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 tion was inversely correlated with that of 5-methylcytosine.

3 binding to chromatin primarily depends on 5-methylcytosine.

4 as determined by an immunoassay that detects methylcytosine.

5 crease in both 5-hydroxymethylcytosine and 5-methylcytosine.

6 er Fe(II) concentration than the reference 3-methylcytosine.

7 to the C5 position of the cytosine to form 5-methylcytosine.

8 es because of imperfect repair of deaminated methylcytosines.

9 or decreases) methylation levels of specific methylcytosines.

10 major energetic coupling between the two CpG 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 forms, including unmodified cytosine (C), 5-methylcytosine (5 mC), 5-hydroxymethylcytosine (5 hmC),

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

18 tic genomes occur primarily in the form of 5-methylcytosine (5 mC).

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

20 5-methylcytosine (5-mC) and 5-hydroxymethylcytosine (5-hmC

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

22 jor epigenetic modifications of cytosines, 5-methylcytosine (5-mC) and 5-hydroxymethylcytosine (5-hmC

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

24 n are needed as many of the techniques for 5-methylcytosine (5-mC) determination, including methyl-se

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

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

27 ction of ascorbate in the hydroxylation of 5-methylcytosine (5-mC) to 5-hydroxymethylcytosine (5-hmC)

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

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

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

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

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

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

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

35 generate the first combined genomic map of 5-methylcytosine, 5hmC and 5fC in mouse embryonic stem cel

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

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

38 5-Methylcytosine (5mC) and 5-hydroxymethylcytosine (5hmC)

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

40 ional DNA glycosylase/lyase, which excises 5-methylcytosine (5mC) and 5-hydroxymethylcytosine (5hmC)

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

42 tween the mammalian cytosine modifications 5-methylcytosine (5mC) and 5-hydroxymethylcytosine (5hmC),

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

44 yme to exhibit specificity toward hmC over 5-methylcytosine (5mC) and cytosine.

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

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

47 5-Methylcytosine (5mC) and its oxidized derivative 5-hydro

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

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

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

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

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

53 5hmC is converted from 5-methylcytosine (5mC) by Tet methylcytosine dioxygenases,

54 ydroxymethylcytosine (5hmC) converted from 5-methylcytosine (5mC) by the ten-eleven translocation (TE

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

56 The role of the 5-methylcytosine (5mC) dioxygenases Tet1 and Tet2 in the i

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

58 Dynamic changes in 5-methylcytosine (5mC) have been implicated in the regulat

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

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

61 mmalian genome, produced upon oxidation of 5-methylcytosine (5mC) in a process catalyzed by TET prote

62 5-Methylcytosine (5mC) in DNA can be oxidized stepwise to

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

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

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

66 TET dioxygenases successively oxidize 5-methylcytosine (5mC) in mammalian genomes to 5-hydroxyme

67 restriction endonuclease AspBHI recognizes 5-methylcytosine (5mC) in the double-strand DNA sequence c

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

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

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

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

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

73 5-methylcytosine (5mC) is a widely studied epigenetic modi

74 Methylcytosine (5mC) is mostly symmetrically distributed

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

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

77 TET proteins oxidize 5-methylcytosine (5mC) on DNA and play important roles in

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

79 46 is known to contact the methyl group of 5-methylcytosine (5mC) or thymine (5-methyluracil).

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

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

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

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

84 are 5-methylcytosine oxidases that convert 5-methylcytosine (5mC) to 5-hydroxymethylcytosine (5hmC) a

85 Tet enzymes (Tet1/2/3) convert 5-methylcytosine (5mC) to 5-hydroxymethylcytosine (5hmC) a

86 ytosine dioxygenases catalyze oxidation of 5-methylcytosine (5mC) to 5-hydroxymethylcytosine (5hmC) a

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

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

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

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

91 Tet enzymes (Tet1/2/3) convert 5-methylcytosine (5mC) to 5-hydroxymethylcytosine (5hmC) i

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

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

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

99 Demethylation involves oxidation of 5-methylcytosine (5mC) to 5-hydroxymethylcytosine (5hmC),

100 TET proteins oxidize 5-methylcytosine (5mC) to 5-hydroxymethylcytosine (5hmC),

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

102 even translocation) enzymes, which convert 5-methylcytosine (5mC) to 5-hydroxymethylcytosine (5hmC).

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

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

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

106 matic activity that catalyses oxidation of 5-methylcytosine (5mC) to generate 5-hydroxymethylcytosine

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

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

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

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

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

112 ian DNA occur in five forms: cytosine (C), 5-methylcytosine (5mC), 5-hydroxymethylcytosine (5hmC), 5-

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

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

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

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

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

118 oteins, which have the capacity to oxidize 5-methylcytosine (5mC), specifically expressed in reprogra

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

120 rm direct methylation of cytosine to yield 5-methylcytosine (5mC), which serves as part of the epigen

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

122 volves TET-mediated iterative oxidation of 5-methylcytosine (5mC)/5-hydroxymethylcytosine (5hmC) and

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

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

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

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

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

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

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

130 In mammals, paternal 5-methylcytosines (5mCs) have been proposed to be actively

131 is involved in these changes by converting 5-methylcytosine (5mec) to 5-hydroxymethylcytosine (5hmec)

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

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

134 denine and 5-methylcytosine, we show that N4-methylcytosine also has a specific kinetic signature and

135 s to obtain N2'-functionalized thymine and 5-methylcytosine amino-LNA phosphoramidites from these key

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

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

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

139 ealed METH-induced decreased enrichment of 5-methylcytosine and 5-hydroxymethylcytosine at GluA1 and

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

141 5-Methylcytosine and 5-Hydroxymethylcytosine in DNA are ma

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

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

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

145 Dnmt3a is required for both 5-methylcytosine and 5-hydroxymethylcytosine patterning wi

146 smegmatis porin A (MspA) to detect and map 5-methylcytosine and 5-hydroxymethylcytosine within single

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

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

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

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

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

152 ROS1 and its homologs remove 5-methylcytosine and incise the sugar backbone at the abas

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

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

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

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

157 Cytosine, 5-methylcytosine, and 5-hydroxymethylcytosine were identif

158 r, reduces the average methylation levels of methylcytosines, and alters (increases or decreases) met

159 xperiment analyzed a mixture of cytosine-, 5-methylcytosine-, and 5-hydroxymethylcytosine-bearing DNA

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

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

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

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

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

165 Methylcytosine-binding proteins containing SRA (SET- and

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

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

168 ytosine (C-C) pair, followed by the cytosine-methylcytosine (C-mC) pair, and the cytosine-hydroxymeth

169 C with a dose (100nM) that decreases total 5-methylcytosine content and reactivates imprinted genes (

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

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

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

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

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

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

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

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

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

179 Tet methylcytosine dioxygenase converts 5-mC to 5-hmC in DNA

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

181 TET2, a methylcytosine dioxygenase highly expressed in these cel

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

183 DNA methylcytosine dioxygenase Ten-eleven translocation 1 (T

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

185 The methylcytosine dioxygenase TET1 ('ten-eleven translocati

186 The enzyme methylcytosine dioxygenase TET1 (TET1) has been shown to

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

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

189 most likely by acting as a co-factor for Tet methylcytosine dioxygenase to generate 5-hmC.

190 most likely by acting as a co-factor for Tet methylcytosine dioxygenase to hydroxylate 5-mC.

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

192 mutations in ten-eleven translocation (TET) methylcytosine dioxygenase-2 (TET2) associated with a hy

193 gen species and Ten Eleven Translocation 1 5-methylcytosine dioxygenase.

194 catalyzed by Tet (ten-eleven translocation) methylcytosine dioxygenase.

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

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

197 The Tet 5-methylcytosine dioxygenases catalyze DNA demethylation b

198 The ten-eleven translocation (Tet) family of methylcytosine dioxygenases catalyze oxidation of 5-meth

199 The ten-eleven translocation (TET) family of methylcytosine dioxygenases initiates demethylation of D

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 the TET (Ten eleven translocation) family of methylcytosine dioxygenases, thereby inhibiting demethyl

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

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

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

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

208 REPRESSOR OF SILENCING 1 (ROS1) family of 5-methylcytosine DNA glycosylases to protect these genes f

209 of the ROS1 subfamily of genes that encode 5-methylcytosine DNA glycosylases/lyases.

210 t, providing an improved efficiency in the 5-methylcytosine enrichment and genome-wide profiling.

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

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

213 slocation (TET) family enzymes can oxidize 5-methylcytosine has greatly advanced our understanding of

214 ng the ten-eleven translocation (TET) family methylcytosine hydroxylase TET1.

215 re potently inhibits enzymes, such as the 5'-methylcytosine hydroxylase TET2, that have previously be

216 hanism of NANOG and uncover a new role for 5-methylcytosine hydroxylases in the establishment of naiv

217 omain-containing histone demethylases, TET 5-methylcytosine hydroxylases, and EglN prolyl-4-hydroxyla

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

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

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

221 ion epigenetically by directly deaminating 5-methylcytosine in concert with base-excision repair to e

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

223 Oxidation of 5-methylcytosine in DNA by ten-eleven translocation (Tet)

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

225 y dioxygenases, which successively oxidize 5-methylcytosine in DNA.

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

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

228 5-hydroxymethylcytosine (5hmC) and oxidized methylcytosines in DNA.

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

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

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

232 5-methylcytosine is an epigenetic mark that affects a broa

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

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

235 We also assessed 5-methylcytosine levels (an indicator of global DNA methyl

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

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

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

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

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

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

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

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

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

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

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

247 5-Methylcytosine (mC) is an epigenetic mark that impacts t

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

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

250 c G.T mispairs generated by deamination of 5-methylcytosine (mC), and downstream base excision repair

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

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

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

254 Because 5-methylcytosine methyltransferase DNMT1 is also a potenti

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

256 of these motifs as well as for one of two 5-methylcytosine motifs.

257 An elp2 mutation increases the total methylcytosine number, reduces the average methylation l

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

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

260 The methylcytosine oxidase TET proteins play important roles

261 Ten-Eleven Translocation (TET) family are 5-methylcytosine oxidases that convert 5-methylcytosine (5

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

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

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

265 EGCs, whereas Tet1 was necessary to induce 5-methylcytosine oxidation specifically at ICRs.

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

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

268 enzymes catalyse DNA demethylation through 5-methylcytosine oxidation.

269 emethylation process can be deamination of 5-methylcytosine producing the TpG alteration and T:G misp

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

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

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

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

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

275 and consistency, or incapable of analysing 5-methylcytosine specifically.

276 ost current approaches for the analysis of 5-methylcytosine still have limitations of being either de

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

278 translocation (TET) family enzymes convert 5-methylcytosine to 5-hydroxylmethylcytosine.

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

280 es, including TET1, TET2 and TET3, convert 5-methylcytosine to 5-hydroxymethylcytosine and regulate g

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

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

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

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

285 which catalyse the iterative oxidation of 5-methylcytosine to 5-hydroxymethylcytosine, 5-formylcytos

286 on status of DNA by successively oxidizing 5-methylcytosine to 5-hydroxymethylcytosine, 5-formylcytos

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

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

289 family of enzymes (TET1/2/3) that convert 5-methylcytosine to 5-hydroxymethylcytosine.

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

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

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

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

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

295 ed SMRT sequencing of N6-methyladenine and 5-methylcytosine, we show that N4-methylcytosine also has

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

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

298 lcytosine (hmC) is an oxidation product of 5-methylcytosine which is present in the deoxyribonucleic

299 ition date shows in-situ de-methylation of 5-methylcytosine, which can be described as a diagenetic p

300 approach, TAmC-Seq, which selectively tags 5-methylcytosine with an azide functionality that can be f