ライフサイエンスコーパス: tetrahydrobiopterin

1 ic heme oxygenase domain (P450-type heme and tetrahydrobiopterin).

2 have impaired ability to bind L-arginine and tetrahydrobiopterin.

3 s of the substrate arginine, or the cofactor tetrahydrobiopterin.

4 dulated by the availability of its cofactor, tetrahydrobiopterin.

5 ctivated by phosphorylation and inhibited by tetrahydrobiopterin.

6 the abundant cofactor (6R)-L-erythro-5,6,7,8-tetrahydrobiopterin.

7 tein or decreased concentrations of cofactor tetrahydrobiopterin.

8 y reconstituted rapidly upon incubation with tetrahydrobiopterin.

9 nzyme activity via chemical stabilization of tetrahydrobiopterin.

10 ffect vascular NOS activity or metabolism of tetrahydrobiopterin.

11 e dihydroxypropyl side chain of (6R)-5,6,7,8-tetrahydrobiopterin.

12 rough interactions between peroxynitrite and tetrahydrobiopterin.

13 the synthesis of the catecholamine co-factor tetrahydrobiopterin.

14 gulated by its substrates, phenylalanine and tetrahydrobiopterin.

15 ost unaffected by L-arginine or the cofactor tetrahydrobiopterin.

16 c conditions even in the presence of Arg and tetrahydrobiopterin.

17 ble precursor of NO synthase (NOS) cofactor, tetrahydrobiopterin.

18 an enzyme important for the biosynthesis of tetrahydrobiopterin.

19 2 of the experiment, rats were treated with tetrahydrobiopterin (20 mg/kg) 5 mins before and 30 mins

20 1000 U/mL), chelerythrine (3 micromol/L), or tetrahydrobiopterin (20 micromol/L).

21 primarily decreased the Km for the cofactor tetrahydrobiopterin (3-fold).

22 (6R)-L-Erythro 5,6,7,8 tetrahydrobiopterin (6BH(4)) is crucial in the hydroxyla

23 recycling process of 6(R)-L-erythro 5,6,7,8 tetrahydrobiopterin (6BH(4)), has extremely low activiti

24 y unveils a defective (6R)-L-erythro-5,6,7,8-tetrahydrobiopterin (6BH4) de novo synthesis/recycling f

25 he essential cofactor (6R)-L-erythro-5,6,7,8-tetrahydrobiopterin (6BH4) for the aromatic amino acid h

26 ulation of the pterin (6R)-L-erythro-5,6,7,8-tetrahydrobiopterin (6BH4).

27 upon oral administration of the PAH cofactor tetrahydrobiopterin [(6R)-L-erythro-5,6,7,8-tetrahydrobi

28 l perfusion is regulated by nNOS and whether tetrahydrobiopterin, a co-factor and stabilizer of nNOS,

29 DCoH also catalyzes the recycling of tetrahydrobiopterin, a cofactor of aromatic amino acid h

30 with an associated severe deficiency of CSF tetrahydrobiopterin, a critical cofactor for monoamine n

31 s not affected by intracellular depletion of tetrahydrobiopterin, a critical cofactor required for iN

32 Supplementation with tetrahydrobiopterin, a nitric oxide synthase cofactor, m

33 ulating genes, including those that regulate tetrahydrobiopterin, a requisite cofactor in dopamine sy

34 We studied whether tetrahydrobiopterin administration exerts beneficial eff

35 The presence of tetrahydrobiopterin affects oxygen metabolism by lowerin

36 ment with folinic acid; the patient with low tetrahydrobiopterin also received sapropterin.

37 e exacerbated by sepiapterin, a precursor of tetrahydrobiopterin, an essential cofactor of (.)NO bios

38 degrees C in WT cells, leak was decreased by tetrahydrobiopterin, an essential NOS cofactor.

39 Treatment with sapropterin, a tetrahydrobiopterin analogue, led to dramatic and long-l

40 stituted with tetrahydrobiopterin (H(4)B) or tetrahydrobiopterin analogues (5-methyl-H(4)B and 4-amin

41 e substrate l-Arg and the cofactors heme and tetrahydrobiopterin and a carboxyl-terminal reductase do

42 Our results demonstrate a central role of tetrahydrobiopterin and alkylglycerol monooxygenase in e

43 omatography analysis revealed a reduction in tetrahydrobiopterin and an increase in dihydrobiopterin

44 MPA depletes tetrahydrobiopterin and decreases NO production by induc

45 nthase oxygenase domains (NOS(ox)) must bind tetrahydrobiopterin and dimerize to be active.

46 al structures that in NOSoxy bind Zn(2+) and tetrahydrobiopterin and help form an active dimer.

47 Interestingly, vitamin C also increased tetrahydrobiopterin and NOS activity in aortas of C57BL/

48 prevents and reverses these effects on TH of tetrahydrobiopterin and reactive nitrogen species.

49 ears to be mediated in part by protection of tetrahydrobiopterin and restoration of eNOS enzymatic ac

50 ed that ONOO- uncouples eNOS by oxidation of tetrahydrobiopterin and that ascorbate does not fully pr

51 The N-terminal oxidase domain binds heme and tetrahydrobiopterin and the arginine substrate.

52 om the NADPH oxidase leading to oxidation of tetrahydrobiopterin and uncoupling of endothelial NO syn

53 diminished cellular levels of L-arginine or tetrahydrobiopterin, and alterations in membrane signali

54 of an oxygenase domain that binds heme, (6R)-tetrahydrobiopterin, and Arg, coupled to a reductase dom

55 as dimeric, bound substrate Arg and cofactor tetrahydrobiopterin, and had a normal heme environment,

56 ontains an oxygenase domain that binds heme, tetrahydrobiopterin, and L-arginine, and a reductase dom

57 for tyrosine, 6-methyltetrahydropterin, and tetrahydrobiopterin are unaffected by replacement of eit

58 rogen peroxide had no effect on the decay of tetrahydrobiopterin, as monitored spectrophotometrically

59 ators of these processes and their impact on tetrahydrobiopterin availability and function have not y

60 These observations indicate that endothelial tetrahydrobiopterin availability modulates neointimal hy

61 Under conditions of tetrahydrobiopterin (BH 4) depletion eNOS also generates

62 omain, which also contains binding sites for tetrahydrobiopterin (BH(4)) and l-Arg.

63 itrite is dictated by the bioavailability of tetrahydrobiopterin (BH(4)) and L-arginine during eNOS c

64 ilizing the cofactors (6R)-l-erythro-5,6,7,8 tetrahydrobiopterin (BH(4)) and molecular oxygen.

65 alanine, its hydroxylation to tyrosine using tetrahydrobiopterin (BH(4)) and O(2).

66 Changes in the steady-state kinetics for tetrahydrobiopterin (BH(4)) and tryptophan for TPH NDelt

67 We tested the hypotheses that differences in tetrahydrobiopterin (BH(4)) bioactivity are key mechanis

68 -dependent dilation; EDD), nitric oxide (NO)/tetrahydrobiopterin (BH(4)) bioavailability, and oxidati

69 Levels of tetrahydrobiopterin (BH(4)) bound to nitric-oxide syntha

70 Reduced availability of tetrahydrobiopterin (BH(4)) contributes to the age-relat

71 Tetrahydrobiopterin (BH(4)) deficiency is a cause of dys

72 Under conditions of L-arginine or tetrahydrobiopterin (BH(4)) depletion, nNOS also generat

73 Tetrahydrobiopterin (BH(4)) diminishes the formation of

74 The role of PPARdelta in metabolism of tetrahydrobiopterin (BH(4)) has not been studied in the

75 at localized supplementation of tyrosine and tetrahydrobiopterin (BH(4)) in aged human skin could aug

76 Tetrahydrobiopterin (BH(4)) is an essential co-factor fo

77 Since tetrahydrobiopterin (BH(4)) is an essential cofactor for

78 upling eNOS, characterized by a reduction in tetrahydrobiopterin (BH(4)) levels and a decrease in the

79 However, the selective presence of tetrahydrobiopterin (BH(4)) makes dopaminergic neurons m

80 led when oxidative depletion of its cofactor tetrahydrobiopterin (BH(4)) occurs.

81 MPP(+) caused a time-dependent depletion of tetrahydrobiopterin (BH(4)) that was mediated by H(2)O(2

82 ity of 5-methyltetrahydrofolate (5-MTHF) and tetrahydrobiopterin (BH(4)) to modulate nitric oxide (NO

83 g enzyme in the biosynthesis of 6(R)-5,6,7,8-tetrahydrobiopterin (BH(4)), a cofactor required for iNO

84 Synthesis of 6(R)-5,6,7,8-tetrahydrobiopterin (BH(4)), a required cofactor for ind

85 ction was associated with elevated levels of tetrahydrobiopterin (BH(4)), a TNF-alpha-stimulated cofa

86 he final step in the biosynthetic pathway of tetrahydrobiopterin (BH(4)), an essential cofactor for a

87 function is compromised due to depletion of tetrahydrobiopterin (BH(4)), an essential cofactor requi

88 Tetrahydrobiopterin (BH(4)), not dihydrobiopterin or bio

89 synthases (NOS) are thiolate-ligated heme-, tetrahydrobiopterin (BH(4))-, and flavin-containing mono

90 The effect of ascorbate was tetrahydrobiopterin (BH(4))-dependent, because ascorbate

91 ated, is dependent on the essential cofactor tetrahydrobiopterin (BH(4)).

92 e (L-arginine) binding site, and a cofactor, tetrahydrobiopterin (BH(4)).

93 , eNOS requires the redox-sensitive cofactor tetrahydrobiopterin (BH(4)); however, the role of BH(4)

94 c-thiolate cluster, rather than the cofactor tetrahydrobiopterin (BH(4)); however, this remains highl

95 presence of the mtNOS cofactor (6R)-5,6,7,8,-tetrahydrobiopterin (BH(4); 100 microm) mitochondrial RO

96 her NOS substrate (L-arginine) and cofactor (tetrahydrobiopterin; BH(4)) concentrations are reduced.

97 e, depending on the availability of cofactor tetrahydrobiopterin (BH4) and l-arginine during catalysi

98 It has been suggested that decreased tetrahydrobiopterin (BH4) availability may be a useful t

99 n are correlated with changes in NO cofactor tetrahydrobiopterin (BH4) biosynthetic enzymes (guanosin

100 was stable in the presence of L-arginine or tetrahydrobiopterin (BH4) but was converted to a five-co

101 We tested whether tetrahydrobiopterin (BH4) can recouple NOS and reverse p

102 acid decarboxylase (AADC) or the TH cofactor tetrahydrobiopterin (BH4) could account for the loss of

103 Tetrahydrobiopterin (BH4) deficiency is reported to unco

104 e (PAH), and a small proportion (2%) exhibit tetrahydrobiopterin (BH4) deficiency with additional neu

105 Tetrahydrobiopterin (BH4) is a cofactor of a number of r

106 Tetrahydrobiopterin (BH4) is a key redox-active cofactor

107 Tetrahydrobiopterin (BH4) is a key regulator of endothel

108 Tetrahydrobiopterin (BH4) is a major endogenous vasoprot

109 Tetrahydrobiopterin (BH4) is a required cofactor for nit

110 Tetrahydrobiopterin (BH4) is a required cofactor for the

111 Tetrahydrobiopterin (BH4) is an absolute requirement for

112 5,6,7,8-Tetrahydrobiopterin (BH4) is an essential cofactor for a

113 Tetrahydrobiopterin (BH4) is an essential cofactor for e

114 Tetrahydrobiopterin (BH4) is an essential cofactor of en

115 Tetrahydrobiopterin (BH4) is an essential cofactor of ni

116 Recent evidence suggests that the cofactor tetrahydrobiopterin (BH4) is an important regulator of n

117 Although the eNOS cofactor tetrahydrobiopterin (BH4) is depleted, its repletion onl

118 e endothelial nitric oxide synthase cofactor tetrahydrobiopterin (BH4) is essential for maintenance o

119 Tetrahydrobiopterin (BH4) is the natural cofactor of sev

120 Physiological control of the co-factor tetrahydrobiopterin (BH4) is tight in normal circumstanc

121 clohydrolase 1 polymorphisms, which decrease tetrahydrobiopterin (BH4) levels, and reduced pain in pa

122 NOS (eNOS) uncoupling, reflected in reduced tetrahydrobiopterin (BH4) levels, increased BH2 levels,

123 Treatment with the eNOS cofactor tetrahydrobiopterin (BH4) or the BH4 precursor sepiapter

124 e endothelial nitric oxide synthase cofactor tetrahydrobiopterin (BH4) plays a pivotal role in mainta

125 We hypothesized that decreased tetrahydrobiopterin (BH4) plays a role in the pathogenes

126 Tetrahydrobiopterin (BH4) serves as a critical co-factor

127 drolase (GCH1), the rate-limiting enzyme for tetrahydrobiopterin (BH4) synthesis, is a key modulator

128 the first step for the de novo production of tetrahydrobiopterin (BH4), a cofactor for nitric oxide s

129 Tetrahydrobiopterin (BH4), a potent reducing molecule wi

130 ry cytokines also up-regulate the amounts of tetrahydrobiopterin (BH4), an enzyme cofactor essential

131 talyzes the last step in the biosynthesis of tetrahydrobiopterin (BH4), an essential cofactor of nitr

132 is dependent on adequate cellular levels of tetrahydrobiopterin (BH4), an important cofactor for the

133 the rate-limiting enzyme for biosynthesis of tetrahydrobiopterin (BH4), an obligate cofactor for NO s

134 ations of l-arginine (Arg), NADPH, FAD, FMN, tetrahydrobiopterin (BH4), and calmodulin, indicating th

135 imiting enzyme in biosynthesis as well as of tetrahydrobiopterin (BH4), and concentration of BH4, whi

136 assayed for phospho-AMPK (Thr172), GTPCH I, tetrahydrobiopterin (BH4), and endothelial functions.

137 e detected from eNOS in the absence of added tetrahydrobiopterin (BH4), and these were quenched by su

138 g related to deficiency of the eNOS cofactor tetrahydrobiopterin (BH4), but whether this mechanism is

139 efficacy of sapropterin, a synthetic form of tetrahydrobiopterin (BH4), for reduction of blood phenyl

140 e heart, reflected by reduced NOS3 dimer and tetrahydrobiopterin (BH4), increased NOS3-dependent gene

141 When 3 is reduced by tetrahydrobiopterin (BH4), instead of an externally supp

142 nstrated lower cerebrospinal fluid levels of tetrahydrobiopterin (BH4), neopterin, and homovanillic a

143 enzyme in BH4 synthesis, increased levels of tetrahydrobiopterin (BH4), reduced endothelial superoxid

144 c BB (BBd) rat is due to decreased levels of tetrahydrobiopterin (BH4), secondary to decreased expres

145 at convert L-Arg to L-citrulline and NO in a tetrahydrobiopterin (BH4)-dependent manner, using NADPH

146 y hypercholesterolemia and, if so, whether a tetrahydrobiopterin (BH4)-dependent mechanism is respons

147 dulator of cardiac function, is the cofactor tetrahydrobiopterin (BH4).

148 on availability of the cofactor (6R)-5,6,7,8-tetrahydrobiopterin (BH4).

149 secondary to oxidation of the NOS cofactor, tetrahydrobiopterin (BH4).

150 tion of NO that is dependent on the cofactor tetrahydrobiopterin (BH4).

151 ent, although some patients can benefit from tetrahydrobiopterin (BH4).

152 tetrahydrobiopterin [(6R)-L-erythro-5,6,7,8-tetrahydrobiopterin (BH4)].

153 dent N-hydroxyarginine oxidation, or Arg and tetrahydrobiopterin binding.

154 n maintaining the integrity of the cofactor (tetrahydrobiopterin) binding site of NOS-2.

155 Oral atorvastatin increased vascular tetrahydrobiopterin bioavailability and reduced basal an

156 ents, atorvastatin rapidly improved vascular tetrahydrobiopterin bioavailability by upregulating GTP-

157 -mediated eNOS phosphorylation and increased tetrahydrobiopterin bioavailability, improving eNOS coup

158 lkylglycerol monooxygenase expression and of tetrahydrobiopterin biosynthesis affecting not only vari

159 ing the NOS substrate L-arginine or cofactor tetrahydrobiopterin blocked the formation of reactive ox

160 Supplementation with tetrahydrobiopterin blocked these MTX-induced effects.

161 Supplementation with tetrahydrobiopterin blocked these MTX-mediated effects.

162 The first bolus of tetrahydrobiopterin blunted the increase in heart rate a

163 frequency is insensitive to the presence of tetrahydrobiopterin, but it shifts to 1126 cm-1 upon bin

164 e-coordinated heme cofactor and, uniquely, a tetrahydrobiopterin cofactor, are used to deliver electr

165 rocycle and a cation radical centered on the tetrahydrobiopterin cofactor.

166 e stimulating hormone/6(R)-L-erythro 5,6,7,8 tetrahydrobiopterin complex.

167 m-dependent relaxation of coronary arteries, tetrahydrobiopterin concentrations, ratio of endothelial

168 binding of substrate l-arginine or cofactor tetrahydrobiopterin converts nitric oxide synthases (NOS

169 ere cerebral folate deficiency, and cerebral tetrahydrobiopterin deficiency due to a germline missens

170 O(2), yielding a recovery of epidermal 4a-OH-tetrahydrobiopterin dehydratase activities and physiolog

171 yielding only wild-type sequences for 4a-OH-tetrahydrobiopterin dehydratase and therefore ruling out

172 inant enzyme activities, together with 4a-OH-tetrahydrobiopterin dehydratase expression in the epider

173 ier it was demonstrated that epidermal 4a-OH-tetrahydrobiopterin dehydratase, an important enzyme in

174 Targeting tetrahydrobiopterin-dependent endothelial NO synthase re

175 Phenylalanine hydroxylase (PAH) is a tetrahydrobiopterin-dependent, nonheme iron enzyme that

176 Tetrahydrobiopterin-derived radical species formed by re

177 Furthermore, levels of tetrahydrobiopterin, dihydrobiopterin, and the key enzym

178 C57BL/6 mice, concomitant with decreases in tetrahydrobiopterin, dimeric and phosphorylated neuronal

179 a/reperfusion injury in db/db mice through a tetrahydrobiopterin/endothelial nitric oxide synthase/ni

180 amma interferon (IFN-gamma), l-arginine, and tetrahydrobiopterin enhanced expression of NOS2 and NOS3

181 In the presence of both L-arginine and tetrahydrobiopterin, eNOS is highly coupled (>90%), and

182 ed in nNOS(-/-) myocytes, whereas myocardial tetrahydrobiopterin, eNOS Thr-495 phosphorylation, and a

183 te limiting in the provision of the cofactor tetrahydrobiopterin for biosynthesis of catecholamines a

184 induced protein thiyl radical formation from tetrahydrobiopterin-free enzyme or following exposure to

185 in the micromolar to nanomolar range) to the tetrahydrobiopterin-free oxidase domain of inducible nit

186 to regenerate alpha-tocopherol, and possibly tetrahydrobiopterin, from its radical species.

187 ival time was significantly prolonged in the tetrahydrobiopterin group (25.0 vs. 17.8 hrs, p<.01).

188 ) is a dimer that binds heme, L-arginine and tetrahydrobiopterin (H(4)B) and is the site for nitric o

189 the structural integrity of the (6R)-5,6,7,8-tetrahydrobiopterin (H(4)B) binding site located at the

190 In nitric oxide synthase (NOS), (6R)-tetrahydrobiopterin (H(4)B) binds near the heme and can

191 rolling electron transfer between bound (6R)-tetrahydrobiopterin (H(4)B) cofactor and the enzyme heme

192 In the first step, a tetrahydrobiopterin (H(4)B) cofactor bound near one of t

193 rg) and display a novel utilization of their tetrahydrobiopterin (H(4)B) cofactor.

194 Ss) are flavo-heme enzymes that require (6R)-tetrahydrobiopterin (H(4)B) for activity.

195 Tetrahydrobiopterin (H(4)B) is a critical element in the

196 oxide synthase (iNOS) was reconstituted with tetrahydrobiopterin (H(4)B) or tetrahydrobiopterin analo

197 How 6R-tetrahydrobiopterin (H(4)B) participates in Arg hydroxyl

198 er than nitric oxide (NO*), upon loss of the tetrahydrobiopterin (H(4)B) salvage enzyme dihydrofolate

199 ncode for the synthetic machinery to produce tetrahydrobiopterin (H(4)B), a cofactor of NOS required

200 ession of GTP cyclohydrolase, which produces tetrahydrobiopterin (H(4)B), an essential cofactor for N

201 NOSs) catalyze two mechanistically distinct, tetrahydrobiopterin (H(4)B)-dependent, heme-based oxidat

202 omains (NOSoxy) that each bind heme and (6R)-tetrahydrobiopterin (H4B) and catalyze NO synthesis from

203 t could not be converted to active dimers by tetrahydrobiopterin (H4B) and l-arginine (Arg).

204 of a thiolate-coordinated heme macrocycle, a tetrahydrobiopterin (H4B) cofactor, and an l-arginine (l

205 nthase (iNOS) is a hemeprotein that requires tetrahydrobiopterin (H4B) for activity.

206 redox role for the enzyme-bound cofactor 6R-tetrahydrobiopterin (H4B) in the second reaction of NO s

207 Here, we establish tetrahydrobiopterin (H4B) levels as an important factor

208 s demonstrate that oxidative inactivation of tetrahydrobiopterin (H4B) may cause uncoupling of endoth

209 How the bound cofactor (6R)-tetrahydrobiopterin (H4B) participates in Arg hydroxylat

210 me-dioxy species and with the formation of a tetrahydrobiopterin (H4B) radical in the enzyme, whereas

211 ers dimerized when incubated with Arg and 6R-tetrahydrobiopterin (H4B), as shown previously.

212 OSox) in each subunit binds heme, L-Arg, and tetrahydrobiopterin (H4B), is the site of NO synthesis,

213 ure of the heme domain of endothelial NOS in tetrahydrobiopterin (H4B)-free and -bound forms at 1.95

214 We studied catalysis by tetrahydrobiopterin (H4B)-free neuronal nitric-oxide syn

215 cofactor for the endothelial NO synthase is tetrahydrobiopterin (H4B).

216 of the substrate L-arginine and the cofactor tetrahydrobiopterin (H4B).

217 f the nitric oxide synthases (NOS) co-factor tetrahydrobiopterin has been shown to prevent IRI.

218 ropionate ensues and eliminates the cofactor tetrahydrobiopterin-heme interaction.

219 Bmal1-KO mice, whereas supplementation with tetrahydrobiopterin improved endothelial function in the

220 ide dismutase or sepiapterin, a precursor to tetrahydrobiopterin, improved endothelium-dependent vaso

221 Less is known about the role of tetrahydrobiopterin in lipid metabolism, although it is

222 ling of the cofactor 6(R)-L- erythro 5,6,7,8 tetrahydrobiopterin in melanocytes.

223 els of the endothelial NO synthase cofactor, tetrahydrobiopterin, in an EC-specific manner and reduce

224 Various tetrahydro- and dihydro-analogs of tetrahydrobiopterin, including 6,7-dimethyl-tetrahydropt

225 luding one with low CSF levels of 5-MTHF and tetrahydrobiopterin intermediates, showed improvement in

226 Tetrahydrobiopterin is a cofactor synthesized from GTP w

227 Tetrahydrobiopterin is a critical cofactor for the NO sy

228 Herein, we analysed whether tetrahydrobiopterin is also involved in TV development.

229 ase 1 (GTPCH1) with consequent deficiency of tetrahydrobiopterin is considered the primary cause for

230 The reducing cofactor tetrahydrobiopterin is not oxidized, nor does it prevent

231 Significantly higher tetrahydrobiopterin levels were detected in aortas of ap

232 itogen-activated protein kinase and elevates tetrahydrobiopterin levels, the dimerization and phospho

233 Peroxynitrite oxidation of tetrahydrobiopterin may represent a pathogenic cause of

234 ive chemicals and consequent deficiencies in tetrahydrobiopterin, may contribute to tissue injury.

235 amined the direct effects of atorvastatin on tetrahydrobiopterin-mediated endothelial nitric oxide (N

236 bility and reduces vascular O(2)(.-) through tetrahydrobiopterin-mediated endothelial NO synthase cou

237 the effect of vitamin C on NOS function and tetrahydrobiopterin metabolism in vivo.

238 nthase inhibitor), sepiapterin (precursor of tetrahydrobiopterin), MitoTEMPO (mitochondria-targeted a

239 ed, and the sheep were randomized to receive tetrahydrobiopterin (n=7), given intravenously as 20 mg/

240 OS, guanosine triphosphate cyclohydrolase I, tetrahydrobiopterin, NO formation, and nitro-oxidative s

241 We then examined the protective effect of tetrahydrobiopterin on PAF-induced bowel injury, mesente

242 e binding is not affected by the presence of tetrahydrobiopterin or arginine.

243 pentachloride (10 micromol/L), but not with tetrahydrobiopterin or L-arginine.

244 Treatment strategies that increase tetrahydrobiopterin or prevent its oxidation may prove u

245 Activity required bound tetrahydrobiopterin or tetrahydrofolate and was linked t

246 NO and citrulline in the presence of either tetrahydrobiopterin or tetrahydrofolate.

247 s did not greatly alter binding of Arg, (6R)-tetrahydrobiopterin, or alter the electronic properties

248 ble by increased concentrations of arginine, tetrahydrobiopterin, or calmodulin.

249 uction, deficiencies in either L-arginine or tetrahydrobiopterin, or reduced membrane fluidity.

250 oxynitrite strikingly increased the decay of tetrahydrobiopterin over 500 seconds.

251 Diabetic heart disease is associated with tetrahydrobiopterin oxidation and high arginase activity

252 from NO synthase is markedly increased, and tetrahydrobiopterin oxidation is evident.

253 Tetrahydrobiopterin oxidation may represent an important

254 subjects had the same novel mutation in the tetrahydrobiopterin pathway involving sepiapterin reduct

255 GTP cyclohydrolase 1 (GCH1) and its product tetrahydrobiopterin play crucial roles in cardiovascular

256 The cofactor tetrahydrobiopterin plays critical roles in the modulati

257 Sepiapterin (2 mg/kg, stable tetrahydrobiopterin precursor) also attenuated PAF-induc

258 Sepiapterin (SEP) is a tetrahydrobiopterin precursor, and L-citrulline (L-Cit)

259 n arterial pressure, and the second bolus of tetrahydrobiopterin prevented the decreases in cardiac i

260 tored renal tissue levels of glutathione and tetrahydrobiopterin; prevented significant accumulation

261 Tetrahydrobiopterin prevents PAF-induced intestinal inju

262 These results indicate that tetrahydrobiopterin prevents the tyrosine-nitrating prop

263 hat have increased or decreased dopamine and tetrahydrobiopterin production exhibit variation in susc

264 In part 2, tetrahydrobiopterin protected against PAF-induced intest

265 The presence of 5,6,7,8-tetrahydrobiopterin quenched the uncoupled reactions and

266 arginine, is fully functional in forming the tetrahydrobiopterin radical upon mixing with oxygen as d

267 With tetrahydrobiopterin-reconstituted eNOS, eNOS protein rad

268 Treatment of mice with oral tetrahydrobiopterin reduces vascular ROS production, inc

269 Tetrahydrobiopterin reduces wild-type TyrH following a s

270 allosteric regulator 6(R)-L-erythro 5,6,7,8 tetrahydrobiopterin resulting in a stable alpha-melanocy

271 TX inhibits reduction of dihydrobiopterin to tetrahydrobiopterin, resulting in increased production o

272 biopterin, 5,6-dihydrobiopterin, and 5,6,7,8-tetrahydrobiopterin reveal that PTR1 does not undergo an

273 l effect on the light absorbance spectrum of tetrahydrobiopterin-saturated nNOS, their binding was mo

274 ddition of PEG-SOD, PEG-SOD+PEG-catalase, or tetrahydrobiopterin significantly (P<0.05) improved NO l

275 Tetrahydrobiopterin significantly attenuated the deterio

276 Donor pretreatment with tetrahydrobiopterin significantly minimised these change

277 te into dimers when incubated with l-Arg and tetrahydrobiopterin, suggesting inadequate subunit inter

278 educe ferric TyrH, but much more slowly than tetrahydrobiopterin, suggesting that the pterin is a phy

279 In this clinically relevant model of sepsis, tetrahydrobiopterin supplementation attenuated the impai

280 Tetrahydrobiopterin supplementation of the donor prevent

281 synthase that was corrected by intracellular tetrahydrobiopterin supplementation.

282 nt genomes contain an unusual paralog of the tetrahydrobiopterin synthesis enzyme 6-pyruvoyltetrahydr

283 predicted a single high-affinity allostere, tetrahydrobiopterin (THB), an essential cofactor in mono

284 erior wall thickness, cardiac contractility, tetrahydrobiopterin, the dimers of nitric oxide synthase

285 presence of methotrexate by the addition of tetrahydrobiopterin, there was no change in susceptibili

286 1 in RNAi lines ((oe)RNAi) or by addition of tetrahydrobiopterin to cultures.

287 form L-dihydroxyphenylalanine (L-DOPA), and tetrahydrobiopterin to form 4a-hydroxybiopterin, in the

288 ere assessed 1 hr after PAF with and without tetrahydrobiopterin treatment.

289 Tetrahydrobiopterin was associated with better preserved

290 eporter of intracellular tyrosine nitration, tetrahydrobiopterin was found to prevent NO2-induced tyr

291 Vascular tetrahydrobiopterin was increased by ATII infusion but w

292 ffectively regulates TH through synthesis of tetrahydrobiopterin, was also upregulated by inositol de

293 dihydrobiopterin levels, an oxidized form of tetrahydrobiopterin, were decreased and vascular endothe

294 s may be due to a reduction of intracellular tetrahydrobiopterin, which is a critical cofactor for NO

295 rbic acid (ascorbate) is required to recycle tetrahydrobiopterin, which is necessary for neurotransmi

296 link between DHFR and metabolism of cerebral tetrahydrobiopterin, which is required for the formation

297 Tetrahydrobiopterin, which is the essential cofactor for

298 Depletion of intracellular tetrahydrobiopterin with an inhibitor of de novo pterin

299 , and renal tissue levels of glutathione and tetrahydrobiopterin with further elevation in dihydrobio

300 bsNOS was dimeric, bound l-Arg and 6R-tetrahydrobiopterin with similar affinity as mammalian N