ライフサイエンスコーパス: NOS

1 NOS activity decreased significantly after reperfusion (

2 NOS(g) converts NO to NO(3) (-) in the presence of O(2)

3 NOS-dependent cytosolic NO release was quantified by aut

4 through increasing activation of PKC-Erk1/2-NOS axis via VEGFR1, while HG-induced elevation of VEGF

5 sest target to Nox4 Indeed, when combining a NOS and a NOX inhibitor at subthreshold concentrations,

6 For example, a NOS protein in the marine cyanobacterium Synechococcus s

7 ET-1, 10 mm N(G) -nitro-l-arginine (l-NNA; a NOS inhibitor) or a combination of 400 nm ET-1 and 10 mm

8 phils exposed to a NOX inhibitor (Nox2ds), a NOS-2 inhibitor (1400 W), or with cells from mice lackin

9 ining enzyme, this is the first example of a NOS that catalyzes an S-demethylation reaction; the nove

10 ic and environmental bacteria also produce a NOS that is evolutionary related to the mammalian enzyme

11 Previously, we demonstrated that a NOS inhibitor targeting both the active and pterin sites

12 ttenuates cutaneous vasodilatation through a NOS-independent mechanism, possibly through a vascular s

13 e-induced cutaneous vasodilatation through a NOS-independent mechanism.

14 A long-standing controversy is whether a NOS exists within mitochondria.

15 As Ca(2+) also activates NOS, we hypothesized that Trpc6 would help to mediate ni

16 ty, whereas PDE5A inhibition requires active NOS.

17 cies by means of specific antibodies against NOS and NADPH-diaphorase (NADPH-d) histochemistry, which

18 as blocked by inhibitors of Gbetagamma, Akt, NOS, and soluble guanylate cyclase.

19 We found that calmodulin alters NOS conformational behaviors in several ways: It changes

20 Although NOS catalysis relies on domain motions, and is activated

21 Furthermore, although NOS and KCa channels contribute to the prostacyclin-indu

22 We also found that, although NOS and KCa channels contribute to prostacyclin-induced

23 9 cm/s vs. 15.1 +/- 4.7 cm/s; p < 0.001) and NOS activity (2.27 +/- 0.96 vs. 1.77 +/- 0.59 vs. 1.30 +

24 PIN), calmodulin, heat shock protein 90, and NOS interacting protein.

25 depletion in the media using l-arginase and NOS inhibition in cancer cells using N(G)-nitro-l-argini

26 a reduced antioxidant capacity of cells and NOS uncoupling.

27 s, in one preparation, a COX-2 inhibitor and NOS substrate that could act to negate the harmful cardi

28 Vasodilation required neuronal NMDARs and NOS stimulation and subsequent guanylyl cyclase activati

29 bjectives of this work are to study NOS1 and NOS-related counterparts involved in regulating physiolo

30 ic process is essentially driven by NOX1 and NOS of the tumor cells, and finally leads to intercellul

31 rate-limiting enzyme in BH4 synthesis), and NOS activity ((14)C L-arginine to L-citrulline conversio

32 agnoses with subthreshold criteria (coded as NOS) with proportions of diagnoses reaching full criteri

33 rs (free SNOs or nitrosated proteins such as NOS), which promote NADPH-dependent reduction of NBT to

34 Staphylococcus aureus NOS (saNOS) has previously been shown to affect virulenc

35 Unlike other bacterial NOSs, syNOS cannot function with tetrahydrofolate and re

36 didates for Parkinson's disease (PD) because NOS enzymes produce nitric oxide (NO), a pro-oxidant tha

37 Sequencing of the beewolf NOS gene revealed no conspicuous differences to related

38 Blocking NOS-mediated BBB dysfunction during this acute/subacute

39 Our findings indicate that syNOS has both NOS and NO oxygenase activities, requires H(4)B, and may

40 cell bodies inside CGRP+ baskets lacked both NOS and CALR, while two overlapping populations containi

41 sis from L-arginine), which were affected by NOS inhibitors confirming the presence of functional enz

42 dentified by neuroimaging and ameliorated by NOS inhibition.

43 ioavailability was additionally indicated by NOS blockade ablating both the positive vascular effects

44 ilic leukemia, not otherwise specified (CEL, NOS) is assigned to patients with MPN with eosinophilia

45 Metazoa and the preservation of conservative NOS architecture from prokaryotic ancestors.

46 g mice treated post-IR with the constitutive NOS inhibitor N(G)-nitro-l-arginine methyl ester (L-NAME

47 Bacteria also contain NOS proteins, but the role of NO production within these

48 t NOS genes, including PDZ domain-containing NOS.

49 while two overlapping populations containing NOS and/or CALR comprised the remainder.

50 /EBPdelta as well as inflammatory cytokines, NOS 2, increased phagocytic activity, and a greater oste

51 es in 66 serum proteins and caused decreased NOS activity and increased VCAM-1 expression in RAECs.

52 Specific common psychiatric diagnoses NOS compared with full-criteria psychiatric diagnoses.

53 In addition, anxiety disorder NOS increased from 44.6% in the 1999-2002 period to 58.1

54 Among visits for bipolar disorder, NOS visits increased more than 18-fold, from 3.6% in the

55 Among all visits for mood disorders, NOS visits grew proportionally 1.5-fold from 45.3% in th

56 Trichoplax and Hoilungia have three distinct NOS genes, including PDZ domain-containing NOS.

57 situ hybridization, we showed that distinct NOSs are expressed in different subpopulations of cells,

58 of chromosome 7, 11q12.3-q25, whereas DLBCL, NOS was predominantly of germinal center B-cell (GCB) su

59 t also contains an N-terminal globin domain (NOS(g)) homologous to bacterial flavohemoglobin proteins

60 t not shear stress-stimulated endothelial (e)NOS activity.

61 5 population controls, we investigated eight NOS SNPs and interactions with both household and ambien

62 tivity and, in the wild-type group, elevated NOS-derived superoxide.

63 h our recent work implicating the endogenous NOS inhibitor asymmetric dimethylarginine (ADMA), a card

64 inducible NOS (macrophages) and endothelial NOS in vitro (aorta) and in vivo (blood pressure).

65 lation and activation of AKT and endothelial NOS.

66 ) m, respectively, whereas human endothelial NOS was hardly affected at all.

67 y protein oxidation and impaired endothelial NOS homodimer formation as plausible mechanistic explana

68 BL/6J mice resulted in increased endothelial NOS (eNOS) protein levels and NO production in the inner

69 Instead, we identified increased endothelial NOS s-glutathionylation as the main mechanism for NOS un

70 c oxide synthase (NOS) isoforms (endothelial NOS and inducible NOS).

71 nd tested against purified nNOS, endothelial NOS (eNOS), and inducible NOS (iNOS) enzymes.

72 t nNOS and inducible NOS but not endothelial NOS are irreversibly inhibited by H2S/NO at modest conce

73 of inducible NOS (iNOS) but not endothelial NOS.

74 educed mRNA expression levels of endothelial NOS (eNOS), Nrf2, and Phase II enzymes (heme oxygenase-1

75 that NOX5-induced uncoupling of endothelial NOS is a causal mechanism and theragnostic target of an

76 tion and increased occurrence of endothelial NOS monomers in the aortic grafts already during graft p

77 L-NIO, and genetic inhibition of endothelial NOS, implicating peroxynitrous acid as a key damaging ag

78 Therefore, targeting endothelial NOS in the donor represents a promising strategy to mini

79 membrane depolarization, reduced endothelial-NOS expression and desensitization of endothelial-derive

80 ated resting flow that is linked to enhanced NOS activity.

81 regulate the nitric oxide synthase enzymes (NOS) are of interest in biology and medicine.

82 creased by tetrahydrobiopterin, an essential NOS cofactor.

83 (18)F-NOS can be used to image iNOS activity in acute lung inf

84 In this study, we tested whether (18)F-NOS could quantify iNOS expression from endotoxin-induce

85 (18)F-NOS imaging was performed again approximately 16 h after

86 eers underwent a baseline, 1-h dynamic (18)F-NOS PET/CT scan.

87 (18)F-NOS uptake was quantified as the distribution volume rat

88 er for PET that binds to iNOS in vivo, (18)F-NOS.

89 Few NOS+ varicosities occurred in baskets.

90 othelial (260-fold), and inducible (41-fold) NOS isoforms and also showed potential for oral bioavail

91 ion, rather than BH4 depletion, accounts for NOS dysfunction in patients after cardiac surgery and ca

92 -glutathionylation as the main mechanism for NOS uncoupling after reperfusion.

93 nnotated gene in the biosynthetic operon for NOS, as an acyl carrier protein that delivers 3-methylin

94 The DMIA moiety is required for NOS efficacy and is synthesized from l-tryptophan in a s

95 ibuprofen arginate served as a substrate for NOS.

96 differed in abundance between cFSGS and FSGS-NOS, 41 were more abundant in cFSGS and 17 in FSGS-NOS.

97 1 were more abundant in cFSGS and 17 in FSGS-NOS.

98 ents with FSGS not otherwise specified (FSGS-NOS) or cFSGS and from normal controls were distinguishe

99 ficantly greater in cFSGS compared with FSGS-NOS.

100 Furthermore, NOS-specific inhibition rescued both measures.

101 We delineate a pathway (Cav1.1--> CaMKII--> NOS) in normal skeletal muscle that regulates the intrac

102 We also found that syNOS does not have NOS activity in E. coli (which lacks H(4)B) and that the

103 cases of high-grade B-cell lymphoma (HGBCL), NOS in patients <=25 years using an integrated approach,

104 A subset of HGBCL, NOS displayed recurrent alterations of Burkitt lymphoma-

105 activated B-cell (ABC) DLBCL profile, HGBCL, NOS, high genetic complexity, 1q21-q44 gains, 2p16/REL g

106 in the presence of O(2) and NADPH; however, NOS(g) did not protect Escherichia coli strains against

107 oinflammatory cytokines (TNF-alpha, MIP-1, i-NOS) were decreased significantly and restoration of tis

108 ns a challenge because of the near identical NOS active sites.

109 cipation, unmedicated individuals with BD II/NOS had decreased activity within the DS (but not VS).

110 ity among unmedicated individuals with BD II/NOS.

111 TAFRO) or iMCD-not otherwise specified (iMCD-NOS).

112 tein content was measured by immunoblotting; NOS activity was evaluated with high-performance liquid

113 s, resulting in a dose-dependent decrease in NOS activity and, in the wild-type group, elevated NOS-d

114 The results also show a decrease in NOS and BH4 biosynthetic enzyme in submandibular glands.

115 ac NOS1 is not accompanied by an increase in NOS activity, due in part to the alterations found in mo

116 We also found that rs2297518 in NOS (NO synthase) 2 (odds ratio, 2.25 [95% CI, 1.21-4.19

117 for the electron transfer (ET) reactions in NOSs.

118 ine complex or nitrosated proteins including NOS.

119 Repletion of NADPH after I/R increased NOS-dependent coronary flow well above that with BH4 alo

120 nNOS, endothelial NOS (eNOS), and inducible NOS (iNOS) enzymes.

121 an increased production of TNF and inducible NOS (iNOS) in the lungs.

122 ments with neuronal NOS (nNOS) and inducible NOS (iNOS) variants (nNOS W409F and iNOS K82A and V346I)

123 hese results suggest that nNOS and inducible NOS but not endothelial NOS are irreversibly inhibited b

124 everal flavones inhibit Muc5AC and inducible NOS up-regulation as well as cytokine release in primary

125 NOS) isoforms (endothelial NOS and inducible NOS).

126 Tadalafil rapidly augmented inducible NOS (iNOS) expression by increasing its mRNA, and siRNA

127 clear factor kappaB and consequent inducible NOS (iNOS)-mediated overproduction of NO, which in combi

128 CSF by engaging Cathepsin S-CX3CR1-inducible NOS signaling.

129 Interestingly, inducible NOS mRNA levels showed a significant (P <0.05) increase

130 nthase (nNOS) and mouse macrophage inducible NOS was inhibited by the hydrogen sulfide (H2S) donor Na

131 ctedly augmented the expression of inducible NOS (iNOS) but not endothelial NOS.

132 )-nitro-l-arginine methyl ester on inducible NOS (macrophages) and endothelial NOS in vitro (aorta) a

133 is not accompanied by TNFalpha or inducible NOS (iNOS) expression.

134 Co-administration of the inducible NOS inhibitor S-methylisothiourea or the proteasome inhi

135 A mechanism involving NOS activity was responsible for the observed phenomena.

136 Together, these results suggest that post-IR NOS inhibition improves radiation tumor response via Th1

137 ortion of US medical visits reporting DSM-IV NOS psychiatric diagnoses compared with the proportion r

138 or (1400 W), or with cells from mice lacking NOS-2 or the gp91(phox) component of NOX.

139 while no evidence for a mitochondria-located NOS was obtained.

140 ic oxide synthase (nNOS) protein and lowered NOS activity in the MPG, which were prevented by ROCK-I.

141 a consensus feline myristoylation motif (MA(NOS)) and examined the impact of MA mutations on virus a

142 nexpectedly, myristoylation efficiency of MA(NOS) in Escherichia coli by co-expressed mammalian NMT w

143 protein but partially sequestered in the MA(NOS) chimera, suggesting that the unusual FIV sequence i

144 virus assembly studies indicate that the MA(NOS) mutation does not affect virus assembly, but does p

145 tase (NOS(red)) domains present in mammalian NOS enzymes (mNOSs), but also contains an N-terminal glo

146 r specificity toward bNOS over the mammalian NOS (mNOS) isoforms remains a challenge because of the n

147 A total of 209 studies were included (mean NOS quality score of 4.8); 112 high- to medium-quality o

148 s were high quality/low risk of bias [median NOS: 8 (range 5 to 9)]; Cochrane risk: "low risk" (9/9,

149 The median NOS score (IQR) was 5 (4-6) out of 8 points and the bias

150 lthy controls to evaluate: (i) ADMA-mediated NOS uncoupling reduces epithelial production of NO and i

151 almodulin, which regulates NOS(red)-mediated NOS(ox) reduction in mNOSs.

152 urthermore, the existence of a mitochondrial NOS is controversial.

153 pressed specifically in mdx skeletal muscle, NOS-M significantly attenuates force loss owing to damag

154 nosis of "362.16: Retinal Neovascularization NOS." RESULTS: The estimated diopter-adjusted prevalence

155 nosis of "362.16: Retinal Neovascularization NOS." Type of initial treatment for mCNV was categorized

156 This NO stems from neuronal NOS (nNOS), but not endothelial (eNOS).

157 nsfer domains in a FRET dye-labeled neuronal NOS reductase domain, and to understand how calmodulin a

158 s concept, we utilized a "Cys-lite" neuronal NOS flavoprotein domain and substituted Cys for two resi

159 ducible NO synthase (NOS2), but not neuronal NOS (NOS1), partially restored the evoked secretory resp

160 re proposed for the inactivation of neuronal NOS (nNOS) by (S)-2-amino-5-(2-(methylthio)acetimidamido

161 ine the subcellular distribution of neuronal NOS (nNOS).

162 loop in cytochrome P450 BM3 and the neuronal NOS mutant (DeltaGly-810).

163 present additional experiments with neuronal NOS (nNOS) and inducible NOS (iNOS) variants (nNOS W409F

164 ed; proportions of other submucosal neurons (NOS-, GABA-, and CGRP-expressing), are also deficient.

165 esence of L-NG-monomethyl arginine (L-NMMA) (NOS inhibitor) but not of D-NG-monomethyl arginine (D-NM

166 this, we designed a modified form of nNOSmu (NOS-M) that is targeted to the sarcolemma by palmitoylat

167 Crucially, normal NOS function depends on availability of the cofactor (6R

168 Nosiheptide (NOS) is a highly modified thiopeptide antibiotic that di

169 It is thought that the catalytic activity of NOS promotes NADPH-dependent reduction of nitro-blue tet

170 cal and temporal conformational behaviors of NOS.

171 Colocalization of NOS and tyrosine hydroxylase was observed in numerous ce

172 tomycin and demonstrates the conservation of NOS-derived NO(*)-haem receptor signalling between bacte

173 Here, we investigated contributions of NOS genes and OP pesticides to PD risk, controlling for

174 istry was used for simultaneous detection of NOS with catecholaminergic, cholinergic, and serotonergi

175 was conducted for simultaneous detection of NOS with tyrosine hydroxylase, choline acetyltransferase

176 young were nearly ablated, with no effect of NOS inhibition in the old.

177 inoguanidine; in addition, the expression of NOS isoforms was analysed.

178 These results suggest that the expression of NOS-M in skeletal muscle may be therapeutically benefici

179 Distinct groups of NOS-immunoreactive cells were observed in pallial and su

180 or without combination with an inhibitor of NOS (l-NAME).

181 dimethylarginine, an endogenous inhibitor of NOS, and maintain vascular homeostasis; however, the reg

182 tro-l-arginine methyl ester, an inhibitor of NOS.

183 ndicate that blast provokes delayed-onset of NOS-dependent pathogenic cascades that can later emerge

184 NADPH and BH4 repletion, full restoration of NOS-dependent coronary flow occurred.

185 nd p=0.0002, respectively) and uncoupling of NOS activity.

186 ultiple lineage-specific diversifications of NOSs and NO/nitrite/nitrate sensors from the common ance

187 30 nM) and very high selectivity over other NOS isoforms, especially human eNOS (hnNOS/heNOS = 2799,

188 at levels similar to those produced by other NOSs but does not require Ca(2+)-calmodulin, which regul

189 Overall, NOS visits constituted 35.0% of the total psychiatric vi

190 syNOS retains the oxygenase (NOS(ox)) and reductase (NOS(red)) domains present in mam

191 The ratio of ENKCL to PCTL-NOS among Native Americans, Asians/Pacific Islanders, an

192 d expression patterns, whereas AS and AD/PDD-NOS were convergent for aspects of candidate genes and f

193 AS was divergent to AD and PDD-NOS for aspects of functional DNMs and expression patter

194 It is revealed that AD and PDD-NOS were broadly convergent in terms of all four genetic

195 iagnoses of autism, Asperger syndrome or PDD-NOS (pervasive developmental disorder not otherwise spec

196 mental disorder not otherwise specified (PDD-NOS), 276 from 247 subjects with Asperger's syndrome (AS

197 ic conditions (pH, PN concentrations, and PN/NOSs ratios) to probe the formation of I435.

198 In the upright-seated posture, NOS inhibition attenuated the FPP-induced augmentation o

199 fits of sarcolemmal-localized NO production, NOS-M also increased the surface membrane levels of utro

200 tive Americans had a lower incidence of PTCL-NOS (all P < .05).

201 In a training cohort of 49 cases of PTCL-NOS with corresponding GEP data, the 2 subtypes identifi

202 y defined 2 major molecular subtypes of PTCL-NOS, PTCL-GATA3 and PTCL-TBX21, which have distinct biol

203 hologists and was validated in a second PTCL-NOS cohort (n = 124), where a significant difference in

204 idence of PTCL not otherwise specified (PTCL-NOS), anaplastic large-cell lymphoma, and adult T-cell l

205 gnated as PTCL-not otherwise specified (PTCL-NOS).

206 ere synthesized and assayed against purified NOS isoforms.

207 iew and only 8 (15%) were both good quality (NOS >= 7) and used a well-validated frailty measure.

208 vatives and assayed them against recombinant NOS enzymes.

209 ine can reverse this mechanism by recoupling NOS, restoring NO production and reducing oxidative and

210 tains the oxygenase (NOS(ox)) and reductase (NOS(red)) domains present in mammalian NOS enzymes (mNOS

211 t require Ca(2+)-calmodulin, which regulates NOS(red)-mediated NOS(ox) reduction in mNOSs.

212 iothreitol (100 mumol/L) completely restored NOS activity after reperfusion (p=0.34).

213 Reversing NOS s-glutathionylation with dithiothreitol (100 mumol/L

214 addition to a central hydroxypyridine ring, NOS contains several other modifications, including mult

215 reactive oxygen and/or nitrogen species (ROS/NOS) could be achieved, detrimental side effects are lik

216 e Newcastle-Ottawa Quality Assessment Scale (NOS).

217 ity according to the Newcastle-Ottawa Scale (NOS) and risk of bias according to a predefined scale.

218 ded studies based on Newcastle-Ottawa Scale (NOS).

219 s was assessed using Newcastle-Ottawa Scale (NOS)/Cochrane risk of bias tool.

220 was assessed using Newcastle-Ottawa scores (NOS) and quality of evidence using Grading of Recommenda

221 ox/flox); LysMCre(+/-) mice with a selective NOS inhibitor or knockout of Nos2, encoding iNOS, signif

222 as a template for next generation selective NOS inhibitor design but also opens new prospects for th

223 ster shell, namely the natural oyster shell (NOS), the calcined natural oyster shell (CNOS), and biom

224 G) -nitro-l-arginine (l-NNA), a non-specific NOS inhibitor; (iii) 50 mm tetraethylammonium (TEA), a n

225 ls with BD II or BD not-otherwise specified (NOS) and 20 matched healthy comparison individuals parti

226 use LBCLs (DLBCLs), not otherwise specified (NOS); 20 LBCL-IRF4 cases; and 12 cases of high-grade B-c

227 The expansion of subthreshold (NOS) DSM-IV diagnoses of mood disorder, bipolar disorder

228 r nonphosphorous neutral organic superbases (NOS).

229 quinoxalin-1-one, inhibitors of NO synthase (NOS) and soluble guanylyl cyclase, respectively, abolish

230 To determine the role of NO synthase (NOS) isoforms in NO generation following exposure to LAs

231 ed from arginine and oxygen via NO synthase (NOS).

232 t vasodilation due to uncoupled NO synthase (NOS).

233 NO(*) generated by mammalian NO(*) synthase (NOS) result from targeting of the haem moiety of soluble

234 We provide evidence that a NO-synthase (NOS) is involved in the generation of the extraordinary

235 upling of endothelial nitric oxide synthase (NOS) activity secondary to oxidation of the NOS cofactor

236 to acetylcholine, and nitric oxide synthase (NOS) activity was defined as the inverse of FBF reserve

237 isease independent of nitric oxide synthase (NOS) activity, whereas PDE5A inhibition requires active

238 and sweating through nitric oxide synthase (NOS) and calcium-activated potassium (KCa) channels in y

239 induced activation of nitric oxide synthase (NOS) and calcium-activated potassium (KCa) channels.

240 e labeling with CGRP, nitric oxide synthase (NOS) and calretinin (CALR) antibodies.

241 eceptors (NMDARs) and nitric oxide synthase (NOS) and is therefore much more suitable for effective N

242 Nitric oxide synthase (NOS) catalyzes the conversion of l-arginine to l-citrull

243 hile NO production by nitric oxide synthase (NOS) enzymes in the eye has been characterized, the more

244 acid l-arginine, via nitric oxide synthase (NOS) enzymes, research in recent years has established t

245 robiopterin (BH(4) )/ nitric oxide synthase (NOS) expression in primary human aortic endothelial cell

246 ly abolishes muscular nitric-oxide synthase (NOS) function as a regulator of blood flow during muscle

247 Nitric oxide synthase (NOS) genes are candidates for Parkinson's disease (PD) b

248 ic system with neural nitric oxide synthase (NOS) immunohistochemistry and NADPH-diaphorase (NADPH-d)

249 stochemical marker of nitric oxide synthase (NOS) in aldehyde-treated tissues.

250 estigated the role of nitric oxide synthase (NOS) in mediating blood-brain barrier (BBB) disruption a

251 are inhibited by the nitric oxide synthase (NOS) inhibitor L-NIO, and genetic inhibition of endothel

252 Nitric oxide synthase (NOS) inhibitors rescue this pathology.

253 ty over the other two nitric oxide synthase (NOS) isoforms (endothelial NOS and inducible NOS).

254 defective endothelial nitric oxide synthase (NOS) produces reactive oxygen and nitrogen free radicals

255 n complex delocalizes nitric oxide synthase (NOS) to alter its signaling, and augments mechanosensiti

256 Oxidative stress and nitric oxide synthase (NOS) uncoupling are thought to contribute to Fabry cardi

257 is imbalance leads to nitric oxide synthase (NOS) uncoupling with reduced nitric oxide (NO) formation

258 (L -NMMA) to inhibit nitric oxide synthase (NOS), the posture-induced increases in the PLM responses

259 drogenase release and nitric oxide synthase (NOS)-dependent cGMP production.

260 nd sweating through a nitric oxide synthase (NOS)-dependent mechanism.

261 nd sweating through a nitric oxide synthase (NOS)-dependent mechanism.

262 to citrulline through nitric oxide synthase (NOS).

263 by activating type 2 nitric-oxide synthase (NOS-2) and NADPH oxidase (NOX).

264 H oxidase, and type 2 nitric-oxide synthase (NOS-2) and resulted in S-nitrosylation of actin.

265 esence of l-arginine (nitric-oxide synthase [NOS] substrate), and it decreased in the presence of L-N

266 rons (with the enzyme nitric oxide synthase; NOS) has helped in understanding important aspects of br

267 Here, we analyzed NO synthases (NOS) in four different species of placozoans-one of the

268 controlling the expression of NO synthases (NOS) in innate and adaptive immune cells, but have also

269 A, 1) is the best substrate of NO synthases (NOS).

270 Nitric oxide synthases (NOS) are important mediators of progrowth signaling in t

271 dministration of the nitric oxide synthases (NOS) co-factor tetrahydrobiopterin has been shown to pre

272 While NO synthases (NOSs) are also expressed in cardiac myocytes, it is uncl

273 nimals by structurally related NO synthases (NOSs), which contain NADPH/FAD- and FMN-binding domains.

274 Nitric oxide (NO) synthases (NOSs) catalyze the formation of NO from l-arginine.

275 Nitric oxide synthases (NOSs) are heme-based monooxygenases that convert l-Arg t

276 up of I435 occurs in nitric oxide synthases (NOSs) upon their reaction with excess PN.

277 ydroxylases (AAAHs), nitric oxide synthases (NOSs), and alkylglycerol monooxygenase (AGMO).

278 utic efficacy could be improved by targeting NOS following tumor irradiation.

279 rgued that a proteinaceous factor other than NOS is responsible for producing diformazan in aldehyde-

280 Here, we show that NOS of the human pathogen Staphylococcus aureus, in conc

281 Our findings suggest that NOS s-glutathionylation, rather than BH4 depletion, acco

282 The NOS inhibitor N(G)-nitro-L-arginine methyl ester (L-NAME

283 hanges the distance distribution between the NOS domains, shortens the lifetimes of the individual co

284 One key structural difference between the NOS isoforms is the amino acid composition of the pterin

285 rs of the FMN domain impact catalysis by the NOS flavoprotein domain and how these behaviors are gove

286 his dilatation was partially reversed by the NOS inhibitor l-NAME.

287 We observed a significant decrease in the NOS substrate l-arginine in plasma from CRPS patients, s

288 Interestingly, the NOS isoforms vary in their capacity to detoxify/activate

289 In knockouts, the NOS activity, caspase-3 expression/activity and the numb

290 (NOS) activity secondary to oxidation of the NOS cofactor, tetrahydrobiopterin (BH4).

291 particular heme-thiolate environment of the NOS enzymes can stabilize an N-bound Fe(III)-N(O)OO(-) i

292 Administration of the NOS inhibitor l-NAME to pregnant mice recapitulated the

293 riments were repeated in the presence of the NOS inhibitors, N(G)-nitro-L-arginine methyl ester and a

294 nor pentaerythritol tetranitrate (PETN), the NOS inhibitor l-nitroarginine (L-NA), plasma pool C1-INH

295 However, due to alternative splicing, the NOS-mRNA in beewolf eggs lacks an exon near the regulato

296 We have shown previously that the NOS enzyme catalytic cycle involves a large number of re

297 nnectomic analyses and specifically that the NOS-1 AC mediates long-range inhibition during night vis

298 ofactor binding site that is adjacent to the NOS active site.

299 primarily on a single interneuron type, the NOS-1 AC: a multistratified, axon-bearing GABAergic cell

300 rom PDE5A inhibition being more sensitive to NOS activation.