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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

25 -1 (MCP-1), we have observed the presence of endothelial NO synthase and platelet endothelial cell ad

26 Endothelial NO synthase and Ser-1177-phosphorylated endo

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

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

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

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

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

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

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

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

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

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

37 Inhibitors of endothelial NO synthase, blocking antibodies to interleu

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

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

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

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

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

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

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

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

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

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

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

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

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

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

52 0.05), decreased phospho-AKT/AKT and phospho-endothelial NO synthase/endothelial NO synthase (NC vers

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

82 Endothelial NO synthase (eNOS) is an enzyme responsible

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

84 Endothelial NO synthase (eNOS) is critically modulated b

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

189 Mice with transgenic endothelial NO synthase overexpression were protected ag

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

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

192 Endothelial NO synthase phosphorylation by VEGF was also

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

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

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

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

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

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

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

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

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

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

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

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

205 Platelets lacking endothelial NO synthase show increased rolling on venule

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

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

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

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

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