ライフサイエンスコーパス: eNOS

1 eNOS and nNOS mutant mice show comparable M1 macrophage

2 eNOS dysfunction observed in platelets and liver tissue

3 nd colocalized with nitric oxide synthase 3 (eNOS) in wild-type cardiac myocytes.

4 hosphorylation of eNOS at threonine 497/495 (eNOS-pThr497/495) in the mouse aorta and HAECs.

5 the ability of GIT1 to bind to and activate eNOS.

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

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

8 Akt phosphorylation activated eNOS (at Ser(1177)), and Akt also regulated the ability

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

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

11 e, impairing phosphorylation of ERK1/2, Akt, eNOS, JNK, cell proliferation, cell migration, and capil

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

13 The BRS up-regulation is associated with Akt-eNOS-NO signaling activation in the NTS and NG induced b

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

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

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

17 naling pathways: angiopoietin/Tie2, PI3K/Akt/eNOS, and syndecan/syntenin, which play important roles

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

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

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

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

22 Although eNOS derangement has been demonstrated in experimental m

23 An eNOS inhibitor phenocopied PLD2 loss and had no further

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

25 ed tonic cardiomyocyte cGMP synthesis via an eNOS/soluble guanylate cyclase pathway.

26 d dysfunction as mice either treated with an eNOS inhibitor (LNAME) or lacking eNOS were no longer re

27 eta2 activation-induced eNOS-pThr497/495 and eNOS inactivation.

28 transcytosis via FcgammaRIIB activation and eNOS antagonism.

29 glutathione peroxidase and GR activities and eNOS, iNOS and TNF-alpha levels (p<0.05).

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

31 2 to 3 weeks had impaired i) aortic Akt and eNOS phosphorylation to infused VEGF, ii) ear angiogenic

32 ding von Willebrand factor, VE-cadherin, and eNOS were observed when compared to CD34+CD146- cells, a

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

34 s-induced NO generation, iNOS expression and eNOS expression compared with normal groups.

35 oscopy revealed that both vascular iNOS- and eNOS-dependent NO formation were normalized in ATII-infu

36 The increased association between PP2A and eNOS at the plasma membrane promotes dissociation of an

37 ed HG-suppressed nitric oxide production and eNOS activity in HAECs, which were prevented by calpain

38 interaction between the myocyte receptor and eNOS, a mediator of HF protection.

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

40 protein levels were similar in eNOS(tg) and eNOS(-/-) as compared to transgene-negative littermates.

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

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

43 Aortic eNOS(Ser1177) phosphorylation was enhanced approximately

44 Ang-II treatment decreased aortic eNOS(Ser1177) phosphorylation in the WT and RBP4-KO mice

45 uces it, with commensurate changes in aortic eNOS(Ser1177) phosphorylation.

46 WT mice fed chow and had no effect on aortic eNOS(Ser1177) phosphorylation.

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

48 ation, and nitro-oxidative stress as well as eNOS uncoupling in the vessel wall, which can be prevent

49 The increase in CVC at eNOS-inhibited (41 +/- 3%CVCmax) and non-selective NOS-i

50 ic lung endothelial monolayer and attenuates eNOS-beta-actin association, peroxynitrite formation, en

51 ditions) but there was no difference between eNOS-inhibited and non-selective NOS-inhibited sites.

52 Under basal conditions, Cav-1 binds eNOS and inhibits nitric oxide (NO) production via the C

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

54 ion, with effects mediated by NO produced by eNOS.

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

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

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

58 ncreased GRK2-CAV1 interaction and decreased eNOS activity.

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

60 ased levels of Trx led to deglutathionylated eNOS.

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

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

63 lease, indicating the presence of a distinct eNOS binding domain within CAV.

64 Exenatide elicited eNOS activation and NO production in endothelial cells,

65 usive, in part due to the lack of endogenous eNOS-specific NO release activators.

66 e data are the first to show that endogenous eNOS activation can provide atheroprotection in diabetes

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

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

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

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

71 ) levels vs. C, but reduced the endothelial (eNOS) and increased the inducible nitric oxide synthase

72 se enzymes (neuronal [nNOS] and endothelial [eNOS]) are altered in the onset of diabetic xerostomia;

73 Lowering RBP4 may reduce BP through enhanced eNOS-mediated vasodilatation and may be a novel therapeu

74 endothelial-specific overexpression of eNOS (eNOS(tg) ), (ii) in eNOS(-/-) mice and (iii) in C57BL/6

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

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

77 Akt-Hsp90-eNOS complex that is required for eNOS phosphorylation and activation.

78 n that CAV residue Phe-92 is responsible for eNOS inhibition, the "inactive" F92A Cav-1 mutant unexpe

79 e found that S1179D substitution in CaM-free eNOS had multiple effects; it increased the rate of flav

80 ing the basal activity of NO production from eNOS.

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

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

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

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

85 r L-NG-nitroarginine methyl ester or genetic eNOS deficiency abolished the sex-related differences.

86 of Src to phosphorylate GIT1 as well as GIT1-eNOS association.

87 ation, prevented disruption of the Akt-Hsp90-eNOS complex in the vasculature, preserved arterial func

88 mbrane promotes dissociation of an Akt-Hsp90-eNOS complex that is required for eNOS phosphorylation a

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

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

91 S activity, and low selectivity versus human eNOS.

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

93 ditional pathological features, including i) eNOS-independent enlargement, ii) altered expression of

94 on from the endothelium, triggering impaired eNOS function and limiting BH4 rescue through NADPH-depe

95 cysteines partially rescued the decrease in eNOS activity, whereas mutation of a distal site, Cys-38

96 mbrane thickening and podocyte effacement in eNOS(-/-) mice with podocyte-specific VEGF(164) gain of

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

98 overexpression of eNOS (eNOS(tg) ), (ii) in eNOS(-/-) mice and (iii) in C57BL/6 mice treated with th

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

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

101 T also significantly reduced the increase in eNOS-beta-actin association and protein tyrosine nitrati

102 sed glomerular S-nitrosylation of laminin in eNOS(-/-) mice.

103 H2S therapy fails to protect against I/R in eNOS phosphomutant mice (S1179A).

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

105 B2R protein levels were similar in eNOS(tg) and eNOS(-/-) as compared to transgene-negative

106 owever, tau phosphorylation was unchanged in eNOS(-/-) mice (P>0.05).

107 ity to bradykinin was investigated including eNOS(-/-) mice.

108 a time-efficient alternative to ET, increase eNOS protein content and the eNOS/NADP(H)oxidase protein

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

110 resistance to CavNOxin treatment, indicating eNOS specificity.

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

112 G via mu-calpain/PKCbeta2 activation-induced eNOS-pThr497/495 and eNOS inactivation.

113 HHcy/HG-induced eNOS-pThr497/495 was reversed by micro-calpsiRNA and ade

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

115 erpermeability was not rescued by inhibiting eNOS activity.

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

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

118 ustering eNOS within a complex that inhibits eNOS activity.

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

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

121 s that the immunosuppressive effects involve eNOS.

122 ve inhibition of nNOS over related isoforms (eNOS and iNOS) is therapeutically desirable.

123 " F92A Cav-1 mutant unexpectedly retains its eNOS binding ability and can increase NO release, indica

124 and endothelial NO synthase (eNOS) knockout (eNOS(-/-)) mice after a swim training period.

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

126 rotein (APP)/PSEN1dE9(+/-) (PS1) that lacked eNOS (APP/PS1/eNOS(-/-)) to examine expression of tau ki

127 In contrast, mice lacking eNOS show resistance to CavNOxin treatment, indicating e

128 ed with an eNOS inhibitor (LNAME) or lacking eNOS were no longer responsive to transgenic endothelial

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

130 HS augmented ANG-(1-7) signaling via the Mas/eNOS/SIRT1 pathway.

131 ssed on intracellular membranes and mediated eNOS activation and NO formation, partially accounting f

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

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

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

135 RK2) that also post-translationally modifies eNOS.

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

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

138 We found modulating eNOS regulated pericyte alpha-SMA phenotype transformati

139 Protein phosphatase 2A (PP2A) became more eNOS-associated in PA-treated cells; the PP2A inhibitor

140 trogen via a mechanism that involves myocyte eNOS-dependent cGMP synthesis and the cGMP-dependent pro

141 2) to determine whether the changes in nNOS/eNOS protein expression or dimerization are correlated w

142 mice resulted in increased endothelial NOS (eNOS) protein levels and NO production in the inner medu

143 sted against purified nNOS, endothelial NOS (eNOS), and inducible NOS (iNOS) enzymes.

144 inst purified nNOS enzymes, endothelial NOS (eNOS), and inducible NOS (iNOS).

145 in subcutaneous adipose tissue of WT but not eNOS(-/-) mice.

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

147 actin were abolished by a genetic absence of eNOS.

148 tions, as this pathway induces activation of eNOS, the expressions of HO-1 and VEGF, and the reductio

149 sis and cytochrome c reductase activities of eNOS, thereby enhancing its participation in biological

150 me c reductase and NO synthase activities of eNOS.

151 Harnessing the atheroprotective activity of eNOS in diabetic settings remains elusive, in part due t

152 n, whereas the phosphorylation and amount of eNOS was not influenced by GLO1-knockdown.

153 However, the protective aspect of eNOS in diabetes-associated atherosclerosis remains cont

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

155 oscopy methods to measure protein content of eNOS and NAD(P)Hoxidase specifically in the endothelial

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

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

158 vascular Trx-mediated deglutathionylation of eNOS protects against ischemia-reperfusion-mediated myoc

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

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

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

162 kinase is a major regulatory determinant of eNOS activity.

163 xport of SENP2, leading to downregulation of eNOS expression and upregulation of proinflammatory adhe

164 tenuated TNFalpha-mediated downregulation of eNOS in human aortic endothelial cells than did untreate

165 ivity through ERRalpha induced expression of eNOS.

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

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

168 othelial gene expression were independent of eNOS activity.

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

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

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

172 (high) leukocytes and up-regulated levels of eNOS glutathionylation in aortas of C57BL/6 mice.

173 with endothelial-specific overexpression of eNOS (eNOS(tg) ), (ii) in eNOS(-/-) mice and (iii) in C5

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

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

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

177 y aggravated HG-increased phosphorylation of eNOS at threonine 497/495 (eNOS-pThr497/495) in the mous

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

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

180 corresponding to the actin binding region of eNOS residues 326-333 has been shown to reduce the hyper

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

182 bution of estrogen through its regulation of eNOS expression and nitric oxide production to vascular

183 10 and changes in ED:EI by MAC regulation of eNOS in endothelial cells.

184 roatherogenic mediator through repression of eNOS-dependent pathways.

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

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

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

188 of I/R injury is dependent in large part on eNOS activation and NO generation.

189 2S relieves the inhibitory effect of PYK2 on eNOS, allowing the latter to produce greater amounts of

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

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

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

193 sed interaction of endothelial nitric oxide (eNOS) with beta-actin.

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

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

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

197 this dose, insulin significantly increased p-eNOS(Ser1177) levels in mIMCD cells.

198 nd neuronal NO synthase (nNOS) mRNA, phospho-eNOS protein, nNOS, and phospho-nNOS protein were signif

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

200 method to compute p-value for a polymorphism eNOS -786T>C which was shown to be associated with breas

201 Trx deficiency in endothelial cells promoted eNOS glutathionylation and reduced its enzymatic activit

202 Mechanistically, PGC-1alpha promotes eNOS expression and activity, which is necessary for pro

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

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

205 SEN1dE9(+/-) (PS1) that lacked eNOS (APP/PS1/eNOS(-/-)) to examine expression of tau kinases and tau

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

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

208 .0 g/kg/d) for 12 weeks remarkably recoupled eNOS and reduced the size of carotid atherosclerotic pla

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

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

211 of the kidney, had approximately 50% reduced eNOS protein levels in their inner medulla along with a

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

213 hypertension that was accompanied by reduced eNOS activation.

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

215 hatidylinositol 3-kinase and Akt to regulate eNOS and the second showing that eNOS directly bound to

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

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

218 rify how Ser(1179) phosphorylation regulates eNOS and provides a foundation to compare its regulation

219 cell maintenance and function by regulating eNOS activity.

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

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

222 l cellular redox protein, is shown to rescue eNOS from glutathionylation during ischemia-reperfusion

223 In CSE KO mice, acute H2S therapy restored eNOS function and NO bioavailability and attenuated I/R

224 leted, its repletion only partially restores eNOS-mediated coronary vasodilation, indicating that oth

225 Ibuprofen arginate retains eNOS substrate activity and reverses endothelial dysfunc

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

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

228 However, apoE4 does not stimulate eNOS or endothelial cell migration or dampen cell adhesi

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

230 o ApoER2 stimulates endothelial NO synthase (eNOS) and endothelial cell migration, and it also attenu

231 nor administration; endothelial NO synthase (eNOS) and neuronal NO synthase (nNOS) mRNA, phospho-eNOS

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

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

234 mice deficient for endothelial NO synthase (eNOS) because their NO metabolite levels are similar to

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

236 wild-type (WT) and endothelial NO synthase (eNOS) knockout (eNOS(-/-)) mice after a swim training pe

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

238 , activation of the endothelial NO synthase (eNOS), phosphorylation of PECAM-1 and VEGFR-2, as well a

239 bioavailability of endothelial NO synthase (eNOS)-derived NO, is a critical inducer of atheroscleros

240 ylates and inhibits endothelial NO synthase (eNOS).

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

242 ated endothelial nitric oxide (NO) synthase (eNOS) were significantly greater in the Tg mice fed NC t

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

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

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

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

247 Endothelial nitric oxide synthase (eNOS) expression was decreased, and activities of protei

248 Endothelial nitric oxide synthase (eNOS) expression was studied in human aortic endothelial

249 increased endothelial nitric oxide synthase (eNOS) expression.

250 o loss of endothelial nitric oxide synthase (eNOS) function.

251 vation of endothelial nitric oxide synthase (eNOS) in an endothelial cell.

252 lished by endothelial nitric oxide synthase (eNOS) inhibitor N(G)-nitro-L-arginine methyl ester.

253 ted Cav-1/endothelial nitric-oxide synthase (eNOS) interaction, which occurs specifically in vascular

254 cells by endothelial nitric-oxide synthase (eNOS) is regulated in response to activation of endothel

255 notype of endothelial nitric oxide synthase (eNOS) knockout mice.

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

257 impairing endothelial nitric oxide synthase (eNOS) phosphorylation and promoting oxidative stress in

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

259 he Asp298 endothelial nitric oxide synthase (eNOS) polymorphism and at moderate risk of cardiovascula

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

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

262 y and for endothelial nitric-oxide synthase (eNOS) specifically.

263 Endothelial nitric-oxide synthase (eNOS) uncoupling and increased inducible NOS (iNOS) acti

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

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

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

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

268 lation of endothelial nitric oxide synthase (eNOS).

269 ession of endothelial nitric oxide synthase (eNOS).

270 domain of endothelial nitric oxide synthase (eNOS, 494-513) and a peptide spanning the N-terminal 20

271 ys (e.g., endothelial nitric oxide synthase [eNOS], Rho-kinase, and dimethylarginine dimethylaminohyd

272 phorylation of Akt and its downstream target eNOS.

273 However, whether targeting eNOS using this peptide can attenuate diabetes-associate

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

275 to regulate eNOS and the second showing that eNOS directly bound to the G-protein-coupled receptor ki

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

277 We have recently shown in vitro that eNOS-derived NO release can be increased by blocking its

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

279 Although the eNOS cofactor tetrahydrobiopterin (BH4) is depleted, its

280 to ET, increase eNOS protein content and the eNOS/NADP(H)oxidase protein ratio in previously sedentar

281 el data analysis workflow, we identified the eNOS peptide as the only calmodulin binding peptide and

282 We observed that depletion of the eNOS substrate NADPH occurs in the postischemic heart wi

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

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

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

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

287 on (S1179D) may impact electron flux through eNOS and the conformational behaviors of its reductase d

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

289 in the RBP4-KO mice, with no change in total eNOS protein.

290 bined contribution of these effects to total eNOS activity.

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

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

293 to those caused by CaM binding to wild-type eNOS, and the S1179D substitution together with CaM bind

294 activates the NOX1-NOXO1 complex to uncouple eNOS.

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

296 We used eNOS knockout ((-/-)) mice as well as an Alzheimer's dis

297 ependent NO formation was increased, whereas eNOS-dependent NO formation was decreased in aortas of A

298 ceramide initiates PP2A colocalization with eNOS and demonstrate that PP2A activation precipitates v

299 5% O2, resulting in greater interaction with eNOS in response to histamine.

300 urther show that Trx directly interacts with eNOS, and we confirmed that Cys-691 and Cys-910 are the