ライフサイエンスコーパス: eNOS

1 eNOS dysfunction observed in platelets and liver tissue

2 eNOS is a major target protein of the primary calcium-se

3 eNOS is tightly regulated at various levels, including t

4 eNOS phosphorylation can be easily measured in cells by

5 capillaries P = 0.311), but eNOS ser(1177) /eNOS content ratio decreased significantly following tra

6 changes in the endothelial GSK-3beta/BH(4) /eNOS/Nrf2 pathways, which may lead to impaired vascular

7 At GD18.5, eNOS(-/-) fetuses were significantly smaller than WT ani

8 tivates the NOX2-p47phox complex to activate eNOS phosphorylation and NO production.

9 minutes concentration-dependently activated eNOS, improved cell viabilities, increased NO generation

10 nock-in mice harboring constitutively active eNOS, elevated CRP did not invoke insulin resistance.

11 Modulating eNOS also affected eNOS expression, eNOS activity and NO availability after

12 h the beta2AR to activate the Gbetagamma-Akt-eNOS-sGC pathway to induce MB.

13 pain in mediating VEGF-induced PI3K/AMPK/Akt/eNOS activation through Ezrin.

14 pathway of VEGF/VEGFR2/calpain/PI3K/AMPK/Akt/eNOS.

15 ated with the phosphorylation of ERK and AKT/eNOS, and promoted microvessel sprouting from an angioge

16 ation of NF-kappaB and activation of the Akt/eNOS survival pathways.

17 unction, and increased activation of the AKT/eNOS/NO signaling pathway in the kidney.

18 The VEGF/VEGFR2/Akt/eNOS/NO pathway is essential to VEGF-induced angiogenesi

19 ent lipid-induced endothelial damage via Akt/eNOS signaling and reduced oxidative stress.

20 Although eNOS derangement has been demonstrated in experimental m

21 An eNOS inhibitor phenocopied PLD2 loss and had no further

22 (PP1c) and MP target subunit-1 (MYPT1) as an eNOS(pThr497) phosphatase.

23 EDR of aortas from wild-type (WT) mice by an eNOS-dependent mechanism.

24 l vein endothelial cells (HUVECs), PAI-1 and eNOS colocalize and proximity ligation assays demonstrat

25 The interaction between PAI-1 and eNOS is a direct interaction as supported in experiments

26 rotein-protein interaction between PAI-1 and eNOS.

27 transcytosis via FcgammaRIIB activation and eNOS antagonism.

28 cient to suppress insulin-stimulated Akt and eNOS phosphorylation and to decrease IkappaBalpha (inhib

29 AMP-activated protein kinase (AMPK), Akt and eNOS, and inhibits iNOS and NADPH oxidase isoform 4 (NOX

30 to similar increases in capillarisation and eNOS/NAD(P)Hoxidase protein ratio within the muscle micr

31 Ablation of both caveolae and eNOS completely abolished neurovascular coupling, wherea

32 ich also induced direct binding of CCR10 and eNOS resulting in inhibition of eNOS activity.

33 endothelial defects with decreased CD31 and eNOS and an increased iNOS and COX2 expression.

34 hannels in ECs, leading to SK/IK channel and eNOS activation, hyperpolarization, vasodilation and a r

35 teries with predominantly IK/SK channel- and eNOS-dependent vasodilatation, respectively.

36 t, co-localization of TRPV4(EC) channels and eNOS at MEPs, and the absence of Hbalpha, favour TRPV4(E

37 ium influx that activates SK/IK channels and eNOS serine 1176 phosphorylation in ECs.

38 eletal muscle microvascular eNOS content and eNOS ser(1177) phosphorylation in terminal arterioles an

39 GF (vascular endothelial growth factor), and eNOS (endothelial nitric oxide synthase) protein content

40 fication in altering calmodulin function and eNOS activation has not been investigated.

41 use endothelial dysfunction through MAPK and eNOS signaling in DN.

42 ectively activated IK/SK channels in MAs and eNOS in PAs, revealing preferential TRPV4(EC) -IK/SK cha

43 HSP70-1 suppressed angiogenic responses and eNOS phosphorylation induced by IL-5.

44 e the relationships between NO synthesis and eNOS phosphorylation in cultured endothelial cells.

45 Loss of TM and eNOS causes endothelial dysfunction, which results in su

46 ion, declined KLF2 binding ability to TM and eNOS promoters, enhanced ICAM-1 expression, and decrease

47 diation-induced suppression of KLF2, TM, and eNOS expression.

48 adiation profoundly suppressed KLF2, TM, and eNOS levels, subdued APC generation, declined KLF2 bindi

49 y upregulates lung HIF-1a, HIF-2a, VEGF, and eNOS expression after ETX exposure.Conclusions: HIF augm

50 concentrations were increased in both WT and eNOS(-/-) mice supplemented with BRJ+ (P < 0.001), where

51 Pregnant wildtype (WT) and eNOS(-/-) mice were supplemented with nitrate-containing

52 of H2S production increased PYK2 (Y402) and eNOS (Y656) phosphorylation.

53 n species levels, as well as PYK2 (Y402) and eNOS (Y656) phosphorylation.

54 As eNOS produces nitric oxide (NO) and NAD(P)Hoxidase produ

55 CBD7) peptide and showed that this can block eNOS interaction with CCR10, but not with calmodulin, re

56 ioles P = 0.802; capillaries P = 0.311), but eNOS ser(1177) /eNOS content ratio decreased significant

57 ve effects produced by XMJ were abolished by eNOS inhibitor L-NAME or specific eNOS siRNA in H2O2-tre

58 Consequently, E2 doubles CaM-eNOS interaction and also promotes dual phosphorylation

59 healing by disrupting CCL28-activated CCR10-eNOS interaction.

60 n mouse dermal wounds not only blocked CCR10-eNOS interaction, but also enhanced expression of eNOS,

61 n by expression of EC markers such as CD144, eNOS, CD31, and VEGFR2.

62 g and GRK2-CAV1 interaction, thus clustering eNOS within a complex that inhibits eNOS activity.

63 ells (HUVECs) treated with dextrin confirmed eNOS uncoupling, as verified by the reduced eNOS dimer/m

64 s were transduced with adenovirus containing eNOS promoter driving secreted alkaline phosphatase (SEA

65 scle microvascular endothelial eNOS content, eNOS serine(1177) phosphorylation, NOX2 content and capi

66 ncreased GRK2-CAV1 interaction and decreased eNOS activity.

67 tion, increased MAPK activity, and decreased eNOS activity.

68 paired mitochondrial integrity and decreased eNOS phosphorylation.

69 d the PLD2-deficiency phenotype of decreased eNOS expression and activity could be rescued by cholest

70 gen sulfide (H(2)S) could dehomocysteinylate eNOS to protect the kidney.

71 Puerarin treatment of diabetic eNOS(-/-) mice significantly attenuated albuminuria and

72 DH oxidase 4 (NOX4) in glomeruli of diabetic eNOS(-/-) mice.

73 nd the absence of Hbalpha, favour TRPV4(EC) -eNOS coupling in PAs.

74 IK/SK channel coupling in MAs and TRPV4(EC) -eNOS coupling in PAs.

75 s determines TRPV4(EC) -IK/SK vs. TRPV4(EC) -eNOS coupling in resistance arteries.

76 anometer proximity to eNOS limits TRPV4(EC) -eNOS signalling in MAs.

77 rotein, haemoglobin alpha, limits TRPV4(EC) -eNOS signalling in mesenteric arteries.

78 sence of haemoglobin alpha favour TRPV4(EC) -eNOS signalling in pulmonary arteries.

79 increases in capillarisation and endothelial eNOS content, while reducing endothelial NOX2 content in

80 y and muscle capillarisation and endothelial eNOS/NAD(P)Hoxidase protein ratio in young obese men.

81 to measure muscle microvascular endothelial eNOS content, eNOS serine(1177) phosphorylation, NOX2 co

82 matory pathways independently of endothelial eNOS activation and NO production.

83 om neuronal NOS (nNOS), but not endothelial (eNOS).

84 hosphorylated endothelial NO synthase (eNOS)/eNOS protein expression with adropin incubation only in

85 ted endothelial nitric oxide synthase (eNOS)/eNOS ratio in an age-dependent manner in the SMFAs.

86 patic p-eNOS have been performed to evaluate eNOS function in platelets and liver specimens.

87 dulating eNOS also affected eNOS expression, eNOS activity and NO availability after SAH.

88 hat nitroTyr-calmodulin retains affinity for eNOS under resting physiological calcium concentrations.

89 as been difficult, and surrogate markers for eNOS activation are widely utilized.

90 ing the basal activity of NO production from eNOS.

91 n, and altered gene expression resulted from eNOS instability, possibly due to enhanced miR-155 expre

92 Brain tissue from eNOS(-/-) mice had statistically higher ratios of p25/p3

93 EMPs were found to carry functional eNOS and to protect against oxidative stress by positive

94 se data indicate that EMPs harbor functional eNOS and potentially play a role in the feedback loop of

95 rtner, localizes in SECs with eNOS in a GIT1/eNOS/NO signaling module.

96 We also found that beta-Arr2-mediated GIT1/eNOS complex formation is dependent on Erk1/2 and Src, t

97 ression is reduced and formation of the GIT1/eNOS/NO signaling module is interrupted during liver inj

98 ta-Arr2 is an integral component of the GIT1/eNOS/NO signaling pathway and have implications for the

99 ty over other NOS isoforms, especially human eNOS (hnNOS/heNOS = 2799, the highest hnNOS/heNOS ratio

100 sayed them against rat and human nNOS, human eNOS, and murine and (in some cases) human iNOS.

101 0-fold selectivity for human nNOS over human eNOS.

102 NOS inhibition, low selectivity versus human eNOS, and significant binding to other CNS targets.

103 S activity, and low selectivity versus human eNOS.

104 In support of this finding are: (i) eNOS and MYPT1 interacts in various endothelial cells (E

105 only in the Middle Aged and Old SMFAs; (ii) eNOS blockade ablating both the positive vascular effect

106 n nNOS-specific aspartate residue (absent in eNOS).

107 There was no change in eNOS ser(1177) phosphorylation (arterioles P = 0.802; ca

108 a rapid onset of hypertension, a decrease in eNOS expression, and an increase in endothelin-1 plasma

109 e liver, has been associated with defects in eNOS protein-protein interactions and posttranslational

110 egative regulator of eNOS and disruptions in eNOS-PAI-1 binding promote increases in NO production an

111 and UtA endothelial function was enhanced in eNOS(-/-) mice supplemented with either BRJ+ or BRJ-, in

112 n of PlGF and RGS4, or by PlGF expression in eNOS(-/-) mice.

113 rin function did not further decrease FMD in eNOS-deficient mice.

114 Improvements in endothelial function in eNOS(-/-) mice were abrogated in the presence of 25 mm K

115 atment was associated with an improvement in eNOS activity and increased L-arginine/ADMA ratio and DD

116 mma- and PI3K-dependent, and the increase in eNOS phosphorylation was Gbetagamma- and Akt-dependent.

117 tment was associated with 2-fold increase in eNOS protein (P < 0.0001) and gene (P = 0.0009) expressi

118 P) and histamine promoted rapid increases in eNOS phosphorylation, as did the receptor tyrosine kinas

119 itrite concentrations were increased only in eNOS(-/-) mice (P < 0.001).

120 sion inversely correlated with reductions in eNOS phosphorylation in placental tissue of human preecl

121 educes nitric-oxide production and increases eNOS decoupling compared with WT calmodulin.

122 by which Ser(1179) phosphorylation increases eNOS activity is not understood.

123 ent SECs rescued eNOS function by increasing eNOS complex formation and NO production.

124 quired to coordinate the PGC-1alpha -induced eNOS expression.

125 n the magnitude of effect of adropin-induced eNOS-mediated vasodilatation with advancing age.

126 asing magnitude of effect of adropin-induced eNOS-mediated vasodilatation with ageing.

127 or loss of functions for calmodulin-induced eNOS activation.

128 t cholesterol depletion with dextrin induced eNOS phosphorylation at Serine(1177) (Ser(1177)) and boo

129 ved insulin-induced and shear stress-induced eNOS activation in hIRECO EC.

130 arginine, or BH(4) plus L-arginine inhibited eNOS monomerization.

131 i-VEGF/VEGFR drugs act in part by inhibiting eNOS, causing vasocontraction, MV collapse to GMP, and s

132 ely these findings reveal that by inhibiting eNOS, endothelial FcgammaRIIB activation by CRP blunts i

133 Moreover, PAI-1 directly inhibits eNOS activity, reducing NO synthesis, and the knockdown

134 ustering eNOS within a complex that inhibits eNOS activity.

135 Intriguingly, eNOS activity is regulated by nitric-oxide synthase traf

136 The aim of this study is to investigate eNOS function in NAFLD patients.

137 n pregnant endothelial NO synthase knockout (eNOS(-/-) ) mice, which exhibit hypertension, endothelia

138 endothelial nitric oxide synthase knockout (eNOS(-/-) ) mice.

139 hesized that caveolin 1 (CAV1), a well-known eNOS interactor, regulates eNOS activity in sinusoidal e

140 icantly suppressed atherogenesis in Ldlr(-/-)eNOS(-/-) mice, demonstrating that athero-suppression is

141 in humans, that NAFLD patients show a marked eNOS dysfunction, which may contribute to a higher CV ri

142 unexpected stimulatory role in GPCR-mediated eNOS signaling.

143 imulates both NO synthesis and PP2A-mediated eNOS dephosphorylation, thus constituting a novel negati

144 the ability of H2S to relieve PYK2-mediated eNOS inhibition and evaluated the importance of the H2S/

145 MICT increased skeletal muscle microvascular eNOS content and eNOS ser(1177) phosphorylation in termi

146 on capillarisation and muscle microvascular eNOS/NAD(P)Hoxidase ratio.

147 RK2) that also post-translationally modifies eNOS.

148 w that MACs were able to positively modulate eNOS expression in human endothelial cells in vitro, an

149 iking discordance between receptor-modulated eNOS phosphorylation and NO formation in endothelial cel

150 Modulating eNOS also affected eNOS expression, eNOS activity and NO

151 ignaling pathways such as VEGFR2, Akt, mTOR, eNOS, and Notch, and reduces EC migration, proliferation

152 d mRNA expression levels of endothelial NOS (eNOS), Nrf2, and Phase II enzymes (heme oxygenase-1, cat

153 and others have previously identified novel eNOS interactors, including G protein-coupled receptor (

154 the endothelial nitric oxide synthase-null (eNOS(-/-)) mice.

155 actin were abolished by a genetic absence of eNOS.

156 lling characterized by greater activation of eNOS relative to MAPK.

157 calmodulin and on binding and activation of eNOS.

158 tubules, where it transduces the activity of eNOS in reprogramming intermediary metabolism, thereby p

159 ly nonlinear, biphasic transient behavior of eNOS activation and NO production: a rapid initial activ

160 BH(4) (cofactor of eNOS) biosynthesis enzyme dihydrofolate reductase (DHFR,

161 However, the contribution of eNOS activation and NO production in the athero-protecti

162 glutaredoxin-mediated deglutathionylation of eNOS has been shown to confer protection in a model of h

163 Thioredoxin-mediated deglutathionylation of eNOS in the coronary artery in vivo protected against re

164 Moreover, increased dephosphorylation of eNOS in 5% O2 was Ca(2+)-sensitive and reversed by okada

165 es MP activity inducing dephosphorylation of eNOS(pThr497) and the 20 kDa myosin II light chains.

166 hanisms involved in the dephosphorylation of eNOS(pThr497) have not yet been clarified.

167 kinase is a major regulatory determinant of eNOS activity.

168 Triple-knockout mouse lacking expression of eNOS, Cav1, and Ldlr were generated to explore the role

169 interaction, but also enhanced expression of eNOS, CD31, and IL-4 with reduction of CCL28 and IL-6 le

170 ivity through ERRalpha induced expression of eNOS.

171 lude that during Hhcy, homocysteinylation of eNOS and disruption of caveolin-mediated regulation lead

172 cy was associated with homocysteinylation of eNOS, reduced enzyme activity and upregulation of caveol

173 nd endothelin-1; (d) immunohistochemistry of eNOS, endothelin-1, P-selectin, intercellular adhesion m

174 l Dysfunction (ED) through the impairment of eNOS function.

175 NAFL showed a higher impairment of eNOS phosphorylation in comparison to NASH (p < 0.01).

176 othelial gene expression were independent of eNOS activity.

177 of CCR10 and eNOS resulting in inhibition of eNOS activity.

178 disruption or pharmacological inhibition of eNOS attenuates angiogenesis during tissue repair, resul

179 Inhibition of eNOS reduces synthesis of its vasodilatory product, nitr

180 cription suppression and mRNA instability of eNOS complemented by upregulation of MCP1 and VCAM1 Thes

181 Overexpression of eNOS and HA-tagged PAI-1 in COS7 cells confirmed the col

182 the loss of flow-induced phosphorylation of eNOS and Akt, as well as inhibition of NO generation.

183 ted by increased tyrosine phosphorylation of eNOS and excess Nox2-derived superoxide.

184 on and also promotes dual phosphorylation of eNOS at Ser-617 and Ser-1179.

185 The second is phosphorylation of eNOS by protein kinases PKC and AKT.

186 Previous reports in which phosphorylation of eNOS has been studied as a surrogate for enzyme activati

187 odulin complexes, followed by recruitment of eNOS from caveolae.

188 nction in SLE, focusing on its regulation of eNOS and NO production in endothelial cells.

189 dings place PAI-1 as a negative regulator of eNOS and disruptions in eNOS-PAI-1 binding promote incre

190 roatherogenic mediator through repression of eNOS-dependent pathways.

191 erfusion injury, motivating further study of eNOS deglutathionylation in general.

192 of TGFbeta signaling, EndMT, suppression of eNOS, and induction of endothelin-1 expression.

193 ith calmodulin, resulting in upregulation of eNOS activity.

194 horylation at the inhibitory residue Y657 of eNOS and expression of proline-rich tyrosine kinase 2 th

195 PT1(pThr696)) controls the activity of MP on eNOS(pThr497).

196 2S relieves the inhibitory effect of PYK2 on eNOS, allowing the latter to produce greater amounts of

197 Knockdown of PAI-1 or eNOS eliminates the proximity ligation assay (PLA) signa

198 PKCalpha-deficient, mast cell-deficient, or eNOS-deficient mice.

199 or genetic disruption of endogenous nNOS or eNOS during workload transitions in cardiac myoctyes.

200 independently of mast cells, or PKCalpha or eNOS expression and rapidly reversed established broncho

201 for platelet-derived phosphorylated-eNOS (p-eNOS) and immunohistochemistry for hepatic p-eNOS have b

202 eNOS) and immunohistochemistry for hepatic p-eNOS have been performed to evaluate eNOS function in pl

203 s (p < 0.001), associated with an impaired p-eNOS in both platelets and liver (p < 0.001).

204 t assays for platelet-derived phosphorylated-eNOS (p-eNOS) and immunohistochemistry for hepatic p-eNO

205 Finally, caveolae disruption promotes eNOS uncoupling in normotensive and hypertensive rat ves

206 Importantly, APP/PS1/eNOS(-/-) mice also had significantly increased tau phos

207 r neuroinflammation were observed in APP/PS1/eNOS(-/-) mice as compared with APP/PS1 mice.

208 d the role of NO in tau pathology in APP/PS1/eNOS(-/-).

209 and evaluated the importance of the H2S/PYK2/eNOS axis on cardiomyocyte injury in vitro and in vivo.

210 .0 g/kg/d) for 12 weeks remarkably recoupled eNOS and reduced the size of carotid atherosclerotic pla

211 In conclusion, XMJ recouples eNOS to prevent the growth of atherosclerosis in rats.

212 Chinese medicine xin-mai-jia (XMJ) recouples eNOS to exert anti-atherosclerotic effects.

213 n enhanced CAV1-GRK2 interaction and reduced eNOS activity.

214 In addition, PYK2 overexpression reduced eNOS activity in a H2S-reversible manner.

215 ial cell (SEC) injury with resultant reduced eNOS activity and NO production within the liver, has be

216 on injury (BDL) led to significantly reduced eNOS activity and to a dramatic increase in portal hyper

217 eNOS uncoupling, as verified by the reduced eNOS dimer/monomer ratio.

218 nockdown of CCR10 with siRNA lead to reduced eNOS expression and tube formation suggesting the involv

219 MRTFA binds to the Nos3 promoter and reduces eNOS expression, thereby mediating a profibrotic paracri

220 V1), a well-known eNOS interactor, regulates eNOS activity in sinusoidal endothelial cells (SECs) via

221 HMG Co-A reductase negatively regulates eNOS, and the PLD2-deficiency phenotype of decreased eNO

222 cell maintenance and function by regulating eNOS activity.

223 novel negative feedback mechanism regulating eNOS activity not present in response to shear stress.

224 st oxidative stress by positively regulating eNOS/Akt signaling, which restored NO production, increa

225 injured or beta-Arr2-deficient SECs rescued eNOS function by increasing eNOS complex formation and N

226 MRTFA inhibition rescues eNOS levels and ameliorates the profibrotic effect of en

227 fficking inducer (NOSTRIN), which sequesters eNOS, thereby attenuating NO production.

228 ass spectrometry (MS), we identified several eNOS interactors, including the protein plasminogen acti

229 olished by eNOS inhibitor L-NAME or specific eNOS siRNA in H2O2-treated cells.

230 sulin-stimulated and shear stress-stimulated eNOS activations were blunted.

231 portantly, we show that beta-Arr2 stimulates eNOS activity, and that beta-Arr2 expression is reduced

232 llular NO or Ca(2+)-despite eliciting strong eNOS phosphorylation responses.

233 tensive rat and SHR vessels, which suggested eNOS uncoupling.

234 ammation, including endothelial NO synthase (eNOS) and NO bioavailability, are unknown.

235 between the loss of endothelial NO synthase (eNOS) and tau phosphorylation in neuronal tissue.

236 n kinase (MAPK) and endothelial NO synthase (eNOS) in EA.hy926 cells treated with conditioned medium

237 The activity of endothelial NO synthase (eNOS) is triggered by calmodulin (CaM) binding and is of

238 insulin stimulates endothelial NO synthase (eNOS) to generate the antiatherosclerotic signaling radi

239 her Abeta42 reduced endothelial NO synthase (eNOS), cyclic GMP (cGMP), and protein kinase G (PKG) act

240 independent of the endothelial NO synthase (eNOS)-mediated NO pathway.

241 ylates and inhibits endothelial NO synthase (eNOS).

242 ased phosphorylated endothelial NO synthase (eNOS)/eNOS protein expression with adropin incubation on

243 n of endothelial nitric oxide (NO) synthase (eNOS) and increased production of NO and reduced inflamm

244 n of endothelial nitric oxide (NO) synthase (eNOS) at Thr497 (eNOS(pThr497)) by protein kinase C or R

245 Endothelial cell nitric oxide (NO) synthase (eNOS), the enzyme responsible for synthesis of NO in end

246 h blunted endothelial nitric oxide synthase (eNOS) activation in skeletal muscle.

247 regulated endothelial nitric-oxide synthase (eNOS) activity is linked to vascular dysfunction.

248 einylates endothelial nitric oxide synthase (eNOS) and alters caveolin-1 expression to decrease nitri

249 action of endothelial nitric oxide synthase (eNOS) and endothelin-1; (d) immunohistochemistry of eNOS

250 Endothelial nitric-oxide synthase (eNOS) and its bioactive product, nitric oxide (NO), medi

251 levels of endothelial nitric oxide synthase (eNOS) and NO.

252 ty of the endothelial nitric-oxide synthase (eNOS) and that Cavin-2 knockdown cells produce much less

253 ened with endothelial nitric oxide synthase (eNOS) antagonist L-NNA and its agonist scutellarin, hemo

254 nnels and endothelial nitric oxide synthase (eNOS) are present in the endothelium of mesenteric and p

255 increased endothelial nitric oxide synthase (eNOS) expression.

256 beds and endothelial nitric oxide synthase (eNOS) in others.

257 ndothelial isoform of nitric oxide synthase (eNOS) is a critical determinant of vascular homeostasis.

258 oduced by endothelial nitric oxide synthase (eNOS) is a critical mediator of vascular function.

259 Endothelial nitric oxide synthase (eNOS) is protective against kidney injury, but the molec

260 ations of endothelial nitric oxide synthase (eNOS) lead to impaired nitric oxide synthesis.

261 timulated endothelial nitric oxide synthase (eNOS) phosphorylation in skeletal muscle and increased a

262 ract with endothelial nitric oxide synthase (eNOS) present in blood.

263 esponsive endothelial nitric oxide synthase (eNOS) promoter, we tested effects of shear stress and el

264 inhibited endothelial nitric oxide synthase (eNOS) serine 1179 phosphorylation, whereas PEG-catalase

265 caused by endothelial nitric oxide synthase (eNOS) uncoupling, is an initial step in atherosclerosis.

266 ptor, and endothelial nitric oxide synthase (eNOS), an enzyme that generates nitric oxide (NO).

267 Endothelial nitric oxide synthase (eNOS), an enzyme that synthesizes nitric oxide (NO) by c

268 vation of endothelial nitric oxide synthase (eNOS), enhanced levels of reactive oxygen species, and a

269 PK), Akt, endothelial nitric oxide synthase (eNOS), nuclear factor erythroid 2-related factor 2 (Nrf2

270 ession of endothelial nitric oxide synthase (eNOS), which generates the potent vasodilator nitric oxi

271 s through endothelial nitric oxide synthase (eNOS)-dependent Src, PI3K, and MAPK signaling.

272 diated by endothelial nitric oxide synthase (eNOS).

273 MCA), and endothelial nitric-oxide synthase (eNOS).

274 horylated endothelial nitric oxide synthase (eNOS)/eNOS ratio in an age-dependent manner in the SMFAs

275 lectin B4, endothelial nitric oxide synthase(eNOS), von Willebrand factor(vWF), and CD31 after cardia

276 phorylation of Akt and its downstream target eNOS.

277 These observations emphasize that eNOS-derived NO can promote angiogenesis.

278 models, no studies have directly shown that eNOS dysfunction is associated with NAFLD in humans.

279 The eNOS inhibitor N(G)-Nitro-l-arginine methyl ester mimick

280 This should impair the eNOS function and diminish NO bioavailability.

281 ring Abeta42 reversed the DIO deficit in the eNOS/cGMP/PKG pathway and decreased endothelin-1.

282 Therefore, by targeting the eNOS and pericyte alpha-SMA phenotype, our present data

283 (O2 (-) , quenching NO) we propose that the eNOS/NAD(P)Hoxidase protein ratio is a marker of vasodil

284 timulating the expression of HSP70-1 via the eNOS signaling pathway.

285 nitric oxide (NO) synthase (eNOS) at Thr497 (eNOS(pThr497)) by protein kinase C or RhoA-activated kin

286 ntributes to the EDR impairment through TLR4/eNOS pathway in the setting of diabetes.

287 ter effect was eliminated when normalised to eNOS content (P = 0.217).

288 lpha (Hbalpha) within nanometer proximity to eNOS limits TRPV4(EC) -eNOS signalling in MAs.

289 scopy revealed comparable increases in total eNOS content in terminal arterioles and capillaries (P <

290 ii) MYPT1 targets and stimulates PP1c toward eNOS(pThr497) substrate (iii) phosphorylation of MYPT1 a

291 the human PLD2 polymorphism does not trigger eNOS loss, but rather creates another effect, suggesting

292 activates the NOX1-NOXO1 complex to uncouple eNOS.

293 fied, for the first time, that OSS uncouples eNOS, which was corrected by RNAi of NOXO1.

294 Results from in vitro eNOS assays with calmodulin nitrated at Tyr-99 revealed

295 /SK channels in mesenteric arteries and with eNOS in pulmonary arteries.

296 Spatial proximity of TRPV4(EC) channels with eNOS and the absence of haemoglobin alpha favour TRPV4(E

297 urce of intracellular PAI-1 interacting with eNOS was shown to be endocytosis derived.

298 5% O2, resulting in greater interaction with eNOS in response to histamine.

299 potentially via functional interaction with eNOS.

300 CR signaling partner, localizes in SECs with eNOS in a GIT1/eNOS/NO signaling module.