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 ts by specifically cleaving and inactivating SNAP25.

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

5 s responding to KCl depolarization expressed SNAP25.

6 in in PC12 cells, which specifically cleaves SNAP25.

7 ire SNARE domains without the involvement of SNAP25.

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

9 ly similar on syntaxin-only bilayers lacking SNAP25.

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

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

12 d through the interaction of Gbetagamma with SNAP25.

13 action between TRIM9 and the SNARE component SNAP25.

14 orms tight links with both synaptobrevin and SNAP25.

15 ol associated with membrane microdomains and SNAP25.

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

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

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

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

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

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

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

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

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

25 Double labeling with SNAP25 and calbindin antibodies demonstrated that horizo

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

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

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

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

30 SNAP25 and SNAP23 are plasma membrane SNARE proteins ess

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

93 SNAP25 endosomes, which exclude the plasma membrane SNAR

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

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

96 SNAP25 expression in mammalian horizontal cells along wi

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

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

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

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

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

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

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

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

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

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

107 The SNAP25 immunoreactivity in the plexiform layers and oute

108 2+) sensor for exocytosis, was found to bind SNAP25 in a Ca(2+)-stimulated manner.

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

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

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

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

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

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

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

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

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

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

119 SNAP25 internalization occurs by constitutive, dynamin-i

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

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

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

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

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

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

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

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

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

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

130 y, suggesting a differential distribution of SNAP25 isoforms.

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

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

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

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

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

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

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

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

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

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

141 mber of these receptors in heterozygote null Snap25 mutants.

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

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

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

145 The Snap25 null mutant mouse provides an opportunity to test

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

181 syntaxin and SNAP25.syntaxin.VAMP SNARE complexes.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

198 9769 C allele was sufficient to increase the SNAP25 transcription level.

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

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

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

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

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

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

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

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

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

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

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

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

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

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