ライフサイエンスコーパス: fusion pore

1 mediates (stalks, hemifusion diaphragms, and fusion pores).

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

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

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

5 eleased immediately after the formation of a fusion pore.

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

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

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

9 catecholamine through a restricted secretory fusion pore.

10 nonlamellar lipidic intermediate states to a fusion pore.

11 ntrolled through regulation of the secretory fusion pore.

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

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

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

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

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

17 hemifusion, and the opening of an expanding fusion pore.

18 ole in the transition from hemifusion to the fusion pore.

19 assembling or disassembling a proteinaceous fusion pore.

20 initial permeance and expansion rate of the fusion pore.

21 lls at rates proportional to the size of the fusion pore.

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

23 mifusion intermediate and the opening of the fusion pore.

24 nsistent with the delayed enlargement of the fusion pore.

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

26 fusion step before opening of the productive fusion pore.

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

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

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

30 endent effects on dilation of the exocytotic fusion pore.

31 nly associated with large dense core granule fusion pores.

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

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

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

35 that SNARE/lipid complexes form proteolipid fusion pores.

36 ity of initially opened but not yet expanded fusion pores.

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

38 in the membrane-distal half stabilized open fusion pores.

39 ssembled complex drives the dilation of open fusion pores.

40 RE complex drive transitions leading to open fusion pores.

41 aracteristic of hemifusion intermediates and fusion pores.

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

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

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

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

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

47 s entails prolonged maintenance of a dilated fusion pore and assembly of actin filament (F-actin) coa

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

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

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

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

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

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

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

55 Hemifusion, flickering of fusion pores, and kinetic transitions between intermedia

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

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

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

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

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

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

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

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

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

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

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

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

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

69 The dynamics of fusion pores between yeast cells were analyzed by follow

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

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

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

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

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

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

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

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

78 ntration ([Glu]v), vesicle volume, ultrafast fusion pore closure, the postsynaptic receptor, and the

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

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

81 For full collapse, the initial fusion pore conductance (G(p)) was usually >375 pS and i

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 strongly impairs exocytosis and decelerates 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 flects the need to bend more membrane during fusion pore dilation.

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

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

106 into the PM; or by "kiss-and-run," where the fusion pore does not dilate and instead rapidly reseals

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

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

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

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

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

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

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

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

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

116 inhibitory effect occurs at a late stage in fusion pore enlargement.

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

118 impaired the release process by compromising fusion pore enlargement.

119 ficial increase of membrane tension restored fusion pore enlargement.

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

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

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

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

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

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

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

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

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

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

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

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

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

133 Slower fusion pore expansion rates and longer fusion pore lifet

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

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

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

137 Fusion pore expansion was measured by two independent me

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

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

140 -dependent dynamin dephosphorylation, limits fusion pore expansion.

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

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

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

144 usion pore opening probabilities and reduced fusion pore expansion.

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

146 pairs, possibly as a consequence of retarded fusion pore expansion.

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

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

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

150 c term to the free energy of Q(II) phase and fusion pores explains some features of fusion pore stabi

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

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

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

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

155 Variations in fusion pore formation and closure cause deviations from

156 However, efficient fusion pore formation and expansion require synaptotagmi

157 Fusion pore formation and expansion, crucial steps for n

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

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

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

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

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

163 PIP2 within the membrane interface regulates fusion pore formation during exocytosis.

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

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

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

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

168 re capable of promoting hemifusion and small fusion pore formation, as shown by a dye redistribution

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

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

171 of the intermediate state directly preceding fusion pore formation.

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

173 the vesicular membrane continuity leading to fusion pore formation.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

189 fusion neck widening and formation of a full fusion pore in our simulation data.

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

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

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

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

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

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

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

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

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

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

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

201 If the lifetime of the fusion pore is comparable to the time required for the s

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

203 At synapses, the size of the fusion pore is unclear, 'kiss-and-run' remains controver

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

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

206 Here, by recording fusion pore kinetics during single vesicle fusion, we fo

207 dence of release, short-term plasticity, and fusion pore kinetics.

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

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

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

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

212 ntitatively accounted for the nonexponential fusion pore lifetime distribution.

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

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

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

216 Assuming 1), fusion pore lifetimes are exponentially distributed (tau

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

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

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

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

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

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

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

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

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

226 he consequences using amperometry to measure fusion pore opening and dilation.

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

228 utants of SCAMP2 decrease the probability of fusion pore opening and the stability of initially opene

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

230 ion of FM dye molecules lost during a single fusion pore opening event.

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

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

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

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

235 x reduced two distinct rate processes before fusion pore opening to different degrees.

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

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

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

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

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

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

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

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

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

245 -like intermediate can either rapidly form a fusion pore or remain in a metastable hemifused state th

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

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

248 emodeling defects had more modest effects on fusion pore permeance.

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

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

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

252 lar Alexa-647, indicating the formation of a fusion pore, prior to loss of fluorescent contents.

253 Fusion pore properties also were unaffected.

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

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

256 or dyes may be released from vesicles via a fusion pore, rather than by full fusion of the vesicle w

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

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

259 tsynaptic currents, and suggest that various fusion pore sizes help to control the kinetics and ampli

260 e and fusion pores explains some features of fusion pore stability and dynamics, and some peculiar ob

261 25B or Syt1 had complex effects on transient fusion pore stability in a stimulus-specific manner.

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

263 iate states (I(1) and I(2)) and then on to a fusion pore state (FP).

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

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

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

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

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

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

270 Hemifusion then proceeds to the fusion pore that connects the two internal contents.

271 le fuses with the plasma membrane (PM) via a fusion pore that then dilates until the secretory vesicl

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 Aside from regulation of the fusion pore, these mechanisms fall into two general cate

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

295 nd 2), vesicle contents are lost through the fusion pore with an exponential time course (tauD), we d

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

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

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

299 kiss-and-run" features fusion by a transient fusion pore without complete loss of vesicle identity an

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