ライフサイエンスコーパス: SNAP25

1 of synaptosome-associated protein of 25 kD (SNAP25).

2 he synaptosome-associated protein of 25 kDa (SNAP25).

3 LK6) and synaptosomal-associated protein 25 (SNAP25).

4 (Ng) and synaptosomal-associated protein 25 (SNAP25).

5 arates the zDABM and S-acylated cysteines in SNAP25.

6 s responding to KCl depolarization expressed SNAP25.

7 in in PC12 cells, which specifically cleaves SNAP25.

8 ire SNARE domains without the involvement of SNAP25.

9 was shorter, comprising residues 167-186 of SNAP25.

10 ly similar on syntaxin-only bilayers lacking SNAP25.

11 ivo with the use of a fluorescent version of SNAP25.

12 or Ca(2+)-dependent synaptotagmin binding to SNAP25.

13 actions between full-length Gbeta1gamma2 and SNAP25.

14 gyrus granule cells in male mice by ablating SNAP25.

15 wo classical SNARE proteins, syntaxin 1A and SNAP25.

16 hogenic variant I67N in the SNAREopathy gene SNAP25.

17 ts by specifically cleaving and inactivating SNAP25.

18 BRB2, CLTC, DHDDS, NUS1, RAB11A, GABBR2, and SNAP25.

19 NAP25-zDHHC17 interaction and S-acylation of SNAP25.

20 d through the interaction of Gbetagamma with SNAP25.

21 action between TRIM9 and the SNARE component SNAP25.

22 orms tight links with both synaptobrevin and SNAP25.

23 ol associated with membrane microdomains and SNAP25.

24 97) epitope was used to quantify the cleaved SNAP25(1-197).

25 ain with subsequent specific cleavage of the SNAP25(1-206) substrate.

26 DHHC ankyrin repeat-binding motif (zDABM) in SNAP25 ((112)VVASQP(117)), which is downstream of its S-

27 rane, colocalizing with the cleaved product, SNAP25(197).

28 identify the central cysteine-rich region of SNAP25/23 as an important regulatory domain.

29 ternary complexes could underlie some of the SNAP25/23 differential ability to control the exocytotic

30 ctor) or synaptosomal-associated protein 25 (SNAP25) (a key component of calcium-triggered transmitte

31 evidence that the interaction of Snapin with SNAP25, a component of the SNARE complex, is also involv

32 hese results show that amino acids 93-111 in SNAP25 act as a flexible molecular spacer that ensures e

33 ype A (BoNT/A) cuts a single peptide bond in SNAP25, an activity used to treat a wide range of diseas

34 SNAP25, an essential component of the soluble NSF (N-eth

35 and biochemical analyses of Rabphilin-3A C2B-SNAP25 and C2B-phosphatidylinositol 4,5-bisphosphate (PI

36 Double labeling with SNAP25 and calbindin antibodies demonstrated that horizo

37 etagamma interaction sites on syntaxin1A and SNAP25 and demonstrated an overlap of the Gbetagamma- an

38 By knocking down SNAP25 and imaging slow endocytosis at a conventional sy

39 d generic markers of secretory cells such as Snap25 and Nefm, but neither synaptic markers such as Sy

40 BoNT/A(RYM) was noncatalytic for SNAP25 and nontoxic for mice.

41 In addition, some synaptic genes, such as Snap25 and Nrxn1, are strongly regulated by deficiency o

42 c amino acids in the cysteine-rich region of SNAP25 and SNAP23 are essential for plasma membrane targ

43 SNAP25 and SNAP23 are plasma membrane SNARE proteins ess

44 The SNAREs SNAP25 and SNAP23 are proteins that are initially cytoso

45 It was reported that SNAP25 and SNAP23 have distinct roles in exocytotic rele

46 faster rate than LC/A1, while LC/A4 cleaved SNAP25 and SNAPtide at slower rates than LC/A1.

47 the first evidence showing the dual role of SNAP25 and synaptobrevin in both exocytosis and slow end

48 yt-1) and indirectly with the SNARE proteins SNAP25 and Syntaxin (Stx-1).

49 antity of two markers of synaptic integrity: SNAP25 and SYT-1.

50 d syntaxin do not assemble in the absence of SNAP25 and that the SN2 segment of SNAP25 is the last to

51 The decreased abundance of SNAP25 and the increased abundance of GPI, PTPN11, OLR1,

52 obust elevations in the presynaptic protein, SNAP25 and the post-synaptic proteins NR2b and PSD95.

53 hobic interactions between the P3 residue of SNAP25 and the S3 pocket optimize alignment of the sciss

54 r, coimmunoprecipitation experiments between SNAP25 and VLGR1 show a physical interaction of these tw

55 ences of synaptosomal-associated protein 25 (SNAP25) and cysteine string protein alpha (CSPalpha).

56 proteins-synaptosomal-associated protein 25 (SNAP25) and cysteine-string protein (CSP).

57 id peroxidation (MDA), and synaptic density (SNAP25) and in IL-6(-/-) and WT C57Bl/6 mice.

58 f the 25-kDa synaptosome-associated protein (SNAP25) and is downstream of the well known inhibition o

59 xin, and synaptosomal-associated protein 25 (SNAP25) and is thought to execute a large conformational

60 nd synaptosome-associated protein of 25 kDa (SNAP25) and the vesicle SNARE protein vesicle-associated

61 3 (STX3), synaptosome-associated protein 25 (SNAP25), and interphotoreceptor matrix proteoglycan 2 (I

62 ), synaptosome-associated protein of 25 kDa (SNAP25), and synaptobrevin 2 (Sb2).

63 yntaxin, 25K synaptosome-associated protein (SNAP25), and vesicle-associated membrane protein (VAMP)/

64 in, synaptosome-associated protein of 25 kD (SNAP25), and vesicle-associated membrane protein/synapto

65 axonal levels of KHSRP target mRNAs, Gap43, Snap25, and Fubp1, following sciatic nerve injury and th

66 ed protein 25 (SNAP25), but not human or rat SNAP25, and microinjection of PG1 and PG2 caused paralys

67 ceptor (SNARE) complex formed by syntaxin-1, SNAP25, and synaptobrevin.

68 ry, including SNARE proteins (synaptobrevin, SNAP25, and syntaxin), is needed to coinitiate endocytos

69 eptor) complex consisting of synaptobrevin2, SNAP25, and syntaxin1.

70 Neurotoxins and an anti-SNAP25 antibody inhibited exocytosis less effectively af

71 Herein, we show that (1) Mef2c and Snap25 are positively regulated by Maf and Mafb to drive

72 Its components, syntaxin-1 and SNAP25, are largely present in individual clusters and p

73 itoylated, cysteine string protein (CSP) and SNAP25, are severely mislocalized at hip14 mutant synaps

74 orted several mutations in the gene encoding SNAP25 as a causative factor for developmental and epile

75 etion mapping identified residues 156-202 of SNAP25 as the optimal cleavage domain for BoNT/A, wherea

76 K binding motif (zDABM) in substrate protein SNAP25, as a mechanism of substrate recruitment prior to

77 due of LC/E, Lys224, binds the P2 residue of SNAP25, Asp179, through ionic interactions.

78 LC/A3 cleaved SNAP25 at 50% of the rate of LC/A1 but cleaved SNAPtide

79 neurotoxin (BoNT) E, a protease that cleaves SNAP25 at Arg(180)-Ile(181), completely inhibits this la

80 ell membranes, whereas BoNT A, which cleaves SNAP25 at Gln(197)-Arg(198), is only partially inhibitor

81 BoNT serotype A and serotype E cleave SNAP25 at residues 197-198 and 180-181, respectively.

82 We describe chimeric SNAP25-based ubiquitin ligases that target BoNT/A LC for

83 LC/A cleaves SNAP25 between residues Gln197-Arg198 and, unlike thermo

84 , the plasma membrane SNAREs syntaxin 1a and SNAP25 bind to VAMP2 found on neurotransmitter-containin

85 ufficiently different from BoNT/A1 to affect SNAP25 binding and cleavage.

86 ynaptotagmin-1 that mediate Ca(2+)-dependent SNAP25 binding by zero-length cross-linking.

87 SNAP25-binding deficient RPH3A did not rescue DCV exocyt

88 e insect synaptosomal-associated protein 25 (SNAP25), but not human or rat SNAP25, and microinjection

89 h similar techniques, we found that not only SNAP25, but also synaptobrevin is involved in slow endoc

90 distinct roles in exocytotic release, where SNAP25, but not SNAP23, supports an exocytotic burst.

91 to cleave SNAP23, and the natural substrate, SNAP25, but not SNAP29 or SNAP47.

92 e exact order of each step of recognition of SNAP25 by BoNT/A at the active site is not clear, the in

93 ep mechanism for recognition and cleavage of SNAP25 by BoNT/A.

94 usly been shown that proteolytic cleavage of SNAP25 by botulinum toxin A reduces the ability of Gbeta

95 ues participate in scissile bond cleavage of SNAP25 by LC/E.

96 we define the multiple pocket recognition of SNAP25 by LC/E.

97 cells, we tracked conformational changes in SNAP25 by total internal reflection fluorescence resonan

98 that mutation of hydrophobic residues of the SNAP25 C-terminal coil that contribute to SNARE core int

99 Syntaxin 1a H3 (syn1aH3) and SNAP25 can form a stable assembly, which can then be bou

100 Overall, pathogenic mutations in SNAP25 cause complex changes in the energy landscape for

101 In a short-term lick test, Snap25 cKO (sour taste absent) and Snap25/ transient rec

102 dine-positive post-mitotic type III cells in Snap25 cKO mice was significantly lower on tracing day 1

103 olished ammonium and sour taste responses in Snap25 cKO mice, which concludes sour-dependent synapse

104 he terminal led to a significant increase in SNAP25 cleavage detected in the soma chamber compared wi

105 but have different catalytic capacities for SNAP25 cleavage, SNAPtide cleavage, and autocatalysis.

106 much lower binding affinity for the t-SNARE SNAP25 compared with syntaxin 1A.

107 Comparison with the syn1aH3-SNAP25 complex suggests that the linkage of the N- and C

108 PC12 cells, we found evidence for a syntaxin-SNAP25 complex that formed with high affinity, required

109 obrevin 2 and the plasma membrane syntaxin1A/SNAP25 complex that initiate the fusion event.

110 inhibition is mediated via tomosyn-syntaxin-SNAP25 complexes and not tomosyn-syntaxin complexes.

111 these mechanisms preserve active syntaxin 1A-SNAP25 complexes at the plasma membrane.

112 ift the equilibrium between tomosyn-syntaxin-SNAP25 complexes on the PM to tomosyn-syntaxin complexes

113 tion that blocks formation of other syntaxin-SNAP25 complexes, and assembled reversibly when Ca2+ ent

114 ar to that of the core SNARE and the syn1aH3-SNAP25 complexes.

115 ere, we demonstrated that epithelia-specific Snap25 conditional knockout (cKO) mice exhibited a signi

116 The chorda tympani nerve of Snap25 conditional knockout mice shows reduced electroph

117 The lack of SNAP25 in sour taste cells (Snap25 conditional knockout) significantly reduces the n

118 Both full-length SNAP25 constructs and the combination of its separated,

119 However, only full-length SNAP25 constructs enabled robust secretion from intact c

120 chain interaction(s) of residues 182-186 of SNAP25 contribute to substrate recognition by LC/E.

121 the AS domains, the P1', P3, and P5 sites of SNAP25 contributed to scissile bond cleavage by LC/A, wh

122 age by LC/A, whereas the P1' and P2 sites of SNAP25 contributed to scissile bond cleavage by LC/E.

123 ay 14, but not at day 7, which suggests that SNAP25 contributes to the maintenance of type III cells.

124 tributes one such region, designated H3, and SNAP25 contributes two SNARE regions to the fusogenic co

125 ate that vesicles containing syntaxin 3B and SNAP25 could fuse with vesicles containing synaptobrevin

126 Despite this, zDHHC3/zDHHC7 could S-acylate SNAP25/CSP more efficiently than zDHHC17, whereas zDHHC1

127 iated strong and selective interactions with SNAP25/CSP, whereas binding of zDHHC3 and zDHHC7 to thes

128 priming step increases with vesicle size and SNAP25 density in the plasma membrane and equals the num

129 ofilament light subunit) and fast transport (snap25) do not accumulate in retinas and are distributed

130 SNAP25 endosomes, which exclude the plasma membrane SNAR

131 -interfering RNA-mediated down-regulation of SNAP25 exerted effects similar to those of BoNT E expres

132 SD-pQTLs for proteins APOE (rs157581) and SNAP25 exhibited sex-dimorphic associations with dementi

133 The N-terminal SN1 segment of SNAP25 exhibits a pronounced increase in backbone orderi

134 To evaluate the significance of the SNAP25-expressing cells, we used RNA amplification from

135 SNAP25 expression in mammalian horizontal cells along wi

136 Here, we generate a SNAP25 extreme C-terminal mutant that is deficient in it

137 tein kinase C family member pkc-2 and by the SNAP25 family member aex-4 in the intestine.

138 ane-mediated disorder-to-order transition of SNAP25 flexible linker facilitates its interaction with

139 hermolysin, recognizes an extended region of SNAP25 for cleavage.

140 ses, the BoNTs recognize extended regions of SNAP25 for cleavage.

141 oteases, BoNTs recognize extended regions of SNAP25 for cleavage; however, the molecular basis for th

142 nse to sour tastants, confirming the role of SNAP25 for sour sensation.

143 Vs), forms helix bundles with syntaxin-1 and SNAP25 for the SNARE assembly.

144 ex, composed of synaptobrevin, syntaxin, and SNAP25, forms the essential fusion machinery for neurotr

145 although structurally clustered mutations in SNAP25 give rise to related synaptic transmission phenot

146 ynaptic (synaptosomal-associated protein 25, SNAP25; growth-associated protein 43, GAP43), postsynapt

147 Our results indicate that SNAP25 has a second function as an endosomal Q-SNARE in

148 he functional and structural implications of SNAP25 having two SNARE motifs (SN1 and SN2).

149 found that prenatal exposure to nicotine in Snap25 heterozygote null mice produced a deficit in the

150 eceptor (GPCR) and aex-4 encodes an exocytic SNAP25 homologue.

151 , or synaptotagmin, were twofold enriched in SNAP25 immunoprecipitated products from schizophrenia OF

152 albumin antibodies in monkey retina verified SNAP25 immunoreactivity in all horizontal cells.

153 The SNAP25 immunoreactivity in the plexiform layers and oute

154 2+) sensor for exocytosis, was found to bind SNAP25 in a Ca(2+)-stimulated manner.

155 sensor synaptotagmin 1 (Syt1) for binding to SNAP25 in a calcium-dependent manner.

156 We report the robust expression of SNAP25 in both plexiform layers.

157 was associated with lower Abeta42 and higher SNAP25 in CSF.

158 Reduced GFAP and SNAP25 in ex-forwards has an uncertain basis, while elev

159 opy in rabbit retina confirmed expression of SNAP25 in lateral elements within photoreceptor triad sy

160 cleavage of the exocytic machinery component SNAP25 in motor nerve terminals.

161 atible with possible intracellular roles for SNAP25 in neuroendocrine cells.

162 e identified a dynamic recycling pathway for SNAP25 in PC12 cells through which plasma membrane SNAP2

163 that an essential role for the C terminus of SNAP25 in regulated exocytosis is to mediate Ca(2+)-depe

164 The lack of SNAP25 in sour taste cells (Snap25 conditional knockout)

165 which suggested a role for the C terminus of SNAP25 in the Ca(2+) regulation of exocytosis.

166 ed the same intracellular localization as WT SNAP25, indicating that the amino acid composition of th

167 SNAP25 initially binds along the belt region of BoNT/A,

168 The P3 site residues, Ile178, of SNAP25 interacted with the S3 pocket in LC/E through hyd

169 SNAP25 internalization occurs by constitutive, dynamin-i

170 We conclude that the extreme C terminus of SNAP25 is a critical region for the Gbetagamma-SNARE int

171 The synaptosomal-associated protein SNAP25 is a key player in synaptic vesicle docking and f

172 cultured hippocampal synapse, we found that SNAP25 is involved in slow, clathrin-dependent endocytos

173 However, a substantial intracellular pool of SNAP25 is maintained by endocytosis.

174 The initial recognition of SNAP25 is mediated by the binding of the B region of SNA

175 SNAP25 is one of three neuronal SNAREs driving synaptic

176 Endocytosis of SNAP25 is regulated by ADP-ribosylation factor (ARF)6 (t

177 Instead, the interaction of RPH3A with SNAP25 is relevant for inhibiting DCV exocytosis.

178 e to sorting endosomes, which indicates that SNAP25 is required for its own endocytic trafficking.

179 bsence of SNAP25 and that the SN2 segment of SNAP25 is the last to enter the SNARE complex.

180 e synaptosomal-associated protein of 25 kDa (SNAP25) is a key downstream effector of Gbetagamma subun

181 Synaptosome-associated protein of 25 kDa (SNAP25) is a plasma membrane Q (containing glutamate)-SN

182 s, synaptosome-associated protein of 25 kDa (SNAP25) is localized to the plasma membrane where it fun

183 y, suggesting a differential distribution of SNAP25 isoforms.

184 target, synaptosomal-associated protein 25 (SNAP25), last only several weeks.

185 o effects of IL-6 deficiency on GFAP, MDA or SNAP25 levels in females, but IL-6 deficiency was associ

186 including CACNA1D, and significantly reduced SNAP25 levels, leading to uncoordinated oscillations and

187 trophenylphosphatase domain and non-neuronal SNAP25-like protein homolog 1 (NIPSNAP1) and NIPSNAP2 ac

188 trophenylphosphatase domain and non-neuronal SNAP25-like protein homolog 1, pyruvate carboxylase, and

189 tion of the mini-linker is not important for SNAP25 localization.

190 static interaction between C-terminal of the SNAP25 loop and syx-1, suggesting that the SNAP25 loop r

191 ed interaction between the C-terminal of the SNAP25 loop and syx-1.

192 We found that the N-terminal of the SNAP25 loop region binds with membrane, and this interac

193 e SNAP25 loop and syx-1, suggesting that the SNAP25 loop region facilitates SNARE-complex assembly th

194 eneath the plasma membrane, monitored with a SNAP25-luciferase fusion protein.

195 ved in vesicle docking and/or fusion through SNAP25-mediated interactions.

196 Synaptosome-associated protein 25 (SNAP25) might contribute to synaptic vesicular release i

197 n addition to the ternary complex containing SNAP25, might enable vesicular docking.

198 The number of SNAP25 molecules changing conformation in the priming st

199 ting the fusion of newcomer SGs (Syn-3/VAMP8/SNAP25/Munc18b) and predocked SGs (Syn-1A/VAMP2/SNAP25/M

200 P25/Munc18b) and predocked SGs (Syn-1A/VAMP2/SNAP25/Muncn18a).

201 A SNAP25 mutant in which the mini-linker region was substi

202 ocking exocytosis, using a dominant-negative SNAP25 mutant in Xenopus oocytes, releases meiotic arres

203 us peptide array experiments, we generated a SNAP25 mutant predicted to have a higher-affinity zDABM.

204 unc18 promoted redistribution of a cytosolic SNAP25 mutant to the membrane, a result indicative of sy

205 mber of these receptors in heterozygote null Snap25 mutants.

206 However, it remains unclear how SNAP25 mutations give rise to these disorders.

207 The interaction with SNAP25 negatively regulates SNARE-mediated exocytosis an

208 terminals of both transmitter phenotypes in Snap25-/- neurons.

209 We utilized mice heterozygous for a Snap25 null allele and deficient in SNAP-25 expression t

210 The Snap25 null mutant mouse provides an opportunity to test

211 Patch-clamp recordings in fetal Snap25-null mutant cortex demonstrated that ablation of

212 al consequences of this allelic variation of SNAP25 on modulating the development and plasticity of t

213 onal consequences of an allelic variation of SNAP25 on modulating the development and plasticity of t

214 sembly of three SNARE proteins, syntaxin and SNAP25 on the plasma membrane and synaptobrevin on the v

215 educed to SNARE complexes containing cleaved SNAP25 or by Ca(2+)-dependent synaptotagmin binding.

216 some-associated protein of 25 kDa or 23 kDa (SNAP25 or SNAP23), is essential in this process.

217 the ternary SNARE complex, containing either SNAP25 or SNAP23, or perhaps due to the differential ass

218 e genes, we used pharmacologic inhibitors of Snap25 or vesicle-associated membrane protein (VAMP)/syn

219 is was rescued by expressing toxin-resistant SNAP25 or wild-type SNAP23, which is naturally toxin-res

220 on of presynaptic SNARE proteins syntaxin-1, SNAP25, or MUNC18-1.

221 hydrophobic and steric interactions with the SNAP25 P1' residue Ile181.

222 Saccharomyces cerevisiae contains two SNAP25 paralogues, Sec9 and Spo20, which mediate vesicle

223 everal studies imply that the loop region of SNAP25 plays important roles in SNARE-complex assembly.

224 We show that SNAP25-positive cells also express typical presynaptic p

225 Remarkably, a mutant SNAP25 protein with an increased affinity for rafts disp

226 the SNARE complex, and more specifically the SNAP25 protein, may be involved in psychiatric disorders

227 These truncated SNAP25 proteins sustain a low level of exocytosis but ar

228 The molecular basis for SNAP25 recognition and cleavage by BoNT serotype E is cu

229 in PC12 cells through which plasma membrane SNAP25 recycles in approximately 3 h.

230 LC/A3 and LC/A4 had similar K(m) values for SNAP25 relative to LC/A1, while the k(cat) for LC/A4 was

231 Approximately 20% of the SNAP25 resides in a perinuclear recycling endosome-trans

232 We recently identified a promoter variant in SNAP25, rs6039769, that is associated with early-onset b

233 complex with the N-terminal SNARE region of SNAP25 (S25N).

234 Given the absence of wt SNAP25, SCORE2 allows determination of the number of mol

235 -terminus that is not seen in the C-terminal SNAP25 segment SN2.

236 on altered the intracellular distribution of SNAP25, shifting it from a perinuclear recycling endosom

237 sequences of a [VIAP][VIT]XXQP consensus in SNAP25, SNAP23, cysteine string protein, Huntingtin, cyt

238 Here, we have employed cysteine mutants of SNAP25/SNAP23, which have modified affinities for raft d

239 membrane, a result indicative of syntaxin1A-SNAP25 SNARE pairing.

240 ts that the linkage of the N- and C-terminal SNAP25 SNARE regions is kinetically advantageous in prev

241 cellular Ca2+, and mutations of syntaxin and SNAP25 (soluble N-ethylmaleimide-sensitive factor attach

242 proteins included all family members of the SNAP25, sprouty, cornifelin, ankyrin, and SLAIN-motif co

243 chroism spectropolarimetry, we characterized SNAP25 structure and interactions with other SNAREs in a

244 By co-coating microtiter plates with SNAP25 substrate and a monoclonal antibody specific for

245 r on the PM and exhibited reduced binding to SNAP25, suggesting that these mutants shift the equilibr

246 ARE show that both proteins contact the same SNAP25 surface, but Rabphilin-3A uses a unique structura

247 yzed the interactions among syntaxin, SNAP23/SNAP25, synaptobrevin, and complexin by employing a newl

248 exes, ternary assemblies of syntaxin, SNAP23/SNAP25 (synaptosomal-associated protein of 23 or 25 kDa)

249 tal cells, we investigated the expression of SNAP25 (synaptosomal-associated protein of 25 kDa), a ke

250 antigen 1), Rab11-interacting proteins, and SNAP25 (synaptosomal-associated protein of 25 kDa)-like

251 ein receptors) complex proteins syntaxin and SNAP25 (synaptosome-associated protein 25), which enable

252 S-Acylation of the SNARE protein SNAP25 (synaptosome-associated protein of 25 kDa) is med

253 f 15 VHH inhibited the cleavage of substrate SNAP25 (synaptosome-associated protein of 25,000 Da) by

254 es synaptosome-associated protein of 25 kDa (SNAP25), syntaxin-1a (syx-1), and synaptobrevin 2, which

255 omprises synaptosomal-associated protein-25 (SNAP25), syntaxin-1A, and synaptobrevin-2.

256 syntaxin and SNAP25.syntaxin.VAMP SNARE complexes.

257 was an endosomal SNARE complex comprised of SNAP25/syntaxin 13/vesicle-associated membrane protein 2

258 ions of the Syt1-C2B domain with the t-SNARE SNAP25/Syntaxin1 complex and/or plasma membrane phosphol

259 nsitive manner with binding of Gbetagamma to SNAP25, syntaxin1A, and the assembled SNARE complex.

260 The insertion of AMPA receptors requires SNAP25-syntaxin1A/B-VAMP2 complexes, whereas insertion o

261 tep toward this goal, recombinant syntaxin1A/SNAP25 (t-SNARE) was reconstituted into polymer-supporte

262 The integral membrane protein syntaxin1A/SNAP25 (t-SNARE) was reconstituted into tethered polymer

263 cb2, Trpm5) and type III (e.g. Pkd2l1, Ncam, Snap25) taste cells.

264 gene for a synaptosomal-associated protein (SNAP25) that interacts with HVA channels, reveals abnorm

265 otein of 23 kDa (SNAP23), but not of 25 kDa (SNAP25), these glial cells exhibited a slow burst of exo

266 operate in cooperation with PIP2/Ca(2+) and SNAP25 to bind the plasma membrane, adopting a conformat

267 nd the plasma membrane proteins syntaxin and SNAP25 to drive membrane fusion.

268 could subsequently orient the P4'-residue of SNAP25 to form a salt bridge with the S4'-residue, which

269 dues) is a zinc metalloprotease that cleaves SNAP25 to inhibit the fusion of neurotransmitter-carryin

270 nge of specificity from its native substrate SNAP25 to the selective degradation of alpha-Synuclein.

271 s mediated by the binding of the B region of SNAP25 to the substrate-binding (B) region of LC/E compr

272 uired only the amino-terminal SNARE motif of SNAP25, tolerated a mutation that blocks formation of ot

273 both syntaxin-tomosyn complexes and syntaxin-SNAP25-tomosyn complexes.

274 9769 C allele was sufficient to increase the SNAP25 transcription level.

275 ick test, Snap25 cKO (sour taste absent) and Snap25/ transient receptor potential vanilloid 1 double

276 Snap25/Trpv1 double knockout mice exhibit increased lick

277 tion of the cytosolic domains of syntaxin1A, SNAP25 (two peptides) and synaptobrevin 2.

278 teins and two SNARE proteins (Syntaxin1A and SNAP25) using electron tomography.

279 and cohort 2 (OFC: +40%), with lower 70-kDa SNAP25-VAMP dimer (-37%) in the OFC.

280 dy uncovers the postsynaptic function of the SNAP25-VAMP1-syntaxin4 complex in mediating the constitu

281 We also identified the SNAP25-VAMP1-syntaxin4 complex mediating the constitutiv

282 n-1A and synaptosomal-associated protein 25 (SNAP25), VAMP2 mediates fusion of synaptic vesicles to r

283 yntaxin, synaptosomal-associated protein 25 [SNAP25], vesicle-associated membrane protein [VAMP]) for

284 In aboBoNT-A-treated animals cleaved SNAP25 was absent in the skin and DRG, but present in th

285 The C terminus of SNAP25 was also essential for Ca(2+)-dependent synaptota

286 ulinum neurotoxin; in these cells all of the SNAP25 was cleaved to a lower molecular weight form, and

287 t-SNAREs (anchored syntaxin associated with SNAP25) was observed in real time by wide-field fluoresc

288 To assess the role of endosomal SNAP25, we expressed botulinum neurotoxin E (BoNT E) lig

289 SNPs in either the region of NEUROD6 or SNAP25 were significantly associated with AD, in APOE4+

290 Different commercial antibodies to SNAP25 were tested on vertical sections of retina.

291 trocyte marker GLAST and the synaptic marker SNAP25, whereas CD11b, a microglial marker, was largely

292 t interaction of this site with syntaxin and SNAP25 which has a biphasic dependence on Ca2+, with max

293 nism that maintains an intracellular pool of SNAP25, which is compatible with possible intracellular

294 Both the SN1 and SN2 segments of SNAP25 will assemble with syntaxin; however, while the a

295 mice expressing a form of the SNARE protein SNAP25 with premature truncation of the C terminus and t

296 Thus, the four subtypes of BoNT/A bind SNAP25 with similar affinity but have different catalyti

297 appeared to align the P1' and P2 residues of SNAP25 with the S1' and S2 pockets of LC/E.

298 ing that a lower-affinity interaction of the SNAP25 zDABM with zDHHC17 is optimal for S-acylation eff

299 pacer that ensures efficient coupling of the SNAP25-zDHHC17 interaction and S-acylation of SNAP25.

300 hortening the mini-linker did not affect the SNAP25-zDHHC17 interaction but blocked S-acylation.