ライフサイエンスコーパス: methylcytosine

1 ther 5- GAG CA-3 or 5- GAG CA-3 (where M = 5-methylcytosine).

2 binding to chromatin primarily depends on 5-methylcytosine.

3 chemistry extended to enable detection of 5-methylcytosine.

4 n: N6-methyladenine, N4-methylcytosine and 5-methylcytosine.

5 the levels of 5-hydroxymethylcytosine over 5-methylcytosine.

6 ich can be assigned to the nucleobases and 5-methylcytosine.

7 tion was inversely correlated with that of 5-methylcytosine.

8 major energetic coupling between the two CpG methylcytosines.

9 5-hydroxymethylcytosine and further oxidize methylcytosines.

10 es because of imperfect repair of deaminated methylcytosines.

11 is active site can accommodate and excise N3-methylcytosine (3mC) and N1-methyladenine (1mA), which a

12 enine (6mA), 5-methylcytosine (5mC) and N(4)-methylcytosine (4mC), will enable strategies to make the

13 on direct hydrophobic interactions with the methylcytosine 5-methyl group.

14 even translocation (Tet) proteins catalyze 5-methylcytosine (5 mC) conversion to 5-hydroxymethylcytos

15 Modification of DNA resulting in 5-methylcytosine (5 mC) or 5-hydroxymethylcytosine (5hmC)

16 thylcytosine (5 hmC), the oxidized form of 5-methylcytosine (5 mC), is a base modification with emerg

17 closely related variants, cytosine (C) and 5'methylcytosine (5'mC), relies on a combination of nucleo

18 5-methylcytosine (5-mC) and 5-hydroxymethylcytosine (5-hmC

19 We measured the percentage of 5-methylcytosine (5-mC) and 5-hydroxymethylcytosine (5-hmC

20 ytosine can undergo modifications, forming 5-methylcytosine (5-mC) and its oxidized products 5-hydrox

21 the impact of arsenic on the oxidation of 5-methylcytosine (5-mC) mediated by the Ten-eleven translo

22 on results from the enzymatic oxidation of 5-methylcytosine (5-mC) to 5-hydroxymethylcytosine (5-hmC)

23 e sensitive to base modifications, such as 5-methylcytosine (5-mC).

24 DNA methylation, detected as 5-methylcytosine (5-MeC) immunofluorescence in isolated IC

25 The methylation of cytosine to 5-methylcytosine (5-meC) is an important epigenetic DNA mo

26 NMT-3a]; DNA methyltransferase-1 [DNMT-1]; 5-methylcytosine [5-mC]; and 5-hydroxymethylcytosine [5-hm

27 proton-bound heterodimers of cytosine and 5-methylcytosine, 5-fluorocytosine, 5-bromocytosine, and 5

28 n DNA polymerase beta is not affected when 5-methylcytosine, 5-hydroxmethylcytosine, and 5-formylcyto

29 apply a statistical algorithm to estimate 5-methylcytosine, 5-hydroxymethylcytosine and unmethylated

30 tion detection revealed an accumulation of 5-methylcytosine, 5-hydroxymethylcytosine, and 5-formylcyt

31 ed DNA bases in mammalian genomes, such as 5-methylcytosine ((5m)C) and its oxidized forms, are impli

32 ation (TET) proteins catalyze oxidation of 5-methylcytosine ((5m)C) residues in nucleic acids to 5-hy

33 The modifications 5-methylcytosine (5mC) and 5-hydroxymethylcytosine (5hmC)

34 5-Methylcytosine (5mC) and 5-hydroxymethylcytosine (5hmC)

35 uantitative and qualitative assessments of 5-methylcytosine (5mC) and 5-hydroxymethylcytosine (5hmC)

36 rd for mapping DNA modifications including 5-methylcytosine (5mC) and 5-hydroxymethylcytosine (5hmC)

37 er, this method cannot distinguish between 5-methylcytosine (5mC) and 5-hydroxymethylcytosine (5hmC).

38 suggested that Tet3-mediated oxidation of 5-methylcytosine (5mC) and DNA replication-dependent dilut

39 ily enzymes (TET1, TET2, and TET3) oxidize 5-methylcytosine (5mC) and generate 5-hydroxymethylcytosin

40 aegleria Tet-like protein, NgTet1, acts on 5-methylcytosine (5mC) and generates 5-hydroxymethylcytosi

41 as an intermediate in the demethylation of 5-methylcytosine (5mC) and in the reactivation of silenced

42 5-Methylcytosine (5mC) and its oxidized derivative 5-hydro

43 stems, including N(6)-methyladenine (6mA), 5-methylcytosine (5mC) and N(4)-methylcytosine (4mC), will

44 DNA base modifications, such as C5-methylcytosine (5mC) and N6-methyldeoxyadenosine (6mA),

45 EPIC) is a common method for interrogating 5-methylcytosine (5mC) at single nucleotide resolution.

46 tosine (5hmC) and a concurrent increase in 5-methylcytosine (5mC) at the eight-cell stage.

47 new methods to quantitatively map oxidized 5-methylcytosine (5mC) bases at high resolution.

48 hmC) is produced by enzymatic oxidation of 5-methylcytosine (5mC) by 5mC oxidases (the Tet proteins).

49 Successive oxidations of 5-methylcytosine (5mC) by Tet dioxygenases generate 5-hydr

50 5hmC is converted from 5-methylcytosine (5mC) by Tet methylcytosine dioxygenases,

51 In mammals, DNA methylation in the form of 5-methylcytosine (5mC) can be actively reversed to unmodif

52 n in the Protein Data Bank (PDB) shows how 5-methylcytosine (5mC) can be recognized in various ways b

53 The TET family of 5-methylcytosine (5mC) dioxygenases plays critical roles i

54 The Arabidopsis ROS1/DEMETER family of 5-methylcytosine (5mC) DNA glycosylases are the first gene

55 This impact of p53 loss on 5-methylcytosine (5mC) heterogeneity was also evident in h

56 We show that 5-methylcytosine (5mC) hypomethylation in hypoxic regions

57 Oxidation of 5-methylcytosine (5mC) in DNA by the ten-eleven translocat

58 5-Methylcytosine (5mC) in DNA CpG islands is an important

59 TET-family dioxygenases oxidize 5-methylcytosine (5mC) in DNA, and exert tumour suppressor

60 anslocation proteins, enzymes that oxidize 5-methylcytosine (5mC) in DNA, has revealed novel mechanis

61 r oxidation of the 5-methyl substituent on 5-methylcytosine (5mC) in DNA.

62 While the role of 5-methylcytosine (5mC) in FMR1 gene silencing has been stu

63 has long been argued that the emergence of 5-methylcytosine (5mC) in many species was driven by the r

64 iated (SRA) domains bind to DNA containing 5-methylcytosine (5mC) in the hemi-methylated CpG sequence

65 initiates DNA demethylation by converting 5-methylcytosine (5mC) into 5-hydroxymethylcytosine (5hmC)

66 initiates DNA demethylation by converting 5-methylcytosine (5mC) into 5-hydroxymethylcytosine (5hmC)

67 emethylation through iteratively oxidizing 5-methylcytosine (5mC) into 5-hydroxymethylcytosine (5hmC)

68 ioxygenases that catalyze the oxidation of 5-methylcytosine (5mC) into 5-hydroxymethylcytosine (5hmC)

69 tion (TET) family of enzymes which oxidize 5-methylcytosine (5mC) into 5-hydroxymethylcytosine (5hmC)

70 ymes are responsible for the conversion of 5-methylcytosine (5mC) into its hydroxymethylated (5hmC),

71 Methylation of cytosine to 5-methylcytosine (5mC) is a prevalent DNA modification fou

72 5-methylcytosine (5mC) is a widely studied epigenetic modi

73 5-Methylcytosine (5mC) is an epigenetic modification invol

74 ss of genic 5hmC was independent of global 5-methylcytosine (5mC) levels and could be partially rescu

75 oach provides the direct quantification of 5-methylcytosine (5mC) levels at single genomic nucleotide

76 Whereas the increase of genomic 5-methylcytosine (5mC) levels during exit from pluripotenc

77 riction enzymes that cleave DNA containing 5-methylcytosine (5mC) or 5-hydroxymethylcytosine (5hmC).

78 46 is known to contact the methyl group of 5-methylcytosine (5mC) or thymine (5-methyluracil).

79 cs to analyze heterogeneity of genome-wide 5-methylcytosine (5mC) patterns within mouse liver.

80 oocytes, characterized by gamete-specific 5-methylcytosine (5mC) patterns, are reprogrammed during e

81 5-methylcytosine (5mC) represents the most common chemical

82 ished that mammalian SRA domain recognizes 5-methylcytosine (5mC) through a base-flipping mechanism.

83 ch promotes DNA demethylation by oxidizing 5-methylcytosine (5mC) to 5-hydroxymethycytosine (5hmC) an

84 leven translocation (Tet) proteins convert 5-methylcytosine (5mC) to 5-hydroxymethylcytosine (5hmC) a

85 family dioxygenases catalyze conversion of 5-methylcytosine (5mC) to 5-hydroxymethylcytosine (5hmC) a

86 TET) enzymes can catalyze the oxidation of 5-methylcytosine (5mC) to 5-hydroxymethylcytosine (5hmC) a

87 ha-KG)-dependent dioxygenases that oxidize 5-methylcytosine (5mC) to 5-hydroxymethylcytosine (5hmC) a

88 hylation by DNMTi and active conversion of 5-methylcytosine (5mC) to 5-hydroxymethylcytosine (5hmC) b

89 Tet1 and Tet2 catalyzed conversion of 5-methylcytosine (5mC) to 5-hydroxymethylcytosine (5hmC) i

90 ion (Tet) family-mediated DNA oxidation on 5-methylcytosine (5mC) to 5-hydroxymethylcytosine (5hmC) r

91 DNA methylcytosine oxidases that converts 5-methylcytosine (5mC) to 5-hydroxymethylcytosine (5hmC) t

92 TET proteins, by converting 5-methylcytosine (5mC) to 5-hydroxymethylcytosine (5hmC),

93 ays a part in these processes by oxidizing 5-methylcytosine (5mC) to 5-hydroxymethylcytosine (5hmC),

94 TET is able to oxidise 5-methylcytosine (5mC) to 5-hydroxymethylcytosine (5hmC),

95 on (TET) enzymes mediate the conversion of 5-methylcytosine (5mC) to 5-hydroxymethylcytosine (5hmC),

96 thylation in mammals involves oxidation of 5-methylcytosine (5mC) to 5-hydroxymethylcytosine (5hmC),

97 ent dioxygenases that successively oxidize 5-methylcytosine (5mC) to 5-hydroxymethylcytosine (5hmC),

98 involves global TET3-mediated oxidation of 5-methylcytosine (5mC) to 5-hydroxymethylcytosine (5hmC),

99 TET enzymes oxidize 5-methylcytosine (5mC) to 5-hydroxymethylcytosine (5hmC),

100 eleven translocation (TET) enzymes oxidize 5-methylcytosine (5mC) to 5-hydroxymethylcytosine and othe

101 p, the TET family of enzymes which convert 5-methylcytosine (5mC) to 5hmC are responsive to the prese

102 er show that TET1, an enzyme that converts 5-methylcytosine (5mC) to 5hmC, responds to DNA damage and

103 TET proteins catalyzing the conversion of 5-methylcytosine (5mC) to 5hmC.

104 t least 10-fold less efficient at mutating 5-methylcytosine (5mC) to thymine than APOBEC3A in a genet

105 ylcytosine (5hmC), a DNA base derived from 5-methylcytosine (5mC) via oxidation by ten-eleven translo

106 ethylation at selective cytosine residues (5-methylcytosine (5mC)) and their removal by TET-mediated

107 group in the 5-carbon position (thymine or 5-methylcytosine (5mC)).

108 c and epigenomic analyses, we investigated 5-methylcytosine (5mC), 5-hydroxymethylcytosine (5hmC) and

109 Such DNA modifications include canonical 5-methylcytosine (5mC), 5-hydroxymethylcytosine (5hmC), 5-

110 ylcytosine (5hmC), a DNA base derived from 5-methylcytosine (5mC), accounts for ~40% of modified cyto

111 tion rate in CpG sites has been related to 5-methylcytosine (5mC), an epigenetically modified base wh

112 ep process that erases the epigenetic mark 5-methylcytosine (5mC), and derivatives thereof, convertin

113 riation, particularly of the modified base 5-methylcytosine (5mC), but taxonomic sampling of disparat

114 5-Methylcytosine (5mC), generated through the covalent add

115 alyze up to three successive oxidations of 5-methylcytosine (5mC), generating 5-hydroxymethylcytosine

116 cytosine (5hmC), an oxidized derivative of 5-methylcytosine (5mC), has been implicated as an importan

117 ating that N6-methyladenine (6mA), and not 5-methylcytosine (5mC), is the main DNA methylation mark i

118 le Decitabine reduces the global levels of 5-methylcytosine (5mC), it results in paradoxical increase

119 ET) dioxygenases catalyze the oxidation of 5-methylcytosine (5mC), the central epigenetic regulator o

120 5-Methylcytosine (5mC), the major modified DNA base in mam

121 Although 5fC is an oxidation product of 5-methylcytosine (5mC), the two epigenetic marks show dist

122 d mainly at CHH sites and characterized by 5-methylcytosine (5mC), there were significant differences

123 together with a reduction in the level of 5-methylcytosine (5mC).

124 importance of eukaryotic DNA methylation [5-methylcytosine (5mC)] in transcriptional regulation and

125 lobal 5-hydroxymethylcytosine (%-5hmC) and 5-methylcytosine (%-5mC) DNA content in blood collected at

126 Cytosine methylation (5-methylcytosine [5mC]) of DNA is the quintessential epige

127 mined the contribution of DNA methylation (5-methylcytosine [5mC]) to AATD liver disease heterogeneit

128 ensor for the detection of methylated DNA (5-methylcytosine, 5mC) and its oxidation derivatives namel

129 Altered DNA methylation (5-methylcytosine, 5mC) might be one underlying mechanism.

130 DNA methylation (5-methylcytosine, 5mC) plays critical biological functions

131 C)8 and (GGCCCC)8 strands with and without 5-methylcytosine (5mCpG) or 5-hydroxymethylcytosine (5hmCp

132 ology, the dynamic addition and removal of 5-methylcytosines (5mCs) are necessary for lineage differe

133 The genome-wide depletion of 5-methylcytosines (5meCs) caused by passive dilution throu

134 served that TP caused a global decrease in 5-methylcytosine abundance in both sexes, a transmissible

135 Remodelling of histones and genomic 5'-methylcytosine and 5'-hydroxymethylcytosine following em

136 , in particular the cytosine modifications 5-methylcytosine and 5-hydroxymethylcytosine (5hmC).

137 level was accompanied by an enrichment of 5-methylcytosine and 5-hydroxymethylcytosine at Bdnf gene

138 t1 to genomic binding sites to orchestrate 5-methylcytosine and 5-hydroxymethylcytosine dynamics.

139 5-Methylcytosine and 5-Hydroxymethylcytosine in DNA are ma

140 Here, we resolve genome-wide 5-methylcytosine and 5-hydroxymethylcytosine in glioblasto

141 ation, we performed genome-wide mapping of 5-methylcytosine and 5-hydroxymethylcytosine in purified m

142 ired irradiated mice we observed increased 5-methylcytosine and 5-hydroxymethylcytosine levels in the

143 al modifications on DNA molecules, such as 5-methylcytosine and 5-hydroxymethylcytosine, play importa

144 e types of methylation: N6-methyladenine, N4-methylcytosine and 5-methylcytosine.

145 e associated with the oxidative conversion 5-methylcytosine and 5hmC, during cytosine demethylation.

146 Intragenic 5-methylcytosine and CTCF mediate opposing effects on pre-

147 ed the MCF-7 and MCF-10A methylomes to map 5-methylcytosine and found the majority of sequences were

148 cytosine and H3K4m3 and an increase in DNA 5-methylcytosine and H3K9m2 in the promoter and enhancer r

149 tive enough to distinguish between cytosine, methylcytosine and hydroxymethylcytosine.

150 A rejection and restriction) recognizes both methylcytosine and methyladenine.

151 st in the genomic distributions of 6mA and 5-methylcytosine and reinforce a distinct role for 6mA as

152 n the modification status of two DNA bases 5-methylcytosine and thymine (5-methyluracil).

153 These two elements share the feature that 5-methylcytosine and thymine both have a methyl group in t

154 ptomic modifications N(1)-methyladenosine, 5-methylcytosine, and pseudouridine (Psi) via bisulfite tr

155 xylcytosine (5caC); together, these oxidized methylcytosines are intermediates in DNA demethylation.

156 al exchange of 5-hydroxymethylcytosine and 5-methylcytosine at downstream CTCF-binding sites is a gen

157 binding specificity and genome occupancy of methylcytosine binding protein 2 (MeCP2).

158 mic DNA methylation pattern is translated by methylcytosine binding proteins like MeCP2 into chromati

159 Although highly homologous to other methylcytosine-binding domain (MBD) proteins, MBD3 does

160 The methylcytosine-binding domain 2 (MBD2) protein recruits

161 Methylcytosine-binding proteins containing SRA (SET- and

162 global DNA methylation, Dnmt activity, and 5-methylcytosine but decreased Tet activity and 5-hydroxym

163 iyama et al. (2015) show that oxidation of 5-methylcytosine by the methylcytosine dioxygenase Tet2 re

164 Oxidation of 5-methylcytosine by the Ten-eleven translocation (TET) fam

165 tes containing extended derivatives of the 5-methylcytosine carrying linear carbon chains and adjacen

166 The iterative oxidation of 5-methylcytosine catalyzed by ten-eleven translocation enz

167 roceed at very similar rates for cytosine, 1-methylcytosine, cytidine, and cytidine 5'-phosphate, and

168 lio-ME3 remarkably boost gene activation and methylcytosine demethylation of targeted loci.

169 ysis showed that homeodomain specificity for methylcytosine depends on direct hydrophobic interaction

170 ylated cytosines (stage I) followed by a Tet methylcytosine dioxygenase (Tet)-dependent decrease in m

171 trated that loss of ten-eleven translocation methylcytosine dioxygenase (TET2)-mediated 5-hydroxymeth

172 ng factor Y-box binding protein 1 (YB-1) and methylcytosine dioxygenase 1 (Tet1), bind to BDNF chroma

173 The contribution of Tet methylcytosine dioxygenase 2 (TET2) and nuclear factor k

174 Tet methylcytosine dioxygenase 2 (Tet2) is an epigenetic reg

175 , DNA methyltransferase 3 Beta (DNMT3B), Tet methylcytosine dioxygenase 2 (TET2), and Thymine DNA gly

176 of gene expression: ten-eleven translocation methylcytosine dioxygenase 2 (TET2).

177 ts interaction with ten-eleven translocation methylcytosine dioxygenase 3 (TET3), a protein responsib

178 occurs, suggesting rapid concomitant loss of methylcytosine dioxygenase activity.

179 TET1 is a 5-methylcytosine dioxygenase and its DNA demethylating act

180 seq with genetic perturbation identifies DNA methylcytosine dioxygenase as an epigenetic barrier into

181 rt diminished ten-eleven translocation (TET) methylcytosine dioxygenase expression and loss of the DN

182 alysed by the ten eleven translocation (Tet) methylcytosine dioxygenase family members, and the roles

183 en translocation-2 (TET2) is a member of the methylcytosine dioxygenase family of enzymes and has bee

184 TET2, a methylcytosine dioxygenase highly expressed in these cel

185 In this article, we demonstrate that the methylcytosine dioxygenase ten-eleven translocation (TET

186 DNA methylcytosine dioxygenase Ten-eleven translocation 1 (T

187 nt functions of opioids were not observed in methylcytosine dioxygenase ten-eleven translocation 1 (T

188 tic alterations in metastatic tumours in the methylcytosine dioxygenase ten-eleven translocation 2 (T

189 The methylcytosine dioxygenase TET1 ('ten-eleven translocati

190 In contrast, methylcytosine dioxygenase TET1 (TET1) expression was su

191 ow that oxidation of 5-methylcytosine by the methylcytosine dioxygenase Tet2 regulates cytokine produ

192 Ten-Eleven-Translocation-2 (Tet2) is a DNA methylcytosine dioxygenase that functions as a tumor sup

193 TET3 is a methylcytosine dioxygenase that initiates DNA demethylat

194 lts show that ten eleven translocation (TET) methylcytosine dioxygenase, predominantly TET1 in HCC ce

195 Mechanistically, this involves TET1, a 5-methylcytosine dioxygenase.

196 Mechanistically, Lin28A recruits 5-methylcytosine-dioxygenase Tet1 to genomic binding sites

197 Somatic mutations of Tet-methylcytosine-dioxygenase-2 (TET2), a key enzyme in DNA

198 Ten-eleven translocation (TET) methylcytosine dioxygenases are enzymes that catalyze th

199 The Tet 5-methylcytosine dioxygenases catalyze DNA demethylation b

200 Here, we reveal the methylcytosine dioxygenases TET1 and TET2 as active regu

201 H2S maintained expression of methylcytosine dioxygenases Tet1 and Tet2 by sulfhydrati

202 converted from 5-methylcytosine (5mC) by Tet methylcytosine dioxygenases, for which Fe(II) is an esse

203 generation by serving as a cofactor for TET methylcytosine dioxygenases.

204 riptional regulator ten-eleven translocation methylcytosine dioxygenease 1 (TET1) has not been well c

205 sing gene regulatory circuit centered on a 5-methylcytosine DNA glycosylase gene is required for long

206 The 5-methylcytosine DNA glycosylase/lyase REPRESSOR OF SILENC

207 facilitate active DNA demethylation by the 5-methylcytosine DNA glycosylase/lyase ROS1.

208 ies of cytosine DNA methyltransferases and 5-methylcytosine DNA glycosylases interact to maintain epi

209 Casilio-ME, that enables not only RNA-guided methylcytosine editing by targeting TET1 to genomic site

210 through RNA polymerase II pausing, whereas 5-methylcytosine evicts CTCF, leading to exon exclusion.

211 o the rate of acid-catalyzed hydrolysis of 1-methylcytosine, for which it furnishes a satisfactory ki

212 While some DNA base modifications such as 5-methylcytosine have been known and studied for decades,

213 minal T hydroxylase (TH) homologous to the 5-methylcytosine hydroxylase domain in TET proteins and a

214 3a, and Dnmt3b) and Ten-eleven translocation methylcytosine hydroxylases (Tet2) in nephron progenitor

215 hydroxylases, including the TET family of 5'-methylcytosine hydroxylases.

216 r-guanine-domain binding proteins, reduced 5-methylcytosine immunoreactivity in the molecular and Pur

217 ic pattern in the content of mitochondrial 5-methylcytosine in amyloid precursor protein/presenilin 1

218 study shows the presence of mitochondrial 5-methylcytosine in CpG and non-CpG sites in the entorhina

219 TET proteins oxidize 5-methylcytosine in DNA to 5-hydroxymethylcytosine and oth

220 slocation 2 (TET2) protein, which oxidizes 5-methylcytosine in DNA, can also bind RNA; however, the t

221 ved in DNA methylation, was localized with 5-methylcytosine in the prophase nucleus of a subset of KI

222 ons through the recognition of symmetrical 5-methylcytosines in CpG (mCG) dinucleotides.

223 5-hydroxymethylcytosine (5hmC) and oxidized methylcytosines in DNA.

224 o 5-hydroxymethylcytosine and other oxidized methylcytosines in DNA.

225 n silico structural modeling, we show that 5-methylcytosine indeed causes steric hindrance in the HIF

226 leven Translocation) family produce oxidized methylcytosines, intermediates in DNA demethylation, as

227 o 5-hydroxymethylcytosine and other oxidized methylcytosines, intermediates in DNA demethylation.

228 y enzymes, which catalyze the oxidation of 5-methylcytosine into 5-hydroxymethylcytosine and further

229 DNA conversions by TET family proteins of 5-methylcytosine into 5-hydroxymethylcytosine, 5-formylcyt

230 hylation at the PWS-IC where a decrease in 5-methylcytosine is observed in association with a concomi

231 5-methylcytosine is the most studied DNA epigenetic modifi

232 It has been widely accepted that 5-methylcytosine is the only form of DNA methylation in ma

233 One such modification, 5-methylcytosine, is relatively abundant in mammalian mRNA

234 Moreover, increased mitochondrial 5-methylcytosine levels are found in the D-loop region of

235 Finally, a loss of mitochondrial 5-methylcytosine levels in the D-loop region is found in t

236 1) A), N(1) -methylguanosine (m(1) G), N(3) -methylcytosine (m(3) C), and N(2) ,N(2) -dimethylguanosi

237 panosoma brucei tRNA(Thr) is methylated to 3-methylcytosine (m(3)C) as a pre-requisite for C-to-U dea

238 tions than the average cellular mRNA, with 5-methylcytosine (m(5)C) and 2'O-methyl modifications bein

239 ccurrence of N(6)-methyladenosine (m(6)A), 5-methylcytosine (m(5)C) and pseudouridine (Psi) in RNA, a

240 For 5-methylcytosine (m(5)C) however, it is largely unknown ho

241 al methylation of RNA cytosine residues to 5-methylcytosine (m(5)C) is an important modification with

242 We found that 5-methylcytosine (m(5)C) is highly enriched in viral genom

243 target for the previously uncharacterized 5-methylcytosine (m(5)C) methyltransferase NSun3 and link

244 NA (mRNA) N(6)-methyladenosine (m(6)A) and 5-methylcytosine (m(5)C), and DNA N(6)-methyldeoxyadenosin

245 er RNAs with N(6)-methyladenosine (m(6)A), 5-methylcytosine (m(5)C), and pseudouridine (Psi).

246 y the METTL2 methyltransferase to form the 3-methylcytosine (m3C) modification.

247 denine (m6A), 5-methylcytosine (m5C), and N4-methylcytosine (m4C).

248 esidues to include N6-methyladenine (m6A), 5-methylcytosine (m5C), and N4-methylcytosine (m4C).

249 Cytosine (C) modifications such as methylcytosine (mC) and hydroxymethylcytosine (hmC) are

250 e from mutagenic G .: T mispairs caused by 5-methylcytosine (mC) deamination and other lesions includ

251 However, deamination of 5-methylcytosine (mC) generates thymine, a canonical DNA b

252 Tet enzymes catalyze stepwise oxidation of 5-methylcytosine (mC) in CpGs to 5-hydroxymethylcytosine (

253 Methylation of cytosine to 5-methylcytosine (mC) is a prevalent reversible epigenetic

254 5-Methylcytosine (mC) is an epigenetic mark that is writte

255 NA demethylation via deamination of either 5-methylcytosine (mC) or TET-oxidized mC bases (ox-mCs), w

256 ved, as has discrimination among cytosine, 5-methylcytosine (mC), and 5-hydroxymethylcytosine (hmC).

257 individual selectivities for cytosine (C), 5-methylcytosine (mC), and hmC at user-defined DNA sequenc

258 .T mismatches that arise by deamination of 5-methylcytosine (mC), and it excises 5-formylcytosine and

259 c G.T mispairs arising from deamination of 5-methylcytosine (mC), and it processes other deamination-

260 Because 5-methylcytosine methyltransferase DNMT1 is also a potenti

261 esults show that TET-mediated oxidation of 5-methylcytosine modulates Lefty-Nodal signalling by promo

262 enzymes that catalyze the demethylation of 5-methylcytosine on DNA.

263 ain, preferentially cleaved DNA containing 5-methylcytosine or 5-hydroxymethylcytosine.

264 In mammals, the oxidized methylcytosines (oxi-mCs) function as epigenetic marks a

265 (TET) dioxygenases oxidize 5mC into oxidized methylcytosines (oxi-mCs): 5-hydroxymethylcytosine (5hmC

266 The methylcytosine oxidase TET proteins play important roles

267 2) encodes a member of the TET family of DNA methylcytosine oxidases that converts 5-methylcytosine (

268 ased Tet1 heterochromatin localization and 5-methylcytosine oxidation are dependent on the CXXC3 doma

269 s system of mammals and which results from 5-methylcytosine oxidation by TET enzymes.

270 ivering TET1 and protein factors that couple methylcytosine oxidation to DNA repair activities, and/o

271 oxygenase that catalyses multiple steps of 5-methylcytosine oxidation.

272 monstrate that Mbd1 enhances Tet1-mediated 5-methylcytosine oxidation.

273 enzymes catalyse DNA demethylation through 5-methylcytosine oxidation.

274 Here, we focus on the interplay of the 5-methylcytosine reader Mbd1 and modifier Tet1 by analyzin

275 n of YTH and SRA domains (the latter a DNA 5-methylcytosine reader) revealed them to be diverse membe

276 Like 5-methylcytosine residues from which they are derived, oxi

277 The hydrolytic deamination of cytosine and 5-methylcytosine residues in DNA appears to contribute sig

278 Reduced TET levels culminate in increased 5-methylcytosine, resulting in CTCF eviction and exon excl

279 de analysis of N(6) -methyladenine and N(4) -methylcytosine revealed high methylation levels in both

280 ly distinguish the taxonomic forms of life-5-methylcytosine separates prokaryotes from eukaryotes and

281 levels and that Lux can process any oxidized methylcytosine sequencing data sets to quantify all cyto

282 on, placing the methyl group comparable to 3-methylcytosine, the prototypic substrate of AlkB.

283 talyze methylation through modification of 5-methylcytosine to 5-hmC.

284 These TETs convert 5-methylcytosine to 5-hydroxymethylcytosine (5-hmC) in DNA

285 TET enzymes oxidize 5-methylcytosine to 5-hydroxymethylcytosine and other oxid

286 TET2 enzymatically converts 5-methylcytosine to 5-hydroxymethylcytosine as well as oth

287 s, on the other hand, blocks Tet1-mediated 5-methylcytosine to 5-hydroxymethylcytosine conversion, in

288 TET) proteins are involved in oxidation of 5-methylcytosine to 5-hydroxymethylcytosine which can be f

289 TET proteins oxidize 5-methylcytosine to 5-hydroxymethylcytosine, 5-formylcytos

290 slocation (Tet) family of enzymes converts 5-methylcytosine to 5-hydroxymethylcytosine, which promote

291 ins are active CpG demethylases converting 5-methylcytosine to 5-hydroxymethylcytosine, with loss of

292 ion of TET2 in promoting the conversion of 5-methylcytosine to hm5C on tRNA and regulating the proces

293 Tet family proteins oxidize 5-methylcytosine to initiate active DNA demethylation thro

294 alternative splicing through conversion of 5-methylcytosine to its oxidation derivatives.

295 The TET enzymes convert methylcytosine to the newly discovered base hydroxymethy

296 les the detection of N6-methyladenine and N4-methylcytosine, two major types of DNA modifications com

297 ylcytosine (5hmC), a DNA base derived from 5-methylcytosine, via oxidation by ten-eleven translocatio

298 ecause genomic DNA used in DAP-seq retains 5-methylcytosines, we determined that >75% (248/327) of Ar

299 etics (histone H3 Lys-4 trimethylation and 5-methylcytosine) were evaluated in samples from 11 22qDS

300 ly reduced affinity for DNA that contains 5'-methylcytosine, which may have implications for the role