ライフサイエンスコーパス: NSF

1 NSF (N-ethylmaleimide sensitive factor) and its yeast co

2 NSF can also disassemble an engineered double-length SNA

3 NSF developed within 3 months after the last gadopenteta

4 NSF develops in patients with renal impairment after exp

5 NSF disassembles soluble N-ethylmaleimide-sensitive fact

6 NSF patients were identified between January 2000 and De

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

8 ormed in the presence of Munc18-1, Munc13-1, NSF and alphaSNAP, which coordinate the assembly-disasse

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

10 comparison between newer and older GBCAs, 37 NSF cases developed after exposure to older GBCAs (exact

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

12 Although NSF occurrence after exposure to newer GBCAs is very rar

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

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

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

16 M adhesion were independent of apoptosis and NSF.

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

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

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

20 ative relationship between GBCA exposure and NSF.

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

25 to developing the technology through NIH and NSF grants.

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

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

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

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

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

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

32 Age at NSF symptom onset was reported for 177 patients (mean, 4

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

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

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

36 by N-ethylmaleimide-sensitive fusion ATPase (NSF), which associates with ASIC1a-NT under acidosis, fa

37 only be closed by the action of the ATPase, NSF.

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 y prevent trans-SNARE complex disassembly by NSF-alphaSNAP, which can lead to de-priming.

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

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 mediated by the membrane fusion protein Comt/NSF and ESCRT-III components Shrub/CHMP4B and CHMP2B, fa

50 Eighteen patients with biopsy-confirmed NSF were identified, none of whom were exposed to GA.

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

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

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

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

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

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

60 expression of either dysbindin or Drosophila NSF.

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

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

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

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

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

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

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

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

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

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

71 soluble N -ethylmaleimide-sensitive factor (NSF) attachment protein receptors (SNAREs).

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

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

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

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

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

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

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

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

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

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

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

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

84 protein, N-ethylmaleimide-sensitive factor (NSF/Sec18), and its co-chaperone alpha-SNAP/Sec17.

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

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

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

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

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

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

91 ound Although nephrogenic systemic fibrosis (NSF) affects the use of gadolinium-based contrast agents

92 The risk for nephrogenic systemic fibrosis (NSF) after exposure to newer versus older gadolinium-bas

93 reactions and nephrogenic systemic fibrosis (NSF) but had lower confidence for risk of NSF because of

94 The risk of nephrogenic systemic fibrosis (NSF) from group II GBCM in patients with advanced kidney

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

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

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

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

99 ata regarding nephrogenic systemic fibrosis (NSF) risk, but there are few if any unconfounded cases o

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

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

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

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

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

105 incidence 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 Associated factors reported for NSF included exposure to GBCA group I (P < .001), dialys

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

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

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

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

114 d: We thank the National Science Foundation (NSF grant IIS-1902617) for the financial support of ICIB

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 ts as a typical National Science Foundation (NSF) Research Experiences for Undergraduates (REU) progr

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

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

120 with seizure free (SF) and non-seizure-free (NSF) outcomes.

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

122 the Funding section should be corrected from NSF grant IIS-7811367 to NSF grant IIS-1902617.

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

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

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

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

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

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

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

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

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

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

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

134 ate in the development of tissue fibrosis in NSF.

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

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

137 IPA more potently and specifically inhibits NSF/Sec18 activity than does N-ethylmaleimide, requiring

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

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

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

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

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

143 dogenous TRX1 removes NO from S-nitrosylated NSF.

144 g 83 291 patients exposed to newer GBCAs, no NSF cases developed (exact 95% CI, 0.0001 to 0.0258 case

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

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

147 with the SNARE-activated ATPase activity of NSF.

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 No unconfounded cases of NSF have been reported for the only available group III

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

154 8 to September 2010 revealed no new cases of NSF resulting from GBCA exposure.

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

156 t there are few if any unconfounded cases of NSF.

157 r institution were surveyed for any cases of NSF.

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

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

160 No patients received diagnoses of NSF.

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

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

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

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

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

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

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

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

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

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

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

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

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

177 1 gene knocked out, the expression levels of NSF and other synapse-enriched components, including vGL

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

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

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

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

182 obtained, along with incidence percentage of NSF.

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

184 s-SNARE complex formation in the presence of NSF-alphaSNAP requires both Munc18-1 and Munc13-1, as pr

185 led trans-SNARE complexes in the presence of NSF-alphaSNAP.

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

187 ed GBCA after 2008, yielding a lower rate of NSF after 2008 (P < .001).

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

189 Rates of NSF were compared through 2008 versus after 2008 and for

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

191 lecular mechanism and energy requirements of NSF.

192 Purpose To perform a systematic review of NSF.

193 s (NSF) but had lower confidence for risk of NSF because of fewer administrations in patients with se

194 e To evaluate safety of GA regarding risk of NSF in patients with impaired kidney function.

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

196 ysis, the upper bound 95% CI for the risk of NSF was 2.8%.

197 of 95% confidence interval (CI) for risk of NSF was determined.

198 alanced against and may outweigh the risk of NSF.

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

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

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

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

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

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

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

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

207 ependent of a key alphaSNAP binding partner, NSF.

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

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

210 luding immediate hypersensitivity reactions, NSF, and intracranial gadolinium retention.

211 Reducing NSF activity by inhibiting PKCepsilon could help restore

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

213 tions revealed that IPA induces a more rigid NSF/Sec18 conformation, which potentially disables the f

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

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

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

217 ec1/Munc18 (SM), Sec17/alpha-SNAP, and Sec18/NSF families.

218 erones of the SM, Sec17/alphaSNAP, and Sec18/NSF families; Rab-GTPases (Rabs); and Rab effectors.

219 nsitive factor, vesicle-fusing ATPase (Sec18/NSF)-driven disassembly that enables a new round of memb

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

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

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

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

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

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

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

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

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

238 grade Golgi Q-SNAREs (where SNARE is soluble NSF-attachment protein receptor).

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

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

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

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

243 yst and fusion driven by assembly of soluble NSF attachment protein receptor (SNARE) proteins from th

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

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

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

267 Time-resolved measurements revealed that NSF-mediated pore closure occurred via a complex 'stutte

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

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

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

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

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

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

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

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

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

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

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

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

280 d be corrected from NSF grant IIS-7811367 to NSF grant IIS-1902617.

281 Four deaths were attributed to NSF.

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

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

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

285 ified for Pb and particulate reduction under NSF/ANSI Standards 53 and 42 to residential homes in tha

286 ression (DE) analysis performed on SF versus NSF groups revealed 24 significantly differentially expr

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

288 Using a three-wave NSF-funded longitudinal survey of 559 engineering and co

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

296 eporting details on individual patients with NSF diagnosis on the basis of both clinical presentation

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

298 In patients with NSF, all MRI examinations performed and contrast agents

299 was also performed to identify patients with NSF.

300 because of the small number of patients with NSF.

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