ライフサイエンスコーパス: nNOS

1 nNOS can be found also in the nucleus; however, its exac

2 nNOS depletion from mdx mice prevented compensatory skel

3 nNOS is expressed in approximately 1% of NAcore neurons.

4 nNOS mediates physiological sympatholysis, thus ensuring

5 rated atomic models of the dystrophin R16-17.nNOS-PDZ complex that correlated well with the alanine s

6 we generated an adeno-associated virus (AAV) nNOS vector and tested its therapeutic efficacy in the a

7 lation reinstates drug seeking by activating nNOS, but activating mGluR5 did not promote reinstated s

8 Importantly, full active nNOS lacking PDZ domain (nNOSbeta) does not localize in

9 neuropeptides CGRP and substance P, and also nNOS-derived NO.

10 Overall, our results indicate that altered nNOS splicing and nuclear localization could be contribu

11 Although nNOS is a heme-containing enzyme, this is the first exam

12 at partial transduction can still ameliorate nNOS delocalization-associated functional deficiency.

13 approach to study both chaperone binding and nNOS ubiquitination in intact HEK293 cells.

14 ificantly attenuated compared to control and nNOS-inhibited (P < 0.001 all conditions) but there was

15 erence between control (58 +/- 2%CVCmax) and nNOS-inhibited (56 +/- 3%CVCmax) sites in response to ex

16 ng to a profound reduction in atrial DYS and nNOS protein content and in nitric oxide availability.

17 human atrial fibrillation recovered DYS and nNOS, and normalised APD and APD rate-dependency.

18 4 and 21 days after ischemia, dystrophin and nNOS levels recovered, and class IIa HDACs relocalized t

19 In goats, a reduction in dystrophin and nNOS protein content was associated with upregulation of

20 hanism causing atrial loss of dystrophin and nNOS; this loss leads to the electrical phenotype induce

21 Gene expression of miR-31, dystrophin, and nNOS was assessed by quantitative RT-PCR; protein conten

22 c treatment with HOE-140 diminished eNOS and nNOS as well as M1-M4 muscarinic receptor expression and

23 eNOS and nNOS mutant mice show comparable M1 macrophage polarizat

24 onal nitric-oxide synthases (iNOS, eNOS, and nNOS) revealed that FcgammaR stimulation in unprimed mac

25 PDE5 and nNOS were deficient in 5 of 5 biopsies.

26 protein complex of NMDA receptor, PSD95 and nNOS.

27 m mediator of nuclear nNOS translocation and nNOS-dependent mitochondrial biogenesis.

28 OS inhibitor); (3) 5 mm N-propyl-l-arginine (nNOS inhibitor); and (4) 10 mm N(5)-(1-iminoethyl)-l-orn

29 and selective monocationic pyrrolidine-based nNOS inhibitors reported to date, and 10 shows improved

30 have developed a series of pyrrolidine-based nNOS inhibitors that exhibit excellent potencies and iso

31 The NOS1AP PDZ motif does not bind nNOS as measured by multiple methods.

32 inoquinolines showed promise as bioavailable nNOS inhibitors but suffered from low human nNOS inhibit

33 after mGluR2/3 blockade reduced by blocking nNOS.

34 miR-31 binding to nNOS 3'UTR recovered both nNOS protein and gene expression but had no effect on th

35 Inhibition of ERK reduced both nNOS activation and NO secretion.

36 ough the calmodulin (CaM)-free and CaM-bound nNOS to cytochrome c, whereas hinge lengthening relieved

37 ct or slowed electron flux through CaM-bound nNOS to cytochrome c.

38 gnals (mostly mitochondrial) were blocked by nNOS deletion, but not by inhibiting the mitochondrial C

39 Overproduction of NO by nNOS is implicated in the pathogenesis of diverse neuron

40 expectedly, muscle fatigue was unaffected by nNOS depletion, revealing a novel latent compensatory me

41 romotes the mechanical activation of cardiac nNOS by acting as a mechanosensor to regulate AMPK activ

42 Preincubation of concentrated nNOS with H2S under turnover conditions decreased activi

43 onclude that under physiological conditions, nNOS is the most relevant source for NO in cardiac myocy

44 urons in the myenteric plexus also contained nNOS.

45 onstrated that nearly all NK1IP -n contained nNOS (96.43%) and that 84.59% of nNOSIP -n co-expressed

46 particular, overexpression of PDZ-containing nNOS (nNOSalpha) increases S-nitrosylated CREB with cons

47 Conversely, nNOS knockout mice show reduced NREM sleep time, shorter

48 at, although sleep is necessary for cortical nNOS/NK1 neuron activation, the proportion of cells acti

49 ously that the proportion of Fos(+) cortical nNOS/NK1 neurons is correlated with established electrop

50 find that the proportion of Fos(+) cortical nNOS/NK1 neurons was minimal when sleep pressure was low

51 y sleep, we show that activation of cortical nNOS/NK1 neurons is directly related to non-rapid eye mo

52 In contrast, a large proportion of cortical nNOS/NK1 neurons was Fos(+) when an equivalent amount of

53 indings support the hypothesis that cortical nNOS/NK1 neurons translate homeostatic sleep drive into

54 sleep, it remained unclear whether cortical nNOS/NK1 neurons are activated to the same degree throug

55 0 promotes nNOS ubiquitination and decreases nNOS protein, and overexpression of Hsp90 inhibits nNOS

56 new therapeutic avenues to restore defective nNOS homeostasis in dystrophin-null Duchenne muscular dy

57 A PDZ domain-deleted nNOS gene (DeltaPDZ nNOS) was packaged into tyrosine mut

58 the therapeutic efficacy of the AAV DeltaPDZ nNOS vector in a symptomatic Duchenne cardiomyopathy mod

59 A PDZ domain-deleted nNOS gene (DeltaPDZ nNOS) was packaged into tyrosine mutant AAV-9 and delive

60 t that the cardioprotective role of DeltaPDZ nNOS is likely through reduced apoptosis, enhanced phosp

61 Supra-physiological DeltaPDZ nNOS expression significantly reduced myocardial fibrosi

62 treat Duchenne cardiomyopathy with DeltaPDZ nNOS gene transfer.

63 ompounds, such as cis-(+)-37, exhibited dual nNOS and NET inhibition (IC(50) of 0.56 and 1.0 muM, res

64 The deletion of the gene encoding nNOS or its pharmacological inhibition in the preoptic r

65 ological or genetic disruption of endogenous nNOS or eNOS during workload transitions in cardiac myoc

66 reactive cells of the OV/MEPO also expressed nNOS.

67 xamined the distribution of cells expressing nNOS in the postnatal and adult female mouse hypothalamu

68 r the R17 alpha1 helix, were dispensable for nNOS interaction.

69 lices of both R16 and R17 were essential for nNOS binding in muscle.

70 s have a glutamatergic phenotype, except for nNOS neurons of the ARH, which are GABAergic.

71 nanomolar inhibitory potency (Ki = 5 nM for nNOS) and good isoform selectivities (nNOS over eNOS [44

72 of this study, exhibiting a Ki of 24 nM for nNOS, with 273-fold and 2822-fold selectivity against iN

73 compound 7, displayed nanomolar potency for nNOS (Ki = 19 nM), good selectivity over endothelial (26

74 x landscape of conformations is required for nNOS catalysis beyond the simple models derived from sta

75 er structural features that are required for nNOS interaction, we replaced an individual alpha-helix

76 eved repression of electron flux in CaM-free nNOS and had no impact or slowed electron flux through C

77 all gradient and inhibits NO production from nNOS.

78 suppress adventitious electron transfer from nNOS to molecular oxygen and thereby preventing accumula

79 nzonitriles conferred the best rat and human nNOS inhibition.

80 specially potent and selective rat and human nNOS inhibitors.

81 a similar binding mode in both rat and human nNOS, in which the 2-aminopyridine and the fluorobenzene

82 ed high potency, selectivity, and good human nNOS inhibition, and retained some permeability in a Cac

83 We aimed to improve human nNOS potency and selectivity and reduce off-target bindi

84 pounds had decreased permeability, low human nNOS activity, and low selectivity versus human eNOS.

85 nNOS inhibitors but suffered from low human nNOS inhibition, low selectivity versus human eNOS, and

86 the potency and isoform selectivity of human nNOS inhibitors bearing a 2-aminopyridine scaffold.

87 still preserves excellent potency with human nNOS (Ki = 30 nM) and very high selectivity over other N

88 macophore and promote interaction with human nNOS-specific His342.

89 d that, like GnRH neurons, most hypothalamic nNOS neurons have a glutamatergic phenotype, except for

90 We tested the hypothesis that CHF impairs nNOS-mediated PO(2)mv control.

91 the crystal structure of lead compound 1 in nNOS.

92 r N-nitro-l-arginine (l-NNA, 200 mum) and in nNOS-knockout (KO) mouse preparations, PAG shifted the t

93 7, driven by the critical residue Asp597 in nNOS, offers compelling insight to explain its isozyme s

94 ; and 2) to determine whether the changes in nNOS/eNOS protein expression or dimerization are correla

95 much lower inhibitor binding free energy in nNOS than in eNOS.

96 that mimicked mGluR5 signaling through Gq in nNOS interneurons, we recapitulated cue-induced reinstat

97 Reductions in muscle integrity in nNOS-null mdx mice were accompanied by decreases in spec

98 of the two chaperones as they participate in nNOS quality control in the cell.

99 the cyano group to a new auxiliary pocket in nNOS.

100 nsient response to beta(3)-AR stimulation in nNOS(-/-) mice.

101 This is accompanied by increased nNOS levels in the AD mice and is reversed upon normaliz

102 by miR-31; recovery of DYS protein increased nNOS protein but not mRNA in keeping with a stabilising

103 carboxamide riboside or salicylate increased nNOS S1412 phosphorylation and was sufficient to enhance

104 0 inhibits nNOS ubiquitination and increases nNOS protein, showing the opposing effects of the two ch

105 rotein, and overexpression of Hsp90 inhibits nNOS ubiquitination and increases nNOS protein, showing

106 ree-dimensional reconstruction of the intact nNOS-CaM complex reveals a closed conformation and a cro

107 Intriguingly, nNOS was seen only after the second week of life in the

108 site of interaction but ignored the involved nNOS residues, and the R17 binding site has not been des

109 ize the full-length of the neuronal isoform (nNOS) complex and determine the structural mechanism of

110 ir of dual AAV vectors that expressed a 6 kb nNOS-binding mini-dystrophin gene.

111 In CSE-KO-nNOS-KO mice, the gradient was shifted in the depolarizi

112 evels is desirable therapeutically, but many nNOS inhibitors are poorly bioavailable.

113 Nonetheless, many nNOS inhibitors mimic l-arginine and are poorly bioavail

114 amounts of NO produced by non-mitochondrial nNOS were insufficient to regulate respiration during be

115 Most nNOS inhibitors mimic l-arginine and have poor bioavaila

116 Muscle nNOS and PDE5 were tested with Western blotting in 5 pat

117 In normal muscles, nNOS function is ensured by its localization at the sarc

118 In both adults and neonates, nNOS was largely restricted to regions of the hypothalam

119 eration of NO is likely to be via a neuronal nNOS-sGC dependent pathway.

120 eration of NO is likely to be via a neuronal nNOS/sGC-dependent pathway.

121 merization of NO synthase enzymes (neuronal [nNOS] and endothelial [eNOS]) are altered in the onset o

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

123 oposed for the inactivation of neuronal NOS (nNOS) by (S)-2-amino-5-(2-(methylthio)acetimidamido)pent

124 the FMN-FAD/NADPH hinge in rat neuronal NOS (nNOS) by constructing mutants that either shortened or l

125 ogical selective inhibition of neuronal NOS (nNOS) has the potential to be therapeutically beneficial

126 reas endothelial NOS (eNOS) or neuronal NOS (nNOS) mutant mice showed comparable T(H)17 cell differen

127 17) are required for anchoring neuronal NOS (nNOS) to the sarcolemma.

128 Neuronal NOS (nNOS) was localized primarily in puncta in the inner ple

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

130 associated proteins, including neuronal NOS (nNOS), in dorsal horn.

131 In neuronal NOS (nNOS), protein domain dynamics and calmodulin binding ar

132 he subcellular distribution of neuronal NOS (nNOS).

133 NOS1AP/nNOS interaction regulates small GTPases, iron transport

134 These data suggest eNOS, not nNOS, mediate NO synthesis during reflex cutaneous vasod

135 unctions as the upstream mediator of nuclear nNOS translocation and nNOS-dependent mitochondrial biog

136 ivation in these mice but, in the absence of nNOS, they are unable to up-regulate NREM delta power ap

137 amate transport and subsequent activation of nNOS by synaptic glutamate spillover is not shared.

138 nadal axis in vivo through the activation of nNOS in neurons of the preoptic region.

139 However, chemogenetic activation of nNOS interneurons in the NAcore reinstated sucrose seeki

140 reviously reported 2-aminoquinoline class of nNOS inhibitors, although orally bioavailable and brain-

141 vel (consistent with the mRNA degradation of nNOS by miR-31).

142 arge part, the CHIP-dependent degradation of nNOS in HEK293 cells, as well as in in vitro studies wit

143 pression and accelerated mRNA degradation of nNOS leading to a profound reduction in atrial DYS and n

144 generative disorders, but the development of nNOS inhibitors is often hindered by poor pharmacokineti

145 splanted cells, including the development of nNOS(+) neurons and subsequent restoration of nitrergic

146 en recently suggested that the PDZ domain of nNOS binds with very low affinity to the C termini of ta

147 poorly understood because the PDZ domain of nNOS can apparently exhibit class I, class II, and class

148 We describe herein that the PDZ domain of nNOS can behave as a bona fide class III PDZ domain and

149 e that competes for the unique PDZ domain of nNOS that interacts with NOS1AP.

150 gh affinity association of the PDZ domain of nNOS to claudin-3 and claudin-14, two tight junction tet

151 7201 do not interact with the PDZ domains of nNOS or PSD-95, nor inhibit the nNOS-PDZ/PSD-95-PDZ inte

152 confirmed that PDE10A operates downstream of nNOS to limit cGMP production and excitatory corticostri

153 xidative muscle and that vascular effects of nNOS-derived NO are manifest principally within glycolyt

154 ype-selective peripheral vascular effects of nNOS-derived NO during high-speed treadmill running.

155 with the extent of selective elimination of nNOS interneurons.

156 Further evaluation of nNOS binding mini-dystrophin dual AAV vectors is warrant

157 shown that supra-physiological expression of nNOS-binding mini-dystrophin restores normal blood flow

158 rface by interacting with the beta-finger of nNOS-PDZ.

159 ognize and ubiquitinate the altered forms of nNOS.

160 While the heterogeneity of nNOS-expressing neurons has been studied in various brai

161 t probable mechanism for the inactivation of nNOS involves oxidative demethylation with the resulting

162 interventions in assessing the influence of nNOS.

163 As a result, inhibition of nNOS and reduction of NO levels is desirable therapeutic

164 Moreover, the relatively weak inhibition of nNOS by Na2S in the absence of Arg and/or BH4 was marked

165 iological functions, selective inhibition of nNOS over other isoforms is essential to minimize side e

166 small molecules for selective inhibition of nNOS over related isoforms (eNOS and iNOS) is therapeuti

167 Conversely, inhibition of nNOS resulted in a loss of S-nitrosylation of gephyrin a

168 Inhibition of nNOS was not affected by the concentrations of l-arginin

169 al highly potent and selective inhibitors of nNOS were discovered.

170 y unrecognized heterodivalent interaction of nNOS with NOS1AP may therefore provide distinct opportun

171 and suggests that functional interaction of nNOS with NOS1AP might be targetable at two distinct sit

172 ever, the relative importance of the loss of nNOS from the sarcolemma versus the importance of loss o

173 OSmu and nNOSbeta to discern how the loss of nNOS impacts dystrophic skeletal muscle pathology.

174 atent compensatory mechanism for the loss of nNOS in mdx mice.

175 ion and pain, the structure and mechanism of nNOS, and the use of this information to design selectiv

176 Overexpression of nNOS decreased the size of postsynaptic gephyrin cluster

177 erein our studies to improve permeability of nNOS inhibitors as measured by both PAMPA-BBB and Caco-2

178 itical involvement of a sparse population of nNOS-expressing interneurons in cue-induced cocaine seek

179 A great proportion of nNOS-immunoreactive neurons in the OV/MEPO and ARH were

180 hat the PDZ domain allows the recruitment of nNOS to nuclei, thus favoring local NO production, nucle

181 In mice lacking dystrophin, restoration of nNOS effects by a phosphodiesterase 5 (PDE5) inhibitor (

182 ons are consistent with the proposed role of nNOS neurons in physiological processes.

183 amino acids involved in the binding site of nNOS-PDZ with dystrophin R16-17 using combined experimen

184 onships in multiple conformational states of nNOS.

185 s) and selective chemogenetic stimulation of nNOS interneurons recapitulated MMP activation and t-SP

186 Simple models based on crystal structures of nNOS reductase have invoked a role for large scale motio

187 ls derived from static crystal structures of nNOS reductase.

188 The interaction surface of nNOS-PDZ involves its main beta-sheet and its specific C

189 is associated with nuclear translocation of nNOS.

190 9 is a major site for poly-ubiquitination of nNOS in vitro and regulates, in large part, the CHIP-dep

191 this landscape advances our understanding of nNOS catalysis/electron transfer, and could provide new

192 keeping with a stabilising effect of DYS on nNOS protein.

193 output nitric oxide (NO) synthase 1 (NOS1 or nNOS) plays a critical role in the inflammatory response

194 ining immunoreactivity for VIP, CGRP, SP, or nNOS were found.

195 ell as more specialized markers (peripherin, nNOS) in ES-NS, both at the transcriptional and protein

196 RNA, phospho-eNOS protein, nNOS, and phospho-nNOS protein were significantly decreased; angiogenic an

197 nt increase in both total and phosphorylated nNOS and slightly elevated levels of phosphorylated eNOS

198 simple, but even more selective and potent, nNOS inhibitors.

199 Overexpression of Hsp70 promotes nNOS ubiquitination and decreases nNOS protein, and over

200 synthase (nNOS) mRNA, phospho-eNOS protein, nNOS, and phospho-nNOS protein were significantly decrea

201 was synthesized and assayed against purified nNOS enzymes, endothelial NOS (eNOS), and inducible NOS

202 was synthesized and tested against purified nNOS, endothelial NOS (eNOS), and inducible NOS (iNOS) e

203 ctly phased R16/17 was sufficient to recruit nNOS to the sarcolemma in mouse muscle.

204 SP (26 +/- 8% and 27 +/- 12%, respectively), nNOS (21 +/- 4% and 26 +/- 7%, respectively), NF200 (75

205 ociated virus (AAV) gene therapy can restore nNOS-binding mini-dystrophin expression and mitigate mus

206 ss defective mechanical signaling to restore nNOS activity in dystrophin-deficient cardiomyocytes.

207 suitable therapeutic strategy for restoring nNOS activity in dystrophin-deficient hearts and muscle.

208 ytes obtained from patients in sinus rhythm, nNOS inhibition was sufficient to recapitulate hallmark

209 Seven months later, we observed robust nNOS expression in the myocardium.

210 es the vasoregulatory actions of sarcolemmal nNOS in BMD patients, and constitutes a putative novel t

211 in(-1)) before (control) and after selective nNOS inhibition with 0.56 mg kg(-1) SMTC.

212 ds are the first highly potent and selective nNOS inhibitory agents that exhibit excellent in vitro e

213 re, we present a structure-guided, selective nNOS inhibitor design based on the crystal structure of

214 We tested the hypothesis that selective nNOS inhibition via S-methyl-l-thiocitrulline (SMTC) wou

215 nM for nNOS) and good isoform selectivities (nNOS over eNOS [440- and 540-fold, respectively] and ove

216 tory potency and good isoform selectivities (nNOS over eNOS and iNOS are 472-fold and 239-fold, respe

217 tly different immunoreactivity for CGRP, SP, nNOS, and TRPV1 (56 +/- 9%, 39 +/- 15%, 17 +/- 13%, 62 +

218 pain hypersensitivity, and increased spinal nNOS expression.

219 We suggest that, at the basal state, nNOS is maximally engaged.

220 cytes, we identified a neuronal NO synthase (nNOS) as the most relevant source of intracellular NO du

221 xide (NO) derived from neuronal NO synthase (nNOS) does not contribute to the hyperaemic response wit

222 ough the activation of neuronal NO synthase (nNOS) in these neurons.

223 xide (NO) generated by neuronal NO synthase (nNOS) initiates penile erection, but has not been though

224 servations, studies in neuronal NO synthase (nNOS) knock-out (KO) mice confirmed that PDE10A operates

225 NO synthase (eNOS) and neuronal NO synthase (nNOS) mRNA, phospho-eNOS protein, nNOS, and phospho-nNOS

226 oss of stretch-induced neuronal NO synthase (nNOS) S1412 phosphorylation.

227 hat neurons containing neuronal NO synthase (nNOS), which are morphologically associated with kisspep

228 tion via activation of neuronal NO synthase (nNOS).

229 urons expressing nitric oxide (NO) synthase (nNOS) and thus capable of synthesizing NO play major rol

230 ropathy, the neuronal nitric oxide synthase (nNOS(-/-)) deficient mouse model, which displays slow tr

231 y both human neuronal nitric-oxide synthase (nNOS) and mouse macrophage inducible NOS was inhibited b

232 Neuronal nitric oxide synthase (nNOS) and p38MAPK are strongly implicated in excitotoxic

233 e neuronal isoform of nitric oxide synthase (nNOS) and reduction of NO levels are therapeutically des

234 he potency for neural nitric oxide synthase (nNOS) and selectivity over the other two nitric oxide sy

235 nhibitors of neuronal nitric oxide synthase (nNOS) and soluble guanylyl cyclase (sGC), and can be mim

236 reactive for neuronal nitric oxide synthase (nNOS) and the neurokinin-1 receptor (NK1) have been prop

237 reactive for neuronal nitric oxide synthase (nNOS) and the receptor NK1, express the functional activ

238 nhibitors of neuronal nitric oxide synthase (nNOS) are regarded as valuable and powerful agents with

239 strophin and neuronal nitric-oxide synthase (nNOS) down-regulation and decreased protein phosphatase

240 Neuronal nitric-oxide synthase (nNOS) has various splicing variants and different subcel

241 izing enzyme neuronal nitric oxide synthase (nNOS) in nerve fibers of the murine vaginal wall.

242 Neuronal nitric oxide synthase (nNOS) inhibition is a promising strategy to treat neurod

243 (mGluR5) on neuronal nitric oxide synthase (nNOS) interneurons.

244 nhibition of neuronal nitric oxide synthase (nNOS) is a promising therapeutic approach to treat neuro

245 Neuronal nitric oxide synthase (nNOS) is a target for development of antineurodegenerati

246 nhibition of neuronal nitric oxide synthase (nNOS) is an important therapeutic approach to target neu

247 produced by neuronal nitric oxide synthase (nNOS) is implicated in neurodegenerative disorders.

248 e neuronal isoform of nitric oxide synthase (nNOS) is one of the fundamental causes underlying neurod

249 ata suggests neuronal nitric oxide synthase (nNOS) mediates the NO component of reflex cutaneous vaso

250 Neuronal nitric oxide synthase (nNOS) membrane delocalization contributes to the pathoge

251 mer ratio of neuronal nitric oxide synthase (nNOS) protein and lowered NOS activity in the MPG, which

252 dary loss of neuronal nitric oxide synthase (nNOS) that occurs in dystrophic muscle is the basis of n

253 95 (PSD-95), neuronal nitric oxide synthase (nNOS), and the N-methyl-D-aspartate (NMDA) receptor is a

254 ance P (SP), neuronal nitric oxide synthase (nNOS), neurofilament 200kDa (NF200), transient receptor

255 els (VGCCs), neuronal nitric oxide synthase (nNOS), oxidative stress from reactive oxygen species, an

256 ociated with neuronal nitric oxide synthase (nNOS), the major source of the ubiquitous and important

257 ase (ChAT)-, neuronal nitric oxide synthase (nNOS)-, and parvalbumin (PV)-positive neurons.

258 Cs of rat or neuronal nitric oxide synthase (nNOS)-Cre-tdTomato mouse recorded in vitro.

259 tive role of neuronal nitric oxide synthase (nNOS).

260 strophy lack neuronal nitric oxide synthase (nNOS).

261 ctivation of neuronal nitric oxide synthase (nNOS).

262 strophin and neuronal nitric oxide synthase (nNOS, also known as NOS1) on atrial electrical propertie

263 construct packaged into a lentiviral system, nNOS was restored.

264 We tested the hypothesis that nNOS inhibition would attenuate reflex cutaneous vasodil

265 tudies we sought to test the hypothesis that nNOS is involved in excitation of baroreflex pathways in

266 We have identified that nNOS adopts an ensemble of open and closed conformationa

267 They also indicate that nNOS has a more complex role as a modifier of dystrophic

268 lthough most current evidence indicates that nNOS localization at the sarcolemma is not required to a

269 These results suggest that nNOS and inducible NOS but not endothelial NOS are irrev

270 tion of muscle stem cells do not contain the nNOS binding site, an important functional motif within

271 domain back into utrophin did not convey the nNOS binding activity.

272 itial cells of Cajal that are reduced in the nNOS(-/-) colon.

273 Z domains of nNOS or PSD-95, nor inhibit the nNOS-PDZ/PSD-95-PDZ interface by interacting with the be

274 However, the majority of the nNOS inhibitors developed are arginine mimetics and, the

275 een presented as efficient inhibitors of the nNOS/PSD-95 protein-protein interaction and shown great

276 e highly unusual sequence specificity of the nNOS:NOS1AP interaction and involvement in excitotoxic s

277 regions of utrophin R15/16 suggests that the nNOS binding site is located in a 10-residue fragment in

278 inity of the dystrophin interaction with the nNOS-PDZ.

279 onal death are reduced by competing with the nNOS:NOS1AP interaction and by knockdown with NOS1AP-tar

280 The crystal structures of these nNOS-inhibitor complexes reveal a new hot spot that expl

281 source for NO in cardiac myocytes, but this nNOS is not located in mitochondria and does not control

282 Thus, nNOS mediates both initiation and maintenance of penile

283 Prevention of miR-31 binding to nNOS 3'UTR recovered both nNOS protein and gene expressi

284 istent with the good selectivity, 7 binds to nNOS and eNOS with different binding modes.

285 the alpha1 helix of dystrophin R17 binds to nNOS in a way uniquely defined by two pairs of the flank

286 tal structures of our NHA analogues bound to nNOS have been determined, revealing the presence of an

287 hibits NMDA-induced recruitment of NOS1AP to nNOS and in vivo in rat, doubles surviving tissue in a s

288 ic stimulus induces recruitment of NOS1AP to nNOS in rat cortical neuron culture.

289 lemma versus the importance of loss of total nNOS from dystrophic muscle remains unknown.

290 des obtained from the in vitro ubiquitinated nNOS identified 12 ubiquitination sites.

291 a new conceptual framework for understanding nNOS signaling and the benefits of NO therapies in dystr

292 However, it remains unclear whether nNOS-mediated heart protection can be translated to gene

293 It is unknown whether nNOS-mediated PO(2)mv regulation is altered in CHF.

294 Many mechanisms through which nNOS deficiency contributes to misregulation of muscle d

295 All compounds were assayed with nNOS, their IC50, KI, and kinact values were obtained, a

296 cc and the extent of NK1 colocalization with nNOS.

297 ough crystal structures of 8R complexed with nNOS and eNOS revealed a similar binding mode, the selec

298 ystrophin display selective interaction with nNOS.

299 P forms an unusually stable interaction with nNOS.

300 we show that the interaction of NOS1AP with nNOS differs radically from the classical PDZ docking as