ライフサイエンスコーパス: NOS

1 NOS activity decreased significantly after reperfusion (

2 NOS activity in murine macrophages has a protective role

3 NOS activity modulates beta-catenin post-translational m

4 NOS inhibitor L-NAME also significantly attenuated RGS4

5 NOS inhibitor N(G)-nitro-L-arginine methyl ester attenua

6 NOS is a large homodimer with well characterized reducta

7 NOS isoforms adopt many conformations enabled by three f

8 NOS-dependent cytosolic NO release was quantified by aut

9 NOSs are homodimeric multidomain enzymes responsible for

10 , macrophage inflammatory protein 2 (MIP-2), NOS-2, interleukin-6 (IL-6), and IL-17a.

11 ylyl cyclase (NO-sGC) receptor antagonist, a NOS inhibitor, and NO donors, suggested that NO released

12 aled that UVA-induced NO release occurs in a NOS-independent, dose-dependent manner, with the majorit

13 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

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

15 domains have been reported, a structure of a NOS holoenzyme has remained elusive.

16 ase inhibition was lost in the presence of a NOS inhibitor.

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

18 ils exposed to a NOX inhibitor (Nox2ds) or a NOS-2 inhibitor (1400W) or with cells from mice lacking

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

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

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

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

23 stimulation in vivo and in vitro, through a NOS-mediated mechanism.

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

25 proteins with small inhibitory RNA abrogates NOS-2 activation, reactive species generation, actin pol

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

27 n transfer at a time, and that CaM activates NOS by constraining rotational motions and by directly b

28 ty, whereas PDE5A inhibition requires active NOS.

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

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

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

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

33 Although NOS has long been proposed to adopt distinct conformatio

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

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

36 ctice in patients with newly diagnosed "AML, NOS" with available FAB information undergoing curative-

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

38 etween percentage DNA methylation in ARG and NOS genes with CIMT was evaluated using linear regressio

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

40 a reduced antioxidant capacity of cells and NOS uncoupling.

41 inhibition of soluble guanylate cyclase and NOS activity rapidly induces neurite retraction of MGE c

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

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

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

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

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

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

48 elopment of antimicrobials against bacterial NOS-containing bacteria.

49 Nitric oxide (NO) produced by bacterial NOS functions as a cytoprotective agent against oxidativ

50 within a single polypeptide chain, bacterial NOS is only composed of an oxygenase domain and must rel

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

52 es is released and is further metabolized by NOS.

53 required cofactor for the synthesis of NO by NOS.

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

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

56 e mass spectrometry was used to map critical NOS interaction surfaces.

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

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

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

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

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

62 5 population controls, we investigated eight NOS SNPs and interactions with both household and ambien

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

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

65 lates EC migration by activating endothelial NOS (eNOS).

66 DL-mediated arginase activation, endothelial NOS uncoupling, endothelial dysfunction, and atherogenes

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

68 lation and activation of AKT and endothelial NOS.

69 yl)-l-ornithine dihydrochloride [endothelial NOS (eNOS) inhibitor].

70 d against purified nNOS enzymes, endothelial NOS (eNOS), and inducible NOS (iNOS).

71 of the constitutively expressed endothelial NOS (eNOS) is unclear.

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

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

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

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

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

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

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

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

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

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

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

83 or T(H)2 cell lineages, whereas endothelial NOS (eNOS) or neuronal NOS (nNOS) mutant mice showed com

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

85 creased by tetrahydrobiopterin, an essential NOS cofactor.

86 was used to evaluate a series of established NOS inhibitors.

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

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

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

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

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

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

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

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

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

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

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

98 ibuprofen arginate served as a substrate for NOS.

99 ans feeds on Bacilli that possess functional NOS.

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

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

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

103 ity among unmedicated individuals with BD II/NOS.

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

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

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

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

108 ght of the dynamic structural transitions in NOS enzymes during enzyme catalysis is lacking.

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

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

111 ral high-resolution structures of individual NOS domains have been reported, a structure of a NOS hol

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

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

114 zymes, endothelial NOS (eNOS), and inducible NOS (iNOS).

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

116 NAME and in mice with neuronal and inducible NOS deficiency, suggesting that excessive nitric oxide r

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

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

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

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

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

122 se (eNOS) uncoupling and increased inducible NOS (iNOS) activity amplify vascular oxidative stress.

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

124 Crystal structures of the mouse inducible NOS oxygenase domain reveal a homologous BH4-binding sit

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

126 -nitrosylase complex consisting of inducible NOS (iNOS), S100A8, and S100A9.

127 al inhibition or gene silencing of inducible NOS abrogated LPS-induced LKB1 degradation, whereas expo

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

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

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

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

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

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

134 itor (1400W) or with cells from mice lacking NOS-2.

135 d, no structure is available for full-length NOS.

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

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

138 Mammalian NOS isoforms are homodimers composed of two domains conn

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

140 Unlike mammalian NOS that contain both FAD and FMN binding domains within

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

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

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

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

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

146 (R16/17) are required for anchoring neuronal NOS (nNOS) to the sarcolemma.

147 ial nitric oxide synthase (NOS) and neuronal NOS in adult transgenic myocytes, which constitutively p

148 ures of inducible, endothelial, and neuronal NOS with and without CaM bound are similar, consisting o

149 oforms--inducible, endothelial, and neuronal NOS--that are composed of an N-terminal oxidase domain a

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

151 In neuronal NOS (nNOS), protein domain dynamics and calmodulin bindi

152 ance-associated proteins, including neuronal NOS (nNOS), in dorsal horn.

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

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

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

156 mined by differential expression of neuronal NOS (nNOS) and postsynaptic PKC activity, both of which

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

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

159 , whereas endothelial NOS (eNOS) or neuronal NOS (nNOS) mutant mice showed comparable T(H)17 cell dif

160 t low dose Iso, and by preferential neuronal NOS inhibition at high-dose Iso.

161 correlates with loss of sarcolemmal neuronal NOS localization in mdx muscle, whereas loss of in vivo

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

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

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

165 uced hypertrophy was reversed by nonspecific NOS inhibition at low dose Iso, and by preferential neur

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

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

168 n of the higher-order domain architecture of NOS is essential to elucidate the molecular underpinning

169 cal and temporal conformational behaviors of NOS.

170 Blockage of NOS activity with the inhibitor L-NG-nitroarginine methy

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

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

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

174 As dimerization of NOS is required for its activity, several dimerization i

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

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

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

178 eir mitochondrial function, as inhibition of NOS partially reverses this effect.

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

180 e previously proposed catalytic mechanism of NOS.

181 In the nucleus of NOS activated cells, nitration levels of beta-catenin in

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

183 e propose a mechanism for the second step of NOS catalysis in which a methylated nitric oxide species

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

185 expressing B2, but has only minor effects on NOS-negative B1 neurons.

186 Hypertrophy was restored on NOS or protein kinase G inhibition.

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

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

189 Caenorhabditis elegans, which lacks its own NOS.

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

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

192 tion was found with Asperger syndrome or PDD-NOS, but power was limited.

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

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

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

196 TA-3 expression identified a subset of PTCL, NOS with distinct clinical features, including inferior

197 45% of PTCLs, not otherwise specified (PTCL, NOS) and was associated with distinct molecular features

198 monstrated distinct clustering of ALCL, PTCL-NOS, and the AITL subtype of PTCL.

199 en percent of morphologically diagnosed PTCL-NOS cases were reclassified into other specific subtypes

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

201 oups can be identified in the remaining PTCL-NOS cases characterized by high expression of either GAT

202 44 (18%) PTCL, not otherwise specified (PTCL-NOS) samples.

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

204 We studied 244 PTCLs, including 158 PTCLs NOS, 63 AITLs, and 23 ALK-negative ALCLs.

205 ere synthesized and assayed against purified NOS isoforms.

206 vatives and assayed them against recombinant NOS enzymes.

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

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

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

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

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

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

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

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

215 ne methyl ester hydrochloride (non-selective NOS inhibitor); (3) 5 mm N-propyl-l-arginine (nNOS inhib

216 nhibited (41 +/- 3%CVCmax) and non-selective NOS-inhibited (40 +/- 4%CVCmax) sites were significantly

217 nce between eNOS-inhibited and non-selective NOS-inhibited sites.

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

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

220 classifiable: PTCL-not otherwise specified (NOS).

221 as (PTCLs; ie, PTCL not otherwise specified [NOS], angioimmunoblastic T-cell lymphoma [AITL], and ana

222 ito, ingested TGF-beta1 induces A. stephensi NOS (AsNOS), which limits parasite development and which

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

224 native redox partners for Bacillus subtilis NOS (bsNOS) and a novel chimera that promotes bsNOS acti

225 of the National Organic Chemistry Symposium (NOS) and, in doing so, traces the development of organic

226 sed blood flow independently of NO synthase (NOS) activity, suggesting involvement of pre-formed cuta

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

228 pterin, the stable precursor of NO synthase (NOS) cofactor, tetrahydrobiopterin.

229 Epigenetic regulation of NO synthase (NOS), the genes responsible for NO production, may affec

230 S-nitrosylases can use NO synthase (NOS)-derived NO to modify selected cysteines in target p

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

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

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

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

235 alcohol inhibition of nitric oxide synthase (NOS) and a direct suppression of the activity of postsyn

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

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

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

239 veolin-3, endothelial nitric oxide synthase (NOS) and neuronal NOS in adult transgenic myocytes, whic

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

241 Nitric oxide synthase (NOS) catalyzes the conversion of L-arginine to L-citrull

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

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

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

245 administration of the nitric oxide synthase (NOS) inhibitor L-NAME and in mice with neuronal and indu

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

247 Nitric-oxide synthase (NOS) is required in mammals to generate NO for regulatin

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

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

250 nitric oxide (NO) by nitric oxide synthase (NOS) requires electrons to reduce the heme iron for subs

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

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

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

254 neuropeptide Y (NPY), nitric oxide synthase (NOS), serotonin, substance P (SP), vasoactive intestinal

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

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

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

258 to citrulline through nitric oxide synthase (NOS).

259 ster, an inhibitor of nitric oxide synthase (NOS).

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

261 gases activate type-2 nitric-oxide synthase (NOS-2) and NADPH oxidase (NOX).

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

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

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

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

266 ransfer reactions catalyzed by NO synthases (NOS).

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

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

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

270 of dedicated enzymes known as NO synthases (NOSes).

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

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

273 Nitric oxide synthases (NOSs) comprise three closely related isoforms that catal

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

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

276 eling for PKCalpha, nitric oxide synthetase (NOS), and either GABA(C) or CtBP2 indicated GABAergic fe

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

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

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

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

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

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

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

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

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

286 Logistical aspects of the NOS and their historical trends are reviewed.

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

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

289 The first step of the NOS reaction has been well-characterized and is presumed

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

291 The role the NOS played in the launch of The Journal of Organic Chemi

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

293 hermore, systemic treatment of mice with the NOS inhibitor NG-monomethyl-l-arginine delayed weight lo

294 igher-order domain organization of all three NOS holoenzymes.

295 Mammals possess three NOS isoforms--inducible, endothelial, and neuronal NOS--

296 ermodynamic analysis of substrate binding to NOS.

297 s endothelial caveolae, which contributes to NOS uncoupling, and, hence, reduced NO-mediated coronary

298 e the transfer of NADPH derived electrons to NOS.

299 rom PDE5A inhibition being more sensitive to NOS activation.

300 2 indicated GABAergic feedback onto RBCs via NOS-immunoreactive ACs.