ライフサイエンスコーパス: endothelial NO synthase

1 nd ONOO- generation by NAD(P)H and uncoupled endothelial NO synthase.

2 donor or from endogenous production of NO by endothelial NO synthase.

3 had no effect on the activity of arterial or endothelial NO synthase.

4 ore NO-mediated responses by upregulation of endothelial NO synthase.

5 lability of tetrahydrobiopterin may activate endothelial NO synthase.

6 Piezo1 was required for normal expression of endothelial NO synthase.

7 ding the endothelium, in which they activate endothelial NO synthase.

8 (NO) production and angiogenesis mediated by endothelial NO synthase, a substrate of AMPK in vascular

9 from hIGFREO had reduced insulin-stimulated endothelial NO synthase activation (mean [SEM] wild type

10 The combined effects of conventional PKC and endothelial NO synthase activation by PST can suppress i

11 ncreased cardiac VEGF expression and Akt and endothelial NO synthase activation were observed by comp

12 ive properties of the lipoprotein, including endothelial NO synthase activation, NO production, and a

13 Such phosphorylation results in endothelial NO synthase activation, which provides a nov

14 linositol-3-kinase pathway, leading to eNOS (endothelial NO synthase) activation both in resistance a

15 ing in endothelium through src that promotes endothelial NO synthase activity and cell migration.

16 tery at concentrations sufficient to inhibit endothelial NO synthase activity, has little effect on h

17 an be involved in important EC functions and endothelial NO synthase activity, we sought to investiga

18 flux for stimulation of calmodulin-dependent endothelial NO synthase activity.

19 dothelium and required for HDL activation of endothelial NO synthase and cell migration; in contrast,

20 onal importance of B2R-induced activation of endothelial NO synthase and cyclooxygenase.

21 In response to TAC, myocardial endothelial NO synthase and iNOS was expressed as both m

22 pathway describing actual NO production from endothelial NO synthase and its various protein partners

23 es, and it is required for HDL activation of endothelial NO synthase and migration in cultured endoth

24 ducer (NOSTRIN) is an interaction partner of endothelial NO synthase and modulates its subcellular lo

25 H(2)O(2) elicited severalfold elevations of endothelial NO synthase and neuronal NO synthase express

26 analysis revealed expression of Ca-dependent endothelial NO synthase and neuronal NO synthase isoform

27 -1 (MCP-1), we have observed the presence of endothelial NO synthase and platelet endothelial cell ad

28 Endothelial NO synthase and Ser-1177-phosphorylated endo

29 Although the altered function of endothelial NO synthase and the overproduction of reacti

30 favorable pharmacodynamic profile depends on endothelial NO synthase and xanthine oxidoreductase -cat

31 tant change in Ca(2+)-dependent NO synthase (endothelial NO synthase and/or neuronal NO synthase) act

32 t ApoE(-/-) mice of insulin receptors, eNOS (endothelial NO synthase) and ETBR (endothelin receptor t

33 ably expressing ETB receptor with or without endothelial NO synthase, and 3) application of antisense

34 cultured cells, which expressed neuronal and endothelial NO synthases, and in cells with elevated NO

35 may inhibit O2- production generated also by endothelial NO synthase at diminished local L-arginine c

36 n of acetyl-CoA carboxylase at Ser-79 and of endothelial NO synthase at Ser-1177, 2 putative downstre

37 ase, have been demonstrated to phosphorylate endothelial NO synthase at Ser-1177.

38 oduction with concomitant phosphorylation of endothelial NO synthase at Ser-1177.

39 is essential in allowing proper function of endothelial NO synthase because GPTCH-1 blockade with 2,

40 Inhibitors of endothelial NO synthase, blocking antibodies to interleu

41 ular endothelial growth factor activation of endothelial NO synthase by altering endothelial NO synth

42 Feedback inhibition of endothelial NO synthase by NO may inhibit O2- production

43 clohydrolase (GCH) I increased levels of the endothelial NO synthase cofactor, tetrahydrobiopterin, i

44 Endothelial GCH overexpression increased endothelial NO synthase coupling and enhanced the prolif

45 of the circadian clock, Bmal1, can influence endothelial NO synthase coupling and reactive oxygen spe

46 pression and activity, resulting in improved endothelial NO synthase coupling and reduced vascular O(

47 o date, the impact of the circadian clock on endothelial NO synthase coupling and vascular reactive o

48 (2)(.-) through tetrahydrobiopterin-mediated endothelial NO synthase coupling.

49 ed vasodilation is unaffected by blockade of endothelial NO synthase, cyclooxygenase, or capsaicin re

50 y endothelium-derived nitric oxide (NO), and endothelial NO synthase-deficient (eNOS-deficient; eNOS(

51 Erythrocytes isolated from endothelial NO synthase-deficient mice exhibited a reduc

52 priapic phenotype due to double neuronal and endothelial NO synthase deletion (dNOS(-/-)) or human si

53 nflammatory cytokines by CD11+ cells, and to endothelial NO synthase-derived NO by d7EB cells, leadin

54 ysiological processes act in concert to make endothelial NO synthase-derived NO potentially important

55 Using western-type diet-fed apoE and apoE/endothelial NO synthase double knockout mice as models o

56 wn whether they can also directly upregulate endothelial NO synthase (ecNOS) activity.

57 0.05), decreased phospho-AKT/AKT and phospho-endothelial NO synthase/endothelial NO synthase (NC vers

58 Because endothelial NO synthase (eNOS and NOS3), beta-adrenergic

59 ow in cultured endothelium that CRP prevents endothelial NO synthase (eNOS) activation by diverse ago

60 Basal and insulin-stimulated endothelial NO synthase (eNOS) activities in endothelial

61 ilatation independently of IGF and increased endothelial NO synthase (eNOS) activity in arterial segm

62 Because endothelial NO synthase (eNOS) activity is largely regul

63 tor (VEGF)-stimulated and hypoxia-stimulated endothelial NO synthase (eNOS) activity.

64 y increases in nitric oxide (NO) release and endothelial NO synthase (eNOS) activity.

65 ial cells apoE3 binding to ApoER2 stimulates endothelial NO synthase (eNOS) and endothelial cell migr

66 the expression of the NO-generating enzymes endothelial NO synthase (eNOS) and inducible NOS (iNOS)

67 d by nitric oxide (NO) donor administration; endothelial NO synthase (eNOS) and neuronal NO synthase

68 ilation and modulate inflammation, including endothelial NO synthase (eNOS) and NO bioavailability, a

69 rvention with antioxidants and l-arginine on endothelial NO synthase (eNOS) and oxidation-sensitive g

70 nd activity, we quantified the expression of endothelial NO synthase (eNOS) and phosphorylated eNOS.

71 However, immunoblots for endothelial NO synthase (eNOS) and soluble guanylyl cycl

72 termine the relationship between the loss of endothelial NO synthase (eNOS) and tau phosphorylation i

73 we report that statin-induced expression of endothelial NO synthase (eNOS) and thrombomodulin is KLF

74 male versus male hearts, there was also more endothelial NO synthase (eNOS) associated with cardiomyo

75 ell (sRBC) adhesion using mice deficient for endothelial NO synthase (eNOS) because their NO metaboli

76 Recent literature indicates that endothelial NO synthase (eNOS) can modulate cancer-relat

77 Nitric oxide (NO) derived from the endothelial NO synthase (eNOS) contributes to regulation

78 ed nitric oxide (NO) availability because of endothelial NO synthase (eNOS) dysfunction are critical

79 ave examined the role of IL-17 in regulating endothelial NO synthase (eNOS) expression in human vascu

80 Plasma NO metabolites and aortic endothelial NO synthase (eNOS) expression were also elev

81 g molecule nitric oxide (NO) by upregulating endothelial NO synthase (eNOS) expression, by maintainin

82 c TNF-alpha expression, and decreased aortic endothelial NO synthase (eNOS) expression.

83 investigate the impact of H2S deficiency on endothelial NO synthase (eNOS) function, NO production,

84 sustained transcriptional activation of the endothelial NO synthase (eNOS) gene, presumably due to s

85 effects differ by apolipoprotein E (APOE) or endothelial NO synthase (eNOS) Glu298Asp gene polymorphi

86 sculature, nitric oxide (NO) is generated by endothelial NO synthase (eNOS) in a calcium/calmodulin-d

87 Aortic VEC, but not VIC, expressed endothelial NO synthase (eNOS) in both porcine and human

88 lar concentrations) release NO by activating endothelial NO synthase (eNOS) in bovine and inducible N

89 mitogen-activated protein kinase (MAPK) and endothelial NO synthase (eNOS) in EA.hy926 cells treated

90 Endothelial NO synthase (eNOS) is an enzyme responsible

91 Nitric oxide (NO) derived from endothelial NO synthase (eNOS) is an integral mediator o

92 Endothelial NO synthase (eNOS) is critically modulated b

93 The expression of the endothelial NO synthase (eNOS) is dramatically influence

94 ys an important role in airway function, and endothelial NO synthase (eNOS) is expressed in airway ep

95 The endothelial NO synthase (eNOS) is regulated by diverse p

96 nthesis to understand how activity of bovine endothelial NO synthase (eNOS) is regulated.

97 The activity of endothelial NO synthase (eNOS) is triggered by calmoduli

98 nd that endothelial cells, which express the endothelial NO synthase (eNOS) isoform, constitutively p

99 taneous adipose tissue of wild-type (WT) and endothelial NO synthase (eNOS) knockout (eNOS(-/-)) mice

100 , an effect reversed by L-NAME and absent in endothelial NO synthase (eNOS) KO mice or angiotensin co

101 ne receptor(s), leading to the activation of endothelial NO synthase (eNOS) NO production through a s

102 whether adenovirus-mediated gene transfer of endothelial NO synthase (eNOS) or Cu/Zn superoxide dismu

103 e with an expression vector containing human endothelial NO synthase (eNOS) or murine inducible NOS (

104 stimulated phosphatidylinositol 3-kinase/Akt/endothelial NO synthase (eNOS) pathway activation, a pos

105 anger 1 (NHE-1) and activated AKT kinase and endothelial NO synthase (eNOS) pathways to ameliorate AL

106 was lost in ESMIRO mice, and insulin-induced endothelial NO synthase (eNOS) phosphorylation was blunt

107 Nitric oxide (NO) produced by endothelial NO synthase (eNOS) plays an essential role i

108 Nitric oxide (NO) produced by endothelial NO synthase (eNOS) plays an essential role i

109 There were significantly reduced levels of endothelial NO synthase (eNOS) protein and constitutive

110 for 24 h showed an increase in the amount of endothelial NO synthase (eNOS) protein and the release o

111 VR increased endothelial NO synthase (eNOS) protein expression (P < 0

112 y several mechanisms, including upregulating endothelial NO synthase (eNOS) protein expression and bl

113 ing basal NO production were lysed, and both endothelial NO synthase (eNOS) protein expression and eN

114 Endothelial NO synthase (eNOS) protein in arteries and a

115 s well as a 49% decrease in immunodetectable endothelial NO synthase (eNOS) protein.

116 NALE: In the endothelium, insulin stimulates endothelial NO synthase (eNOS) to generate the antiather

117 n vascular disease states are due in part to endothelial NO synthase (eNOS) uncoupling related to def

118 Endothelial NO synthase (eNOS) via the production of NO

119 mRNA expression of endothelial NO synthase (eNOS) was increased (P < 0.05)

120 Endothelial NO synthase (eNOS) was present in SEC based

121 t drainage in transgenic mice overexpressing endothelial NO synthase (eNOS) was studied.

122 NO is produced by endothelial NO synthase (eNOS) whose function is modulat

123 We hypothesized that overexpression of endothelial NO synthase (eNOS) within the endothelium wo

124 d, respectively, by exposing wild-type (WT), endothelial NO synthase (eNOS)(-/-) and inducible NO syn

125 sion, and the phosphorylation states of Akt, endothelial NO synthase (eNOS), and p70S6K were determin

126 nd is S-nitrosylated at a single cysteine by endothelial NO synthase (eNOS), and that S-nitrosylation

127 Endothelial NO synthase (eNOS), but not the inducible is

128 Protein expression of endothelial NO synthase (eNOS), caveolin, and calmodulin

129 Mechanistically, higher Abeta42 reduced endothelial NO synthase (eNOS), cyclic GMP (cGMP), and p

130 NO, produced by endothelial NO synthase (eNOS), is a key mediator of pul

131 helin-1 (ET-1) and a significantly decreased endothelial NO synthase (eNOS), mRNA, and protein levels

132 luding [Ca2+]i transients, activation of the endothelial NO synthase (eNOS), phosphorylation of PECAM

133 Nitric oxide (NO), which is derived from endothelial NO synthase (eNOS), provides crucial signals

134 eptor (EpoR) ligand-binding, which activates endothelial NO synthase (eNOS), regulates the prosurviva

135 Nitric oxide (NO), generated by the endothelial NO synthase (eNOS), regulates vascular tone

136 kt kinase-dependent calcium sensitization of endothelial NO synthase (eNOS), stimulating NO productio

137 In endothelia, NO is synthesized by endothelial NO synthase (eNOS), which is negatively regu

138 emains unclear whether it can be produced by endothelial NO synthase (eNOS), which is present in RBCs

139 f the endothelium including NO production by endothelial NO synthase (eNOS), which it stimulates via

140 ell culture, CRP decreases the expression of endothelial NO synthase (eNOS), which regulates diverse

141 NO is produced by endothelial NO synthase (eNOS), whose expression is down

142 ial cells, we addressed the possibility that endothelial NO synthase (eNOS)-dependent NO production w

143 Oral D-4F restored endothelium- and endothelial NO synthase (eNOS)-dependent vasodilation in

144 Therefore, we investigated the role of endothelial NO synthase (eNOS)-derived NO on in vivo reg

145 in vivo approaches, we studied the effect of endothelial NO synthase (eNOS)-derived NO on liver tumor

146 lungs demonstrated a significant increase in endothelial NO synthase (eNOS)-derived NO production rel

147 racterized by the lowered bioavailability of endothelial NO synthase (eNOS)-derived NO, is a critical

148 In endothelium, NO is derived from endothelial NO synthase (eNOS)-mediated L-arginine oxida

149 eolae function in aECs is independent of the endothelial NO synthase (eNOS)-mediated NO pathway.

150 This was prevented by inhibiting endothelial NO synthase (eNOS).

151 kinase, directly phosphorylates and inhibits endothelial NO synthase (eNOS).

152 ons using nitric oxide (NO) derived from the endothelial NO synthase (eNOS).

153 + influx which may cause some stimulation of endothelial NO synthase (eNOS).

154 s include the upregulation and activation of endothelial NO synthase (eNOS).

155 zyme activity assays for NAD(P)H-oxidase and endothelial NO synthase (eNOS).

156 sphatidylinositol 3-Akt kinase pathways, and endothelial NO synthase (eNOS).

157 ule nitric oxide (NO), which is generated by endothelial NO synthase (eNOS).

158 ion of tetrahydrobiopterin and uncoupling of endothelial NO synthase (eNOS).

159 rast, few if any ECs in atheroma stained for endothelial NO synthase (eNOS).

160 ssociated estrogen receptors (ER) coupled to endothelial NO synthase (eNOS).

161 ER) alpha-mediated, nongenomic activation of endothelial NO synthase (eNOS).

162 ism involving the selective up-regulation of endothelial NO synthase (eNOS).

163 cofactor for nitric oxide (NO) production by endothelial NO synthase (eNOS).

164 on of vascular tone is considered to involve endothelial NO synthase (eNOS).

165 ) regulate nitric oxide (NO) production from endothelial NO synthase (eNOS).

166 as supported by (i) increased phosphorylated endothelial NO synthase (eNOS)/eNOS protein expression w

167 l lines demonstrated that NO* down-regulated endothelial NO* synthase (eNOS) but up-regulated TNFalph

168 al endothelial nitric oxide (NO) production (endothelial NO synthase [eNOS] and phosphorylated eNOS)

169 e levels in blood reflect NO production from endothelial NO synthase enzymes, and recent data suggest

170 We have shown that CRP decreases endothelial NO synthase expression and bioactivity in hu

171 A-285222 treatment enhanced dermis endothelial NO synthase expression and plasma NO levels

172 IGFBP-3 increased endothelial NO synthase expression in human EPCs leading

173 ) levels and caused a transient reduction in endothelial NO synthase expression.

174 ial NO synthase inhibition) without changing endothelial NO synthase expression/activation (Ser 1177

175 Vascular endothelial growth factor and endothelial NO synthase expressions were also significan

176 The impairment of endothelial NO synthase function was likely due to post-

177 via a receptor-mediated pathway, upregulates endothelial NO synthase gene expression, leading to incr

178 etinoblastoma, which is dependent in part on endothelial NO synthase-generated NO.

179 pathophysiological mechanisms that regulate endothelial NO synthase in endothelial regeneration rema

180 of antisense oligodeoxynucleotides targeting endothelial NO synthase in human umbilical vein endothel

181 g phosphorylation and Golgi translocation of endothelial NO synthase in response to the M3R agonist c

182 caveolin-1, a putative negative regulator of endothelial NO synthase, in mediating deficient intrahep

183 ne during shear inhibited dimer formation of endothelial NO synthase, increased endothelial cell supe

184 NO-mediated EDD (greater DeltaFBF(ACh) with endothelial NO synthase inhibition) without changing end

185 que granulomas had upregulated inducible and endothelial NO synthase (iNOS and eNOS) and arginase (Ar

186 In these pathways, endothelial NO synthase is activated 1), via calcium rel

187 An essential cofactor for the endothelial NO synthase is tetrahydrobiopterin (H4B).

188 Using endothelial NO synthase knockout (eNOS KO) mice, inducib

189 nction and increase fetal growth in pregnant endothelial NO synthase knockout (eNOS(-/-) ) mice, whic

190 ne whether prolonged loss of NO activity, in endothelial NO synthase knockout (eNOS(-/-)) mice, influ

191 Thus, shear stress not only increases endothelial NO synthase levels but also stimulates produ

192 to post-translational mechanisms, given that endothelial NO synthase mRNA and protein levels did not

193 ort that human NK cells express constitutive endothelial NO synthase mRNA and protein, but not detect

194 NO, synthesized in endothelial cells by endothelial NO synthase (NOS 3), is believed to be an im

195 The protein levels of endothelial NO synthase (NOS) and inducible NOS were inc

196 Endothelial NO synthase (NOS3) localizes to caveolae, wh

197 ated the effects of congenital deficiency of endothelial NO synthase (NOS3) on the pulmonary vascular

198 wed that there was a significant decrease in endothelial NO synthase (NOS3)-labeled, serotonin (5-HT)

199 yper-responsiveness was seen in mice lacking endothelial NO synthase (NOS3).

200 Although exhaled NO and NO2- were increased, endothelial NO synthase or inducible NO synthase express

201 ate and nitrite were reduced in mice lacking endothelial NO synthase or treated with the xanthine oxi

202 ference in Cu/Zn or Mn superoxide dismutase, endothelial NO synthase, or inducible NO synthase protei

203 Indeed, both NO donors and endothelial NO synthase overexpression promoted HSC apop

204 Mice with transgenic endothelial NO synthase overexpression were protected ag

205 anisms leading to migration and that the Akt/endothelial NO synthase pathway is necessary for VEGF-st

206 Ts stimulated keratinocyte proliferation via endothelial NO synthase phosphorylation and NO productio

207 Endothelial NO synthase phosphorylation by VEGF was also

208 increased AMPK, acetyl-CoA carboxylase, and endothelial NO synthase phosphorylation in mouse aorta a

209 Insulin-stimulated aortic endothelial NO synthase phosphorylation was also signifi

210 ion, acceleration of endothelial repair, and endothelial NO synthase phosphorylation were abrogated i

211 tracellular signal-regulated kinase 1/2, and endothelial NO synthase phosphorylation, upregulation of

212 ation of endothelial NO synthase by altering endothelial NO synthase phosphorylation.

213 In nondiabetic vessels, endothelial NO synthase produced NO that scavenged super

214 in the vasculature, to regulate coupling of endothelial NO synthase, production of superoxide, and m

215 O synthase isoforms revealed the presence of endothelial NO synthase protein in healthy and PVL rats

216 ion caused a left versus right difference in endothelial NO synthase protein levels after 4 weeks tha

217 lial NO synthase and Ser-1177-phosphorylated endothelial NO synthase protein levels were upregulated

218 ves activation of phosphoinositide-3-kinase, endothelial NO synthase, protein kinase C, glycogen synt

219 nstrate increased expression and activity of endothelial NO synthase, reduced oxidative damage associ

220 Targeting tetrahydrobiopterin-dependent endothelial NO synthase regulation in the endothelium is

221 chemically using L-NMMA, or genetically, in endothelial NO synthase serine to alanine (S1176A) mutan

222 Platelets lacking endothelial NO synthase show increased rolling on venule

223 peroxide production because of dysfunctional endothelial NO synthase that was corrected by intracellu

224 phorylation and GFRP downregulation prevents endothelial NO synthase uncoupling in response to oscill

225 uggest important roles for NAD(P)H oxidases, endothelial NO synthase uncoupling, and protein kinase C

226 ming subunits were not affected by IR, while endothelial NO synthase was upregulated in the ZO arteri

227 Effects of IgG on endothelial NO synthase were assessed in human aortic en

228 king down the expression of Rap1A, HSPB6, or endothelial NO synthase, which serve as PKA-activatable