ライフサイエンスコーパス: VAMP2

1 , and Vesicle-Associated Membrane Protein 2 (VAMP2).

2 2 and 3, but at a novel site (Arg66-Ala67 in VAMP2).

3 ) and vesicle-associated membrane protein 2 (VAMP2).

4 osis, vesicle-associated membrane protein 2 (VAMP2).

5 in of vesicle-associated membrane protein 2 (VAMP2).

6 of a soluble SNARE coil domain derived from VAMP2.

7 P-25 heterodimers were able to interact with VAMP2.

8 SNARE regions to the fusogenic complex with VAMP2.

9 es containing syntaxin1A, but not SNAP-25 or VAMP2.

10 ampus, but females expressed lower levels of VAMP2.

11 of 200 kDa (FIP200), as a binding partner of VAMP2.

12 Munc18-1 and 2 SNARE proteins-syntaxin 1 and VAMP2.

13 complexes containing syntaxin4, SNAP23, and VAMP2.

14 addition, septin 7 coimmunoprecipitates with VAMP2.

15 as not able to interact with synaptobrevin-2/VAMP2.

16 otein and compared the relative abundance of VAMP2/3 in JG cells versus total mouse kidney mRNA by qu

17 Genetic inactivation of VAMP2/3 in myelinating oligodendrocytes caused severe hy

18 Overall, our results show that functional VAMP2/3 in OL lineage cells is essential for proper myel

19 age of the vesicle associated SNARE proteins VAMP2/3 in the OL lineage of both male and female mice i

20 We found that OLs with cleaved VAMP2/3 in the spinal cord white matter showed significa

21 igodendrocyte surface proteins revealed that VAMP2/3 incorporates axon-myelin adhesion proteins that

22 In this study, we show that VAMP2/3, SNARE proteins involved in vesicular traffickin

23 In the developing mouse spinal cord, many VAMP2/3-cleaved OLs appeared to stall in the premyelinat

24 Through live imaging, we discovered that VAMP2/3-mediated exocytosis drives membrane expansion wi

25 Together, our results demonstrate that VAMP2/3-mediated membrane expansion in oligodendrocytes

26 sis mediated by the vesicular SNARE proteins VAMP2/3.

27 on of vesicle-associated membrane protein 2 (VAMP2)-a component of the SNARE complex that resides on

28 ), show impaired Kif1a-mediated transport of Vamp2, a cargo of Kif1a, with decreased run length.

29 C2b with YES kinase and increased content of VAMP2, a protein on insulin secretory granules, at the p

30 n the final maturation of many peptides, and VAMP2, a vesicle soluble N-ethylmaleimide-sensitive fact

31 hat helix 12 provides a folding template for VAMP2, accelerating SNAREpin assembly and membrane fusio

32 In one, alpha-syn binds to VAMP2, acting as a SNARE chaperone-but with no effect on

33 VAMP2 acts together with mycolate structure to inhibit p

34 VAMP2 encodes the vesicular SNARE protein VAMP2 (also called synaptobrevin-2).

35 n VAMP8 knock-out (-/-) acini confirmed that VAMP2 and -8 are the primary VAMPs for regulated exocyto

36 vesicle-associated membrane protein family (VAMP2 and -8) thought to regulate exocytosis.

37 vesicle-associated membrane proteins (VAMP), VAMP2 and -8, each controlling 50% of stimulated secreti

38 nstrate that TRPC3-N terminus interacts with VAMP2 and alphaSNAP.

39 ve alpha-synuclein with both synaptobrevin-2/VAMP2 and anionic lipids.

40 l lethality of the syb mutations, as can rat VAMP2 and cellubrevin.

41 Condensate formation is specific for R-SNARE VAMP2 and dependent on alphaSYN lipid membrane binding.

42 Additionally, we showed that both VAMP2 and FIP200 are critical for murine keratinocyte en

43 we used tetanus toxin to chronically cleave VAMP2 and inhibit SNARE-mediated neurotransmitter releas

44 Depletion of both VAMP2 and NCS1 individually resulted in the reduced upta

45 of two endogenous axonal membrane proteins, VAMP2 and NgCAM, in order to elucidate the cellular even

46 f endogenous fluorescent labeled presynaptic VAMP2 and postsynaptic PSD95 in long-term cultured live

47 y of SNAP-25 to interact with syntaxin 1 and VAMP2 and prevents the assembly of the SNARE complex.

48 entified a first phase (0-2 min) mediated by VAMP2 and second (2-10 min) and third phases (10-30 min)

49 of beta-cells, interact with SNARE proteins VAMP2 and SNAP25, colocalize with insulin granules, and

50 complex with two synaptic vesicle proteins, VAMP2 and synapsin-I, both of which must be phosphorylat

51 Fusions of miniSOG to VAMP2 and synaptophysin enabled disruption of presynapti

52 resynaptic neurotransmitter release proteins VAMP2 and synaptophysin.

53 ts suggest that the transmembrane domains of VAMP2 and syntaxin 1A contribute to complex assembly and

54 nal fragments of SNAP-25, when combined with VAMP2 and syntaxin 1A, were sufficient for stable comple

55 er GLUT4-vesicle proteins including IRAP and VAMP2 and that GLUT4 sequestration is saturable.

56 unilamellar vesicles containing the v-SNARE VAMP2 and the Ca(2+) sensor synaptotagmin 1.

57 ssion of the presynaptic proteins SNAP25 and VAMP2 and the postsynaptic protein SYNGAP1.

58 croscopy confirms both the SNARE identity as VAMP2 and the proteolysis of VAMP2 as a marked decrease

59 d to determine the specific cleavage site in VAMP2 and the susceptibility of VAMP8 (endobrevin).

60 We conclude that VAMP2 and VAMP3 are expressed in JG cells, but only VAMP

61 We found that VAMP2 and VAMP3 mRNA are expressed and enriched in JG ce

62 Cleavage of VAMP2 and VAMP3 with tetanus toxin blocked cAMP-stimulat

63 Assembled BoNT/X cleaves VAMP2 and VAMP4 in cultured neurons and causes flaccid p

64 this approach, we confirm the requirement of VAMP2 and VAMP7 for insulin and osmotic shock traffickin

65 The unique cleavages of VAMP2 and VAMP8 may be linked to pancreatitis that devel

66 Thus, we hypothesized that VAMP2 and/or -3 mediate cAMP-stimulated renin release fr

67 e, we investigated whether overexpression of VAMP2 and/or VAMP3 could protect insulin-stimulated GLUT

68 with vesicle-associated membrane protein 2 (VAMP2) and plasma membrane proteins syntaxin 1A and syna

69 vin-2/vesicle-associated membrane protein 2 (VAMP2) and promoted SNARE-complex assembly.

70 ysin, vesicle-associated membrane protein 2 (VAMP2), and the vacuolar proton pump as components of th

71 on of syntaxin 1A, the cytoplasmic domain of VAMP2, and amino- and carboxyl-terminal regions of SNAP-

72 osed of syntaxin-1, SNAP-25, synaptobrevin-2/VAMP2, and Munc18-1.

73 etalloprotease from fraction nu that cleaves VAMP2, and report its amino acid sequence.

74 18c binding, increased syntaxin 4 binding to VAMP2, and significantly enhanced glucose-stimulated sec

75 ze and coprecipitate with Rab11a, myosin Vb, VAMP2, and syntaxin 4, components of the plasma membrane

76 regulated interactions between the v-SNARE, VAMP2, and the t-SNARE, syntaxin 4.

77 DM4, NME7, RAB8B, TFE3, TNFAIP3, TNK1, TOP1, VAMP2, and YY1.

78 her, these data demonstrate that syntaxin 4, VAMP2, and/or VAMP3/cellubrevin can function as target m

79 lasma membrane in 3T3L1 adipocytes through a VAMP2- and syntaxin 4-dependent mechanism.

80 Together, our results identify VAMP2 as a cargo-selective v-SNARE and suggest that surf

81 ARE identity as VAMP2 and the proteolysis of VAMP2 as a marked decrease in secondary antibody-conjuga

82 ime in individual fusion events, we identify VAMP2 as a selective v-SNARE for GPCR delivery.

83 nd SNAP23, and whereas many studies identify VAMP2 as the v-SNARE, others suggest that either VAMP3 o

84 ified vesicle-associated membrane protein 2 (VAMP2) as a critical factor involved in skin differentia

85 ner to facilitate the increase in Syntaxin 4-VAMP2 association and to promote vesicle/granule fusion.

86 wever, no increase in basal level Syntaxin 4-VAMP2 association occurred with either latrunculin treat

87 as in triggering Syntaxin 4 accessibility to VAMP2 at a step preceding vesicle docking/fusion.

88 ided with increased binding of syntaxin 4 to VAMP2 at the plasma membrane.

89 L348R) within helix 12 selectively abolishes VAMP2 binding and the stimulatory function of Munc18-1 i

90 Moreover, VAMP2 binding protects alpha-Syn against forming aggrega

91 ed to exhibit glucose-induced activation and VAMP2 binding, and failed to potentiate insulin release

92 ARE complex, positioning them for productive VAMP2 binding.

93 We found that silencing VAMP2 blocked cAMP-induced renin release by ~50%.

94 Furthermore, VAMP2 bound both GST-Cdc42-GTPgammaS and GST-Cdc42-GDP,

95 In vitro binding analyses showed that VAMP2 bound directly to Cdc42 and that a heterotrimeric

96 Cav-1 associated with Cdc42-VAMP2-bound granules present near the plasma membrane un

97 Through its interaction with the Cdc42-VAMP2-bound insulin granule complex, Cav-1 may contribut

98 In vivo silencing of VAMP2 but not VAMP3 in TALs blunted cAMP-stimulated stea

99 We concluded that VAMP2 but not VAMP3 selectively mediates cAMP-stimulated

100 of primary cultures of JG cells showed that VAMP2 (but not VAMP3) co-localized with renin-containing

101 of exocytic and endocytic vesicles, such as Vamp2, Clathrin and Dynamin, are sequestered in unreleas

102 The VAMP2 cleavage site is between the transmembrane anchor

103 ntaining cognate proteins (for instance, the VAMP2 cognate syntaxin1/SNAP-25 complex), the fluorescen

104 Overexpression of VAMP3, but not VAMP2, completely prevented lipid-induced inhibition of

105 hibited formation of the syntaxin 13-SNAP-25-VAMP2 complex by displacing VAMP2 from the complex.

106 and GST-Cdc42-GDP, indicating that the Cdc42-VAMP2 complex could form under both cytosolic GDP-bound

107 induced the dissociation of Cav-1 from Cdc42-VAMP2 complexes, coordinate with the timing of Cdc42 act

108 AMPA receptors requires SNAP25-syntaxin1A/B-VAMP2 complexes, whereas insertion of GABAA receptors re

109 ABAA receptors relies on SNAP23-syntaxin1A/B-VAMP2 complexes.

110 SNARE-dependent liposome fusion assay using VAMP2-containing donor and syntaxin-1/SNAP-25-containing

111 d, tomosyns extensively bind synaptobrevin-2/VAMP2-containing template complexes and prevent SNAP-25

112 The TMD of the SNARE protein synaptobrevin2/VAMP2 contains two highly conserved small amino acids, G

113 ontrast, the R-SNARE protein synaptobrevin-2/VAMP2 contributes to both regulated and constitutive AMP

114 hydrophobic energies by which this domain of VAMP2 could bind to the adjacent lipid bilayer in an ins

115 The genetic synaptopathy caused by VAMP2 de novo mutations highlights the key roles of this

116 fuse with vesicles containing synaptobrevin2/VAMP2, demonstrating that syntaxin 3B can function as a

117 ge of vesicle-associated membrane protein 2 (VAMP2)-dependent exocytosis from tanycytes.

118 In aggregate, these data suggest that VAMP2-dependent exocytosis regulates plasma membrane ins

119 When VAMP2-dependent exocytosis was silenced in single axons,

120 demonstrated that insulin stimulates SOCE by VAMP2-dependent Orai1 trafficking to the plasma membrane

121 Interestingly, VAMP2 did not show preferential localization on MOR-cont

122 its SNARE motif with that of synaptobrevin-2/VAMP2 did not.

123 of its hexamer structure and its binding of VAMP2 dimers, both of which we demonstrate in detergent

124 Here, we investigated nine synaptobrevin-2 (VAMP2) disease-causing variants and uncovered their spec

125 ost identical to vesicle-associated protein (VAMP2-EGFP), and these proteins are often transported to

126 VAMP2 encodes the vesicular SNARE protein VAMP2 (also ca

127 after vesicle-associated membrane protein 2 (VAMP2) enters the SNARE complex.

128 oforms of synaptobrevin, Syb1/VAMP1 and Syb2/VAMP2, exhibit distinct but partially overlapping patter

129 cAMP stimulation enhanced VAMP2 exocytic delivery to the plasma membrane of renal

130 demonstrated that cAMP stimulation enhances VAMP2 exocytosis and promotes VAMP2 interaction with NKC

131 be, biosyn, which consists of a biotinylated VAMP2 expressed at presynaptic terminals.

132 aptic vesicle fusion and Munc18-3:Syntaxin-4:VAMP2 for GLUT4 translocation and insulin release, which

133 ane fusion by competing with synaptobrevin-2/VAMP2 for SNARE-complex assembly.

134 , VAMP8, for plasma membrane endocytosis and VAMP2 for sorting to the specialized insulin-responsive

135 ary template complexes - Munc18-1:Syntaxin-1:VAMP2 for synaptic vesicle fusion and Munc18-3:Syntaxin-

136 NARE motif and competes with synaptobrevin-2/VAMP2 for the SNARE-complex assembly.

137 lipidomic profiling, and further reveal that VAMP2 forms distinctive conformations in different membr

138 mbrane SNAREs syntaxin 1a and SNAP25 bind to VAMP2 found on neurotransmitter-containing vesicles.

139 taxin 13-SNAP-25-VAMP2 complex by displacing VAMP2 from the complex.

140 ealed a parallel redistribution of Cdc42 and VAMP2 from the granule fraction to the plasma membrane i

141 When VAMP2 function was disrupted, oligodendrocytes exhibited

142 tion correlated with parallel alterations in VAMP2 granule docking with Syntaxin 4.

143 Here, we use the yeast VAMP2 homologue Snc1 to investigate the pathways and sig

144 on of syntaxin-4's putative cognate receptor VAMP2 in aquaporin-2-containing vesicles, supports the v

145 riments showed that TeNT efficiently cleaved VAMP2 in depolarized neurons and neurons blocked for syn

146 ings establish a role for both myosin Va and VAMP2 in oligodendrocyte function as it relates to myeli

147 report that NKCC2 co-immunoprecipitates with VAMP2 in rat TALs, and they co-localize in discrete doma

148 protein that is part of a fusion machinery, VAMP2 in the example detailed herein, are included in th

149 eport five heterozygous de novo mutations in VAMP2 in unrelated individuals presenting with a neurode

150 Expression of tetanus toxin to cleave VAMP2 in VAMP8 knock-out (-/-) acini confirmed that VAMP

151 n interacts with the vesicular SNARE protein VAMP2 in vitro and ex vivo (using yeast-2 hybrid and coi

152 ated protein of 23 kilodaltons [SNAP23], and VAMP2) in rat pancreatic acini.

153 reported that a mutation in synaptobrevin 2 (Vamp2) in restless (rlss) mice results in a marked incre

154 iation of SNAP-23 or syntaxin 4 but promoted VAMP2 insertion into plasma membrane rafts.

155 induce the targeting of intracellular Cdc42-VAMP2-insulin granule complexes to Syntaxin 1A at the pl

156 18 within domain 3a leads to synaptobrevin-2/VAMP2 interaction and SNARE complex formation.

157 ation enhances VAMP2 exocytosis and promotes VAMP2 interaction with NKCC2.

158 cating a functional importance for the Cdc42-VAMP2 interaction.

159 Here, we show that alpha-syn-VAMP2 interactions are necessary for alpha-syn-induced s

160 Moreover, proteins (Rab3a, syntaxin-1A, and VAMP2) involved in exocytosis also localize with alpha-s

161 We found that VAMP2 is delivered to the surface of both axons and dend

162 VAMP2 is essential for vesicular exocytosis and activity

163 Furthermore, VAMP2 is shown to be concentrated in lipid rafts isolate

164 at of the ternary SNARE complex, except that VAMP2 is substituted to the second copy of syntaxin 1A.

165 nd VAMP3 are expressed in JG cells, but only VAMP2 is targeted to renin-containing granules and media

166 ecipitation analyses lead us to propose that VAMP2 is the major v-SNARE involved in GLUT4 trafficking

167 rior to the SNARE assembly, the structure of VAMP2 is unclear.

168 revin/vesicle-associated membrane protein 2 (VAMP2) is an essential soluble N-ethyl maleimide-sensiti

169 ce in the interaction between syntaxin 4 and VAMP2, leading to the dysfunction of the SNARE complex.

170 Deletion of VAMP2 leads to aberrant skin stratification and enucleat

171 s VAMP8-mediated mid- and late-phase but not VAMP2-mediated early-phase secretion.

172 SP-regulated actin dynamics coordinated with VAMP2-mediated exocytosis and involves a novel role for

173 etory pathway is required for VAMP8- but not VAMP2-mediated ZG exocytosis.

174 ystem to follow secretion over time revealed VAMP2 mediates an early rapid phase peaking and falling

175 synaptosomal-associated protein 25 (SNAP25), VAMP2 mediates fusion of synaptic vesicles to release ne

176 IRAP and VAMP2 mRNA levels were unaffected in aP2-GLUT4-Tg, sugge

177 celerated fusion kinetics of TMD-rigidifying VAMP2 mutants.

178 hin the juxtamembrane domain that reduce the VAMP2 net positive charge, and thus its interaction with

179 renal cells, and stimulation of PKA enhanced VAMP2-NKCC2 co-immunoprecipitation in TALs.

180 NTRK1 in glioblastoma, MSN-ROS1, TRIM4-BRAF, VAMP2-NRG1, TPM3-NTRK1 and RUFY2-RET in lung cancer, FGF

181 with vesicle-associated membrane protein 2 (VAMP2) on GLUT4 storage vesicles (GSVs) and facilitates

182 Loss of VAMP2 or FIP200 enhances cutaneous carcinogenesis in viv

183 ir recruitment was sensitive to depletion of VAMP2 or NCS1, whereas recruitment of the recycling endo

184 Then we specifically knocked down VAMP2 or VAMP3 by adenoviral-mediated delivery of short

185 Unlike VAMP8 silencing, knockdown of VAMP2 or VAMP3 did not affect mucin secretion.

186 iomyocytes transiently overexpressing either VAMP2 or VAMP3 were cultured for 16 h with elevated conc

187 te, expression of the cytoplasmic domains of VAMP2 or VAMP3/cellubrevin also resulted in an inhibitio

188 25 (t-SNAREs) and the delivery-vesicle SNARE VAMP2 (or v-SNARE) contain the "SNARE regions" that esse

189 orin on vesicle-associated membrane protein (VAMP2)) or CalipHluorin (pHluorin on an L-type Ca(2+) ch

190 that vesicle-associated membrane protein 2 (VAMP2) orchestrates alphaSYN phase separation both in vi

191 etion exclusively from the VAMP8 but not the VAMP2 pathway.

192 Expression of this 28-residue VAMP2 peptide in MIN6 beta cells resulted in the specifi

193 ssing vesicle-associated membrane protein 2 (VAMP2)-pHluorin with 36-nm localization precision.

194 We use a new GSV reporter, VAMP2-pHluorin, and bypass insulin signaling by disrupti

195 Our results showed that, once internalized, VAMP2-pHluorin/Atto647N-tagged nanobodies exhibited a ma

196 We conclude that the TMD of VAMP2 plays a critical role in membrane fusion and that

197 rease in the total number of synapses and/or VAMP2 positive neurons.

198 rged juxtamembrane domain of a reconstituted VAMP2 protein and inhibit membrane fusion.

199 hat overexpression of GLUT4 affects IRAP and VAMP2 protein stability.

200 VAMP2 protein was also decreased by 60% in aP2-GLUT4-/-

201 Syntaxin6 and other accessory molecules like VAMP2, Rab6, and Rab8 on Salmonella-containing phagosome

202 Deletion analyses of VAMP2 revealed that only the N-terminal 28 residues were

203 complete loss of the VAMP8 pathway, whereas VAMP2-secretion remains intact.

204 l domain: selective retention in the case of VAMP2, selective delivery in the case of NgCAM.

205 P8/SNAP25/Munc18b) and predocked SGs (Syn-1A/VAMP2/SNAP25/Muncn18a).

206 describe the dynamic membrane association of VAMP2 SNARE motif in mammalian cells, and the structural

207 markedly weakens the membrane association of VAMP2 SNARE motif, which releases the SNARE motif and fa

208 served residues within the C terminus of the VAMP2 SNARE motif.

209 regulation of different membrane regions on VAMP2 structure and sheds light on the spatial regulatio

210 With the exception of synaptobrevin2, or VAMP2 (syb2), which is directly involved in vesicle fusi

211 In contrast, the apparent number of VAMP2/synaptobrevin 2, synaptophysin, and synaptogyrin d

212 rizers." MISTs based on the vesicle proteins VAMP2/Synaptobrevin and Synaptophysin induced rapid ( ap

213 interact with the dual prenylated rab3A and VAMP2/Synaptobrevin II receptor PRA1.

214 ions with the synaptic vesicle SNARE protein VAMP2/synaptobrevin-2, the synaptic vesicle-attached syn

215 the levels and localization of SNARE-protein VAMP2/synaptobrevin-2.

216 Vesicle associated membrane protein 2 (VAMP2/synaptobrevin2), a core SNARE protein residing on

217 teins synaptobrevin II (sybII, also known as VAMP2), syntaxin, and SNAP-25, generating a force transf

218 sitive attachment protein receptors (SNAREs) VAMP2, Syntaxin-1A, and SNAP-25 in membrane fusion.

219 itive vesicular transport machinery, namely, VAMP2, syntaxin-4, and IRAP, the last of these being the

220 18c depletion ablated the glucose-stimulated VAMP2-Syntaxin 4 association as well as Syntaxin 4 activ

221 mutations confirmed that the Munc18-Syntaxin-VAMP2 "template" complex is a functional intermediate in

222 A mutation in the cytoplasmic domain of VAMP2 that inhibits endocytosis abolished its axonal pol

223 y by activating the synaptic vesicle protein VAMP2 to form SNARE fusion complexes, the molecular mech

224 NARE motif cannot substitute synaptobrevin-2/VAMP2 to form template complexes with Munc18-1 and synta

225 stable assembly, which can then be bound by VAMP2 to form the full SNARE complex.

226 smission by cooperating with synaptobrevin-2/VAMP2 to prevent SNAP-25 binding during SNARE assembly,

227 25, holding them in a conformation ready for VAMP2 to replace it to mediate the membrane fusion event

228 ntaining vesicles by blocking the binding of VAMP2 to syntaxin 4.

229 protein n-Sec1p, competed for the binding of VAMP2 to syntaxin 4.

230 1 and vesicle-associated membrane protein 2 (VAMP2) to form a ternary soluble N-ethylmaleimide-sensit

231 er sequence (e.g., W146C, K174E) alter Kif1a/Vamp2 transport by disrupting Dcx/Kif1a interactions wit

232 ammalian cells, and the structural change of VAMP2 upon the change of intracellular lipid environment

233 to phosphorylated tau (e.g. synaptic protein VAMP2, vacuolar-ATPase subunit ATP6V0D1); therefore, we

234 egulating the endocytosis of SNAREs, such as VAMP2, VAMP3 and VAMP8, which have diverse effects on di

235 The vesicle SNARE proteins VAMP2 (vesicle associated membrane protein 2) and VAMP3

236 fusion factor attachment receptor) proteins VAMP2 (vesicle-associated membrane protein 2) and syntax

237 5 (excitatory amino acid transporter 5), and VAMP2 (vesicle-associated membrane protein 2), are marke

238 additional interaction with synaptobrevin-2/VAMP2 (vesicle-associated membrane protein 2), leading t

239 synaptosome-associated protein of 25 kD) and VAMP2 (vesicle-associated membrane protein 2), precludes

240 idification by live-cell imaging of pHluorin-VAMP2 (vesicle-associated membrane protein-2), a pH-sens

241 ced the fusion rate, whereas its addition to VAMP2 vesicles was inhibitory.

242 ted the fusion reaction, and its addition to VAMP2 vesicles was stimulatory.

243 tatic interactions, specifically mediated by VAMP2 via its juxtamembrane domain and the alphaSYN C-te

244 rther analysis revealed that the majority of VAMP2 was associated with a distinct class of raft with

245 When miniSOG-VAMP2 was expressed panneuronally in Caenorhabditis eleg

246 VAMP2 was not involved in constitutive NKCC2 delivery.

247 VAMP2 was preferentially enriched in vesicles that media

248 ricosities, but the vesicular SNARE protein, vamp2, was present in a fraction of those varicosities.

249 SNAP-25, syntaxin 13, and VAMP2 were bound from rat brain membranes to the Hrs coi

250 Moreover, within these fractions Cdc42 and VAMP2 were found to co-immunoprecipitate under basal and

251 ransmembrane anchors of both syntaxin 1A and VAMP2 were protected from trypsin digestion.

252 uroendocrine cells, syntaxin 1, SNAP-25, and VAMP2, were not involved in homotypic ISG fusion.

253 ind a reconstituted integral membrane cargo (VAMP2), which has been covalently linked to mono-ubiquit

254 on of vesicle-associated membrane protein 2 (VAMP2), which is known to associate with myosin Va.

255 esicles containing IRAP, LRP1, sortilin, and VAMP2, which are sequestered by TUG, Ubc9, and other pro

256 singly, application of the soluble domain of VAMP2, which blocks SNARE assembly by competing for bind

257 we show that the R-SNAREs VAMP8, VAMP3, and VAMP2, which cycle between the plasma membrane and endos

258 um tuberculosis, VTI1B and STX8 complex with VAMP2, which in turn decreases VAMP8 binding.

259 own of septin 7 increased the interaction of VAMP2 with nephrin and syntaxin 4.

260 omplexes of greater thermostability than can VAMP2 with syntaxin 1a and SNAP-25 in vitro, but it lack

261 Cleavage of VAMP2 with tetanus toxin (TeNT) did not prevent delivery

262 e fusion protein attachment protein receptor VAMP2 with the target soluble N-ethyl-maleimide-sensitiv

263 e vesicle-associated membrane SNARE protein (VAMP2) with Cdc42 and compared these structural interact

264 However, sorting and trafficking of VAMP2 within the endosomal system is not well understood