ライフサイエンスコーパス: cell fusion

1 trated that alpha(2)M* induced trophoblastic cell fusion.

2 ules and mechanisms regulating trophoblastic cell fusion.

3 with target cells and also Env-mediated cell-cell fusion.

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

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

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

7 stomatitis virus results in homotypic virus-cell fusion.

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

9 educes HIV-1 infectivity by inhibiting virus-cell fusion.

10 ent programme for the induction of mammalian cell fusion.

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

12 ur glycoproteins essential for HSV entry and cell fusion.

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

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

15 removed the inhibitor to study synchronized cell fusion.

16 system that begins to reconstitute mammalian cell fusion.

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

18 rol on the plasma membrane to suppress virus-cell fusion.

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

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

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

22 severely limited our ability to reconstitute cell fusion.

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

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

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

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

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

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

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

30 nated cell-cell communication and suppresses cell fusion.

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

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

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

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

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

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

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

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

39 inucleate states after failed cytokinesis or cell fusion.

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

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

42 ge spike conformational changes required for cell fusion.

43 essed to overcome energetic barriers to cell-cell fusion.

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

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

46 lings show chemotropic interactions and cell-cell fusion.

47 elated with diminished B cell and epithelial cell fusion.

48 independently of dynamin also prevented cell-cell fusion.

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

50 lex series of interactions that culminate in cell fusion.

51 a specific gH motif required for epithelial cell fusion.

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

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

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

55 rectly represses genes promoting trophoblast cell fusion.

56 on of nuclei within myofibers after myogenic cell fusion.

57 and bone resorption, suggesting a defect in cell fusion.

58 d actin assembly is sufficient to drive cell-cell fusion.

59 hoblastic cells, which, in turn, may promote cell fusion.

60 of the fusion protein (F) to mediate cell-to-cell fusion.

61 f virus-induced cell-to-cell spread and cell-cell fusion.

62 furin and a reduced ability to mediate cell-cell fusion.

63 eneficial by preventing reinfection and cell-cell fusion.

64 xis alerts the cell of potentially dangerous cell fusion.

65 his binding is associated with inhibition of cell fusion.

66 atic neuronal morphological changes and cell-cell fusion.

67 ezygotes) and colocalization is required for cell fusion.

68 and cellular receptors to initiate virus and cell fusion.

69 comparable levels of homologous HEK293T cell-cell fusion.

70 i formation, and death of chemically induced cell fusions.

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

72 metalloproteases that block S-mediated cell-cell fusion, a process that contributes to the destructi

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

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

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

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

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

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

79 1V mutant had a large increase in epithelial cell fusion activity of up to 300% greater than that of

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

81 1-DeltaDAG1 cells, despite efficient cell-to-cell fusion activity.

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

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

84 l of a required accessory protein will block cell fusion, again forcing cell-free spread.

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 e CWI kinase Pkc1p ( PKC1*) caused decreased cell fusion and Cdc42p localization in prezygotes.

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

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

92 Somatic cell fusion and conspecific cooperation are crucial soci

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

94 Nevertheless, the mechanisms involved in cell fusion and differentiation are yet to be fully eluc

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

96 versity of the known proteins mediating cell-cell fusion and highlight their different working mechan

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

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

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

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

101 transitions between which are delineated by cell fusion and meiotic division.

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

103 was mediated primarily at the level of virus-cell fusion and not binding.

104 consecutive prolines are important for cell-cell fusion and pathogenesis.

105 Mutant NiV-MNESmut caused increased cell-cell fusion and produced lower virus titers.

106 and stemness-associated genes, but inhibits cell fusion and production of syncytiotrophoblast (STB)-

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

108 ive pressure towards the evolution of sexual cell fusion and reciprocal recombination during early eu

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

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

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

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

113 thentic LASV, inhibits LASV GP-mediated cell-cell fusion and virus-cell fusion, and, reminiscent of i

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

115 skeletal development, viral infection, cell-cell fusion, and ataxia.

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

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

118 g triggers to initiate mating, mechanisms of cell fusion, and DNA exchange, have yet to be characteri

119 ded for gKsyn-, UL20syn-, or UL24syn-induced cell fusion, and hence it was of interest to ascertain w

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

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

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

123 d fusogenicity accelerate viral entry, cause cell fusion, and thereby compromise genome stability.

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

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

126 ression of fusogens in neurons leads to cell-cell fusion, and, if so, whether this affects neuronal f

127 LASV GP-mediated cell-cell fusion and virus-cell fusion, and, reminiscent of its activity on influen

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

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

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

131 This finding suggests that cell fusion, as macroevolution event, favours specific s

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

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

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

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

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

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

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

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

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

141 nhancer of SARS-CoV-2 infection, and cell-to-cell fusion assays confirmed the ability of endocytic mu

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

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

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

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

146 Using stripe migration assays, chimeric cell-cell fusion assays, and a Sema3a transgenic mouse model,

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

148 time-of-addition studies, transient cell-to-cell fusion assays, and chimeric vesicular stomatitis vi

149 oop that were confirmed in transient cell-to-cell fusion assays.

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

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

152 MO catalytic activity abolished the block in cell fusion between formerly incompatible strains.

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

154 We show here that cell fusion between immortalized myoblasts and transform

155 C lineages indicated the possibility of cell-cell fusion between these two lineages.

156 239 with N173Q mediated CD4-independent cell-cell fusion but could not infect CD4-negative cells in s

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

158 sterol plays an important role in this virus-cell fusion, but molecular structural information about

159 otease inhibitors suppressed S-mediated cell-cell fusion, but not virus entry.

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

161 chanisms in syncytial fungi regulate somatic cell fusion by operating precontact during chemotropic i

162 suggest that IFITM3 oligomers inhibit virus-cell fusion by promoting membrane rigidity.

163 gp41-cholesterol interaction mediates virus-cell fusion by recruiting gp41 to the boundary of the li

164 Cell fusion can occur between mesenchymal stem cells (MS

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

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

167 wr-2, were necessary and sufficient to block cell fusion: cwr-1 encodes a polysaccharide monooxygenas

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

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 echanical stress and exhibit defects in cell-cell fusion during mating, which is exacerbated by simul

172 romone signaling, polarized growth, and cell-cell fusion during mating.

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

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

175 cental protein that negatively regulates the cell fusion essential for trophoblast syncytialization v

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

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

178 sed lineage tracing experiments, we rule out cell fusion events and confirm that hematopoietic lineag

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

180 Cell fusion experiments establish that increased cellula

181 Cell fusion experiments further reveal that the ratio of

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

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

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

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 n identified as necessary and sufficient for cell fusion (fusogens) use diverse mechanisms.

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

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

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

191 -induced death is suppressed by mutations in cell fusion genes ( FUS1, FUS2, RVS161, CDC42), implying

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

193 arriers, neuronal contacts and sites of cell-cell fusion have identified a core set of features share

194 Ever since the discovery of cell-cell fusion, how cells join together to form zygotes and

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

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

197 egulate cell wall dissolution during somatic cell fusion in a wild population of the filamentous fung

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

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

200 as encapsulation of invading pathogens, cell-cell fusion in response to foreign bodies, and their sel

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

202 inery so that the mutated F protein mediated cell fusion in the absence of known MeV cellular recepto

203 ividual cells, rejecting the process of cell-cell fusion in the normal development and function of th

204 hesized that SUPYN may thereby regulate cell-cell fusion in the placenta.

205 well with the capability of HSV-1 to induce cell fusion in the UL24syn background, suggesting that t

206 y with the capability of the virus to induce cell fusion in the UL24syn background.

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

208 model to unravel mechanisms underlying cell-cell fusion in vivo.

209 show that these compounds inhibit HIV-target cell fusion independently of viral tropism.

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

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

212 les of cell-surface Env recognition and cell-cell fusion inhibition by antibodies differed for the DS

213 family and has previously been implicated in cell fusion, interacts with Mac-1.

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

215 ls in the tumor microenvironment; and cancer cell fusion is a direct route to tumor cell heterogeneit

216 Cell-cell fusion is a physiological process that is hijacked

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

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

219 Cell-cell fusion is an evolutionarily conserved process that

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

221 Cell-cell fusion is essential for fertilization.

222 Cell fusion is essential for the development of multicel

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 indispensable for creating life and build

226 Cell-cell fusion is inherent to sexual reproduction.

227 Here, we find that yeast cell fusion is negatively regulated by components of the

228 The main known impact of cell fusion is to promote the formation of metastatic hy

229 Cell fusion is ubiquitous in eukaryotic fertilization an

230 Transcription induction, needed for cell-cell fusion, is mediated by Gbetagamma and the mitogen-a

231 V) spike (S) protein, involved in viral-host cell fusion, is the primary immunogenic target for virus

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

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

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

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

236 mechanically induced stress and during cell-cell fusion, leading to inhibition of the MAPK Fus3.

237 Cell fusion likely drives tumor evolution by undermining

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

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

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

244 adation would cause lysis, the initiation of cell fusion must be highly regulated.

245 n in each mating partner, and sustained once cell fusion occurred until the fungus enter the plant ti

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

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

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

249 SOS Env supported virus entry and cell-cell fusion only after exposure to a reducing agent, dit

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

251 While different cell fusion processes appear to proceed via similar memb

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

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

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

255 Cell-cell fusion remains the least understood type of membran

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

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

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

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

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

261 tion, "stabilizing" MAbs also inhibited cell-cell fusion, suggesting a unique mechanism by which the

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

263 cause a second type of membrane fusion, cell-cell fusion (syncytium formation), which is linked to pa

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

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

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

267 s and targeted an epitope critical for virus-cell fusion. Therefore, unlike the leading EBV gp350 vac

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

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

270 ltative intracellular bacterium induces host cell fusion through its type VI secretion system 5 (T6SS

271 that the cGAS-STING pathway senses unnatural cell fusion through micronuclei formation as a danger si

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

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

274 Near cell fusion to take place, the increase on pheromone sig

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

276 a with numerous centrosomes, suggesting that cell fusion triggered caspase-2 activation.

277 We report that bacterial T6SS5-dependent cell fusion triggers type I IFN gene expression in the h

278 ts cooperative behavior in fungi by blocking cell fusion upon contact, contributing to fungal immunit

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

280 1 Envelope protein (Env) mediates viral-host cell fusion via a network of conformational transitions,

281 ude that Mid2p and Pkc1p negatively regulate cell fusion via Cdc42p and Fus2p.

282 ey players mediating early events in cell-to-cell fusion, vital for intercellular viral spread.

283 However, virus-cell fusion was more efficient for F proteins harboring

284 Cell fusion was selectively inhibited by the hexapeptide

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

286 ion protocols that allow tracking of ex vivo cell fusion, we present transcription and translation dy

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

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

289 nable a rapid spread of infection by cell-to-cell fusion, whereas viruses harboring L or S at P8 spre

290 Cell-cell fusion, which is essential for tissue development a

291 ired for viral entry into cells and for cell-cell fusion, which is pathognomonic of henipaviral infec

292 er, thymol, were shown to block virus-target cell fusion while not perturbing other stages of the vir

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

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 multicellularity is associated with somatic cell fusion within and between colonies.

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