ライフサイエンスコーパス: deoxycytidine

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

20 2'-C-methylcytidine (MeFdC) and 2'-fluoro-2'-deoxycytidine (2'-FdC).

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

43 5-Aza-2'-deoxycytidine (5-aza-dC) is a nucleoside analogue with c

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

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

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

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

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

49 Using the methylation inhibitor 5-aza-2'-deoxycytidine (5-aza-dC), we investigated whether DNA me

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

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

52 B and pharmacologic inhibition with 5-Aza-2'-deoxycytidine (5-Aza-dC, decitabine) to demonstrate that

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

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

55 Previous studies have shown that 5-Aza-2'deoxycytidine (5-AzadC), a DNMT1 inhibitor, induces re-e

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

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

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

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

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

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

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

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

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

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

66 5-Aza-2'-deoxycytidine (5azaC-dR) has been employed as an inhibit

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

83 3 (Pit-1/0 cells) were treated with 5-aza-2'-deoxycytidine, a demethylating reagent.

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

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

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

87 For LG-deoxycytidine adducts, the initial dihydroxypyrrolidine

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

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

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

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

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

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

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

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

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

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

98 3,N(4)-etheno-2'-deoxycytidine and 1,N(6)-etheno-2'-deoxyadenosine, forme

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

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

101 5-Aza-2'-deoxycytidine and diesel exhaust particle exposure in hu

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

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

104 different positions of the DNA (5-methyl-2'-deoxycytidine and N(6)-methyl-2'-deoxyadenosine) represe

105 ses to the DNMT and HDAC inhibitors 5-Aza-2'-deoxycytidine and suberoylanilide hydroxamic acid in vit

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

123 nditioned media was mediated by secretion of deoxycytidine, but not other deoxynucleosides, through e

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

141 6S) (generated by reaction of bisulfite with deoxycytidine (dC)) to uracil (dU).

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

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

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

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

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

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

148 Activation-induced deoxycytidine deaminase (AID) initiates somatic hypermut

149 2 stems from mutations in activation-induced deoxycytidine deaminase (AID) that abolish immunoglobuli

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

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

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

153 APOBEC3H is a deoxycytidine deaminase that can restrict the replicatio

154 nfectivity, is a single-stranded DNA (ssDNA) deoxycytidine deaminase with two domains, a catalyticall

155 tetrahydrouridine, an inhibitor of cytidine/deoxycytidine deaminase, in patients with a variety of s

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

157 The APOBEC3 family of deoxycytidine deaminases has the ability to restrict HIV

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

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

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

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

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

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

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

165 5-Aza-2'-deoxycytidine decreased, whereas folate-depleted/high-me

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

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

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

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

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

171 hynyl-2'-deoxyuridine (EdU) and 5-ethynyl-2'-deoxycytidine (EdC).

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

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

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

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

176 In preclinical studies, 5-fluoro-2'-deoxycytidine (FdCyd), an inhibitor of DNA methyltransfe

177 an TDG bound to DNA with cadC (5-carboxyl-2'-deoxycytidine) flipped into its active site.

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

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

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

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

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

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

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

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

186 inhibitors (DNMTi) 5-azacytidine and 5-aza-2-deoxycytidine have been approved for the treatment of di

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

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

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

190 ncorporated pyrrolo-deoxycytidine to replace deoxycytidine in another loop.

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

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

193 5-Aza-2'-deoxycytidine induced demethylation of several CpG nucle

194 sarcoma cells with decitabine (DAC, 5-Aza-2'-deoxycytidine) induces expression of ERalpha and leads t

195 Deoxycytidine inhibited the processing of gemcitabine in

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

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

198 t a 2'-endo sugar conformation of the target deoxycytidine is favored for substrate binding and deami

199 ion and MS-based analysis, we measured heavy deoxycytidine isotope incorporation into newly synthesiz

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

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

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

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

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

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

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

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 or activation, 2'-AzCyd is phosphorylated by deoxycytidine kinase (dCK), and we find that expression

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

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

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

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

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

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

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 Low deoxycytidine kinase expression in tumour biopsies from

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

245 3G (A3G) specifically targets and deaminates deoxycytidine nucleotides, generating deoxyuridine, in s

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

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

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

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

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

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

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

253 These results suggest that reducing deoxycytidine production in PSCs may increase the effica

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

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

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

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

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

262 t with the DNA hypomethylating agent 5-aza-2-deoxycytidine restored the ability of Tyk2(-/-) NK cells

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

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

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

266 rophages with methylation inhibitor 5-Aza-2'-deoxycytidine resulted in increased levels of IL-10 when

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

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

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

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

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

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

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

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

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

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

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

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

279 t MUC1-mediated CDA activity corresponded to deoxycytidine to deoxyuridine metabolic reprogramming up

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

281 in one loop region and incorporated pyrrolo-deoxycytidine to replace deoxycytidine in another loop.

282 version of a clinically used drug (5-aza-2'-deoxycytidine) to alter the catalytic activity of DNA me

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

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

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

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

287 5-Aza-2'-deoxycytidine treatment, bisulfite DNA sequencing, and m

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

289 Recently, human dCTPase (deoxycytidine triphosphatase), also known as DCTPP1 (hum

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 A stable heavy isotope of 2'-deoxycytidine was used as an internal standard and one-s

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

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

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