ライフサイエンスコーパス: 5-azacytidine

1 s, which could be reversed by treatment with 5-azacytidine.

2 d by growth in the DNA methylation inhibitor 5-azacytidine.

3 was also achieved by treatment of cells with 5-Azacytidine.

4 sion on treatment with a demethylating drug, 5-azacytidine.

5 e presence of ribavirin and another mutagen, 5-azacytidine.

6 ed by treatment with the demethylating agent 5-azacytidine.

7 after treatment with the demethylating agent 5-azacytidine.

8 chostatin A or the DNA methylation inhibitor 5-azacytidine.

9 h all reexpressed hMLH1 after treatment with 5-azacytidine.

10 fter the addition of the demethylating agent 5-azacytidine.

11 leles, both of which could be reactivated by 5-azacytidine.

12 ression by the inhibitor of DNA methylation, 5-azacytidine.

13 dium butyrate or trichostatin A but not with 5-azacytidine.

14 ed by treatment with the demethylating agent 5-azacytidine.

15 methylating agents, 5-azacytidine or 2-deoxy-5-azacytidine.

16 nd 5 controls with the hypomethylating agent 5-azacytidine.

17 d was significantly decreased in response to 5-azacytidine.

18 ntiation of MSCs in culture was induced with 5-azacytidine.

19 lls was restored with a demethylation agent, 5-azacytidine.

20 pression of GADD45alpha or pretreatment with 5-azacytidine.

21 t epithelial cells by the demethylating drug 5-azacytidine.

22 A, but not with the DNA demethylation agent, 5-azacytidine.

23 ells, treatment with the demethylating agent 5-azacytidine (10 microM for 6 days) did not activate CY

24 tment of AML blasts with decitabine (DAC) or 5-azacytidine, 2 hypomethylating agents that show effica

25 division, we find that the 3 drugs studied, 5-azacytidine (5 micromol/L), hydroxyurea (40 micromol/L

26 mRNA, and treatment of these cell lines with 5-azacytidine (5-AC), a demethylation reagent, induced p

27 o heavy metals only after demethylation with 5-azacytidine (5-AsaC).

28 5-azacytidine (5-Aza) is a potent inducer of fetal hemog

29 Cells primed to produce IFN by 5-azacytidine (5-aza) underwent endoplasmic reticulum (E

30 5-Azacytidine (5-Aza), a DNA demethylating agent, induce

31 rs by treatment with the demethylating agent 5-azacytidine (5-Aza).

32 LNCaP PCA cells: treatment of the cells with 5-azacytidine (5-aza-C), an inhibitor of DNA methyltrans

33 rapped when conducted on the cytosine analog 5-azacytidine (5-aza-C).

34 a few CpG dinucleotides by brief exposure to 5-azacytidine (5-AzaC) but persisted even after prolonge

35 ently, TSA and the DNA demethylating reagent 5-azacytidine (5-AzaC) caused marked synergistic activat

36 The cytosine analog 5-azacytidine (5-AzaC) is a demethylating agent that is

37 5-Azacytidine (5-azaC) is an azanucleoside approved for

38 thylation and that the methylation inhibitor 5-azacytidine (5-AzaC) potently blocks the increased cel

39 MDAMB468 with the DNA methylation inhibitor, 5-azacytidine (5-AzaC) results in growth arrest, whereas

40 oic acid (VPA) and DNA methylation inhibitor 5-azacytidine (5-azaC) specifically reversed the repress

41 Following 5-azacytidine (5-azaC) treatment of siJKA, aberrant RNA

42 lites, such as the DNA-hypomethylating agent 5-azacytidine (5-AzaC), have been shown to lower maligna

43 by heavy metals only after demethylation by 5-azacytidine (5-AzaC).

44 Within this study, 5-azacytidine (5-azaC, a DNMT inhibitor) was used as a p

45 e also demonstrate resistance to the mutagen 5-azacytidine (5-AZC) and decreased accumulation of muta

46 iral mechanism for the ribonucleoside analog 5-azacytidine (5-AZC).

47 1 (HIV-1) by use of chemical mutagens [i.e., 5-azacytidine (5-AZC)] as well as by host factors with m

48 lar activity of the 5-azacytidine derivative 5-azacytidine-5'-elaidate (CP-4200), a nucleoside transp

49 eviated by preventing methylation, either by 5-azacytidine (5AC) treatment or by introduction of a mu

50 s been treated with the demethylating agent, 5-azacytidine (5aC).

51 methyl-N'-nitro-N-nitrosoguanidine (NTG) and 5-azacytidine (5AZ).

52 ites of action (methotrexate, actinomycin D, 5-azacytidine, 8-thioguanosine).

53 Treatment with 5-azacytidine, a demethylating agent, causes Th2 cells t

54 Treatment of the hepatoma bearing rats with 5-azacytidine, a demethylating agent, induced basal as w

55 ment of two of the resistant cell lines with 5-azacytidine, a known inhibitor of methylation, results

56 Treatment with 5-azacytidine, a methylation inhibitor, partially revers

57 ment of two clonal lines of Ku-80 cells with 5-azacytidine, a potent DNA demethylating agent, rendere

58 posure of proliferating 10T1/2 stem cells to 5-azacytidine, a potent DNA methylation inhibitor, gave

59 ansplanted hepatoma after demethylation with 5-azacytidine, a potent inhibitor of DNA methyltransfera

60 Decitabine, but not 5-azacytidine, also produced a G(2)/M cell-cycle arrest

61 5'-Azacytidine, an inhibitor of DNA methylation that der

62 le in the sibling cultures by treatment with 5-azacytidine, an inhibitor of DNA methylation, and the

63 as relieved upon treatment of the cells with 5-azacytidine, an inhibitor of DNA methyltransferase, wi

64 e with the DNA methyltransferase inhibitors, 5'-azacytidine and 5'-aza-2'-deoxycytidine, activated ba

65 Treatment of breast cancer MCF7 cells with 5'azacytidine and Trichostatin A resulted in expression

66 ng genes that affect drug sensitivity, using 5-azacytidine and 2'-deoxy-5-azacytidine (DAC, decitabin

67 ed DNA methylation, led to widespread use of 5-azacytidine and 5-aza-2'-deoxycytidine (Decitabine) to

68 The DNA-hypomethylating agents 5-azacytidine and 5-aza-2'-deoxycytidine are effective t

69 h concentrations of the pyrimidine analogues 5-azacytidine and 5-azacytosine.

70 Except for 5-azacytidine and 8-thioguanosine, all compounds examine

71 tly, cytosine arabinoside, ethidium bromide, 5-azacytidine and aspirin all significantly reduced the

72 s demonstrating that drugs like hydroxyurea, 5-azacytidine and butyric acid each yielded increases in

73 lls with the DNA methyltransferase inhibitor 5-azacytidine and comparing gene expression with oligonu

74 Together, 5-azacytidine and decitabine exert growth-inhibitory and

75 mined the effects of 2 demethylating agents, 5-azacytidine and decitabine on growth and survival of n

76 pleted a minimum of 4 cycles of therapy with 5-azacytidine and entinostat.

77 n response to both methylation inhibition by 5-azacytidine and exposure to Pseudomonas aeruginosa lip

78 tomatoes to the methyltransferase inhibitor 5-azacytidine and find that they ripen prematurely.

79 The cellular toxicity of 5-azacytidine and its DNA demethylating activity were st

80 the mutational specificity of two mutagens, 5-azacytidine and N-methyl-N'-nitro-N-nitroso-guanidine.

81 ted with 2 DNA methyltransferase inhibitors (5-azacytidine and procainamide) and 3 ERK pathway inhibi

82 ith active lupus and in T cells treated with 5-azacytidine and procainamide.

83 med using two additional nucleoside analogs, 5-azacytidine and ribavirin.

84 in the presence of the epigenetic modifiers 5-azacytidine and suberoyl bis-hydroxamic acid and under

85 A combination of the DNMT inhibitor 5-azacytidine and the HDAC inhibitor butyrate markedly r

86 AML) patients enrolled in a phase 1 trial of 5-azacytidine and the histone deacetylase inhibitor enti

87 s had relapsed disease or were refractory to 5-azacytidine and/or lenalidomide, and 3 had received in

88 s using three nucleoside analogs, ribavirin, 5-azacytidine, and 5-fluorouracil.

89 of cNJ101 cells with a demethylating agent, 5-azacytidine, and a histone deacetylase inhibitor, tric

90 was achieved using the demethylating agent, 5-azacytidine, and the HDAC inhibitor, valproic acid.

91 5-Azacytidine- and 5-aza-deoxycytidine (5-aza-CdR)-media

92 Finally, we identified 5'-azacytidine as a new P-TEFb-releasing agent.

93 Patients received 5-azacytidine (AZA) 75 mg/m(2) intravenously daily for 7

94 5-Azacytidine (AZA) is a nucleoside analog that is used

95 w correlation (R = 0.44, P = .11) to that of 5-azacytidine (AZA), but a good correlation to that of c

96 ls using the DNA methyltransferase inhibitor 5-azacytidine (Aza).

97 in vivo antitumorigenic actions of the DNMTi 5-azacytidine (AZA).

98 5-Azacytidine (aza-C) and its derivatives are cytidine a

99 Anticancer drug 5-azacytidine (aza-C) induces DNA-protein cross-links (D

100 ibiting DNA methyltransferase activity using 5-azacytidine (Aza; a cytosine analog) to limit HSV-1-in

101 rse transcriptase activity was produced with 5-azacytidine (AzaC) and with 5'-iodo-2'-deoxyuridine (I

102 f R2 seedlings germinated in the presence of 5-azacytidine (AzaC) were herbicide-resistant and also c

103 (TGF-beta) cytokine, a demethylating agent (5-azacytidine), B cell receptor engagement with anti-IgG

104 derived by treating 10T1/2 fibroblasts with 5-azacytidine, but not in parental 10T1/2 cells.

105 that clinically relevant, nontoxic doses of 5-azacytidine can restore erythropoietin production and

106 Treatment of LNCaP-LN3 cells with 5'-azacytidine caused re-expression of LDHB transcripts.

107 te that gemcitabine and doxorubicin (but not 5-azacytidine, cis-platinum, or 5-fluorouracil) induce l

108 ted whether the demethylating agent 2'-deoxy-5-azacytidine (DAC) can be used in vivo to sensitize MMR

109 , GPC3 expression was restored after 2-deoxy 5-azacytidine (DAC)-mediated demethylation of its promot

110 ensitivity, using 5-azacytidine and 2'-deoxy-5-azacytidine (DAC, decitabine) as demethylating agents.

111 se DNA methylation is reversible, drugs like 5'-azacytidine, decitabine, and histone deacetylase inhi

112 Demethylation agent 5'-azacytidine decreased BMPER expression in fibroblasts

113 Transport assays using [(1)(4)C]5-azacytidine demonstrated Na(+)-independent uptake of t

114 In contrast, the cellular activity of the 5-azacytidine derivative 5-azacytidine-5'-elaidate (CP-4

115 ular carcinoma (HCC) cell lines treated with 5-azacytidine (DNA hypomethylating agent) and/or trichos

116 vity was maximally rescued by treatment with 5-azacytidine (DNA methyltransferase inhibitor) compared

117 iate to a myofibroblast-like phenotype using 5-azacytidine do not promote tumor cell growth as effici

118 th exposure to the DNA methylation inhibitor 5-azacytidine, enforces astrocyte dedifferentiation.

119 tion of egg production and egg maturation by 5-azacytidine establishes an essential role for 5-methyl

120 ion could be turned on, off, and on again by 5-azacytidine exposure, washout, and reexposure.

121 ate-passage clones only by pretreatment with 5-azacytidine followed by trichostatin A, suggesting tha

122 18 h to the DNA methyltransferase inhibitor 5-azacytidine, followed by a three-step protocol for the

123 ethylated cells with the demethylating agent 5-azacytidine had a modest effect on COX-2 expression, b

124 d inhibition of beta-globin mRNA levels, and 5-azacytidine had little effect on beta-globin mRNA leve

125 hat were unmethylated at the COX-2 promoter, 5-azacytidine had no effect on H. pylori-stimulated COX-

126 xample, we have previously demonstrated that 5-azacytidine has its greatest antiviral potency during

127 d with inhibitors of DNA methyltransferases (5-Azacytidine), histone deacetylases (valproic acid), an

128 We examine trials of agents, including 5-azacytidine, hydroxyurea, and short-chain fatty acids.

129 Treatment of mice with 5-azacytidine (i.p.) resulted in a significant dose-depe

130 a key transporter for the cellular uptake of 5-azacytidine in leukemia cells and raise the possibilit

131 ent with the DNA methyltransferase inhibitor 5-azacytidine in the context of a mouse containing the e

132 Demethylation of DNA with 5-azacytidine in two cell lines induced expression of hT

133 ued by treatment with a demethylation agent (5-azacytidine) in two NSCLC cell lines lacking DMBT1 exp

134 .5 but differentiate in vitro in response to 5'-azacytidine, in part depending on Bmpr1a, a receptor

135 obin expression was induced upon exposure to 5-azacytidine, in cells derived from -117 Greek heredita

136 ar concentrations of the demethylating agent 5-azacytidine increased basal expression and hypoxic ind

137 eviously observed that the nucleoside analog 5-azacytidine increased the spleen necrosis virus (SNV)

138 moter in vivo by treatment of the cells with 5-azacytidine increased transglutaminase expression and

139 ls with the DNA methyltransferase inhibitor, 5 azacytidine induced RI expression and restored TGF-bet

140 prostatic carcinoma cell line cultures with 5-azacytidine induced ETB mRNA expression, suggesting th

141 case, treatment with the demethylating agent 5-azacytidine induced expression of the absent hMLH1 pro

142 Treatment with the hypomethylating agent 5-azacytidine induced PLS3 expression in Jurkat cells an

143 asts with CEF culture supernatants from both 5-azacytidine-induced and noninduced CEF led to ALV infe

144 A strong dependence of 5-azacytidine-induced DNA demethylation on hENT1 activit

145 in HD cells relative to control, as well as 5-azacytidine-induced hypomethylation.

146 ease in vitiliginous SL101 birds and also in 5-Azacytidine-induced vitiliginous BL101 parental contro

147 80/cp70 with the demethylating agent 2-deoxy-5'-azacytidine induces resensitization to cisplatin and

148 L), treatment with the hypomethylating agent 5-azacytidine induces chromosome breakage in root tips.

149 Finally, treatment of MBD2-null mice with 5-azacytidine induces only a small, nonadditive inductio

150 Demethylation agent 5-azacytidine inhibited the deletion of the penultimate

151 he responsible proteins for the transport of 5-azacytidine into MDS/AML cells are unknown.

152 The nucleoside analog 5-azacytidine is an archetypical drug for epigenetic can

153 ersy over the mechanism of Hb F induction by 5-azacytidine led to the identification of hydroxyurea a

154 Here we describe 5-azacytidine-mediated RNA immunoprecipitation (Aza-IP),

155 Neither 5-azacytidine nor decitabine induced substantial apoptos

156 D133- cell subpopulations were cultured with 5'-azacytidine or vascular endothelial growth factor (VE

157 e treated with the DNA demethylating agents, 5-azacytidine or 2-deoxy-5-azacytidine.

158 Similarly, inhibiting methylation with 5-azacytidine or knocking down the DNA methyltransferase

159 RNA-seq analysis of CSCs treated with 5-azacytidine plus butyrate provided evidence that inhib

160 nsitive cells with the methylation inhibitor 5-azacytidine prevented the emergence of resistant cells

161 rsely, global inhibition of methylation with 5-azacytidine promoted eotaxin-3 production in associati

162 eexpression by demethylation treatment using 5-azacytidine reduced the proliferation and colony forma

163 nd for the modulation of transporter-related 5-azacytidine resistances.

164 atment of cells with the methylase inhibitor 5-azacytidine restored CREB binding to the Wnt10b gene p

165 atment of R2 progeny of silenced plants with 5-azacytidine resulted in demethylation of the Ubi1 prom

166 Experimental DNA demethylation with 5'-azacytidine results in a similar increase of H3-K4me.

167 gitudinal analysis in a patient treated with 5-azacytidine revealed that karyotypically abnormal HSCs

168 T-116 cells with the DNA demethylating agent 5-azacytidine reverses promoter methylation, promotes no

169 When seedlings are treated with 5-azacytidine, root growth of epi-lines is restored to w

170 However, because of 5-azacytidine's general toxicity, other nucleoside analo

171 lls with the DNA methyltransferase inhibitor 5-azacytidine selectively demethylated this area and inc

172 NA level, and the DNA methylation inhibitor, 5-Azacytidine, significantly elevated the Drg-1 gene exp

173 5-Azacytidine, the first such agent in clinical use, was

174 After these cells were treated with 5-azacytidine, they regained the ability to clone in hyp

175 NA methyltransferase and the cytidine analog 5-azacytidine to recover RNA targets by immunoprecipitat

176 Clonogenic assays demonstrate that the 5-azacytidine treated cells show increased sensitivity t

177 modest effect on COX-2 expression, but when 5-azacytidine-treated cells were subsequently stimulated

178 Stroma derived from 5-azacytidine-treated patients lacked aberrant methylati

179 5'-azacytidine treatment additionally regulated BMPER ex

180 T beta RII message, which was reversed upon 5'-azacytidine treatment, indicating that the promoter m

181 Furthermore, 5-azacytidine treatment activated CIITA expression in cl

182 y methylated and silenced mir-124 gene loci, 5-azacytidine treatment allowed miR-124 re-expression an

183 Similar to mouse NPC1L1, 5-azacytidine treatment also increased the level of huma

184 Rescue of DNA repair gene expression by 5-azacytidine treatment identified DNA methylation as a

185 Bisulfite analysis of cells in which 5-azacytidine treatment induced GFP expression revealed

186 Increasing dosages of 5-azacytidine treatment led to higher levels of firefly

187 Demethylation of the gene by deoxy-5-azacytidine treatment led to its reactivation in a lun

188 2-Deoxy-5-azacytidine treatment of cell lines with aberrant meth

189 The 5-azacytidine treatment of OSCC cells led to an up-regul

190 Last, although 5-azacytidine treatment of Rael cells results in a G1 ar

191 Experimental demethylation by either 5-azacytidine treatment or DNMT1 depletion diminished bo

192 ggressive cells by promoter methylation, but 5-azacytidine treatment reactivated the expression.

193 mma-globin gene at a level commensurate with 5-azacytidine treatment, 10- to 20-fold over that observ

194 When methylation of the MITEs was blocked by 5-azacytidine treatment, a threefold increase in the end

195 Following 5-azacytidine treatment, RA and trichostatin A markedly

196 tides were demethylated in Ku-80 cells after 5-azacytidine treatment.

197 n pericytes; these effects were prevented by 5-azacytidine treatment.

198 5-Azacytidine treatments also resulted in stabilization

199 seful biomarker to predict the efficiency of 5-azacytidine treatments.

200 vation of silenced tumor suppressor genes by 5-azacytidine (Vidaza) and its congener 5-aza-2'-deoxycy

201 gulation of MGMT in HeLa S3 cells induced by 5-azacytidine was accompanied by progressive demethylati

202 5-Azacytidine was first synthesized almost 40 years ago.

203 The finding that 5-azacytidine was incorporated into DNA and that, when p

204 Cells treated with 5-azacytidine were monitored for 2 wk compared with 1 wk

205 n associated with RIP by taking advantage of 5-azacytidine, which prevents most methylation in Neuros

206 m+ did not occur when conidia were plated on 5-azacytidine, which reduces DNA methylation.

207 iR2 after the treatment of HCT116 cells with 5-azacytidine, which resulted in differential expression