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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
14 even translocation (Tet) proteins catalyze 5-methylcytosine (5 mC) conversion to 5-hydroxymethylcytos
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
19 closely related variants, cytosine (C) and 5'methylcytosine (5'mC), relies on a combination of nucleo
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)
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
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)
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).
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
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.
52 hmC) is produced by enzymatic oxidation of 5-methylcytosine (5mC) by 5mC oxidases (the Tet proteins).
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
57 The Arabidopsis ROS1/DEMETER family of 5-methylcytosine (5mC) DNA glycosylases are the first gene
61 mmalian genome, produced upon oxidation of 5-methylcytosine (5mC) in a process catalyzed by TET prote
64 anslocation proteins, enzymes that oxidize 5-methylcytosine (5mC) in DNA, has revealed novel mechanis
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)
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
78 riction enzymes that cleave DNA containing 5-methylcytosine (5mC) or 5-hydroxymethylcytosine (5hmC).
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
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
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
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),
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
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
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
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
131 is involved in these changes by converting 5-methylcytosine (5mec) to 5-hydroxymethylcytosine (5hmec)
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
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.
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
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.
150 cytosine and H3K4m3 and an increase in DNA 5-methylcytosine and H3K9m2 in the promoter and enhancer r
154 st in the genomic distributions of 6mA and 5-methylcytosine and reinforce a distinct role for 6mA as
156 These two elements share the feature that 5-methylcytosine and thymine both have a methyl group in t
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
162 mic DNA methylation pattern is translated by methylcytosine binding proteins like MeCP2 into chromati
166 iyama et al. (2015) show that oxidation of 5-methylcytosine by the methylcytosine dioxygenase Tet2 re
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
176 , DNA methyltransferase 3 Beta (DNMT3B), Tet methylcytosine dioxygenase 2 (TET2), and Thymine DNA gly
180 alysed by the ten eleven translocation (Tet) methylcytosine dioxygenase family members, and the roles
182 In this article, we demonstrate that the methylcytosine dioxygenase ten-eleven translocation (TET
184 tic alterations in metastatic tumours in the methylcytosine dioxygenase ten-eleven translocation 2 (T
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
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
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
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
205 sing gene regulatory circuit centered on a 5-methylcytosine DNA glycosylase gene is required for long
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
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
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
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
226 ved in DNA methylation, was localized with 5-methylcytosine in the prophase nucleus of a subset of KI
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
233 hylation at the PWS-IC where a decrease in 5-methylcytosine is observed in association with a concomi
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
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 (
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-
255 esults show that TET-mediated oxidation of 5-methylcytosine modulates Lefty-Nodal signalling by promo
259 (TET) dioxygenases oxidize 5mC into oxidized methylcytosines (oxi-mCs): 5-hydroxymethylcytosine (5hmC
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
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
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
276 ost current approaches for the analysis of 5-methylcytosine still have limitations of being either de
280 es, including TET1, TET2 and TET3, convert 5-methylcytosine to 5-hydroxymethylcytosine and regulate g
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
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
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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