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 exists as two developmentally regulated alternat

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

9 SNAP-25 is an essential component of SNARE complexes dri

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

11 SNAP-GST pull-down assays demonstrate SCRIB binds multip

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

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

14 y of the SNARE complex formed by syntaxin-1, SNAP-25 and synaptobrevin, allowing exquisite regulation

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

16 ring Munc18-1 binding; binding to syntaxin-1-SNAP-25 heterodimers, precluding SNARE complex formation

17 s with the neuronal SNAREs, using syntaxin-1-SNAP-25-containing liposomes and liposomes containing sy

18 ntaxin-1 but also in the t-SNARE (syntaxin-1/SNAP-25) complex.

19 that the closed syntaxin-1 in the syntaxin-1/SNAP-25/Munc18-1 complex is less stable than that in the

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

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

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

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

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

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

26 ssibly related to the difference in SNAP-25a/SNAP-25b ratios, suggesting that the splicing switch may

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

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

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

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

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

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

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

34 ected membrane proteins were labeled using a SNAP-tag, which allowed us to visually inspect the enric

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 New adult SNAP recipients had higher socioeconomic status, better

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

41 uman O(6)-alkylguanine-DNA alkyltransferase (SNAP-tag).

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

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

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

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

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

47 three genes including one encoding an alpha-SNAP protein.

48 These results indicate that STX5 and alpha-SNAP facilitate cholesterol trafficking from PMs to mito

49 Immunodepletion of STX5 and alpha-SNAP from PMs decreased steroidogenesis supported by PMs

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

51 e treatment of rats recruited STX5 and alpha-SNAP to adrenal PMs and mitochondria.

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

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

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

55 ctor (NSF/Sec18), and its co-chaperone alpha-SNAP/Sec17.

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

57 Furthermore, alpha-SNAP depletion significantly reduces fluorescence resona

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

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

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

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

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

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

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

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

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

67 Knockdown of either STX5 or alpha-SNAP in Y1 cells decreased stimulated steroidogenesis.

68 decreased, whereas recombinant STX5 or alpha-SNAP restored, the PMs' ability to support steroidogenes

69 e-sensitive factor attachment protein (alpha-SNAP) are enriched in adrenal PMs, and adrenocorticotrop

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

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

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

73 Although the Rhg1 alpha-SNAP is known to play an important role in vesicle traff

74 In this report, we show that the Rhg1 alpha-SNAP strongly interacts with two syntaxins of the t-SNAR

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

76 perones of the Sec1/Munc18 (SM), Sec17/alpha-SNAP, and Sec18/NSF families.

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

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

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

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

81 escent visualization revealed that the alpha-SNAP and the two interacting syntaxins localize to the p

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

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

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

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

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

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

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

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

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

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

92 42]; stage 1, beta = -0.242 [SE, 0.051]; and SNAP, beta = -0.157 [SE, 0.044]; P </= .001), whereas th

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

94 s a stable SNARE complex with syntaxin-1 and SNAP-25 through its C-terminal SNARE motif and competes

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

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

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

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

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

100 mal levels of total SNAP-25, Syntaxin 1A and SNAP-47 in the hippocampus, but females expressed lower

101 1, preventing binding to synaptobrevin-2 and SNAP-25 to form the ternary SNARE complex.

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

103 We explored the function of SNAP-25a and SNAP-25b at Schaffer collateral-CA1 synapses in hippocam

104 alternatively spliced isoforms, SNAP-25a and SNAP-25b.

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

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

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

108 Confocal microscopy imaging analysis and SNAP-tag sucrose density fractionation assays revealed t

109 XS8 cross-linking reactions between Halo and SNAP proteins and verified lattice dynamics in purified

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

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

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

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

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

115 pocampus using 4-week-old wild-type (WT) and SNAP-25b-deficient (MT) mice.

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

117 ired by nature's engineered proteins such as SNAP receptor [soluble N-ethylmale-imide-sensitive facto

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

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

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

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

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

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

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

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

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

127 New child SNAP recipients were less likely to eat all meals and ha

128 ing crude membrane extracts of chromosomally SNAP-tagged and wild-type B. subtilis strains with prote

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

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

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

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

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

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

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

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

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

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

139 The MUN-bound template complex enhances SNAP-25 binding to the templated SNAREs and subsequent f

140 el algorithm for predicting new and existing SNAP recipiency that can be applied to other data sets,

141 istic algorithm to identify new and existing SNAP recipients using the 1999-2013 waves of the Panel S

142 We sought to identify new and existing SNAP recipients, and to examine differences in sociodemo

143 tary quality was similar to that of existing SNAP households.

144 a population that differed from the existing SNAP population and that may benefit from different type

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

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

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

148 al and temporal cortices, and no changes for SNAP-25, PSD-95, VAMP, and syntaxin in frontal cortex.

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

150 elay of the alternative splicing switch from SNAP-25a to SNAP-25b.

151 amics in purified VLPs incorporating 10% Gag-SNAP, 10% Gag-Halo, and 80% Gag proteins.

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

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

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

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

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

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

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

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

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

161 nsity of presynaptic stimuli was affected in SNAP-25b-deficient mice.

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

163 males, possibly related to the difference in SNAP-25a/SNAP-25b ratios, suggesting that the splicing s

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

165 or these, which generally show reductions in SNAP-25, PSD-95, synapsin and rab3A protein levels in th

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

167 erizing the protein expression of individual SNAP-25 isoforms revealed that WT females had higher lev

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

169 ly regulated alternatively spliced isoforms, SNAP-25a and SNAP-25b.

170 ITK-SNAP was used for linear, 2-D and 3-D manual CC measures

171 E, synaptosome-associated protein of 25 kDa (SNAP-25/SN25), serves as a PKA substrate, implying a pot

172 g protocol with fluorescent ligands to label SNAP/CLIP-tags fused to claudins and occludin to identif

173 amate-based photoswitch via a self-labelling SNAP tag.

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

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

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

177 ly labeled the nucleoporin Nup96 with mEGFP, SNAP-tag, HaloTag or the photoconvertible fluorescent pr

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

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

180 protein of interest (POI) through a modular SNAP-Tag/benzylguanine covalent interaction.

181 Each month, SNAP provides assistance to 40 million low-income Americ

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

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

184 New SNAP households exhibited differences in food access and

185 dict which individuals were likely to be new SNAP recipients.

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

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

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

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

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

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

192 25 drastically decreased the cleavability of SNAP-25.

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

194 The etiology of SNAP in this population remains unclear.

195 The expansion of SNAP since the Great Recession enrolled a population tha

196 ted by the expression of an inactive form of SNAP-25.

197 We explored the function of SNAP-25a and SNAP-25b at Schaffer collateral-CA1 synapse

198 et quality, and, subsequently, the health of SNAP participants.

199 l to strengthen the public health impacts of SNAP, organized into three areas: (a) food production an

200 ould strengthen the public health impacts of SNAP.

201 -1 inhibits Ca(2+) currents independently of SNAP-25.

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

203 evealed that WT females had higher levels of SNAP-25a than WT males, suggesting a sex-dependent delay

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

205 ch in vivo in mice, where photoactivation of SNAP-mGluR2 in the medial prefrontal cortex reversibly m

206 ividual is a new or established recipient of SNAP.

207 avior between new and existing recipients of SNAP after the recession.

208 tween new, existing, and never recipients of SNAP in FoodAPS.

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

210 implications of the tandem-like structure of SNAP-25 are unclear.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

229 e Supplemental Nutrition Assistance Program (SNAP) expanded significantly after the Great Recession o

230 ) Supplemental Nutrition Assistance Program (SNAP) is the cornerstone of the US nutrition safety net.

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

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

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

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

235 nd Supplemental Nutrition Assistant Program [SNAP] status).

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

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

238 leimide-sensitive factor attachment protein (SNAP).

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

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

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

242 Single Nuclei Adipocyte RNA-sequencing (SNAP-seq) of subcutaneous adipose tissue defined a metab

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

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

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

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

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

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

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

250 n MT mice, strengthening the conclusion that SNAP-25b is important for cognitive performance by alter

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

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

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

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

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

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

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

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

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

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

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

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

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

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 we identify two synergistic functions of the SNAP-25 linker: First, linker motifs support t-SNARE int

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

268 ns are tagged with either the HaloTag or the SNAP-tag, permitting a multistep affinity enrichment of

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

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

273 alternative splicing switch from SNAP-25a to SNAP-25b.

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 MT mice expressed normal levels of total SNAP-25, Syntaxin 1A and SNAP-47 in the hippocampus, but

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

278 mproved by modulating their activity towards SNAP-25.

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

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

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

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

283 librated by targeted mass spectrometry using SNAP as an anchor protein, and an enrichment factor was

284 VAMP3, SNAP-29, and syntaxin 4 proved important in driving cyto

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

286 6 were stage 1, 28 were stage 2, and 46 were SNAP.

287 work describing the mechanisms through which SNAP policy can influence public health, particularly by

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

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

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

297 6%) were also seen in patients with MCI with SNAP subtypes compared with their Abeta+ counterparts.

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

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

300 hat concatenates the two SNARE motifs within SNAP-25.