ライフサイエンスコーパス: syntaxin

1 function of UNC-13/Munc13 in opening UNC-64/ syntaxin.

2 fficking of FasII and synaptobrevin, but not syntaxin.

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

4 x formation through high-affinity binding to syntaxin.

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

6 opening of a 'closed' conformation of UNC-64/syntaxin.

7 s that are otherwise completely unrelated to syntaxins.

8 GSIS, and we have identified SUMOylation of syntaxin 1 A as a potential component of this brake.

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

10 ate containing Munc18-1 and 2 SNARE proteins-syntaxin 1 and VAMP2.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

25 gth amisyn forms a stable SNARE complex with syntaxin-1 and SNAP-25 through its C-terminal SNARE moti

26 tic vesicles (SVs), forms helix bundles with syntaxin-1 and SNAP25 for the SNARE assembly.

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

28 ible linker facilitates its interaction with syntaxin-1 and SNARE-complex assembly.

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

30 formation of syntaxin-1 not only in the free syntaxin-1 but also in the t-SNARE (syntaxin-1/SNAP-25)

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

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

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

34 ex is biased toward the open conformation of syntaxin-1 compared with the binary complex.

35 1 catalyzes the transition from the Munc18-1/syntaxin-1 complex to the SNARE complex, the molecular m

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

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

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

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

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

41 rnary SNARE complex formation by locking the syntaxin-1 in a cleft of Munc18-1.

42 protein Munc18-1 traps the Qa-SNARE protein syntaxin-1 in an autoinhibited closed conformation.

43 g/closing transition reveals that the closed syntaxin-1 in the syntaxin-1/SNAP-25/Munc18-1 complex is

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

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

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

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

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

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

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

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

52 1 proteins induce the closed conformation of syntaxin-1 not only in the free syntaxin-1 but also in t

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

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

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

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

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

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

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

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

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

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

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

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

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

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

67 ntly inhibits liposome fusion by: binding to syntaxin-1, hindering Munc18-1 binding; binding to synta

68 is avoided only when Munc18-1 binds first to syntaxin-1, leading to Munc18-1-Munc13-1-dependent lipos

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

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

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

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

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

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

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

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

77 rate assembly of the SNARE complex formed by syntaxin-1, SNAP-25 and synaptobrevin, allowing exquisit

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

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

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

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

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

83 in-1, hindering Munc18-1 binding; binding to syntaxin-1-SNAP-25 heterodimers, precluding SNARE comple

84 ution assays with the neuronal SNAREs, using syntaxin-1-SNAP-25-containing liposomes and liposomes co

85 brevin and the target (t)-SNAREs Snap-25 and syntaxin-1.

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

87 mplex is less stable than that in the closed syntaxin-1/Munc18-1 complex, which is manifested by the

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

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

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

91 at septin 7 interacts with the SNARE protein syntaxin 11 and facilitates its interaction with syntaxi

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

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

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

95 1; and a SNAP receptor complex consisting of Syntaxin 13, Snap29, and Vamp7 are all required for the

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

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

98 We found that Syntaxin 16 (Stx16) and its cognate SNARE partners all h

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

100 Syntaxin 17 (Stx17) has been implicated in autophagosome

101 We show that autophagosomal syntaxin 17 (Stx17) heterotrimerizes with synaptosome-as

102 markably, LAMP-2B functions independently of syntaxin 17 (STX17), a protein that is essential for aut

103 Syntaxin 17 (Stx17), a SNARE with major roles in autopha

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 tochondria communication through cleavage of syntaxin 17.

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

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

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

112 Syntaxin-17 remains associated with mature MDVs and form

113 eviously identified NBAS, a component of the Syntaxin 18 complex involved in Golgi-to-ER trafficking,

114 ogenic proteins, including the SNARE protein syntaxin-18.

115 an pseudoislets showed reduced SNARE protein syntaxin 1a (STX1A), a key SNARE component.

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

117 (5RK) of the plasma membrane neuronal SNARE, syntaxin 1A (Syx), in vesicle exocytosis, although widel

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

119 ce expressed normal levels of total SNAP-25, Syntaxin 1A and SNAP-47 in the hippocampus, but females

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 factor activating protein receptor) protein syntaxin 1A.

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

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

128 osome-associated protein of 25 kDa (SNAP25), syntaxin-1a (syx-1), and synaptobrevin 2, which is essen

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

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

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

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

137 Together with its partners syntaxin-1A and synaptosomal-associated protein 25 (SNAP

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

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

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

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

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

153 Moreover, proteins (Rab3a, syntaxin-1A, and VAMP2) involved in exocytosis also loca

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

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

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

159 Here, we report that the H(abc) domain of syntaxin 3 (Stx3) indeed binds to monomeric ubiquitin wi

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

161 Here we evaluate the role of syntaxin 3 (STX3), in trafficking of OS membrane protein

162 segment plasma membrane proteins, including syntaxin 3 (STX3), synaptosome-associated protein 25 (SN

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

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

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

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

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

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

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

170 SNAREs involved remain highly controversial; syntaxin-3 and syntaxin-4 are leading candidates for the

171 recordings in hippocampal slices showed that syntaxin-3 cKO did not exhibit significant changes in CA

172 Syntaxin-3 cKO mice performed similarly as the controls

173 Here, we generated and analyzed syntaxin-3 cKO mice.

174 Consistent with the minimal effects of syntaxin-3 cKO, syntaxin-3 mRNA level was very low in hi

175 However, this does not exclude a role for syntaxin-3 in such processes.

176 Together, our data suggest that syntaxin-3 is dispensable for hippocampal basal neurotra

177 with the minimal effects of syntaxin-3 cKO, syntaxin-3 mRNA level was very low in hippocampal and co

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

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

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

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

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

183 ated interference in the interaction between syntaxin 4 and VAMP2, leading to the dysfunction of the

184 assays indicate that Fer1l6 colocalizes with syntaxin 4 and vinculin, and that the putative C2 domain

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

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

187 VAMP3, SNAP-29, and syntaxin 4 proved important in driving cytokine release

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

189 e identify an endosomal trafficking protein, Syntaxin 4, which is specifically involved in the presen

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

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

192 18c) regulates membrane fusion by activating syntaxin-4 (STX-4) to bind cognate SNARE proteins to for

193 remain highly controversial; syntaxin-3 and syntaxin-4 are leading candidates for the syntaxin isofo

194 ticity, and further supports the notion that syntaxin-4 is the major isoform mediating these processe

195 euron specific conditional knockout (cKO) of syntaxin-4 significantly reduces basal transmission, syn

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

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

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

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

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

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

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

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

204 Overall, syntaxin 6 could be a prognostic biomarker for patients

205 exhibited a significant correlation between syntaxin 6 expression and survival.

206 rall survival (OS) between groups, with high syntaxin 6 expression correlating with decreased surviva

207 Next, syntaxin 6 expression was evaluated in clear cell (786-O

208 Syntaxin 6 expression was higher in Caki-1 and ACHN RCC

209 ) was queried for clinicopathologic data and syntaxin 6 expression.

210 Silencing of syntaxin 6 in ACHN cells significantly decreased the cel

211 Here, we examined the tumorogenic role of syntaxin 6 in renal cell carcinoma (RCC).

212 iomarker for patients with papillary RCC and syntaxin 6 inhibitors hold promise as a novel therapy ag

213 Syntaxin 6 is a SNARE family protein known to play an im

214 the curve (AUC) to determine the ability of syntaxin 6 to predict 3-year overall survival.

215 The AUC for syntaxin 6 was 0.73, significantly higher compared to 0.

216 calised with the trans-Golgi network protein syntaxin 6, but after 5 hours BFA treatment, TPD52 showe

217 aminopeptidase (IRAP) and the SNARE protein Syntaxin 6.

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

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

220 corticotropes, SSTR2 moves to a juxtanuclear syntaxin-6-positive compartment, where it remains until

221 F), whereupon SSTR2 exits the compartment on syntaxin-6-positive vesicular/tubular carriers that depe

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

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

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

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

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

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

228 Syntaxin, a transmembrane protein on the plasma membrane

229 However, open syntaxin aggravates the defects of unc-18/Munc18 mutants

230 It cleaves the mosquito syntaxin and employs a unique receptor recognition strat

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

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

233 The two syntaxins and their two homeologs were mutated, individu

234 n of raga-1 mutant longevity requires UNC-64/syntaxin, and promotes mitochondrial fission cell nonaut

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

236 eceptor) complex, composed of synaptobrevin, syntaxin, and SNAP25, forms the essential fusion machine

237 Syntaxins are a family of membrane-anchored SNARE protei

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 axin 11 and facilitates its interaction with syntaxin binding protein 2 to promote lytic granule fusi

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

243 Syntaxin-binding protein 1 (STXBP1, also known as MUNC18

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

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

246 (2+) channels, whereas overexpression of the syntaxin-binding protein Doc2B or ubMunc13-2 increases s

247 Here, we revisit the effects of open unc-64/syntaxin by generating knockin (KI) worms.

248 ding of the molecular mechanism by which the syntaxin cluster regulates membrane fusion.

249 lants; importantly, the genes encoding these syntaxins co-localize with SCN resistance quantitative t

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

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

252 Syntaxins contain an N-terminal regulatory domain, terme

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

254 ur results show that facilitating opening of syntaxin enhances exocytosis in a wide range of genetic

255 Other syntaxin family members also bind to K63-linked poly-ubi

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

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

258 Peking roots with deletions introduced into syntaxin genes exhibited significantly reduced resistanc

259 We conclude that the syntaxin H(abc) domain and the GAT domain are both struc

260 The syntaxin H(abc) domain has previously been found to be s

261 While syntaxin homodimerization is supposed to promote the tra

262 nd no changes for SNAP-25, PSD-95, VAMP, and syntaxin in frontal cortex.

263 e H(abc) domain may regulate the function of syntaxins in membrane fusion or may suggest additional f

264 nd syntaxin-4 are leading candidates for the syntaxin isoform underlying postsynaptic plasticity.

265 Unexpectedly, the open syntaxin KI partially suppresses exocytosis defects of v

266 e, we show that the plasma membrane-resident syntaxin-like glutamine-soluble N-ethylmaleimide-sensiti

267 that the alpha-SNAP and the two interacting syntaxins localize to the plasma membrane and perinuclea

268 in we hypothesized that the H(abc) domain of syntaxins may also bind to ubiquitin.

269 wed that these three genes converge onto the syntaxin-mediated neurotransmitter release pathway, whic

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

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

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

273 otein attachment protein receptor (Q-SNARE), SYNTAXIN OF PLANTS121 (SYP121), interacts with QUIRKY (Q

274 psis (Arabidopsis thaliana) Qa-SNARE SYP132 (Syntaxin of Plants132) as a key factor in H(+)-ATPase tr

275 le map describing the glycome profile of the SYNTAXIN OF PLANTS61 (SYP61) trans-Golgi network compart

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

277 association of several residents, including SYNTAXIN OF PLANTS61, and altered vesicle morphology in

278 Rhg1 alpha-SNAP strongly interacts with two syntaxins of the t-SNARE family (Glyma.12G194800 and Gly

279 Correspondingly, open syntaxin partially bypasses the requirement of Munc13 bu

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

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

282 taxin1A with respect to the membrane hosting syntaxin's transmembrane domain was investigated with na

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

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

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

286 /Munc18 (SM) protein VPS33A, mirroring other syntaxin-SM interactions and therefore suggesting a unif

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

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

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

290 Syntaxin (STX)-5 and alpha-soluble N-ethylmaleimide-sens

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

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

293 cess that requires SNARE proteins, including syntaxins (Stxs).

294 tant phenotypes by overexpressed open UNC-64/syntaxin suggested a specific function of UNC-13/Munc13

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

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

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

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

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

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

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