ライフサイエンスコーパス: HT-29 cell

1 16 cells but were 22 and 4, respectively, in HT-29 cells.

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

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

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

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

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

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

8 lactosyltransferase, previously described on HT-29 cells.

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

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

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

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

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

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

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

16 125I and examined for the ability to bind to HT-29 cells.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

34 supernatants from nonpolarized and polarized HT-29 cells.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

62 18a was more potent than irinotecan against HT-29 cells and was as potent as irinotecan against A549

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

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

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

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

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

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

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

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

71 1beta and IL-8 expression in both Caco-2 and HT-29 cells as assayed by electrophoretic mobility shift

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

98 0-fold less potent MGMT inhibitor than BG in HT-29 cell extracts, these results illustrate the capaci

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

128 11B, isolated from the human colon carcinoma HT-29 cell line.

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

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

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

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

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

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

135 HT-29 cells mediated specific uptake and degradation of

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

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

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

139 HT-29 cells produce a functional apically located asialo

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

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

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

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

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

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

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

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

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

149 32P-labeling of HT-29 cells showed that the 30 KDa protein was phosphory

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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