ライフサイエンスコーパス: 5-aza-2'-deoxycytidine

1 lated tumour cell lines after treatment with 5-aza 2-deoxycytidine.

2 recovered in tumour cell lines treated with 5-aza 2-deoxycytidine.

3 n and could be restored after treatment with 5-aza-2-deoxycytidine.

4 reast tumour cell lines after treatment with 5'-aza-2'deoxycytidine.

5 ion, which was restored after treatment with 5-aza 2'-deoxycytidine.

6 vated by the DNA methyltransferase inhibitor 5-aza-2'-deoxycytidine.

7 et gene for RAs and the demethylation agent, 5-aza-2'-deoxycytidine.

8 fter inhibition of DNA methyltransferases by 5-aza-2'-deoxycytidine.

9 orated into viral DNA following reduction to 5-aza-2'-deoxycytidine.

10 ly elicited by demethylation agents, such as 5-Aza-2'-deoxycytidine.

11 be reactivated by the hypomethylating agent 5-aza-2'-deoxycytidine.

12 tin A, or a DNA methyltransferase inhibitor, 5-Aza-2'-deoxycytidine.

13 and reactivated by the demethylating agent, 5-aza-2'-deoxycytidine.

14 ell lines with the DNA methylation inhibitor 5-Aza-2'-deoxycytidine.

15 d was reactivated by the demethylating agent 5-aza-2'-deoxycytidine.

16 ion with the DNA methyltransferase inhibitor 5-aza-2'-deoxycytidine.

17 ed by treatment with DNA-demethylating agent 5-aza-2'-deoxycytidine.

18 ine xenografts by systemic administration of 5-aza-2'-deoxycytidine.

19 ssion are induced by the demethylating agent 5-aza-2'-deoxycytidine.

20 after treatment with the demethylating agent 5-Aza-2'-deoxycytidine.

21 east cancer cells with a demethylating agent 5-aza-2'-deoxycytidine.

22 ved by chemically induced demethylation with 5-aza-2'-deoxycytidine.

23 econstituted when cells were pretreated with 5-aza-2'-deoxycytidine.

24 iated cells with the DNA demethylating agent 5-aza-2'-deoxycytidine.

25 locus, was induced following treatment with 5-aza-2'-deoxycytidine.

26 fter treatment with a methylation inhibitor, 5-aza-2'-deoxycytidine.

27 significantly by treatment of the cells with 5-aza-2'-deoxycytidine.

28 after treatment with the demethylating agent 5-aza-2'-deoxycytidine.

29 sts treated with the DNA demethylating agent 5-aza-2'-deoxycytidine.

30 F-7 breast cancer cells synergistically with 5-aza-2'-deoxycytidine.

31 tro treatment with the hypomethylating agent 5-aza-2'-deoxycytidine.

32 r treatment with the DNA demethylating agent 5-aza-2'-deoxycytidine.

33 sure to AH or by the DNA demethylating agent 5-aza-2'-deoxycytidine.

34 r cell line with the DNA demethylating agent 5-aza-2'-deoxycytidine.

35 lated glioma cell lines after treatment with 5-aza-2'-deoxycytidine.

36 expressed in cell lines after treatment with 5'-aza-2'-deoxycytidine.

37 peutic potential of the demethylating agent, 5'-aza-2'-deoxycytidine.

38 es; furthermore, the DNA demethylating agent 5 aza-2'deoxycytidine (5-Aza-dC) antagonizes the effects

39 However, treatment with 5'-aza-2'-deoxycytidine (5'-aza-dC) restored IGFBP-3 exp

40 that treatment with the demethylating agent 5'-aza-2'-deoxycytidine (5-Aza-dC) significantly inhibit

41 Treatment with 5'-aza-2'-deoxycytidine (5-azaC), a DNA methyltransferas

42 sociated with gene silencing, treatment with 5'-aza-2-deoxycytidine (5'-aza-dC) (an inhibitor of DNA

43 RNA (6-fold) in human HCC cells treated with 5'aza-2'deoxycytidine (5-Aza-CdR, DNA methylation inhibi

44 reatment with epigenetic silencing modifiers 5-aza-2'-deoxycytidine (5-aza) and trichostatin A (TSA).

45 uated whether the DNA methylation inhibitor, 5-aza-2'-deoxycytidine (5-Aza) could modulate extracellu

46 ner with the DNA methyltransferase inhibitor 5-aza-2'-deoxycytidine (5-aza), 0 of 14 mice developed p

47 ), and of HCT-116 colonocytes incubated with 5-aza-2'-deoxycytidine (5-AZA).

48 ent with the DNA methyltransferase inhibitor 5-aza-2'-deoxycytidine (5-aza-CdR) and the histone deace

49 DNA methylation inhibitors such as 5-aza-2'-deoxycytidine (5-Aza-CdR) are currently used fo

50 PTX with the DNA methyltransferase inhibitor 5-Aza-2'-deoxycytidine (5-aza-CdR) induced higher levels

51 mor cell lines MDA-MB-231 and UACC 1179 with 5-aza-2'-deoxycytidine (5-aza-CdR) induced transcription

52 The DNA methyltransferase inhibitor 5-aza-2'-deoxycytidine (5-aza-CdR) inhibits DNA methyltr

53 and Molt 3, with the methylation inhibitor, 5-aza-2'-deoxycytidine (5-aza-CdR) resulted in increased

54 5-Aza-2'-deoxycytidine (5-aza-CdR), an inhibitor of DNA

55 Treatment of prostate cancer cell lines with 5-aza-2'-deoxycytidine (5-Aza-CdR), an inhibitor of DNA

56 Decitabine, or 5-aza-2'-deoxycytidine (5-aza-CdR), is a well-characteri

57 Treatment with 5-aza-2'-deoxycytidine (5-Aza-CdR), previously known for

58 ysiological levels to low doses of the DNMTi 5-aza-2'-deoxycytidine (5-aza-CdR), there is a synergist

59 t was decreased by the methylation inhibitor 5-aza-2'-deoxycytidine (5-aza-CdR).

60 tic target of methylation inhibitors such as 5-Aza-2'-deoxycytidine (5-Aza-CdR).

61 ncer cell lines with the methylase inhibitor 5-aza-2'-deoxycytidine (5-aza-CdR).

62 ent with the DNA methyltransferase inhibitor 5-aza-2'-deoxycytidine (5-aza-CdR).

63 The nucleoside analog 5-aza-2'-deoxycytidine (5-aza-CdR, decitabine) is a pote

64 ment of these cells with demethylating agent 5-aza-2'-deoxycytidine (5-aza-dC) increased mRNA levels

65 ent with the DNA methyltransferase inhibitor 5-aza-2'-deoxycytidine (5-aza-dC) increases the expressi

66 5-Aza-2'-deoxycytidine (5-aza-dC) is a nucleoside analog

67 with the DNA demethylating nucleoside analog 5-AZA-2'-deoxycytidine (5-AZA-dC) synergistically augmen

68 , showed induction of ABCG2 expression after 5-aza-2'-deoxycytidine (5-aza-dC) treatment, suggesting

69 ponents was restored with either IFNgamma or 5-aza-2'-deoxycytidine (5-aza-dC) treatment.

70 on dependency of silencing was determined by 5-aza-2'-deoxycytidine (5-aza-dC) treatment.

71 , treatment with the DNA demethylating agent 5-aza-2'-deoxycytidine (5-Aza-dC) was sufficient to reac

72 We thus determined the role of 5-aza-2'-deoxycytidine (5-Aza-dC), an inhibitor of DNA m

73 ore, treatment with the demethylating agent, 5-Aza-2'-deoxycytidine (5-Aza-dC), restored TSP-1 expres

74 Using the methylation inhibitor 5-aza-2'-deoxycytidine (5-aza-dC), we investigated wheth

75 CRC) cell lines with or without treatment of 5-aza-2'-deoxycytidine (5-aza-dC).

76 nes with the DNA methyltransferase inhibitor 5-Aza-2'-deoxycytidine (5-aza-dC).

77 iminate use of demethylating agents, such as 5-aza-2'-deoxycytidine (5-Aza-dC).

78 east cancer cells with demethylating agents [5-aza-2'-deoxycytidine (5-aza-dC)] and histone deacetyla

79 and DNMT3B and pharmacologic inhibition with 5-Aza-2'-deoxycytidine (5-Aza-dC, decitabine) to demonst

80 A (TSA), a histone deacetylase inhibitor, or 5-aza-2'-deoxycytidine (5-AzaC), a DNA methyltransferase

81 aP(CS) and PC-3 with the demethylating agent 5-aza-2'-deoxycytidine (5-AZAdC) reactivated PMP24 mRNA

82 by methylation, the DNA demethylating agent 5-aza-2'-deoxycytidine (5-AZAdC) was assessed.

83 /activated status induced in normal cells by 5-aza-2'-deoxycytidine (5-azadC) was mimicked by conditi

84 l human bronchial epithelial cells following 5-aza-2'-deoxycytidine (5-azadC), Depsipeptide FK228 (DP

85 sing nucleoside analogs of cytosine, such as 5-aza-2'-deoxycytidine (5-azadC).

86 Treatment of cells with 5-aza-2'deoxycytidine (5-aza-dC) increases CDKN2A expres

87 The DNA methyltransferase inhibitor, 5-Aza-2'deoxycytidine (5-AzaCdR) is an approved epigenet

88 Previous studies have shown that 5-Aza-2'deoxycytidine (5-AzadC), a DNMT1 inhibitor, indu

89 Treatment with either 5-Aza-2-deoxycytidine (5-Aza) or trichostatin A (TSA) wa

90 fter treatment with trichostatin A (TSA) and 5-Aza-2-deoxycytidine (5-Aza).

91 ated with a DNA methyltransferase inhibitor, 5-Aza-2-deoxycytidine (5-Aza-2dC), and an RAW294.7 cell

92 The DNA-demethylating drug 5-Aza-2-deoxycytidine (5-azadC) induced rapid nuclear ac

93 which have no detectable TFPI-2 expression, 5-aza-2'-deoxycytidine (5aC), an inhibitor of DNA methyl

94 permethylated genes following treatment with 5'-aza 2'-deoxycytidine (5Aza-dC).

95 reduction of DNMT with either the inhibitor 5-aza-2'-deoxycytidine (5Aza) or siRNA markedly reduced

96 after treatment with the demethylating agent 5-aza-2'-deoxycytidine (5Aza-dC) and/or the histone deac

97 r, the use of DNA-demethylating agents (e.g. 5-aza-2'-deoxycytidine (5aza-dC)) to study epigenetic re

98 eously immortal Li-Fraumeni fibroblasts with 5-aza-2'-deoxycytidine (5AZA-dC), an inhibitor of DNA me

99 upled it with a cell based loss-of-function (5-Aza-2'-deoxycytidine (5Aza-dC)-induced senescence bypa

100 Demethylation treatment with 5-aza-2'-deoxycytidine (5aza2dc) increased the sensitivi

101 xpressing reduced gamma-catenin protein with 5-aza-2'-deoxycytidine (5aza2dc), a DNA methylation inhi

102 5-Aza-2'-deoxycytidine (5azaC-dR) has been employed as a

103 However, we have developed a strategy using 5-aza-2'-deoxycytidine (5azaD) and trichostatin A (TSA),

104 4+ cells with the chromatin-modifying agents 5-aza-2'-deoxycytidine (5azaD) and trichostatin A (TSA),

105 ) cells with the chromatin-modifying agents, 5-aza-2'-deoxycytidine (5azaD) and trichostatin A (TSA).

106 DNA methyltransferase inhibitor, decitabine [5-aza-2'-deoxycytidine (5azaD)], followed by the histone

107 ut not normal CD34(+) cells with decitabine (5-aza-2'-deoxycytidine [5azaD]), followed by suberoylani

108 rone (DHT) and the DNA methylation inhibitor 5'-aza-2'-deoxycytidine (5AzadC) were introduced into th

109 5-Aza-2'-deoxycytidine (5azadC) inhibits DNA methyltrans

110 ls with the DNA methyltransferase inhibitor, 5-aza-2'-deoxycytidine (5azadC).

111 the AM cell line (MHS) after treatment with 5-aza-2'-deoxycytidine (a methyltransferase inhibitor).

112 press Lhx3 (Pit-1/0 cells) were treated with 5-aza-2'-deoxycytidine, a demethylating reagent.

113 Treatment with 5-aza-2'-deoxycytidine, a demethylation agent, and knock

114 Our reporter assays and gene reactivation by 5-aza-2'-deoxycytidine, a DNA demethylating agent, show

115 s of tetradecanoyl phorbol acetate (TPA) and 5-aza-2'-deoxycytidine, a DNA methyltransferase inhibito

116 In vitro methylation of MAO B promoter with 5-aza-2'-deoxycytidine, a DNA methyltransferase inhibito

117 Treatment with 5-aza-2'-deoxycytidine, a methyltransferase inhibitor, c

118 yltransferase inhibitors, 5'-azacytidine and 5'-aza-2'-deoxycytidine, activated basal expression leve

119 h the DNA methyltransferase (DNMT) inhibitor 5-aza-2'-deoxycytidine (ADC) to reactivate DNA methylati

120 ce treated with the DNA demethylating agent, 5-aza-2'-deoxycytidine, after UVB exposure.

121 with 10 muM DNA-methyltransferase inhibitor 5-aza-2'-deoxycytidine, again correlating with increased

122 ptide or the DNA methyltransferase inhibitor 5-aza-2'-deoxycytidine alone or concomitantly did not re

123 that manipulating MGPC DNA methylation with 5-aza-2'-deoxycytidine altered their properties.

124 antly, treatment of immortal cell lines with 5-aza-2'-deoxycytidine, an inhibitor of DNA methyltransf

125 reduced LIF responsiveness were treated with 5-aza-2'-deoxycytidine, an inhibitor of DNA methyltransf

126 Treatment with 5-aza-2'-deoxycytidine, an inhibitor of DNA methyltransf

127 bination of DNA methyl transferase inhibitor 5-Aza 2-deoxycytidine and histone deacetylase inhibitor

128 after treatment with the demethylating drug 5-aza-2 deoxycytidine and histone deacetylation inhibiti

129 ot CXCR4 or SOX17, was strongly inhibited by 5-aza-2'-deoxycytidine and by knockdown of DNMT3b.

130 5-Aza-2'-deoxycytidine and diesel exhaust particle expos

131 ar responses to the DNMT and HDAC inhibitors 5-Aza-2'-deoxycytidine and suberoylanilide hydroxamic ac

132 ation and histone deacetylation because both 5-aza-2'-deoxycytidine and trichostatin A partially resc

133 demonstrating that promoter demethylation by 5-aza-2'-deoxycytidine and trichostatin A reactivated TI

134 is, we identified >160 genes up-regulated by 5-aza-2'-deoxycytidine and trichostatin A treatment.

135 cell line UACC3199 following treatment with 5-aza-2'-deoxycytidine and trichostatin A.

136 reatment with the DNA methylation inhibitors 5-aza-2'-deoxycytidine and zebularine as well as DNA met

137 Treatment with the DNA demethylating agent 5-aza-2'-deoxycytidine and/or the histone deacetylase in

138 l lines with the methyltransferase inhibitor 5-aza-2-deoxycytidine and the histone deacetylase inhibi

139 and Jurkat) before and after treatments with 5-aza-2-deoxycytidine and trichostatin A.

140 etic repression of PDLIM2 can be reversed by 5-aza-2-deoxycytidine and vitamin D to suppress KSHV-ass

141 ed when Neuro2A cells were demethylated with 5-aza-2'-deoxycytidine, and increasing Sp3 levels in Sch

142 DNA-hypomethylating agents 5-azacytidine and 5-aza-2'-deoxycytidine are effective treatments for pati

143 ed by treatment with the demethylating agent 5-aza-2'-deoxycytidine as well as by down-modulation of

144 te using the DNA methyltransferase inhibitor 5-aza-2'-deoxycytidine (Aza) induced acetylation of hist

145 0.01) increase in expression after 2 days of 5-aza-2'-deoxycytidine (AZA) treatment and a significant

146 ecific genetic Xist ablation with short-term 5-aza-2'-deoxycytidine (Aza) treatment models the synerg

147 Our purpose was to investigate whether 5-aza-2'-deoxycytidine (Aza), a DNA methyltransferase (D

148 Treatment with 5-aza-2'-deoxycytidine (AZA), a DNA methyltransferase in

149 s natively methylated, and subjected them to 5-aza-2'-deoxycytidine (Aza-C) treatment.

150 shock, but rather by the demethylating agent 5-aza-2'-deoxycytidine (Aza-C).

151 but not hexamethylene bisacetamide (HMBA) or 5-aza-2'-deoxycytidine (Aza-CdR), reactivate latent HIV-

152 d selectively bind to genomic DNA containing 5-aza-2'-deoxycytidine (aza-dC) in vivo.

153 The DNA methylation inhibitor, 5-aza-2'-deoxycytidine (aza-dC) increases collagen gene

154 MIS increases p16 protein levels, and 5'-Aza-2'-deoxycytidine (AzadC) induces p16 mRNA; theref

155 treatment, and combined treatment of TSA and 5-aza-2'-deoxycytidine (AzadC) synergistically induced e

156 B cells with the methyltransferase inhibitor 5-aza-2'-deoxycytidine before and at early stages of rep

157 The addition of 5-aza-2'-deoxycytidine blocked the hypoxia-induced incre

158 permethylated, and the DNA methylation agent 5'-aza-2'-deoxycytidine, but not the histone deacetylase

159 ls with the DNA methyltransferase inhibitor, 5-aza-2'-deoxycytidine, caused a dramatic increase in KI

160 Treatment of cells with 5-aza-2'-deoxycytidine causes restoration of Cosmc trans

161 and treatment with the methylation inhibitor 5-Aza-2'-deoxycytidine could partially restore ASIC2 exp

162 460 lung cancer cells mediated by sequential 5-aza 2'-deoxycytidine (DAC)/depsipeptide FK228 (DP) exp

163 ent with the DNA methyltransferase inhibitor 5-aza-2'-deoxycytidine (DAC) activates CYP24A1 expressio

164 eating lung cancer cell lines using low-dose 5-aza-2'-deoxycytidine (DAC) caused an accumulation of p

165 s cancer, we used the DNA demethylating drug 5-aza-2'-deoxycytidine (DAC) in an aggressive mouse mode

166 5-aza-2'-deoxycytidine (DAC) is approved for the treatme

167 hese cell lines with the demethylating agent 5-aza-2'-deoxycytidine (DAC) up-regulated SOCS-1 express

168 Treatment with a demethylating agent, 5-aza-2'-deoxycytidine (DAC), restored IL-6 induction of

169 0 cell line with the DNA demethylating agent 5-aza-2'-deoxycytidine (DAC)-enhanced HER4 expression, c

170 combination with the DNA-demethylating agent 5-aza-2'-deoxycytidine (DAC).

171 enocarcinoma cell lines after treatment with 5-aza-2'-deoxycytidine (DAC).

172 5 in cancer cells by three epigenetic drugs: 5-aza-2'-deoxycytidine (DAC; decitabine), arsenic trioxi

173 ation experiments of two CC cell lines using 5-aza-2'deoxycytidine (DAC) treatment.

174 lines treated with the methylation inhibitor 5-aza-2'deoxycytidine (DAC), where we found a 1-16% decr

175 cted a phase 1/2 study of the combination of 5-aza-2'-deoxycytidine (decitabine) and the histone deac

176 n in AML cell lines and patient blasts using 5-aza-2'-deoxycytidine (decitabine) and trichostatin A i

177 The cytidine analogues azacytidine and 5-aza-2'-deoxycytidine (decitabine) are commonly used to

178 s by 5-azacytidine (Vidaza) and its congener 5-aza-2'-deoxycytidine (decitabine) has provided an alte

179 The cytosine analog 5-aza-2'-deoxycytidine (decitabine) hypomethylates DNA b

180 The DNA methyltransferase inhibitor 5-aza-2'-deoxycytidine (decitabine) induces DNA demethyl

181 5-Aza-2'-deoxycytidine (decitabine) is postulated to hav

182 Lung cancer cells are sensitive to 5-aza-2'-deoxycytidine (decitabine) or midostaurin (PKC4

183 e CpG island methylation, and treatment with 5-aza-2'-deoxycytidine (decitabine) resulted in up-regul

184 , led to widespread use of 5-azacytidine and 5-aza-2'-deoxycytidine (Decitabine) to demonstrate the c

185 the efficacy of arsenic trioxide (As2O3) or 5-aza-2-deoxycytidine (decitabine) alone and in combinat

186 Treatment with the DNA methylation inhibitor 5-aza-2'-deoxycytidine decreased cell proliferation, gro

187 ce with low doses of the demethylating agent 5-aza-2'-deoxycytidine decreased the incidence of neopla

188 5-Aza-2'-deoxycytidine decreased, whereas folate-deplete

189 Sequential 5-aza-2'deoxycytidine/depsipeptide FK228 treatment marke

190 chromatin modulation with trichostatin A or 5-aza-2'-deoxycytidine elevates USP9X expression in huma

191 Treatment of NPD cell lines with 5-aza-2'-deoxycytidine enhanced the expression of the pa

192 Furthermore, the DNA demethylating agent 5-aza-2-deoxycytidine failed to upregulate GAS5-AS1 in N

193 after treatment of cells with retinoic acid, 5-aza-2'-deoxycytidine, folate-depleted/high-methionine

194 Last, sequential treatment with 5-aza-2'-deoxycytidine followed by zebularine hindered t

195 ent with the DNA methyltransferase inhibitor 5-aza-2'-deoxycytidine for 5 days restored TIG1 expressi

196 sing ChIP-chip analysis, Trichostatin A, and 5-aza-2'-deoxycytidine further support an epigenetically

197 However, 5-aza-2'-deoxycytidine had no effect on the inflammatory

198 sferase inhibitors (DNMTi) 5-azacytidine and 5-aza-2-deoxycytidine have been approved for the treatme

199 Treatment with 5'-aza-2'-deoxycytidine in a murine bleomycin-induced pu

200 macologic inhibition of DNA methylation with 5-aza-2'-deoxycytidine in combination with restoration o

201 These sites were screened by treatment with 5-aza-2'-deoxycytidine in four TN and five non-TNBC cell

202 or, Bob1 (OCA-B, OBF-1), were reactivated by 5-aza-2'-deoxycytidine, indicating that gene silencing i

203 evels in BT549 and MDA-MB-231 cells, whereas 5'-aza-2'-deoxycytidine induced expression in MDA-MB-231

204 Treatment with the DNA hypomethylating agent 5-aza-2'-deoxycytidine induced and up-regulated the mRNA

205 5-Aza-2'-deoxycytidine induced demethylation of several

206 Treatment of cells with 30 mumol/L 5-aza-2'-deoxycytidine induced Gal-3 mRNA and protein ex

207 methylation, rather than genomic deletion as 5-aza-2'-deoxycytidine induced reactivation of DLC-1 exp

208 onexpressing cells and of T-cell clones with 5-aza-2'deoxycytidine induced IL-1alpha expression in th

209 The DNA methylase inhibitor, 5-aza-2'-deoxycytidine, induced KIR DNA hypomethylation

210 of AtT20 cells with the demethylating agent, 5-Aza-2'-deoxycytidine, induced the re-expression of thi

211 43B osteosarcoma cells with decitabine (DAC, 5-Aza-2'-deoxycytidine) induces expression of ERalpha an

212 Moreover, zebularine and 5-aza-2-deoxycytidine, inhibitors of DNMT activity, bloc

213 Decitabine (5-aza-2'-deoxycytidine) inhibits DNA methylation and has

214 therapy, the demethylating drug decitabine (5-aza-2'-deoxycytidine) is increasingly used to treat ac

215 One such molecule is 5,6-dihydro-5-aza-2'-deoxycytidine (KP1212), a selective mutagen tha

216 Treatment of HepG2 cells with 5-aza-2'-deoxycytidine led to partial demethylation of t

217 of DNA methyltransferase (Dnmt) enzymes with 5-aza-2'-deoxycytidine or genetic ablation of both Dnmt1

218 ferentiated cells, exposure of DAOY cells to 5-aza-2'-deoxycytidine or their growth as stem cell-like

219 sed and hypomethylated genes, treatment with 5-aza-2'-deoxycytidine or with trichostatin A, either al

220 ld also be induced by a demethylating agent (5'-aza-2'-deoxycytidine) or histone deacetylase inhibito

221 Treatment with methylation (5-aza-2'-deoxycytidine) or deacetylation (trichostatin A

222 d with inhibition of methylation with either 5-Aza-2-Deoxycytidine, or siRNA to DNA Methyltransferase

223 Treatment with 5-aza-2'-deoxycytidine partially reactivated ARHI expres

224 (GSK126), or the DNA methylation inhibitor, 5-Aza-2'-deoxycytidine, partially restored miR-34a level

225 vation of the methylation-dependent genes by 5-aza-2'-deoxycytidine plus trichostatin A revealed a fu

226 upregulated by DNA demethylation induced by 5-aza-2'-deoxycytidine plus trichostatin A treatment and

227 ent with the DNA methyltransferase inhibitor 5'-aza-2'-deoxycytidine promoted demethylation of the OP

228 ent with the DNA methyltransferase inhibitor 5-aza-2'-deoxycytidine rapidly decreased the level of H3

229 tin A, but not the DNA methylation inhibitor 5'-aza-2'-deoxycytidine, re-established the expression o

230 y the data that demethylation of promoter by 5-aza-2'-deoxycytidine reactivated Betaig-h3 and restore

231 vitro treatment with the demethylating agent 5-aza-2'-deoxycytidine reactivated CRBP1 expression.

232 n and treatment with the demethylating agent 5-aza-2'-deoxycytidine reactivated SLIT2 gene expression

233 linical samples (P=0.004) and treatment with 5-aza-2'-deoxycytidine reactivated Spry2 expression in L

234 tment of KYSE220 ESCC and BIC EAC cells with 5-aza-2'-deoxycytidine reduced NELL1 methylation and inc

235 h the DNA methyltransferase (DNMT) inhibitor 5-aza-2'-deoxycytidine reduces cytosine methylation of t

236 l lines treated with the demethylating agent 5-AZA-2'-deoxycytidine reexpressed IGFBP3 at the mRNA an

237 melanoma cells with the demethylating agent 5-aza-2'-deoxycytidine reinduces Rap1GAP expression, fol

238 unoglobulin G (anti-IgG), and, surprisingly, 5-aza-2'-deoxycytidine require short exposures of 15 min

239 DEC with the DNA methyltransferase inhibitor 5-aza-2'-deoxycytidine restored calcitriol-mediated indu

240 The demethylating agent 5-aza-2'-deoxycytidine restored caspase-8 expression and

241 Treatment with 5-aza-2'-deoxycytidine restored expression; dense methyl

242 xposure to the chromatin demethylating agent 5-aza-2'-deoxycytidine restored HSPA1A expression.

243 eatment of SMCs with the demethylating agent 5-aza-2'-deoxycytidine restored MCT3 expression and norm

244 nes with the DNA methyltransferase inhibitor 5-aza-2'-deoxycytidine restored PDLIM2 expression and re

245 Treatment with 5-aza-2'-deoxycytidine restored RA response in two of th

246 whereas the DNA methyltransferase inhibitor 5-aza-2'-deoxycytidine restored the down-regulation of E

247 In vitro treatment of NK cells with 5-aza-2'-deoxycytidine restored the IL-2 signaling pathw

248 cells and treatment with demethylating agent 5-aza-2-deoxycytidine restored DOC2B expression.

249 Treatment with the DNA hypomethylating agent 5-aza-2-deoxycytidine restored the ability of Tyk2(-/-)

250 cell lines with a DNA methylation inhibitor, 5-aza-2' deoxycytidine, restored hypoxia-induced BNIP3 e

251 ethylated at CpG islands, and treatment with 5'-aza-2'-deoxycytidine restores near-normal levels of m

252 ation by the DNA methyltransferase inhibitor 5'-aza-2'-deoxycytidine restores SP1 binding and STAT5A

253 Moreover, treatment with 5-aza-2'-deoxycytidine restores WIF-1 expression.

254 ersed by the DNA methyltransferase inhibitor 5-aza-2'-deoxycytidine, restoring both SOD2 expression a

255 Treatment of myeloid cell lines with 5-aza-2'-deoxycytidine resulted in a significant decreas

256 tment of methylated/silenced cell lines with 5-aza-2'-deoxycytidine resulted in gene re-expression.

257 5-Aza-2'-deoxycytidine resulted in increased Cables expr

258 ating macrophages with methylation inhibitor 5-Aza-2'-deoxycytidine resulted in increased levels of I

259 f the cell lines with the demethylating drug 5-aza-2'-deoxycytidine resulted in increased LXN express

260 Treatment of OV207 and SKOV3 by 5-aza-2'-deoxycytidine resulted in increased transcripti

261 Blocking methylation by treatment with 5-aza-2'-deoxycytidine resulted in reduced H3K4me3 bindi

262 Treatment with 5-Aza-2'-deoxycytidine resulted in restoration of gene t

263 Treatment with the demethylating agent 5-aza-2'-deoxycytidine resulted in TIMP-2 upregulation i

264 ression with the methyltransferase inhibitor 5-aza-2'deoxycytidine resulted in partial demethylation

265 ells with a DNA methyltransferase inhibitor, 5-aza-2'-deoxycytidine, resulted in lower methylation an

266 exon 1 hypermethylation, is re-expressed by 5-aza-2'deoxycytidine resulting in the restoration of a

267 d HBECs treated with the demethylating agent 5-aza-2'deoxycytidine revealed miR-196b and miR-34c-5p t

268 lls with the DNA methyltransferase inhibitor 5-aza-2'-deoxycytidine reverses the methylation of the P

269 eatment with the methyltransferase inhibitor 5-aza-2'-deoxycytidine, suggesting a role for DNA methyl

270 on1a and PLCepsilon1b by demethylating agent 5-aza-2'-deoxycytidine, suggesting epigenetic silencing

271 ated with a DNA methyltransferase inhibitor, 5-Aza-2'-Deoxycytidine, the APC expression in these cell

272 Upon extended growth in the absence of 5-aza-2'-deoxycytidine, the cells exhibit partial revers

273 SC-22 deregulation was reversed in vivo by a 5-aza-2'-deoxycytidine therapy of T or NK LGL leukemia,

274 ; when treated with the demethylating agent, 5-aza-2'-deoxycytidine, these five cell lines all showed

275 Combined with the induction of revertants by 5-aza-2'-deoxycytidine, this result suggested that stabi

276 -tuneable version of a clinically used drug (5-aza-2'-deoxycytidine) to alter the catalytic activity

277 )1 and DNMT3b3 proteins were undetectable in 5-Aza-2'-deoxycytidine-treated and untreated nondividing

278 We profiled mRNAs in control and 5-aza-2'-deoxycytidine-treated parents and allotetraploi

279 -G transcriptional activity was dependent of 5-aza-2'-deoxycytidine treatment and enhanced by interfe

280 tumors and cancer cell lines but induced by 5-aza-2'-deoxycytidine treatment in a dose-dependant man

281 We show that 5-aza-2'-deoxycytidine treatment not only reactivates ge

282 WIF1 re-expression upon 5-aza-2'-deoxycytidine treatment or WIF1 gene transfer i

283 ypomethylation of these promoters induced by 5-aza-2'-deoxycytidine treatment reactivated or enhanced

284 The 5-aza-2'-deoxycytidine treatment restored MB-COMT expres

285 5-aza-2'-deoxycytidine treatment resulted in demethylati

286 Gene expression analyses and 5-aza-2'-deoxycytidine treatment showed that promoter hy

287 tion in 25% to 93% of the HNSCC samples, and 5-aza-2'-deoxycytidine treatment was able to restore exp

288 C tumor samples, and DNA demethylation using 5-aza-2'-deoxycytidine treatment was able to significant

289 5-Aza-2'-deoxycytidine treatment, bisulfite DNA sequenci

290 s DNA demethylated and reexpressed following 5-aza-2'-deoxycytidine treatment, H3K9me1 and H3K9me2 ar

291 After 5-aza-2'-deoxycytidine treatment, increased expression o

292 ced HLA-G transcriptional activity following 5-aza-2'-deoxycytidine treatment.

293 (n = 15) and 9% of NSCLCs (n = 11), whereas 5-aza-2'deoxycytidine treatment restored CAV1 expression

294 gastric cancer (IGC) cell lines treated with 5-aza-2'-deoxycytidine using microarrays containing 22,2

295 Importantly, when 5-aza-2'-deoxycytidine was combined with the histone dea

296 lowing treatment with a demethylating agent, 5-aza-2'-deoxycytidine, was shown.

297 Using 5-aza-2'-deoxycytidine, we show that DNA methylation is

298 The DNA methyltransferase inhibitor 5-aza-2'-deoxycytidine, which inhibits DNA methylation,

299 lls with the DNA methyltransferase inhibitor 5-aza-2'-deoxycytidine, which reduced DNA methylation fr

300 Treating Jurkat T cells with 5-aza-2'-deoxycytidine, which reduced DNA methylation, i