ライフサイエンスコーパス: 5-azacytidine

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

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

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

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

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

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

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

8 after treatment with the demethylating agent 5-azacytidine.

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

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

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

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

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

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

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

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

17 ells from female donors and were reversed by 5-azacytidine.

18 uced Kawasaki disease mice were treated with 5-azacytidine.

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

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

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

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

23 pression of GADD45alpha or pretreatment with 5-azacytidine.

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

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

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

27 ken before, during, and after treatment with 5-azacytidine (40 patients; 15 nonresponders, 25 respond

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

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

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

31 5-azacytidine (5-Aza) is a potent inducer of fetal hemog

32 ty of DNA methyltransferase (Dnmt) inhibitor 5-azacytidine (5-aza) to generate outer hair cells (OHCs

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

34 5-Azacytidine (5-Aza), a DNA demethylating agent, induce

35 In contrast to 5-azacytidine (5-aza), allogeneic stem-cell transplantat

36 treatment with the DNA demethylating agent, 5-azacytidine (5-aza), was significantly more toxic to T

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

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

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

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

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

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

43 5-Azacytidine (5-azaC) is an azanucleoside approved for

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

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

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

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

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

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

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

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

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

53 1 (HIV-1) by use of chemical mutagens [i.e., 5-azacytidine (5-AZC)] as well as by host factors with m

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

55 roved DNA hypomethylating agents (DHAs) like 5-azacytidine (5AC) and decitabine (DAC) demonstrate eff

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

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

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

59 revious work has demonstrated that the DNMTi 5-Azacytidine (5AZA-C) activates type I interferon signa

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

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

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

63 Treatment of CP myoblasts with 5-azacytidine, a DNA hypomethylating agent, reduced this

64 Treatment with 5-Azacytidine, a DNMT1 inhibitor, led to demethylation o

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

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

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

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

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

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

71 A class switch, and inhibition of RNA 5mC by 5-azacytidine ameliorated progression of IgA nephropathy

72 5'-Azacytidine, an inhibitor of DNA methylation that der

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

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

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

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

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

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

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

80 side DNA methyltransferase (DNMT) inhibitors 5-azacytidine and 5-aza-2'-deoxycytidine lack selectivit

81 The DNA methyltransferase inhibitors (DNMTi) 5-azacytidine and 5-aza-2-deoxycytidine have been approv

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

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

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

85 cells treated with the small molecule drugs 5-azacytidine and bisperoxovanadium (HOpic), which inhib

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

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

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

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

90 nsferase and histone deacetylase inhibitors, 5-azacytidine and entinostat, disrupts the premetastatic

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

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

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

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

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

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

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

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

99 In a phase 1 trial, we found oral 5-azacytidine and romidepsin to be safe and effective, w

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

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

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

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

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

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

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

107 5-Azacytidine- and 5-aza-deoxycytidine (5-aza-CdR)-media

108 he DNA hypomethylating agents decitabine and 5-azacytidine are the only two drugs approved for treatm

109 The 5-azacytidines are approved inhibitors of DNMT1, but the

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

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

112 models, we conducted a phase 1 study of oral 5-azacytidine (AZA) and romidepsin (ROMI) in patients wi

113 5-Azacytidine (AZA) is a nucleoside analog that is used

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

115 the DNA methyltransferase inhibitor (DNMTi) 5-azacytidine (AZA), have profound effects on transcript

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

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

118 5-Azacytidine (aza-C) and its derivatives are cytidine a

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

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

121 ent using a DNA methyltransferase inhibitor (5-azacytidine, AZA), methylation-specific PCR (MSP) and

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

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

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

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

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

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

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

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

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

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

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

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

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

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

136 Methylation inhibitor 5-azacytidine diminishes the differences between memory

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

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

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

140 ted with the DNA methyltransferase inhibitor 5-Azacytidine during seed germination and early growth.

141 DNA methylation inhibitor 5-azacytidine effectively reverses expression of the TSG

142 mon targets (TE) activated by the same drug (5-azacytidine) elicit an immune response, which may be i

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

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

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

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

147 18 h to the DNA methyltransferase inhibitor 5-azacytidine, followed by a three-step protocol for the

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

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

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

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

152 porter mouse embryonic stem cells (mESCs) to 5-Azacytidine, HDAC inhibitors, BET inhibitors or GSK-J4

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

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

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

156 Inhibition of DNA methyltransferase by 5-azacytidine in 786-O and Caki-2 cells resulted in Wnt-

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

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

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

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

161 .5 but differentiate in vitro in response to 5'-azacytidine, in part depending on Bmpr1a, a receptor

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

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

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

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

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

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

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

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

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

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

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

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

174 80/cp70 with the demethylating agent 2-deoxy-5'-azacytidine induces resensitization to cisplatin and

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

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

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

178 induces wound-edge gene methylation and that 5'-azacytidine, inhibitor of methylation, improved wound

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

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

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

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

183 Neither 5-azacytidine nor decitabine induced substantial apoptos

184 PegIFN-alpha combined with 5-azacytidine only partially overcame resistance in VF;D

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

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

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

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

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

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

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

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

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

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

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

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

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

198 Treatment with 5-azacytidine reverted DNA hypermethylation but did not

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

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

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

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

203 5-Azacytidine, the first such agent in clinical use, was

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

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

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

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

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

209 5'-azacytidine treatment additionally regulated BMPER ex

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

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

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

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

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

215 hylation state of its proximal enhancer, and 5-azacytidine treatment increased IGFBP2 expression.

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

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

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

219 2-Deoxy-5-azacytidine treatment of cell lines with aberrant meth

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

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

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

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

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

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

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

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

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

229 5-Azacytidine treatments also resulted in stabilization

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

231 ic methylation in human and mouse cells, and 5-azacytidine triggered DNA demethylation is more pronou

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

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

234 5-Azacytidine was first synthesized almost 40 years ago.

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

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

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

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

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