ライフサイエンスコーパス: NSF

1 NSF can also disassemble an engineered double-length SNA

2 NSF developed within 3 months after the last gadopenteta

3 NSF develops in patients with renal impairment after exp

4 NSF disassembles soluble N-ethylmaleimide-sensitive fact

5 NSF interacts directly with MuSK with nanomolar affinity

6 NSF patients were identified between January 2000 and De

7 NSF/Sec18 disrupts these cis-SNARE complexes, allowing r

8 er, our data reveal key roles for the miR-33-NSF axis during hepatic secretion and suggest that cauti

9 Accumulating information about NSF risks led to revision of the labeling text for all o

10 of Drosophila double mutant for comatose (an NSF mutant) and Kum (a SERCA mutant), and present an ana

11 , orchestrating SNARE complex assembly in an NSF-SNAP-resistant manner together with Munc18-1.

12 tablish in vivo contributions of SNAP-25 and NSF to synaptic vesicle trafficking and define molecular

13 M adhesion were independent of apoptosis and NSF.

14 Thus, we propose that the Arr1 and NSF interaction is important for modulating normal synap

15 , but Arr1 also enhances both NSF ATPase and NSF disassembly activities.

16 ents with stage 5 chronic kidney disease and NSF were treated with oral imatinib mesylate at a dosage

17 ents with stage 5 chronic kidney disease and NSF, despite the persistence of gadolinium in the tissue

18 educed anxiety-like behavior in the EPMZ and NSF tests.

19 ative relationship between GBCA exposure and NSF.

20 rthermore, suppression of NSF expression and NSF mutation attenuate MuSK downstream signaling.

21 red to access the CIPRES Science Gateway and NSF XSEDE's large computational resources.

22 y or blocking interactions between GluR2 and NSF, or GluR2 and GRIP/PICK1 results in LTP mediated by

23 Common associations of GBCA MR imaging and NSF were acute and severe chronic renal failure and live

24 rval between contrast material injection and NSF onset was 29 days +/- 25 (standard deviation) (range

25 s detailed mutagenesis analyses of NSF-N and NSF-D1, dissecting their roles in ATP hydrolysis, SNAP.S

26 d by searching for grants awarded by NIH and NSF from inception to 2015.

27 to developing the technology through NIH and NSF grants.

28 uction were found to associate with NSF, and NSF was detected within the assembled BV.

29 fined as soluble NSF attachment protein, and NSF is defined as N-ethylmaleimide-sensitive factor) com

30 de-sensitive factor) attachment protein] and NSF proteins are conserved across eukaryotes and sustain

31 The secretomes of both SSc and NSF fibroblasts display a pattern of shared changes comp

32 ease of reticulocalbin-1 in affected SSc and NSF skin, and Western blot findings demonstrated its pre

33 three cell strains each of normal, SSc, and NSF dermal fibroblasts were pooled separately, and each

34 O increases the interaction between TRX1 and NSF, and endogenous TRX1 removes NO from S-nitrosylated

35 east in part, through existing mechanisms at NSF, NIH, and other agencies.

36 The ATPase NSF (N-ethylmaleimide sensitive factor), together with S

37 The ATPase NSF (N-ethylmaleimide-sensitive factor) and the adaptor

38 The interfaces between NSF, SNAPs, and SNAREs exhibit characteristic electrosta

39 with a median interval of 18 months between NSF symptom onset and death.

40 manner in vitro, but Arr1 also enhances both NSF ATPase and NSF disassembly activities.

41 had increased by the greatest extent in both NSF and SSc secretomes.

42 e we report structures of ATP- and ADP-bound NSF, and the NSF/SNAP/SNARE (20S) supercomplex determine

43 differences exist between ATP- and ADP-bound NSF.

44 lasma membranes and that are disassembled by NSF-SNAPs.

45 P and the ternary SNARE complex, followed by NSF binding.

46 ta directs AMPAR trafficking, as measured by NSF/GluR2-dependent increases of GluR2/3-containing rece

47 ain (NSF-N) and two AAA domains, a catalytic NSF-D1 and a structural NSF-D2.

48 We also compare NSF with other known AAA+ family members.

49 ls to identify all cases of biopsy-confirmed NSF and all patients administered a GBCA from January 1,

50 In contrast, NSF is shown here not to be required for WT PP depressio

51 ed on fluorescence dequenching, we correlate NSF-driven disassembly rates with the SNARE-activated AT

52 TRX1 promotes exocytosis by denitrosylating NSF.

53 ysis who experienced renal failure developed NSF after administration of gadobenate dimeglumine after

54 Fifteen patients developed NSF after gadolinium-enhanced MR imaging.

55 Five patients developed NSF in the peritransplant period, and four underwent a c

56 ne which patients were at risk of developing NSF appear to reduce the incidence of this complication

57 lumine doses had a higher risk of developing NSF than did those who received lower doses (odds ratio

58 The presence of a DN NSF protein resulted in low-efficiency entry of BV and t

59 nalysis of infections in cells expressing DN NSF revealed that progeny nucleocapsids were retained in

60 In cells expressing DN NSF, entering virions were trapped in the cytoplasm or t

61 The presence of DN NSF also moderately reduced trafficking of the viral env

62 NSF protomer contains an N-terminal domain (NSF-N) and two AAA domains, a catalytic NSF-D1 and a str

63 expression of either dysbindin or Drosophila NSF.

64 Each NSF protomer contains an N-terminal domain (NSF-N) and t

65 mplexes), N-ethylmaleimide-sensitive factor (NSF) (disassembles SNARE complexes after each membrane f

66 which the N-ethylmaleimide-sensitive factor (NSF) acts during synaptic vesicle (SV) trafficking was i

67 orporates N-ethylmaleimide sensitive factor (NSF) and alpha-SNAP, which disassemble syntaxin-1 and SN

68 proteins, N-ethylmaleimide sensitive factor (NSF) and O(6)-alklyguanine-DNA alkyltransferase (AGT), w

69 Soluble N-ethylmaleimide-sensitive factor (NSF) attachment protein (alpha-SNAP) is a multifunctiona

70 , soluble N-ethylmaleimide-sensitive factor (NSF) attachment protein (gamma-SNAP), and the transmembr

71 Soluble N-ethylmaleimide-sensitive factor (NSF) attachment protein alpha (alphaSNAP) is a well know

72 A soluble N-ethylmaleimide-sensitive factor (NSF) attachment protein alpha (alphaSNAP) is an essentia

73 g soluble N-ethylmaleimide-sensitive factor (NSF) attachment protein receptor (SNARE) complexes and m

74 e soluble N-ethylmaleimide-sensitive factor (NSF) attachment protein receptor (SNARE) proteins compri

75 (soluble N-ethylmaleimide-sensitive factor (NSF) attachment protein receptor)-catalyzed membrane fus

76 r soluble N-ethylmaleimide-sensitive factor (NSF) attachment protein receptors (SNAREs), phospholipid

77 [soluble N-ethylmaleimide-sensitive factor (NSF) attachment protein; alpha-SNAP] and Sec18 (NSF) per

78 a role of N-ethylmaleimide sensitive factor (NSF) in regulating MuSK endocytosis and subsequent signa

79 N-Ethylmaleimide-sensitive factor (NSF) is a homo-hexameric member of the AAA(+) (ATPases a

80 ng enzyme N-ethylmaleimide-sensitive factor (NSF) is known to be crucial for intracellular membrane f

81 Arr1 and N-ethylmaleimide-sensitive factor (NSF) that is enhanced in a dark environment when mouse p

82 modifying N-ethylmaleimide-sensitive factor (NSF), a key component of the exocytic machinery.

83 lates the N-ethylmaleimide-sensitive factor (NSF), an ATPase critical for membrane fusion events, and

84 targeting N-ethylmaleimide-sensitive factor (NSF), both in vivo and in primary hepatocytes.

85 N-ethylmaleimide-sensitive factor (NSF), first discovered in 1988, is a key factor for euka

86 prised of N-ethylmaleimide-sensitive factor (NSF), soluble NSF attachment proteins (SNAPs), and SNARE

87 se called N-ethylmaleimide-sensitive factor (NSF).

88 them the N-ethylmaleimide-sensitive factor (NSF).

89 ersistent N-ethylmaleimide-sensitive factor (NSF)/glutamate receptor subunit 2 (GluR2)-dependent traf

90 n p97 and N-ethylmaleimide sensitive factor (NSF); N1 of Pex1 is mobile, but the others are packed ag

91 can be modulated by two additional factors: NSF and alpha-SNAP.

92 ming test (FST), novelty suppressed feeding (NSF) test, and open field test (OFT).

93 maze (EPMZ) and novelty-suppressed feeding (NSF) tests, as compared with nonseparated (NS) controls,

94 ypophagia (NIH), novelty-suppressed feeding (NSF), social defeat stress, and learned helplessness.

95 t 3% body mass d(-1) (non-satiation feeding, NSF) for 4 weeks, fasted for 4d (F) and then fed to sati

96 C) O157:H7 that are non-sorbitol fermenting (NSF) and beta-glucuronidase negative (GUD(-)) carry a la

97 ognomonic for nephrogenic systemic fibrosis (NSF) in the setting of chronic renal disease with associ

98 Nephrogenic systemic fibrosis (NSF) is a fibrosing skin disorder that develops in patie

99 Nephrogenic systemic fibrosis (NSF) is a severe fibrosing disorder occurring in patient

100 Nephrogenic systemic fibrosis (NSF) is associated with gadolinium-based magnetic resona

101 sis (SSc) and nephrogenic systemic fibrosis (NSF) was performed to identify proteins that reflect the

102 diagnosis of nephrogenic systemic fibrosis (NSF), a rare disease occurring after administration of g

103 sociated with nephrogenic systemic fibrosis (NSF), a severe systemic fibrosing disorder that predomin

104 ts, including nephrogenic systemic fibrosis (NSF), the untreatable condition recently linked to gadol

105 e the risk of nephrogenic systemic fibrosis (NSF).

106 se resembling nephrogenic systemic fibrosis (NSF-like) and a broader set of rheumatological, inflamma

107 ose a processive helicase-like mechanism for NSF in which approximately 1 residue is unwound for ever

108 h no MRI (n = 1418451), the hazard ratio for NSF-like outcomes was not statistically significant.

109 sonance at each center, patients at risk for NSF at center A, and dialysis patients at center B were

110 synaptic function, we examined the role for NSF in dysbindin/BLOC-1-dependent synaptic homeostatic p

111 These findings support a role for NSF in replenishing active zone t-SNAREs for subsequent

112 These findings identify new roles for NSF and PKCepsilon in regulating synaptic inhibition thr

113 ns between 2007 and 2008 after screening for NSF risk was instituted (Fisher exact test, P = .001).

114 EPMZ on P40-41, while others were tested for NSF on P50-52.

115 6 survey of 704 National Science Foundation (NSF) Biological Sciences Directorate principal investiga

116 rts of previous National Science Foundation (NSF) projects provided for the generation of parallel mo

117 Supported by National Science Foundation (NSF), International Society of Intelligent Biological Me

118 h (NIH) and the National Science Foundation (NSF).

119 Navier and Fourier in Navier-Stokes-Fourier (NSF) equations.

120 izure-free (SF, n = 14) or non-seizure-free (NSF, n = 10).

121 f soluble N-ethylmaleimide-sensitive fusion (NSF) attachment protein receptor (SNARE) proteins, which

122 GUD(+) NSF O157:H7 strains are presumed to be precursors of GUD

123 d, pO157-2 (89,762 bp), isolated from GUD(+) NSF O157:H7 strain G5101.

124 ce of pO157-2 in six other strains of GUD(+) NSF O157:H7.

125 These results indicated that GUD(+) NSF O157:H7 strains might not be direct precursors to GU

126 ains are presumed to be precursors of GUD(-) NSF O157:H7 strains that also carry pO157.

127 ins might not be direct precursors to GUD(-) NSF O157:H7 as previously proposed but rather have evolv

128 at center C, and one patient at center D had NSF and had undergone gadolinium chelate-enhanced MR ima

129 Neither patient had NSF, while only 1 of these patients had renal disease.

130 Arginine Fingers (Arg(385) and Arg(388)) in NSF-D1 shows that each region plays a discrete role.

131 ect and independent of its known activity in NSF dependent SNARE complex disassembly.

132 ere differentially increased or decreased in NSF fibroblasts compared with normal fibroblasts.

133 ate in the development of tissue fibrosis in NSF.

134 gadodiamide) either in the sclerotic skin in NSF or in GAP.

135 serine 460 and threonine 461, and increased NSF ATPase activity, which was required for GABA(A) rece

136 lectron microscopy structures of full-length NSF and 20S supercomplex have been reported over the yea

137 in (SNAP), the adaptor protein that mediates NSF binding to the SNARE complex, did not interact with

138 maintains late-LTP by persistently modifying NSF/GluR2-dependent AMPAR trafficking to favor receptor

139 -nitrosylated NSF levels, but S-nitrosylated NSF levels decrease within 3 h after exposure to NO.

140 usly synthesized NO increases S-nitrosylated NSF levels, but S-nitrosylated NSF levels decrease withi

141 f TRX1 increases the level of S-nitrosylated NSF, prolongs the inhibition of exocytosis, and suppress

142 dogenous TRX1 removes NO from S-nitrosylated NSF.

143 he adoption of restrictive GBCA policies, no NSF cases were observed at either center.

144 e trafficking, induced elevated abundance of NSF, and caused cytotoxicity.

145 with the SNARE-activated ATPase activity of NSF.

146 dy presents detailed mutagenesis analyses of NSF-N and NSF-D1, dissecting their roles in ATP hydrolys

147 The association of NSF development with gadolinium chelate contrast agent a

148 iscoveries include gene-based association of NSF with triglyceride levels and several genes (ACSM3, E

149 We report a case of NSF developing 10 years after exposure to gadolinium.

150 mbiguously diagnose the patient as a case of NSF.

151 were searched for biopsy-confirmed cases of NSF during the same study periods.

152 MATERIALS AND A review of all cases of NSF observed at an institution from 2003 to 2008 was con

153 8 to September 2010 revealed no new cases of NSF resulting from GBCA exposure.

154 inistration were instituted, no new cases of NSF were identified among 52,954 contrast-enhanced MR ex

155 seases, timing of NSF symptom onset, date of NSF diagnosis, and clinical outcome.

156 munication were evaluated for development of NSF through September 2014.

157 No patients received diagnoses of NSF.

158 atures of this case support the diagnosis of NSF 10 years after exposure to gadolinium.

159 Patients who had a diagnosis of NSF between January 2000 and December 2006 were identifi

160 The diagnosis of NSF was confirmed histopathologically in all patients.

161 n in the dermis, supporting the diagnosis of NSF.

162 ctive on the appearance and disappearance of NSF, including its initial recognition as a discrete cli

163 In keeping with this role, disruption of NSF function results in activity-dependent redistributio

164 AR expression via the direct dissociation of NSF from GluA2.

165 structures of individual N and D2 domains of NSF and low-resolution electron microscopy structures of

166 Plk2 engagement of NSF, but not Plk2 kinase activity, was required for this

167 rms of NSF or knockdown of the expression of NSF, the key regulator of the SNARE system, significantl

168 xpression of dominant-negative (DN) forms of NSF or knockdown of the expression of NSF, the key regul

169 The incidence of NSF after gadolinium-enhanced MR imaging without screeni

170 Respective total benchmark incidence of NSF at both centers, at-risk incidence of NSF at center

171 of NSF at both centers, at-risk incidence of NSF at center A, and dialysis incidence of NSF at center

172 f NSF at center A, and dialysis incidence of NSF at center B were 37 of 65 240, 28 of 925, and nine o

173 The overall incidence of NSF was 36.5 cases per 100,000 gadolinium-enhanced magne

174 The incidence of NSF was compared before and after implementation of an i

175 The benchmark incidence of NSF was determined and expressed as the ratio of the num

176 The benchmark incidence of NSF was much greater at the two centers where gadodiamid

177 The incidence of NSF was one in 2913 patients who underwent gadodiamide-e

178 The incidences of NSF during the pre-guidelines adoption and transitional

179 Plk2 disrupted the interaction of NSF with the GluA2 subunit of AMPARs, promoting extensiv

180 Not only does Arr1 bind to the junction of NSF N-terminal and its first ATPase domains in an ATP-de

181 1 gene knocked out, the expression levels of NSF and other synapse-enriched components, including vGL

182 supercomplex and the molecular mechanism of NSF-mediated SNARE complex disassembly remained unclear

183 We propose a model of NSF-mediated disassembly in which the reaction is initia

184 NSF inhibitor N-ethylmaleimide, mutation of NSF, or suppression of NSF expression all inhibited agri

185 sk is designed to decrease the occurrence of NSF and to enhance the safe use of GBCAs in radiologic p

186 hs and up to 11 years preceding the onset of NSF, respectively.

187 ntetate dimeglumine and the time to onset of NSF.

188 As the pathogenesis of NSF is still largely unknown particularly with regard to

189 obtained, along with incidence percentage of NSF.

190 dentified by time-controlled perturbation of NSF function with a photoactivatable inhibitory peptide.

191 he conserved residues in the central pore of NSF-D1 (Tyr(296) and Gly(298)) are involved in SNAP.SNAR

192 o gadolinium and the initial presentation of NSF is typically weeks to months but has been documented

193 Neuronal SNAREs activate the ATPase rate of NSF by approximately 26-fold.

194 However, neither reduction of NSF alone or in combination with dysbindin haploinsuffic

195 lecular mechanism and energy requirements of NSF.

196 titutional policy designed to assess risk of NSF prior to GBCA use.

197 temia were associated with increased risk of NSF.

198 us study from our group, support the role of NSF in the susceptibility to cocaine dependence.

199 e N domain and of the D1 ATP-binding site of NSF.

200 tion or near-atomic resolution structures of NSF and of the 20S supercomplex, as well as recent insig

201 Structural studies of NSF and its complex with SNAREs and SNAPs (known as 20S

202 aleimide, mutation of NSF, or suppression of NSF expression all inhibited agrin-induced AChR clusteri

203 Furthermore, suppression of NSF expression and NSF mutation attenuate MuSK downstrea

204 enal status, concomitant diseases, timing of NSF symptom onset, date of NSF diagnosis, and clinical o

205 identify conserved sequences in the 3'UTR of NSF as miR-33 responsive elements and show that Nsf is s

206 ts show that a positively charged surface on NSF-N, bounded by Arg(67) and Lys(105), and the conserve

207 c electrostatic patterns, suggesting how one NSF/SNAP species can act on many different SNARE complex

208 ependent of a key alphaSNAP binding partner, NSF.

209 Cepsilon associated with NSF, phosphorylated NSF at serine 460 and threonine 461, and increased NSF A

210 an 15 mL/min, hemodialysis helped to prevent NSF.

211 n N-ethylmaleimide-sensitive fusion protein (NSF), an ATPase involved in membrane fusion events and s

212 Reducing NSF activity by inhibiting PKCepsilon could help restore

213 n related to those of the protein remodelers NSF and p97, while its overall hexameric architecture an

214 ecycling in presynaptic terminals and reveal NSF as a potential target for rapid regulation of transm

215 ated with the National Science Foundation's (NSF) National Nanotechnology Infrastructure Network (NNI

216 ) attachment protein; alpha-SNAP] and Sec18 (NSF) perform ATP-dependent disassembly of cis-SNARE comp

217 Operating independently of Sec18 (NSF) catalysis, Sec17 (alpha-SNAP) either inhibits or st

218 cofactors, including Sec17/alpha-SNAP, Sec18/NSF, and Sec1/Munc18 (SM) proteins.

219 Karyogamy requires both the Sec18p/NSF ATPase and ER/NE luminal homeostasis.

220 s are that sperm SNAREs engage in alpha-SNAP/NSF-sensitive complexes at a post-fusion stage.

221 Soluble NSF attachment protein receptors (SNAREs) are the core p

222 function of synaptotagmin-1 (syt-1):soluble NSF attachment protein receptor (SNARE) interactions dur

223 At this concentration of PI 4,5-P(2) soluble NSF attachment protein receptor (SNARE)-dependent liposo

224 We show in human cells that a soluble NSF attachment protein receptor (SNARE) complex comprise

225 transport machinery component, alpha soluble NSF attachment protein (alpha-SNAP), occurring during de

226 n analyses that identified the alpha soluble NSF attachment protein (Gm-alpha-SNAP) resistance gene b

227 amino acid transporter and an alpha soluble NSF attachment protein gene specifically in syncytia und

228 Importantly, alpha-soluble NSF attachment protein (SNAP), the adaptor protein that

229 an effect that was rescued by alpha-soluble NSF attachment protein.

230 sed screen, we identified alphaSNAP (soluble NSF [N-ethylmalemeide-sensitive factor] attachment prote

231 nsitive fusion protein 2 (dNSF2) and soluble NSF attachment protein (Snap) as strong genetic modifier

232 lasma membrane SNAREs syntaxin-1 and soluble NSF attachment protein (SNAP)-25.

233 Munc18-1 and soluble NSF attachment protein receptors (SNAREs) are critical f

234 tor (SNARE, where SNAP is defined as soluble NSF attachment protein, and NSF is defined as N-ethylmal

235 at platelet secretion is mediated by Soluble NSF Attachment Protein Receptor (SNARE) proteins from gr

236 functional trafficking steps used by soluble NSF attachment protein receptor (SNARE) proteins have be

237 Neurotransmission is achieved by soluble NSF attachment protein receptor (SNARE)-driven fusion of

238 have not been shown to use canonical soluble NSF attachment protein receptor (SNARE) machinery for fu

239 ogically, alpha-synuclein chaperones soluble NSF attachment protein receptor (SNARE) complex assembly

240 , giving rise to two target-membrane soluble NSF attachment protein receptor (t-SNARE) isoforms.

241 hylmaleimide-sensitive factor (NSF), soluble NSF attachment proteins (SNAPs), and SNAREs in synaptic

242 gh its binding to and disassembly of soluble NSF attachment protein (SNAP) receptor (SNARE) complexes

243 nderstanding the fundamental role of soluble NSF attachment protein receptor (SNARE) complexes in mem

244 ) have linked genes encoding several soluble NSF attachment protein receptor (SNARE) regulators to ca

245 and the adaptor protein alpha-SNAP (soluble NSF attachment protein) disassemble all SNARE complexes

246 alpha-SNAP [soluble NSF (N-ethylmaleimide-sensitive factor) attachment prote

247 nd that yeast vacuolar SNAREs (SNAP [Soluble NSF attachment protein] Receptors) increase the permeabi

248 sitive factor), together with SNAPs (soluble NSF attachment protein), disassembles the SNARE complex

249 The two SNAPs (soluble NSF attachment proteins) differ by only five amino acids

250 eraction of HOPS with certain SNARE (soluble NSF attachment protein receptor) proteins ensures the fu

251 s by cleaving their cytosolic SNARE (soluble NSF attachment protein receptor) substrates.

252 is mediated by assemblies of SNARE (soluble NSF-attachment protein receptor) and SM (Sec1/Munc18-lik

253 hanism that requires a unique SNARE (soluble NSF-attachment protein receptor)-dependent fusion machin

254 NAP25, an essential component of the soluble NSF (N-ethylmaleimide-sensitive factor) attachment prote

255 tor protein Myosin Vb (Myo5B) or the soluble NSF attachment protein receptor Syntaxin 3 (Stx3) distur

256 ween synaptotagmin-1 (syt-1) and the soluble NSF attachment protein receptors (SNAREs) are required d

257 In this study, the Soluble NSF-Attachment Protein (SNAP) subfamily of TPR containin

258 domains, a catalytic NSF-D1 and a structural NSF-D2.

259 anism, a skin biopsy sample from a suspected NSF patient was investigated.

260 In the photoreceptor synapse, NSF functions to sustain a higher rate of exocytosis, in

261 n, SM19712) or by inhibiting exocytosis (TAT-NSF, N-ethylmaleimide-sensitive factor inhibitor).

262 s abolished by endothelium denudation or TAT-NSF.

263 tem is involved in AcMNPV infection and that NSF is required for efficient entry and nuclear egress o

264 lication and further support the belief that NSF is associated with GBCA administration.

265 We present evidence that NSF uses a processive unwinding mechanism to disassemble

266 ions in native yeast vacuoles, we found that NSF/Sec18 activates the vacuolar cis-SNARE complex by se

267 To test the hypothesis that NSF and dysbindin/BLOC-1 participate in a pathway-regula

268 igations of substrate requirements show that NSF is capable of disassembling a truncated SNARE substr

269 The NSF incidence associated with a high dose of GBCA increa

270 The NSF incidence in the patients with acute renal failure w

271 s observed between the present study and the NSF results for continuum cases.

272 tructures of ATP- and ADP-bound NSF, and the NSF/SNAP/SNARE (20S) supercomplex determined by single-p

273 benchmark and experimental data than are the NSF results in all studied cases of rarefied problems.

274 risk haplotype for cocaine dependence in the NSF gene, encoding the protein N-Ethylmaleimide-Sensitiv

275 One model that appears to work is the NSF-funded synthesis center, an incubator for community-

276 transitioning from six-fold symmetry of the NSF ATPase domains to pseudo four-fold symmetry of the S

277 r variant (CNV) that encompasses part of the NSF gene.

278 lenges, given the evolutionary nature of the NSF risk evidence.

279 sma membrane insertion of GluA2 requires the NSF binding site within its intracellular cytoplasmic do

280 entral nodes in the SF group compared to the NSF group, preoperatively.

281 nity, and treatment of muscle cells with the NSF inhibitor N-ethylmaleimide, mutation of NSF, or supp

282 it enhanced AMPAR association with Thorase, NSF, and Nicalin.

283 his synaptic enhancement is mediated through NSF/GluR2 interactions but not vesicle-associated membra

284 f they were performed within 1 year prior to NSF onset.

285 xposed to gadopentetate dimeglumine prior to NSF onset.

286 Six1 and WASp expression, which returned to NSF levels within 16h of SF.

287 expression and found that the levels of two NSF transcripts were significantly increased in peripher

288 ith between-subject factor 'outcome' (SF vs. NSF) and within-subject factor 'treatment' (pre-operatio

289 rion production were found to associate with NSF, and NSF was detected within the assembled BV.

290 baculovirus proteins closely associate with NSF, and these results suggest their involvement in the

291 Activated PKCepsilon associated with NSF, phosphorylated NSF at serine 460 and threonine 461,

292 Human dysbindin/BLOC-1 coprecipitates with NSF and vice versa, and both proteins colocalized in a D

293 Es can be unwound in a single encounter with NSF.

294 alpha-SNAP is defective in interaction with NSF.

295 rast agent administered to each patient with NSF were determined at each center by using the standard

296 All 33 patients with NSF (mean age, 49 years; age range, 15-78 years) had adv

297 More patients with NSF had proinflammatory events, and compared with patien

298 ords was performed to identify patients with NSF that was diagnosed between January 1998 and December

299 as the ratio of the number of patients with NSF who had undergone gadolinium chelate-enhanced magnet

300 s should be aware that GAP can occur without NSF or renal disease and is associated with the use of r

301 y events, and compared with patients without NSF, these patients had lower pH, younger age, lower eGF