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

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

5 of a soluble SNARE coil domain derived from VAMP2.

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

7 SNARE regions to the fusogenic complex with VAMP2.

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

9 complexes containing syntaxin4, SNAP23, and VAMP2.

10 addition, septin 7 coimmunoprecipitates with VAMP2.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

29 resynaptic neurotransmitter release proteins VAMP2 and synaptophysin.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

50 18c binding, increased syntaxin 4 binding to VAMP2, and significantly enhanced glucose-stimulated sec

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

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

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

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

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

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

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

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

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

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

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

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

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

64 ARE complex, positioning them for productive VAMP2 binding.

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

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

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

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

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

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

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

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

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

74 The VAMP2 cleavage site is between the transmembrane anchor

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

99 When VAMP2 function was disrupted, oligodendrocytes exhibited

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

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

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

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

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

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

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

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

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

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

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

111 18 within domain 3a leads to synaptobrevin-2/VAMP2 interaction and SNARE complex formation.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

133 25 (t-SNAREs) and the delivery-vesicle SNARE VAMP2 (or v-SNARE) contain the "SNARE regions" that esse

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

154 18c depletion ablated the glucose-stimulated VAMP2-Syntaxin 4 association as well as Syntaxin 4 activ

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

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

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

158 25, holding them in a conformation ready for VAMP2 to replace it to mediate the membrane fusion event

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

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

161 1 and vesicle-associated membrane protein 2 (VAMP2) to form a ternary soluble N-ethylmaleimide-sensit

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

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

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

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

166 5 (excitatory amino acid transporter 5), and VAMP2 (vesicle-associated membrane protein 2), are marke

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

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

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

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

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

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

173 When miniSOG-VAMP2 was expressed panneuronally in Caenorhabditis eleg

174 VAMP2 was not involved in constitutive NKCC2 delivery.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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