ライフサイエンスコーパス: deoxycytidine

1 derived and have a strong bias for a 5'-end deoxycytidine.

2 ential of the demethylating agent, 5'-aza-2'-deoxycytidine.

3 ed with the DNA demethylating agent 5-aza-2'-deoxycytidine.

4 t cancer cells synergistically with 5-aza-2'-deoxycytidine.

5 ment with the hypomethylating agent 5-aza-2'-deoxycytidine.

6 nt with the DNA demethylating agent 5-aza-2'-deoxycytidine.

7 H or by the DNA demethylating agent 5-aza-2'-deoxycytidine.

8 ne with the DNA demethylating agent 5-aza-2'-deoxycytidine.

9 (rather than a purine) flanking the targeted deoxycytidine.

10 oma cell lines after treatment with 5-aza-2'-deoxycytidine.

11 ivation resulted in trapping of 2'-fluoro-2'-deoxycytidine.

12 the DNA methyltransferase inhibitor 5-aza-2'-deoxycytidine.

13 or RAs and the demethylation agent, 5-aza-2'-deoxycytidine.

14 g is similar as that of 5-(hydroxymethyl)-2'-deoxycytidine.

15 bition of DNA methyltransferases by 5-aza-2'-deoxycytidine.

16 to viral DNA following reduction to 5-aza-2'-deoxycytidine.

17 uld be restored after treatment with 5-aza-2-deoxycytidine.

18 ed by demethylation agents, such as 5-Aza-2'-deoxycytidine.

19 h was restored after treatment with 5-aza 2'-deoxycytidine.

20 ivated by the hypomethylating agent 5-aza-2'-deoxycytidine.

21 our cell lines after treatment with 5'-aza-2'deoxycytidine.

22 d with efficiencies up to 3-fold higher than deoxycytidine.

23 a DNA methyltransferase inhibitor, 5-Aza-2'-deoxycytidine.

24 tment with a methylation inhibitor, 5-aza-2'-deoxycytidine.

25 g composed of dimethylaniline (DMA) fused to deoxycytidine.

26 C1' with a hydroxide ion in 5-substituted 2'-deoxycytidines.

27 2'-C-methylcytidine (MeFdC) and 2'-fluoro-2'-deoxycytidine (2'-FdC).

28 gs in addition to its natural substrates, 2'-deoxycytidine, 2'-deoxyguanosine, and 2'-deoxyadenosine.

29 modified bases (2'-Fluoro-Uridine, 5-Methyl-deoxyCytidine, 2,6-Diaminopurine or Iso-deoxyGuanosine)

30 io of 5-methyl-2'-deoxycytidine (5mdC) to 2'-deoxycytidine (2dC) in the enzymatic hydrolysate of full

31 ridin-6-yl)-3-aminopropionyl]aminoet hyl}-2'-deoxycytidine 5'-monophosphate) analogue is located to t

32 ternary complexes reveal that relative to D-deoxycytidine 5'-triphosphate (D-dCTP) in the canonical

33 orming a Watson-Crick base pair with correct deoxycytidine 5'-triphosphate (dCTP) and its syn-conform

34 inactivated by 1 equiv of 2',2'-difluoro-2'-deoxycytidine 5'-triphosphate (F(2)CTP) in <2 min.

35 inactivated by 1 equiv of 2',2'-difluoro-2'-deoxycytidine 5'-triphosphate (F(2)CTP).

36 s of human DNA polymerase lambda, DNA, and L-deoxycytidine 5'-triphosphate (L-dCTP), or the triphosph

37 om the DNA helix and the pairing of incoming deoxycytidine 5'-triphosphate with a surrogate arginine

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

39 increased A3G's 5' nucleoside preference for deoxycytidine (5'-CC).

40 derivatives of thymidine (1) and 5-methyl-2'-deoxycytidine (5) produce interstrand cross-links in dup

41 ther the DNA methylation inhibitor, 5-aza-2'-deoxycytidine (5-Aza) could modulate extracellular matri

42 Treatment with either 5-Aza-2-deoxycytidine (5-Aza) or trichostatin A (TSA) was used t

43 HCT-116 colonocytes incubated with 5-aza-2'-deoxycytidine (5-AZA).

44 h a DNA methyltransferase inhibitor, 5-Aza-2-deoxycytidine (5-Aza-2dC), and an RAW294.7 cell line tra

45 DNA methylation inhibitors such as 5-aza-2'-deoxycytidine (5-Aza-CdR) are currently used for the tre

46 human EC cells are highly sensitive to 5-aza-deoxycytidine (5-aza-CdR) compared with somatic solid tu

47 Decitabine, or 5-aza-2'-deoxycytidine (5-aza-CdR), is a well-characterized drug

48 al levels to low doses of the DNMTi 5-aza-2'-deoxycytidine (5-aza-CdR), there is a synergistic inhibi

49 t of methylation inhibitors such as 5-Aza-2'-deoxycytidine (5-Aza-CdR).

50 old) in human HCC cells treated with 5'aza-2'deoxycytidine (5-Aza-CdR, DNA methylation inhibitor) and

51 hermore, the DNA demethylating agent 5 aza-2'deoxycytidine (5-Aza-dC) antagonizes the effects of AID

52 the DNA methyltransferase inhibitor 5-aza-2'-deoxycytidine (5-aza-dC) increases the expression of PTC

53 5-Aza-2'-deoxycytidine (5-aza-dC) is a nucleoside analogue with c

54 ency of silencing was determined by 5-aza-2'-deoxycytidine (5-aza-dC) treatment.

55 as restored with either IFNgamma or 5-aza-2'-deoxycytidine (5-aza-dC) treatment.

56 nt with the DNA demethylating agent 5-aza-2'-deoxycytidine (5-Aza-dC) was sufficient to reactivate BA

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

58 herapeutic and DNA-demethylating agent 5-aza-deoxycytidine (5-aza-dC), transgenic expression of macro

59 se of demethylating agents, such as 5-aza-2'-deoxycytidine (5-Aza-dC).

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

61 The DNA methyltransferase inhibitor, 5-Aza-2'deoxycytidine (5-AzaCdR) is an approved epigenetic cance

62 The DNA-demethylating drug 5-Aza-2-deoxycytidine (5-azadC) induced rapid nuclear accumulati

63 rm the 5hmC into glucosyl-5-hydroxymethyl-2'-deoxycytidine (5-gmC) and achieved 20% 5-gmC in the geno

64 l, 5-formyl and 5-carboxyl derivatives of 2'-deoxycytidine (5-HmdC, 5-FodC and 5-CadC).

65 family dioxygenases can oxidize 5-methyl-2'-deoxycytidine (5-mdC) in DNA to yield the 5-hydroxymethy

66 S) for direct measurement of the 5-methyl-2'-deoxycytidine, 5-(hydroxymethyl)-2'-deoxycytidine, 5-for

67 ine, 5-formyl-2'-deoxycytidine, 5-carboxy-2'-deoxycytidine, 5-(hydroxymethyl)-2'-deoxyuridine, 2'-deo

68 hydroxymethyl)-2'-deoxycytidine, 5-formyl-2'-deoxycytidine, 5-carboxy-2'-deoxycytidine, 5-(hydroxymet

69 ethyl-2'-deoxycytidine, 5-(hydroxymethyl)-2'-deoxycytidine, 5-formyl-2'-deoxycytidine, 5-carboxy-2'-d

70 n of DNMT with either the inhibitor 5-aza-2'-deoxycytidine (5Aza) or siRNA markedly reduced OS-induce

71 e of DNA-demethylating agents (e.g. 5-aza-2'-deoxycytidine (5aza-dC)) to study epigenetic regulation

72 with a cell based loss-of-function (5-Aza-2'-deoxycytidine (5Aza-dC)-induced senescence bypass) scree

73 5-Aza-2'-deoxycytidine (5azaC-dR) has been employed as an inhibit

74 with the chromatin-modifying agents 5-aza-2'-deoxycytidine (5azaD) and trichostatin A (TSA), but not

75 rmal CD34(+) cells with decitabine (5-aza-2'-deoxycytidine [5azaD]), followed by suberoylanilide hydr

76 and the DNA methylation inhibitor 5'-aza-2'-deoxycytidine (5AzadC) were introduced into the medium a

77 he DNA methyltransferase inhibitor, 5-aza-2'-deoxycytidine (5azadC).

78 ormy-2'deoxycytidine (5fdC) and 5-carboxyl-2'deoxycytidine (5cadC).

79 oxymethyl-2'deoxycytidine (5hmdC), 5-formy-2'deoxycytidine (5fdC) and 5-carboxyl-2'deoxycytidine (5ca

80 '-deoxycytidine (dC) with 5-hydroxymethyl-2'-deoxycytidine (5hmC) in the E. coli genome and approxima

81 thods to assess levels of 5-hydroxymethyl-2'-deoxycytidine (5hmdC) and 5-methyl-2'-deoxycytidine (5md

82 ed oxidized forms of 5mdC: 5-hydroxymethyl-2'deoxycytidine (5hmdC), 5-formy-2'deoxycytidine (5fdC) an

83 icated by an increase of genomic 5-methyl-2'-deoxycytidine (5mdC) content and more importantly, by an

84 Although the salvage mechanism of 5-methyl-2'deoxycytidine (5mdC) has been investigated before, it re

85 hyl-2'-deoxycytidine (5hmdC) and 5-methyl-2'-deoxycytidine (5mdC) in genomic DNA, we investigated whe

86 nalysis using the molar ratio of 5-methyl-2'-deoxycytidine (5mdC) to 2'-deoxycytidine (2dC) in the en

87 umn, 2'-deoxyguanosine (2dG) and 5-methyl-2'-deoxycytidine (5mdC) were resolved in less than 1 min wi

88 to form stable Watson-Crick base pairs with deoxycytidine (8-oxoG:dC) and Hoogsteen base pairs with

89 ell line (MHS) after treatment with 5-aza-2'-deoxycytidine (a methyltransferase inhibitor).

90 3 (Pit-1/0 cells) were treated with 5-aza-2'-deoxycytidine, a demethylating reagent.

91 Treatment with 5-aza-2'-deoxycytidine, a demethylation agent, and knockdown of D

92 ter assays and gene reactivation by 5-aza-2'-deoxycytidine, a DNA demethylating agent, show that DNA

93 adecanoyl phorbol acetate (TPA) and 5-aza-2'-deoxycytidine, a DNA methyltransferase inhibitor, on his

94 eoxyadenosine, N(2)-deoxyguanosine, and N(4)-deoxycytidine adducts in vitro.

95 For LG-deoxycytidine adducts, the initial dihydroxypyrrolidine

96 d with the DNA demethylating agent, 5-aza-2'-deoxycytidine, after UVB exposure.

97 muM DNA-methyltransferase inhibitor 5-aza-2'-deoxycytidine, again correlating with increased MMP13 ex

98 ipulating MGPC DNA methylation with 5-aza-2'-deoxycytidine altered their properties.

99 The deoxycytidine analog decitabine (DAC) can deplete DNA me

100 citabine is a new, safely administered, oral deoxycytidine analog that has encouraging activity in le

101 Gemcitabine is a deoxycytidine analog that is widely used in the chemothe

102 Gemcitabine is a deoxycytidine analog used in the treatment of various so

103 s or RTs has not been established although L-deoxycytidine analogs (lamivudine and emtricitabine) and

104 Although lamivudine and emtricitabine, two L-deoxycytidine analogs, have been widely used as antivira

105 While the therapeutic activity of the deoxycytidine analogue decitabine is thought to reflect

106 The corresponding 2'-deoxycytidine analogue is not as well-accommodated in du

107 3,N(4)-etheno-2'-deoxycytidine and 1,N(6)-etheno-2'-deoxyadenosine, forme

108 ne from the tumor's margin; also 5-formyl-2'-deoxycytidine and 5-carboxy-2'-deoxycytidine were lower

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

110 5-Aza-2'-deoxycytidine and diesel exhaust particle exposure in hu

111 urally related cytidine analogues, such as 2'deoxycytidine and gemcitabine, occurs through a saturabl

112 of DNA methyl transferase inhibitor 5-Aza 2-deoxycytidine and histone deacetylase inhibitor trichost

113 icantly improved activity with 5-substituted deoxycytidine and thymidine analogues.

114 sphate leads to accumulation of radiolabeled deoxycytidine and thymidine nucleotides within the mitoc

115 , formed via ionizing radiation damage to 2'-deoxycytidine and thymidine, respectively, under anoxic

116 ression of PDLIM2 can be reversed by 5-aza-2-deoxycytidine and vitamin D to suppress KSHV-associated

117 with the DNA methylation inhibitors 5-aza-2'-deoxycytidine and zebularine as well as DNA methyltransf

118 Treatment with demethylating agent 5-aza-deoxycytidine and/or histone deacetylation inhibitor tri

119 of combining gemcitabine (2',2'-difluoro 2'-deoxycytidine) and 7-ethyl-10-hydroxycamptothecin (SN-38

120 bstrate, the S-adenosyl-l-methionine and the deoxycytidine, and linking them together.

121 ethylating agents 5-azacytidine and 5-aza-2'-deoxycytidine are effective treatments for patients with

122 ethyl-2'-deoxyuridine and 5-hydroxymethyl-2'-deoxycytidine are predicted to be efficient mutagens.

123 theno-2'-deoxyadenosine and 3,N(4)-etheno-2'-deoxycytidine arising from reaction of DNA with lipid pe

124 atment with the demethylating agent 5-aza-2'-deoxycytidine as well as by down-modulation of Dnmt1 exp

125 the DNA methyltransferase inhibitor 5-aza-2'-deoxycytidine (Aza) induced acetylation of histone 3, in

126 atment with the DNA-demethylating drug 5-Aza-deoxycytidine (AZA) restores high-risk neuroblastoma sen

127 rease in expression after 2 days of 5-aza-2'-deoxycytidine (AZA) treatment and a significant (P < 0.0

128 netic Xist ablation with short-term 5-aza-2'-deoxycytidine (Aza) treatment models the synergy in vivo

129 purpose was to investigate whether 5-aza-2'-deoxycytidine (Aza), a DNA methyltransferase (DNMT1) inh

130 examethylene bisacetamide (HMBA) or 5-aza-2'-deoxycytidine (Aza-CdR), reactivate latent HIV-1 in HPCs

131 ith the methyltransferase inhibitor 5-aza-2'-deoxycytidine before and at early stages of reprogrammin

132 The addition of 5-aza-2'-deoxycytidine blocked the hypoxia-induced increase in me

133 ted, and the DNA methylation agent 5'-aza-2'-deoxycytidine, but not the histone deacetylase inhibitor

134 ing a deoxyuridine to the 3' position of the deoxycytidine C13 in the catalytic core of the same DNAz

135 rmyl-2'-deoxycytidine (fdC) and 5-carboxy-2'-deoxycytidine (cadC) were recently discovered in mammali

136 Treatment of cells with 5-aza-2'-deoxycytidine causes restoration of Cosmc transcripts, r

137 the DNA methyltransferase inhibitor 5-aza-2'-deoxycytidine (DAC) activates CYP24A1 expression in pros

138 we used the DNA demethylating drug 5-aza-2'-deoxycytidine (DAC) in an aggressive mouse model of stro

139 5-aza-2'-deoxycytidine (DAC) is approved for the treatment of mye

140 periments of two CC cell lines using 5-aza-2'deoxycytidine (DAC) treatment.

141 ne with the DNA demethylating agent 5-aza-2'-deoxycytidine (DAC)-enhanced HER4 expression, confirming

142 on with the DNA-demethylating agent 5-aza-2'-deoxycytidine (DAC).

143 oma cell lines after treatment with 5-aza-2'-deoxycytidine (DAC).

144 er cells by three epigenetic drugs: 5-aza-2'-deoxycytidine (DAC; decitabine), arsenic trioxide (ATO),

145 Although [(18)F]CFA uptake was reduced by deoxycytidine (dC) competition, this inhibition required

146 eoxyadenosine (dA), deoxyguanosine (dG), and deoxycytidine (dC) into their monophosphate forms, with

147 DNA with four or more contiguous runs of 2'-deoxycytidine (dC) nucleotides have the potential to ado

148 dine deaminase that catalyzes deamination of deoxycytidine (dC) on single-stranded DNA (ssDNA).

149 Deoxycytidine (dC) triphosphate (dCTP) can be produced b

150 achieve approximately 63% replacement of 2'-deoxycytidine (dC) with 5-hydroxymethyl-2'-deoxycytidine

151 6S) (generated by reaction of bisulfite with deoxycytidine (dC)) to uracil (dU).

152 dFdC), a structural analog of the nucleoside deoxycytidine (dC), derives its primary antitumor activi

153 de monophosphates to deoxythymidine (dT) and deoxycytidine (dC), we hypothesized that: (1) deoxynucle

154 e (AID) initiates CSR and SHM by deaminating deoxycytidines (dCs) in switch (S) and V(D)J region DNA,

155 ctronic excited states of the DNA nucleoside deoxycytidine (dCyd) and its methylated analogue 5-methy

156 Activation-induced deoxycytidine deaminase (AID) deaminates C to U on singl

157 Activation-induced deoxycytidine deaminase (AID) generates antibody diversi

158 2 stems from mutations in activation-induced deoxycytidine deaminase (AID) that abolish immunoglobuli

159 Applying this model to activation-induced deoxycytidine deaminase (AID), which catalyzes C-->U dea

160 We show here that deoxycytidine deaminase (DCD)-deficient mutants of Esche

161 Human deoxycytidine deaminase APOBEC3A (Apo3A) acts as an HIV-

162 APOBEC3H is a deoxycytidine deaminase that can restrict the replicatio

163 G (Apo3G) is a single-stranded DNA-dependent deoxycytidine deaminase, which, in the absence of the hu

164 ng these enzymes are the seven human APOBEC3 deoxycytidine deaminases, each with unique target sequen

165 of the viral infectivity factor Vif, through deoxycytidine deamination and a deamination-independent

166 he major active agents and (2) inhibition of deoxycytidine deamination might enhance dTMP+dCMP therap

167 cell lines and patient blasts using 5-aza-2'-deoxycytidine (decitabine) and trichostatin A increased

168 cytidine analogues azacytidine and 5-aza-2'-deoxycytidine (decitabine) are commonly used to treat my

169 acytidine (Vidaza) and its congener 5-aza-2'-deoxycytidine (decitabine) has provided an alternate app

170 The DNA methyltransferase inhibitor 5-aza-2'-deoxycytidine (decitabine) induces DNA demethylation and

171 Lung cancer cells are sensitive to 5-aza-2'-deoxycytidine (decitabine) or midostaurin (PKC412), beca

172 5-Aza-2'-deoxycytidine decreased, whereas folate-depleted/high-me

173 We found that LGE(2) reacted with deoxycytidine, deoxyadenosine, or deoxyguanosine in vitr

174 Each enzyme class (deoxycytidine, deoxyguanosine, and deoxythymidine kinase

175 lipoteichoic acid and synthetic unmethylated deoxycytidine-deoxyguanosine dinucleotides, which mimic

176 ults showed that, among the 5-substituted 2'-deoxycytidine derivatives examined [XdC, where X = H (dC

177 ticancer drug gemcitabine (2',2'-difluoro-2'-deoxycytidine; dFdC) was severely compromised in Mycopla

178 n modulation with trichostatin A or 5-aza-2'-deoxycytidine elevates USP9X expression in human PDA cel

179 hermore, the DNA demethylating agent 5-aza-2-deoxycytidine failed to upregulate GAS5-AS1 in NSCLC cel

180 ymethyl-2'-deoxycytidine (hmdC), 5-formyl-2'-deoxycytidine (fdC) and 5-carboxy-2'-deoxycytidine (cadC

181 sphorylated form of araC, dFdC, 2'-fluoro-2'-deoxycytidine (FdC), and cytidine into two nicked DNA su

182 atment of cells with retinoic acid, 5-aza-2'-deoxycytidine, folate-depleted/high-methionine medium, a

183 conversion of Ig genes by the deamination of deoxycytidine, followed by error-prone mismatch- or base

184 -chip analysis, Trichostatin A, and 5-aza-2'-deoxycytidine further support an epigenetically altered

185 ticancer drug gemcitabine (2',2'-difluoro-2'-deoxycytidine, GEM) which is used in treatment of pancre

186 ons with the RNR inhibitor 2',2'-difluoro-2'-deoxycytidine (gemcitabine).

187 ine (cytarabine, araC) and 2',2'-difluoro-2'-deoxycytidine (gemcitabine, dFdC), are effective cancer

188 xt, we assessed the formation of 5-methyl-2'-deoxycytidine glycol in the form of its deaminated produ

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

190 erived DNA modifications, 5-hydroxymethyl-2'-deoxycytidine (hmdC), 5-formyl-2'-deoxycytidine (fdC) an

191 ntified the nucleotide as 5-hydroxymethyl-2'-deoxycytidine (hmdC).

192 Treatment with 5'-aza-2'-deoxycytidine in a murine bleomycin-induced pulmonary fi

193 eaminase (AID), an enzyme that can deaminate deoxycytidine in DNA in vitro, where its activity is sen

194 tes were screened by treatment with 5-aza-2'-deoxycytidine in four TN and five non-TNBC cell lines.

195 ovide the reducing equivalent to the 3'-keto-deoxycytidine intermediate by the class I and II RNRs pr

196 We find that 5-carboxyl-2'-deoxycytidine ionizes with pK(a) values of 4.28 (N3) and

197 the nucleoside salvage pathway (NSP) enzymes deoxycytidine kinase (dCK) and thymidine kinase (TK1).

198 the cytosol of human cells is carried out by deoxycytidine kinase (dCK) and thymidine kinase 1 (TK1).

199 Deoxycytidine kinase (DCK) controls the rate-limiting st

200 We hypothesized that PET probes for deoxycytidine kinase (dCK) could be used to differentiat

201 ch as cladribine, require phosphorylation by deoxycytidine kinase (dCK) for pharmacological activity.

202 d inhibition of ribonucleotide reductase and deoxycytidine kinase (dCK) in multiple cancer cell lines

203 Deoxycytidine kinase (dCK) is a rate limiting enzyme cri

204 Deoxycytidine kinase (dCK) is a rate-limiting enzyme in

205 Deoxycytidine kinase (dCK) is an essential nucleoside ki

206 Human deoxycytidine kinase (dCK) is responsible for the phosph

207 The physiological role of human deoxycytidine kinase (dCK) is to phosphorylate deoxynucl

208 pancreatic cancer cells, HuR associates with deoxycytidine kinase (dCK) mRNA, which encodes the enzym

209 human-derived reporter genes based on human deoxycytidine kinase (dCK) suitable for clinical PET.

210 nucleotide purine analog, is a substrate for deoxycytidine kinase (dCK), a key enzyme in the deoxyrib

211 (18)F-FAC retention in cells requires deoxycytidine kinase (dCK), a rate-limiting enzyme in th

212 Deoxycytidine kinase (dCK), a rate-limiting enzyme in th

213 ilibrative nucleoside transporter 1 (hENT1), deoxycytidine kinase (dCK), and ribonucleotide reductase

214 In this article, we describe a deficiency in deoxycytidine kinase (DCK), one of the major enzymes of

215 enzymes, ribonucleotide reductase (RNR) and deoxycytidine kinase (dCK), via distinct molecular mecha

216 We wanted to understand why human deoxycytidine kinase (dCK), which is related to HSV1-TK

217 oximately by 2 orders of magnitude in the 2'-deoxycytidine kinase (dCK)-deficient CEM/dCK(-) cell lin

218 step in which they are monophosphorylated by deoxycytidine kinase (dCK).

219 tivation was significantly less dependent on deoxycytidine kinase and on nucleoside transporters, and

220 dine (RO-9187) were excellent substrates for deoxycytidine kinase and were phosphorylated with effici

221 We used a human deoxycytidine kinase containing three amino acid substit

222 o more cytotoxic than gemcitabine HCl in the deoxycytidine kinase deficient (CCRF-CEM/dCK(-/-)) tumor

223 uman sodium-iodide symporter (hNIS), a human deoxycytidine kinase double mutant (hdCKDM), and herpes

224 ncy on the nucleoside salvage pathway enzyme deoxycytidine kinase for the maintenance of a proper bal

225 Inhibition of adenosine kinase and deoxycytidine kinase prevented the accumulation of dATP

226 Human deoxycytidine kinase triple mutant (hdCK3mut) is a nonim

227 s a poor phosphorylation substrate for human deoxycytidine kinase, a pro-nucleotide form of the 4-bro

228 EGF and the gemcitabine metabolizing enzyme, deoxycytidine kinase, are specifically bound by HuR in p

229 One such molecule is 5,6-dihydro-5-aza-2'-deoxycytidine (KP1212), a selective mutagen that induces

230 ding the drug candidate 5-aza-5,6-dihydro-2'-deoxycytidine (KP1212), which causes A-to-G and G-to-A m

231 2'-deoxyadenosine, 2'-deoxyguanosine, and 2'-deoxycytidine led to accelerated rates of glycoside clea

232 Treatment of HepG2 cells with 5-aza-2'-deoxycytidine led to partial demethylation of the promot

233 samples showed that the 5-(hydroxymethyl)-2'-deoxycytidine level was 5-fold lower in colorectal carci

234 em mass spectrometry of a stable levuglandin-deoxycytidine (LG-dC) adduct that forms upon reaction of

235 (>500 samples in 4 days) assay for measuring deoxycytidine methylation in genomic DNA.

236 Deoxycytidine methylation may regulate cell differentiat

237 sed previously to measure percentage genomic deoxycytidine methylation, a lack of a secure source of

238 w building blocks, 5-(5-phenylfuran-2-yl)-2'-deoxycytidine monomer Y and 5-(1-phenyl-1H-pyrazol-3-yl)

239 onomer Y and 5-(1-phenyl-1H-pyrazol-3-yl)-2'-deoxycytidine monomer Z, that emulate the conformation o

240 ecular bypass therapy with the TK2 products, deoxycytidine monophosphate (dCMP) and deoxythymidine mo

241 inhibition of thymidylate synthase (TS) and deoxycytidine monophosphate (dCMP) deaminase by dZMP, wh

242 The pre-steady-state rate constant of deoxycytidine monophosphate (dCMP) insertion opposite th

243 in (MBP)-fused AID alone and in complex with deoxycytidine monophosphate, we surprisingly identify a

244 nosine (N(6)-CMdA) and N(4)-carboxymethyl-2'-deoxycytidine (N(4)-CMdC), liquid chromatography-ESI tan

245 drazone between a non-natural N(4) -amino-2'-deoxycytidine nucleobase and the aldehyde residue of an

246 Sapacitabine is an oral deoxycytidine nucleoside analog with a unique mechanism

247 , activation-induced deaminase (AID) mutates deoxycytidine on single-stranded DNA (ssDNA) generated b

248 ed cells, exposure of DAOY cells to 5-aza-2'-deoxycytidine or their growth as stem cell-like spheres

249 ion reaction with the opposing thymidine, 2'-deoxycytidine, or 2'-deoxyadenosine.

250 nhibition of methylation with either 5-Aza-2-Deoxycytidine, or siRNA to DNA Methyltransferase (DNMT)

251 , or the DNA methylation inhibitor, 5-Aza-2'-deoxycytidine, partially restored miR-34a levels in huma

252 A new fluorescent base analog, pyrrolo-deoxycytidine (PdC), can now be routinely incorporated i

253 ted by DNA demethylation induced by 5-aza-2'-deoxycytidine plus trichostatin A treatment and the DNA

254 reated with the demethylating agent 5-AZA-2'-deoxycytidine reexpressed IGFBP3 at the mRNA and protein

255 cells with the demethylating agent 5-aza-2'-deoxycytidine reinduces Rap1GAP expression, followed by

256 in G (anti-IgG), and, surprisingly, 5-aza-2'-deoxycytidine require short exposures of 15 min or less.

257 ctivation-induced deaminase (AID) deaminates deoxycytidine residues in immunoglobulin genes, triggeri

258 AID deaminates deoxycytidine residues in single-stranded DNA to deoxyur

259 ngle-domain cytidine deaminase that converts deoxycytidine residues to deoxyuridine in single-strande

260 g of those that contained densely methylated deoxycytidine residues within CpGs and those that were l

261 d treatment with demethylating agent 5-aza-2-deoxycytidine restored DOC2B expression.

262 o the chromatin demethylating agent 5-aza-2'-deoxycytidine restored HSPA1A expression.

263 the DNA methyltransferase inhibitor 5-aza-2'-deoxycytidine restored PDLIM2 expression and resulted in

264 the DNA methyltransferase inhibitor 5-aza-2'-deoxycytidine restored the down-regulation of E-cadherin

265 at CpG islands, and treatment with 5'-aza-2'-deoxycytidine restores near-normal levels of methylation

266 the DNA methyltransferase inhibitor 5-aza-2'-deoxycytidine, restoring both SOD2 expression and the ra

267 reatment of myeloid cell lines with 5-aza-2'-deoxycytidine resulted in a significant decrease in the

268 l lines with the demethylating drug 5-aza-2'-deoxycytidine resulted in increased LXN expression.

269 cking methylation by treatment with 5-aza-2'-deoxycytidine resulted in reduced H3K4me3 binding in the

270 treated with the demethylating agent 5-aza-2'deoxycytidine revealed miR-196b and miR-34c-5p to be epi

271 the DNA methyltransferase inhibitor 5-aza-2'-deoxycytidine reverses the methylation of the PDLIM2 pro

272 adaptive cell types differ in glycolytic and deoxycytidine salvage demands during an immune response

273 D-(arabinofuranosyl)cytosine ([18F]-FAC) for deoxycytidine salvage.

274 ethyl-2'-deoxyuridine and 5-hydroxymethyl-2'-deoxycytidine, should be mutagenic.

275 Treatment of cells with 5-aza-deoxycytidine stimulated the expression of miR-148a in t

276 for the endogenous nucleosides thymidine and deoxycytidine than wild type TK2, and its ectopic expres

277 The furanose ring within the deoxycytidine that is the methylation target displays th

278 egulation was reversed in vivo by a 5-aza-2'-deoxycytidine therapy of T or NK LGL leukemia, which sig

279 d to the 5-position of 2'-deoxyuridine or 2'-deoxycytidine through a propyne linker.

280 Activation-induced deaminase converts deoxycytidine to deoxyuridine at the Ig loci.

281 ficiency virus type 1 virions and deaminates deoxycytidine to deoxyuridine on nascent minus-strand re

282 cytidine derivative, proposed to be 3'-keto-deoxycytidine, to dCTP and a small amount of cytosine.

283 riptional activity was dependent of 5-aza-2'-deoxycytidine treatment and enhanced by interferon-gamma

284 We show that 5-aza-2'-deoxycytidine treatment not only reactivates genes but d

285 WIF1 re-expression upon 5-aza-2'-deoxycytidine treatment or WIF1 gene transfer induces si

286 5% to 93% of the HNSCC samples, and 5-aza-2'-deoxycytidine treatment was able to restore expression i

287 amples, and DNA demethylation using 5-aza-2'-deoxycytidine treatment was able to significantly restor

288 5-Aza-2'-deoxycytidine treatment, bisulfite DNA sequencing, and m

289 transcriptional activity following 5-aza-2'-deoxycytidine treatment.

290 ow that inactivation of dCK in mice depletes deoxycytidine triphosphate (dCTP) pools and induces RS,

291 synthesis to enhance the intrinsic levels of deoxycytidine triphosphate (dCTP).

292 Escherichia coli involves DNAP IV inserting deoxycytidine triphosphate opposite [+ta]-B[a]P-N(2)-dG

293 (dCK) in multiple cancer cell lines depletes deoxycytidine triphosphate pools leading to DNA replicat

294 DNA chlorination damage product, 5-chloro-2'-deoxycytidine, was quantified in diseased human colon sa

295 ethyl-2'-deoxyuridine and 5-hydroxymethyl-2'-deoxycytidine were found to increase the mutation freque

296 se cytosine, and nucleosides cytidine and 2'-deoxycytidine were immobilized by soft landing on plasma

297 o 5-formyl-2'-deoxycytidine and 5-carboxy-2'-deoxycytidine were lower in colorectal carcinoma tissue

298 the DNA methyltransferase inhibitor 5-aza-2'-deoxycytidine, which reduced DNA methylation from 3.1% i

299 -deaza-2'-deoxyguanosine and 5-octadiynyl-2'-deoxycytidine with unsymmetrical 2,5-bis(azidomethyl)pyr

300 protonation of N3 in deoxythymidine and not deoxycytidine would facilitate hydrogen bonding of dTTP