ライフサイエンスコーパス: syntaxin

1 sertion of a tail-anchored protein, SYP72, a syntaxin.

2 ted, there was no activity toward SNAP-25 or syntaxin.

3 x formation through high-affinity binding to syntaxin.

4 arily through one type of SNARE protein, the syntaxins.

5 ave been found for different SM proteins and syntaxins.

6 the original binding mode of SM proteins and syntaxins.

7 -embedded t-SNAREs consisting of full-length syntaxin 1 and SNAP-25B at the membrane, as measured by

8 Here we report that cleavage of syntaxin 1 by BoNT/C, and cleavage of SNAP-25 by BoNT/E

9 Also, calcium was shown to promote syntaxin 1 clustering in the plasma membrane, but the mo

10 racted with ER and Golgi syntaxin 5 and with syntaxin 1 in the absence of Munc18a, when syntaxin 1 is

11 h syntaxin 1 in the absence of Munc18a, when syntaxin 1 is retained in the ER.

12 tory interaction between Munc18-1 and closed syntaxin 1 is well described, the mechanism of how Munc1

13 Recently, it was shown that PI(4,5)P2and syntaxin 1, a SNARE protein that catalyzes regulated exo

14 Munc18 binds to the closed conformation" of syntaxin 1, the ER-Golgi SM protein Sly1 interacts only

15 pecifically and reversibly connects multiple syntaxin 1/PI(4,5)P2complexes into larger mesoscale doma

16 g and trafficking the central SNARE protein, syntaxin-1 (i.e. chaperoning function), by its domain-1;

17 Syntaxin-1 (Stx1) is a component of the synaptic vesicle

18 receptor (SNARE) complexes by SNARE proteins syntaxin-1 (Stx1), synaptosomal-associated protein 25 (S

19 We observed that endogenous syntaxin-1 accumulates at the Golgi of Munc18-1 KO neuro

20 attachment protein receptor (SNARE) protein syntaxin-1 adopts a closed conformation when bound to Mu

21 We conclude that clustering of syntaxin-1 allows the cell to maintain a high syntaxin-1

22 3a of Munc18-1 abolishes its ability to bind syntaxin-1 and fails to rescue the level and trafficking

23 quires the polybasic juxtamembrane region of syntaxin-1 and is not affected by the superclamp mutatio

24 thereby increasing the immunoavailability of syntaxin-1 and leading indirectly to Ca(2+) current inhi

25 Syntaxin-1 and Munc18-1 depend on each other for normal

26 mutant of P335A reduces the ability to bind syntaxin-1 and rescue syntaxin-1 levels.

27 ronal SM protein Munc18-1 and SNARE proteins syntaxin-1 and SNAP-25 (25 kDa synaptosome-associated pr

28 ibody targeting otoferlin immunoprecipitated syntaxin-1 and SNAP-25 but not synaptobrevin-1.

29 ctor (NSF) and alpha-SNAP, which disassemble syntaxin-1 and SNAP-25 heterodimers.

30 Its components, syntaxin-1 and SNAP25, are largely present in individual

31 tially containing the plasma membrane SNAREs syntaxin-1 and soluble NSF attachment protein (SNAP)-25.

32 bility of the Munc18-1 variants to chaperone syntaxin-1 and to rescue exocytosis is strongly impaired

33 ays a significant role in the chaperoning of syntaxin-1 and, if so, how these dual functions of domai

34 fails to rescue the level and trafficking of syntaxin-1 as well as to restore exocytosis in Munc18-1/

35 at the preferential binding of CAPS1 to open syntaxin-1 can contribute to the stabilization of the op

36 alpha-helix containing Pro-335 promotes the syntaxin-1 chaperoning function, whereas the P335A mutat

37 ion could not be explained by differences in syntaxin-1 chaperoning/localization or vesicle docking,

38 l cholesterol depletion, leading directly to syntaxin-1 cluster dispersal and Ca(2+) current inhibiti

39 te Ca(2+) influx by expanding or contracting syntaxin-1 clusters.

40 1 catalyzes the transition from the Munc18-1/syntaxin-1 complex to the SNARE complex, the molecular m

41 te to the stabilization of the open state of syntaxin-1 during its transition from "closed" state to

42 yntaxin-1 allows the cell to maintain a high syntaxin-1 expression level without compromising Ca(2+)

43 Exocytosis likely starts with Syntaxin-1 folded into a self-inhibited closed conformat

44 mpromising Ca(2+) influx, and recruitment of syntaxin-1 from clusters by SNAP-25 expression makes it

45 ous or exogenous SNAP-25 expression recruits syntaxin-1 from clusters on the plasma membrane, thereby

46 inding protein Doc2B or ubMunc13-2 increases syntaxin-1 immunoavailability and concomitantly down-reg

47 In contrast, syntaxin-1 inhibits Ca(2+) currents independently of SNA

48 more potent than the A-isoform, but not when syntaxin-1 is cleaved by botulinum neurotoxin C.

49 yx-of-Held synapse from mutant mice in which syntaxin-1 is rendered constitutively open and SNARE-com

50 Syntaxin-1 is the central SNARE protein for neuronal exo

51 es the ability to bind syntaxin-1 and rescue syntaxin-1 levels.

52 d two conserved residues (R151, I155) in the syntaxin-1 linker region as key sites for the MUN domain

53 ation tightly bound to Munc18-1, whereas the syntaxin-1 linker region changes its conformation, simil

54 uggest that the conformational change of the syntaxin-1 linker region induced by Munc13-1 initiates t

55 Cell death was too rapid after syntaxin-1 loss to study Golgi abnormalities.

56 ults reveal a striking interplay between the syntaxin-1 N-peptide and the conformational state of the

57 presynaptic, GB(1a)-containing receptors on syntaxin-1 opening and calcium entry to enhance probabil

58 , which activates SNARE complexes containing syntaxin-1 or -3, but not complexes containing syntaxin-

59 te Munc18-1/syntaxin-1/MUN complex, in which syntaxin-1 still adopts a closed conformation tightly bo

60 chanisms: First, neuronal silencing promotes syntaxin-1 switch from a closed to an open conformation

61 e and requires that the target-SNARE protein syntaxin-1 switches from a closed to an open conformatio

62 C2D-F domains interact with the syntaxin-1 t-SNARE motif with maximum binding within the

63 veral other phenotypes as causal (defects in syntaxin-1 targeting and synaptic transmission).

64 The mutants rescued vesicle docking and syntaxin-1 targeting to the plasma membrane, with the ex

65 morphology, but not synaptic transmission or syntaxin-1 targeting.

66 ception of P335A that only supported partial syntaxin-1 targeting.

67 nformational states ("closed" vs. "open") of syntaxin-1 using PC12 cells and Caenorhabditis elegans.

68 rmation, similar to that of the LE mutant of syntaxin-1 when bound to Munc18-1.

69 Expression of Munc18-1, which recruits syntaxin-1 within the exocytotic pathway, does not modul

70 lethargy of unc-64 (C. elegans orthologue of syntaxin-1)-null mutants.

71 quires Munc18-1, which binds to the released syntaxin-1, and Munc13-1, which, together with Munc18-1,

72 ly of the SNARE complex composed of SNAP-25, syntaxin-1, and synaptobrevin-2 (sybII) proteins.

73 ermolecular interactions among the receptor, syntaxin-1, and the Ca(V)2.2 channel.

74 Munc18-1 reclustering was independent of syntaxin-1, but required calcium influx and protein kina

75 and its binding partner, the t-SNARE-protein Syntaxin-1, by approximately 30% and decrease spontaneou

76 yrosine (Y337A), which interacts with closed syntaxin-1, mildly increased secretory amplitude.

77 th occurs in cultured neurons upon depleting syntaxin-1, Munc18-1, and/or SNAP-25, well before synaps

78 As proteins, such as syntaxin-1, Munc18-1, or SNAP-25, modulate alpha-synucle

79 proteins involved in synaptic transmission (syntaxin-1, Munc18-1, SNAP-25), whereas other proteins i

80 n-neuronal Munc18 isoform that does not bind syntaxin-1, Munc18-3, in Munc18-1 KO neurons prevented c

81 The loss of presynaptic proteins Munc18-1, syntaxin-1, or SNAP-25 is known to produce cell death, b

82 a demonstrate that cell death upon Munc18-1, syntaxin-1, or SNAP-25 loss occurs via a degenerative pa

83 Munc13s open Syntaxin-1, orchestrating SNARE complex assembly in an N

84 nesis, within 1-4 DIV upon loss of t-SNAREs (syntaxin-1, SNAP-25) or Munc18-1, but not v-SNAREs (syna

85 lease depends on the SNARE complex formed by syntaxin-1, synaptobrevin and SNAP-25, as well as on com

86 The SNAREs Syntaxin-1, Synaptobrevin, and SNAP-25 play a central ro

87 ritical role in intracellular trafficking of syntaxin-1, which is dependent on the conformational sta

88 et of Munc18-1 rescues impaired secretion in syntaxin-1-depleted PC12 cells and the lethality and let

89 synapses via lateral diffusion together with syntaxin-1.

90 ction is important for a tripartite Munc18-1/syntaxin-1/MUN complex, in which syntaxin-1 still adopts

91 The atypical lipid-anchored Syntaxin 11 (STX11) and its binding partner, the Sec/Mun

92 n the ability to interact with and stabilize syntaxin 11.

93 AMP8-dependent recycling endosomes deposited syntaxin-11 at immune synapses, facilitating assembly of

94 ns in the two degranulation genes Rab27a and syntaxin-11, impaired the dynamics and secretion of cyto

95 enes, those coding for perforin, Rab27a, and syntaxin-11.

96 core secretion machinery complexes, such as syntaxin-11/SNAP23 heterodimers, and fractionation studi

97 1; and a SNAP receptor complex consisting of Syntaxin 13, Snap29, and Vamp7 are all required for the

98 ates in intracellular compartments including Syntaxin-13- and RAB-14-labeled endosomes.

99 We show that the Medicago truncatula SYNTAXIN 132 (SYP132) gene undergoes alternative cleavag

100 nsitive factor attachment protein receptors) syntaxin 17 (STX17) and SNAP29, and the vesicle (v)-SNAR

101 ind that HOPS colocalizes and interacts with Syntaxin 17 (Syx17), the recently identified autophagoso

102 interact with the ER-specific SNARE proteins Syntaxin 17 and 18, however only Syntaxin 18 was require

103 aken different routes to discover a role for Syntaxin 17 in the maturation of autophagosomes.

104 Cleavage of syntaxin 17 inhibits not only autophagy but also stauros

105 binding of Vamp8 to the autophagosomal SNARE Syntaxin 17 to modulate the fusion of autophagosomes wit

106 secretion is unaffected by downregulation of syntaxin 17, a SNARE promoting autophagosome-lysosome fu

107 Lpg1137 binds to and cleaves syntaxin 17, a soluble N-ethylmaleimide-sensitive factor

108 ch in turn actively promote LC3 degradation, Syntaxin 17-positive autophagosome formation, and lysoso

109 tochondria communication through cleavage of syntaxin 17.

110 In this study, we identify syntaxin-17 as a core mitochondrial SNARE required for t

111 Syntaxin-17 can be traced to the last eukaryotic common

112 McLelland et al. show that the SNARE Syntaxin-17 mediates MDV fusion with endolysosomes, prom

113 Syntaxin-17 remains associated with mature MDVs and form

114 RE proteins Syntaxin 17 and 18, however only Syntaxin 18 was required for Procollagen VII export.

115 Neither SLY1 nor Syntaxin 18 was required for the export of the equally b

116 Along with the t-SNARE Syntaxin 18, we now reveal the complete complement of SN

117 stimulation by Ca(2+)SIGNIFICANCE STATEMENT Syntaxin 1A (Syx) is a central protein component of the

118 (5RK) of the plasma membrane neuronal SNARE, syntaxin 1A (Syx), in vesicle exocytosis, although widel

119 All tdTomato fluorescent cells expressed syntaxin 1A and GABA-immunoreactivity indicating they we

120 Syntaxin 1A and syntaxin 3 inhibit the membrane expressi

121 taC318) that retains electrical function and syntaxin 1A binding, but lacks the ability to form clust

122 of Kv2.1, specifically its interaction with syntaxin 1A, could lead to neuroprotection following isc

123 the closed conformation and the N-peptide of syntaxin 1a, thereby inhibiting SNARE complex formation,

124 ollowing ischemic injury in vivo The minimal syntaxin 1A-binding sequence of Kv2.1 C terminus (C1aB)

125 ansporters are modulated by interaction with syntaxin 1A.

126 factor activating protein receptor) protein syntaxin 1A.

127 ype-2 diabetes (T2D), severely reduced islet syntaxin-1A (Syn-1A) levels contribute to insulin secret

128 The core SNARE protein syntaxin-1a (syn1a) was expressed by murine ileal L cell

129 Changing the stoichiometry of syntaxin-1a and d-SNAP-25 in the target bilayer had sign

130 In the second procedure, monomeric syntaxin-1a and dodecylated (d-)SNAP-25 are separately r

131 lightly weakens the binding between "closed" syntaxin-1A and Munc18-1, whereas the same mutation in t

132 le proteins (SV), including synaptotagmin-1, syntaxin-1A and Rab3, in the brain of this LRRK2 fly mod

133 y 50% when the vesicles bearing the t-SNAREs syntaxin-1A and SNAP-25 were preincubated with Munc18 fo

134 o the 1:1 plasma membrane t-SNARE complex of syntaxin-1a and SNAP-25 while simultaneously binding the

135 naptobrevin-2 and the plasma membrane SNAREs syntaxin-1a and SNAP-25 with a 1:1:1 stoichiometry.

136 ain and a binary SNARE complex consisting of syntaxin-1A and SNAP-25A via the accessory domain.

137 l change in the Munc18-1 hinge-loop controls syntaxin-1A and subsequent SNARE complex assembly.

138 bility increased in response to stimulation, syntaxin-1A became less mobile.

139 ciation is a consequence of sequestration of syntaxin-1A by Munc18a and subsequent release of SNAP-25

140 We show that expression of "closed" syntaxin-1A carrying N-terminal single point mutations (

141 Accordingly, syntaxin-1A confinement was prevented by expression of b

142 Munc18-1 and syntaxin-1A control SNARE-dependent neuroexocytosis and

143 These Munc18-1 and syntaxin-1A diffusional switches were blocked by the exp

144 8-1, whereas the same mutation in the "open" syntaxin-1A disrupts it.

145 18-1 domain 3a hinge-loop therefore controls syntaxin-1A engagement into SNARE complex formation duri

146 Conversely, expression of the "open" syntaxin-1A harboring the same mutations fails to rescue

147 led nonhomogeneous diffusion of Munc18-1 and syntaxin-1A in and out of partially overlapping nanodoma

148 the solution NMR structure of micelle-bound syntaxin-1A in its prefusion conformation.

149 In the first procedure, syntaxin-1a is purified in a strictly monomeric form and

150 c mutant of Munc18a with reduced affinity to syntaxin-1A results in less reduction of vesicle associa

151 Ca(2+)-dependent manner with syntaxin-3 and syntaxin-1A soluble N-ethylmaleimide-sensitive factor at

152 nt release of SNAP-25 (i.e. Munc18a captures syntaxin-1A via its high affinity interaction).

153 l SNARE acceptor complex consisting of 1:1:1 syntaxin-1a(residues 183-288):SNAP-25:syb(residues 49-96

154 indered by the spontaneous assembly of a 2:1 syntaxin-1a:SNAP-25 complex on target membranes that kin

155 ta-synuclein, synaptogyrin-3, synaptophysin, syntaxin 1B, synaptotagmin, and synapsin 1), we performe

156 Wild-type human syntaxin-1B but not a mutated protein rescued the effect

157 entification of mutations in STX1B, encoding syntaxin-1B, that are associated with both febrile seizu

158 ation selectively promotes interactions with syntaxin 2 (but not syntaxins 3 or 4) and that these int

159 R-mutated rab17 led to the redistribution of syntaxin 2 and 5' nucleotidase from the apical membrane

160 distribution further suggests that rab17 and syntaxin 2 mediate fusion of transcytotic vesicles at th

161 tify syntaxin-binding protein 1 (STXBP1) and syntaxin-2 and -3 as endogenous Slp4-a binding partners

162 ipitations showed that STXBP1 interacts with syntaxin-2 and -3, but not with syntaxin-4.

163 Silencing of its SNARE-binding partner syntaxin 3 (STX3) also markedly inhibited degranulation,

164 the soluble NSF attachment protein receptor Syntaxin 3 (Stx3) disturb epithelial polarity and cause

165 Syntaxin 3 (Stx3), a SNARE protein located and functioni

166 ID showed homozygous truncating mutations in syntaxin 3 (STX3).

167 , Sec22b in combination with plasma membrane syntaxin 3 and syntaxin 4 as well as SNAP-23 and SNAP-29

168 ion and overexpression of syntaxin 4 but not syntaxin 3 in oligodendrocyte progenitor cells but not i

169 Syntaxin 1A and syntaxin 3 inhibit the membrane expression of B(0)AT1 by

170 The expression of synaptobrevin and syntaxin 3, TA proteins essential for vesicle fusion, wa

171 rotein receptor (SNARE) machinery components syntaxins 3 and 4, localizing to the cell body and the m

172 omotes interactions with syntaxin 2 (but not syntaxins 3 or 4) and that these interactions are nucleo

173 ssociation in a Ca(2+)-dependent manner with syntaxin-3 and syntaxin-1A soluble N-ethylmaleimide-sens

174 the Q-SNARE syntaxin-4, whereas LTP utilized syntaxin-3; both additionally required the Q-SNARE SNAP-

175 A Glycine max syntaxin 31 homolog (Gm-SYP38) was identified as being e

176 Syntaxin 31 is a protein that resides on the cis face of

177 The analysis demonstrates a role for syntaxin 31-like genes in resistance that until now was

178 rmore, we observed that GMFG interacted with syntaxin 4 (STX4) and syntaxin-binding protein 4 (STXBP4

179 stigated the interaction between Munc18c and syntaxin 4 (Syx4).

180 rize one candidate, the postsynaptic t-SNARE Syntaxin 4 (Syx4).

181 ion between dysferlin and the SNARE proteins syntaxin 4 and SNAP-23.

182 bination with plasma membrane syntaxin 3 and syntaxin 4 as well as SNAP-23 and SNAP-29 completes carg

183 Thus, downregulation and overexpression of syntaxin 4 but not syntaxin 3 in oligodendrocyte progeni

184 s to increased FRET of fluorescently labeled syntaxin 4 with VAMP3 specifically at the plasma membran

185 of the biosynthesis of MBP mRNA relies on a syntaxin 4-dependent mechanism, which likely involves ac

186 escue the block of MBP mRNA transcription in syntaxin 4-downregulated cells.

187 ells and colocalizes with and interacts with syntaxin 4.

188 g assays indicate that dysferlin accelerates syntaxin 4/SNAP-23 heterodimer formation and SNARE-media

189 18c) regulates membrane fusion by activating syntaxin-4 (STX-4) to bind cognate SNARE proteins to for

190 Rab17 co-localizes with Syntaxin-4 in the soma, dendritic shaft, the tips of dev

191 Syntaxin-4 knockdown reduced GluK2 but had no effect on

192 Rab17 knockdown caused Syntaxin-4 redistribution away from dendrites and into a

193 Rab17 mediates the dendritic trafficking of Syntaxin-4 to selectively regulate dendritic surface ins

194 tic surface expression of GluK2 by enhancing Syntaxin-4 translocation to dendrites.

195 ntaxin-1 or -3, but not complexes containing syntaxin-4, whereas LTP required complexin.

196 duced AMPAR trafficking utilized the Q-SNARE syntaxin-4, whereas LTP utilized syntaxin-3; both additi

197 teracts with syntaxin-2 and -3, but not with syntaxin-4.

198 The SNARE syntaxin 5 (Stx5) was extremely sensitive to disruption

199 tein level of a cellular trafficking factor, syntaxin 5 (STX5), a member of the syntaxin family of SN

200 port the identification of the Golgi t-SNARE syntaxin 5 (Syn5) as the ubiquitinated substrate.

201 SNAP-47 also interacted with ER and Golgi syntaxin 5 and with syntaxin 1 in the absence of Munc18a

202 On the other hand, inhibition of syntaxin 5 function by small interfering RNA silencing o

203 We identify a cellular protein, syntaxin 5, important for generating this compartment, a

204 Together, our data strongly suggest that syntaxin 5-mediated retrograde transport to the Golgi ap

205 e also demonstrate that the microtubule- and syntaxin 6-mediated Golgi translocation of EGFR is neces

206 with dynein and fuses with the Golgi through syntaxin 6-mediated membrane fusion.

207 with previous studies, the microtubule- and syntaxin 6-mediated trafficking pathway from cell surfac

208 ansduction is unaffected by the knockdown of syntaxins 6 and 16, which are two major effectors in the

209 with vesicular trafficking proteins, such as syntaxin-6 (STX6) and vesicular-associated membrane prot

210 d that elevated AnxA6 levels interfered with syntaxin-6 (Stx6)-dependent recycling of integrins to th

211 ular proteins, but it is highly enriched for syntaxin-6 and Rab11.

212 PICK1 colocalized with syntaxin-6, a marker for immature granules.

213 ns-Golgi network, partially overlapping with syntaxin-6.

214 x and endosomal glutamine-containing SNAREs [syntaxin 7 (STX7), STX8, and vesicle transport through t

215 Colocalization of Munc13-4 and syntaxin 7 at late endosomes was demonstrated by high-re

216 Munc13-4 binding to syntaxin 7 was significantly increased by calcium.

217 ction between the tethering factor Munc13-4, syntaxin 7, and VAMP8.

218 scued by expression of Munc13-4 but not by a syntaxin 7-binding-deficient mutant.

219 Here, we show that syntaxin 8 (MoSyn8), a Qc-SNARE protein homolog, also pl

220 tudy we identified expression of the t-SNARE syntaxin 8 (STX8) (Qc SNARE) in mouse and human platelet

221 results suggest that the unassembled form of syntaxin-8 and the potassium channel TASK-1 are internal

222 Coexpression of syntaxin-8 caused a fourfold reduction in TASK-1 current

223 TASK-1 and syntaxin-8 colocalized in the early endosomal compartmen

224 The endosomal SNARE protein syntaxin-8 interacts with the acid-sensitive potassium c

225 A syntaxin-8 mutant that cannot assemble with other SNARE

226 This implies that syntaxin-8 regulates the endocytosis of TASK-1.

227 ignal in TASK-1 and an endocytosis signal in syntaxin-8 were mutated.

228 fluorescence-tagged clathrin, TASK-1, and/or syntaxin-8.

229 s had virtually the same effect as wild-type syntaxin-8.

230 identify unique roles for isoforms of UNC-64/Syntaxin, a protein required for synaptic vesicle fusion

231 32A, P334L) map exclusively to the predicted syntaxin and soluble N-ethylmaleimide-sensitive factor a

232 Acceptor vesicles contain reconstituted syntaxin and synaptosomal-associated protein 25 (SNAP-25

233 ynaptic vesicle proteins synapsin I, SV2, or syntaxin and the neuropeptide calcitonin gene-related pe

234 eract with the N-peptide of their partnering syntaxins and are thought to instead promote SNARE compl

235 ynaptosomal-associated protein 25 (SNAP-25), syntaxin, and shortened peptides representing the substr

236 sists of the three proteins synaptobrevin-2, syntaxin, and synaptosomal-associated protein 25 (SNAP25

237 roteins (synaptosomal-associated protein 25, syntaxin, and vesicular glutamate transporter type 1), t

238 We showed that multiple syntaxins are present on the peri-arbuscular membrane.

239 Syntaxins are target-SNAREs that crucially contribute to

240 The selectivity in syntaxin binding and apical protein redistribution furth

241 he C1a peptide, we were able to localize the syntaxin binding site on Kv2.1 to the most plasma membra

242 crease in currents by interfering with Kv2.1/syntaxin binding.

243 reen for targets for Slp4-a, we now identify syntaxin-binding protein 1 (STXBP1) and syntaxin-2 and -

244 Heterozygous mutations in the syntaxin-binding protein 1 (STXBP1) gene, which encodes

245 t GMFG interacted with syntaxin 4 (STX4) and syntaxin-binding protein 4 (STXBP4); however, only knock

246 e association studies (GWAS) have identified syntaxin-binding protein 5 (STXBP5) as a candidate gene

247 ve consistently identified the gene encoding syntaxin-binding protein 5 (STXBP5) in this context.

248 Syntaxin-binding protein 5 (STXBP5; also known as tomosy

249 nts, identified a unique missense variant in syntaxin-binding protein 5-like (STXBP5L c.3127G>A, p.Va

250 (2+) channels, whereas overexpression of the syntaxin-binding protein Doc2B or ubMunc13-2 increases s

251 mediated process, and that the SNARE protein syntaxin binds directly to Kv2.1 channels.

252 o be organized in small clusters adjacent to syntaxin clusters.

253 f the Munc18-1 domain 3a within the Munc18-1:syntaxin complex result in an additional interaction wit

254 lix 12 leads to opening of a closed Munc18-1:syntaxin complex, followed by productive SNARE complex a

255 yn-syntaxin-SNAP25 complexes and not tomosyn-syntaxin complexes.

256 ntaxin-SNAP25 complexes on the PM to tomosyn-syntaxin complexes.

257 xpression of a constitutively open mutant of syntaxin could only minimally restore neurotransmitter r

258 g factor, syntaxin 5 (STX5), a member of the syntaxin family of SNARE proteins.

259 Munc13 catalyzes the transit of syntaxin from a closed complex with Munc18 into the tern

260 While syntaxin homodimerization is supposed to promote the tra

261 l layer (GCL), and RBPMS is not expressed in syntaxin (HPC-1)-immunoreactive cells in the inner nucle

262 t of tomosyn to vesicle fusion sites through syntaxin interaction.

263 is generally thought to suppress assembly of syntaxin into the SNARE complex.

264 Syntaxin is known to bind to Kv2.1 in a domain comprisin

265 g SNARE proteins (synaptobrevin, SNAP25, and syntaxin), is needed to coinitiate endocytosis, likely t

266 es and is positioned to stabilize a putative syntaxin-like bundle motif.

267 Using clustered syntaxin molecules as an example, we study the influence

268 sufficient) to the binding of tomosyn to the syntaxin monomer, indicating that full-length tomosyn po

269 In the first cohort, syntaxin, Munc18-1, and Cplx1, but not VAMP, Cplx2, or s

270 From these, we identified SYNTAXIN OF PLANTS 13II (SYP13II) as a t-SNARE that is e

271 by the trans-Golgi network-localized protein SYNTAXIN OF PLANTS61 (SYP61) was increased under CESTRIN

272 at the nearly essential Aspergillus nidulans syntaxin PepA(Pep12) , present in all endocytic compartm

273 neral control the accessibility of the bound syntaxin, probably preparing it for SNARE complex assemb

274 ther disrupting the interaction of Kv2.1 and syntaxin promoted the survival of cortical neurons follo

275 iana involves specific interactions with two syntaxin proteins, namely, the Qc-SNARE SYP61 and the Qa

276 eins might interact simultaneously with both syntaxin regions.

277 wth but becomes essential if the early Golgi syntaxin SedV(Sed5) is compromised, showing that the Gol

278 ng that the Golgi can function with a single syntaxin, SedV(Sed5) .

279 Further, mRNAs for several Syntaxins show CELF2 dependent regulation.

280 nc18, Munc13 additionally ensures the proper syntaxin/SNAP-25 subconfiguration.

281 t tomosyn inhibition is mediated via tomosyn-syntaxin-SNAP25 complexes and not tomosyn-syntaxin compl

282 utants shift the equilibrium between tomosyn-syntaxin-SNAP25 complexes on the PM to tomosyn-syntaxin

283 esent in both syntaxin-tomosyn complexes and syntaxin-SNAP25-tomosyn complexes.

284 ing of Sec1/Munc18 (SM) proteins to specific syntaxin SNARE proteins.

285 Of the four syntaxins specialized for exocytosis, syntaxin (Syn)-2 i

286 ndirectly with the SNARE proteins SNAP25 and Syntaxin (Stx-1).

287 ptic markers involved in exocytosis, such as syntaxin (Stx1b), Ras-related proteins (Rab3a/c), and ra

288 In beta-cells, syntaxin (Syn)-1A interacts with SUR1 to inhibit ATP-sen

289 e four syntaxins specialized for exocytosis, syntaxin (Syn)-2 is the least understood.

290 ndependent of Munc18: it promotes the proper syntaxin/synaptobrevin subconfiguration during assembly

291 ttachment protein receptor (SNARE) proteins (syntaxin, synaptosomal-associated protein 25 [SNAP25], v

292 microtubule-dependent pathway involving the syntaxin SYX-5.

293 2 (syb2) and the two plasma membrane SNAREs syntaxin (syx) and SNAP-25 draws the two membranes toget

294 ophila mutant, which has a point mutation in syntaxin that causes increased spontaneous fusion.

295 Three syntaxins, Tlg2p, Pep12p and Vam3p, organize the yeast e

296 The syntaxin TlgB(Tlg2) localizing to the TGN appears to med

297 These results establish that binding of syntaxin to Kv2.1 is crucial for the manifestation of ox

298 ion, we show that tomosyn is present in both syntaxin-tomosyn complexes and syntaxin-SNAP25-tomosyn c

299 e splicing of two mRNA isoforms of the SNARE Syntaxin/unc-64.

300 gi lack the equivalent of the yeast vacuolar syntaxin Vam3p, making unclear how these organisms regul