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1 ction, presumably by counteracting inducible nitric oxide synthase.
2 ice with a genetic deficiency of endothelial nitric oxide synthase.
3 ic mediators VEGF receptor 2 and endothelial nitric oxide synthase.
4 ) and preventing its formation by inhibiting nitric oxide synthase.
5 eases in shear and activation of endothelial nitric oxide synthase.
6 rons ( approximately 1%) expressing neuronal nitric oxide synthase.
7 rom erythrocytic xanthine oxidoreductase and nitric-oxide synthase.
8 terin (BH4) is an essential cofactor for all nitric oxide synthases.
10 beta-, and gamma-splice variants of neuronal nitric oxide synthase 1 (NOS1), and NOS1beta expression
11 codes for the main NO-producing enzyme, the nitric oxide synthase 1 (NOS1), have been found to conve
12 factor for the production of nitric oxide by nitric oxide synthase 1 (NOS1), major modulator of cardi
13 we have chosen to study the long isoform of nitric oxide synthase 1 adaptor protein (NOS1AP), a prot
14 e with macula densa-specific knockout of all nitric oxide synthase 1 isoforms (MD-NOS1KO) had a signi
15 tulates the previously reported phenotype of nitric oxide synthase 1-deficient mice, which have achal
17 taglomerular apparatus of wild-type (WT) and nitric oxide synthase 1alpha-knockout (NOS1alphaKO) mice
18 in 6 (IL6), tumor necrosis factor (TNF), and nitric oxide synthase 2 (NOS2) were studied further.
19 ssue inhibitor of metalloproteinase 1, Dpp4, nitric oxide synthase 2 (Nos2), interleukin 1beta (Il1b)
20 Furthermore, we identified the activity of nitric oxide synthase 2 (NOS2, also known as iNOS) origi
22 of IL-1beta, TNF-alpha, IL-12, and inducible nitric oxide synthase 2 and downregulation of genes asso
23 that therapy requires induced expression of nitric oxide synthase 2 in monocyte-derived dendritic ce
24 decreased the expression of NADPH oxidase 2, nitric oxide synthase 2, and nuclear factor-kappaB1 mRNA
26 )) and triple-negative breast cancer (TNBC), nitric oxide synthase-2 (NOS2) and cyclooxygenase-2 (COX
28 h is located at 11p14, potentially affecting nitric oxide synthase 3 (NOS3) expression, as shown by m
29 2 genes that mediate nitric oxide signaling (Nitric Oxide Synthase 3 [NOS3] and Guanylate Cyclase 1,
31 d indomethacin and inhibition of endothelial nitric oxide synthase abolished the effects of therapeut
32 nd isoform-specific endothelial and neuronal nitric oxide synthase activation and nitric oxide produc
33 ribe a new mechanism for reduced endothelial nitric oxide synthase activation during renal IR that ca
34 m channel activation, attenuated endothelial nitric oxide synthase activation, increased oxidative st
37 homeostasis, along with reduced endothelial nitric oxide synthase activity, endothelial dysfunction,
38 ons of nuclear factor kappaB and endothelial nitric oxide synthase/Akt/inducible nitric oxide synthas
39 in capillary/arteriole density, endothelial nitric oxide synthase/Akt/vascular endothelial growth fa
40 obese type 2 diabetic mice by an endothelial nitric oxide synthase/Akt/vascular endothelial growth fa
41 tream targets, including Akt and endothelial nitric oxide synthase, although incremental activation b
42 Pathway analysis identified association with nitric oxide synthase and adenosine monophosphate-activa
43 lated from liver expressed reduced inducible nitric oxide synthase and arginase 1 and displayed a red
44 l-MDSC contact and was mediated by inducible nitric oxide synthase and cationic amino acid transporte
45 ated closely with their immunoreactivity for nitric oxide synthase and choline acetyltransferase.
46 EDH), ACh trials were repeated with combined nitric oxide synthase and cyclooxygenase inhibition.
47 ts downstream effectors CD36 and endothelial nitric oxide synthase and cyclooxygenase-2 activity.
48 pregulation of interleukin-1 beta, inducible nitric oxide synthase and cyclooxygenase-2 in the cortex
49 gen species, nitric oxide release, inducible nitric oxide synthase and cycloxygenase-2 expression.
50 nucleotide phosphate-oxidase 2 and inducible nitric oxide synthase and enhanced lung concentrations o
53 ased glutathione levels, increased inducible nitric oxide synthase and heme-oxygenase 1 expression, a
54 ased glutathione levels, increased inducible nitric oxide synthase and heme-oxygenase 1 expression, a
55 is attributable to preservation of neuronal nitric oxide synthase and sarcoplasmic reticulum Ca(2+)
57 n) of Protein kinase B (Akt) and endothelial nitric oxide synthase and the phosphorylation (inhibitio
58 n) of Protein kinase B (Akt) and endothelial nitric oxide synthase and the phosphorylation (inhibitio
59 1; 2) suppressed the expression of inducible nitric oxide synthase and type I IFN and 3) induced auto
60 e availability of BH4 leads to uncoupling of nitric oxide synthases and production of highly oxidativ
61 lammatory markers (TNFalpha, IL-6, inducible nitric oxide synthase) and a gene for glucose absorption
62 -induced signaling, because Akt, endothelial nitric oxide synthase, and extracellular regulated kinas
63 , involving c-Jun-N-terminal kinases (JNKs), nitric oxide synthase, and intracellular cGMP, exerts a
64 al cell levels of phosphorylated endothelial nitric oxide synthase, and of nitrates and nitrites in c
65 acrophages that expressed IL10 and inducible nitric oxide synthase, and reduced serum levels of inter
66 ltransferase, tyrosine hydroxylase, neuronal nitric oxide synthase, and vasoactive intestinal polypep
67 glial fibrillary acidic protein and neuronal nitric-oxide synthase, and Abeta and p-Tau(Ser-202) also
68 matory proteins (e.g. cyclophilin, inducible nitric oxide synthase, annexins, galectin, cathepsins an
70 ther IL-17/arginase I or IFN-gamma/inducible nitric oxide synthase axis as suppressor mechanisms.
71 e factor-1alpha, heme oxygenase-1, inducible nitric oxide synthase, B-cell lymphoma-extra large, and
74 ar endothelial growth factor and endothelial nitric oxide synthase, but the expression of endothelial
77 (AAV) expressing cKL to diabetic endothelial nitric oxide synthase-deficient mice or alphaKL-null mic
78 wild-type (WT), NO/redox imbalance (neuronal nitric oxide synthase-deficient mice-1 [NOS1(-/-)]), and
81 opterin concentrations, ratio of endothelial nitric oxide synthase dimers/monomers, and nitric oxide
83 n, shedding of procoagulant MPs, endothelial nitric oxide synthase downregulation, and reduced nitric
85 d it was associated with blunted endothelial nitric oxide synthase (eNOS) activation in skeletal musc
86 s were used, and intervened with endothelial nitric oxide synthase (eNOS) antagonist L-NNA and its ag
90 ear stress-induced activation of endothelial nitric oxide synthase (eNOS) in an endothelial cell.
91 hich was completely abolished by endothelial nitric oxide synthase (eNOS) inhibitor N(G)-nitro-L-argi
92 t-translational modifications of endothelial nitric oxide synthase (eNOS) lead to impaired nitric oxi
93 ty and hypertension by impairing endothelial nitric oxide synthase (eNOS) phosphorylation and promoti
94 re suppressed insulin-stimulated endothelial nitric oxide synthase (eNOS) phosphorylation in skeletal
96 ndeed, RNAi of p47phox inhibited endothelial nitric oxide synthase (eNOS) serine 1179 phosphorylation
97 dysfunction, which is caused by endothelial nitric oxide synthase (eNOS) uncoupling, is an initial s
98 s to AMPK-mediated activation of endothelial nitric oxide synthase (eNOS), enhanced levels of reactiv
102 the calmodulin binding domain of endothelial nitric oxide synthase (eNOS, 494-513) and a peptide span
104 he stability and activity of the endothelial nitric-oxide synthase (eNOS) and that Cavin-2 knockdown
108 phosphorylation, and a decrease in inducible nitric oxide synthase expression both at the cardiac and
112 39 prevented the induction of both inducible nitric-oxide synthase expression and nitric oxide releas
113 crosis factor alpha (TNFalpha) and inducible nitric-oxide synthase expression, indicative of enhanced
114 atter hampered the detachment of endothelial nitric oxide synthase from caveolin-1, leading to an imp
115 ignaling and enhanced myocardial endothelial nitric oxide synthase function and nitric oxide signalin
117 genetic (5-mC, DNMTs), vascular (endothelial nitric oxide synthase), glial (connexin-43, glial fibril
119 emodelling by over-expression of endothelial nitric oxide synthase in the fat pad of the adult rat me
120 ry cytokines and the mRNA encoding inducible nitric-oxide synthase in both LRP1-expressing and -defic
121 ls, transiently transfected with endothelial nitric oxide synthase, in patients with PAH refractory t
122 de production and muscle phospho-endothelial nitric oxide synthase increased in a stepwise fashion by
123 of pro-inflammatory cytokines and inducible nitric-oxide synthase induction in BV2 cells in a concen
124 in young adults with VVS can be corrected by nitric oxide synthase inhibition, demonstrated with our
129 not corrected by the addition of a neuronal nitric oxide synthase inhibitor indicating that the incr
132 ist phenylephrine (PE), with and without the nitric oxide synthase inhibitor N(G)-monomethyl-L-argini
133 However, in preparations pretreated with the nitric oxide synthase inhibitor N-nitro-l-arginine (l-NN
134 l death in vitro, which was prevented by the nitric oxide synthase inhibitor NG-nitro-l-arginine meth
135 as FoxO4 inactivation and administration of nitric oxide synthase inhibitor to FoxO4 KO mice reverse
137 AME (N(omega)-nitro-L-arginine methyl ester; nitric oxide synthase inhibitor) abolished flow-mediated
138 etric dimethylarginine (ADMA), an endogenous nitric oxide synthase inhibitor, are associated with mit
139 a, including those regulating the endogenous nitric oxide synthase inhibitors asymmetrical dimethylar
140 6 (1.5 +/- 0.2-fold; p = 0.02) and inducible nitric oxide synthase (iNOS) (2.4 +/- 0.4-fold; p = 0.01
141 flammatory input through increased inducible nitric oxide synthase (iNOS) activity causes S-nitrosyla
143 ne metabolizing enzymes, including inducible nitric oxide synthase (iNOS) and arginase (ARG), are typ
146 adical scavenger and inhibitors of inducible nitric oxide synthase (iNOS) and cathepsin B also revers
148 ionally, the protein expression of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2
149 1 target genes, such as TNF-alpha, inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2
150 to exhibit prolonged expression of inducible nitric oxide synthase (iNOS) and enhanced killing of per
151 ay that requires the expression of inducible nitric oxide synthase (iNOS) and generation of high leve
152 complex 1 (mTORC1), HIF1alpha and inducible nitric oxide synthase (iNOS) coordinates DC metabolism a
153 Obesity results in perilymphatic inducible nitric oxide synthase (iNOS) expression and accumulation
154 used mainly by enhanced microglial inducible nitric oxide synthase (iNOS) expression and NO release,
157 by genetic deletion of inducible isoform of nitric oxide synthase (iNOS) from VCP TG mouse and by ph
159 ported that Sal-1 targets cellular inducible nitric oxide synthase (iNOS) in a miRNA manner, leading
160 lyze the role of NADPH oxidase and inducible nitric oxide synthase (iNOS) in a murine model of A. act
162 ce nitric oxide (NO) or upregulate inducible nitric oxide synthase (iNOS) mRNA following Toll-like re
164 -gamma), and TNF-alpha, as well as inducible nitric oxide synthase (iNOS) were significantly upregula
165 interferon (IFN)gamma induction of inducible nitric oxide synthase (iNOS), a gene linked to bile duct
166 Both subsets produced Arginase-1, inducible nitric oxide synthase (iNOS), and transforming growth fa
167 ith rapid induction of nitrite and inducible nitric oxide synthase (iNOS), followed by induction of T
168 aB p65-responsive genes, including inducible nitric oxide synthase (iNOS), interleukin-6 (IL-6), and
169 t a nitric oxide-producing enzyme, inducible nitric oxide synthase (iNOS), is overexpressed under the
170 d HIF-2alpha, leading to decreased inducible-nitric oxide synthase (iNOS), NO-production, and VEGF.
171 endothelial growth factor (VEGF), inducible nitric oxide synthase (iNOS), nuclear factor-kappa B (NF
181 872, P < 0.0005) and expression of inducible nitric oxide synthase (iNOS; r = 0.9986, P < 0.0001).
182 , complement factor D, lactotransferrin, and nitric oxide synthase interacting protein) by quantitati
183 lysaccharide-induced expression of inducible nitric oxide synthase, interleukin-1beta, and interleuki
184 s factor alpha, interleukin-1beta, inducible nitric oxide synthase, interleukin-6, and gamma interfer
185 Finally, treatment of diabetic endothelial nitric oxide synthase knockout mice with selexipag augme
186 Furthermore, macrophages from inducible nitric oxide synthase knockout mice, which had intact RO
190 dichlorofluorescein diacetate dye, inducible nitric oxide synthase levels determined by Western blot,
192 neuronal (neuron-specific enolase, neuronal nitric oxide synthase) markers in IR(Akita) compared wit
193 ated signalling through Akt, the endothelial nitric oxide synthase mediated pathway, regulates anabol
195 triggers calmodulin-dependent activation of nitric oxide synthase, nitric oxide (NO) production, NO-
197 el of human enteric neuropathy, the neuronal nitric oxide synthase (nNOS(-/-)) deficient mouse model,
198 itors while retaining the potency for neural nitric oxide synthase (nNOS) and selectivity over the ot
199 agonist mecamylamine, inhibitors of neuronal nitric oxide synthase (nNOS) and soluble guanylyl cyclas
200 al interneurons, immunoreactive for neuronal nitric oxide synthase (nNOS) and the receptor NK1, expre
201 he nitric oxide synthesizing enzyme neuronal nitric oxide synthase (nNOS) in nerve fibers of the muri
207 xcess nitric oxide (NO) produced by neuronal nitric oxide synthase (nNOS) is implicated in neurodegen
208 se in the dimer to monomer ratio of neuronal nitric oxide synthase (nNOS) protein and lowered NOS act
210 pendent reduction in dystrophin and neuronal nitric oxide synthase (nNOS, also known as NOS1) on atri
211 Citrulline formation by both human neuronal nitric-oxide synthase (nNOS) and mouse macrophage induci
212 scle is the muscle-specific form of neuronal nitric oxide synthase (nNOSmu) produced by the NOS1 gene
213 tuberculosis esxL induced the expression of nitric-oxide synthase, NO production, and p38 MAPK pathw
214 as associated with uncoupling of endothelial nitric oxide synthase (NOS) activity secondary to oxidat
215 pre-established heart disease independent of nitric oxide synthase (NOS) activity, whereas PDE5A inhi
216 utaneous vasodilatation and sweating through nitric oxide synthase (NOS) and calcium-activated potass
217 diated by prostacyclin-induced activation of nitric oxide synthase (NOS) and calcium-activated potass
218 nt expression of NMDA receptors (NMDARs) and nitric oxide synthase (NOS) and is therefore much more s
220 oduction from the amino acid l-arginine, via nitric oxide synthase (NOS) enzymes, research in recent
222 ytotoxic effects, which are inhibited by the nitric oxide synthase (NOS) inhibitor L-NIO, and genetic
223 se (nNOS) and selectivity over the other two nitric oxide synthase (NOS) isoforms (endothelial NOS an
224 ase, during hyperoxia, defective endothelial nitric oxide synthase (NOS) produces reactive oxygen and
225 e dystrophin-sarcoglycan complex delocalizes nitric oxide synthase (NOS) to alter its signaling, and
228 -monomethyl-L -arginine (L -NMMA) to inhibit nitric oxide synthase (NOS), the posture-induced increas
234 rophin protein completely abolishes muscular nitric-oxide synthase (NOS) function as a regulator of b
235 lytic cascade triggered by activating type 2 nitric-oxide synthase (NOS-2) and NADPH oxidase (NOX).
236 s by mitochondria, NADPH oxidase, and type 2 nitric-oxide synthase (NOS-2) and resulted in S-nitrosyl
237 ion increased in the presence of l-arginine (nitric-oxide synthase [NOS] substrate), and it decreased
238 is of the nitrergic neurons (with the enzyme nitric oxide synthase; NOS) has helped in understanding
239 ary to mRNA encoding the neuronal isoform of nitric oxide synthase (Nos1) is expressed in the mouse b
240 hat protein kinase Cbeta (PKCbeta) and brain nitric oxide synthase (NOS1), both identified by proteom
241 the metalloproteinase ADAMTS1 and inducible nitric oxide synthase (NOS2) as therapeutic targets in i
242 racellular adhesion molecule 1 (ICAM-1), and nitric oxide synthase (NOS2), developed leukostasis and
243 -regulated genes in BV-2 microglia including nitric oxide synthase (NOS2), interleukin-6 (IL-6), and
244 ells are phenotypically similar to inducible nitric oxide synthase (NOS2)- and tumor necrosis factor
245 thyl transferase (COMT(-/-)) and endothelial nitric oxide synthase (Nos3(-/-)) knockout mice, would b
246 y intact cells, is controlled by endothelial nitric oxide synthase (NOS3) and is crucial for attenuat
247 ation to pregnancy, as knockout mice lacking nitric oxide synthase (NOS3) have abnormal utero-placent
248 in, apelin receptor (APLNR), and endothelial nitric oxide synthase (NOS3) in HA adaptation and HA pul
249 etes was induced in hypertensive endothelial nitric oxide synthase (Nos3)-deficient mice by five low-
250 ochromes P450, the buildup of I435 occurs in nitric oxide synthases (NOSs) upon their reaction with e
251 ng aromatic amino acid hydroxylases (AAAHs), nitric oxide synthases (NOSs), and alkylglycerol monooxy
252 e improves insulin resistance in endothelial nitric oxide synthase null mice, and multiple studies ha
254 eam signaling pathways involving endothelial nitric oxide synthase or prostanoid production (indometh
255 crosis factor-alpha (P = 0.04) and inducible nitric oxide synthase (P = 0.02) in skin biopsy specimen
256 anifested by decreased levels of endothelial nitric oxide synthase (P< .005) and Kruppel-like factor
258 othelial nitric oxide synthase/Akt/inducible nitric oxide synthase pathways were assessed by Western
259 by siRNA significantly increased endothelial nitric oxide synthase phosphorylation at threonine 495 l
260 c oxide production and decreased endothelial nitric oxide synthase phosphorylation at threonine 495 l
261 cardiac GLUT4 translocation and endothelial nitric oxide synthase phosphorylation were blunted 7 day
262 tivation, an increase in Akt and endothelial nitric oxide synthase phosphorylation, and a decrease in
263 nels (K(Ca)3.1 and K(Ca)2.3) and endothelial nitric oxide synthase, produces additive tone, which is
264 s an activated endothelium and for inducible nitric oxide synthase production upon HGF stimulation.
266 of capon (C-terminal PDZ ligand of neuronal nitric-oxide synthase protein), apoptosis-associated spe
267 opterin, dimeric and phosphorylated neuronal nitric oxide synthase, sarcoplasmic reticulum Ca(2+) han
268 dimerization and phosphorylation of neuronal nitric oxide synthase, sarcoplasmic reticulum Ca(2+) rel
269 actility, tetrahydrobiopterin, the dimers of nitric oxide synthase, sarcoplasmic reticulum Ca(2+) rel
270 activation by fluvoxamine triggered the Akt-nitric oxide synthase signaling pathway, resulting in ti
272 sociated variant-BPIFB4 restores endothelial nitric oxide synthase signaling, rescues endothelial dys
273 ivity for vasoactive intestinal polypeptide, nitric oxide synthase, somatostatin, and vesicular gluta
276 volves the activation of the Akt-endothelial nitric oxide synthase survival pathway, and the inhibiti
277 volves the activation of the Akt-endothelial nitric oxide synthase survival pathway, and the inhibiti
278 6, multiple PDZ protein 1, Tamalin, neuronal nitric oxide synthase, syntrophins, protein interacting
279 ry cytokine tumor necrosis factor, inducible nitric oxide synthase, the M1 activator interferon gamma
280 effects alter the expression of endothelial nitric oxide synthase, the stability of atherosclerotic
281 Intriguingly, eNOS activity is regulated by nitric-oxide synthase trafficking inducer (NOSTRIN), whi
283 ssion of proinflammatory proteins (inducible nitric oxide synthase, tumor necrosis factor-alpha, and
284 ssion of proinflammatory proteins (inducible nitric oxide synthase, tumor necrosis factor-alpha, and
285 t radiation disrupted BH4, which resulted in nitric oxide synthases uncoupling and augmented radiatio
288 relevant changes in the vascular endothelial nitric oxide synthase vasodilatory response, which is a
289 tion that could be restored by inhibition of nitric oxide synthase via the inhibitor N-nitro-l-methyl
292 progenitor cells overexpressing endothelial nitric oxide synthase was tolerated hemodynamically in p
293 ression of Nos2, the gene encoding inducible nitric oxide synthase, was elevated in the absence of PP
294 e dismutase were increased, whereas those of nitric oxide synthase were decreased, in 7- to 10-week-o
295 , cyclooxygenase 2 and inducible endothelial nitric oxide synthase, were assessed in peripheral blood
296 adhesion molecule-1 (VCAM-1) and endothelial nitric oxide synthase, whereas PDEs had significantly hi
297 activation of a phagosomal enzyme, inducible nitric oxide synthase, which is necessary for NO product
298 he production of nitric oxide by endothelial nitric-oxide synthase, which ascorbate is known to activ
299 c contractions persisted until inhibition of nitric oxide synthase with N(omega) -nitro-l-arginine me
300 howed higher levels of phosphorylated neural nitric oxide synthase within neural stem cells (NSCs).
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