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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

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