ライフサイエンスコーパス: fusion pore

1 aflets (stalk formation), and formation of a fusion pore.

2 mifusion intermediate and the opening of the fusion pore.

3 g of the SNARE complex to the opening of the fusion pore.

4 fusion step before opening of the productive fusion pore.

5 fusion starts with the formation of a narrow fusion pore.

6 t transition (expansion) of the stalk into a fusion pore.

7 both initiation of fusion and formation of a fusion pore.

8 the plasma membranes, and the formation of a fusion pore.

9 together, thus allowing their TMRs to form a fusion pore.

10 ion of the molecular control of the platelet fusion pore.

11 eleased immediately after the formation of a fusion pore.

12 ell into the collapsed vesicle to expand the fusion pore.

13 content through a transient, nanometer-sized fusion pore.

14 st likely due to the flickering of a dilated fusion pore.

15 catecholamine through a restricted secretory fusion pore.

16 nonlamellar lipidic intermediate states to a fusion pore.

17 ntrolled through regulation of the secretory fusion pore.

18 it becomes leaky and unable to form a clean fusion pore.

19 nd appear to be involved in formation of the fusion pore.

20 d to the presynaptic membrane by a transient fusion pore.

21 in which holes in the membrane evolve into a fusion pore.

22 nsistent with the delayed enlargement of the fusion pore.

23 endent effects on dilation of the exocytotic fusion pore.

24 a stalk, hemifusion and the completion of a fusion pore.

25 and a hemifusion-stalk pathway leading to a fusion pore.

26 aracteristic of hemifusion intermediates and fusion pores.

27 t and transient openings and closings of the fusion pores.

28 ot gather information about the formation of fusion pores.

29 nly associated with large dense core granule fusion pores.

30 als the dynamic formation and dissolution of fusion pores.

31 r the syt-PS interaction in stabilizing open fusion pores.

32 r frequency of fusion events and more stable fusion pores.

33 and duration of DCV fusion pores but not MV fusion pores.

34 that SNARE/lipid complexes form proteolipid fusion pores.

35 and promote the stabilization of exocytotic fusion pores.

36 blockage is due to the stabilization of open fusion pores.

37 re elastic energies of stalks and catenoidal fusion pores according to recent models.

38 ticipates in the enlargement or expansion of fusion pores after hemifusion.

39 The rate of enlargement of a fusion pore also correlated with the extent and kinetics

40 Remarkably, these synaptic fusion pores also open spontaneously in the absence of s

41 y to play a crucial role in formation of the fusion pore, an essential structure required in the fina

42 a shift fragment that shifted to expand the fusion pore and 2) a fall-in fragment that fell into the

43 s occurs because of premature closure of the fusion pore and is modulated by the activity of clathrin

44 However, the formation of a fusion pore and its expansion has been difficult to dete

45 orrelated temporally with the opening of the fusion pore and not with its dilation.

46 , CpxII attenuates fluctuations of the early fusion pore and slows its expansion but is functionally

47 ives rise to an unequal distance between the fusion pore and the electrode as well as fusion pore siz

48 s from virion tips disrupts the formation of fusion pores and infection kinetics.

49 ease transmitter, but instead to close their fusion pores and survive intact for future use (kiss-and

50 sion, Kar5p may help dilation of the initial fusion pore, and Kar2p and Kar8p act after outer NE fusi

51 interplay between diffusion, flux through a fusion pore, and possibly dissociation from a vesicle's

52 consistent descriptions for the shape of the fusion pore, and the deviation between the continuum and

53 these events arise due to the formation of a fusion pore approximately 12 nm in diameter.

54 er that a vesicle, when activated, opens its fusion pore approximately 3 times out of 4 and that the

55 )(-)), the expansion and closing time of the fusion pore are longer, suggesting chaotropes can extend

56 The effects of syt IV on fusion pores are discussed in terms of structural models

57 o stall the fusion process before productive fusion pores are formed.

58 Regulated exocytosis establishes a narrow fusion pore as initial aqueous connection to the extrace

59 These exhibited a wider fusion pore as measured by increased fusion pore conduct

60 the structure and composition of the initial fusion pore, as well as the question of whether SNAREs m

61 e greater stability of an initial exocytotic fusion pore associated with larger vesicles reflects the

62 that involves rapid opening and closure of a fusion pore at the release site.

63 d kiss and run exocytosis opens synaptic DCV fusion pores away from active zones that readily conduct

64 They efficiently formed fusion pores based on virus replication and quantitative

65 at the cAMP-sensor Epac2 (Rap-GEF4) controls fusion pore behavior by acutely recruiting two pore-rest

66 esterol opens pores directly by reducing the fusion-pore bending energy, and indirectly by concentrat

67 Formation of a fusion pore between a vesicle and its target membrane is

68 g to the formation of a single-channel macro fusion pore between the two muscle cells.

69 sence of Nef inhibits the formation of small fusion pores between viruses and cells.

70 mine molecules that are escaping through the fusion pore but favor its interaction with the vesicle m

71 ncreased the conductance and duration of DCV fusion pores but not MV fusion pores.

72 own that second messenger cAMP modulates the fusion pore, but the detailed mechanisms remain elusive.

73 indicate a role for the syb2 TMD in nascent fusion pores, but in a very different structural arrange

74 pt and preceded the opening of an exocytotic fusion pore by approximately 90 ms.

75 y, we studied the stability of the transient fusion pore by measuring its dwell time, relation to ves

76 icle docking and fusion and the promotion of fusion pores by negative intrinsic spontaneous curvature

77 one- or neurotransmitter-filled vesicle -the fusion pore- can flicker open and closed repeatedly befo

78 A-dependent control of vesicles with unusual fusion pore characteristics.

79 fter exocytosis, SVs are recovered by either fusion pore closure (kiss-and-run) or clathrin-mediated

80 A fusion pore composed of lipid is an obligatory kinetic i

81 d at a late step in exocytosis and modulates fusion pores composed of SNARE complexes.

82 a wider fusion pore as measured by increased fusion pore conductance and a prolonged fusion pore dwel

83 To determine how fusion pore conductance and dynamics depend on these res

84 ing full-fusion of DCVs syt IV increased the fusion pore conductance but not the duration.

85 charge of TMD residues near the N terminus; fusion pore conductance was altered by substitutions at

86 re, consistent with the observed decrease of fusion pore conductance.

87 mperometric "foot-current" currents, reduced fusion pore conductances, and lower fusion pore expansio

88 ranule exocytosis measurements) in which the fusion pore connecting the granule lumen to the exterior

89 ulforhodamine 101 imaging showed that double fusion pores could simultaneously occur in a single vesi

90 o expand the hemifusion diaphragm and form a fusion pore decreases rapidly as the radius decreases.

91 ipid mixing always preceded the opening of a fusion pore, demonstrating that VSV G-mediated fusion pr

92 It is believed that immediately afterward, fusion pores dilate spontaneously.

93 pore opening, and slowing a later step when fusion pores dilate.

94 al fusion pore opening probabilities but the fusion pores dilated extensively.

95 er elevated stimulation frequencies inhibits fusion pore dilation and maintains the granule in a kiss

96 at membrane tension is the driving force for fusion pore dilation and that Cdc42 is a key regulator o

97 , while showing no change in the kinetics of fusion pore dilation or morphological vesicle docking.

98 riggered exocytosis membrane bending opposes fusion pore dilation rather than fusion pore formation.

99 mulation (action potentials at 15 Hz) evokes fusion pore dilation, full granule collapse, and additio

100 tatin decreased membrane tension, as well as fusion pore dilation.

101 fusion, and a graded slowing of the rate of fusion pore dilation.

102 cent probes was used to assess the extent of fusion pore dilation.

103 strongly impairs exocytosis and decelerates fusion pore dilation.

104 flects the need to bend more membrane during fusion pore dilation.

105 Conductance through single, voltage-clamped fusion pores directly reported sub-millisecond pore dyna

106 cies, slower release kinetics, and prolonged fusion pore duration that were correlated with reduced p

107 Together, they probe the continuum of the fusion-pore duration, from milliseconds to many seconds

108 The opening of a fusion pore during exocytosis creates the first aqueous

109 tion, expansion, and closing of the membrane fusion pore during exocytosis was found to be strongly d

110 o promote membrane deformation and stabilize fusion pores during exocytotic events.

111 Flickering of fusion pores during exocytotic release of hormones and n

112 ionship between the formation of hundreds of fusion pores during the acrosome reaction in spermatozoa

113 ased fusion pore conductance and a prolonged fusion pore dwell time.

114 retation of amperometric current in terms of fusion pore dynamics and provides a, to our knowledge, n

115 v-SNARE TMD variants differentially regulate fusion pore dynamics in mouse chromaffin cells, indicati

116 To explore the possible role of fusion pore dynamics, a transformation of amperometry cu

117 OPHN1 requires its Rho-GAP domain to control fusion pore dynamics.

118 flection fluorescence microscopy to quantify fusion-pore dynamics in vitro and to separate the roles

119 assays show a strain-independent failure of fusion pore enlargement among H2 (A/Japan/305/57), H3 (A

120 impaired the release process by compromising fusion pore enlargement.

121 ficial increase of membrane tension restored fusion pore enlargement.

122 alk formation, to pore creation, and through fusion pore enlargement.

123 affold proteins restrain pore expansion, the fusion pore eventually reseals.

124 d Syt-1 and Syt-7 impose distinct effects on fusion pore expansion and granule cargo release.

125 cAMP elevation restricts and slows fusion pore expansion and peptide release, but not when

126 e hydrolase (GTPase) activity in controlling fusion pore expansion and postfusion granule membrane to

127 ion demonstrate a novel mechanism underlying fusion pore expansion and provide a new explanation for

128 Ca(2+) also promotes fusion pore expansion and Syts have been implicated in t

129 We conclude that Epac2/cAMP controls fusion pore expansion and thus the balance of hormone an

130 MD restores normal secretion but accelerates fusion pore expansion beyond the rate found for the wild

131 a(2+)-dependent Syt-effector interactions in fusion pore expansion by expressing Syt-1 mutants select

132 ctivity of dynamin regulates the rapidity of fusion pore expansion from tens of milliseconds to secon

133 min I in the regulation of activity-mediated fusion pore expansion in mouse adrenal chromaffin cells.

134 Therefore, fusion pore expansion is a key control point for the act

135 Fusion pore expansion is an essential step for full-coll

136 Our results suggest that fusion pore expansion is regulated by a calcineurin-depe

137 that pharmacological interventions promoting fusion pore expansion may be effective in diabetes thera

138 Slower fusion pore expansion rates and longer fusion pore lifet

139 reduced fusion pore conductances, and lower fusion pore expansion rates.

140 the view that membrane bending occurs during fusion pore expansion rather than during fusion pore for

141 y early F-triggering but also late extensive fusion pore expansion steps in the membrane fusion casca

142 tivity, experienced under stress, results in fusion pore expansion to evoke maximal catecholamine rel

143 Fusion pore expansion was measured by two independent me

144 Surprisingly, insulin promotes fusion pore expansion, blocked by acute perturbation of

145 with either membrane merger (hemifusion) or fusion pore expansion.

146 -dependent dynamin dephosphorylation, limits fusion pore expansion.

147 syndapin substrate) limits activity-mediated fusion pore expansion.

148 embrane insertion and SNARE binding to drive fusion pore expansion.

149 ial role in vesicle priming, triggering, and fusion pore expansion.

150 usion pore opening probabilities and reduced fusion pore expansion.

151 actively promotes membrane fusion as well as fusion pore expansion.

152 al flexibility, actively setting the pace of fusion pore expansion.

153 Ca(2+)-affinity of release, and accelerates fusion-pore expansion during individual vesicle fusion e

154 We have investigated the role of fusion-pore expansion in determining the contrasting dis

155 reased, consistent with a prolonged delay of fusion-pore expansion.

156 peared ~6 s after initial opening, as if the fusion pore fluctuated in size, flickered, and resealed.

157 The TMD of syx influences fusion pore flux in a manner that suggests it lines the

158 Fusion pore flux was sensitive to the size and charge of

159 he aligned myoblasts, cell-cell contacts and fusion pores form.

160 us conclude that the content release, i.e., fusion pore formation after the merger of the two lipid

161 Variations in fusion pore formation and closure cause deviations from

162 However, efficient fusion pore formation and expansion require synaptotagmi

163 Fusion pore formation and expansion, crucial steps for n

164 ARE force-generated membrane bending promote fusion pore formation and expansion.

165 Our results on fusion pore formation and lipid diffusion from the PSM i

166 Moreover, we show that fusion pore formation and PIP2 redistribution precedes a

167 current models, the experiments suggest that fusion pore formation begins with molecular rearrangemen

168 The effect of cholesterol on fusion pore formation between synaptobrevin-2 (VAMP-2)-c

169 The triggering of fusion pore formation by Ca(2+) is mediated by specific

170 Two modes of fusion pore formation demonstrate a novel mechanism unde

171 tion of the plasma membrane might facilitate fusion pore formation during exocytosis.

172 The results suggest a mechanism whereby fusion pore formation is induced by movement of the char

173 chanism by which this force transfer induces fusion pore formation is still unknown.

174 s and the substantial reduction in energy of fusion pore formation provided by this spread indicate t

175 sts that HA acylation, while not critical to fusion pore formation, contributes to pore expansion in

176 viral membranes mix (lipid mixing) prior to fusion pore formation, enlargement, and completion of fu

177 mifusion stalk to transmembrane contact, and fusion pore formation.

178 urn, increases cortical tension and promotes fusion pore formation.

179 ing fusion pore expansion rather than during fusion pore formation.

180 which was only rarely observed (<0.01%), and fusion pore formation.

181 of the intermediate state directly preceding fusion pore formation.

182 invades the adjacent founder cell to promote fusion pore formation.

183 the vesicular membrane continuity leading to fusion pore formation.

184 ing opposes fusion pore dilation rather than fusion pore formation.

185 force transfer to the membranes and inducing fusion pore formation.

186 fluorescence was recovered, presumably after fusion-pore formation and exposure of the core to the ph

187 endent fusion of isolated VLPs to liposomes: fusion pores formed and expanded, as demonstrated by the

188 y smaller vesicles dilated more rapidly than fusion pores formed by larger vesicles.

189 ing exocytosis in chromaffin and PC12 cells, fusion pores formed by smaller vesicles dilated more rap

190 med to probe the function of the syb2 TMD in fusion pores formed during catecholamine exocytosis in m

191 SB-JMR-TMD enhanced the rates of stalk and fusion pore (FP) formation in a sharply sigmoidal fashio

192 cell-attached patches and dense-core vesicle fusion pores had conductances that were half as large as

193 brane, but the role of this vesicle SNARE in fusion pores has yet to be tested.

194 curvature energies of stalks and catenoidal fusion pores have almost the same dependence on monolaye

195 n of a stalk, and triggered expansion of the fusion pore, here we introduce a synthetic fusogen that

196 The productive fusion pore in membrane fusion is generally thought to b

197 ls, indicating that expansion of the initial fusion pore in tPA granules was delayed.

198 The effects of syt IV on fusion pores in PC12 cells resembled the effects on fusi

199 pores in PC12 cells resembled the effects on fusion pores in peptidergic nerve terminals.

200 orrespond to the initial opening of a narrow fusion pore, in adrenal chromaffin cells of wild-type an

201 vents dilation and reveals properties of the fusion pore induced by SNARE (soluble N-ethylmaleimide-s

202 cus, which in turn promotes PLS invasion and fusion pore initiation during myoblast fusion.

203 ion along pathways involving Pn3m phase-like fusion pore intermediates rather than pathways involving

204 Fusion pores involving the SNAP-25Delta9 mutant will be

205 Formation of the fusion pore is a central question for regulated exocytos

206 cent prediction of continuum models that the fusion pore is a metastable structure and that its optim

207 ly 3 times out of 4 and that the area of the fusion pore is approximately 4 nm(2).

208 f genetic material shortly after the initial fusion pore is formed.

209 e is no mechanistic model explaining how the fusion pore is opened by conformational changes in the S

210 an aqueous channel-like structure, termed a fusion pore, is formed.

211 vesicles and a novel regulatory site at the fusion pore itself.

212 mental observation of flickering and closing fusion pores (kiss-and-run) is very well explained by th

213 ithout any accessory proteins can expand the fusion pore large enough to transmit ~11 kDa cargoes.

214 ver, repetitive stimuli induce a more stable fusion pore, leading to an increased amount of neurotran

215 l fusion was most efficient and the extended fusion pore lifetime (0.7 s) enabled notable detection o

216 on Ca(2+)-triggered exocytosis revealed that fusion pore lifetime (tau) varies with vesicle content (

217 ntitatively accounted for the nonexponential fusion pore lifetime distribution.

218 The vesicle size dependence of fusion pore lifetime quantitatively accounted for the no

219 The logarithm of 1/(fusion pore lifetime) varied linearly with vesicle curva

220 size failed to alter the size dependence of fusion pore lifetime.

221 lower fusion pore expansion rates and longer fusion pore lifetimes were observed after inhibition of

222 Once formed, the initially stable and narrow fusion pore may reversibly widen (transient exocytosis)

223 sion pore properties, suggesting a model for fusion pore mechanics that couple C terminal zipping of

224 ges in mepcs that would be consistent with a fusion pore mechanism.

225 ovide further support for the existence of a fusion pore mediated mode of exocytosis, and demonstrate

226 l features (e.g., dimension and shape of the fusion pore near the pore center) are consistent among i

227 rate in supporting membrane curvature at the fusion pore neck.

228 IP2/BAR assembly that regulates the exocytic fusion pore of dense-core vesicles in cultured endocrine

229 ed by depolarization, with shortening of the fusion pore open time.

230 plasma membranes dock at multiple sites and fusion pores open at the contact points.

231 of the lipid membrane that are necessary for fusion pore opening and expansion.

232 mediate is the main factor that favors rapid fusion pore opening at high cholesterol.

233 Fusion pore opening at resting synapses provides a mecha

234 ion between changes in the SNARE complex and fusion pore opening is, however, still unknown.

235 This structure is generated from fusion pore opening or closure (fission) at the plasma m

236 +)-dependent SNARE binding exhibited reduced fusion pore opening probabilities and reduced fusion por

237 ependent membrane insertion exhibited normal fusion pore opening probabilities but the fusion pores d

238 two ways, enhancing an early step leading to fusion pore opening, and slowing a later step when fusio

239 Brief spiking activity triggered a transient fusion pore opening, followed by immediate retrieval of

240 -SNARE membrane favors a mechanism of direct fusion pore opening, whereas low cholesterol favors a me

241 mbrane to the plasma membrane and subsequent fusion pore opening.

242 n suggested that C-terminal zipping triggers fusion pore opening.

243 coat that forms on the vesicle shortly after fusion pore opening.

244 ent signal enables detection of DCV docking, fusion-pore opening, and vesicle collapse into the plana

245 se indicate that G100V/C103V retards initial fusion-pore opening, hinders its expansion and leads to

246 Here, synaptic DCV fusion pore openings are imaged without interference fro

247 chanisms for activity-evoked and spontaneous fusion pore openings with the latter sharing features of

248 reformation; (b) kiss-and-run, in which the fusion pore opens and closes; and (c) compound exocytosi

249 At the final stage of exocytotis, a fusion pore opens between the plasma and a secretory ves

250 espond to the rapid opening and closing of a fusion pore (or "kiss-and-run") with a median opening ti

251 explained by a direct action of Rab3A on the fusion pore, or by Rab3A-dependent control of vesicles w

252 perometry current was introduced that yields fusion pore permeability divided by vesicle volume (g/V)

253 Unlike syx, the syb2 residues that influence fusion pore permeation fell along two alpha-helical face

254 mpare the shape and energies of the membrane fusion pore predicted by coarse-grained (MARTINI) and co

255 clusion, cAMP-mediated stabilization of wide fusion pores prevents vesicles from proceeding to the fu

256 Fusion pore properties also were unaffected.

257 inal residues (SNAP-25Delta9) showed changed fusion pore properties, suggesting a model for fusion po

258 HCN channel blocker (ZD7288), show modulated fusion pore properties.

259 sms such as incomplete cytokinesis or muscle fusion pore regulators.

260 sm by which this force leads to opening of a fusion pore remains elusive.

261 etrieval of vesicles without dilation of the fusion pore, resulting in very little BDNF secretion at

262 The estimated pore-electrode distance and fusion pore size for disk electrodes are 239 and 11.5 nm

263 the fusion pore and the electrode as well as fusion pore size, which leads to different average spike

264 25B or Syt1 had complex effects on transient fusion pore stability in a stimulus-specific manner.

265 A fusion pore stably forms and expands in Phase III, there

266 rmediate (I2 state) that converts to a final fusion pore state with a combined rate k3.

267 influences the transitions between different fusion pore states remains unclear.

268 less tightly zipped and may lead to a longer fusion pore structure, consistent with the observed decr

269 e the curvature and therefore stabilizes the fusion pore structure.

270 ned with vesicles until full dilation of the fusion pore, supporting potential coupling with SNARE fu

271 Syt I produced more rapid dilation of fusion pores than syt VII or syt IX, consistent with its

272 are released through fluctuating exocytotic fusion pores that can flicker open and shut multiple tim

273 f-width mEPCs are caused by reduced diameter fusion pores that remain open longer.

274 lter small molecules through a size-limiting fusion pore, the activation of isoforms that favor kiss-

275 a manner that suggests it lines the nascent fusion pore through the plasma membrane.

276 partner to syx in completing a proteinaceous fusion pore through the vesicle membrane, but the role o

277 This supports the view of an initial fusion pore through two relatively flat membranes formed

278 nd the host membrane, and the formation of a fusion pore through which the viral genome is transferre

279 ell membranes, resulting in the formation of fusion pores through which the viral genome is released.

280 mplex assembly and rapid (micro-millisecond) fusion pore transitions, and to define the role of acces

281 s on fusion event frequency and the rates of fusion pore transitions.

282 id stalk and also drive its expansion into a fusion pore upon the addition of excess calcium.

283 Here, we probed the dilation of single fusion pores using v-SNARE-reconstituted 23-nm-diameter

284 s or in approximately 1 s by the reversal of fusion pores via 'kiss-and-run' endocytosis.

285 oscopy imaging, we found that the exocytotic fusion pore was generated from the SNARE-dependent fusio

286 of observing rhythmic reopening of transient fusion pores was elevated by dbcAMP.

287 the quantity necessary for the formation of fusion pores, we treat cells with ATP to stimulate Ca2+-

288 loss of Rab3A could be due to malfunctioning fusion pores, we used carbon fibre amperometry to record

289 on and fusion were significantly shorter and fusion pores were larger in dynamic endosomes than in mo

290 bility that a synaptic vesicle will open its fusion pore when the fusion machinery of the vesicle is

291 urotransmitters are released through nascent fusion pores, which ordinarily dilate after bilayer fusi

292 of cell-cell contact, giving rise to nascent fusion pores whose expansion establishes full cytoplasmi

293 transient deformations consistent with rapid fusion pore widening after exocytosis; a Dyn1 mutant wit

294 a Dyn1 mutant with decreased activity slowed fusion pore widening by stabilizing postfusion granule m

295 membrane to the point of rupture, promoting fusion pore widening for RNP release.

296 f highly curved structures, and, eventually, fusion pore widening.

297 hat, additionally, tPA itself stabilizes the fusion pore with dimensions that restrict its own exit.

298 gered exocytosis begins with a proteinaceous fusion pore with less stressed membrane, and becomes lip

299 n, while direct transition from a stalk to a fusion pore without a hemifusion intermediate is highly

300 he stalk energy and the energy of catenoidal fusion pores would decrease by tens of k(B)T relative to