ライフサイエンスコーパス: hemifusion

1 tween Env-expressing cells and target cells (hemifusion).

2 id not progress beyond a lipid mixing stage (hemifusion).

3 on events are now reclassified as productive hemifusion.

4 largement or expansion of fusion pores after hemifusion.

5 ytoplasmic content between cells, resembling hemifusion.

6 ex (gHL) mediated lipid mixing indicative of hemifusion.

7 bit prompt, full fusion while others exhibit hemifusion.

8 sogenic conformation or had induced membrane hemifusion.

9 nsive stages following rather than preceding hemifusion.

10 ature created an intermediate state of local hemifusion.

11 ceding prehairpin intermediate formation and hemifusion.

12 ion time for fusion was faster than that for hemifusion.

13 ng after the onset is faster for fusion than hemifusion.

14 lasmic mixing, indicating that GS can induce hemifusion.

15 were deleted (from either end) mediated only hemifusion.

16 icles, apposition and contact formation, and hemifusion.

17 ooking intermediate structures like membrane hemifusion.

18 ipid-anchored Vam3 interfered already before hemifusion.

19 t membrane does not significantly affect IAV hemifusion.

20 enching that cannot be ascribed to fusion or hemifusion.

21 membrane makes trimerization a bottleneck in hemifusion.

22 etric giant unilamellar vesicles (aGUVs) via hemifusion.

23 ctedly long lag phases between pH change and hemifusion.

24 omplexes have the capacity to drive membrane hemifusion.

25 contacting monolayers in a process known as hemifusion.

26 for measuring the free energy of adhesion or hemifusion.

27 e in all steps of membrane fusion, including hemifusion.

28 sion proceeds through an intermediate called hemifusion(1,2).

29 oposed that membrane fusion transits through hemifusion, a condition in which the outer leaflets of t

30 e lipid composition, productive and dead-end hemifusion account for 65% of all fusion events.

31 All mutants retained normal hemifusion activity, i.e., lipid mixing between the oute

32 terodimer gH-gL has been proposed to mediate hemifusion after the interaction of another required gly

33 n adjacent membranes and stimulates membrane hemifusion, an event that may mimic expansion of the aut

34 These findings strongly imply that hemifusion and a small pore are the key intermediates of

35 or HA function; G1S and G1V mutant HAs cause hemifusion and abolish fusion, respectively.

36 ignificantly suppressed Env-induced membrane hemifusion and caspase-3 activation and augmented Hsp70

37 Hemifusion and complete fusion depend on HAP2/GCS1 prese

38 our system therefore differentiates between hemifusion and complete fusion of interacting vesicle pa

39 lexes on intact organelles in the absence of hemifusion and content mixing.

40 Importantly, both hemifusion and full fusion are leakage-free.

41 ring of protein-free liposomes, and enhances hemifusion and full fusion of proteoliposomes reconstitu

42 vesicle fusion assay can distinguish between hemifusion and full fusion with only a single lipid dye,

43 eled hemifusion of synthetic vesicles, where hemifusion and fusion are most commonly driven by calciu

44 But both cell-cell hemifusion and fusion pore formation were pH dependent.

45 This allowed both hemifusion and fusion to be monitored.

46 ive regulator of lipid mixing during vacuole hemifusion and fusion.

47 SV entry glycoproteins are required for both hemifusion and fusion.

48 n to postfusion conformations encircling the hemifusion and initial fusion pores in a distinct conica

49 e, but cationic probes are excluded; and (3) hemifusion and lipid mixing of contacting monolayers of

50 (l-Opa1) is sufficient for membrane docking, hemifusion and low levels of content release.

51 10 mol%) in a process mainly associated with hemifusion and membrane tension increase, commonly leadi

52 e membrane spans only half the bilayer: upon hemifusion and mixing of the outer leaflets, the DNA-lip

53 E11A and W14A expressed hemagglutinins with hemifusion and no fusion activities, and F9A and N12A ha

54 te (BMP), greatly enhanced the efficiency of hemifusion and permitted full fusion.

55 imeric HA proteins were capable of promoting hemifusion and small fusion pore formation, as shown by

56 ts that the six-helix bundle can form before hemifusion and that subsequent conformational changes, s

57 ding transient fusion, formation of a stalk, hemifusion and the completion of a fusion pore.

58 elieved to undergo rapid lipid mixing during hemifusion and then a slow, rate-limiting completion of

59 In cells, this hemifusion and transfer process did not disrupt the surf

60 erior enabled detection of the lipid mixing (hemifusion) and content transfer (full fusion) steps of

61 entiates between single-vesicle interaction, hemifusion, and complete fusion, the latter mimicking qu

62 increase, that is, monomeric probe transfer, hemifusion, and complete fusion.

63 Nyv1 permitted the reaction to proceed up to hemifusion, and lipid-anchored Vam3 interfered already b

64 fusion-defective mutations G1S, which causes hemifusion, and particularly G1V, which blocks fusion, h

65 be used to detect substages such as docking, hemifusion, and pore expansion and full fusion.

66 esumptive early step in the fusion reaction, hemifusion, and the final stage of fusion, content mixin

67 major stages in the fusion pathway: contact, hemifusion, and the opening of an expanding fusion pore.

68 These reveal how bilayer hemifusion-and thus lubrication breakdown-depends on the

69 n inhibitory lipid that blocks fusion before hemifusion, applying low pH at 37 degrees C created an i

70 The exchange and hemifusion are seen with anionic vesicles; the effect of

71 e first experimental evidence for fusion and hemifusion arising from different machines.

72 erpret the series of intermediates preceding hemifusion as a result of the requirement that multiple

73 ition to complete fusion SNAREs also promote hemifusion as an alternative outcome.

74 nuation of Env-mediated cell-cell fusion and hemifusion, as well as viral infectivity mediated by bot

75 Furthermore, results from a hemifusion assay indicate that cleavage of SP plays an i

76 To verify that our hemifusion assay was capable of detecting hemifusion, we

77 xing in both cell-cell- and virus-cell-based hemifusion assays.

78 is intermediate had been reached resulted in hemifusion at low temperature and fusion at physiologica

79 e gp41 dependent and related to the membrane hemifusion between envelope-expressing cells and target

80 sphatidylcholine, were here found to promote hemifusion between fluorescently labeled liposomes and p

81 ation of stalks, the essential precursors of hemifusion, between bilayers of the different lipid mixt

82 estabilizing drug chlorpromazine rescued the hemifusion block and allowed entry and subsequent replic

83 eptors, becoming internalized and initiating hemifusion but failing to uncoat the viral nucleocapsid

84 es and planar membranes could cause not only hemifusion, but also complete fusion when internal press

85 alcohol to the surface of membranes promotes hemifusion by facilitating the transient breakage of the

86 Promotion of membrane hemifusion by short-chain alcohol was also observed for

87 The finding that a state of transitional hemifusion can be readily obtained via a point mutation

88 with the planar bilayer membranes as target, hemifusion can precede pore formation, and the occurrenc

89 ween adjacent bilayers and then to the stalk hemifusion configuration.

90 We also observed enhanced hemifusion, content mixing, and syncytium formation in S

91 We observed that the hemifusion, cytoplasmic content mixing, and syncytium fo

92 mic tail, 824L gH, is incapable of executing hemifusion despite normal cell surface expression.

93 ial pore formed near the rim of the extended hemifusion diaphragm (HD), a rim-pore.

94 e fused while the inner leaflets engage in a hemifusion diaphragm (HD).

95 rmined two distinct hemifusion structures: a hemifusion diaphragm and a novel structure termed a 'lip

96 t elastic stresses, which propagate into the hemifusion diaphragm and accelerate the fusion pore form

97 vesicle, but that the barrier to expand the hemifusion diaphragm and form a fusion pore decreases ra

98 pic hemifused vesicles featuring an extended hemifusion diaphragm consistently associated with a 42-n

99 The rupture frequency and hemifusion diaphragm diameter were not affected by G1S m

100 Hemifusion diaphragm expansion is spontaneous for distal

101 mechanism, while isolated enlargement of the hemifusion diaphragm leads to the formation of a metasta

102 In contrast, pathways that involved a stable hemifusion diaphragm only resulted in fusion after many

103 between small vesicles proceeds via a small hemifusion diaphragm rather than a fully expanded one.

104 The fusion process also features a large hemifusion diaphragm that transitions to a wide pore for

105 stalk formation, splay within the expanding hemifusion diaphragm, and fissure widening initiating po

106 usion pore, created when a hole forms in the hemifusion diaphragm, expands without bound.

107 n-free membrane point contact, rather than a hemifusion diaphragm, using a single vesicle-vesicle lip

108 limited radial expansion of the stalk into a hemifusion diaphragm.

109 sure widening initiating pore formation in a hemifusion diaphragm.

110 usion pore develops in a local and transient hemifusion diaphragm.

111 formed by the inner leaflets that compose a hemifusion diaphragm.

112 d fusion than they generated within a stable hemifusion diaphragm.

113 ive spontaneous curvature to leaflets of the hemifusion diaphragm.

114 ng electron microscopy, we present images of hemifusion diaphragms that form as stalks expand and pro

115 e stability of fusion intermediates (stalks, hemifusion diaphragms, and fusion pores).

116 fusion after treatments known to destabilize hemifusion diaphragms.

117 known to promote or inhibit the creation of hemifusion did not significantly alter the lipid dye spr

118 eeds through stages of adhesion, flattening, hemifusion, elimination of the intervening septum, and u

119 Hemifusion events are roughly half productive (leading t

120 ore fusion rate k(core), and the fraction of hemifusion events increases with increasing percentage o

121 kinetics of R18 dequenching and thus single hemifusion events initiated by a fast low-pH trigger.

122 vides more sensitive detection of productive hemifusion events than do lipid labels alone.

123 the reaction drives progression beyond early hemifusion events to complete fusion.

124 Single hemifusion events were detected by fluorescence microsco

125 ncluded in the t-SNARE bilayer gives rise to hemifusion events.

126 aused a 5-50 times increase in the number of hemifusion events.

127 primarily involving liposome attachment and hemifusion events.

128 Hemifusion, flickering of fusion pores, and kinetic tran

129 and the results provide clear evidence that hemifusion followed by full fusion requires a parallel o

130 long-lived kinetic intermediates leading to hemifusion, followed by a single, rate-limiting step to

131 model in which SNARE pairing leads to rapid hemifusion, followed by slow further lipid rearrangement

132 the same pattern of dye spread as in stable hemifusion, for this "stunted" fusion, lower concentrati

133 s and synaptotagmin-1 begins from an initial hemifusion-free membrane point contact, rather than a he

134 dle and, in doing so, sequentially catalyzes hemifusion, fusion pore opening, and enlargement.

135 utralizing antibodies (BNAbs) to block viral hemifusion/fusion establish the MPER as a prime vaccinat

136 not yet folded into six-helix bundles after hemifusion has been achieved.

137 domain creates fusion pores after a stage of hemifusion has been achieved.

138 d the inner leaflets remain intact; however, hemifusion has been observed only as an end point rather

139 that both Syt1 and Doc2b are able to induce hemifusion; however, significantly higher Syt1 concentra

140 we test the stability of the aGUVs formed by hemifusion in preserving their contents during the proce

141 may be a fusion protein capable of inducing hemifusion in the absence of gB, the recently solved cry

142 nce dye redistribution assays also showed no hemifusion in the Env proteins which did not induce fusi

143 ane by means of AFM and by the occurrence of hemifusion in the SFA, which is an indicator of defectiv

144 AB domain and induces membrane tethering and hemifusion in this cell-free model.

145 tion that it mediates liposome tethering and hemifusion in vitro.

146 iological systems is thought to pass through hemifusion, in which the outer leaflets are fused while

147 ntial, providing a direct demonstration that hemifusion induced by class II and class III viral prote

148 Correct channel formation was blocked by the hemifusion inhibitor lysophosphatidylcholine (LPC), but

149 usion at steps following the creation of the hemifusion intermediate and may have inhibited fusion at

150 Es might make different contributions to the hemifusion intermediate and the opening of the fusion po

151 ts to indicate that fusion progressed to the hemifusion intermediate but fusion pore formation was in

152 membrane lipid composition, this restricted hemifusion intermediate either transformed into a fusion

153 tion from a stalk to a fusion pore without a hemifusion intermediate is highly improbable.

154 nd content mixing defining the lifetime of a hemifusion intermediate were significantly shorter for B

155 rive membrane fusion is thought to involve a hemifusion intermediate, a condition in which the outer

156 ed by HSV-1 glycoproteins occurred through a hemifusion intermediate.

157 membrane leaflets leading to formation of a hemifusion intermediate.

158 membrane fusion of Moloney MLV occurs via a hemifusion intermediate.

159 either the fully fused state or a long-lived hemifusion intermediate.

160 ediated fusion proceeds through a long-lived hemifusion intermediate.

161 Fusion is thought to proceed through a "hemifusion" intermediate in which the outer membrane lea

162 Gaussian curvature that is characteristic of hemifusion intermediates and fusion pores.

163 We also show that hemifusion intermediates can be trapped, likely as unpro

164 mbrane may be important for the formation of hemifusion intermediates in the membrane fusion pathway.

165 azine, an agent that induces fusion pores in hemifusion intermediates to complete fusion, suggesting

166 mbrane disruption by promoting highly curved hemifusion intermediates, leading to fusion.

167 native formation and dilation of microscopic hemifusion intermediates.

168 eeded to complete fusion without discernible hemifusion intermediates.

169 ransitioned to complete fusion, showing that hemifusion is a true intermediate.

170 the first direct evidence that gp41-mediated hemifusion is both required and sufficient for induction

171 Our results demonstrate that hemifusion is dominant at the early stage of the fusion

172 t is when lysophosphatidylcholine is added), hemifusion is inhibited.

173 This intermediate stage, called hemifusion, is a critical event shared by exocytosis, pr

174 that, while gp41 fusion peptide does affect hemifusion, it mainly affects pore formation.

175 an intermediate with properties expected of hemifusion just as the membranes are about to transit to

176 eflection fluorescence microscopy to compare hemifusion kinetics among these pairings.

177 dy/Fab coverage display significantly slower hemifusion kinetics.

178 These results support a hemifusion-like model of the short NC gp41 in which the

179 f model parameters it was possible to induce hemifusion-like structural changes by a tension increase

180 ich segment to promote extensive contact and hemifusion-like structure formation between the endoplas

181 inal calculations from those of the standard hemifusion mechanism, which was studied in detail in the

182 ding endothelial and cancer cells, through a hemifusion mechanism.

183 g wild-type haemagglutinin or haemagglutinin hemifusion mutant G1S(5) and liposome mixtures were stud

184 ence or a single arginine to Delta12 HA, the hemifusion mutant that terminates with 15 (hydrophobic)

185 redict that a tightly coordinated process of hemifusion neck expansion and pore formation is responsi

186 ids to compute dynamic relationships between hemifusion neck widening and formation of a full fusion

187 Both full fusion and hemifusion occur with a time constant of 5-10 ms.

188 Hemifusion occurred independent of polarity.

189 sphatidylinositol-anchored ectodomain of HA, hemifusion occurred, but no fully enlarged pores were ob

190 low temperature supports the hypothesis that hemifusion occurs before pore formation.

191 Hemifusion of giant unilamellar vesicles and a supported

192 For aGUVs prepared from the hemifusion of giant unilamellar vesicles composed of 1,2

193 esults show that the energies of adhesion or hemifusion of lipid bilayers could vary over 2 orders of

194 brane contact are imaged in real time during hemifusion of model lipid membranes, together with simul

195 Here we mathematically modeled hemifusion of synthetic vesicles, where hemifusion and f

196 as two temporally distinct waves, presumably hemifusion of the outer leaflet followed by inner leafle

197 icates that on a somewhat slower time scale, hemifusion of vesicles is triggered by salt, with mixing

198 g the conformational transition by following hemifusion of WNV virus-like particles (VLPs) in a singl

199 sitol-anchored analogue of HA only mediates "hemifusion" of membranes, i.e., the merging of the proxi

200 sed on our new calculations, the energies of hemifusion, of complete fusion, and of the pore in a bil

201 ted in full fusion, and the remaining 35% in hemifusion; of those, approximately two thirds were perm

202 are associated with either membrane merger (hemifusion) or fusion pore expansion.

203 tructs detected at the cell surface mediated hemifusion (outer leaflet merger) upon low-pH treatment,

204 The hemifusion phenotype of Ser HA was confirmed by electrop

205 Ser HA, therefore, displayed a hemifusion phenotype.

206 is supports a model in which partial fusion (hemifusion) proceeds by a mechanism that is independent

207 of protein-free vesicle-vesicle fusion, the hemifusion rate k(hemi) is 15-20 times faster than the c

208 Hemifusion requires a small amount of energy independent

209 Hemifusion requires at least two adjacent trimers.

210 ixing is consistent with the hypothesis that hemifusion requires just a portion of the energy release

211 usion were simply a less probable event than hemifusion, requiring a larger number of identical fusio

212 sistent with previous reports, we found that hemifusion results in large variation in outer leaflet e

213 The load and contact time-dependent hemifusion results show that the domain rearrangements d

214 ntly belong to the same family of restricted hemifusion (RH) structures.

215 anges such as poration, stalk formation, and hemifusion rupture are essential to cellular function, b

216 on time of lipid mixing after it begins than hemifusion, since the full event cannot be faster than t

217 hould have a shorter average delay time than hemifusion, since there are more machines.

218 at vesicle fusion typically passes through a hemifusion stage and that the time from vesicle contact

219 useful model fusion system, at least to the hemifusion stage in which the viral and target cell lipi

220 s by mediating the transition from the early hemifusion stage to complete fusion.

221 in the DNA-lipid system are arrested at the hemifusion stage, whereas only 5% eventually go to full

222 9) caused a block in fusion promotion at the hemifusion stage.

223 The control of post-hemifusion stages by shifting the spontaneous curvature

224 rane fusion: initialization, transition from hemifusion stalk to transmembrane contact, and fusion po

225 athway leading to the lipidic junction and a hemifusion-stalk pathway leading to a fusion pore.

226 uired to form the T-phase and the subsequent hemifusion-stalk-resembling R-phase.

227 limiting cases; the analysis indicates that hemifusion started at about 15 degrees C and increased o

228 ole in the progression from the intermediate hemifusion state to a complete fusion.

229 As demonstrated by recent findings on the hemifusion state, identifying intermediates of membrane

230 ine, agents that induce pores in an arrested hemifusion state, rescued infection by H8R virus to with

231 r how its substitution arrests fusion at the hemifusion state.

232 rted here also arrest membrane fusion at the hemifusion state.

233 ection by arresting virus-cell fusion at the hemifusion state.

234 s a mechanism leading to a long-lived (>5 s) hemifusion state.

235 accepted that membrane fusion proceeds via a hemifusion step before opening of the productive fusion

236 For viral fusion, the hemifusion structures are not determined(3).

237 We determined two distinct hemifusion structures: a hemifusion diaphragm and a nove

238 The surprising finding that Ser HA displays hemifusion suggests that the HA ectodomain functions not

239 A stable intermediate of hemifusion that could transit to fusion was also generat

240 Hemifusion, the linkage of contacting lipid monolayers o

241 propose that after the HA-ectodomain induces hemifusion, the transmembrane domain causes pore formati

242 Hemifusion then proceeds to the fusion pore that connect

243 n is supposed to promote the transition from hemifusion to complete fusion, the role of synaptobrevin

244 ixing but not the subsequent transition from hemifusion to full fusion.

245 ution of each leaflet in the transition from hemifusion to fusion.

246 The discovered progression from transient hemifusion to small, and then expanding, fusion pores up

247 lay an essential role in the transition from hemifusion to the fusion pore.

248 of gp41 (D589L) mediated transfer of lipids (hemifusion) to bystander cells but was defective in cell

249 Over time, hemifusion transitioned to complete fusion, showing that

250 icantly in the robustness of the bilayers to hemifusion under physiological loads (when lubrication b

251 GS(HA) virus, demonstrating that GS-mediated hemifusion was a functional intermediate in the membrane

252 In other words, by using DiI as probe, hemifusion was clearly observed to occur before pore for

253 The extent of hemifusion was deduced from the total R18 dequenching da

254 Alcohol-induced hemifusion was inhibited by lysophosphatidylcholine.

255 ur hemifusion assay was capable of detecting hemifusion, we used glycosylphosphatidylinositol (GPI)-l

256 of contacting monolayers to create a zone of hemifusion where continuity between the two adherent mem

257 ed influenza hemagglutinin (GPI-HA) mediates hemifusion, whereas chimeras with foreign transmembrane

258 No hemifusion with only lipid dye flux was detected.

259 HA) of influenza virus was thought to induce hemifusion without pore formation.

260 fusion pore or expanded into an unrestricted hemifusion, without pores but with unrestricted lipid mi

261 eral segregation of cardiolipin and membrane hemifusion would be critical for explaining the effects