ライフサイエンスコーパス: HT-29 cell

1 pholinos permit LIGHT to induce apoptosis in HT-29 cells.

2 of the sipA sopABDE2 mutant for nonpolarized HT-29 cells.

3 lecular alterations in human colon carcinoma HT-29 cells.

4 (control) and 36 (100 micro M celecoxib) in HT-29 cells.

5 16 cells but were 22 and 4, respectively, in HT-29 cells.

6 in cytosol following silibinin treatment of HT-29 cells.

7 pression and enzyme activity in colon cancer HT-29 cells.

8 testinal epithelial cells, namely Caco-2 and HT-29 cells.

9 rting measurable toxic effects on HEK293 and HT-29 cells.

10 ivity were both diminished in differentiated HT-29 cells.

11 ered bacteria displayed induced adherence to HT-29 cells.

12 ivation of the EGF receptor or Akt kinase in HT-29 cells.

13 lactosyltransferase, previously described on HT-29 cells.

14 bited no cytotoxicity on kidney (HEK293) and HT-29 cells.

15 expressed on the surface of roughly half of HT-29 cells.

16 n was also inhibited in Ad5dnTRAF-2-infected HT-29 cells.

17 TRAF-2 is involved in IL-1 beta signaling in HT-29 cells.

18 loops and an in vitro cytotoxic response in HT-29 cells.

19 toxicity production by lysis of 51Cr-labeled HT-29 cells.

20 on of all isolates was confirmed in vitro in HT-29 cells.

21 125I and examined for the ability to bind to HT-29 cells.

22 te 10- to 15-fold increase in penetration of HT-29 cells.

23 cultured human intestinal epithelial cells, HT-29 cells.

24 sent, the 26 KDa Bcl-2 protein was absent in HT-29 cells.

25 l lines treated, the most sensitive were the HT-29 cells.

26 cells such as HT-29-MTX than to the parental HT-29 cells.

27 ping of intracellular Na(+) dynamics in live HT-29 cells.

28 ontrol of necroptosis in La-RIPK3-transduced HT-29 cells.

29 emination process was much more efficient in HT-29 cells.

30 aling increased E. coli O157:H7 adherence to HT-29 cells.

31 bovine, goat, buffalo, yak and camel milk in HT-29 cells.

32 this pathway by inhibiting p65 activation in HT-29 cells.

33 the transcriptional change induced by CA in HT-29 cells.

34 ing apoptosis and reduction the viability of HT-29 cells.

35 Wiskott-Aldrich Syndrome protein (N-WASP) in HT-29 cells.

36 they did not show any effect on apoptosis in HT-29 cells.

37 endogenous muscarinic M3 receptor in native HT-29 cells.

38 tergent-resistant membrane (DRM) vesicles in HT-29 cells.

39 ivity in tumor necrosis factor-alpha-treated HT-29 cells.

40 ssion and MAT2A promoter activity in RKO and HT-29 cells.

41 ivated Src rescues RACK1-inhibited growth of HT-29 cells.

42 n of the epidermal growth factor receptor in HT-29 cells.

43 xoS-GAP on Rac1 inactivation were evident in HT-29 cells.

44 supernatants from nonpolarized and polarized HT-29 cells.

45 antly reduced Act-induced IL-8 production in HT-29 cells.

46 cer-derived cell lines, including Caco-2 and HT-29 cells.

47 ates COX-2 expression and PGE2 production in HT-29 cells.

48 DLD1, and SW480 cell lines and antagonism in HT-29 cells.

49 tes activation of endogenous procaspase-9 in HT-29 cells.

50 icity of the cisplatin/17-AAG combination in HT-29 cells.

51 eam proteins and, subsequently, apoptosis in HT-29 cells.

52 ition of protein synthesis in human colonic (HT-29) cells.

53 f SCP-2 overexpressing hepatoma cells (72%), HT-29 cells (58%), and SCP-2 overexpressing L-cells (37%

54 ot analysis of apical side-treated polarized HT-29 cells, Act induced phosphorylation of p38, c-Jun N

55 HT-29 cells activated the endogenous TNF gene in respons

56 or a heparin fragment to effectively inhibit HT-29 cell adhesion to Ang was determined to be 6 disacc

57 gative regulator for the formation of stable HT-29 cell adhesion to extracellular matrix.

58 ife of the time course of induction of TR in HT-29 cells after adding selenium was 10 h.

59 imerize to form an amino acid transporter in HT-29 cells after bacterial infection; levels of SLC7A5-

60 of ATP/carbachol-stimulated iodide influx in HT-29 cells after lentiviral infection with the yellow f

61 Chinese magnolia-vine), was investigated in HT-29 cells against DON-induced cytotoxicity, oxidative

62 ell differentiated HCA-7, Moser, LS-174, and HT-29 cells, albeit at different levels.

63 cells, whereas gp120 strains not activating HT-29 cells also did not activate Bob-transfected cells.

64 Cultured HT-29 cells also had high activity for this kinase.

65 Gp120 strains that induced signaling in HT-29 cells also induced calcium fluxes in Bob-transfect

66 x was also induced by IFN-gamma treatment of HT-29 cells and may be a second point of transcriptional

67 on factor IFN regulatory factor-1 (IRF-1) in HT-29 cells and that IRF-1 binds to an element in exon 1

68 A similar reduction was also observed with HT-29 cells and U251 cells.

69 18a was more potent than irinotecan against HT-29 cells and was as potent as irinotecan against A549

70 the generation of reactive oxygen species in HT-29 cells and was suppressive in the CCD-18Co cells wh

71 eaflet of the plasma membrane in intestinal (HT-29) cells and thereby reduce CT uptake into the cells

72 ting with anti-Bcl-2 antibodies was found in HT-29 cells, and also in human colon, tonsil, and some o

73 d apoptosis inducer in human colon carcinoma HT-29 cells, and justify further studies to investigate

74 protect against DON-induced cytotoxicity in HT-29 cells, and significantly lessened the DON-stimulat

75 a induced NF-kappa B DNA binding activity in HT-29 cells, and the activated NF-kappa B complex was el

76 owed that silibinin doses found effective in HT-29 cells are achievable in plasma, which increases th

77 spheroids of human colorectal adenocarcinoma HT-29 cells are generated by culturing the cells in 96-w

78 The aim of this study was to examine HT-29 cells as a polarized cell model for studying apica

79 -FFAU) has been synthesized and evaluated in HT-29 cells as a potential PET agent for herpes simplex

80 1beta and IL-8 expression in both Caco-2 and HT-29 cells as assayed by electrophoretic mobility shift

81 llent activation of the MTX prodrugs to kill HT-29 cells as efficiently as MTX itself.

82 d IL-8 gene expression was also inhibited in HT-29 cells as measured by Northern blot and ELISA.

83 o direct DNA damage in colon adenocarcinoma (HT-29) cells as a result of treatment with all extracts,

84 entration of CPT required to kill 50% of the HT-29 cells, as determined by clonogenic assays.

85 emokine CXCL1 were upregulated in cocultured HT-29 cells at 4 h compared to levels in control cells.

86 , a geldanamycin delivative, radiosensitized HT-29 cells at a relatively low dose of irradiation, and

87 ion of induced COX-2 messenger RNA (mRNA) in HT-29 cells at concentrations of < or =1 micromol/L.

88 ly, overexpression of the core3 structure in HT-29 cells attenuated cell surface expression of both e

89 ressed using an inducible expression system, HT-29 cells became sensitive to apoptosis in response to

90 uberoylanilide hydroxamic acid than SW620 or HT-29 cells (both expressing mutant APC).

91 njugates were nontoxic (IC(50) > 100 muM) to HT-29 cells, both in the dark and upon light activation

92 showed low cytotoxicity (IC(50) > 94 muM) in HT-29 cells, both in the dark and upon light activation

93 trol L-selectin-immunoglobulin also bound to HT-29 cells but had no effect on tumor cell lung coloniz

94 p27 protein levels or apoptosis in HCT-15 or HT-29 cells but induced keratin 18 in both cell lines.

95 with high basal activities of ERK1/2 such as HT-29 cells, but not in cells with low basal activities,

96 41% and 55%, and co-culture with HCT-116 and HT-29 cells by 39% and 26% (C3G) and 50% and 51% (D3G),

97 In vitro studies were performed in HT-29 cells by incubation at various time points.

98 and pIgR mRNA are coordinately regulated in HT-29 cells by TNF-alpha, IFN-gamma, and IL-1beta.

99 ignificant levels of interleukin-8 (IL-8) in HT-29 cell culture supernatants by 4 h, which increased

100 reonine kinase STK11 (also known as LKB1) in HT-29 cells decreased the efficiency of protrusion resol

101 y detected was CXCR4 (fusin/LESTR), although HT-29 cells did not express mRNA for its ligand, stromal

102 In HT-29 cells, endogenous DNAS1L3 localized to the endopla

103 was also demonstrated in human colon cancer HT-29 cells, esophageal cancer KYSE 150 cells, and prost

104 Cell cycle analysis of HT-29 cells exposed with indomethacin showed a partial G

105 We also found that human colonic epithelial HT-29 cells express CRHR2alpha mRNA, whereas expression

106 Undifferentiated and proliferating human HT-29 cells express hGATA-6 but not hGATA-4 or hGATA-5.

107 eported O6-BG-induced degradation of MGMT in HT-29 cell extracts and showed the extracts to be active

108 The proteolysis of O6-BG-inactivated MGMT in HT-29 cell extracts was energy-dependent and was markedl

109 0-fold less potent MGMT inhibitor than BG in HT-29 cell extracts, these results illustrate the capaci

110 spase-9 that was immunoprecipitated from the HT-29 cell extracts.

111 similar lack of IkappaB alpha degradation in HT-29 cells followed TNF-alpha and bacterial polymer sti

112 ains of enteric bacteria were incubated with HT-29 cells for 1 hr.

113 d that sulindac and sulindac sulfide prevent HT-29 cells from progressing from the G0/G1 into the S p

114 d signaling could rescue colonic epithelial (HT-29) cells from apoptosis induced by proapoptotic cyto

115 Comparisons of alterations in HT-29 cell function caused by P. aeruginosa strains that

116 ExoS was also found to cause alterations in HT-29 cell function, leading to the loss of cell adhesio

117 Results from the present study in HT-29 cells further demonstrate the correlation between

118 ocytes during allogeneic responses, inhibits HT-29 cell growth, and weakly stimulates NF-kappaB-depen

119 HT-29 cells had a 7-fold increase in sensitivity to AraC

120 lipopolysaccharide-stimulated differentiated HT-29 cells (HT-29/MTX, where MTX is methotrexate) compa

121 d strong antitelomerase activity in PC-3 and HT-29 cells (IC(50) values ranging from 5.2 to 9.1 muM).

122 ing preparations of native FAK and PTEN from HT-29 cells in a specific Tyr-phosphatase assay FAK was

123 MUC5AC mucins secreted by HT-29 cells in culture are oligomeric glycoproteins with

124 hiazoles, inhibited by >95% iodide influx in HT-29 cells in response to multiple calcium-elevating ag

125 (GlcNAc)2 structures was obtained by growing HT-29 cells in the presence of glycoprotein processing i

126 An additional investigation of sorting live HT-29 cells in the spiral microfluidic channel indicated

127 nase was not degraded in IL-1beta-stimulated HT-29 cells, in contrast to Caco-2 cells.

128 hibitors on the IkappaB-NF-kappaB systems in HT-29 cells, in which proteasome inhibitors activate rat

129 y was unaltered by PI 3-kinase inhibition in HT-29 cells, in which TNF-alpha was shown to activate PI

130 ated PGE(2)-induced EP4 receptor activity in HT-29 cells increased resistance to spontaneous apoptosi

131 Rotavirus infection of HT-29 cells induced mRNA for several C-C and C-X-C chemo

132 with M. avium suppressed IL-8 production by HT-29 cells infected with Salmonella typhimurium.

133 ate pretreatment of a human colon cell line (HT-29 cells) inhibited the tumor necrosis factor-alpha (

134 f 511 glycans, and that virus infectivity in HT-29 cells is abrogated by anti-A-type antibodies as we

135 st that, since the toxin rapidly intoxicates HT-29 cells, it may be internalized.

136 In HT-29 cells, ITF increased the stability of DAF mRNA.

137 In HT-29 cells, K+ efflux was 2.0 +/- 0.1 micromol/cm2/s, i

138 Overexpression of the EP4 receptor in HT-29 cells led to basal EP4 receptor signalling in the

139 S. flexneri dissemination in HT-29 cells led to the local phosphorylation of tyrosine

140 urvival rate) and higher adhesion ability to HT-29 cell line after digestion (528 +/- 29 cells per 10

141 11B, isolated from the human colon carcinoma HT-29 cell line.

142 brid nanocrystals were conducted with KB and HT-29 cell lines and characterized by confocal microscop

143 ession was determined in LS174T, Caco-2, and HT-29 cell lines in response to stimulation with interle

144 G allele and transfected into either HeLa or HT-29 cell lines showed less promoter activity than comp

145 The studies with Caco-2 and HT-29 cell lines showed that digested coffee extracts ha

146 colorectal adenocarcinoma cells (Caco-2 and HT-29 cell lines) were investigated.

147 exerted cytotoxic activity against HeLa and HT-29 cell lines, but were inactive towards MRC-5 and MC

148 inoma (HeLa) and human colon adenocarcinoma (HT-29) cell lines than CRE.

149 al (RGM1) and colon cancer (Caco-2, LoVo and HT-29) cell lines.

150 emonstrated using proteome-wide reactions of HT-29 cell lysates with a model probe of threonine beta-

151 HT-29 cells mediated specific uptake and degradation of

152 In HT-29 cells, miR-627 was the only miRNA significantly up

153 In neither the HT-29 cells nor any of the other five human cell lines d

154 synthesized, radiolabeled, and evaluated on HT-29 cells (NTS(1)(+)).

155 OPN mRNA levels increased after infection of HT-29 cells, peaking in 4 to 6 h.

156 HT-29 cells produce a functional apically located asialo

157 Tapcin reduced colorectal adenocarcinoma HT-29 cell proliferation and tumor volume in mouse hollo

158 and dose-dependent high inhibitory effect on HT-29 cell proliferation.

159 ds present in rosemary, against colon cancer HT-29 cells proliferation is investigated using a compre

160 The induction of IRF-1 mRNA by IFN-gamma in HT-29 cells reaches a maximum at 6 h and is superinduced

161 DNA binding activity in differentiated HT-29 cells relative to HT-29/p cells was strongly reduc

162 Reduced CAP-D3 in HT-29 cells resulted in earlier recruitment of SLC7A5 to

163 crosis factor alpha (TNF-alpha) treatment of HT-29 cells resulted in increased expression of inflamma

164 Adenoviral-mediated expression of ZBP-89 in HT-29 cells revealed that ZBP-89 potentiates butyrate in

165 B. fragilis enterotoxin was associated with HT-29 cell rounding and with augmented internalization o

166 We conclude that cellular differentiation of HT-29 cells selectively impairs the IL-1beta signaling p

167 32P-labeling of HT-29 cells showed that the 30 KDa protein was phosphory

168 Overexpression of GKLF in HT-29 cells significantly reduced ODC mRNA and protein l

169 In HT-29 cells stimulated with IL-1beta, IkappaB alpha was

170 leukaemia (HL-60) and colon adenocarcinoma (HT-29) cells suggest an increase in apoptosis following

171 R4 expression and induced differentiation of HT-29 cells, suggesting a role for CXCR4 in maintenance

172 We then tested these mutants in human HT-29 cells that, in contrast to the MDCK cells, were re

173 are not involved in TNF-induced necrosis in HT-29 cells, the target of MLKL during TNF-induced necro

174 s motile bacteria reached the cell cortex in HT-29 cells, they formed membrane protrusions that resol

175 e that IL-1 beta induces COX-2 expression in HT-29 cells through multiple signaling pathways and NF-k

176 Greater sensitivity of HT-29 cells to a calpain inhibitor, as measured by IL-8

177 erfere with E-selectin-dependent adhesion of HT-29 cells to activated vascular endothelium and to blo

178 Exposure of HT-29 cells to butyrate eliminated their constitutive NF

179 ct of 2f-LI and increased the sensitivity of HT-29 cells to cytokine-induced apoptosis.

180 The exposure of HT-29 cells to SN-38 for a limited period of time (<2 h)

181 lished epithelial monolayers using polarized HT-29 cells transduced to express CCR5, and an explant s

182 In HT-29 cells transfected with HuR and CUGBP2, a switch in

183 Kinetic studies in HT-29 cells treated with O6-BG indicated a slow and grad

184 ses on RNA from human intestinal epithelial (HT-29) cells treated with the cytotoxic enterotoxin (Act

185 pe and cyclophosphamide-resistant MCF-7, and HT-29 cells under aerobic conditions and HT-29 cells und

186 F-7 cells and were also selectively toxic to HT-29 cells under hypoxic conditions (selectivity ratios

187 and HT-29 cells under aerobic conditions and HT-29 cells under hypoxic conditions.

188 ion of endogenous procaspase-9 occurs in the HT-29 cells under normal conditions and that denitrosati

189 as assessed in lipopolysaccharide-stimulated HT-29 cells using ELISA assay.

190 ion ([Ca2+]i) was monitored in fura-2-loaded HT-29 cells using microscope-based fluorescence imaging.

191 The adhesion of radiolabeled E. cloacae to HT-29 cells was concentration and temperature dependent

192 The CXCR4 receptor in HT-29 cells was functionally coupled, as demonstrated by

193 MUC2 expression in HT-29 cells was increased by TNF-alpha treatment and by

194 nterestingly, silibinin-induced apoptosis in HT-29 cells was independent of caspases activation, as a

195 strin-releasing peptide receptor on PC-3 and HT-29 cells was investigated.

196 shRNA library in human colon adenocarcinoma HT-29 cells, we found that knockdown of MLKL blocked TNF

197 the previously reported studies on Gd-tex in HT-29 cells, we tested five other human tumor cell lines

198 s are expressed in human colonic epithelium, HT-29 cells were examined by RT-PCR for the expression o

199 Confluent HT-29 cells were exposed to 10(6) bacteria for 1 h and t

200 , recombinant GKLF and nuclear extracts from HT-29 cells were found to bind to the Sp1 motif on the C

201 HT-29 cells were incubated with cell stressors such as D

202 The gp120-induced effects on HT-29 cells were inhibited by anti-Bob neutralizing anti

203 Caco-2 and HT-29 cells were pretreated with various cytokines befor

204 on at G2-M, and a fraction of the SW-480 and HT-29 cells were specifically arrested in mitosis.

205 HT-29 cells were subjected to 12 Gy gamma-irradiation in

206 IELs lysed more 51Cr-labeled HT-29 cells when cultured for 72 hours with IL-15 (48% +

207 in these cell lines and inhibited growth of HT-29 cells, which express wild-type PPARgamma but not H

208 bitory effect against MCF-7, MDA-MB 231, and HT-29 cells, which is more than 10-fold higher than that

209 Treatment of HT-29 cells with 15d-PGJ2 resulted in up-regulation of b

210 sal of SPARC gene suppression after treating HT-29 cells with 5-Aza.

211 Human IgA1 bound specifically to HT-29 cells with a molar ratio of 0.26 compared with asi

212 The extract inhibited the proliferation of HT-29 cells with an IC50 of 87mug/ml.

213 Transfection of HT-29 cells with an IRF-1 expression plasmid (pAct-1) tr

214 Treatment of HT-29 cells with cisplatin in the absence or presence of

215 Treatment of HT-29 cells with IL-1 beta induced expression of COX-2 m

216 Treatment of colonic epithelial HT-29 cells with IL-17 increased pIgR expression.

217 Preincubation of HT-29 cells with oltipraz enhanced the rate of removal o

218 Moreover, in HT-29 cells with silenced Foxo3a, the amount of IkappaBa

219 LPS-induced IL-8 is increased in HT-29 cells with silenced Foxo3a.

220 Treatment of HT-29 cells with the tyrosine kinase inhibitor imatinib

221 but not in HeLa cells, and the treatment of HT-29 cells with U0126 enhanced radiation sensitivity po

222 Moreover, treatment of HT-29 cells with UcnII, which binds exclusively to CRHR2

223 f gamma-oryzanol-loaded gliadin particles on HT-29 cells, with IC(50) values of 0.47 and 0.40 mg/mL f