ライフサイエンスコーパス: nNOS

1 nNOS and its receptor, guanylate cyclase (NO-GC), are ex

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

3 nNOS depletion from mdx mice prevented compensatory skel

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

5 nNOS serine1412 (S1412) phosphorylation may reduce the a

6 nNOS(S1412A) ileum expressed less phosphodiesterase-5 an

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

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

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

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

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

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

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

14 occupy a water-filled pocket surrounding an nNOS-specific aspartate residue (absent in eNOS).

15 The calbindin and nNOS immunostained neurons were the most commonly observ

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

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

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

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

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

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

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

23 eNOS and nNOS mutant mice show comparable M1 macrophage polarizat

24 iven the widespread expression of NMDARs and nNOS in the mammalian brain, we speculate that NO contro

25 ate a significant reduction in ER, Nrf2, and nNOS expression in gastric specimens.

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

27 protein complex of NMDA receptor, PSD95 and nNOS.

28 ially ubiquitinates heme-deficient nNOS (apo-nNOS) over heme-containing nNOS (holo-nNOS).

29 ed several classes of 2-aminoquinoline-based nNOS inhibitors, but these compounds had drawbacks inclu

30 However, no association was detected between nNOS DNA methylation and gene expression.

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

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

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

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

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

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

41 urons in the myenteric plexus also contained nNOS.

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

43 ficient nNOS (apo-nNOS) over heme-containing nNOS (holo-nNOS).

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

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

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

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

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

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

50 welve hours of cast immobilization decreased nNOS gene expression, whereas nNOS DNA methylation level

51 preferentially ubiquitinates heme-deficient nNOS (apo-nNOS) over heme-containing nNOS (holo-nNOS).

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

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

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

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

56 Supra-physiological DeltaPDZ nNOS expression significantly reduced myocardial fibrosi

57 treat Duchenne cardiomyopathy with DeltaPDZ nNOS gene transfer.

58 sitive ELISA to measure Hsp70:CHIP-dependent nNOS ubiquitination without interference from direct ubi

59 NOS DNA methylation levels and downregulated nNOS gene expression in atrophic slow-twitch soleus musc

60 nce the ubiquitination of only dysfunctional nNOS while leaving the native functional nNOS untouched.

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

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

63 t neuronal depolarization stimulates enteric nNOS phosphorylation by Akt to promote normal GI motilit

64 at all neurons in the ICc do in fact express nNOS in the form of discrete puncta found at the cell me

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

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

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

68 set of neurons show cytoplasmic labeling for nNOS, whereas in the central nucleus (ICc), such neurons

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

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

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

72 human nNOS, and only modest selectivity for nNOS over related enzymes.

73 At higher frequencies, nNOS S1412 had no effect.

74 all gradient and inhibits NO production from nNOS.

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

76 nal nNOS while leaving the native functional nNOS untouched.

77 S (apo-nNOS) over heme-containing nNOS (holo-nNOS).

78 -bound BH(4) triggers ubiquitination of holo-nNOS by the Hsp70:CHIP complex.

79 rget promiscuity, low activity against human nNOS, and only modest selectivity for nNOS over related

80 nzonitriles conferred the best rat and human nNOS inhibition.

81 specially potent and selective rat and human nNOS inhibitors.

82 oline and assayed them against rat and human nNOS, human eNOS, and murine and (in some cases) human i

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

84 up to nearly 900-fold selectivity for human nNOS over human eNOS.

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

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

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

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

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

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

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

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

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

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 ot only excellent potency ( K(i) < 30 nM) in nNOS inhibition but also a significantly low P-glycoprot

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

100 ty of the Hsp70:CHIP complex for inactivated nNOS.

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

102 Low-frequency depolarization increased nNOS S1412 phosphorylation and relaxed WT ileum but only

103 that 1 week of cast immobilization increased nNOS DNA methylation levels and downregulated nNOS gene

104 that 1 week of cast immobilization increased nNOS DNA methylation levels in Sol, although only a mino

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

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

107 (EFS) of wild-type (WT) mouse ileum induced nNOS S1412 phosphorylation that was blocked by tetrodoto

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

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

110 ssion in cast immobilized muscle may involve nNOS DNA methylation.

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

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

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

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

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

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

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

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

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

120 iquitination of dysfunctional but not native nNOS, and it suggests that this therapeutic strategy wil

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

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

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

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

125 In this study, we synthesized new nNOS inhibitors based on 7-phenyl-2-aminoquinoline and a

126 t cell type-specific expression of the NMDAR/nNOS complex in the mammalian brain, our data suggest th

127 ) and neuronal nitric oxide synthase (nNOS), nNOS enzymatic activity, activation of MK2 (MAPK-activat

128 oped and characterized a nonphosphorylatable nNOS(S1412A) knock-in mouse and evaluated its enteric ne

129 nt additional experiments with neuronal NOS (nNOS) and inducible NOS (iNOS) variants (nNOS W409F and

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

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

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

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

134 he subcellular distribution of neuronal NOS (nNOS).

135 NOS1AP/nNOS interaction regulates small GTPases, iron transport

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

137 egulate nitrergic function by improving Nrf2/nNOS expression in experimental hyperglycemia.

138 the ICc is solely mediated by activation of nNOS and sGC.

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

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

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

142 Modulation of the activity of nNOS-expressing neurons drove changes in the basal and e

143 We concluded that chronic adaptation of nNOS gene expression in cast immobilized muscle may invo

144 This response is abolished by blockade of nNOS or sGC, indicating that the NMDA effect is mediated

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

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

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

148 Moreover, depletion of nNOS-bound BH(4) triggers ubiquitination of holo-nNOS by

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

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

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

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

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

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

155 7201 do not interact with the PDZ domains of nNOS or PSD-95, nor inhibit the nNOS-PDZ/PSD-95-PDZ inte

156 unchanged, suggesting that downregulation of nNOS gene expression by short-term muscle inactivity is

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

158 with the extent of selective elimination of nNOS interneurons.

159 quitous, but highly localized, expression of nNOS throughout the ICc and demonstration of the dramati

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

161 Furthermore, this punctate form of nNOS expression may exist and have gone unnoticed in oth

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

163 em, we have established that inactivation of nNOS by heme or tetrahydrobiopterin (BH(4)) alteration a

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

179 Thus, phosphorylation of nNOS S1412 is a significant regulatory mechanism for nit

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

181 The presence of nNOS throughout this sensory nucleus argues for a major

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

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

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

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

186 o understand the physiologic significance of nNOS S1412 phosphorylation.

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

188 onships in multiple conformational states of nNOS.

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

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

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

192 is associated with nuclear translocation of nNOS.

193 nalog JG-258, enhances the ubiquitination of nNOS 3-fold.

194 nd nNOSu (i.e. the major splicing variant of nNOS in skeletal muscle) decreased.

195 e nNOSbeta gene, another splicing variant of nNOS, in EDL was unchanged by cast immobilization, where

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

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

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

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

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

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

202 Punctate nNOS appears at glutamatergic synapses in a complex with

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

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

205 However, the mechanisms regulating nNOS expression in atrophic muscle remain unclear.

206 relaxed WT ileum but only partially relaxed nNOS(S1412A) ileum.

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

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

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

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

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

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

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

214 pain hypersensitivity, and increased spinal nNOS expression.

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

216 ted by the activity of neuronal NO synthase (nNOS) following Ca(2+) entry through extrasynaptic NMDA-

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

218 Neuronal NO synthase (nNOS) is activated by Ca(2+)/calmodulin to produce NO, w

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

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

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

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

223 Neuronal NO(*) Synthase (nNOS) was examined for levels and localization in neuron

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

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

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

227 Blockers of neuronal nitric oxide synthase (nNOS) and of NMDA receptors blocked potentiation, indica

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

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

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

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

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

233 ke 2 (Nrf2), neuronal Nitric Oxide Synthase (nNOS) expression and nitrergic relaxation in gastric neu

234 sociation of neuronal nitric oxide synthase (nNOS) from postsynaptic density 95 (PSD95) and a reduced

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

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

237 Neuronal nitric oxide synthase (nNOS) in skeletal muscle is a key regulator of skeletal

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

239 netration of neuronal nitric oxide synthase (nNOS) inhibitors toward the development of new drugs for

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

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

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

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

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

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

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

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

248 Neuronal nitric oxide synthase (nNOS) regulates muscle atrophy in skeletal muscle.

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

250 r studies on neuronal nitric oxide synthase (nNOS), a client of the Hsp90 and Hsp70 chaperone system,

251 nhibition of neuronal nitric oxide synthase (nNOS), an enzyme implicated in neurodegenerative disorde

252 protein) and neuronal nitric oxide synthase (nNOS), nNOS enzymatic activity, activation of MK2 (MAPK-

253 We show that neuronal nitric oxide synthase (nNOS), the enzyme that synthesizes nitric oxide (NO), oc

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

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

256 e inhibitory neuronal nitric oxide synthase (nNOS)-expressing cells.

257 yramidal and neuronal nitric oxide synthase (nNOS)-expressing neurons.

258 alretinin, and neural nitric oxide synthase (nNOS).

259 ctivation of neuronal nitric oxide synthase (nNOS).

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

261 the brain by neuronal nitric oxide synthase (nNOS).

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

263 s containing neuronal nitric oxide synthase (nNOS, ~7 million in number, with both small and large so

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

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

266 We hypothesized that nNOS expression in atrophic muscle is regulated by DNA m

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

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

269 Our multi-labeling studies reveal that nNOS puncta form multiprotein complexes with NMDA recept

270 ia porcellus, male and female), we show that nNOS occurs in two distinct cellular distributions.

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

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

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

274 istalsis and segmentation were faster in the nNOS(S1412A) ileum.

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

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

277 uscle is regulated by DNA methylation of the nNOS promotor in soleus (Sol; slow-twitch fibre dominant

278 The abundance of the nNOS protein and cell membrane (especially type IIa fibr

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

280 cle atrophy by epigenetic mechanisms via the nNOS/NO pathway.

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

282 These nNOS, calretinin, and parvalbumin immunopositive WMICs,

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

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

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

286 ansport by NMDARs is also tightly coupled to nNOS activity and NO production, it has yet to be determ

287 hic Sol, the gene expression levels of total nNOS and nNOSu (i.e. the major splicing variant of nNOS

288 on decreased gene expression levels of total nNOS and nNOSu in Sol.

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

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

291 OS (nNOS) and inducible NOS (iNOS) variants (nNOS W409F and iNOS K82A and V346I) and computational me

292 tion decreased nNOS gene expression, whereas nNOS DNA methylation levels were unchanged, suggesting t

293 muscle mass; however, it is unclear whether nNOS expression is regulated by DNA methylation.

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

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

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

297 cc and the extent of NK1 colocalization with nNOS.

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

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