ライフサイエンスコーパス: MDCK cell

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

2 etyllactosamine, was depleted from polarized MDCK cells.

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

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

5 cal determinant of replication efficiency in MDCK cells.

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

7 g spindle orientation during cystogenesis of MDCK cells.

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

9 the two most abundant galectins expressed in MDCK cells.

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

11 an the specific production from the parental MDCK cells.

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

13 table oligomeric complexes in the context of MDCK cells.

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

15 he apical membrane localization in polarized MDCK cells.

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

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

18 osynthetic trafficking pathways in polarized MDCK cells.

19 5-GFP in polarized, but not in subconfluent, MDCK cells.

20 tive apical recycling endosomes of polarized MDCK cells.

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

22 t junction assembly and cell polarization in MDCK cells.

23 of cells to swainsonine inhibits motility of MDCK cells.

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

25 ormation of a tight monolayer from dispersed MDCK cells.

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

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

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

29 ) and nonpermeabilized transfected COS-1 and MDCK cells.

30 A1 abundance in the apical membrane in UT-A1-MDCK cells.

31 n LLC-PK1 cells, but only 40% was present in MDCK cells.

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

33 olocalize extensively with ARNO in migrating MDCK cells.

34 femtomolar concentrations (fM-GAi) in canine MDCK cells.

35 ctivity on polarized biosynthetic traffic in MDCK cells.

36 transcytosis via the basolateral membrane in MDCK cells.

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

38 i and TGN markers in transiently transfected MDCK cells.

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

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

41 ied by heterologous expression in mIMCD3 and MDCK cells.

42 ificant decrease in intracellular calcium in MDCK cells.

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

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

45 AIs oseltamivir carboxylate and zanamivir in MDCK cells.

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

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

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

49 ressure over multiple sequential passages in MDCK cells.

50 zed at the basolateral membrane of polarized MDCK cells.

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

52 chimeric constructs in Rat1 fibroblasts and MDCK cells.

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

54 ogenesis utilizes 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 sheets of motile Madin-Darby canine kidney (MDCK) cells.

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

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

60 Golgi complex in Madin-Darby canine kidney (MDCK) cells.

61 ned morphology in Madin-Darby canine kidney (MDCK) cells.

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

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

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

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

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

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

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

69 ough polarized epithelial cell monolayers of MDCK cells after administration of AR, but not transform

70 The HGF/SF-mediated protection of DU-145 and MDCK cells against ADR (demonstrated using MTT (3-(4,5-d

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

72 MDCK cells also synthesized laminin alpha5, a component

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

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

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

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

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

78 the virus susceptibility to NA inhibitors in MDCK cells and demonstrated that the glycan attached at

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

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

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

82 ced virus that could form plaques on regular MDCK cells and had only moderately decreased replication

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

84 ted for their impact on virus replication in MDCK cells and in embryonated chicken eggs.

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

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

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

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

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

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

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

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

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

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

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 lin mutants inhibit G1/S phase transition of MDCK cells, and depletion of cingulin by regulated RNA i

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

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

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

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

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

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

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 reduced growth and failed to form plaques in MDCK cells but formed wild-type-like plaques in an MDCK

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

148 In MDCK cells, exogenous expression of phosphorylation-defe

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

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

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

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

153 In MDCK cells expressing the pseudophosphorylated FIP2 muta

154 Madin-Darby canine kidney (MDCK) cells expressing enhanced green fluorescent protei

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

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

157 ed (ACR) lipid domain fraction isolated from MDCK cells for the first time revealed unique structural

158 MDCK cells form monoclonal cysts in three-dimensional co

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

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

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

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

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

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

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

166 MDCK cells grown in the presence of a phosphatidylinosit

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

184 shown that expression of the ARF-GEF ARNO in MDCK cells induces robust activation of Rac, the formati

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

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

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

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

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

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

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

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

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

194 Primary cilia of MDCK cells lack interdoublet dynein motors.

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

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

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

198 ells but formed wild-type-like plaques in an MDCK cell line expressing wild-type HA.

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

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

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

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

203 ations of these mutations, we created stable MDCK cell lines expressing these constructs.

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

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

206 We created stable Madin-Darby canine kidney (MDCK) cell lines expressing enhanced green fluorescent p

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

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

209 ha(1) subunit to the basolateral membrane in MDCK cells may determine the differential distribution o

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

211 0 CFTR inhibitor analogs were screened in an MDCK cell model, and near-complete suppression of cyst g

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

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

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

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

216 increase in the paracellular permeability of MDCK cell monolayers.

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

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

219 gene segments following several passages in MDCK cells or embryonated chicken eggs.

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

221 combinant strain in embryonated hen eggs, in MDCK cells, or in vivo in a mouse model.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

238 gly inhibit uPA activity but they also block MDCK cell scattering and in vitro invasion of human glio

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

240 In MDCK cells (showing cation selectivity), claudins 2, 4,

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

242 f structurally diverse organic cations using MDCK cells stably expressing human PMAT.

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

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

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

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

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

248 MDCK cells synthesize LN5 only when subconfluent, and th

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

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

251 rease apical membrane expression of UT-A1 in MDCK cells that were stably transfected with UT-A1 (UT-A

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

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

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

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

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

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

258 ndin dehydrogenase are expressed in the same MDCK cell, they must be compartmentalized because even i

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

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

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

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

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

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

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

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

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

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

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

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

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

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

273 trisphosphate [PtdIns(3,4,5)P3] to polarized MDCK cells was sufficient to increase PAK internalizatio

274 at were stably transfected with UT-A1 (UT-A1-MDCK cells) was tested.

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

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

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

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

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

280 MDCK cells were found suitable for the virus production

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

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

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

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

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

286 nce of junctions, Madin-Darby canine kidney (MDCK) cells were depleted of E-cadherin by RNA interfere

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

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

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

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

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

292 Incubation of surface-attached MDCK cells with an antibody against the extracellular do

293 helial cells, whereas treatment of confluent MDCK cells with an Rac1 inhibitor decreased Mirk activit

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

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

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

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

298 ributes into an intracellular compartment in MDCK cells without any change in primary cilia localizat

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