ライフサイエンスコーパス: syncytia

1 IHCs are electrochemically coupled in 'mini-syncytia'.

2 n and the formation of multinucleated cells (syncytia).

3 aximum 5 days after transfection (100 nuclei/syncytia).

4 rmation of multinucleated giant cells (i.e., syncytia).

5 pathological induction of cell-cell fusion (syncytia).

6 the formation of multinuclear, fused cells (syncytia).

7 animal viruses induce cells to fuse and form syncytia.

8 nd mediates adhesion with FMs and developing syncytia.

9 infected cells to form large multinucleated syncytia.

10 -BL HeLa-based HIV-1 indicator cells to form syncytia.

11 ation of an electromechanical wave along the syncytia.

12 id not yield detectably increased numbers of syncytia.

13 sion, penetrated cells and induced extensive syncytia.

14 ffect and resulted in the formation of large syncytia.

15 MV glycoproteins did not form multinucleated syncytia.

16 d monocytic cells with long-lived osteoclast syncytia.

17 for fusion of epidermal cells into discrete syncytia.

18 ker genes into the heart or other electrical syncytia.

19 proteins, with subsequent formation of cell syncytia.

20 fusion machinery, allowing the formation of syncytia.

21 cle, reenter mitosis, and form multicellular syncytia.

22 or cells are fused into large multinucleated syncytia.

23 pread, surface glycoproteins fuse cells into syncytia.

24 n, and degeneration, of large multinucleated syncytia.

25 d of glial tumor cells throughout astrocytic syncytia.

26 later times, the staining surrounded entire syncytia.

27 characterized by very large, multinucleated syncytia.

28 owever, effected the formation of only small syncytia.

29 ergo inappropriate fusion with the epidermal syncytia.

30 were able to detect and quantify HIV-induced syncytia.

31 eading to formation of lethal multinucleated syncytia.

32 r most conditions, without the appearance of syncytia.

33 ould be detected in multinucleated DC-T cell syncytia.

34 lytic infection with extensive formation of syncytia.

35 nt correlated with the formation of enlarged syncytia.

36 erodera schachtii-induced feeding sites, the syncytia.

37 CMV also spreads cell to cell and can induce syncytia.

38 lls showed cytopathic effects, forming giant syncytia.

39 on of reverse transcriptase and formation of syncytia.

40 nd can direct the formation of multinucleate syncytia.

41 er into large multi-nucleated cells known as syncytia.

42 entral determinant of the local cytoplasm in syncytia.

43 and cause multinucleated giant cells, termed syncytia.

44 germ cells while joined in germline cysts or syncytia.

45 argest cells in the body, and one of its few syncytia.

46 ereas cells expressing F plus TM formed some syncytia.

47 nt membrane and induced prominent epithelial syncytia.

48 ased repression in unicellular organisms and syncytia.

49 ciently in both cell types and induced large syncytia.

50 al cell sloughing, apoptosis, and occasional syncytia.

51 ation and/or maintenance of nematode-induced syncytia.

52 ane breakdown and formation of multinucleate syncytia.

53 receptors are expressed in nematode-induced syncytia.

54 lature into specialized feeding sites called syncytia.

55 ncentrations of auxin increase in developing syncytia.

56 plant root to form feeding cells, so-called syncytia.

57 ion of the cellular antioxidant machinery in syncytia.

58 ein accumulation and by robust expansion via syncytia, a characteristic feature of JHM virus dissemin

59 CedV forms syncytia, a hallmark of henipaviral and paramyxoviral in

60 Syncytia activate macrophages and fusogenic membrane gly

61 ity of vaccinia virus-infected cells to form syncytia after a brief exposure to a pH below 6, known a

62 ions were unable to mediate the formation of syncytia after low-pH treatment.

63 logically active, mediating the formation of syncytia, albeit at a reduced rate.

64 Both uncoordinated motility of syncytia and adhesion to CD4(+) lymph node cells led to

65 usion by the production of fluorescent green syncytia and allowed us to elucidate many aspects of HCV

66 but not their parental bulk viruses, induced syncytia and caused acute death of infected CD8(+) cells

67 VEM in Vero cells also resulted in increased syncytia and enhanced cell-to-cell spread in cells infec

68 d that HIV-infected T cells are motile, form syncytia and establish tethering interactions that may f

69 The infected cells were multinucleated syncytia and expressed the S100 and p55 dendritic cell m

70 mutants, Fcs-5B, formed protease-independent syncytia and grew to 10-fold-higher titers compared to t

71 eveal spatial relationships among nematodes, syncytia and host vascular tissues at the cellular level

72 ro cells with icDelta10aa resulted in larger syncytia and more virions, with reduced numbers of S pro

73 usion of all seam cells with the surrounding syncytia and pronounced defects in molting.

74 In addition, HIV-1-infected T-lymphocyte syncytia and the significance of adhesion molecule/ligan

75 tion of cytosolic contents through the glial syncytia and to the extracellular space, respectively.

76 ly refractory cell lines, induction of large syncytia, and accelerated kinetic properties.

77 endent cell-mediated cytotoxicity, formed no syncytia, and neither underwent nor induced apoptosis in

78 of cell types induces the formation of giant syncytia, and that fusion of a human trophoblastic cell

79 However, it does not form syncytia, and the virus is avirulent in chickens.

80 s strongly activated in the nematode-induced syncytia, and transgenic plants overexpressing SPDS2 sho

81 igand interactions in the formation of these syncytia are described.

82 The consequences of ploidy variation in syncytia are difficult to predict because protein imbala

83 Here, we show that syncytia are highly ordered structures over 24-48 h but

84 rms large syncytia with XC cells, whereas no syncytia are reported for amphotropic virus.

85 is the principal mechanism of T cell death, syncytia are the main source of virus production, and bo

86 Quantitative syncytia assays showed that JPVTM was defective in promo

87 y to support infection still induced massive syncytia at low pH.

88 entry and spread in A56/K2 cells and induced syncytia at neutral pH in HeLa cells despite the express

89 een delivered, consistent with the idea that syncytia, at least in vitro, are not required for HIV-1

90 , allowing neighboring cells to fuse to make syncytia, but this can be prevented by removing various

91 hen combined, enabled formation of extensive syncytia by human cancer cell lines that express the tar

92 tor is required for the induction of XC cell syncytia by the R(+) Env protein.

93 Small syncytia can be readily identified by the two-color cyto

94 The multinucleate cells resembled the syncytia caused by physical wounding.

95 s results in the formation of multinucleated syncytia, causing mitochondrial failure with ATP depleti

96 cells infected with VZVgB-36 form extensive syncytia compared to the relatively small syncytia forme

97 Endothelial syncytia, comprised of multinucleated giant-endothelial

98 ence imaging revealed that the cell walls of syncytia contain cellulose and the hemicelluloses xylogl

99 alysis of various samples, we found that all syncytia contained large amounts of virions and that mos

100 The majority of these syncytia could be double labeled for HIV-1 RNA and a den

101 With these cells, the formation of syncytia could be induced by acidic medium.

102 s where HIV-1 replication can be enhanced in syncytia derived from dendritic cells.

103 g and resulted in the absence of RSV-induced syncytia despite no significant change in viral titer.

104 data suggest that the unique manner in which syncytia develop and die provides a highly effective pat

105 While visible syncytia do not form after MV infection of HAE, the cyto

106 secreted as an effector into the developing syncytia during early plant parasitism.

107 cteristically forms multinucleated cells, or syncytia, during the infection of human tissues, but lit

108 dings and modeling, we propose that IHC-mini-syncytia enhance sensitivity and reliability of cochlear

109 vL1Ri in the absence of inducer did not form syncytia following brief low-pH treatment even though ex

110 The observation of few and delayed syncytia following MHV-A59 infection of hepatocytes more

111 ulated and allowed to develop feeding sites (syncytia) for 8 days.

112 did not spread to neighboring cells nor did syncytia form after low-pH treatment.

113 In the case of CHO/rRAM-1 cells, syncytia form at foci of amphotropic 4070A virus infecti

114 Syncytia form by incorporating neighboring cells into a

115 How syncytia form remains poorly understood.

116 s as measured by inhibition of HIV-1 induced syncytia formation and HIV-1 reverse transcriptase activ

117 Additionally, we find that ESI-09 disrupts syncytia formation and inhibits cell-to-cell transmissio

118 aling through this gBcyt motif regulates VZV syncytia formation and is essential for skin pathogenesi

119 fusion and viral replication as measured by syncytia formation and p24 levels, respectively.

120 onal antibodies that inhibit HTLV-1-mediated syncytia formation and recognize conformational epitopes

121 ys162Ser/gL-Cys144Ser mutations had impaired syncytia formation and reduced interference of HCMV entr

122 on human and rat HCC cells showed extensive syncytia formation and significantly enhanced cytotoxic

123 SA59 (P), significantly affected neural cell syncytia formation and viral titers postinfection in vit

124 ficiently neutralized SARS-CoV and inhibited syncytia formation between cells expressing the S protei

125 ion of a recombinant VSV capable of inducing syncytia formation between tumor cells through membrane

126 3 and CKR-2b support HIV-1 89.6 env-mediated syncytia formation but do not support fusion by any of t

127 showed that an MMP inhibitor interferes with syncytia formation elicited by mutant F proteins and con

128 ocal HCC lesions in their livers resulted in syncytia formation exclusively within the tumors, and th

129 if S-protein expression would also result in syncytia formation in endothelial cells.

130 were generated to establish their effects on syncytia formation in replication in vitro and in the hu

131 Here, we showed that syncytia formation is dependent on proteins of the recen

132 These in vitro effects of aggressive syncytia formation translated to severely impaired skin

133 cells expressing MBG or EBO GP and mediated syncytia formation triggered by MBG GP.

134 helial cells results in cell-cell fusion and syncytia formation triggered by the fusion (F) and attac

135 However, syncytia formation was much greater with coexpression of

136 ddBCNAs also inhibit wild type measles virus syncytia formation with a TCID(50) of 7.5 muM for the le

137 IgM inhibited by >90% syncytia formation with the X4-IIIB infected SupT-1 cell

138 tive in promoting cell-to-cell fusion (i.e., syncytia formation) compared with JPV.

139 mination showed evidence of cytolysis, giant syncytia formation, and apoptotic changes evidenced by o

140 e, as indicated by exit from the cell cycle, syncytia formation, and the presence of muscle myosin fi

141 /920F substitutions in VZV caused aggressive syncytia formation, reducing cell-cell spread.

142 sed a four- to eightfold increase in RD cell syncytia formation, whereas anti-CD9 and anti-CD81 antib

143 progeny virions and prevent back-fusion and syncytia formation.

144 hat Ck-17 expression localized to regions of syncytia formation.

145 and anti-CD81 antibodies markedly delayed RD syncytia formation.

146 V-infected cells into the CNS, and promoting syncytia formation.

147 ed ability to block NiV glycoprotein-induced syncytia formation.

148 esis uncoupled from cytokinesis, whereas the syncytia formed by cyst nematodes arise from coordinated

149 ve syncytia compared to the relatively small syncytia formed during native VZV infection.

150 otif in GALV results in vectors with reduced syncytia forming capabilities.

151 omatitis virus, was previously shown to lose syncytia-forming ability if six residues (GLIIGL) were d

152 ted hepatic arterial infusion of recombinant syncytia-forming VSV vector in advanced multifocal hepat

153 Nuclei in syncytia found in fungi, muscles, and tumors can behave

154 matodes induce host-plant root cells to form syncytia from which the nematodes feed.

155 on, and thus, by preventing the formation of syncytia, Gag helps to secure efficient transfer of vira

156 together to form zygotes and multinucleated syncytia has remained a fundamental question in cell and

157 Similar DC-syncytia have been identified within the mucosal surface

158 This resulted in the formation of larger syncytia, higher production of infectious particles, and

159 gest that mixed ploidy is tolerated in these syncytia; however, there may be costs associated with va

160 ablation in RPE develop pigmentary changes, syncytia, hypoplasia, age-dependent centrifugal and non-

161 xpression, and a wild-type ability to induce syncytia in an XC cell cocultivation assay.

162 and -2 and assayed for the ability to induce syncytia in BJAB cells and HeLa cells.

163 sally linked to the development of extensive syncytia in brain capillary endothelial cells (BCEC).

164 The adapted virus induces large syncytia in cells containing either wild-type or mutant

165 ransported to the cell surface and to induce syncytia in cells expressing the ecotropic receptor.

166 This protein induced extensive syncytia in cells expressing the normal virus receptor C

167 rarity of clinical isolates able to produce syncytia in culture suggests that extensive cell fusion

168 t VZV-induced cell fusion continued to cause syncytia in cultured cells infected with rOka47DeltaC or

169 Alary muscle syncytia in Drosophila larvae undergo a remarkable proce

170 Interestingly, neither RSV nor HMPV formed syncytia in HAE tissues.

171 to Calu-3 cells and, more frequently, formed syncytia in hAOs.

172 ral budding, and self-propagating ability of syncytia in HIV-infected SUP-T1 cell cultures and indivi

173 S protein can also mediate the formation of syncytia in infected cells.

174 halitis and analyzed their ability to induce syncytia in monocyte-derived macrophages (MDM) and neuro

175 ducing the formation of large multinucleated syncytia in Mus dunni cells.

176 pared gene expression profiles of developing syncytia in soybean near-isogenic lines differing at Rhg

177 characteristic cytopathic effect by forming syncytia in susceptible cells.

178 virus was impaired in its ability to induce syncytia in T-cell lines.

179 Adaptation of FIV to replicate and form syncytia in the Crandell feline kidney (CrFK) cell line

180 of multinucleated feeding structures termed syncytia in the roots of host plants.

181 s, with MIBE F-bearing viruses causing large syncytia in these cells.

182 S-CoV-2 are capable of infecting and forming syncytia in Vero/ACE2 cells which lack TMPRSS2 expressio

183 The R(+) Env protein induced syncytia in XC cells expressing a mutant mCAT1 lacking b

184 formation and maintenance of feeding sites (syncytia) in host roots, and these processes are highly

185 345 prevented the formation of typical giant syncytia induced by HIV Bal strain replication in these

186 ed mice were able to reduce the formation of syncytia induced by the envelope glycoprotein of HTLV-1,

187 ficantly suppressed the formation of XC cell syncytia induced by the R(+) Env protein but not that in

188 These results indicate that syncytia induced in the resistant line are undergoing se

189 opic variants, also designated slow/low, non-syncytia-inducer or macrophage-tropic, which dominate th

190 (+) T cells acutely infected with either non-syncytia-inducing (NSI) or syncytia-inducing (SI) HIV-1

191 hat acute infection of CD4+ T cells with non-syncytia-inducing (NSI) viruses generally increased beta

192 is transmitted by macrophage (M)-tropic/non-syncytia-inducing (NSI) viruses, which hyperactivate the

193 d with either non-syncytia-inducing (NSI) or syncytia-inducing (SI) HIV-1 isolates.

194 ent of M-tropic viruses by T cell (T)-tropic/syncytia-inducing (SI) viruses, which are known to be hi

195 nstrated that IL-2 treatment inhibited HIV-1 syncytia-inducing ability and dose-dependently decreased

196 kin 4 (IL-4) inhibits the propagation of non-syncytia-inducing and increases the propagation of syncy

197 ia-inducing and increases the propagation of syncytia-inducing HIV-1 isolates by two mechanisms.

198 lution and in the phenotypic switch from non-syncytia-inducing to syncytia-inducing, which leads to a

199 notypic switch from non-syncytia-inducing to syncytia-inducing, which leads to accelerated disease pr

200 Envelope glycoprotein gp120 of syncytia-inducing/lymphocyte tropic HIV-1 strains induce

201 Death of syncytia is associated with nuclear fusion and premature

202 the longitudinal and circular smooth muscle syncytia is necessary to provide the "mixing" type of mo

203 e potential explanation for the formation of syncytia is viral adaptation for these CD4(+) CNS cells.

204 The formation of multinucleated cells (syncytia) is a hallmark of henipaviral infections and is

205 nd used by some viruses to form pathological syncytia, is typically driven by fusogenic membrane prot

206 appear distinct, rather forming a homogenous syncytia-like arrangement as seen in the domestic dog.

207 used methods do not allow quantification of syncytia, nor do they estimate the number of cells invol

208 le germ cells develop in full synchrony as a syncytia of interconnected cells called germline cysts (

209 Spl574 produces large syncytia of multinucleated giant cells in M. dunni cells

210 Thus, the syncytia of such germaria are filled with mitochondria.

211 Defense-related genes up-regulated within syncytia of the resistant line included those predominan

212 ls and a somewhat enhanced ability to induce syncytia on CHO-C8 cells.

213 DNA had a markedly reduced ability to induce syncytia on CHO-HVEM12 cells and a somewhat enhanced abi

214 d substitution in gK, induced numerous large syncytia on HveA-expressing Chinese hamster ovary cells

215 cystamine-treated cultures lacked the giant syncytia or CPE induced by HIV-1 infection.

216 Of 11 Env variants that failed to induce syncytia or did so poorly, 7 contained changes in amino

217 APMV-7 does not form syncytia or plaques in cell culture, but its replication

218 The Ban/AF vaccine virus did not produce syncytia or plaques in cell culture, even in the presenc

219 of the HIV-1 envelope glycoproteins to form syncytia or to support virus entry.

220 The fusion of myoblasts into multinucleate syncytia plays a fundamental role in muscle function, as

221 Both lower SLP and fewer syncytia positively correlated with fecal STEC numbers.

222 ial dysfunction occurred in GALV-FMG-induced syncytia prior to loss of viability with loss of the mit

223 Dying syncytia produce significantly more syncytiosomes than n

224 When around 50 cells were fused, the syncytia rapidly disintegrated and many of the infected

225 ssays and is debilitated in the formation of syncytia relative to the wild-type F protein, the F Tail

226 In Drosophila, the formation of muscle syncytia requires the cooperative participation of two t

227 ated with apoptosis and/or the generation of syncytia resulting from the direct cell-to-cell transmis

228 es fusion of infected endothelial cells into syncytia, resulting in endothelial disruption and hemorr

229 elopmentally upregulated within giant cells, syncytia, root tips, and lateral root primordia.

230 P-T1 cell cultures and individually isolated syncytia seeded in uninfected SUP-T1 cell cultures.

231 viral proteins, and fuse into multinucleated syncytia several days later.

232 d elevated levels of HIV-1, and formed large syncytia similar to untreated cells.

233 f either causes infected cells to form large syncytia spontaneously.

234 peutic repair or cellular delivery system to syncytia such as the myocardium.

235 ny is rarely observed in naturally occurring syncytia, such as the multinucleate fungus Ashbya gossyp

236 erminal epitope tag induced the formation of syncytia, suggesting partial interference with the funct

237 F or HN does not result in the formation of syncytia, suggesting serotype-specific protein differenc

238 Viruses that infect T-cell lines to form syncytia (syncytium-inducing, SI) are frequently found i

239 The mutant virus also formed larger syncytia than the wild-type virus, linking CKII-mediated

240 the passaged, pathogenic SHIVs induced more syncytia than those of the respective parental SHIV.

241 Cell fusions produce multinucleate syncytia that are crucial to the structure of essential

242 resulting in the formation of multinucleated syncytia that eventually became nonviable.

243 at low density, the BMP4-treated cells form syncytia that express chorionic gonadotrophin (CG).

244 resulted in the formation of multinucleated syncytia that reached a maximum 5 days after transfectio

245 d PLC-sensitive PI(4,5)P(2) pool in the cell syncytia that supports auditory hair cells; (ii) spatial

246 them to fuse with neighboring cells to form syncytia that ultimately die.

247 o target cells and for the cell-cell fusion (syncytia) that results from many paramyxoviral infection

248 ted at a low multiplicity were fused to form syncytia, thereby allowing capsids released from infecte

249 bset of infected cells formed multinucleated syncytia through HIV envelope-dependent cell fusion.

250 rus entry and fusion as well as formation of syncytia through interaction with the EFC.

251 uch as bone, muscle, and placenta, fuse into syncytia to acquire new functions and transcriptional pr

252 Both giant cells and syncytia undergo extensive cell wall architectural modif

253 ix soybean GeneChip directly compared Peking syncytia undergoing a resistant reaction to those underg

254 nematode-induced feeding structures known as syncytia undergoing an incompatible interaction with the

255 ously by RNA-seq experiments as expressed in syncytia undergoing an incompatible reaction.

256 The cytological features of syncytia undergoing susceptible or resistant reactions a

257 NSF attachment protein gene specifically in syncytia undergoing their defense responses.

258 cal herpetic lesions typically contain large syncytia, underscoring the importance of cell-to-cell fu

259 erved that BDV-infected cells form extensive syncytia upon low-pH treatment.

260 ng CD4 and CCR5 formed multinucleated cells (syncytia) upon exposure to BaL, a macrophagetropic strai

261 ssed by counting multinucleated giant cells (syncytia) visualized by light microscopy.

262 tion of cyst nematode EGases into developing syncytia was not detected.

263 Formation of syncytia was observed in tumors treated with retargeted

264 Syncytia were detected by DNA staining with propidium io

265 SLP was lower (P < 0.05) and syncytia were fewer (P < 0.05) in STEC-treated sheep tha

266 ould not be recovered, even though transient syncytia were formed in transfected cells.

267 Regions of metaxylem vessels near syncytia were found to have deviated from classical deve

268 Instead, the S100+ infected syncytia were localized to the surface of tonsil invagin

269 Syncytia were markedly absent, and little or no viral an

270 Differences in the ability to induce syncytia were not due to differences in the levels of to

271 No increase in Ck-17 mRNA expression and no syncytia were observed in RSV-infected cells grown in th

272 After 24 h, syncytia were observed, and cell culture supernatants fr

273 e muscle MAP4 isotype, but the multinucleate syncytia were short and apolar, microtubules were disorg

274 The syncytia were smaller, and they were present in lower nu

275 ines that express the target receptor; these syncytia were substantially larger than the plaques form

276 The syncytia were viable for a period of 2 days and then rap

277 mutant in transfected cells was evident when syncytia were visualized and counted, it was not detecte

278 bridges, which characterize the formation of syncytia, were never observed.

279 their ability to form large, multinucleated syncytia when cocultured with the rat XC cell line.

280 1, respectively, and they then form abundant syncytia when exposed to these viruses.

281 led to the formation of multinucleated cell syncytia when expressed in the absence of other viral pr

282 xpressing F, G, TM, or F plus G did not form syncytia whereas cells expressing F plus TM formed some

283 factor genes were upregulated in developing syncytia, whereas in non-infected plants, these two prom

284 ical constraints govern the integrity of the syncytia which are formed upon extensive cell fusion.

285 of HEp-2 cells, the SH-minus virus produced syncytia which were at least equivalent in size to those

286 lls by fusing them into large multinucleated syncytia, which die by sequestration of cell nuclei and

287 ed (1) the formation of giant multinucleated syncytia, which eventually underwent necrotic lysis, and

288 s expressing the modified Env failed to form syncytia with CD4(+) permissive cells.

289 aging cell line, psi 422, psi 422 cells form syncytia with CD4-positive cells, correctly express HIV-

290 with CD4 enables nonpermissive cells to form syncytia with cells expressing M-tropic, but not T-tropi

291 ncy virus-1 receptors, formed multinucleated syncytia with cells expressing S protein.

292 or the chimeric HIV envelope protein formed syncytia with cells expressing the CD4 receptor for HIV.

293 e show that intact rotavirus and VLPs induce syncytia with cells that are permissive to rotavirus inf

294 Moreover, gB(275Y) caused the formation of syncytia with numerous centrosomes, suggesting that cell

295 contrast, arginine substitutions resulted in syncytia with only 2-fold more nuclei, a -0.5-log10 redu

296 Cells expressing the 89.6 env protein form syncytia with QT6 cells expressing CD4 and either Fusin

297 to correlate the ability of HTLV-2 to induce syncytia with the ability to replicate in BJAB cells.

298 ed to enhanced fusion and formation of giant syncytia with uninfected cells.

299 Ecotropic murine leukemia virus forms large syncytia with XC cells, whereas no syncytia are reported

300 ding domain, formed the large multinucleated syncytia with XC cells.