ライフサイエンスコーパス: cell fusion

1 GCS1 is sufficient to promote mammalian cell-cell fusion.

2 stomatitis virus results in homotypic virus-cell fusion.

3 rusions into the "receiving" cell to promote cell fusion.

4 cell walls at the right place to allow cell-cell fusion.

5 FFWO, while having a modest effect on virus-cell fusion.

6 inucleate states after failed cytokinesis or cell fusion.

7 lanine (N58A) caused extensive virus-induced cell fusion.

8 ent programme for the induction of mammalian cell fusion.

9 on of oMAP4 impairs cell elongation and cell-cell fusion.

10 odulation of integrin signaling, and cell-to-cell fusion.

11 ls expressing 3-OS HS significantly enhanced cell fusion.

12 M HL region plays a critical role in cell-to-cell fusion.

13 C82 and C243 caused extensive virus-induced cell fusion.

14 lings show chemotropic interactions and cell-cell fusion.

15 elated with diminished B cell and epithelial cell fusion.

16 independently of dynamin also prevented cell-cell fusion.

17 ndrome coronaviruses for cell-cell and virus-cell fusion.

18 ur glycoproteins essential for HSV entry and cell fusion.

19 lex series of interactions that culminate in cell fusion.

20 a specific gH motif required for epithelial cell fusion.

21 V-1 envelope-induced CD4/CXCR4-mediated cell-cell fusion.

22 to an important role of endocytosis in cell-cell fusion.

23 irion envelopment, egress, and virus-induced cell fusion.

24 hat DC-STAMP is engaged in the late stage of cell fusion.

25 an that used by class II fusion proteins for cell fusion.

26 ell proteases to mediate virus-cell and cell-cell fusion.

27 n infectivity and ability to mediate cell-to-cell fusion.

28 lication and its spike protein-mediated cell-cell fusion.

29 esis and of diseases resulting from abnormal cell fusion.

30 removed the inhibitor to study synchronized cell fusion.

31 n retroviral pseudotypes and triggering cell-cell fusion.

32 key role in IFN-beta-mediated C2C12 myoblast cell fusion.

33 drebrin in HIV-1 viral infection and cell to cell fusion.

34 fetomaternal interface via trophoblast cell-cell fusion.

35 oxyl-terminal truncated gB, causes extensive cell fusion.

36 ing fusogenic protein engagement during cell-cell fusion.

37 ing endocycles and becoming polyploid, or by cell fusion.

38 Mb) into yeast under conditions that promote cell fusion.

39 tive regulator of HIV entry and HIV-mediated cell fusion.

40 ion of T cells already at the stage of virus-cell fusion.

41 r Yorkie modulates both polyploidization and cell fusion.

42 gK is required for gB-mediated virus-induced cell fusion.

43 virus entry as well as virus-induced cell-to-cell fusion.

44 system that begins to reconstitute mammalian cell fusion.

45 they are formed by incomplete cytokinesis or cell fusion.

46 d not facilitate BV- and CeHV-2-induced cell-cell fusion.

47 ole in cell-to-cell spread and virus-induced cell fusion.

48 dc42-138, which is specifically defective in cell fusion.

49 membrane fusion during virion entry and cell-cell fusion.

50 t, Itgb1D and Cav3, genes important for cell-cell fusion.

51 wild-type levels of infectivity and cell-to-cell fusion.

52 eases markedly decreased both entry and cell-cell fusion.

53 f these lysines contributed to gB/gH-gL cell-cell fusion.

54 severely limited our ability to reconstitute cell fusion.

55 nveloped virus entry into cells, and somatic cell fusion.

56 merged when placed in the same cell by cell-cell fusion.

57 ed from donor marrow cells in the absence of cell fusion.

58 s and not, as previously thought, by cell-to-cell fusion.

59 own about the biophysical regulation of cell-cell fusion.

60 e fusion proteins dedicated to inducing cell-cell fusion.

61 ceptor binding by HN is dispensable for cell-cell fusion.

62 nated cell-cell communication and suppresses cell fusion.

63 tivity, commensurate with the defect in cell-cell fusion.

64 to couple host receptor recognition to virus-cell fusion.

65 way of the cell, resulting in the absence of cell fusion.

66 rus F triggering during viral entry and cell-cell fusion.

67 synthesis zone to shift from cell growth to cell fusion.

68 for viral entry into host cells and for cell-cell fusion, a hallmark of the disease pathobiology.

69 dhesion in suppressing larval epidermal cell-cell fusion--a role that may be conserved in other epith

70 Using the natural cell fusion ability of the halophilic archaeon Haloferax

71 ng of the yolk syncytial nuclei and enhanced cell fusion, accompanied by disruption of microtubule ne

72 ignal peptide peptidase, and is required for cell fusion activities.

73 -I and D-II with C153 of gH/gL, had normal B cell fusion activity but reduced epithelial cell fusion

74 files and may contribute to the high cell-to-cell fusion activity characteristic of the morbillivirus

75 on have been shown to reduce pH-induced cell-cell fusion activity of ectopically expressed GPC to app

76 a possible explanation for the high cell-to-cell fusion activity of morbilliviruses.

77 1V mutant had a large increase in epithelial cell fusion activity of up to 300% greater than that of

78 of gL is involved in restricting epithelial cell fusion activity, strongly correlating with syncytiu

79 cell fusion activity but reduced epithelial cell fusion activity, which was partially restored by tr

80 1-DeltaDAG1 cells, despite efficient cell-to-cell fusion activity.

81 gL in the kinetics of gB-mediated epithelial cell fusion, adding to previous findings indicating a di

82 pression, and the ability to mediate cell-to-cell fusion after low-pH exposure.

83 L are required for epithelial cell fusion; B cell fusion also requires gp42.

84 rmore, there are notable differences in cell-cell fusion among aMPV subtypes.

85 cific glycans on NiV-F to reduce endothelial cell fusion, an effect that may reduce pathophysiologic

86 d extracellular matrix proteins; (2) clastic cell fusion and activation by the RANKL/RANK/OPG and ATP

87 urvature transitions that occur during virus-cell fusion and are broad-spectrum antivirals against en

88 g of the nanoscale biophysical regulation of cell fusion and can be exploited in biomaterials design

89 d sorting, cell washing and patterning, cell-cell fusion and communication, and tissue engineering.

90 ed direct membrane breakdown leading to cell-cell fusion and consequent mixing of cytoplasmic content

91 tion of progeny virus and reduce endothelial cell fusion and damage, depending on timing of galectin-

92 We next imaged single HIV-cell fusion and found that these events were manifested

93 In this study, using cell-cell fusion and HA-pseudovirus infectivity assays, we fo

94 results in attenuation of Env-mediated cell-cell fusion and hemifusion, as well as viral infectivity

95 and alphav integrins are essential for cell-cell fusion and hMPV infection.

96 broad set of genes required for trophoblast cell fusion and hormonogenesis.

97 HS during HCMV plaque formation and cell-to-cell fusion and identify a novel target for future thera

98 or leucine 207 reduces both epithelial and B cell fusion and is accompanied by reduced gp42 binding.

99 nding affinity and 0.2 muM EC50 against cell-cell fusion and live virus replication and was active ag

100 ole for elevated MAPK activity in successful cell fusion and morphogenic reorganization.

101 ene in an expression vector for ex vivo cell-cell fusion and pseudotype assays demonstrated fusogenic

102 n (N48 and N58) sites of gK in virus-induced cell fusion and replication.

103 onstructural viral protein that induces cell-cell fusion and syncytium formation.

104 hMPV infectivity and F protein-mediated cell-cell fusion and that the integrin-binding motif in the F

105 tibody neutralization, while modulating cell-cell fusion and viral entry via multiple mechanisms.

106 and alphav integrins are essential for cell-cell fusion and viral replication, (ii) the first two re

107 ) were essential for S protein-mediated cell-cell fusion and virus entry.

108 that they were essential for mediating cell-cell fusion and virus entry.

109 High RAPGEF2 protein levels promoted cell-cell fusion and, consequently, multinucleation.

110 one of the most important genes involved in cell-fusion and showed decreased gene expression during

111 role of SIV layer 3 in viral entry, cell-to-cell fusion, and CD4 binding.

112 imA to facilitate actin-based motility, host cell fusion, and dissemination.

113 toskeletal rearrangements were necessary for cell fusion, and in combination they were sufficient to

114 Nuclear transplantation, cell fusion, and induced pluripotent stem cell studies h

115 e reversed by somatic cell nuclear transfer, cell fusion, and iPS.

116 ns with resident or tissue-based stem cells, cell fusion, and neurotrophin elaboration--offer renewed

117 the MAbs to FR1 are neutralizing, block cell-cell fusion, and prevent the association of gB with lipi

118 nvasion of one cell into another during cell-cell fusion, and the force-feedback loops that ensure ro

119 racellular transport, G-F interactions, cell-cell fusion, and viral entry.

120 ew compounds were evaluated in binding, cell-cell fusion, and viral replication assays.

121 have been identified that are defective for cell fusion, and yet the molecular mechanism of this pro

122 further mechanistic twist, gB-mediated cell-cell fusion appears restricted by its intraviral or cyto

123 Using a cell fusion approach to generate multinucleate cells, we

124 ies and actin dependences of FFWO versus HIV-cell fusion are consistent with the notion that, except

125 large cells generated by polyploidization or cell fusion are essential because they are better able t

126 ng-term time-lapse microscopy has identified cell fusion as the main route of RS cell formation.

127 key role in the induction of osteoclast (OC) cell fusion, as well as DC-mediated immune regulation.

128 Using a virus-cell fusion assay and live-cell single-molecule force sp

129 We show that a heterologous cell fusion assay in vitro and allelic complementation e

130 demonstrated fusogenicity in an ex vivo cell-cell fusion assay on a panel of mammalian cells.

131 A heterotypic cell fusion assay resulting in productive fusion may pro

132 us-free split-green fluorescent protein cell-cell fusion assay that enables real-time measurements of

133 In a cell-cell fusion assay, line 19 F was more fusogenic than Lon

134 Here, using a reconstituted "flipped" cell-cell fusion assay, we show that lipid-anchored STX11 and

135 red in the presence of FQ as shown in a cell-cell fusion assay.

136 e-like fusion levels in an in vitro gB/gH-gL cell fusion assay.

137 tin gene: It is fusogenic in an ex vivo cell-cell fusion assay; it is specifically expressed in the s

138 Although cell-cell fusion assays are valuable, they do not fully recap

139 Cell-cell fusion assays indicate that a minimum of two events

140 Cell-cell fusion assays indicate that SaHV-1 entry glycoprote

141 Cell-cell fusion assays indicated that nectin-1, an HSV-1 gD

142 Cell-cell fusion assays show a strain-independent failure of

143 ufficient to confer CD4 independence in cell-cell fusion assays, although other mutations were requir

144 the complexin-I inhibitory activity in cell-cell fusion assays, and by the crystal structure of a su

145 n and quantitative cell-to-cell and virus-to-cell fusion assays.

146 show that they are fully functional in cell-cell fusion at shorter coincubation times and at lower t

147 gB and gH/gL are required for epithelial cell fusion; B cell fusion also requires gp42.

148 ides a valuable model for investigating cell-cell fusion because of the importance of this process fo

149 XC cells with chicken fibroblasts, allowing cell fusion between both partners.

150 Cell-cell fusion between gametes is a defining step during de

151 239 with N173Q mediated CD4-independent cell-cell fusion but could not infect CD4-negative cells in s

152 5% and increased the level of F-induced cell-cell fusion but had little impact on assembly of viral s

153 gH to epithelial cells initiating epithelial cell fusion but not for fusion with B cells and gp42 bin

154 was found to be required for virus-mediated cell fusion, but only for mutants that harbor syncytial

155 cells toward pluripotency following cell-to-cell fusion by a mechanism that is rapid but poorly unde

156 Thus, HMPV F is triggered to induce virus-cell fusion by interactions with cellular receptors in a

157 Cell fusion can occur between mesenchymal stem cells (MS

158 This finding means that cell fusion can produce abnormal cell types, including c

159 Virus-induced cell fusion caused by deletion of the carboxyl-terminal

160 device, we revealed the underlying abnormal cell fusion causing defective vulval morphology in mutan

161 y1Delta zygotes accumulate ER at the zone of cell fusion, causing a block in nuclear congression.

162 w these networks reach a consensus, we model cell fusion computationally.

163 Mechanistically, the inefficient muscle cell fusion correlates well with the transcriptional rep

164 e reconstituted a high-efficiency, inducible cell fusion culture system in the normally nonfusing Dro

165 This de novo cell fusion culture system reveals a general role for ac

166 The cell fusion defect is not a secondary consequence of ine

167 rum of congenital myopathies to include cell-cell fusion deficits.

168 titution caused significantly increased cell-cell fusion despite reduced cell-surface gB.

169 scopy methods to study this key form of cell-cell fusion during development of the indirect flight mu

170 parameters, which affected the efficiency of cell fusion during infection.

171 ntial contribution of myomaker-mediated stem cell fusion during physiological adult muscle hypertroph

172 Polyploid cells can originate from cell fusion, endoreplication, and cytokinesis failure.

173 ast cellular mixture with PEG, which induces cell fusion, engulfment, aggregation or lysis.

174 Thus, one cell fusion event can both initiate malignancy and fuel

175 ing phenotypic diversity; however, whether a cell fusion event can initiate malignancy and direct tum

176 ceptor degeneration and observed spontaneous cell fusion events between Muller glia and the transplan

177 yncytium; it can trigger cell-cell and virus-cell fusion ex vivo; and it has been conserved for >25 m

178 Cell fusion experiments establish that increased cellula

179 Cell fusion experiments further reveal that the ratio of

180 Using cell fusion experiments in live embryos, we find that th

181 Virion-cell and cell-cell fusion experiments revealed that LY6E promotes memb

182 Using cell-cell fusion experiments, we found that SaHV-1 uses the e

183 membrane fusion in transient-expression cell-cell fusion experiments.

184 formed: nuclear transfer to eggs or oocytes, cell fusion, extract treatment, direct reprogramming to

185 Despite the importance of cell fusion for mammalian development and physiology, th

186 The cell fusion frequency of both Deltalfd-1 and DeltaPrm1 m

187 es have important roles in viral entry, cell-cell fusion, G-F interactions, G oligomerization, and im

188 However, despite cell fusion generating many useful mAbs questions have b

189 and could form through endoreduplication or cell fusion, generating regular-sized cancer cells quick

190 Although cancer cell fusion has been suggested as a mechanism of cancer

191 rature describing leukocyte/macrophage-tumor cell fusion hybrids, and their role in metastatic progre

192 hat JPVTM was defective in promoting cell-to-cell fusion (i.e., syncytia formation) compared with JPV

193 iruses, EBV, a gammaherpesvirus, can mediate cell fusion if gB and gHgL are expressed in trans.

194 ated by a single protein, such as epithelial cell fusion in Caenorhabditis elegans, the cell fusion s

195 isolated from herpetic lesions cause limited cell fusion in cell culture, clinical herpetic lesions t

196 ata show that Cdc42p acts at a late stage in cell fusion in concert with a key cell fusion regulator,

197 an essential contributor to skeletal muscle-cell fusion in developing mouse embryos.

198 S HS) during HCMV-mediated entry and cell-to-cell fusion in HIS cells.

199 irst host cell-encoded protein that inhibits cell fusion in mammals.

200 ar mechanisms of membrane merger during cell-cell fusion in most eukaryotic organisms remain elusive.

201 novel mechanism involving increased cell-to-cell fusion in the absence of CD4, the primary receptor

202 l mutations in either gB or gK did not cause cell fusion in the absence of UL11.

203 of gH cytotail mutations on virus-free cell-cell fusion in transfected cells to exclude the contribu

204 Suppressyn knock-down promotes cell-cell fusion in trophoblast cells and cell-associated and

205 logically, PEDV strain CV777 induced greater cell fusion in Vero cells than did U.S. PEDV strains.

206 ytia, underscoring the importance of cell-to-cell fusion in virus spread in infected tissues.

207 iral genes drastically enhance virus-induced cell fusion in vitro and in vivo.

208 e gBcyt ITIM regulates gB/gH-gL-induced cell-cell fusion in vitro, tyrosine residues Y881 and Y920 in

209 etal myogenesis involves extensive rounds of cell fusion, in which individual myoblasts are incorpora

210 eletion abrogated gBDelta28syn virus-induced cell fusion, indicating that the amino terminus of gK is

211 use the use of concentrated Sendai virus for cell fusion induced an increase in intracellular calcium

212 Trypsin was required for cell-cell fusion induced by subtype B but not subtypes A and

213 are essential for herpesvirus entry and cell-cell fusion induced syncytium formation, a characteristi

214 bling MyoD accumulation, differentiation and cell fusion into myofibers.

215 Osteoclast and myoblast cell-cell fusion involves the formation of actin-rich protrus

216 Cell-cell fusion is a regulated process that requires merging

217 Previously, we have shown that cell-cell fusion is an asymmetric process in which an "attack

218 Cell-cell fusion is an evolutionarily conserved process that

219 dence that the mechanism of phlebovirus-host cell fusion is conserved among genetically and patho-phy

220 h HN activates the F protein such that virus-cell fusion is controlled and occurs at the right time a

221 Cell-cell fusion is critical for the conception, development,

222 Cell-cell fusion is essential for fertilization.

223 and phenotypic potential of tumors formed by cell fusion is established immediately or within a few c

224 Cell-cell fusion is fundamental to a multitude of biological

225 Cell-cell fusion is inherent to sexual reproduction.

226 AREs mediate nuclear fusion, ER fusion after cell fusion is necessary to complete nuclear congression

227 elineated, but their role in regulating cell-cell fusion is poorly understood.

228 Cell fusion is the key event of fertilization that gives

229 Cell fusion is ubiquitous in eukaryotic fertilization an

230 e pathway (MAK-2), which is also involved in cell fusion, is unaffected.

231 In contrast, for B cell fusion it requires gB and gH/gL with gp42 serving a

232 he actin cytoskeleton are implicated in cell-cell fusion, it remains unclear whether and how they coo

233 and gB work together to modulate epithelial cell fusion kinetics are essential to understand the hig

234 rall relatively slower viral entry than cell-cell fusion kinetics.

235 Cell fusion likely drives tumor evolution by undermining

236 monstrate an excellent performance as a live-cell fusion marker in STED microscopy, using 640 nm exci

237 rst host cell-encoded inhibitor of mammalian cell fusion may encourage improved understanding of cell

238 totail is an essential component of the cell-cell fusion mechanism and show that the N-terminal porti

239 sion may encourage improved understanding of cell fusion mechanisms, of placental morphogenesis and o

240 such as the deadly Nipah virus (NiV), virus-cell fusion mechanistic studies are especially cumbersom

241 such as the deadly Nipah virus (NiV), virus-cell fusion mechanistic studies are notably cumbersome.

242 Here we use cell fusion-mediated pluripotent reprograming to study h

243 et1 and Tet2 proteins have discrete roles in cell-fusion-mediated pluripotent reprogramming and impri

244 n studies have predominantly focused on cell-cell fusion models, largely due to the low availability

245 In the filamentous fungus Neurospora crassa, cell fusion occurs during asexual spore germination, whe

246 ive fusion of CHO-nectin-1 cells but limited cell fusion of CHO-PILRalpha cells.

247 ieved to be the first report of in-vivo cell-cell fusion of human lymphoma and rodent host cells, and

248 aturation of OCLs was abrogated by defective cell fusion of pre-OCLs depleted of Orai1, consistent wi

249 uolar ATPase V(o) domain that is involved in cell fusion of pre-OCLs.

250 us, RS cell generation is related neither to cell fusion of unrelated Hodgkin cells nor to endomitosi

251 to growth-induced formation of giant Hodgkin cells, fusion of small mononuclear cells followed by a s

252 In cone photoreceptors, similar to bipolar cells, fusion of the initial ribbon-associated synaptic

253 A partial dependence of HIV-cell fusion on actin remodeling was observed in CD4(+) T

254 Polyploidy can occur because of cell fusion or abnormal cell division (endoreplication,

255 l infections and neoplasia, spontaneous cell-cell fusion, or syncytialization, is quite restricted in

256 involve permanent donor-host nuclear or cell-cell fusion, or the uptake of free protein or nucleic ac

257 2 at wild-type levels, and the mutant's cell-cell fusion phenotypes generally correlated to viral ent

258 Aberrations during this cell-fusion process are associated with Intrauterine Gro

259 syncytium layer but displays a heterologous cell-fusion process unique among eutherian mammals.

260 f VZV gB (gBcyt) has been implicated in cell-cell fusion regulation because a gB[Y881F] substitution

261 fective VZV propagation is dependent on cell-cell fusion regulation by the conserved gBcyt lysine clu

262 e stage in cell fusion in concert with a key cell fusion regulator, Fus2p, which contains a Dbl-homol

263 family member and DC-STAMP is an osteoclast cell-fusion regulator.

264 It is a long-held paradigm that cell fusion reprograms gene expression but the extent of

265 results establish in vivo role of Anx A1 in cell fusion required for myofiber regeneration and not i

266 Although cell-cell fusion requires the presence of fusogenic membrane

267 ically induced colitis in rodents); commonly cell fusion seems to be responsible for this.

268 In this study, we uncoupled the cell fusion step from both pre-fusion stages of osteocla

269 l cell fusion in Caenorhabditis elegans, the cell fusion step in osteoclastogenesis is controlled by

270 d the scaffold protein HAM-5) to specialized cell fusion structures termed conidial anastomosis tubes

271 rus entry into target cells and for the cell-cell fusion (syncytia) that results from many paramyxovi

272 t fusion, we established a heterologous cell-cell fusion system, in which fibroblasts expressing muta

273 the TNase target antigen were produced using cell fusion techniques.

274 eleased from PI cells induced higher cell-to-cell fusion than the parental virus following infection

275 rminating spores of this fungus undergo cell-cell fusion, thereby forming a highly interconnected sup

276 FFWO occurring at the cell surface with HIV-cell fusion through a conventional entry route, we desig

277 ggers trophoblast fusion, heme inhibits BeWo cell fusion through activation of STAT3.

278 the ability of individual mutants to support cell fusion through each receptor.

279 tions rely on a poorly understood ability of cell fusion to create new cell types.

280 We recently used cell fusion to define a class of silent genes termed "ci

281 Here we use cell fusion to examine the earliest events in the reprog

282 programs to drive tissue-specific functions (cell fusion) to promote a developmental transition.

283 ere, we designed experiments to examine cell-cell fusion using bulk metallic glass (BMG) nanorod arra

284 observations suggest that gB modulates cell-cell fusion via an ITIM-mediated Y881 phosphorylation-de

285 -type-like B cell fusion, whereas epithelial cell fusion was greatly reduced.

286 Cell fusion was selectively inhibited by the hexapeptide

287 tiation and kinetics of gB-driven epithelial cell fusion, we established a virus-free split-green flu

288 f gD remained essential for virus spread and cell fusion, we propose that gH:KV mimics a transition s

289 he conserved DB resulted in wild-type-like B cell fusion, whereas epithelial cell fusion was greatly

290 nd Newcastle disease virus HN abolishes cell-cell fusion, whereas HN retains receptor binding and neu

291 e (329)RGD(331) motif are essential for cell-cell fusion, whereas mutations at D331 did not significa

292 in cleavage efficiency, facilitating cell-to-cell fusion, while HN169R possesses a multifaceted role

293 n inhibits HIV-1 production and HIV-mediated cell fusion, while syntenin depletion specifically incre

294 ibited conidial germination and accompanying cell fusion with different potencies.

295 igate whether the mechanism of breast cancer cell fusion with mesenchymal stem/multipotent stromal ce

296 e motif that is necessary for promoting cell-cell fusion with myomaker.

297 e mutants displayed a 40 to 60% reduction in cell fusion with no effect on gH/gL trafficking.

298 ith a role in the formation--by heterologous cell fusion with uterine cells--of the trinucleate cells

299 the roles of DC-STAMP in promoting local OC cell fusion without affecting adaptive immune responses

300 dependent focus at the center of the zone of cell fusion (ZCF) and remains associated with remnant ce