ライフサイエンスコーパス: syntaxin 1A

1 s of the alpha1B subunit, beta2a subunit and syntaxin 1A.

2 regulating the interaction between GAT1 and syntaxin 1A.

3 t VAMP2 is substituted to the second copy of syntaxin 1A.

4 ynaptosome-associated protein of 23 kDa) and syntaxin 1A.

5 normally, but are no longer able to bind to syntaxin 1a.

6 not require the membrane anchoring domain of syntaxin 1A.

7 dk5 has a significantly reduced affinity for syntaxin 1A.

8 ecipitation of a complex containing GAT1 and syntaxin 1A.

9 mediated interactions with phospholipids and syntaxin 1A.

10 the NO-enhanced association of VAMP/SNAP-25/syntaxin 1a.

11 mplex and inhibited the binding of n-sec1 to syntaxin 1a.

12 ansporters are modulated by interaction with syntaxin 1A.

13 factor activating protein receptor) protein syntaxin 1A.

14 ffinity for the t-SNARE SNAP25 compared with syntaxin 1A.

15 TR trafficking produced by overexpression of syntaxin 1A.

16 ed an intact interaction between tomosyn and syntaxin 1A.

17 ked release induced by the overexpression of syntaxin-1A.

18 be prevented by uncoupling the channels from syntaxin-1A.

19 wed great identity with syntaxin 1-homologs (syntaxin 1A/1B) from various other species.

20 lated by an epithelially expressed syntaxin (syntaxin 1A), a membrane protein that also modulates neu

21 us oocyte expression system are inhibited by syntaxin 1A, a component of the membrane trafficking mac

22 eral ion channels and pumps are regulated by syntaxin 1A, a component of the synaptic vesicle docking

23 ing a molecule with 63-64% identity to human syntaxin 1A, a membrane- anchored protein involved in sy

24 id binding, (2) calcium-dependent binding to syntaxin 1A, a plasma membrane protein critical for vesi

25 Syntaxin 1A, a presynaptic soluble N-ethylmaleimide-sens

26 ly are regulated by direct interactions with syntaxin 1A, a protein involved in vesicle docking and i

27 This domain directly interacted with syntaxin 1A, a SNARE protein involved in both neurotrans

28 Furthermore, syntaxin 1A, a soluble N-ethylmaleimide-sensitive factor

29 Individual t-SNAREs (e.g., syntaxin 1A) also regulate synaptic calcium channels and

30 sults suggest a new target for regulation by syntaxin 1A and a novel mechanism for controlling the ma

31 chment protein receptor complex (SNARE) with syntaxin 1a and a synaptosomal associated protein of 25

32 physical and functional interactions between syntaxin 1A and CFTR are blocked by a syntaxin-binding p

33 m-specific nature of the interaction between syntaxin 1A and CFTR to identify residues in the H3 doma

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

35 Evidence of interactions between syntaxin 1A and GAT1 comes from three experimental appro

36 avity that showed a reduced interaction with syntaxin 1A and impaired chaperone function, but still b

37 components of the vesicle fusion machinery, syntaxin 1A and Munc-18.

38 Syntaxin 1a and neuronal Sec1 (nSec1) form an evolutiona

39 fector proteins to conformational changes in syntaxin 1a and nSec1 that lead to core complex formatio

40 These findings indicate that syntaxin 1A and other members of the SNARE machinery are

41 the level of vesicle SNARE interaction with syntaxin 1a and secretory responsiveness.

42 The plasma membrane SNAREs syntaxin 1A and SNAP-25 (t-SNAREs) and the delivery-vesi

43 ex, composed of the plasma membrane t-SNAREs syntaxin 1A and SNAP-25 and the vesicle v-SNARE synaptob

44 Syntaxin 1A and SNAP-25 binding was reduced by the M46A

45 icles) lie within a domain required for both syntaxin 1A and SNAP-25 binding.

46 Target plasma membrane SNAREs (t-SNAREs) syntaxin 1A and SNAP-25 form the t-SNARE complex that se

47 The native otoferlin C2F domain bound syntaxin 1A and SNAP-25 in a Ca2+-dependent manner (with

48 greater thermostability than can VAMP2 with syntaxin 1a and SNAP-25 in vitro, but it lacks a transme

49 The interaction between the proteins syntaxin 1A and SNAP-25 is a key step in synaptic vesicl

50 Furthermore, the SNARE proteins syntaxin 1A and SNAP-25 were unable to modulate voltage-

51 Assembly of the plasma membrane proteins syntaxin 1A and SNAP-25 with the vesicle protein synapto

52 red in trans to t-SNARE vesicles (containing syntaxin 1A and SNAP-25).

53 proteins of the hair-cell synaptic complex, syntaxin 1A and SNAP-25, as well as the calcium channel,

54 hat amisyn forms nonfusogenic complexes with syntaxin 1a and SNAP-25, holding them in a conformation

55 proteins of the release apparatus, including syntaxin 1A and SNAP-25.

56 lity characteristics to the rafts containing syntaxin 1A and SNAP-25.

57 inated binding to either syntaxin 1A or both syntaxin 1A and SNAP-25.

58 A or SNAP-25 and ternary complexes with both syntaxin 1A and SNAP-25.

59 In the neuron, the plasma membrane SNAREs syntaxin 1a and SNAP25 bind to VAMP2 found on neurotrans

60 Basal ENaC currents were inhibited by syntaxin 1A and stimulated by syntaxin 3.

61 al interaction at the ionic layer by cuffing syntaxin 1A and synaptobrevin 2, similar to the action o

62 e interactions between two synaptic proteins syntaxin 1A and synaptobrevin 2, using an atomic force m

63 ttachment protein receptor (tSNARE) proteins syntaxin 1A and synaptosomal-associated protein of 25 kD

64 otein 2 (VAMP2) and plasma membrane proteins syntaxin 1A and synaptosome-associated protein of 25 kDa

65 2 (VAMP-2) and the plasma membrane proteins syntaxin 1A and synaptosome-associated protein of 25 kDa

66 Both syntaxin 1A and syntaxin 3 could be co-immunoprecipitate

67 Syntaxin 1A and syntaxin 3 inhibit the membrane expressi

68 The interaction of syntaxin 1A and syntaxin 3B with other synaptic proteins

69 Toward this end we show here that both Syntaxin 1A and Syntaxin 4 associated with F-actin in MI

70 il-forming domain that binds specifically to syntaxin 1a and syntaxin 4 both in vitro and in vivo, as

71 ally, it is shown that Cdk5 can also bind to syntaxin 1A and that a complex of Cdk5, p35, Munc-18, an

72 Membrane topologies of syntaxin 1A and the t-SNARE complex were investigated us

73 interactions among the target SNARE protein Syntaxin 1A and the vesicle-associated membrane SNARE pr

74 k5 acts to regulate Munc18a interaction with syntaxin 1a and thereby modulates the level of vesicle S

75 an autonomously folded N-terminal domain in syntaxin 1A and to elucidate its three-dimensional struc

76 boxyl-terminal transmembrane anchors of both syntaxin 1A and VAMP2 were protected from trypsin digest

77 in multiple experimental systems expressing syntaxin 1A and wild-type GAT1 or GAT1 mutants.

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

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

80 between helices B and C that differ between syntaxin-1a and epimorphin/syntaxin-2; through site-dire

81 Interaction between the syntaxin-1A and H+-ATPase is important in the targeted e

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

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

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

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

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

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

88 ne-mimicking vesicles containing full-length syntaxin-1A and SNAP-25A.

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

90 H+-ATPase (subunits E, a, and c) bound to syntaxin-1A and to a lesser extent to synt-1B but not to

91 SNAP-25 and one coiled-coil domain each from syntaxin-1a and VAMP-2.

92 Syntaxins 1A and 1B were present only in intracellular s

93 a chaperone when it interacts with monomeric syntaxin 1A, and it can activate soluble N-ethylmaleimid

94 tive factor attachment protein-25 (SNAP-25), syntaxin 1A, and synaptobrevin.

95 SNAP-25, syntaxin 1A, and synaptobrevin/vesicle-associated membra

96 reviously characterized N-terminal domain of syntaxin 1A, and, unlike syntaxin 1A, the N-terminal dom

97 ) receptor (SNARE) proteins synaptobrevin 2, syntaxin-1A, and SNAP-25 is the key step that leads to e

98 ntaxin-2 based on the published structure of syntaxin-1a, and we use this model to identify the struc

99 es: botulinum toxin cleavage of syntaxin 1A, syntaxin 1A antisense treatments, and coimmunoprecipitat

100 n proposed that interactions of SNAP-25 with syntaxin 1A are required for initial membrane attachment

101 Using yeast two-hybrid selection with syntaxin-1A as bait, we have isolated a cDNA encoding th

102 Using the yeast two-hybrid system with syntaxin-1A as bait, we isolated soluble NSF attachment

103 deletion of this domain both eliminates NET/syntaxin 1A associations and prevents phorbol ester-trig

104 epithelial cells from these tissues express syntaxin 1A at >10-fold molar excess over CFTR.

105 lar Cdc42-VAMP2-insulin granule complexes to Syntaxin 1A at the plasma membrane.

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

107 d by soluble syntaxin 1A peptides and by the syntaxin 1A binding protein, Munc-18.

108 lux was mimicked by mutations in GAT1 at the syntaxin 1A binding site.

109 None of these mutations affected syntaxin 1A binding to other SNAREs or the assembly and

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

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

112 Here we report that the syntaxin-1a-binding protein Munc18a, which interacts wit

113 The present data show that the SNARE protein syntaxin 1A binds the N-terminal tail of SERT, and this

114 Syntaxin 1A binds the NH(2) terminal domain of NET, and

115 Syntaxin 1A binds to and inhibits epithelial cystic fibr

116 We also show that syntaxin 1A binds to and inhibits the activities of dise

117 s revealed increased levels of mRNA encoding syntaxin 1A but decreased Munc18-1 and ZnT8 mRNA.

118 ressed by the simultaneous overexpression of syntaxin-1A but not by the coexpression of SNAP-25.

119 nt at low Gbetagamma concentrations, and (2) syntaxin-1A (but not syntaxin-1B) shifts the ratio in fa

120 The otoferlin C2D domain also bound syntaxin 1A, but with weaker affinity (Kd = 1.7 x 10(-5)

121 alcium channel family were also regulated by syntaxin-1A, but to a smaller extent.

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

123 Here, we report the existence of a syntaxin-1A/Ca(v)3.2 T-type calcium channel signaling co

124 fects on transmitter release of manipulating syntaxin 1A-calcium channel interactions at Xenopus tadp

125 tion in vitro, it has been hypothesized that syntaxin 1A-calcium channel interactions could alter cal

126 nprint peptides, which competitively perturb syntaxin 1A-calcium channel interactions, decreased quan

127 and vesicle recycling and that the affected syntaxin-1A/CaMKII interaction is essential for normal b

128 nd that a complex of Cdk5, p35, Munc-18, and syntaxin 1A can be fashioned in the absence of ATP and p

129 signaling-related proteins such as Gbeta and syntaxin 1A can be in this higher order complex of CFTR

130 -dependent modulation of the Ca2+ current by syntaxin 1A cannot explain the large suppression of Ca2+

131 Thus, syntaxin 1A cannot inhibit Na(+) permeability in the abs

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

133 Syntaxin 1A caused similar reductions in forward and rev

134 indicated that this single point mutation in syntaxin-1A causes abnormal regulation of neuronal plast

135 Conversely, the syntaxin 1A-CFTR interaction was unaffected by mutating

136 ous studies on N- or P/Q-type Ca2+ channels, syntaxin 1A co-expression reduced current amplitudes, in

137 ivated Cdk5 becomes localized to the Munc-18-syntaxin 1A complex by its affinity for both proteins so

138 The Munc-18-syntaxin 1A complex has been postulated to act as a nega

139 The crystal structure of the nSec1-syntaxin 1a complex, determined at 2.6 A resolution, rev

140 aracterize the dynamic properties of tomosyn-syntaxin 1A complexes in live adrenal chromaffin cells.

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

142 rents are effectively inhibited by a minimal syntaxin 1A construct (i.e., the membrane-anchored H3 do

143 that the transmembrane domains of VAMP2 and syntaxin 1A contribute to complex assembly and stability

144 Syntaxin 1a contributes one such region, designated H3,

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

146 nors increased formation of the VAMP/SNAP-25/syntaxin 1a core complex and inhibited the binding of n-

147 Cdc42 and that a heterotrimeric complex with Syntaxin 1A could also be formed.

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

149 R-syntaxin 1A interaction, including soluble syntaxin 1A cytosolic domain and recombinant Munc-18, au

150 protein phosphatase 2A catalytic subunit and syntaxin 1A decreased after PD169316 or beta-PMA treatme

151 of epitope-tagged ENaC subunits showed that syntaxin 1A decreases ENaC current by reducing the numbe

152 egion of the cytoplasmic domain of the SNARE syntaxin 1A, designated H3, contributes one of the four

153 urthermore, expression of a cytosolic mutant syntaxin 1A did not interfere with SNAP-25 membrane inte

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

155 8-1, whereas the same mutation in the "open" syntaxin-1A disrupts it.

156 18-1 domain 3a hinge-loop therefore controls syntaxin-1A engagement into SNARE complex formation duri

157 We have shown previously that syntaxin 1A exerts its effects on GAT1 by decreasing the

158 These data suggest that syntaxin 1A exerts its effects, directly or indirectly,

159 NAP-25 the single-span transmembrane protein syntaxin-1A forms the receptor complex on the plasma mem

160 Using these syntaxin 1A fragments, we demonstrated that blocking tra

161 Immunoprecipitation of syntaxin 1A from the sodium-transporting epithelial cell

162 tic membranes is preserved by the sorting of syntaxin-1A from recycling synaptic vesicles.

163 Syntaxin 1a H3 (syn1aH3) and SNAP25 can form a stable as

164 Soluble syntaxin 1A H3 domain partially blocks Munc18-1 activati

165 In the crystal structure of syntaxin 1A H3, four molecules associate as a homotetram

166 which correspond to sequences located in the syntaxin-1A H3 domain, the C-terminal domain of SNAP-25,

167 d, and 3) the inhibition of ASIC currents by syntaxin 1A had an absolute requirement for either gamma

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

169 Munc18a in vitro within a preformed Munc18a.syntaxin 1a heterodimer complex and that this results in

170 structure is maintained up to residue 259 of syntaxin 1A, identical to that of the ternary complex.

171 NETs colocalize with and bind to syntaxin 1A in both native preparations and heterologous

172 tentiated by disrupting its interaction with syntaxin 1A in cultured epithelial cells.

173 ) that cannot fully substitute for wild-type syntaxin 1A in membrane fusion reactions.

174 blotting and immunofluorescence, we observed syntaxin 1A in native gut and airway epithelial tissues

175 specific residues that map to the surface of syntaxin 1A in the SNARE complex led to the identificati

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

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

178 ) has been shown previously to phosphorylate syntaxin-1A in vitro and we have identified Ser14 as the

179 hilin significantly decreases its binding to syntaxin-1A in vitro.

180 Removal of the N-terminal H(abc) domain of syntaxin 1A increased fusion probability >30-fold compar

181 Of most significance, syntaxin 1A increased voltage-dependent inactivation in

182 resected and cultured high grade gliomas, 2) syntaxin 1A inhibited ASIC currents only when ASIC1 and

183 Here we report that syntaxin 1A inhibits CFTR chloride channels by means of

184 Syntaxin 1A inhibits GABA uptake of an endogenous GABA t

185 Thus, modulation of the tomosyn-syntaxin 1A interaction in response to secretagogue acti

186 s associated with an increase in the tomosyn-syntaxin 1A interaction, including increased cycling of

187 Reagents that disrupt the CFTR-syntaxin 1A interaction, including soluble syntaxin 1A c

188 ein kinase C activation disrupts surface NET/syntaxin 1A interactions and downregulates NET activity

189 that substrate translocation regulates GAT1-syntaxin 1A interactions and provide a mechanism by whic

190 modulated by molecules that disrupt SERT and syntaxin 1A interactions.

191 wo identical copies of the SNARE region from syntaxin 1A intertwine as a coiled coil near the "ionic

192 Here, we have reconstituted syntaxin-1A into lipid model membranes, and we show that

193 Thus, CFTR channel regulation by syntaxin 1A involves hydrophilic interactions that are m

194 Syntaxin 1a is a plasma membrane soluble N-ethylmaleimid

195 to the Habc domain and the configuration of syntaxin 1a is dominated by a closed state.

196 The modulation of CFTR currents by syntaxin 1A is eliminated either by deletion of this tai

197 In the present study, we determined whether syntaxin 1A is expressed in native epithelial tissues th

198 ansporter mutant that fails to interact with syntaxin 1A is not regulated by PKC.

199 Syntaxin 1A is seen near the apical cell surfaces of hum

200 Syntaxin-1A is a t-SNARE that is involved in vesicle doc

201 However, the internal fraction of syntaxin-1A is excluded from synaptic vesicles that unde

202 Syntaxin-1A is part of the SNARE complex that forms in m

203 In this report, we show that syntaxin-1A is phosphorylated in vitro by CKI on Thr21.

204 We report here that syntaxin-1A is predominantly localized to the plasma mem

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

206 entified as a binding partner of the Q-SNARE syntaxin 1A, is thought to be critical in setting the le

207 The CFTR binding site on syntaxin 1A maps to the third predicted helical domain (

208 ation of the interaction between Munc18a and syntaxin 1a may provide an important mechanism controlli

209 The syntaxin 1A-mediated reduction in GABA flux and efflux w

210 d to the plasma membrane, and in particular, syntaxin 1a mediates synaptic vesicle docking in the ner

211 mes, which exclude the plasma membrane SNARE syntaxin 1A, merge with those derived from clathrin-depe

212 on modulation is mimicked by coinjection of syntaxin 1a mRNA and is eliminated by injecting synaptop

213 Injection of wild-type syntaxin 1A mRNA had no effect.

214 in oocytes expressing interaction-deficient syntaxin 1A mutants.

215 n is descended from the same ancestor as the syntaxin 1a N-terminal domain, and that both protein fam

216 Previous studies have shown that syntaxin-1A occurs in clusters that are different from l

217 These two contradictory roles of syntaxin 1A on NET appear to be linked and reveal a dyna

218 dy was undertaken to determine the effect of syntaxin 1A on this weakly inactivating Ca2+ channel.

219 no effect on fusion, and the same change in syntaxin 1A only reduced the extent and rate of fusion b

220 pimorphin/syntaxin-2 is highly homologous to syntaxin-1a, only epimorphin/syntaxin-2 can stimulate ma

221 ENaC cRNA (alpha, beta, gamma subunits) with syntaxin 1A or 3 cRNAs in Xenopus oocytes.

222 omain of VAMP-2 eliminated binding to either syntaxin 1A or both syntaxin 1A and SNAP-25.

223 he formation of binary complexes with either syntaxin 1A or SNAP-25 and ternary complexes with both s

224 eir competence to form complexes with either syntaxin 1A or SNAP-25.

225 Mutagenesis of either syntaxin 1A or the pore-forming alpha(1B) subunit of N-t

226 Hypomorphic mutations in syntaxin-1A or n-synaptobrevin, which also disrupt neuro

227 Biochemical studies suggest that syntaxin 1A participates in multiple protein-protein int

228 of CFTR function can be reversed by soluble syntaxin 1A peptides and by the syntaxin 1A binding prot

229 Syntaxin-1A phosphorylation by DAP kinase or its S188D m

230 Syntaxin 1A physically interacts with CFTR chloride chan

231 Syntaxin 1A plays a central role in neurotransmitter rel

232 interactions and demonstrate that Drosophila syntaxin 1A plays multiple regulatory roles in neurotran

233 As syntaxin-1A plays a key role in the regulation of neurot

234 The SNARE protein syntaxin 1A, primarily known for important interactions

235 nc-64, which encodes the presynaptic protein syntaxin 1A, produce large allele-specific differences i

236 sing effects of synprint peptides and mutant syntaxin 1A provide in vivo support for the hypothesis t

237 axin, we generated mice with a knock-in (KI) syntaxin-1A (R151G) mutation.

238 To further understand the mechanisms of syntaxin 1A regulation of this weakly inactivating chann

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

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

241 We found that ovaries that are mutant for syntaxin-1a, rop, and synaptotagmin are also defective i

242 e implicated a role for the t-SNARE protein, syntaxin 1A (S1A), in the regulation of ENaC current (I(

243 actor attachment protein receptor)) protein, syntaxin 1A (S1A), inhibits ENaC mediated sodium entry.

244 revious results showed that the H3 domain of syntaxin-1A (S1A) binds to ENaC to reduce N, supporting

245 Syntaxin-1A, SNAP-25, and synaptobrevin-2 (also known as

246 ynaptic protein complex, recombinant binary (syntaxin 1A.SNAP-25), recombinant ternary, and native te

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

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

249 Syntaxin 1A stoichiometrically binds to the N-terminal c

250 Here, we report a transport complex linking syntaxin 1a (Stx) and Munc18, two proteins functioning i

251 rons that endogenously express both GAT1 and syntaxin 1A, substrate application results in a decrease

252 etic and biochemical interactions of CSP and syntaxin-1A suggest that CSP may chaperone or modulate p

253 In oocytes expressing GAT1 and syntaxin 1A, superfusion of transporter substrates incre

254 Whereas syntaxin 1A supports the surface trafficking of NET prot

255 teractions between synaptobrevin 2 (Sb2) and syntaxin 1A (Sx1A) can be readily isolated and studied w

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

257 Here we report that syntaxin 1A (syn1A) coexpressed with N-type channels in

258 e factor attachment protein receptor protein syntaxin 1A (SYN1A) interacts with and regulates the fun

259 Recently, we demonstrated that syntaxin 1A (SYN1A) regulates NET surface expression and

260 te for such a regulator is the SNARE protein syntaxin 1A (Syn1A), previously found to interact with h

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

262 The three neuronal SNAREs syntaxin-1A, synaptobrevin-II (VAMP), and SNAP-25A were

263 ntal approaches: botulinum toxin cleavage of syntaxin 1A, syntaxin 1A antisense treatments, and coimm

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

265 (5RK) of the plasma membrane neuronal SNARE, syntaxin 1A (Syx), in vesicle exocytosis, although widel

266 Here, we report that Syntaxin 1A (Syx1A) is required for efficient traffickin

267 We identified two proteins, Rab11 and Syntaxin 1A (Syx1A), that were required for Evi vesicle

268 e compelling evidence for the existence of a syntaxin-1A/T-type Ca(2+) channel signaling complex and

269 ated whether the subcellular localization of syntaxin-1A, tagged with the pH-sensitive fluorescent ta

270 nd branching morphogenesis onto the inactive syntaxin-1a template.

271 ion results in a decrease in the fraction of syntaxin 1A that is bound to GAT1 on a time-scale compar

272 ensitive factor attachment protein receptor) syntaxin 1A that is found in conventional synapses of th

273 direct physical interaction between CFTR and syntaxin 1A that limits the functional activities of nor

274 r interaction with another synaptic protein, syntaxin 1A, that was deposited onto the cantilever tip.

275 etry, included a carboxyl-terminal region of syntaxin 1A, the cytoplasmic domain of VAMP2, and amino-

276 -terminal domain of syntaxin 1A, and, unlike syntaxin 1A, the N-terminal domain of mSec22b has no eff

277 sidues mutated to alanine was assembled with syntaxin 1A, there was significantly reduced affinity of

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

279 asmic domain of GAT1 directly interacts with syntaxin 1A; this interaction induces a decrease in the

280 ry effects by regulating the availability of syntaxin 1A to interact with the transporter, and a tran

281 ransmembrane (TM) domain to the TM domain of syntaxin 1A to trigger transmitter release.

282 dulator of neural plasticity, interacts with syntaxin-1A to regulate exocytosis, and 2) that a syntax

283 known vesicle targeting and fusion proteins syntaxin 1A, Vamp 2, and SNAP23.

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

285 This phenotype was not rescued when syntaxin 1A was co-expressed with SNAP-25.

286 tural similarity to the N-terminal domain of syntaxin 1a was discovered, comprising the entire three-

287 nal conserved domain of the neuronal t-SNARE syntaxin-1A was determined to a resolution of 1.9 A usin

288 site of alpha1B and the C-terminal third of syntaxin 1A were necessary for the reduced current ampli

289 nts of SNAP-25, when combined with VAMP2 and syntaxin 1A, were sufficient for stable complex assembly

290 Finally, we found that SNAP-23/25 and syntaxin 1A, when co-expressed in MDCK cells, do not sta

291 red cells, the plasma membrane SNARE protein syntaxin 1A, when expressed as a full-length protein, di

292 ty interaction with the target SNARE protein syntaxin 1a (where SNARE is derived from SNAP receptor (

293 eractions between SNAP-23 and CFTR depend on syntaxin 1A, which binds to both proteins.

294 st, injecting mRNA for mutant (A240V, V244A) syntaxin 1A, which reduces calcium channel modulation bu

295 agent NEM inhibited the binding of n-sec1 to syntaxin 1a, while beta-ME could reverse the NO-enhanced

296 interaction between known binding partners, syntaxin 1a with neuronal Sec1 (nSec1), and the fibrobla

297 favoring the interaction of the H3 region of syntaxin 1a with other proteins involved in membrane fus

298 Co-expression of syntaxin 1A with the weakly inactivating bovine N-type C

299 and thus permit the positive interaction of syntaxin 1A with upstream protein effectors of the secre

300 or modulate protein-protein interactions of syntaxin-1A with either calcium channels or other compon