ライフサイエンスコーパス: Caco-2 cell

1 FPN-mediated cellular iron efflux (HepG2 and Caco-2 cells).

2 d in response to inflammation and hypoxia in Caco-2 cells.

3 produce CS23 yet was capable of adhering to Caco-2 cells.

4 ractions between FSVs during their uptake by Caco-2 cells.

5 PT/5-FU co-treatment was more effective in Caco-2 cells.

6 hydroperoxide (TBHP)-induced cytotoxicity of Caco-2 cells.

7 that the gene does not direct attachment to Caco-2 cells.

8 cant inhibition against pathogen adhesion to Caco-2 cells.

9 and enhanced FOXO-1 and p27(kip1) levels in Caco-2 cells.

10 tically enhanced cellular uptake of Cy5 into Caco-2 cells.

11 infection for virus isolation in Vero B4 and Caco-2 cells.

12 showed significantly decreased adherence to Caco-2 cells.

13 C human intestinal disease strains attach to Caco-2 cells.

14 mbinant CD0873 protein alone associates with Caco-2 cells.

15 nI sialidase for adhering to enterocyte-like Caco-2 cells.

16 Human intestinal mucosa was modeled using Caco-2 cells.

17 alidase inhibitors reduced F4969 adhesion to Caco-2 cells.

18 howed no sign of cytotoxicity when tested in Caco-2 cells.

19 hen evaluated based on permeability tests on Caco-2 cells.

20 ytic process that moves virus into polarized Caco-2 cells.

21 plaining how GAGs promote iron uptake by the Caco-2 cells.

22 the claudin-1 ECL-2 offered no protection to Caco-2 cells.

23 ize cytotoxicity if CPE had already bound to Caco-2 cells.

24 the apical and basolateral membranes of the Caco-2 cells.

25 (retention, transport and uptake of zinc) in Caco-2 cells.

26 al contents of sorghum on the iron uptake by Caco-2 cells.

27 This phenomenon was also observed with Caco-2 cells.

28 ative stress induced by hydrogen peroxide in Caco-2 cells.

29 ic (DNA strand breaks) effects in intestinal Caco-2 cells.

30 forces in intact human intestinal epithelial Caco-2 cells.

31 in vitro model of intestinal inflammation of Caco-2 cells.

32 vitro was measured by cytotoxicity assays on Caco-2 cells.

33 exhibited reduced invasion into INT-407 and Caco-2 cells.

34 cipitated with SIgA, bound to the surface of Caco-2 cells.

35 nvasive G1 Nal(r) strain were screened using Caco-2 cells.

36 erocytes in biopsy samples and monolayers of Caco-2 cells.

37 observed by electron microscopy in infected Caco-2 cells.

38 ide were analyzed in polarized monolayers of Caco-2 cells.

39 eased attachment of wild-type V. cholerae to Caco-2 cells.

40 educed oxidative stress triggered by H2O2 in CaCo-2 cells.

41 . monocytogenes adhesion but not invasion of Caco-2 cells.

42 m proliferating and differentiated HT-29 and Caco-2 cells.

43 occurred at the apical membrane of polarized Caco-2 cells.

44 cell surface expression of SI and DPP-IV in Caco-2 cells.

45 lized version of a popular model devised for Caco-2 cells.

46 L-2 specifically blocked the cytotoxicity on Caco-2 cells.

47 llular or plasma membrane content of SERT in Caco-2 cells.

48 f Lf is responsible for the interaction with Caco-2 cells.

49 not abolish apoB secretion in differentiated Caco-2 cells.

50 uced up-regulation of occludin expression in Caco-2 cells.

51 din was present in raft fractions of control Caco-2 cells.

52 s with constipation also upregulated SERT in Caco-2 cells.

53 orescent dye to monitor its interaction with Caco-2 cells.

54 rnalization, and targeting to the nucleus of Caco-2 cells.

55 ubdomain of Lf bound as well as intact Lf to Caco-2 cells.

56 d quantifying CTB attached to the surface of Caco-2 cells.

57 phosphorylation of occludin was evaluated in Caco-2 cells.

58 ted defective adhesion and invasion of human Caco-2 cells.

59 G polysaccharides can enhance iron uptake by Caco-2 cells.

60 phosphorylation of mTOR, S6K, and 4E-BP1 in Caco-2 cells.

61 n to bind to differentiated human intestinal Caco-2 cells.

62 lls and, as expected, decreased adherence to Caco-2 cells.

63 osol and pinoresinol) on vitamin D uptake by Caco-2 cells.

64 composition and Fe bioaccessibility to human Caco-2 cells.

65 ive effect against H2O2 induced oxidation in Caco-2 cells.

66 in uptake and secretion was also assessed in Caco-2 cells.

67 with a mix of the 3 polyphenols delivered to Caco-2 cells.

68 inhibitory effects against colon carcinoma (CaCo-2) cells.

69 nanoparticles across intestinal epithelial (Caco-2) cells.

70 frequency in both normal (RPE-1) and tumor (CaCo-2) cells.

71 elicited a significant ferritin response in Caco-2 cells (4.8-fold compared to the other breads) sug

72 We recently demonstrated that Caco-2 cells (a naturally CPE-sensitive enterocyte-like

73 nopus PRMT1 promoter and characterized it in CaCo-2 cells, a human cell line with intestinal stem cel

74 This was an in vitro study using Caco-2 cells, a human-derived intestinal epithelial cell

75 ermined their effect on uptake of mercury in Caco-2 cells, a model of intestinal epithelium, exposed

76 structed in type A SD strain F4969 had lower Caco-2 cell adhesion than wild-type F4969 or a complemen

77 after in vitro gastrointestinal resistance, Caco-2 cell adhesion), bioactivity and microstructure we

78 The effect against oxidative stress in Caco-2 cells, after in vitro digestion was also investig

79 totoxicity test showed that the viability of Caco-2 cells against beta-carotene microemulsions at con

80 neutrophils' oxidative burst and to protect Caco-2 cells against oxidative damage, the peel extract

81 s initiated from MAG is mediated by DGAT1 in Caco-2 cell and rat intestinal mucosal membranes, respec

82 of in vitro digestion and absorption across Caco-2 cells and (ii) the protective role of the oil bio

83 A total of 271 transcripts in Caco-2 cells and 207 transcripts in C. difficile were si

84 +)-dependent, saturable binding to HCT-8 and Caco-2 cells and competitively inhibited C. parvum attac

85 a membrane and intracellular Hsp60 levels in Caco-2 cells and consequently enhanced LAP-mediated L. m

86 Cocultures of CaCo-2 cells and DCs in a "double-layer" model followed

87 tigated the function of TCP in attachment to Caco-2 cells and found that mutants lacking TCP were def

88 transporter-mediated AP but not BL uptake in Caco-2 cells and human and mouse intestinal tissues.

89 AP membrane localization of OCT1 (mOct1) in Caco-2 cells and human and mouse intestine.

90 l changes in the human colorectal epithelial Caco-2 cells and in C. difficile after infection.

91 has revealed fundamental differences between Caco-2 cells and in vivo differentiated enterocytes in r

92 toxic effects of a cocktail of pollutants in Caco-2 cells and increase their tumorigenicity.

93 ies have been used to study proliferation in CaCo-2 cells and intestinal biopsy samples from patients

94 fers significantly from entry into polarized Caco-2 cells and is not influenced by virus binding to D

95 hat ER-beta is expressed at higher levels in Caco-2 cells and its levels are further boosted with PT

96 (ZnT10 gene), and CBWD transcripts in human Caco-2 cells and the ability of zinc to repress reporter

97 holemeal bread, its impact on iron uptake in Caco-2 cells and the predicted bioavailability of iron f

98 milks significantly reduced EAEC adhesion to Caco-2 cells and transgenic milk resulted in less coloni

99 uced a CPE variant that was noncytotoxic for Caco-2 cells and was unable to form CPE pores.

100 owed a significant reduction in adherence to Caco-2 cells and wild-type bacteria preincubated with an

101 invasiveness in human intestinal epithelial (Caco-2) cells and chicken liver (LMH) cells and survival

102 assessed in vitro by using human intestinal (Caco-2) cells and in vivo by using radiolabeled ferritin

103 ermining the localization of OCT1 (mOct1) in Caco-2 cells, and human and mouse enterocytes.

104 l-characterized cell lines, including, HeLa, CaCo-2 cells, and nontransformed human keratinocytes and

105 he uptake of polyphenols from guarana, using Caco-2 cells, and the effect of digested guarana on carb

106 Caco-2 cells as a model of human intestinal epithelia an

107 us-infected polarized intestinal epithelial (Caco-2) cells as well as surrounding noninfected cells.

108 The Caco-2 cell assay indicated that Fe is bioavailable.

109 uation of the bioprotective capacities using Caco-2 cell assay performed in this study makes a novel

110 PPH) radical scavenging and human intestinal Caco-2 cells assays.

111 on of MMP-9 from TNFalpha/IL1beta stimulated Caco-2 cells at 10 muM, which could be attributed to NO

112 The extracts, assayed on Caco-2 cells at a plausible intestinal concentration, si

113 PT also induced a significant increase in Caco-2 cells at pre-G phase coupled with increased Bax/B

114 re gene- and cell context-dependent with the Caco-2 cells being the most responsive cell line.

115 rimary intestinal epithelial cells and human Caco-2 cells; both express CCK receptor 1 and 2 (CCK1R a

116 DOCK1 siRNA reduced its expression >95% in Caco-2 cells but inhibited spreading much less than comb

117 pe A and C human intestinal strains bound to Caco-2 cells, but NanI-producing strains had higher atta

118 rkedly increased in differentiated HT-29 and Caco-2 cells, but the core3 structure was hardly detecta

119 d-type NHE3 was expressed in fibroblasts and Caco-2 cells, but the NHE3-S(719) mutant was fully resis

120 ad a lower uptake and secretion of lutein in Caco-2 cells by 10.0- and 50.5-fold, respectively, compa

121 uptake of hydrophobic drug were explored in Caco-2 cells by fluorescent Cy5 dye as a hydrophobic dru

122 Moreover, adhesion of C. difficile to Caco-2 cells can be partially blocked if cells are pretr

123 In Caco-2 cells, CCK enhanced CCK1R/CCK2R heterodimerizatio

124 eroxidase activities in H2O2 treated CCD and Caco-2 cells compared to PEPS, EPS and control groups.

125 In vitro permeation studies with Caco-2 cells confirmed the transmembrane transport of th

126 TC 11168, and a small percentage of infected Caco-2 cells contained 5 to 20 internalized bacteria per

127 Loss of Notch-1 expression in Caco-2 cells correlated with decreased transepithelial r

128 dherence of Std fimbriated S. Typhimurium to Caco-2 cells could be blocked by co-incubation with H ty

129 ediated binding to human colonic epithelial (Caco-2) cells could be abrogated by removing N-linked gl

130 and nitric oxide (NO) production in a human Caco-2 cell culture assay.

131 ptosis using human adenocarcinoma cell line (Caco-2 cell) cultures.

132 Unlike what we observed in Caco-2 cells, CVB3 entered HeLa cells with CAR.

133 n-110 in native hDAO from amniotic fluid and Caco-2 cells, DAO from porcine kidneys, and rhDAO produc

134 short hairpin RNA-mediated OCT1 knockdown in Caco-2 cells decreased AP uptake of pentamidine by appro

135 he intracellular trafficking of P2Ns in live caco-2 cells demonstrated the involvement of endocytic p

136 -dimensional matrigel model, in which single Caco-2 cells develop to form polarized cysts.

137 Over the course of Caco-2 cell differentiation, macroH2A1.1 was up-regulate

138 al resistance of the IEB were measured using Caco-2 cells; effects on signal transduction proteins we

139 Conversely, overexpression of Hsp60 in Caco-2 cells enhanced WT adhesion and transepithelial tr

140 d 977 genes were differentially expressed in Caco-2 cells exposed to HTy or HTy-Et for 24h, respectiv

141 and vitamin C contents, on human intestinal Caco-2 cells exposed to hydrogen peroxide (H2O2)-induced

142 After Caco-2 cells exposure, no significant differences were o

143 by gentamycin protection assays in HT-29 and Caco-2 cells expressing small hairpin RNAs against CAP-D

144 nt with 0.2% ethanol for two months rendered Caco-2 cells far more susceptible to wound damage and cy

145 ion was reflected by a decreased flux across Caco-2 cells for the drug combinations compared to drug

146 Parental Caco-2 cells formed regular hollow gland-like structures

147 digests differed in their ability to protect Caco-2 cells from H2O2.

148 tion of alpha-humulene, were able to protect Caco-2 cells from oxidative stress induced by tert-butyl

149 ivities (ABTS and DPPH assays) and inhibited Caco-2 cell growth.

150 t abundant gangliosides, GM(3) and GD(3), in Caco-2 cells has been determined using confocal microsco

151 oblast transfectants and naturally sensitive Caco-2 cells have also implicated certain claudins (e.g.

152 sters were effectively activated in HeLa and Caco-2 cell homogenates and were found to be good substr

153 ting that anthocyanins effectively protected Caco-2 cells in a concentration-dependent manner.

154 y were absorbed, metabolized and released by Caco-2 cells in culture media.

155 ssible polyphenols from EVA were absorbed by Caco-2 cells in higher proportions than from EVO, and mi

156 re was a higher cellular uptake of lutein by Caco-2 cells in nanoemulsions (872.9+/-88.3pmol/mgprotei

157 the epithelial barrier in the differentiated Caco-2 cells in vitro.

158 The Caco-2 cells incorporated capsaicin and dihydrocapsaicin

159 butyrate-induced differentiation of HT29 and Caco-2 cells increased the levels of released exosomes a

160 We show that Caco-2 cells incubated with E. coli display an activatio

161 a luciferase reporter gene in human colonic CaCo-2 cells indicating that ISX acts as a transcription

162 gradient fractions of control or CPE-treated Caco-2 cells, indicating a raft-independent association

163 In human colon cancer Caco-2 cells, induction of cellular HD5 expression by fi

164 table short hairpin RNA knockdown of PTEN in Caco-2 cells influenced expression or localization of cd

165 Most mutants with reduced Caco-2 cell invasiveness also showed significantly reduc

166 ral program of gene expression in polarizing Caco-2 cells involved changes in signaling pathways (e.g

167 ar glucosamine at micromolar level in living Caco-2 cells is also demonstrated.

168 nous sodium-dependent succinate transport in Caco-2 cells is also inhibited by ACA.

169 top of the device and first absorbed by the Caco-2 cell layer, and then metabolized by the primary h

170 neity and low transfection efficiency of the Caco-2 cell line prompted the isolation of several sub-c

171 The CaCo-2 cell line was used to study EGF-, IL15-, and P31-

172 activity, all compounds were active against Caco-2 cell line, being the ones with glucose moiety and

173 ant diarrhoea is assessed in vitro using the Caco-2 cell line.

174 the 1761C allele in HepG2, MCF-7, LNCaP, and Caco-2 cell lines (all P<0.001), thus indicating that th

175 Measurement of intracellular Caco-2 cell metabolites revealed a significantly increas

176 The Caco-2 cell method, but not the dialysability assay, pro

177 Stimulation of 5-HT4R increased Caco-2 cell migration and reduced oxidative stress-induc

178 In a Caco-2 cell model of enteritis, culture supernatants of

179 In our study, the Caco-2 cell model of intestinal epithelium was used to d

180 In the CaCo-2 cell model, IL15 and EGF cooperated to induce pro

181 In a Caco-2 cell model, supersaturated solutions of the activ

182 hesive property of extracts was evaluated in Caco-2 cell model.

183 nal barrier based on permeability studies in Caco-2 cell model.

184 ood-brain barrier (BBB) as demonstrated in a Caco-2 cell model.

185 ithelial translocation in an enterocyte-like Caco-2 cell model.

186 and transport studies were conducted using a Caco-2 cell model.

187 mented special-grade maize porridges using a Caco-2 cell model.

188 ransport of TCMPs we used the differentiated Caco-2 cells model.

189 the ABTS radical scavenging test and CCD and Caco-2 cell models.

190 (DPPH and hydroxyl radicals) and biological (Caco-2 cells) models were used.

191 Regulation of LPA1 expression in Caco-2 cells modulated epithelial permeability and the e

192 from both methods) were transported through Caco-2 cell monolayer despite absorption rates being low

193 xpression prevented the C. sakazakii-induced CaCo-2 cell monolayer permeability despite the presence

194 The Caco-2 cell monolayer permeation tests showed that PG-QC

195 found to be absorbed mainly in the ileum and Caco-2 cell monolayer through passive diffusion and bile

196 e original GSE phenolic compounds passed the Caco-2 cell monolayer, since all were recovered in the a

197 r role in transepithelial transport within a Caco-2 cell monolayer-model system and impact on ANC sta

198 vestigate the transport of PHIP-M1 through a Caco-2 cell monolayer.

199 eal and faecal fermented samples, passed the Caco-2 cell monolayer.

200 ted the greatest transport efficiency across Caco-2 cell monolayers (21.4%), two-fold more than that

201 By using polarized epithelial Caco-2 cell monolayers and Shigella flexneri as a model

202 roperoxide (TBH)-induced oxidative damage to Caco-2 cell monolayers as a model system of the human in

203 ermeability through artificial membranes and Caco-2 cell monolayers in vitro and penetrance across th

204 he brush-border membrane of human intestinal Caco-2 cell monolayers showed characteristics of both PA

205 Caco-2 cell monolayers were used to mimic the small inte

206 results were seen in vitro using established Caco-2 cell monolayers wherein acrolein decreased barrie

207 findings showing AP localization of OCT1 in Caco-2 cell monolayers, an established model of human in

208 ate the absorption of resultant oligomers on Caco-2 cell monolayers.

209 acteria-induced damage targeted to polarized Caco-2 cell monolayers.

210 activation and tight junction disruption in Caco-2 cell monolayers.

211 lls and for transcellular permeability using Caco-2 cell monolayers.

212 ydrolysate but enhanced its transport across Caco-2 cell monolayers.

213 taldehyde on the tight junction integrity in Caco-2 cell monolayers.

214 totoxicity or cytoskeleton reorganization of Caco-2 cell monolayers.

215 ly through the basolateral side of polarized Caco-2 cell monolayers.

216 ssion of Hsp60 significantly, which rendered Caco-2 cells more susceptible to subsequent LAP-mediated

217 F) and cytoprotective/cytotoxic effects upon Caco-2 cells (MTT, cell cycle and reactive oxygen specie

218 E1E2 glycoprotein interaction with polarized Caco-2 cells occurred predominantly at the apical surfac

219 red as tea infusions were investigated using Caco-2 cells on the intestinal inflammation and cytochro

220 Caco-2 cells overexpressing full-length TLR2 or mutant T

221 er for the co-culture cell model compared to Caco-2 cells (p<0.01).

222 thesized and displayed high solubilities and Caco-2 cell permeabilities, suggesting high absorption f

223 l and faecal fermentation were combined with Caco-2 cell permeability studies for GSE samples.

224 dition, the effects of the P31-43 peptide on CaCo-2 cell proliferation and downstream signaling were

225 content of PCA and the highest inhibition of Caco-2 cell proliferation with an IC50 (16.11 mug/mL) co

226 The effect of digested juice on Caco-2 cells proliferation was also studied, and the red

227 ures and overexpression of truncated STX3 in Caco-2 cells recapitulated most characteristics of varia

228 larly, knockdown of apoAIV in differentiated Caco-2 cells reduced MTP, FoxA2, and FoxO1 mRNA levels,

229 hairpin RNA (shRNA) suppression of Hsp60 in Caco-2 cells reduced WT adhesion and translocation 4.5-

230 processed at 303 kJ/kg completely increased Caco-2 cells resistance towards oxidative damage by reco

231 Inhibition of PKC zeta in Caco-2 cells resulted in activation of the human apical

232 ss of MarvelD3 expression in differentiating Caco-2 cells resulted in increased cell migration and pr

233 and human colorectal adenocarcinoma-derived Caco-2 cells resulted in significant up-regulation of SO

234 or CD55) at the apical surface of polarized Caco-2 cells results in rapid transport of the virus to

235 aPKC induces robust apoptotic cell death in Caco-2 cells, significantly reducing both cyst size and

236 3E or Y145 mutants were disrupted in colonic Caco-2 cells, similar to ezrin mislocalization in the co

237 in-tagged DOCK5 localized to the membrane of Caco-2 cells spreading on collagen IV.

238 Coculture of STC-1 cells with Caco-2 cells stably expressing CD36 did not alter secret

239 n and invasion of nonpolarized and polarized Caco-2 cells, the adhesion and transcytosis of M-like ce

240 In Caco-2 cells, the ROS levels and, in both cell lines, th

241 reduces S. Typhimurium invasion of HeLa and Caco-2 cells to a level similar to that observed using a

242 ical resistance (TEER) was measured in human Caco-2 cells to assess permeability after application of

243 with and translocation across differentiated Caco-2 cells to better understand Campylobacter's pathog

244 pression of alcohol dehydrogenase sensitized Caco-2 cells to ethanol-induced tight junction disruptio

245 We found Caco-2 cells to significantly enhance isolation success

246 studied the oral absorption of HDTA using a Caco-2 cell transport system and an animal model.

247 In Caco-2 cells treated with IFNgamma and TNFalpha, OEA (vi

248 zed cells, CVB-infected polarized intestinal Caco-2 cells undergo nonapoptotic necrotic cell death tr

249 ptake measured by in vitro dialysability and Caco-2 cell uptake assays to that of iron and zinc absor

250 gestion and translocate across monolayers of Caco-2 cells, used as a model of the intestinal epitheli

251 Levels of proteins were reduced in Caco-2 cells using short-hairpin RNAs or proteins were i

252 Knockdown of EpCAM in T84 and Caco-2 cells using shRNAs led to changes in morphology a

253 f mouse brain, liver, red muscle fibers, and CaCo-2 cells using the TAPEG FASP approach allowed ident

254 showed an increase in ferritin synthesis in Caco-2 cells versus iron sulphate, beta-CN(1-25)4P being

255 10-0.079mgmL(-1) range showed no decrease of Caco-2 cell viability at concentrations lower than 125mu

256 Significant protection of Caco-2 cells was also observed using either rclaudin-4 o

257 -malvidin-3-O-glucoside (Cat-Mv3glc) through Caco-2 cells was assessed by performing transepithelial

258 The ability of Cat-Mv3glc to cross Caco-2 cells was compared with that of malvidin-3-glucos

259 In addition, a transport study with Caco-2 cells was conducted to evaluate the impact of co-

260 ice against H2O2-induced oxidative stress in Caco-2 cells was determined using biomarkers for cellula

261 hydroperoxide (tert-BOOH) induced stress in Caco-2 cells was investigated.

262 more efficient specific cytotoxic effect on Caco-2 cells was observed on the cells incubated with th

263 ic ice cream and the adhesion of L. casei to Caco-2 cells was observed.

264 Phylloquinone uptake by Caco-2 cells was saturable and was significantly impaire

265 and 80% inhibition between Jurkat cells and Caco-2 cells was seen at 90 microM.

266 Binding of ferritin to Caco-2 cells was shown to be saturable, and the kinetics

267 ial cells, whereas invasion of bacteria into Caco-2 cells was significantly inhibited.

268 binding of Ag85 on elastin siRNA-transfected Caco-2 cells was significantly reduced (34.3%), implying

269 e efficiency of C. jejuni 81-176 invasion of Caco-2 cells was two- to threefold less than the efficie

270 u human intestinal enteroids and transformed Caco-2 cells, we report that ExPEC strain CP9 binds to a

271 When Caco-2 cells were employed, more robust antioxidant acti

272 ccharide (LPS) treatment of human intestinal Caco-2 cells were examined, in terms of nitric oxide (NO

273 Caco-2 cells were infected with a lentivirus containing

274 n contrast, only 11 to 17% of differentiated Caco-2 cells were observed to bind and internalize eithe

275 alf-lives and steady-state protein levels in Caco-2 cells were repressed when HuR was silenced but wa

276 dehyde in H2O2 treated CCD 841 CoN (CCD) and Caco-2 cells were significantly inhibited by PEPS, EPS,

277 umarins on [3H]cyclosporine translocation in Caco-2 cells were then compared.

278 Human intestinal Caco-2 cells were treated with multiple concentrations o

279 d mineral retention, transport and uptake by Caco-2 cells were used to assess bioavailability.

280 Caco-2 cells were used to demonstrate the passage of the

281 1A1 was also induced in the human intestinal Caco-2 cells when the cells were cultured in the presenc

282 ate SCFA-AhR ligand interactions in YAMC and Caco-2 cells where SCFAs synergistically enhance basal a

283 -to-apical [3H]cyclosporine translocation in Caco-2 cells, whereas the furanocoumarin-free GFJ extrac

284 (CD133NPs) were efficiently internalized by Caco-2 cells, which abundantly express CD133 (>9-fold hi

285 ed with increased NHE3 surface expression in Caco-2 cells, which also was NHERF2-dependent; was assoc

286 lowered the amounts of fullerene taken up by Caco-2 cells, which are derived from a human colorectal

287 ffect on iron uptake from intact ferritin by Caco-2 cells, which suggests that ferritin-bound iron is

288 lated gastrointestinal tract and adhesion to Caco-2 cells while improved the ACE-inhibitory and antio

289 Moreover, the incubation of differentiated Caco-2 cells with a non-toxic oil concentration (100mug/

290 Infection of Caco-2 cells with EPEC for 30-120 minutes decreased apic

291 1 RNA levels were reduced by pretreatment of Caco-2 cells with IFN-beta1a.

292 Stimulation of Caco-2 cells with IgE-Ag complexes triggered upregulatio

293 Pretreatment of Caco-2 cells with MbetaCD had no appreciable effect on C

294 In contrast, pretreatment of Caco-2 cells with neuraminidase or co-incubation with th

295 B inhibitor alpha (IkBa) was knocked down in Caco-2 cells with small interfering RNAs.

296 Treatment of Caco-2 cells with tumor necrosis factor-alpha and interf

297 re that treatment of human intestine-derived Caco-2 cells with vitamin D(3) markedly increased endoge

298 Treatment of human enterocytes (CaCo-2 cells) with recombinant human PCSK9 (10 mug/mL fo

299 l viability or the cytoskeleton structure of Caco-2 cells (XTT viability assay and confocal microscop

300 Serial blind passage in Caco-2 cells yielded increasing copies of VA1 RNA, and m