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 tion, followed by measurement of ferritin in Caco-2 cells.

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

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

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

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

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

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

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

10 fects of Fermented-AP were highlighted using Caco-2 cells.

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

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

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

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

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

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

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

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

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

20 showed significantly decreased adherence to Caco-2 cells.

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

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

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

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

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

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

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

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

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

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

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

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

33 vitro digestion coupled with transport using Caco-2 cells.

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

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

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

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

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

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

40 the INFOGEST protocol, followed by uptake by Caco-2 cells.

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

42 ession of inflammatory cytokines in infected Caco-2 cells.

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

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

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

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

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

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

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

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

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

52 paB) activation following LPS stimulation in Caco-2 cells.

53 ctive [(57)Co]Cbl in polarized monolayers of Caco-2 cells.

54 ne (50 nM), the tissues resembling polarized Caco-2 cells.

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

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

57 efore and after intestinal metabolization by Caco-2 cells.

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

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

60 short hairpin RNA-mediated DRA knockdown in Caco-2 cells.

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

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

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

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

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

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

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

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

69 decreased in presence of ABCB1 inhibitor in Caco-2 cells (-20.4%; p < 0.05) and increased in Griptit

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

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

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

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

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

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

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

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

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

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

80 he formulations and their ability to protect Caco-2 cells against oxidative stress were confirmed in

81 After incubation with Caco-2 cells, AHR activity of different coffees was betw

82 ition of beef proteins to the apical side of Caco-2 cells, alpha-Gal containing peptides were not det

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

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

95 attenuated human rotavirus strain, CDC-9, in Caco-2 cells and neonatal rats.

96 -higher titers than wild-type virus in human Caco-2 cells and simian Vero cells.

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

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

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

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

101 taken up by human colorectal adenocarcinoma (Caco-2) cells and bestowed CAA, determined by monitoring

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

103 predominant inhibitor of glucose uptake into Caco-2 cells, and gallated catechins the most potent: CG

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

105 esses and the effects of oxidative stress in Caco-2 cells, and preserved the integrity of tight junct

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

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

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

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

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

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

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

113 M13 accelerate the wound recovery process of Caco-2 cells at the concentrations seen in the colon (1.

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 MTP expression in differentiated intestinal Caco-2 cells, but increased expression in hepatic Huh7 c

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

120 totoxic effect and reduced cell viability of Caco-2 cells by 45% and 62%, respectively.

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

122 oxia and bacteria-containing formula, and in Caco-2 cells by media inoculated with LPS.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

142 The vitamin D transport efficiency across Caco-2 cells for small sized nanoemulsions (233 nm) was

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

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

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

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

147 bjected to in vitro digestions, and added to Caco-2 cells grown on permeable supports.

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

149 Experimental NEC in rat pups and Caco-2 cells had increased permeability compared to cont

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

151 yme-enriched homogenates obtained from human Caco-2 cells (IC(50) = 64.75 ug/mL).

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

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

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

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

156 ce (TEER) in primary human colon tissues and Caco-2 cells in vitro through upregulating tight junctio

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

158 The Caco-2 cells incorporated capsaicin and dihydrocapsaicin

159 addition of fructose 1,6-biphosphate to the Caco-2 cells increased iron uptake 2-fold.

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

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

162 MIR200C-3p was rapidly increased in Caco-2 cells incubated with IL1B; the antagomiR-200c pre

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

164 In Caco-2 cells, individual tea catechins reduced the SGLT1

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

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

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

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

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

170 The generation of a ZIP14-deficient CaCo-2 cell line enabled the identification of ZIP14 as

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

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

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

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

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

176 P treatment of BRJ inhibits proliferation of Caco-2 cell lines, exhibiting non-cytotoxic effect for H

177 ces showed no cytotoxicity on HepG2, AGS and Caco-2 cell lines.

178 in preventing the AAPH-mediated oxidation of Caco-2 cells, low-density lipoprotein and deoxyribonucle

179 We show that Caco-2 cell maturation and differentiation into the inte

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

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

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

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

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

185 so carotenoid bioavailability) using a human Caco-2 cell model system.

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

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

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

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

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

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

192 e ferritin response in a simulated digestion/Caco-2 cell model.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

210 Translocation studies of protein across Caco-2 cell monolayers showed a lower translocation rate

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

233 re formation and activity in enterocyte-like Caco-2 cells, reducing the cytotoxicity caused by this t

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

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

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

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

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

239 3E or Y145 mutants were disrupted in colonic Caco-2 cells, similar to ezrin mislocalization in the co

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

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

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

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

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

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

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

247 Moreover, in Caco-2 cells transcellular transport of the known OATP2B

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

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

250 Caco-2 cells treated with the chelate at calcium concent

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

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

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

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

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

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

257 The uptake by Caco-2 cells varied from 130.2 to 131.9 ng/mg cell prote

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

259 For cytotoxicity, the Caco-2 cell viability analysis revealed that these two t

260 10-0.079mgmL(-1) range showed no decrease of Caco-2 cell viability at concentrations lower than 125mu

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

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

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

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

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

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

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

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

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

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

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

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

273 Caco-2 cells were cultured in the TEEI bioreactor under

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

275 induction of AHR- and Nrf2-pathway genes in Caco-2 cells were evaluated by real-time qPCR.

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

277 Instead, when Caco-2 cells were incubated with lipids extracted from b

278 Caco-2 cells were infected with a lentivirus containing

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

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

281 Caco-2 cells were transfected with vectors that express

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

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

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

285 1A1 was also induced in the human intestinal Caco-2 cells when the cells were cultured in the presenc

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

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

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

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

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

291 which together with its high permeability in Caco-2 cells will allow its classification as a BCS clas

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

293 inhibited glucose uptake into the intestinal Caco-2 cells with GT being the most potent inhibitor (IC

294 1 RNA levels were reduced by pretreatment of Caco-2 cells with IFN-beta1a.

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