ライフサイエンスコーパス: SNAP

1 SNAP appears most likely to capture inherent individual

2 SNAP caused a depolarizing shift in voltage-dependent N-

3 SNAP eliminates those errors by calculating the correct

4 SNAP exhibited excellent storage stability when encapsul

5 SNAP is likely heterogeneous, with a subset of this grou

6 SNAP near-infrared imaging and tandem-affinity purificat

7 SNAP-25 is a Q-SNARE protein mediating exocytosis of neu

8 SNAP-25 regulates Ca(2+) channels, with potentially impo

9 SNAP-47 also interacted with ER and Golgi syntaxin 5 and

10 SNAP-47 preferentially interacted with the trans-Golgi n

11 SNAP-47 silencing further shifted the subcellular locali

12 SNAPs interact with the SNARE complex with an opposite s

13 By using an uncapped PLGA (Mw=24,000-38,000) SNAP was slowly released for over 10days, whereas by usi

14 synaptic transmission (syntaxin-1, Munc18-1, SNAP-25), whereas other proteins involved in the same mo

15 n 1-4 DIV upon loss of t-SNAREs (syntaxin-1, SNAP-25) or Munc18-1, but not v-SNAREs (synaptobrevins/V

16 We show that replacement of 10 SNAP-23 residues with their SNAP-25 counterparts effects

17 he spontaneous assembly of a 2:1 syntaxin-1a:SNAP-25 complex on target membranes that kinetically alt

18 phorylate synaptosome-associated protein 23 (SNAP-23), which in turn enables the formation of the SNA

19 to mimic synaptosomal-associated protein 25 (SNAP-25) are utilized in gold nanoparticle-based assays

20 (Stx1), synaptosomal-associated protein 25 (SNAP-25), and synaptobrevin-2 (Syb2).

21 VAMP-2), synaptosomal-associated protein 25 (SNAP-25), syntaxin, and shortened peptides representing

22 cleaves Synaptosomal-Associated Protein 25 (SNAP-25), the substrate of wt BoNT/A, but exhibits slowe

23 bstrate, synaptosomal-associated protein 25 (SNAP-25).

24 RE synaptosomal-associated protein of 25kDa (SNAP-25B), which disrupt neurotransmitter release and ha

25 sting of 1:1:1 syntaxin-1a(residues 183-288):SNAP-25:syb(residues 49-96) was found to greatly acceler

26 dicate that dysferlin accelerates syntaxin 4/SNAP-23 heterodimer formation and SNARE-mediated lipid m

27 The remaining 47,595 SNAP households in the county received usual benefits.

28 Rab2, Rab7, and its effector, PLEKHM1; and a SNAP receptor complex consisting of Syntaxin 13, Snap29,

29 In our approach, a SNAP-tagged cell-surface receptor of interest is conjuga

30 Among participants who received a SNAP benefit </=15 d before being surveyed, energy intak

31 lity of these dye conjugates when bound to a SNAP-tag fused membrane protein in live cells.

32 eling of live cells was demonstrated using a SNAP-tag approach to install the boronic acid reagent on

33 a DNA-linked antibody or covalently using a SNAP-tag.

34 Previous results with a SNAP-25 construct lacking the nine C terminal residues (

35 wild type and QUAD opsins, with or without a SNAP tag for fluorescence labeling.

36 sequences for diseases involving an aberrant SNAP-25 expression level.

37 de (NO) donor S-nitroso-acetylpenicillamine (SNAP) and silicone oil in commercial medical grade silic

38 , and Pelham, and Version IV Scale for ADHD (SNAP-IV), and the neuropsychological function was assess

39 bacter baumannii and Pseudomonas aeruginosa (SNAP and POP studies).

40 of individuals with neurodegeneration alone (SNAP) later demonstrated Abeta+.

41 alpha-SNAP [soluble NSF (N-ethylmaleimide-sensitive factor) at

42 alpha-SNAP is a crucial component of Orai1 channels, and its d

43 osition fusion triggers such as Sec 17/alpha-SNAP and/or synaptotagmin, which insert their apolar "we

44 usion factor attachment protein alpha (alpha-SNAP), but not Galpha13, inhibited both basal and thromb

45 n possess multiple repeat copies of an alpha-SNAP gene (Glyma.18G022500) that encodes atypical amino

46 calcium release activated channel, and alpha-SNAP is necessary for its function.

47 ylmaleimide sensitive factor (NSF) and alpha-SNAP, which disassemble syntaxin-1 and SNAP-25 heterodim

48 f alpha-SNAP with Stim1 and Orai1, and alpha-SNAP-depleted cells show faster and less constrained mob

49 ted by two additional factors: NSF and alpha-SNAP.

50 face of the Golgi apparatus and binds alpha-SNAP-like proteins, but has no known role in resistance.

51 tive factor that requires the cofactor alpha-SNAP to first bind to the assembled SNARE complex.

52 In conclusion, alpha-SNAP plays a critical role in the balance between follic

53 pha12 to alpha-SNAP, and an engineered alpha-SNAP binding-domain minigene peptide blocked basal and e

54 Furthermore, alpha-SNAP depletion significantly reduces fluorescence resona

55 Gm-alpha-SNAP and Gm-SYP38 overexpression induce the transcriptio

56 On the other hand, alpha-SNAP-mutant mice show a reduction in alpha-SNAP protein

57 a-SNAP-mutant mice show a reduction in alpha-SNAP protein levels.

58 Sodium permeation in alpha-SNAP-deficient cells cannot be corrected by tethering mu

59 ic decline in fertility is observed in alpha-SNAP-mutant females.

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

61 ovarian tissue and the consequences of alpha-SNAP (M105I) mutation (hyh mutation) in folliculogenesis

62 we examined the expression pattern of alpha-SNAP in ovarian tissue and the consequences of alpha-SNA

63 er, these data reveal a unique role of alpha-SNAP in the on-site functional assembly of Orai1 subunit

64 We suggest that binding of alpha-SNAP to the SNARE complex affects the ability of the SNA

65 opy reveals sustained coassociation of alpha-SNAP with Stim1 and Orai1, and alpha-SNAP-depleted cells

66 d allele of Glyma18g02590 (a predicted alpha-SNAP [alpha-soluble N-ethylmaleimide-sensitive factor at

67 itive factor (NSF) attachment protein (alpha-SNAP) is a multifunctional protein that participates in

68 itive factor (NSF) attachment protein; alpha-SNAP] and Sec18 (NSF) perform ATP-dependent disassembly

69 Remarkably, alpha-SNAP depletion induces formation of higher-order Orai1 o

70 we found that the resistance-type Rhg1 alpha-SNAP is defective in interaction with NSF.

71 ently of Sec18 (NSF) catalysis, Sec17 (alpha-SNAP) either inhibits or stimulates SNARE-mediated fusio

72 Here we show that alpha-SNAP hypomorph, hydrocephalus with hopping gait, Napa(hy

73 ranules and liposomes we now show that alpha-SNAP on its own interferes with the zippering of membran

74 Our results showed that alpha-SNAP protein is highly expressed in GCs and its expressi

75 i1 C-terminal tail, demonstrating that alpha-SNAP regulates functional assembly and calcium selectivi

76 Here we show that alpha-SNAP regulates on-site assembly of Orai1 dimers into cal

77 15 mediated the binding of Galpha12 to alpha-SNAP, and an engineered alpha-SNAP binding-domain minige

78 nta expression of resistance-type Rhg1 alpha-SNAPs depleted the abundance of SNARE-recycling 20S comp

79 e cytotoxicity of resistance-type Rhg1 alpha-SNAPs.

80 Expression of these alpha-SNAPs counteracted the cytotoxicity of resistance-type R

81 hyperaccumulate relative to wild-type alpha-SNAPs at the nematode feeding site, promoting the demise

82 lization revealed that resistance-type alpha-SNAPs specifically hyperaccumulate relative to wild-type

83 loci that encode canonical (wild-type) alpha-SNAPs.

84 uality of dietary intake in African American SNAP participants.

85 HIP significantly increased FV intake among SNAP participants, closing approximately 20% of the gap

86 relative to stage 0 (t = 4.38; P < .001) and SNAP (t = 4.08; P < .001).

87 P < .001), stage 1 (t = -2.48; P = .03), and SNAP (t = -2.26; P = .03).

88 P < .001), stage 2+ (t = 2.10; P = .04), and SNAP (t = 9.32; P < .001), and those with stage 2+ had a

89 42]; stage 1, beta = -0.242 [SE, 0.051]; and SNAP, beta = -0.157 [SE, 0.044]; P </= .001), whereas th

90 alpha-SNAP, which disassemble syntaxin-1 and SNAP-25 heterodimers.

91 REs consisting of full-length syntaxin 1 and SNAP-25B at the membrane, as measured by fluorescence po

92 Individuals in stage 0, stage 1, and SNAP did not differ from one another in cognitive perfor

93 esicles bearing the t-SNAREs syntaxin-1A and SNAP-25 were preincubated with Munc18 for 30 min.

94 membrane t-SNARE complex of syntaxin-1a and SNAP-25 while simultaneously binding the lipid bilayer a

95 d the plasma membrane SNAREs syntaxin-1a and SNAP-25 with a 1:1:1 stoichiometry.

96 SNARE complex consisting of syntaxin-1A and SNAP-25A via the accessory domain.

97 1, preventing binding to synaptobrevin-2 and SNAP-25 to form the ternary SNARE complex.

98 axin 3 and syntaxin 4 as well as SNAP-23 and SNAP-29 completes cargo secretion.

99 ters, and both splice variants, SNAP-25a and SNAP-25b, can participate in this process.

100 ferlin and the SNARE proteins syntaxin 4 and SNAP-23.

101 umulation relative to stage 0 (t = 8.44) and SNAP (t = 6.61) (P < .001 for all comparisons).

102 umulation relative to stage 0 (t = 4.96) and SNAP (t = 4.06), and those with stage 1 had accelerated

103 e-permeable dyes SiR and ATTO590 as Halo and SNAP substrates.

104 ND-), 1 (Abeta+/ND-), and 2 (Abeta+/ND+) and SNAP (Abeta-/ND+).

105 VD disparities between SNAP participants and SNAP-ineligible individuals, by approximately 8% (10 DPP

106 PVN presympathetic neurons through PKC- and SNAP-25-mediated surface expression of NMDARs.

107 ns) packaged food and beverage purchases and SNAP status [current participant, income-eligible nonpar

108 plex formed by syntaxin-1, synaptobrevin and SNAP-25, as well as on complexins, which bind to the SNA

109 The SNAREs Syntaxin-1, Synaptobrevin, and SNAP-25 play a central role in membrane fusion, forming

110 wo plasma membrane SNAREs syntaxin (syx) and SNAP-25 draws the two membranes together, but the events

111 identified an interaction between VAMP7 and SNAP-47 using a proteomics approach.

112 udies of NSF and its complex with SNAREs and SNAPs (known as 20S supercomplex) started about 20years

113 embrane syntaxin 3 and syntaxin 4 as well as SNAP-23 and SNAP-29 completes cargo secretion.

114 ld level, to examine the association between SNAP status and purchases while controlling for sociodem

115 t potentially reduce CVD disparities between SNAP participants and SNAP-ineligible individuals, by ap

116 hlorfenuron impaired the interaction between SNAP-25 and its chaperone Hsc70, decreasing SNAP-25 leve

117 n assay revealed direct interactions between SNAP-25 and Gbetagamma subunits in retinal synaptic laye

118 improve food and beverage purchases in both SNAP and non-SNAP households.

119 Our findings suggest that both SNAP-25B mutations impair synaptic exocytosis by destabi

120 d recruitment of syntaxin-1 from clusters by SNAP-25 expression makes it available for regulating Ca(

121 ristics, we found significant differences by SNAP status of purchases of fruit, processed meat, salty

122 ility of elasticity measurements provided by SNAP could improve significantly the applicability of ce

123 i-A monoclonal antibodies but did not cleave SNAP-25 as expected for BoNT/A.

124 genic complexes incorporating BoNT/A-cleaved SNAP-25.

125 ever, their serotype A (BoNT/A) that cleaves SNAP-25 (synaptosomal-associated protein of 25 kDa) has

126 sing genetically encoded chemical tags CLIP, SNAP, Halo, and TMP for tissue labeling; this resulted i

127 o-ET/subtomogram averaging with the clonable SNAP tag, a widely used cell biological probe to visuali

128 In contrast, SNAP only slightly inhibited P/Q-type and L-type current

129 nging the stoichiometry of syntaxin-1a and d-SNAP-25 in the target bilayer had significant effects on

130 e, monomeric syntaxin-1a and dodecylated (d-)SNAP-25 are separately reconstituted into proteoliposome

131 SNAP-25 and its chaperone Hsc70, decreasing SNAP-25 levels in cultured neuroendocrine cells, and inh

132 were compared between patients with distinct SNAP (Abeta- and neurodegeneration-positive [Abeta-N+])

133 In this study, NO donors (SNAP and DETA-NONOate) inhibited DC antigen presentation

134 dues with their SNAP-25 counterparts effects SNAP-25-like cleavability.

135 MPNs and model cell lines expressing either SNAP-tagged Notch or vascular endothelial cadherin (VE-c

136 By means of the existing SNAP-25-toxin co-crystal structure, molecular dynamics s

137 staining showed that endogenous or exogenous SNAP-25 expression recruits syntaxin-1 from clusters on

138 We examined five SNAP-25 mutations designed to interfere with syt-1 inter

139 g this technique, we fuse an N-terminal FLAG-SNAP-tag to TERT, which allows us to reliably detect TER

140 an 40S ribosomal subunits with a fluorescent SNAP-tag at ribosomal protein eS25 (RPS25).

141 -molecule performance of various fluorescent SNAP and HALO ligands.

142 as fruit, vegetables, and whole grains, for SNAP participants when their benefits run out.

143 nhibitory activity in a cell-based model for SNAP-25 cleavage and an ex vivo assay for BoNT/A-mediate

144 intrinsic endoprotease activity specific for SNAP-25, a key protein for presynaptic neurotransmitter

145 itive factor (NSF) attachment protein (gamma-SNAP), and the transmembrane protein Nicalin.

146 e ribbon synapses is regulated by Gbetagamma/SNAP-25 interactions indicates that these mechanisms are

147 by BoNT/A, supporting a role for Gbetagamma/SNAP-25 interactions.

148 ides the first demonstration that Gbetagamma/SNAP-25 interactions regulate synaptic function at a rib

149 nces of the target species using GlimmerHMM, SNAP, and AUGUSTUS pipelines, followed by MAKER2 program

150 tyl-S-nitroso-d,l-penicillaminami de (glycol-SNAP-2) were also capable of stimulating native sarcKATP

151 years), 64 (25.9%) were classified as having SNAP.

152 The incorporation of an engineered hCG-SNAP fusion reporter protein (human chorionic gonadotrop

153 assay formats, with either mAb10F12 or His6-SNAP-25 coupled to the biosensor chip.

154 Human SNAP-23 cleaving mutants were isolated using a newly est

155 lyses the reason for the resistance of human SNAP-23, an isoform of SNAP-25.

156 ockets to corresponding amino acids of human SNAP-23.

157 ined food and beverage purchase behaviors in SNAP participants with the use of electronic purchase da

158 f key food, beverage, and nutrient groups in SNAP participants and nonparticipants.Using a data set o

159 associated with synaptic function, including SNAP-25, Rab3A and PSD-95, and with axonal transport and

160 d SNAP status.American households, including SNAP households, show room for improvement in the nutrit

161 Using the time-reporter insulin-SNAP to track age-distinct SGs we now show that their dy

162 Synaptosomal-associated protein of 25 kDa (SNAP-25) is a key molecule in the soluble N-ethylmaleimi

163 Single molecule experiments with labeled SNAP-25 indicate that the reduction of vesicle associati

164 is compatible with subcellular localization SNAP-tag fusion protein methodologies and use appropriat

165 including SLC6A3, DRD5, DRD4, SLC6A4, LPHN3, SNAP-25, HTR1B, NOS1 and GIT1.

166 r Abeta+ counterparts, all patients with MCI SNAP subtypes displayed better preservation of temporopa

167 to O(6)-methylguanine DNA methyltransferase (SNAP-tag) fusion proteins.

168 -methylguanine DNA methyltransferase (MGMT), SNAP-tag, and lactoferrin, with four different probes.

169 of observations with potentially misreported SNAP status.American households, including SNAP househol

170 The Mobyle SNAP Workbench web portal allows end users to (i) execut

171 a membrane requires two classes of molecules-SNAP receptor (SNARE) and Sec1/Munc18 (SM) protein.

172 The highest payload was 0.56(+/-0.01) mumol SNAP/mg microspheres.

173 WT and mutant SNAP-47 overexpression impaired VAMP7 exocytic activity.

174 We mutated SNAP-25 within the recently identified region I and regi

175 and beverage purchases in both SNAP and non-SNAP households.

176 -eligible and higher-income nonparticipants, SNAP participants purchased an additional approximately

177 The interfaces between NSF, SNAPs, and SNAREs exhibit characteristic electrostatic p

178 chestrating SNARE complex assembly in an NSF-SNAP-resistant manner together with Munc18-1.

179 a membranes and that are disassembled by NSF-SNAPs.

180 ectrostatic patterns, suggesting how one NSF/SNAP species can act on many different SNARE complexes.

181 tures of ATP- and ADP-bound NSF, and the NSF/SNAP/SNARE (20S) supercomplex determined by single-parti

182 Phylogenetic analysis of SNAP genes from 22 diverse plant species showed that SNA

183 25 drastically decreased the cleavability of SNAP-25.

184 Cleavage of SNAP-25 by BoNT/A generates neo-epitopes which can be de

185 es assembly of the SNARE complex composed of SNAP-25, syntaxin-1, and synaptobrevin-2 (sybII) protein

186 The inhibitory effect of SNAP on N-type currents was blocked by the sulfhydryl-sp

187 The etiology of SNAP in this population remains unclear.

188 Our data demonstrate that fusion of SNAP with target proteins allowed for protein localizati

189 -1 inhibits Ca(2+) currents independently of SNAP-25.

190 e resistance of human SNAP-23, an isoform of SNAP-25.

191 utant engineered to express normal levels of SNAP-25 but only SNAP-25a.

192 In mammalian systems, loss of SNAP-25 or Syb2 severely impairs neurotransmitter releas

193 suitability in single-molecule microscopy of SNAP-tag fusion proteins in live cells.

194 g., total calories and sodium).Regardless of SNAP status, households had low mean purchases of fruit,

195 axin-1A by Munc18a and subsequent release of SNAP-25 (i.e. Munc18a captures syntaxin-1A via its high

196 In addition, shedding of SNAP-Tac into the medium was greatly influenced by its O

197 To our knowledge, this is the first use of SNAP-tag reactions to modify benzylguanine-functionalize

198 The areas of SNAPs after tactile stimulation recovered to 61 +/- 11%

199 s for the treatment of diseases that rely on SNAP-23-mediated hypersecretion.

200 to express normal levels of SNAP-25 but only SNAP-25a.

201 first abnormality observed upon Munc18-1 or SNAP-25 loss within 3 DIV.

202 resynaptic proteins Munc18-1, syntaxin-1, or SNAP-25 is known to produce cell death, but the underlyi

203 hat cell death upon Munc18-1, syntaxin-1, or SNAP-25 loss occurs via a degenerative pathway unrelated

204 s proteins, such as syntaxin-1, Munc18-1, or SNAP-25, modulate alpha-synuclein neuropathy and/or are

205 upon depleting syntaxin-1, Munc18-1, and/or SNAP-25, well before synapse formation.

206 Our SNAP-25b-deficient mouse may represent a diabesity model

207 d high tau), and suspected non-AD pathology (SNAP) (high Abeta and high tau).

208 a+/ND+) or suspected non-AD pathophysiology (SNAP; Abeta-/ND+).

209 ected non-Alzheimer disease pathophysiology (SNAP) than in Abeta-positive (Abeta+) counterparts.

210 ected non-Alzheimer disease pathophysiology (SNAP), defined as biomarker negative for beta-amyloid (A

211 NO donor S-nitroso-N-acetyl-D-penicillamine (SNAP) was encapsulated within poly(lactic-co-glycolic ac

212 O donor S-nitroso-N-acetyl-DL-penicillamine (SNAP) rapidly reduced N-type currents when Cav2.2 was co

213 he Social Networks among Appalachian People (SNAP) Study (2008-2010).

214 ereas expression of selective phosphomimetic SNAP-23 mutants (Ser95-->Glu95 but not Ser20-->Glu20) re

215 Ectopic expression of non-phosphorylated SNAP-23 mutant (Ser95-->Ala95) significantly reduces PKM

216 pectrometry confirm that PKM2 phosphorylates SNAP-23 at Ser95.

217 The sensory nerve action potentials (SNAPs) remained dispersed and areas recovered to 23 +/-

218 e standardized nanomechanical AFM procedure (SNAP) ensures the precise adjustment of the AFM optical

219 Supplemental Nutritional Assistance Program (SNAP) and recipients' dietary quality during the days an

220 o Supplemental Nutrition Assistance Program (SNAP) participants for purchasing targeted FVs (TFVs).

221 g Supplemental Nutrition Assistance Program (SNAP) participants only.

222 n Supplemental Nutrition Assistance Program (SNAP) participants than in nonparticipants after the 200

223 e Supplemental Nutrition Assistance Program (SNAP), which is the largest federal nutrition assistance

224 rimary neurons, select derivatives protected SNAP-25 by up to 89%.

225 s study, the Soluble NSF-Attachment Protein (SNAP) subfamily of TPR containing proteins is characteri

226 antly, alpha-soluble NSF attachment protein (SNAP), the adaptor protein that mediates NSF binding to

227 ntaxin-1 and soluble NSF attachment protein (SNAP)-25.

228 leimide-sensitive factor attachment protein (SNAP).

229 lecule fluorescence measurements of purified SNAP-tagged constructs revealed that both proteins are m

230 Among participants who received SNAP benefits >15 d before being surveyed, energy intake

231 We found that although both green and red SNAP ligands provide sufficient fluorescent signal, only

232 elling of specific proteins with a reducible SNAP-tag substrate.

233 Conversely, transfer of each of the replaced SNAP-23 residues to SNAP-25 drastically decreased the cl

234 struct lacking the nine C terminal residues (SNAP-25Delta9) showed changed fusion pore properties, su

235 ower for each 1-d increase in the time since SNAP distribution (TSSD).

236 sis of lysosomes using the exocyst and SNARE SNAP-29 to form a large protrusion that invades vulval t

237 in-3; both additionally required the Q-SNARE SNAP-47 and the R-SNARE synatobrevin-2.

238 The C2F domain directly binds the t-SNARE SNAP-25 maximally at 100 muM and with reduction at 0 muM

239 ion Assessor, FATHMM, LRT, PANTHER, PhD-SNP, SNAP, SNPs&GO and MutPred), 3 conservation scores (GERP+

240 leavage of the endogenous protein substrate, SNAP-25, even at low muM concentrations of complexes.

241 c13 additionally ensures the proper syntaxin/SNAP-25 subconfiguration.

242 ost lives, while a 30% F&V subsidy targeting SNAP participants would most reduce socio-economic dispa

243 attributable to a 30% F&V subsidy targeting SNAP participants, the approximately 25,800 (95% UI 24,3

244 We conclude that SNAP-47 plays a role in the proper localization and func

245 ouse adrenal chromaffin cells and found that SNAP-25 inhibits Ca(2+) currents, with the B-isoform bei

246 We found that SNAP-47 mainly localized to cytoplasm, the endoplasmic r

247 nd lipid and glucose homeostases showed that SNAP-25b-deficient mice fed with control diet developed

248 stral lineages, supports the hypothesis that SNAPs were duplicated and derived from a common ancestor

249 es from 22 diverse plant species showed that SNAPs were distributed in six monophyletic clades corres

250 The SNAP (Smoking and Nicotine in Pregnancy) trial compared

251 The SNAP system consists of a self-labelling enzyme tag, whi

252 The SNAP-25 K201Q mutant showed no changes compared with SNA

253 The SNAP-tag is an intrinsically monovalent and highly speci

254 guideRNA and editing enzyme by applying the SNAP-tag technology, a process that we demonstrate here

255 at the positively charged amino acids at the SNAP-25 C terminus promote tight SNARE complex zippering

256 ral lobes were indistinguishable between the SNAP and stage 0 groups (entorhinal cortex, beta = -0.00

257 In soybean, five members constitute the SNAP gene family: GmSNAP18, GmSNAP11, GmSNAP14, GmSNAP02

258 stribution volume ratio, 1.08 [0.05] for the SNAP group; 1.09 [0.05] for the stage 1 group).

259 d introduction of a peptide derived from the SNAP-25 C terminus.

260 Compared with the stage 0 group, the SNAP group was not more likely to have subthreshold PiB

261 However, the SNAP-targeted intervention might potentially reduce CVD

262 Participants in the SNAP and participants in the National School Lunch Progr

263 relation between participants' stages in the SNAP cycle and their macronutrient consumption, Healthy

264 SE, 0.027]; P >/= .88) and were lower in the SNAP group compared with the stage 2 group (entorhinal c

265 d susceptible parents, the divergence of the SNAP gene family is analysed over time.

266 Next, we confirmed the utility of the SNAP-tag for studying protein turnover by pulse-chase la

267 Here we use the SNAP tag system to examine the site of delivery of the a

268 polarized MDCK epithelial cells, we used the SNAP and CLIP labeling systems to fluorescently tag temp

269 -0.157 [SE, 0.044]; P </= .001), whereas the SNAP group showed a diminished practice effect over time

270 Pretreatment with the SNAP-25 cleaving protease BoNT/A inhibited L-AP4 effects

271 s in the very early and late stages of their SNAP cycles.

272 eplacement of 10 SNAP-23 residues with their SNAP-25 counterparts effects SNAP-25-like cleavability.

273 These SNAP-25b-deficient mice were exposed to either a control

274 of each of the replaced SNAP-23 residues to SNAP-25 drastically decreased the cleavability of SNAP-2

275 ssed the power of bioorthogonal tethering to SNAP and CLIP protein tags to create a family of light-g

276 As expected, there was no activity toward SNAP-25 or syntaxin.

277 mproved by modulating their activity towards SNAP-25.

278 A C-terminally truncated SNAP-47 was impaired in interaction with VAMPs and affec

279 The two SNAPs (soluble NSF attachment proteins) differ by only f

280 d reanneal; pulse-chase-pulse analysis using SNAP-tagged claudins showed preferential incorporation o

281 fluorescent competitor of the analyte using SNAP-tag in conjugation with a second fluorophore that i

282 tion with high efficiency and fidelity using SNAP-linked gold nanoparticles, without disrupting the n

283 neurotransmitters, and both splice variants, SNAP-25a and SNAP-25b, can participate in this process.

284 AR (EhBAR), were chosen for localization via SNAP tag labeling and localized to the site of partially

285 6 were stage 1, 28 were stage 2, and 46 were SNAP.

286 serum (0.1 LD50/ml serum) was attained when SNAP-25 was coupled directly to the chip, followed by se

287 In this study, clinically normal adults with SNAP did not exhibit evidence of elevated tau levels, wh

288 nomeric form and subsequently assembled with SNAP-25 in detergent with the correct 1:1 stoichiometry.

289 ster resonance energy transfer combined with SNAP- and ACP-tag labeling in COS7 cells to monitor dime

290 K201Q mutant showed no changes compared with SNAP-25 wild-type.

291 Touch sensation correlated with SNAP areas (p < 0.005) and was negatively related to the

292 rns of neurodegeneration in individuals with SNAP compared with their Abeta+ counterparts.

293 At the group level, individuals with SNAP did not show cognitive decline but did show a dimin

294 ve: To determine whether CN individuals with SNAP show evidence of early Alzheimer disease (AD) proce

295 ss of hippocampal volume in individuals with SNAP were indistinguishable from those without any patho

296 rated that Ub(G76V)-GFP-Syb2 interacted with SNAP-25 and Syntaxin1, the SNARE partners of synaptobrev

297 amma subunits (Gbetagamma) interactions with SNAP-25, a core component of the synaptic vesicle fusion

298 6%) were also seen in patients with MCI with SNAP subtypes compared with their Abeta+ counterparts.

299 In MCI with SNAP, low APOE epsilon4 and high APOE epsilon2 carrier p

300 In MCI with SNAP, sustained glucose metabolism and gray matter volum

301 ylmaleimide sensitive factor), together with SNAPs (soluble NSF attachment protein), disassembles the