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

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

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

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

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

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

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

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

32 We studied whether tetrahydrobiopterin administration exerts beneficial eff

33 The presence of tetrahydrobiopterin affects oxygen metabolism by lowerin

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

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

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

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

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

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

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

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

42 MPA depletes tetrahydrobiopterin and decreases NO production by induc

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

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

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

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

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

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

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

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

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

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

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

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

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

56 These observations indicate that endothelial tetrahydrobiopterin availability modulates neointimal hy

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

58 r factor (erythroid-derived 2)-like 2 (Nrf2)/tetrahydrobiopterin (BH(4) )/ nitric oxide synthase (NOS

59 blished that inactivation of nNOS by heme or tetrahydrobiopterin (BH(4)) alteration and loss triggers

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

79 with a synthetic formulation of the cofactor tetrahydrobiopterin (BH(4)) that partly acts as a pharma

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

100 Tetrahydrobiopterin (BH4) deficiency is reported to unco

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

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

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

104 Tetrahydrobiopterin (BH4) is a key regulator of endothel

105 Tetrahydrobiopterin (BH4) is a major endogenous vasoprot

106 Tetrahydrobiopterin (BH4) is a required cofactor for nit

107 Tetrahydrobiopterin (BH4) is a required cofactor for the

108 Tetrahydrobiopterin (BH4) is an absolute requirement for

109 5,6,7,8-Tetrahydrobiopterin (BH4) is an essential cofactor for a

110 Tetrahydrobiopterin (BH4) is an essential cofactor for e

111 Tetrahydrobiopterin (BH4) is an essential cofactor of en

112 Tetrahydrobiopterin (BH4) is an essential cofactor of ni

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

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

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

116 Tetrahydrobiopterin (BH4) is the natural cofactor of sev

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

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

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

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

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

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

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

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

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

126 Tetrahydrobiopterin (BH4), a potent reducing molecule wi

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

143 , the initiating step in the biosynthesis of tetrahydrobiopterin (BH4).

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

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

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

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

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

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

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

151 Oral atorvastatin increased vascular tetrahydrobiopterin bioavailability and reduced basal an

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

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

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

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

156 Supplementation with tetrahydrobiopterin blocked these MTX-induced effects.

157 Supplementation with tetrahydrobiopterin blocked these MTX-mediated effects.

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

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

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

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

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

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

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

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

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

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

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

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

170 e P450, and four nonheme oxygenases, namely, tetrahydrobiopterin-dependent aromatic amino acid hydrox

171 Targeting tetrahydrobiopterin-dependent endothelial NO synthase re

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

173 Tetrahydrobiopterin-derived radical species formed by re

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

198 er and produces NO from l-Arg and NADPH in a tetrahydrobiopterin (H(4)B)-dependent manner at levels s

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

224 Tetrahydrobiopterin is a cofactor synthesized from GTP w

225 Tetrahydrobiopterin is a critical cofactor for the NO sy

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

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

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

229 Significantly higher tetrahydrobiopterin levels were detected in aortas of ap

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

231 phenylalanine concentrations (n = 6,115) and tetrahydrobiopterin loading test results (n = 4,381), en

232 Peroxynitrite oxidation of tetrahydrobiopterin may represent a pathogenic cause of

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

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

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

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

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

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

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

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

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

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

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

244 Activity required bound tetrahydrobiopterin or tetrahydrofolate and was linked t

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

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

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

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

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

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

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

252 Tetrahydrobiopterin oxidation may represent an important

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

254 t the importance of the GTP Cyclohydrolase I/Tetrahydrobiopterin pathway.

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 of both a genotype-based phenotype (88%) and tetrahydrobiopterin responsiveness (83%).

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

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

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

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

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

276 Tetrahydrobiopterin significantly attenuated the deterio

277 Donor pretreatment with tetrahydrobiopterin significantly minimised these change

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

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

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

281 Tetrahydrobiopterin supplementation of the donor prevent

282 synthase that was corrected by intracellular tetrahydrobiopterin supplementation.

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

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

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

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

287 1 in RNAi lines ((oe)RNAi) or by addition of tetrahydrobiopterin to cultures.

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