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 ytoplasmic content between cells, resembling hemifusion.

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

5 bit prompt, full fusion while others exhibit hemifusion.

6 sogenic conformation or had induced membrane hemifusion.

7 nsive stages following rather than preceding hemifusion.

8 ature created an intermediate state of local hemifusion.

9 ceding prehairpin intermediate formation and hemifusion.

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

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

12 lasmic mixing, indicating that GS can induce hemifusion.

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

14 icles, apposition and contact formation, and hemifusion.

15 ipid-anchored Vam3 interfered already before hemifusion.

16 enching that cannot be ascribed to fusion or hemifusion.

17 membrane makes trimerization a bottleneck in hemifusion.

18 ctedly long lag phases between pH change and hemifusion.

19 omplexes have the capacity to drive membrane hemifusion.

20 contacting monolayers in a process known as hemifusion.

21 for measuring the free energy of adhesion or hemifusion.

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

23 on events are now reclassified as productive hemifusion.

24 largement or expansion of fusion pores after hemifusion.

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

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

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

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

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

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

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

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

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

34 Hemifusion and complete fusion depend on HAP2/GCS1 prese

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

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

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

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

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

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

41 This allowed both hemifusion and fusion to be monitored.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

88 Hemifusion diaphragm expansion is spontaneous for distal

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

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

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

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

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

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

95 sure widening initiating pore formation in a hemifusion diaphragm.

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

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

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

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

100 ive spontaneous curvature to leaflets of the hemifusion diaphragm.

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

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

103 fusion after treatments known to destabilize hemifusion diaphragms.

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

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

106 Hemifusion events are roughly half productive (leading t

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

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

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

110 Single hemifusion events were detected by fluorescence microsco

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

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

113 Hemifusion, flickering of fusion pores, and kinetic tran

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

140 membrane leaflets leading to formation of a hemifusion intermediate.

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

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

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

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

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

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

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

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

149 native formation and dilation of microscopic hemifusion intermediates.

150 eeded to complete fusion without discernible hemifusion intermediates.

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

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

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

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

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

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

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

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

159 dy/Fab coverage display significantly slower hemifusion kinetics.

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

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

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

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

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

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

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

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

168 Hemifusion occurred independent of polarity.

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

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

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

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

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

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

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

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

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

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

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

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

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

182 The hemifusion phenotype of Ser HA was confirmed by electrop

183 Ser HA, therefore, displayed a hemifusion phenotype.

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

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

186 Hemifusion requires a small amount of energy independent

187 Hemifusion requires at least two adjacent trimers.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

213 Hemifusion, the linkage of contacting lipid monolayers o

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

215 Hemifusion then proceeds to the fusion pore that connect

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

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

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

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

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

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

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

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

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

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

226 Alcohol-induced hemifusion was inhibited by lysophosphatidylcholine.

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

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

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

230 No hemifusion with only lipid dye flux was detected.

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

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

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