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1 e not dependent upon endothelial caveolae or endothelial nitric oxide synthase.
2 attenuation of the vasoprotective effects of endothelial nitric oxide synthase.
3 bility and superoxide generated by uncoupled endothelial nitric oxide synthase.
4 ectable in mice with a genetic deficiency of endothelial nitric oxide synthase.
5  proangiogenic mediators VEGF receptor 2 and endothelial nitric oxide synthase.
6 related increases in shear and activation of endothelial nitric oxide synthase.
7 din-1 and inhibited S1177 phosphorylation of endothelial nitric oxide synthase.
8 minished VEGF-mediated activation of Akt and endothelial nitric-oxide synthase.
9 n C57BL/6J mice but not in mice deficient in endothelial nitric-oxide synthase.
10 tion of both Thr-172 of AMPK and Ser-1177 of endothelial nitric oxide synthase, a downstream enzyme o
11 mice showed markedly decreased expression of endothelial nitric oxide synthase, a well-known mediator
12                                Inhibition of endothelial nitric oxide synthase abolished globular adi
13      Combined indomethacin and inhibition of endothelial nitric oxide synthase abolished the effects
14 ice, we tested the hypothesis that a lack of endothelial nitric oxide synthase accelerates renal inju
15 is because of loss of insulin-stimulated Akt/endothelial nitric oxide synthase activation and angiote
16 ndothelial cells, SR-BI mediates HDL-induced endothelial nitric oxide synthase activation and prolife
17 se data describe a new mechanism for reduced endothelial nitric oxide synthase activation during rena
18 etworks, reactive oxygen species production, endothelial nitric oxide synthase activation, and cGMP p
19 nt of circulating angiogenic cells, enhanced endothelial nitric oxide synthase activation, and increa
20 red by approximately 40% with respect to Akt/endothelial nitric oxide synthase activation, and leukoc
21 helial sodium channel activation, attenuated endothelial nitric oxide synthase activation, increased
22 thelin B receptor and consequently decreased endothelial nitric oxide synthase activation.
23 proinflammatory polarization, restoration of endothelial nitric oxide synthase activation.
24 line in endothelial nitric oxide release and endothelial nitric oxide synthase activity and increased
25           MPs from patients with OSA reduced endothelial nitric oxide synthase activity and nitric ox
26 wild-type mice coincident with reduced liver endothelial nitric oxide synthase activity and NO conten
27                              Statins improve endothelial nitric oxide synthase activity and vascular
28 accepted that diabetes mellitus (DM) impairs endothelial nitric oxide synthase activity as well as en
29 ecovery, vascular and capillary density, and endothelial nitric oxide synthase activity were signific
30 ow recovery, vascular and capillary density, endothelial nitric oxide synthase activity, and were ass
31 rdiovascular homeostasis, along with reduced endothelial nitric oxide synthase activity, endothelial
32 tionality via nitrite reduction and red cell endothelial nitric oxide synthase activity, potentially
33 ein expressions of nuclear factor kappaB and endothelial nitric oxide synthase/Akt/inducible nitric o
34  an increase in capillary/arteriole density, endothelial nitric oxide synthase/Akt/vascular endotheli
35 recovery in obese type 2 diabetic mice by an endothelial nitric oxide synthase/Akt/vascular endotheli
36 tion factor Kruppel-like factor 2 as well as endothelial nitric oxide synthase, along with significan
37 f PI3K downstream targets, including Akt and endothelial nitric oxide synthase, although incremental
38 ey endothelial signaling proteins--including endothelial nitric oxide synthase, AMP-activated protein
39 L(Healthy) were observed after inhibition of endothelial nitric oxide synthase and after delipidation
40                                      Because endothelial nitric oxide synthase and Bcl-2 activities a
41 pairment of agonist-stimulated activation of endothelial nitric oxide synthase and cGMP production.
42 kinase and its downstream effectors CD36 and endothelial nitric oxide synthase and cyclooxygenase-2 a
43 ocosahexaenoic acid increased phosphorylated endothelial nitric oxide synthase and endothelial nitric
44                                Additionally, endothelial nitric oxide synthase and extracellular sign
45                         SIRT1-regulated Akt, endothelial nitric oxide synthase and GLUT4 levels were
46 ed heart failure in part via upregulation of endothelial nitric oxide synthase and increased nitric o
47 ase/Akt pathway to inhibit the activation of endothelial nitric oxide synthase and metabolic actions.
48 ates 2 critical antiatherosclerotic enzymes, endothelial nitric oxide synthase and prostacyclin synth
49 activated protein kinase (AMPK) and requires endothelial nitric oxide synthase and soluble guanylyl c
50 ally reduced by inhibition or elimination of endothelial nitric oxide synthase and that the vasodilat
51 n (activation) of Protein kinase B (Akt) and endothelial nitric oxide synthase and the phosphorylatio
52 n (activation) of Protein kinase B (Akt) and endothelial nitric oxide synthase and the phosphorylatio
53 he expression of KLF2 and the KLF2-regulated endothelial nitric oxide synthase and thrombomodulin at
54 Expression of proangiogenic proteins phospho-endothelial nitric oxide synthase and vascular endotheli
55 tream signaling targets of VEGFR2, including endothelial nitric-oxide synthase and soluble guanylate
56 shear stress-induced signaling, because Akt, endothelial nitric oxide synthase, and extracellular reg
57 or CD31, vascular endothelial growth factor, endothelial nitric oxide synthase, and hypoxia-inducible
58 ed endothelial cell levels of phosphorylated endothelial nitric oxide synthase, and of nitrates and n
59 ing phosphodiesterase type 5, phosphorylated endothelial nitric oxide synthase, and phosphorylated va
60 ic AMP/protein kinase A signaling machinery, endothelial nitric oxide synthase, and Rac1.
61 sed the mRNA and protein expression of KLF2, endothelial nitric oxide synthase, and thrombomodulin.
62  activation of AMP-activated protein kinase, endothelial nitric oxide synthase, and vascular endothel
63 d from shear stress-dependent stimulation of endothelial nitric oxide synthase at the remote site of
64 bition of nitric oxide/nitrite generation by endothelial nitric oxide synthase at the remote site or
65 taII-dependent inhibitory phosphorylation of endothelial nitric oxide synthase at Thr-495, leading to
66                                Inhibition of endothelial nitric oxide synthase attenuated flow augmen
67 roup 3, whereas messenger RNA expressions of endothelial nitric oxide synthase, Bcl-2, interleukin-10
68 trosation was associated with increased Cav1-endothelial nitric oxide synthase binding in response to
69 on of vascular endothelial growth factor and endothelial nitric oxide synthase, but the expression of
70 (HUVEC), resulting in the phosphorylation of endothelial nitric oxide synthase, cell migration, and t
71  product dihydrobiopterin (BH2), which lacks endothelial nitric oxide synthase cofactor activity.
72                                          The endothelial nitric oxide synthase cofactor tetrahydrobio
73                                          The endothelial nitric oxide synthase cofactor tetrahydrobio
74 on, obesity-induced perturbations in cardiac endothelial nitric oxide synthase, connexin-43, and mark
75                   Whereas both inducible and endothelial nitric oxide synthase contributed to nitric
76 vascular homocysteine, is a key regulator of endothelial nitric oxide synthase coupling and nitric ox
77 iated virus (AAV) expressing cKL to diabetic endothelial nitric oxide synthase-deficient mice or alph
78 anol-mediated suppression of EPC biology was endothelial nitric oxide synthase-dependent because endo
79                       Neuregulin production, endothelial nitric oxide synthase dimerization, and Bcl-
80 tetrahydrobiopterin concentrations, ratio of endothelial nitric oxide synthase dimers/monomers, and n
81  upregulation, shedding of procoagulant MPs, endothelial nitric oxide synthase downregulation, and re
82 ation and high arginase activity, leading to endothelial nitric oxide synthase dysfunction.
83 including phosphorylated STAT3 (p-STAT3) and endothelial nitric oxide synthase (e-NOS).
84 al dysfunction with ageing via modulation of endothelial nitric oxide synthase (eNOS) acetylation/act
85 ion, IRAK1 degradation, RONS generation, and endothelial nitric oxide synthase (eNOS) activation (as
86 ers membrane-initiated signals, resulting in endothelial nitric oxide synthase (eNOS) activation and
87 delivery, and it was associated with blunted endothelial nitric oxide synthase (eNOS) activation in s
88 tions of Cav1 and NOS3, we show that chronic endothelial nitric oxide synthase (eNOS) activation seco
89 oproteins, aortic pathology, aortic Akt1 and endothelial nitric oxide synthase (eNOS) activities, imm
90 adrenergic receptor (AR) activation promotes endothelial nitric oxide synthase (eNOS) activity and NO
91      Caveolin-1 exerts a tonic inhibition of endothelial nitric oxide synthase (eNOS) activity.
92  factor signaling, which can lead to reduced endothelial nitric oxide synthase (eNOS) activity; the e
93             AMD3100 upregulated BM levels of endothelial nitric oxide synthase (eNOS) and 2 targets o
94 tary wheel running (VWR) on the abundance of endothelial nitric oxide synthase (eNOS) and extracellul
95                                         Both endothelial nitric oxide synthase (eNOS) and inducible n
96  protects the heart, but it is apparent that endothelial nitric oxide synthase (eNOS) and nitric oxid
97 asculogenesis and angiogenesis) we evaluated endothelial nitric oxide synthase (eNOS) and phosphoryla
98 In vitro, Akt1 preferentially phosphorylates endothelial nitric oxide synthase (eNOS) and promotes NO
99      We tested this concept and the roles of endothelial nitric oxide synthase (eNOS) and Src activat
100 t Cav-1 deficiency induced the activation of endothelial nitric oxide synthase (eNOS) and the generat
101 red pericytes were used, and intervened with endothelial nitric oxide synthase (eNOS) antagonist L-NN
102       Deficits in nitric oxide production by endothelial nitric oxide synthase (eNOS) are associated
103             Kruppel-like factor 2 (KLF2) and endothelial nitric oxide synthase (eNOS) are fluid shear
104 e (AMPK), with subsequent phosphorylation of endothelial nitric oxide synthase (eNOS) at Ser-633 and
105 a vasorelaxing agent that acts downstream of endothelial nitric oxide synthase (eNOS) by directly act
106 ty of substrate and/or necessary co-factors, endothelial nitric oxide synthase (eNOS) can generate NO
107  X receptor-alpha (RXRA) chr9:136355885+ and endothelial nitric oxide synthase (eNOS) chr7:150315553+
108                                              Endothelial nitric oxide synthase (eNOS) deficiency may
109      However, the functional significance of endothelial nitric oxide synthase (eNOS) expressed in he
110 , abacavir, and AZT) significantly decreased endothelial nitric oxide synthase (eNOS) expression and
111 mice was altered and associated with reduced endothelial nitric oxide synthase (eNOS) expression and
112 firmed in IRKO mice, consistent with reduced endothelial nitric oxide synthase (eNOS) expression in b
113                                              Endothelial nitric oxide synthase (eNOS) expression was
114                                              Endothelial nitric oxide synthase (eNOS) expression was
115  tumors, Ad-VEGF-A(164) strikingly increased endothelial nitric oxide synthase (eNOS) expression.
116 -VEGFR-2, cyclooxygenase (COX)-1, COX-2, and endothelial nitric oxide synthase (eNOS) expressions as
117 nary vasodilation is impaired due to loss of endothelial nitric oxide synthase (eNOS) function.
118                   Polymorphisms in the human endothelial nitric oxide synthase (eNOS) gene (NOS3) hav
119                               Dysfunction of endothelial nitric oxide synthase (eNOS) has been implic
120                                              Endothelial nitric oxide synthase (eNOS) has been shown
121  the wall shear stress-induced activation of endothelial nitric oxide synthase (eNOS) in an endotheli
122 l of green tea (GT) to improve uncoupling of endothelial nitric oxide synthase (eNOS) in diabetic con
123                                  The role of endothelial nitric oxide synthase (eNOS) in forming nati
124 hich nanomolar resveratrol rapidly activates endothelial nitric oxide synthase (eNOS) in human umbili
125      Using this method, we demonstrated that endothelial nitric oxide synthase (eNOS) in lymphatic en
126 ing via phosphatidylinositol 3-kinase/Akt to endothelial nitric oxide synthase (eNOS) in the vasculat
127                                      Whereas endothelial nitric oxide synthase (eNOS) inhibition had
128 ylcholine, which was completely abolished by endothelial nitric oxide synthase (eNOS) inhibitor N(G)-
129                                              Endothelial nitric oxide synthase (eNOS) is a critical m
130                                              Endothelial nitric oxide synthase (eNOS) is an important
131                                              Endothelial nitric oxide synthase (eNOS) is critical in
132                                      Because endothelial nitric oxide synthase (eNOS) is involved in
133 e that, in glomerular mesangial cells (MCs), endothelial nitric oxide synthase (eNOS) is uncoupled up
134 ss podocyte VEGF-A on the renal phenotype of endothelial nitric oxide synthase (eNOS) knockout mice.
135 in which post-translational modifications of endothelial nitric oxide synthase (eNOS) lead to impaire
136 eduction in apoptosis and an upregulation of endothelial nitric oxide synthase (eNOS) levels in ische
137 with sCD40L showed significant reductions of endothelial nitric oxide synthase (eNOS) mRNA and protei
138              All three kinases phosphorylate endothelial nitric oxide synthase (eNOS) on serine (S) 1
139 Rho kinase (RhoK) / protein kinase B (AKT) / endothelial nitric oxide synthase (eNOS) pathways was an
140 nsin (ANG)-(1-7)-induced vasodilator effect, endothelial nitric oxide synthase (eNOS) phosphorylation
141                      Ranolazine's effects on endothelial nitric oxide synthase (eNOS) phosphorylation
142 xpectedly, we observed 1.7-fold higher basal endothelial nitric oxide synthase (eNOS) phosphorylation
143 thelial growth factor (VEGF)-induced Akt and endothelial nitric oxide synthase (eNOS) phosphorylation
144 Erk phosphorylation and shear stress-induced endothelial nitric oxide synthase (eNOS) phosphorylation
145 T signaling cascade and subsequent increased endothelial nitric oxide synthase (eNOS) phosphorylation
146 y CAP exposure suppressed insulin-stimulated endothelial nitric oxide synthase (eNOS) phosphorylation
147  and this was associated with an increase in endothelial nitric oxide synthase (eNOS) phosphorylation
148 II sensitivity and hypertension by impairing endothelial nitric oxide synthase (eNOS) phosphorylation
149                                              Endothelial nitric oxide synthase (eNOS) plays a central
150 jects prospectively genotyped for the Asp298 endothelial nitric oxide synthase (eNOS) polymorphism an
151 ing upon contact with blood to interact with endothelial nitric oxide synthase (eNOS) present in bloo
152 ed endothelial nitric oxide synthase (PeNOS)/endothelial nitric oxide synthase (eNOS) ratio was measu
153                  The molecular mechanisms of endothelial nitric oxide synthase (eNOS) regulation of m
154            Indeed, RNAi of p47phox inhibited endothelial nitric oxide synthase (eNOS) serine 1179 pho
155 at this process is inhibited by the PI3K/Akt/endothelial nitric oxide synthase (eNOS) signaling pathw
156  hepatic stellate cell contraction), and the endothelial nitric oxide synthase (eNOS) signaling pathw
157                              CRP antagonizes endothelial nitric oxide synthase (eNOS) through process
158 ility to macromolecules via translocation of endothelial nitric oxide synthase (eNOS) to cytosol and
159 nthesis, dysregulated l-arginine metabolism, endothelial nitric oxide synthase (eNOS) uncoupling and
160              Vascular superoxide (O2(-)) and endothelial nitric oxide synthase (eNOS) uncoupling were
161  Endothelial dysfunction, which is caused by endothelial nitric oxide synthase (eNOS) uncoupling, is
162           Endothelin-1 is known to stimulate endothelial nitric oxide synthase (eNOS) via the endothe
163 nd brain in organ specific manners; however, endothelial nitric oxide synthase (eNOS) was not signifi
164  PPARdelta agonist GW501516 on uncoupling of endothelial nitric oxide synthase (eNOS) were determined
165                                Inhibition of endothelial nitric oxide synthase (eNOS) with the specif
166        AKT, AMP-dependent kinase (AMPK), and endothelial nitric oxide synthase (eNOS)(s1179) phosphor
167  genes such as Kruppel-like factor 2 (Klf2), endothelial nitric oxide synthase (eNOS), and bone morph
168 th reduced Kruppel-like factor (KLF)2, KLF4, endothelial nitric oxide synthase (eNOS), and thrombomod
169 (VCAM-1), nuclear factor kappaB (NF-kappaB), endothelial nitric oxide synthase (eNOS), B-cell leukemi
170 n contributes to AMPK-mediated activation of endothelial nitric oxide synthase (eNOS), enhanced level
171 lpha-induced signaling cascade that involves endothelial nitric oxide synthase (eNOS), JNK3, and MAPK
172 ition, liver samples were obtained to assess endothelial nitric oxide synthase (eNOS), phosphorylated
173 tio and upregulated the expression of aortic endothelial nitric oxide synthase (eNOS), phosphorylated
174                       Instead, expression of endothelial nitric oxide synthase (eNOS), which generate
175                                              Endothelial nitric oxide synthase (eNOS)-mediated NO pro
176 mall intestine via the vasodilatory molecule endothelial nitric oxide synthase (eNOS).
177 uced inflammation through phosphorylation of endothelial nitric oxide synthase (eNOS).
178  and requires nitric oxide (NO) derived from endothelial nitric oxide synthase (eNOS).
179 obiopterin (BH4) is an essential cofactor of endothelial nitric oxide synthase (eNOS).
180 tein phosphatase (PP2A) dephosphorylation of endothelial nitric oxide synthase (eNOS).
181   Instead, it increased tissue expression of endothelial nitric oxide synthase (eNOS).
182 tase 2A (PP2A) association directly with the endothelial nitric oxide synthase (eNOS)/Akt/Hsp90 compl
183 type through upregulating proteins including endothelial nitric oxide synthase (eNOS)/inducible nitri
184 othelin-1, endothelin-1 receptor type A, and endothelial nitric oxide synthase (eNOS)], pro-inflammat
185 de spanning the calmodulin binding domain of endothelial nitric oxide synthase (eNOS, 494-513) and a
186                                Activation of endothelial nitric oxide synthase (eNOS, NOS3, or NOS II
187 ion of PPARdelta might prevent uncoupling of endothelial nitric oxide synthase (eNOS, P<0.05, n=6-9).
188 Endothelial dysfunction, including decreased endothelial nitric-oxide synthase (eNOS) activity and lo
189                                              Endothelial nitric-oxide synthase (eNOS) and its bioacti
190 ed H-Ras mediates VEGF-induced activation of endothelial nitric-oxide synthase (eNOS) and migratory r
191 ontrolling the stability and activity of the endothelial nitric-oxide synthase (eNOS) and that Cavin-
192 educed insulin-stimulated phosphorylation of endothelial nitric-oxide synthase (eNOS) at Ser(1177) an
193                        Kallistatin increased endothelial nitric-oxide synthase (eNOS) expression and
194 n of Kruppel-like factor 2 (KLF2), increased endothelial nitric-oxide synthase (eNOS) expression, and
195  Recent evidence suggests that blunted Cav-1/endothelial nitric-oxide synthase (eNOS) interaction, wh
196                                              Endothelial nitric-oxide synthase (eNOS) is a critical r
197 ing of NO production from NADPH oxidation by endothelial nitric-oxide synthase (eNOS) is enhanced in
198 sis of NO in sinusoidal endothelial cells by endothelial nitric-oxide synthase (eNOS) is regulated in
199 ies have shown that the acute stimulation of endothelial nitric-oxide synthase (eNOS) mRNA transcript
200                                              Endothelial nitric-oxide synthase (eNOS) plays a central
201 n important post-translational mechanism for endothelial nitric-oxide synthase (eNOS) regulation.
202 itions of oxidative stress generally and for endothelial nitric-oxide synthase (eNOS) specifically.
203 arginine (ADMA) induces the translocation of endothelial nitric-oxide synthase (eNOS) to the mitochon
204  maintains endothelial function by targeting endothelial nitric-oxide synthase (eNOS) to the plasma m
205                                              Endothelial nitric-oxide synthase (eNOS) uncoupling and
206  we demonstrate that, in MCs, Ang II induces endothelial nitric-oxide synthase (eNOS) uncoupling with
207                                              Endothelial nitric-oxide synthase (eNOS) utilizes l-argi
208 PI3K/Akt pathway to reduce the activation of endothelial nitric-oxide synthase (eNOS).
209 he plasma membrane Ca(2+)-ATPase (PMCA), and endothelial nitric-oxide synthase (eNOS).
210 factors in the angiogenesis pathway (Akt and endothelial nitric oxide synthase [eNOS]) are activated.
211 lved intrahepatic vasoactive pathways (e.g., endothelial nitric oxide synthase [eNOS], Rho-kinase, an
212  artery endothelial cells in vitro increased endothelial nitric oxide synthase expression and activat
213 flow and regulates EC function by increasing endothelial nitric oxide synthase expression and inhibit
214                                A decrease in endothelial nitric oxide synthase expression levels was
215 uent regulation of Kruppel-like factor 2 and endothelial nitric oxide synthase expression represents
216 criptional activity and laminar flow-induced endothelial nitric oxide synthase expression through ERK
217 cally, loss of Nox4 resulted in reduction of endothelial nitric oxide synthase expression, nitric oxi
218 irectly phosphorylated ERK5 S496 and reduced endothelial nitric oxide synthase expression.
219 odulated vascular permeability by increasing endothelial nitric-oxide synthase expression and by down
220 ) expression, apoptosis, and increased eNOS (endothelial nitric oxide synthase) expression.
221        The latter hampered the detachment of endothelial nitric oxide synthase from caveolin-1, leadi
222 thological signaling and enhanced myocardial endothelial nitric oxide synthase function and nitric ox
223 sion) of epigenetic (5-mC, DNMTs), vascular (endothelial nitric oxide synthase), glial (connexin-43,
224 ty of endogenous nitric oxide and upregulate endothelial nitric oxide synthase, have been used to pre
225 methylarginines and subsequent ADMA-mediated endothelial nitric-oxide synthase impairment.
226 f vascular remodelling by over-expression of endothelial nitric oxide synthase in the fat pad of the
227 ogenitor cells, transiently transfected with endothelial nitric oxide synthase, in patients with PAH
228 b nitric oxide production and muscle phospho-endothelial nitric oxide synthase increased in a stepwis
229 a, tumor necrosis factor-alpha, IL-6, IL-10, endothelial nitric oxide synthase, inducible nitric oxid
230 onstitutive isoforms, including neuronal and endothelial nitric oxide synthase, inducible nitric oxid
231                   We identify the endogenous endothelial nitric oxide synthase inhibitor ADMA as a bi
232  D-serine coactivation of NMDA receptors and endothelial nitric oxide synthase is involved in astrocy
233 synthase and that the vasodilatory effect of endothelial nitric oxide synthase is likely mediated by
234 cose delivery in FcgammaRIIB(-/-) mice or in endothelial nitric oxide synthase knock-in mice with pho
235 m wild type mice than those in the aortas of endothelial nitric oxide synthase knock-out mice.
236                                     By using endothelial nitric oxide synthase knockout (eNOSKO) mice
237 cently, we and others reported that diabetic endothelial nitric oxide synthase knockout (eNOSKO) mice
238               Finally, treatment of diabetic endothelial nitric oxide synthase knockout mice with sel
239 AR3 antagonist, affects development of DN in endothelial nitric oxide synthase-knockout db/db mice.
240                    Mice lacking a functional endothelial nitric oxide synthase (KO, NOS3(-/-) ) and w
241 vasodilator dysfunction was due to decreased endothelial nitric oxide synthase levels and impaired sm
242   SIRT1-mediated signalling through Akt, the endothelial nitric oxide synthase mediated pathway, regu
243 ssion in both ApoE(-/-) and WT EPCs, whereas endothelial nitric oxide synthase messenger RNA expressi
244 2(.-) anions, whether derived from uncoupled endothelial nitric oxide synthase, nicotinamide adenine
245 f the vascular endothelial growth factor-Akt-endothelial nitric oxide synthase-nitric oxide-cGMP path
246  in db/db mice through a tetrahydrobiopterin/endothelial nitric oxide synthase/nitric oxide pathway.
247 ysfunction was associated with uncoupling of endothelial nitric oxide synthase (NOS) activity seconda
248        beta3-AR colocalized with caveolin-3, endothelial nitric oxide synthase (NOS) and neuronal NOS
249 enerative phase, during hyperoxia, defective endothelial nitric oxide synthase (NOS) produces reactiv
250 atechol-O-methyl transferase (COMT(-/-)) and endothelial nitric oxide synthase (Nos3(-/-)) knockout m
251  structurally intact cells, is controlled by endothelial nitric oxide synthase (NOS3) and is crucial
252 tion of apelin, apelin receptor (APLNR), and endothelial nitric oxide synthase (NOS3) in HA adaptatio
253               We hypothesized that uncoupled endothelial nitric oxide synthase (NOS3) through upregul
254 opterin (BH(4)) is an essential cofactor for endothelial nitric oxide synthase (NOS3), decreased bioa
255         Diabetes was induced in hypertensive endothelial nitric oxide synthase (Nos3)-deficient mice
256                                Expression of endothelial nitric-oxide synthase (NOS3) was not altered
257 etary nitrate improves insulin resistance in endothelial nitric oxide synthase null mice, and multipl
258 erated DN model, STZ-induced diabetes in the endothelial nitric oxide synthase-null (eNOS(-/-)) mice.
259 lial nitric oxide synthase-dependent because endothelial nitric oxide synthase-null mice displayed an
260 hibitory domain (residues 595-639) in bovine endothelial nitric oxide synthase on enzyme activity and
261 ited downstream signaling pathways involving endothelial nitric oxide synthase or prostanoid producti
262 nction was manifested by decreased levels of endothelial nitric oxide synthase (P< .005) and Kruppel-
263 oronary arterioles, (2) heart phosphorylated endothelial nitric oxide synthase (p-eNOS/eNOS) protein,
264                           The phosphorylated endothelial nitric oxide synthase (PeNOS)/endothelial ni
265 lencing CSE by siRNA significantly increased endothelial nitric oxide synthase phosphorylation at thr
266 stored nitric oxide production and decreased endothelial nitric oxide synthase phosphorylation at thr
267 bular adiponectin dose-dependently increased endothelial nitric oxide synthase phosphorylation but ha
268  selectively inhibited Bcl-xL expression and endothelial nitric oxide synthase phosphorylation but in
269 ulin resistance, including decreased Akt and endothelial nitric oxide synthase phosphorylation in the
270 tion of protein kinase C and loss of Akt and endothelial nitric oxide synthase phosphorylation occurr
271 tion-induced cardiac GLUT4 translocation and endothelial nitric oxide synthase phosphorylation were b
272 or kappaB activation, an increase in Akt and endothelial nitric oxide synthase phosphorylation, and a
273 ce K(+) channels (K(Ca)3.1 and K(Ca)2.3) and endothelial nitric oxide synthase, produces additive ton
274 ssion of inducible nitric oxide synthase and endothelial nitric oxide synthase, production of nitric
275 ylated endothelial nitric oxide synthase and endothelial nitric oxide synthase protein levels and nit
276                     In conclusion, a lack of endothelial nitric oxide synthase resulted in the develo
277 ease in VEGFR2 phosphorylation and increased endothelial nitric oxide synthase Ser(1177) phosphorylat
278 longevity-associated variant-BPIFB4 restores endothelial nitric oxide synthase signaling, rescues end
279 or, and L-citrulline (L-Cit) is converted to endothelial nitric oxide synthase substrate, L-arginine.
280 nism that involves the activation of the Akt-endothelial nitric oxide synthase survival pathway, and
281 nism that involves the activation of the Akt-endothelial nitric oxide synthase survival pathway, and
282  of VE-cadherin, KDR, von Willebrand factor, endothelial nitric oxide synthase, the lack of CD45, CD1
283 udies, these effects alter the expression of endothelial nitric oxide synthase, the stability of athe
284                          Seven to 50 million endothelial nitric oxide synthase-transfected endothelia
285                Metanx ingredients counteract endothelial nitric oxide synthase uncoupling and oxidati
286 link between the transport of l-arginine and endothelial nitric oxide synthase uncoupling in hyperten
287 that is associated with vascular remodeling, endothelial nitric oxide synthase uncoupling, decreased
288                Metanx treatment counteracted endothelial nitric oxide synthase uncoupling, inducible
289                      Caffeine down-regulated endothelial nitric oxide synthase, vascular endothelial
290 observe any relevant changes in the vascular endothelial nitric oxide synthase vasodilatory response,
291 er-reporter episomal transfection assays for endothelial nitric oxide synthase, VE-cadherin, and vWF
292 the islet capillary dilation is modulated by endothelial nitric oxide synthase via complementary sign
293  endothelial progenitor cells overexpressing endothelial nitric oxide synthase was tolerated hemodyna
294  Both retinal protein and mRNA expression of endothelial nitric oxide synthase were decreased by twof
295 e 4, vascular endothelial growth factor, and endothelial nitric oxide synthase were remarkably higher
296 endent genes, cyclooxygenase 2 and inducible endothelial nitric oxide synthase, were assessed in peri
297 scular cell adhesion molecule-1 (VCAM-1) and endothelial nitric oxide synthase, whereas PDEs had sign
298 nd on both the production of nitric oxide by endothelial nitric-oxide synthase, which ascorbate is kn
299 ndomethacin (Indo; 5 microm) nor blockade of endothelial nitric oxide synthase with N(G)-nitro-L-argi
300        Shear stress-dependent stimulation of endothelial nitric oxide synthase within the femoral art

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