ライフサイエンスコーパス: MDCK cell

1 M5081/2012 (H1N1), were passaged in eggs and MDCK cells.

2 ressure over multiple sequential passages in MDCK cells.

3 zed at the basolateral membrane of polarized MDCK cells.

4 ere found to have a higher endosomal pH than MDCK cells.

5 chimeric constructs in Rat1 fibroblasts and MDCK cells.

6 A labeled by PSP can be directly observed in MDCK cells.

7 etyllactosamine, was depleted from polarized MDCK cells.

8 rmed by a site-directed mutagenesis study in MDCK cells.

9 ding and the lumen polarity defects in Par1b MDCK cells.

10 cal determinant of replication efficiency in MDCK cells.

11 lectin chaperone, calnexin, were studied in MDCK cells.

12 g spindle orientation during cystogenesis of MDCK cells.

13 rs of the galectin (Gal) family expressed in MDCK cells.

14 the two most abundant galectins expressed in MDCK cells.

15 an the specific production from the parental MDCK cells.

16 table oligomeric complexes in the context of MDCK cells.

17 basal levels of canine Mrp2/Abcc2 protein in MDCK cells.

18 he apical membrane localization in polarized MDCK cells.

19 ect the basal levels of canine Mrp2/Abcc2 in MDCK cells.

20 pical marker, p75-GFP, after polarization of MDCK cells.

21 osynthetic trafficking pathways in polarized MDCK cells.

22 5-GFP in polarized, but not in subconfluent, MDCK cells.

23 tive apical recycling endosomes of polarized MDCK cells.

24 t junction assembly and cell polarization in MDCK cells.

25 of cells to swainsonine inhibits motility of MDCK cells.

26 lar to those of the parental virus (rWSN) in MDCK cells.

27 ormation of a tight monolayer from dispersed MDCK cells.

28 ompartment that is distinct from the VACs of MDCK cells.

29 secretion and a reversal of its polarity in MDCK cells.

30 D and in the apical plasma membrane of UT-A1-MDCK cells.

31 ifferentially regulate cell-cell adhesion in MDCK cells.

32 , inhibit influenza A virus proliferation in MDCK cells.

33 at the expense of lateral membrane height in MDCK cells.

34 H1N1) and A/Scotland/20/74 (H3N2) virions in MDCK cells.

35 ied by heterologous expression in mIMCD3 and MDCK cells.

36 AIs oseltamivir carboxylate and zanamivir in MDCK cells.

37 e tip of the cilia in transfected mIMCD3 and MDCK cells.

38 th key developmental and renal functions, in MDCK cells.

39 e of 2.1 muM against H1N1 influenza virus in MDCK cells.

40 the first numerical model of this network in MDCK cells.

41 ed expression from cotransfected plasmids in MDCK cells.

42 ell spread area and aspect ratio in pairs of MDCK cells.

43 pment and promoted branching in matrix-grown MDCK cells.

44 bited similar degrees of long-term growth in MDCK cells.

45 ificant decrease in intracellular calcium in MDCK cells.

46 were identified by viral passage in eggs and MDCK cells.

47 phatase 2A (PP2A) expression and activity in MDCK cells.

48 hoA activation, and restricted core level in MDCK cells.

49 ions of polarized Madin-Darby canine kidney (MDCK) cells.

50 ase) viral RNA in Madin-Darby canine kidney (MDCK) cells.

51 rface proteins in Madin-Darby canine kidney (MDCK) cells.

52 ring infection of Madin-Darby canine kidney (MDCK) cells.

53 ogenesis utilizes Madin-Darby canine kidney (MDCK) cells.

54 ated (EXOC5CTS-m) Madin-Darby canine kidney (MDCK) cells.

55 face of polarized Madin-Darby canine kidney (MDCK) cells.

56 l polarization of Madin-Darby canine kidney (MDCK) cells.

57 rane of polarized Madin-Darby canine kidney (MDCK) cells.

58 ain of ECV304 and Madin-Darby canine kidney (MDCK) cells.

59 sheets of motile Madin-Darby canine kidney (MDCK) cells.

60 tion in polarized Madin-Darby canine kidney (MDCK) cells.

61 large plaques in Madin-Darby canine kidney (MDCK) cells.

62 ses GPC in renal [Madin-Darby canine kidney (MDCK)] cells.

63 Strikingly, recently confluent MDCK cells (1-3 d) displayed AP1B-dependence in the bios

64 Using the MDCK cell 3D-tubulogenesis assay, activated G alpha 12 i

65 RP5 were found to colocalize in RPE, CE, and MDCK cells, a general model of polarized epithelia.

66 ally associated with the common endosomes of MDCK cells, accessible to endocytic probes internalized

67 However, MDCK cells also express relatively high levels of cadher

68 MDCK cells also synthesized laminin alpha5, a component

69 hway was important for Env transformation in MDCK cells, although the mechanisms of action differed i

70 We show that in Madin-Darby canine kidney (MDCK) cells, an apical ceramide-enriched compartment (AC

71 rmation assays in Madin-Darby canine kidney (MDCK) cells, an underlying mechanism that leads to the i

72 long the apical and basolateral membranes in MDCK cells and binds the cell polarity protein Par6 in a

73 competitive infection experiments in ST6GalI-MDCK cells and C57/BL6 mice.

74 expression decreased surface EAAT2b in both MDCK cells and cultured astrocytes, suggesting that the

75 virus replication and protein yield in both MDCK cells and eggs by introducing a single substitution

76 ound to be critical for virus replication in MDCK cells and eggs.

77 nsible for the improved growth properties in MDCK cells and eggs.

78 truncation of PA-X increased virus yields in MDCK cells and enhanced viral replication, pathogenicity

79 ymerase PA segment, grew to higher titers in MDCK cells and ferret tissues and caused more-severe dis

80 replicate as well as wild-type (WT) virus in MDCK cells and in embryonated chicken eggs but is highly

81 hoA-GEF required for Shroom3-dependent AC in MDCK cells and in the lens pit.

82 al to the mechanisms identified in QLalpha12-MDCK cells and included loss of Bcl-2, JNK activation, a

83 epsilon-toxin cytotoxicity towards cultured MDCK cells and inhibited the ability of the toxin to for

84 ining the head domain target to junctions in MDCK cells and Rat1 fibroblasts.

85 creased growth of both H3N8 and H3N2 CIVs in MDCK cells and suppressed expression from cotransfected

86 ses derived from plasmids were propagated in MDCK cells and then passaged in mice up to four times.

87 confirm this pathway in Galpha(12)-silenced MDCK cells and utilize MDCK cell lines harboring either

88 ssing the HA and NA of CA09 were passaged in MDCK cells and variants exhibiting large-plaque morpholo

89 viruses, however, showed growth kinetics in MDCK cells and virulence in mice similar to those of wil

90 multistep growth analyses on wild-type (wt) MDCK cells and were able to form plaques only on MDCK ce

91 d in vitro bound strongly to FcRn-expressing MDCK cells and were transcytosed in an FcRn-dependent ma

92 ins in epithelial Madin Darby canine kidney (MDCK) cells and by expression of mutated and chimeric co

93 way of megalin in Madin-Darby canine kidney (MDCK) cells and found that it is a long-lived, fast recy

94 large plaques in Madin-Darby canine kidney (MDCK) cells and grew robustly in vitro and in ovo They h

95 in kidney-derived Madin-Darby canine kidney (MDCK) cells and identified the rho-guanosine triphosphat

96 ene expression in Madin-Darby canine kidney (MDCK) cells and in LLC-PK1 cells using small interfering

97 ned the effect of serial adaptation in eggs, MDCK cells, and guinea pigs.

98 gated the polarity of uptake of taurine into MDCK cells, and our results confirmed that uptake in sit

99 to a higher titer, produced large plaques on MDCK cells, and retained NA activity.

100 ulated during influenza A virus infection in MDCK cells, and the knockout of Bak in mouse embryonic f

101 onstruct inhibits tight junction assembly in MDCK cells, and this defect in tight junction assembly c

102 rowth kinetics in Madin-Darby canine kidney (MDCK) cells, and 5 passages in MDCK cells revealed no re

103 failed to grow in Madin-Darby canine kidney (MDCK) cells, and resulted in fewer dominating mutations

104 In MDCK cells, approximately 60% of AQP1 diffused freely, w

105 MDCK cells are currently being considered as an alternat

106 Madin Darby canine kidney (MDCK) cells are a well characterized epithelial cell lin

107 , although less abundant ceramide species in MDCK cells, are highly enriched in ceramide and Rab11a v

108 ays using defined animal antiserum confirmed MDCK cells as the preferred cell substrate for influenza

109 mutation demonstrated replication defects in MDCK cells as well as in primary differentiated airway e

110 ABCC2 protein in MRP2/ABCC2 gene-transfected MDCK cells as well as the basal levels of canine Mrp2/Ab

111 land of confluent Madin-Darby canine kidney (MDCK) cells as a model system to quantify the collective

112 long-term flow of Madin-Darby canine kidney (MDCK) cells as they moved through microchannels.

113 in both biosynthetic and recycling routes of MDCK cells, as a result of its predominant functional lo

114 18 lacked detectable cytotoxic activity in a MDCK cell assay.

115 ed efficiently in Madin-Darby canine kidney (MDCK) cells at 39 degrees C, but the replication of WSN(

116 3) is arrested in Madin-Darby canine kidney (MDCK) cells at a step subsequent to inclusion developmen

117 to the complete growth of type B viruses in MDCK cells before day three post-infection, resulting in

118 expansion of a radially symmetric colony of MDCK cells, both in the edge migration velocity and in c

119 zed to the basolateral membrane of polarized MDCK cells, but AE1-M909T localized to both the apical a

120 In vitro, X31-sciIV can infect MDCK cells, but infectious virions are not produced unle

121 causes missorting of basolateral proteins in MDCK cells, but only after knockdown of AP-1B, suggestin

122 by signaling from activated Rac1 to MKK3 in MDCK cells, but the mechanism of activation of Mirk in p

123 ripts for Gal-2 and -12 were not detected in MDCK cells, but we found transcript levels for Gal-3 > G

124 mpounds had moderate to high permeability in MDCK cells, but were rapidly metabolized in rodents and

125 anes of polarized Madin-Darby canine kidney (MDCK) cells, but enzyme activity was severely diminished

126 rowth kinetics in Madin-Darby canine kidney (MDCK) cells, but pH1N1low-1 is significantly inhibited b

127 mbranes isolated from L-cell fibroblasts and MDCK cells by detergent-free affinity chromatography and

128 face of polarized Madin-Darby canine kidney (MDCK) cells by transit through apical recycling endosome

129 ruses were not attenuated for replication in MDCK cells, Calu-3 cells, or in primary differentiated m

130 We found that although passage in eggs and MDCK cells can lead to a loss of filaments, an exclusive

131 to deform the pillars, rounding epithelial (MDCK) cells can create space to divide.

132 Furthermore, in MDCK cells co-expressing alpha(1), beta(1), and beta(2)

133 PDZ protein prominent in both astrocytes and MDCK cells, colocalized and coimmunoprecipitated with EA

134 ominantly in TfR-rich endosomal fractions in MDCK cells confluent for 1 and 4 d.

135 rtex in HepG2 cells and Par1b-overexpressing MDCK cells correlated with a single or no LGN-NuMA cresc

136 In cultured MDCK cells, CRB2S associates with apical membranes and d

137 n 2-D culture, and delays but does not block MDCK cell cyst formation and tubulogenesis in 3-D cultur

138 tly than control MDCK cell cysts, EXOC5CTS-m MDCK cell cysts form significantly fewer tubules than co

139 (S227A) elicits a loss in lumen formation in MDCK cell cysts grown in Matrigel, the putative pseudoph

140 s form tubules more efficiently than control MDCK cell cysts, EXOC5CTS-m MDCK cell cysts form signifi

141 nication, we used Madin-Darby canine kidney (MDCK) cell cysts grown in 3D gels of extracellular matri

142 nhibition of N-glycosylation or infection of MDCK cells defective in N-glycosylation resulted in decr

143 A similar effect on the TJ was observed in MDCK cells depleted for either Scribble or Dlg1 by small

144 iogenesis of epithelial lateral membranes in MDCK cells depleted of endogenous AnkG.

145 In contrast, PC1-silenced MDCK cells displayed enhanced thrombin-induced apoptosis

146 Mu1B-knocked down MDCK cells displayed loss of polarity of several endogen

147 clathrin adaptor AP-1 by RNA interference in MDCK cells disrupted apical localization of megalin, cau

148 pression during the formation of polarity in MDCK cells, disrupts polarization of the cell, explainin

149 essed in Huh7 and Madin-Darby canine kidney (MDCK) cells, disrupts apicobasal polarity.

150 However, ciliogenesis-impaired MDCK cells do not undergo continual junction remodeling,

151 ared with control Madin-Darby canine kidney (MDCK) cells, EXOC5 overexpression increases and KD decre

152 In MDCK cells, exogenous expression of phosphorylation-defe

153 ce appearance of newly transfected confluent MDCK cells expressing FLAG-M2-GFP demonstrate that the M

154 uantitative confocal microscopy of polarized MDCK cells expressing GFP chimeras of wild-type and muta

155 Exosomes isolated from MDCK cells expressing individual full-length EGFR ligand

156 The cilia in mIMCD3 and MDCK cells expressing mutant IFT43 were found to be sign

157 In MDCK cells expressing the pseudophosphorylated FIP2 muta

158 ateral surface of Madin-Darby canine kidney (MDCK) cells expressing myristoylation-deficient (G2A) Na

159 ntrol cysts, whereas Exoc5-KD and EXOC5CTS-m MDCK cells failed to form mature cysts.

160 of Y398D/Y402D mutant of occludin sensitized MDCK cells for hydrogen peroxide-induced barrier disrupt

161 MDCK cells form monoclonal cysts in three-dimensional co

162 Here, we demonstrate that MDCK cells form solitary lumina during their first cell

163 Kidney-derived Madin Darby canine kidney (MDCK) cells form lumina at their apices, and target lumi

164 Cholesterol depletion in MDCK cells greatly restricted AQP1 diffusion, consistent

165 uential control of these two phases, we used MDCK cells grown as cysts and treated with hepatocyte gr

166 tdIns(3,4,5)P3 to the basolateral surface of MDCK cells grown as cysts caused basolateral protrusions

167 Using MDCK cells grown as three-dimensional cysts as a model f

168 shes membrane association of 190-kDa AnkG in MDCK cells grown in low calcium.

169 MDCK cells grown in the presence of a phosphatidylinosit

170 HGF treatment of Madin-Darby canine kidney (MDCK) cells grown as cysts in three-dimensional culture

171 lasma membrane in Madin-Darby canine kidney (MDCK) cells grown in low calcium, although these cells l

172 ations of HGF, in Madin-Darby canine kidney (MDCK) cells, grown as cysts in 3D collagen cell culture.

173 Wild-type and knockdown MDCK cells had differing physiological and morphological

174 acingulin constructs in Rat1 fibroblasts and MDCK cells identifies specific sequences within the head

175 nating mutations during viral passaging than MDCK cells.IMPORTANCE Robust in vitro culture systems fo

176 However, in an MDCK cell in vitro model for enterotoxemic effects, supe

177 ransformation in both normal and transformed MDCK cells in 3-D culture.

178 reased pSer(829) basolateral localization in MDCK cells in a time dependent manner and was essential

179 titers in the mouse respiratory tract versus MDCK cells in culture showed that the mutants displayed

180 ay an important role in virus replication in MDCK cells in culture.

181 cessfully isolated in eggs and propagated in MDCK cells in the presence of N-tosyl-l-phenylalanine ch

182 nt of polarity in Madin-Darby canine kidney (MDCK) cells in part through phosphorylation of serine 22

183 ferret antisera for many viruses isolated in MDCK cells, including homologous reference viruses.

184 virus strains in Madin-Darby canine kidney (MDCK) cells, including H3N2 and H1N1 seasonal and 2009 p

185 d to the lower lateral membrane of polarized MDCK cells independent of mu1B adaptin.

186 hat Par1b promotes lateral lumen polarity in MDCK cells independently of Ca(2+)-mediated cell-cell ad

187 MDCK cells to VACs characteristic of control MDCK cells, indicating a novel link between E-cadherin a

188 zonula occludens 1 (ZO-1) family proteins in MDCK cells induces a highly organized contractile actomy

189 ree-dimensional real time PCR, as well as in MDCK cells inducible for the MAPK gene Raf.

190 the expression of multiple viral proteins in MDCK cells infected at a low multiplicity with IAV, we o

191 f generating RT-qPCR-ready cell lysates from MDCK cells infected with influenza virus.

192 Induction of PC1 in MDCK cells inhibited NHA2 expression with concordant inh

193 cantly (P < 0.0001) during serial passage in MDCK cells inoculated with seasonal influenza A (H1N1) v

194 cantly, we show that expression of LM-332 in MDCK cells is an autocrine response to endogenous TGF-be

195 dicate that particle assembly in T3-infected MDCK cells is defective, possibly due to a temperature-s

196 this, overexpression of mammalian IFT52C in MDCK cells is dominant-negative and causes IFT protein m

197 itro, but CRMP-1-dependent actin assembly in MDCK cells is EVL specific.

198 virus strains show that reovirus tropism for MDCK cells is primarily regulated by replication protein

199 Primary cilia of MDCK cells lack interdoublet dynein motors.

200 ively localize to Madin-Darby canine kidney (MDCK) cell lateral membranes.

201 OTL2 in polarized Madin-Darby canine kidney (MDCK) cells leads to YAP activation, as indicated by dec

202 Galpha(13) subunit, and thrombin-stimulated MDCK cells led to increased interaction of Galpha(12) wi

203 V2 receptor agonist (determined by measuring MDCK cell line cAMP accumulation), producing 57% of AVP'

204 The MDCK cell line in which half of the endogenous beta(1) s

205 orm of NS1 in the interferon (IFN)-competent MDCK cell line.

206 l cultures of the mammalian renal epithelial MDCK cell line.

207 influenza virus A/Puerto Rico/8/34 (H1N1) in MDCK cell line.

208 ratio not only in Caco-2 but also in the MDR-MDCK cell line.

209 The Madin Darby canine kidney (MDCK) cell line has been a popular mammalian model to in

210 developed hCK, a Madin-Darby canine kidney (MDCK) cell line that expresses high levels of human infl

211 n Galpha(12)-silenced MDCK cells and utilize MDCK cell lines harboring either overexpressed or silenc

212 was applied for analysis of three different MDCK cell lines used for influenza propagation and where

213 substitution mutants of hCTR1 in HEK293 and MDCK cells localized the site of O-linked glycosylation

214 des on the plasma membrane and, in polarized MDCK cells, localizes to the apical domain.

215 AP1B knock down MDCK cells missorted CAR from recycling endosomes to the

216 Using the MDCK cell model of cystogenesis, it was found that NHA2

217 0 CFTR inhibitor analogs were screened in an MDCK cell model, and near-complete suppression of cyst g

218 Here we overexpressed SGLT1 in MDCK cell monolayers and reconstituted the purified tran

219 and substantially lower permeability across MDCK cell monolayers than mefloquine.

220 mbly and/or maintenance of TJs in Caco-2 and MDCK cell monolayers.

221 nd dose dependence of uptake of taurine into MDCK cell monolayers.

222 increase in the paracellular permeability of MDCK cell monolayers.

223 Relative to MDCK cells, Mv1 Lu reported higher titers and the remain

224 After a single high-multiplicity passage in MDCK cells of an egg-derived stock that lacked detectabl

225 g (OE), Exoc5-knockdown (KD), and EXOC5CTS-m MDCK cells on Transwell filters, we found that primary c

226 n the alpha(1)-beta(1) complex isolated from MDCK cells or the alpha(2)-beta(2) complex isolated from

227 ntroduced here showed that mu1B-knocked down MDCK cells plated on filters at confluency and cultured

228 h in two in vitro cyst models-principal-like MDCK cells (plMDCKs) within a collagen matrix and cultur

229 ynamic role of Rab11-FIP2 phosphorylation on MDCK cell polarity.

230 and B strains, in Madin-Darby canine kidney (MDCK) cells, primary epithelial cells derived from human

231 tate from tilted to parallel positions while MDCK cells progress from prometaphase to metaphase.

232 ntrast, downregulation of DeltaNp63 inhibits MDCK cell proliferation and migration in 2-D culture, an

233 eral sorting adaptor in adenovirus-resistant MDCK cells promoted apical localization of CAR and incre

234 ta(1) or beta(2) subunits expressed in renal MDCK cells replace endogenous beta(1) subunits in the al

235 ontrast, apical surface formation in control MDCK cells required Ca(2+)-dependent cell-cell adhesion,

236 ase at the plasma membrane of kidney-derived MDCK cells, resulting in a virtual Na(+) efflux pump.

237 ttachment to collagen-I, G alpha 12-silenced MDCK cells revealed a more adherent phenotype.

238 ng to immunopurified human MUC1 expressed in MDCK cells revealed a preference for binding GST-Gal-3 a

239 ly isolated caveolae from rotavirus-infected MDCK cells revealed full-length, high-mannose glycosylat

240 anine kidney (MDCK) cells, and 5 passages in MDCK cells revealed no reversion of the I221L substituti

241 EXOC5 control, KD, and EXOC5-overexpressing MDCK cells revealed significant alterations in protein c

242 p fold whose mutation abrogated induction of MDCK cell scatter.

243 ired to stimulate Madin-Darby canine kidney (MDCK) cell scatter.

244 Time-lapse imaging of EB1-GFP in polarized MDCK cells showed microtubule plus ends growing toward t

245 We show that MDCK cells silenced for the polarity gene scribble (scri

246 We purified cellular membranes isolated from MDCK cells stably expressing rat Pannexin1 or Pannexin2

247 cells and were able to form plaques only on MDCK cells stably expressing wt M2 protein.

248 Madin-Darby canine kidney (MDCK) cells stably transfected with human FcRn were used

249 ic-type intracellular luminal compartment in MDCK cells, suggesting a role for Par1b in the branching

250 imilar role was found for mammalian Rab10 in MDCK cells, suggesting that a conserved mechanism regula

251 MDCK cells synthesize LN5 only when subconfluent, and th

252 We generated MDCK cells that constitutively express epitope-tagged F2

253 Similarly, when PIV-5 was grown in MDCK cells that stably expressed dominant negative Cav-1

254 ion, we generated Madin-Darby canine kidney (MDCK) cells that stably express EGFP-EAAT2a or EGFP-EAAT

255 In MDCK cells, the basolateral potassium channel Kv7.1 requ

256 ilon-toxin and mutant proteins were added to MDCK cells, the I51C/A114C and V56C/F118C mutant protein

257 MDCK cells, the most widely used cell line for influenza

258 Unlike the parental MDCK cells, the siat7e-expressing cells were capable of

259 is hypothesis, in Madin-Darby canine kidney (MDCK) cells, the Na,K-ATPase alpha(1) and beta(1) subuni

260 idney epithelial (Madin-Darby canine kidney [MDCK]) cells, the Par1 isoform Par1b/MARK2/EMK1 promotes

261 Megalin enters polarized MDCK cells through segregated apical sorting endosomes a

262 ased apoptosis in Madin-Darby canine kidney (MDCK) cells through Galpha(12) stimulation of JNK and de

263 nt of polarity in Madin-Darby canine kidney (MDCK) cells through phosphorylation of Ser-227 by MARK2.

264 optosis and influenza A virus replication in MDCK cells, thus suggesting a role for Bcl-2 family memb

265 oprecipitation experiments in NCC-expressing MDCK cells to explore protein interactions.

266 especially TAp63, but not p53, decapacitates MDCK cells to form a cyst structure through enhanced epi

267 zed delivery of MUC1 mutants and chimeras in MDCK cells to identify the apical targeting signal.

268 restore susceptibility of sialidase-treated MDCK cells to infection by both recent (A/Victoria/361/1

269 Mechanistic analyses using in vitro MDCK cells to mimic outer bud cell behavior establish th

270 Using three-dimensional cultures of MDCK cells to model cystogenesis in vitro, we showed tha

271 was taken to adapt the H5N1 VN04 ca virus in MDCK cells to select HA variants with larger plaque morp

272 e intracellular luminal compartment in Par1b-MDCK cells to VACs characteristic of control MDCK cells,

273 or (TFR) in endocytic membranes of polarized MDCK cells upon internalization of donor- and acceptor-l

274 in localization were observed in T3-infected MDCK cells using confocal microscopy, TEM revealed marke

275 We depleted ZO-1 in MDCK cells using siRNA methods and observed specific def

276 receptor achieves its apical localization in MDCK cells via transcytosis.

277 Using short-term 3-dimensional culture of MDCK cells, we find that the small GTPase Rab14 is requi

278 ffer in productively and abortively infected MDCK cells, we used confocal immunofluorescence and thin

279 g to replicate in Madin-Darby canine kidney (MDCK) cells, we found that replication efficiency is reg

280 Mutant proteins stably expressed in MDCK cells were analyzed by confocal microscopy and Tran

281 Anchorage-dependent MDCK cells were converted to anchorage-independent cells

282 MDCK cells were found suitable for the virus production

283 MDCK cells were inoculated with tissue lysates, enabling

284 results indicated that JSRV Env-transformed MDCK cells were larger and had full or multiple lumens,

285 Furthermore, G alpha 12-silenced MDCK cells were resistant to thrombin-stimulated cyst de

286 PC1-overexpressing MDCK cells were resistant to thrombin/Galpha(12)-stimula

287 tralization at one day post-infection showed MDCK cells were similar (<1 log(2) lower) or superior (>

288 In contrast, the data obtained with MDCK cells were the least predictive of restricted viral

289 Madin-Darby canine kidney (MDCK) cells were engineered to constitutively produce an

290 n human HT-29 cells that, in contrast to the MDCK cells, were responsive to the internalin domain alo

291 production and reduced virus replication in MDCK cells when expressed in a recombinant virus in whic

292 RNA was detected 2 to 4 h postinoculation of MDCK cells, whereas synthesis of cold-adapted IAV +RNA w

293 In MDCK cells, which produce E-cadherin, a variant lacking

294 ng, wound healing and transwell migration of MDCK cells, while an inactive CA IX variant lacking the

295 rate that G alpha 12 inhibits interaction of MDCK cells with collagen-I, the major ligand for alpha2

296 xin receptors on the apical cell membrane of MDCK cells with Eu-doped oxide nanoparticles coupled to

297 Infection of polarized MDCK cells with the ESEV virus additionally results in f

298 Madin-Darby canine kidney (MDCK) cells with inducible Galpha12 (Galpha12-MDCK) and

299 In MDCK cells, Yap1 was sequestered to cell-cell junctions

300 toplasmic tail in Madin-Darby canine kidney (MDCK) cells yielded a mutant with infectivities somewhat