A novel L-arginine-selective amperometric bi-enzyme biosensor ba

260 d circulating glucagon levels and attenuated l-arginine-stimulated glucagon secretion both in vivo an

261 a nitric oxide synthase (NOS) inhibitor] and l-arginine (substrate for NO production via NOS) were us

262 nt of the mNAGS increased in the presence of L-arginine suggesting smaller hydrodynamic radius due to

263 control, NOS inhibited, arginase inhibited, L-arginine supplemented and arginase inhibited plus L-ar

264 ine supplemented and arginase inhibited plus L-arginine supplemented.

265 However, L-arginine supply can be restricted by arginase activity

266 tandem mass spectrometry, we determined that L-arginine synthesized from L-citrulline was less effect

267 h as the peritoneal injections of caerulein, L-arginine, the retrograde infusion of sodium taurochola

268 ircumvent this by converting L-citrulline to L-arginine, thereby resupplying substrate for NO product

269 itates the export of agmatine in exchange of l-arginine, thus providing substrates for further remova

270 ate-onset asthma phenotype, plasma ratios of L-arginine to ADMA may explain the inverse relationship

271 The L-arginine level and the L-arginine to ADMA ratio (a measure of L-arginine bioava

272 icromol/mL, respectively [P = .0001]; median L-arginine to ADMA ratio, 115, 125, and 187, respectivel

273 ively; P = .018) and was associated with the L-arginine to ADMA ratio.

274 ponsible for consuming the dietary supply of l-arginine to deprive the disease of an essential nutrie

275 f a high-energy phosphoryl group from ATP to l-arginine to form phosphoarginine, which is used as an

276 Given that intravenous administration of L-arginine to human patients is well tolerated, combined

277 ated isoforms that catalyze the oxidation of L-arginine to L-citrulline and the important second mess

278 e synthase (NOS) catalyzes the conversion of l-arginine to l-citrulline and the second messenger nitr

279 ii) The H2O2-mediated oxidation of N-hydroxy-L-arginine to L-citrulline by a series of hemin/G-quadru

280 e in BH4 synthesis), and NOS activity ((14)C L-arginine to L-citrulline conversion) were measured by

281 e synthase (NOS) catalyzes the conversion of L-arginine to L-citrulline through the intermediate N(om

282 required for the synthesis and channeling of L-arginine to nitric oxide synthase (NOS) for nitric oxi

283 The breakdown of L-arginine to ornithine and urea by host arginase suppor

284 Arg1) and nitric oxide synthases compete for l-arginine to produce either polyamines or nitric oxide,

285 Moreover, addition of exogenous L-arginine to the cultures increased deformability of bo

286 decarboxylase, diverting the iNOS substrate l-arginine toward the synthesis of polyamines.

287 ian cells produces higher levels of NO. from l-arginine upon infections to eliminate pathogens.

288 Furthermore, collectrin directly regulates l-arginine uptake and plasma membrane levels of CAT1 and

289 oxide synthase (asymmetrical DMA [ADMA]) and l-arginine uptake into the cell (ADMA and symmetrical DM

290 nd closure and increased cell proliferation, L-arginine uptake, CAT1 and CAT2 protein levels, total p

291 s cell proliferation, scratch wound closure, L-arginine uptake, cationic amino acid transporter activ

292 roughout the vasculature, where it regulates L-arginine uptake.

293 Arginase-II (Arg-II), the type-II L-arginine-ureahydrolase, is highly expressed in pancrea

294 Most animals produce NO from L-arginine via a family of dedicated enzymes known as NO

295 endogenous NO production from the amino acid l-arginine, via nitric oxide synthase (NOS) enzymes, res

296 The effects of l-arginine were blocked by bath application of l-NAME (2

297 treated with the iNOS inhibitor N-monomethyl-l-arginine were largely unable to resolve genital tract

298 /locus of cross-over P strategy; cerulein or L-arginine were used to induce AP.

299 mmetric dimethyl arginine (ADMA) relative to L-arginine, which can lead to greater nitric oxide synth

300 by KCl and the addition of flavor enhancers (l-arginine, yeast and oregano extract) on probiotic Prat