ライフサイエンスコーパス: cytosine

1 when opposite adenine but not when opposite cytosine.

2 model to distinguish 5-mC from unmethylated cytosine.

3 w low to undetectable levels of the modified cytosine.

4 acts at genomic sites containing methylated cytosine.

5 xplain the E446D preference for unmethylated cytosine.

6 derivatives thereof, converting them back to cytosine.

7 ertain bases and certain epigenetic forms of cytosine.

8 een developed beyond the epigenetic marks on cytosine.

9 cleobases and base pairs most favorably with cytosine.

10 rallel profiling of activity on all modified cytosines.

11 s found to proceed at very similar rates for cytosine, 1-methylcytosine, cytidine, and cytidine 5'-ph

12 aguanine as well as 5-substituted uracil and cytosine 2'-deoxyribonucleosides and mono- and triphosph

13 Here we show that cytosine 32 in the anticodon loop of Trypanosoma brucei

14 Methylation at 5-cytosine (5-mC) is a fundamental epigenetic DNA modifica

15 show that inhibition of post-transcriptional cytosine-5 methylation locks tumour-initiating cells in

16 This failed to reveal any known (cytosine-5) DNA methyltransferases, but identified homol

17 Mammalian DNA (cytosine-5) methyltransferase 1 (DNMT1) is essential for

18 e de novo DNA methyltransferase Dnmt3a [DNA (cytosine-5-)-methyltransferase 3 alpha] in this hippocam

19 tely estimate the parameters of unmethylated cytosine (5C), 5mC and 5hmC from Infinium microarray dat

20 f 5-methyl cytosine (5mC) to 5-hydroxymethyl cytosine (5hmC) and play important roles during developm

21 DNA methylation at the 5-position of cytosine (5mC) is an epigenetic modification that regula

22 TET enzymes catalyze conversion of 5-methyl cytosine (5mC) to 5-hydroxymethyl cytosine (5hmC) and pl

23 carbon of the cytosine base to form 5 methyl cytosine (5mC) without altering the DNA sequences.

24 ential to be methylated at the 5-position of cytosine (5mC), or to undergo further oxidation to the 5

25 used by NUCLEOSIDE HYDROLASE1 (NSH1) because cytosine accumulation is strongly reduced in a cda nsh1

26 sion DNA synthesis polymerase to incorporate cytosine across from a replication-stalling G-quadruplex

27 ifying measures that are associated with the cytosine-adenine-guanine (CAG) expansion in individuals

28 ant, but poorly understood, modifications to cytosine affect the local conformational dynamics of a D

29 sferase activity using 5-azacytidine (Aza; a cytosine analog) to limit HSV-1-induced ocular lesions.

30 on first-line therapy with tenofovir plus a cytosine analogue (lamivudine or emtricitabine) plus a n

31 As we have shown previously for our cytosine analogue FRET-pair, FRET between qAN1 and qAnit

32 ance (107 [93%] vs 462 [77%]; p<0.0001), and cytosine analogue resistance (100 [87%] vs 378 [63%]; p=

33 The bright fluorescent cytosine analogue tC(O) stands out among fluorescent bas

34 for the presence of resistance to tenofovir, cytosine analogue, or NNRTIs.

35 Our findings indicate that cytosine analogues restore a balanced haematopoiesis wit

36 ion results in the loss of hydroxymethylated cytosine and a corresponding increase in cytosine methyl

37 In addition, we examined a number of cytosine and adenine methyltransferases to generate doub

38 dates 8-oxoG at the primer terminus opposite cytosine and adenine.

39 We present a framework for mapping cytosine and adenosine methylation with the Oxford Nanop

40 For that, bis-bithiophene derivatized with cytosine and bithiophene derivatized with boronic acid w

41 IS2, MEA, and their paralogs, compared their cytosine and histone methylation patterns, and analyzed

42 etics of hydrolytic deamination reactions of cytosine and its naturally occurring derivatives, we dem

43 The extruded cytosine and last guanine nucleotides form water-mediate

44 ced deaminase (AID) functions by deaminating cytosines and causing U:G mismatches, a rate-limiting st

45 th the natural nucleobases adenine, thymine, cytosine, and guanosine has been performed.

46 ating high amounts of cytidine but also CMP, cytosine, and some uridine in seeds.

47 an display de novo or acquired resistance to cytosine arabinoside (Ara-C), a primary component of ind

48 eferences observed with targeting unmodified cytosine are further exaggerated when deaminating mC.

49 Methylated cytosines are associated with gene silencing.

50 microcin C-like compounds carrying terminal cytosines are biologically active and target aspartyl-tR

51 In mammals, methylated cytosines are found predominantly in CpGs but in plants

52 G sites can only be methylated when internal cytosines are methylated.

53 ts active site such that it is a hybrid of a cytosine as well as a guanine deaminase, thereby conferr

54 haplotype-specific and was most promoted by cytosine at rs609621 in the NSE 3' splice-site (3'ss), w

55 A key finding was that the methylation of cytosine at the specific CpG dinucleotides will particip

56 yl group is located in the same plane as the cytosine base and forms an intra-residue hydrogen bond w

57 yl group is added at the fifth carbon of the cytosine base to form 5 methyl cytosine (5mC) without al

58 of a methyl group at the fifth carbon of the cytosine base.

59 (<6.3), where the protonation of one of the cytosine bases increases the stability of the intrahelic

60 ein are dramatically altered when one of the cytosine bases is replaced with methyl-, hydroxymethyl-,

61 amily enzymes are best known for deaminating cytosine bases to uracil in single-stranded DNA, with ch

62 otides in the human genome are methylated at cytosine bases.

63 DNA cytosine methylation and methyl-cytosine binding domain (MBD) containing proteins are fo

64 MeCP2 is a methyl-cytosine binding protein that is proposed to function as

65 Guanine (G), adenine (A), thymine (T), and cytosine (C) are the four basic constituents of DNA.

66 Methylation of cytosine (C) at C-phosphate-guanine (CpG) sites enhances

67 four out of the seven haplotypes showed high cytosine (C) deaminase activity, with hap V displaying e

68 (5mC) can be actively reversed to unmodified cytosine (C) through TET dioxygenase-mediated oxidation

69 cytidine deaminase APOBEC3F (A3F) deaminates cytosine (C) to uracil (U) and is a known restriction fa

70 POBEC) family of proteins that can deaminate cytosine (C) to uracil (U) on nucleic acids.

71 logical functions mostly through deaminating cytosine (C) to uracil on single-stranded DNA/RNA.

72 e DNA nucleotides (Adenine (A), Guanine (G), Cytosine (C), and Thymine (T)) on single-stranded DNA (s

73 aring the four genetic bases of adenine (A), cytosine (C), thymine (T), and guanine (G).

74 Within MeDIP-Seq libraries, methylated cytosines can be found in both double-stranded (symmetri

75 while the iminohydantoin ring of dIa mimics cytosine; consequently, a dGh/dIa site was synthesized i

76 We characterize rG4 formation relative to cytosine content and alternative RNA structure stability

77 Cyclopentenyl cytosine (CPEC), a CTP synthase inhibitor that has been

78 involves nucleophilic attack of Cys(1226) to cytosine (Cyt) C6, methyl transfer from S-adenosyl-l-met

79 individual DNA duplexes containing a single cytosine-cytosine mismatch.

80 imiting the expression of activation-induced cytosine deaminase (AID).

81 d that requires the activity of two enzymes: cytosine deaminase (CD) and UPRT.

82 C members with two Zn-coordinated homologous cytosine deaminase (CD) domains, with the others being A

83 suggest that Vif binds and inhibits the non-cytosine deaminase activities of intact A3G and intact A

84 thereby causing elevated A3B expression and cytosine deaminase activity in cancer cells.

85 Cancer genome sequencing has implicated the cytosine deaminase activity of apolipoprotein B mRNA edi

86 o elaborate a simple method for assaying DNA cytosine deaminase activity that eliminates potential po

87 A likely cause is the DNA cytosine deaminase APOBEC3B (A3B).

88 n specifically induces the innate immune DNA cytosine deaminase APOBEC3B.

89 Deletion of yeast cytosine deaminase Fcy1 significantly decreased the rate

90 e APOBEC3B (A3B) single-stranded DNA (ssDNA) cytosine deaminase has important roles in innate immunit

91 ain of APOBEC3G (A3G-CTD), an ssDNA-specific cytosine deaminase, was expressed in an Escherichia coli

92 d to the therapeutically useful enzyme yeast cytosine deaminase, we obtained a approximately 3-fold c

93 of a single bifunctional yeast fusion gene, cytosine deaminase/uracil phosphoribosyltransferase (FCU

94 ating that R-loops limit activation-induced (cytosine) deaminase access to the transcribed DNA strand

95 d to remove RNA allowing activation-induced (cytosine) deaminase to promote somatic hypermutation on

96 APOBEC3H and homologous single-stranded DNA cytosine deaminases are unique to mammals.

97 The APOBEC3 family of DNA cytosine deaminases has important roles in innate immuni

98 n cancer genomes have implicated the APOBEC3 cytosine deaminases in oncogenesis, possibly offering a

99 The APOBEC3 family of DNA cytosine deaminases is capable of restricting the replic

100 The designed photocontrolled cytosine deaminases may also aid in improving chemothera

101 sociated with altered CpGs and APOBEC-family cytosine deaminases similar to mutation signatures deriv

102 APOBEC3s (A3s) are single-stranded DNA cytosine deaminases that provide innate immune defences

103 show that the LGST is accessible to cellular cytosine deaminating agents, explains the well-known GC

104 grees C during that period, then half of the cytosine-deaminating events per unit biomass would have

105 e present work, we examined the mechanism of cytosine deamination and the response of the uncatalyzed

106 We find cytosine deamination follows a conventional thermal age

107 The rate of cytosine deamination is much higher in single-stranded D

108 for CAG repeat instability: one mediated by cytosine deamination of DNA engaged in R-loops and the o

109 ll genomics often arise from the artifact of cytosine deamination upon cell lysis.

110 A methyl transferases and spontaneous methyl-cytosine deamination.

111 of co-occurring somatic mutations caused by cytosine deamination.

112 methyltrasferase EZH2, TET2 a key factor in cytosine demethylation and inactive DNMT3L, shown by kno

113 ient in Tet1, a tumor suppressor involved in cytosine demethylation, we observed a similar loss of pr

114 roxymethylcytosine (5hmC), are essential for cytosine demethylation.

115 Mechanistically, CPEC functions as a cytosine derivate to stimulate adenosine receptors A1 an

116 The discovery indicated that these cytosine derivatives in RNA might also play important ep

117 Within gene bodies, H3K36me3 and cytosine DNA methylation are elevated at exons of splice

118 We measured changes in cytosine DNA methylation in single-cell root hairs as co

119 grates histone modification and whole-genome cytosine DNA methylation profiles to identify the precis

120 Cytosine DNA methylation regulates the expression of euk

121 Cytosine DNA methylation, the addition of a chemical mar

122 it is unknown how the dynamic activities of cytosine DNA methyltransferases and 5-methylcytosine DNA

123 en 8-oxoG is at the primer terminus opposite cytosine, DNA centric changes lead to a clash between O8

124 E446D) resulted in preference for unmodified cytosine, due to decreased affinity for 5mC.

125 splice site sequences or mutation of nearby cytosines eliminated ICP27-mediated splicing inhibition,

126 Type I enzymes that modify cytosine exclusively were formed by replacing the adenin

127 of the TYR gene, with the substitution of a cytosine for a thymine nucleotide (C64T) at codon 22, le

128 transferases that have specialized to target cytosines for methylation in specific sequence contexts.

129 , we note that the donor and acceptor of our cytosine FRET-pair, tC(O) and tCnitro, can be convenient

130 (DPA) linker separated from a single guanine-cytosine (G-C) base pair by zero-to-six adenine-thymine

131 everal STR loci that are entirely guanine or cytosines (G or C) have insufficient read evidence for i

132 STs in terms of their genome sizes, guanine-cytosine (GC) content, intron numbers, and gene content.

133 odon bias, which correlates with low guanine-cytosine (GC) content, limits transcription of certain g

134 licular B cells) and also attained increased cytosine guanine dinucleotide responsiveness.

135 he major G allele of rs12041331, an intronic cytosine guanine dinucleotide-single-nucleotide polymorp

136 s, we assayed genome-wide DNA methylation at cytosine-guanine dinucleotides (CpGs) in whole blood fro

137 Modification of cytosine-guanine dinucleotides (CpGs) is a key part of m

138 MBD1 binds to methylated cytosine-guanine dinucleotides (mCGs) within the sequenc

139 etween R2 and DNA methylation in many of the cytosine-guanine dinucleotides.

140 research, we examined DNA methylation at the cytosine-guanine locus cg13989295 as well as DNA methyla

141 distribution, localization, and function of cytosine hydroxymethylation and identifies central roles

142 S) patients and observed widespread aberrant cytosine hypermethylation occurring preferentially outsi

143 yptic binding sites, in conjunction with DNA cytosine hypomethylation, histone hyperacetylation and u

144 whereas hemi-hydroxylation of the equivalent cytosine in an mCG site decreases affinity and specifici

145 Restriction-Modification enzymes that modify cytosine in one DNA strand and adenine in the opposite s

146 mination of four epigenetic modifications to cytosine in the proposed active demethylation cycle is d

147 lication to differing degrees by deaminating cytosine in viral (-)DNA, which forms promutagenic uraci

148 plicates (on average 29.5% of the methylated cytosines in a given replicate), indicating that a large

149 METHYLTRANSFERASE 2 (DRM2), which methylates cytosines in all sequence contexts through an RNA-guided

150 mpensated by interactions involving unpaired cytosines in an upstream, EvoFold-predicted stem loop (t

151 luding 12 million differentially methylated cytosines in domesticated allotetraploid cottons and the

152 tion and variable rates of non-conversion of cytosines in each sample to compute posterior likelihood

153 The AID/APOBEC family enzymes convert cytosines in single-stranded DNA to uracils, causing bas

154 Methylation of 19 cytosines increased the rate constant 3-fold for adducti

155 To access these additional runs of cytosine, increased negative superhelicity is necessary,

156 ger peptide part modified with carboxymethyl-cytosine instead of adenosine was described, but no biol

157 TET1 oxidizes methylated cytosine into 5-hydroxymethylcytosine (5hmC), resulting

158 on-induced cytidine deaminase (AID) converts cytosine into uracil to initiate somatic hypermutation (

159 RNA editing is converting hundreds of cytosines into uridines during organelle gene expression

160 The spontaneous deamination of cytosine is a major source of transitions from C*G to T*

161 Methylation of cytosine is an epigenetic mark involved in the regulatio

162 Methylation of DNA at carbon 5 of cytosine is essential for mammalian development and impl

163 ng in replacement of 5meCs with unmethylated cytosines is a hallmark of primordial germ cells (PGCs).

164 importance of the balance in these modified cytosines is emphasized by the fact that TET2 is mutated

165 le-length HPTs almost exclusively of guanine/cytosines located between genes or affecting the reading

166 re, we examine the genome-wide, C(5) -Methyl-cytosine (m5C) methylome and its correlation to global t

167 ouridylation, and methylation of carbon 5 in cytosine (m5C).

168 Indeed, methylation of cytosines makes attraction between GC-rich DNA as strong

169 Unmethylated cytosines may be converted to uracil through the additio

170 embers, was reported to deaminate methylated cytosine (mC) on DNA, and this mC deamination was propos

171 CpG sites and further flipping of methylated cytosines (mC) by the Set and Ring Associated (SRA) doma

172 sequencing study of the influence of methyl cytosines (MeC) on kinetics of p53 gene adduction by mod

173 We examined two forms of DNA methylation, cytosine methylation (5mC) and hydroxymethylation (5hmC)

174 enetic modifications, such as H3K9me3 and C5 cytosine methylation (5mC).

175 spacer (IGS) structure, they showed altered cytosine methylation and chromatin condensation patterns

176 inactivation, the functional significance of cytosine methylation and demethylation in mouse embryoge

177 h proteins are required for normal levels of cytosine methylation and hydroxymethylation in murine em

178 urthermore, base pair resolution analysis of cytosine methylation and hydroxymethylation with oxidati

179 DNA cytosine methylation and methyl-cytosine binding domain

180 methylome; and (3) TDCIPP-induced impacts on cytosine methylation are localized to CpG islands within

181 ical- and chromosome-specific alterations in cytosine methylation at 2 hpf.

182 ted cytosine and a corresponding increase in cytosine methylation at key regulatory regions on the vi

183 CTCF is sensitive to cytosine methylation at position 2, but insensitive at p

184 undergo epigenetic modifications, including cytosine methylation by DNA methyltransferases (DNMTs).

185 Cytosine methylation has been shown to regulate essentia

186 Although cytosine methylation has key roles in several processes

187 these data, we highlight predicted roles of cytosine methylation in global cellular metabolism provi

188 dingly, the Bdnf promoter exhibited aberrant cytosine methylation in mutant Htt-expressing cortical n

189 presents the first comprehensive picture of cytosine methylation in the epitranscriptome of pluripot

190 The role of cytosine methylation in the structure and function of en

191 Treatment with a cytosine methylation inhibitor completely suppressed the

192 Cytosine methylation is a key epigenetic mark in many or

193 Cytosine methylation is a key mechanism of epigenetic re

194 Cytosine methylation is an epigenetic and regulatory mar

195 Understanding cell-to-cell variability in cytosine methylation is essential for understanding cell

196 hanges post-LPS stimulation, suggesting that cytosine methylation is one of the dominant mechanisms d

197 Cytosine methylation is widespread in most eukaryotic ge

198 These changes include cytosine methylation of DNA at cytosine-phosphate dieste

199 Cytosine methylation of DNA is an epigenetic modificatio

200 Chromatin modifications, such as cytosine methylation of DNA, play a significant role in

201 Cytosine methylation regulates essential genome function

202 Cytosine methylation regulates the length and stability

203 hite, allowing genome-wide quantification of cytosine methylation via high-throughput sequencing.

204 ined epigenetic heterogeneity as assessed by cytosine methylation within defined genomic loci with fo

205 Cytosine methylation within the gene encoding for FK506

206 the loss of H3K4me3 and then subsequent DNA cytosine methylation, changes that were heritable across

207 utating HISTONE DEACETYLASE 6 (HDA6), or the cytosine methyltransferase genes MET1 or CMT3, erases HI

208 e methyltransferase, DIM-5, and a DNMT1-like cytosine methyltransferase, DIM-2.

209 the system having protonated or unprotonated cytosines, mimicking the pH 5.0 and 8.0 conditions, high

210 ic DNA analysis revealed iterative oxidative cytosine modification accumulation in mice exposed to hi

211 mproves the quantification and comparison of cytosine modification levels and that Lux can process an

212 n act as a direct epigenetic sensor of E-box cytosine modification states and that local CpG modifica

213 iotechnological tool to discriminate between cytosine modification states.

214 tic mark 5-hydroxymethylcytosine (5hmC) is a cytosine modification that is abundant in the central ne

215 low disambiguation of 5mC from an additional cytosine modification, 5-hydroxymethylcytosine (5hmC).

216 Lux models all cytosine modifications (C, 5mC, 5hmC, 5fC, and 5caC) sim

217 for epigenetic regulation, in particular the cytosine modifications 5-methylcytosine and 5-hydroxymet

218 We sought to investigate these cytosine modifications and their effect on gene expressi

219 suggesting a gene regulation mechanism where cytosine modifications change the accessibility of nucle

220 Cytosine modifications diversify and structure the genom

221 efficient strategy to achieve locus-specific cytosine modifications in the genome without obvious imp

222 and opposing effects of the two most common cytosine modifications on the frequency of cancer causin

223 Our study provides new insights on how cytosine modifications, their modifiers and readers cros

224 been shown to produce irregular estimates of cytosine modifications.

225 ytosine sequencing data sets to quantify all cytosine modifications.

226 The cytosine moiety undergoes an additional modification-car

227 ansitions dominated, with significantly more cytosines mutated to thymine in the lagging-strand templ

228 r demonstrated that Hsp90 increased both A3G cytosine mutation efficiency on HBV DNA and total HBV mu

229 Cytosine mutations within TCA/T motifs are common in can

230 The introduction of cytosine nucleobase 2 into position 24 of RRM1 increased

231 Cytosine nucleobases are shown to alter the adhesion of

232 nd meZRE2 (5- GAG G A-3), where a methylated cytosine occupies one of the inner thymine residues corr

233 We provide evidence that external cytosines of CpCpG sites can only be methylated when int

234 ts of the epigenetic mark 5-hydroxymethyl on cytosine on the structure of the Dickerson-Drew dodecame

235 f them the edited adenosines mis-paired with cytosines on the pre-miRNA structure.

236 0 deoxy-ribonucleotides of thymine, adenine, cytosine, or guanine results in the growth of four disti

237 interactions would provide a preference for cytosine over thymine, and the latter one could explain

238 rmal stability; sequences with at least five cytosines per tract folded into i-motif at room temperat

239 anges include cytosine methylation of DNA at cytosine-phosphate diester-guanine dinucleotides, histon

240 Of 31 discovery-stage cytosine-phosphate-guanine (CpG) dinucleotides, 13 repli

241 Cytosine-phosphate-guanine (CpG) methylation was assayed

242 ) agonists in vivo In mice, the TLR9 agonist cytosine-phosphate-guanine (CpG) oligodeoxynucleotide fo

243 n adipose tissue.The DNA methylation of 4875 Cytosine-phosphate-guanine (CpG) sites was affected diff

244 ome-wide association study of methylation of cytosine-phosphate-guanine dinucleotide (CpG) sites in r

245 Comparing current versus never smokers, 2623 cytosine-phosphate-guanine sites (CpGs), annotated to 14

246 Cytosine-phosphate-guanine sites for analysis were chose

247 h Toll-like receptor 9 agonist, class B CpG (cytosine-phosphate-guanine) oligodeoxynucleotides (ODNs)

248 tivation via Toll-like receptor 9 using CpG (cytosine-phosphate-guanine) oligodeoxynucleotides (ODNs)

249 pposed to polyinosinic:polycytidylic acid or cytosine-phosphate-guanine, is robustly inhibited by vas

250 he present study, DNA methylation in four 5'-cytosine-phosphate-guanine-3' (CpG) sites of long inters

251 Whereas 7.8% of 473,921 5'-cytosine-phosphate-guanine-3' (CpG) sites were hypomethy

252 irus-induced IL-8 responses and increased 5'-cytosine-phosphate-guanine-3' (CpG)-induced IL-12p40 and

253 lts in DNA demethylation at specific CpG (5'-cytosine-phosphate-guanine-3') sites close to the c-Fos

254 onas gingivalis lipopolysaccharide (LPS) and cytosine-phospho-guanine (CpG) oligodeoxynucleotides for

255 c contributions of five neutral tautomers of cytosine prior to ionization.

256 CpCpG sites methylated in both cytosines promote spreading of methylation in the CpHpG

257 The high degree of similarity among their cytosine-recognizing components (MTase and S) suggest th

258 enine target recognition domain (TRD) with a cytosine-recognizing TRD.

259 In addition, Hsp90 shifted A3G's cytosine region selection in HBV DNA and increased A3G's

260 epeats are added at the 3' or 5' ends of the cytosine-repeats.

261 The removal of methylated cytosines requires the base excision repair enzyme TDG,

262 o acid long peptide with C-terminal modified cytosine residue is produced.

263 ponsible for de novo methylation of specific cytosine residues in CpG dinucleotides during mammalian

264 ine, and cytidine 5'-phosphate, and also for cytosine residues in single-stranded DNA generated from

265 ted to spontaneous deamination of methylated cytosine residues in the colon and small intestine, prob

266 s and RNA-directed DNA methylation (RdDM) at cytosine residues in three DNA sequence contexts (CG, CH

267 s 544 RNA-directed DNA methylation (RdDM) at cytosine residues regulates gene expression, silences tr

268 Posttranscriptional methylation of RNA cytosine residues to 5-methylcytosine (m(5)C) is an impo

269 Here we describe a systematic study of cytosine-rich DNA sequences, with varying numbers of con

270 he pH-responsive microcapsules are made of a cytosine-rich layer cross-linked by nucleic acid bridges

271 as an acceptor of unwound quadruplexes via a cytosine-rich region near the 3'-end of the RNA.

272 This indicated that thousands of cytosine-rich sequences in the human genome may fold int

273 ternative DNA secondary structures formed in cytosine-rich sequences.

274 In contrast, the unmethylated cytosine's exocyclic N4 amino group (NH2) and its ring c

275 ith an initial global decrease in methylated cytosines (stage I) followed by a Tet methylcytosine dio

276 ce, only a handful of bacterial, genome-wide cytosine studies have been conducted, with none for mari

277 zation energies (AIEs) of specific gas-phase cytosine tautomers produced in a molecular beam.

278 tures and energetics of neutral and cationic cytosine tautomers were determined using explicitly corr

279 ffected by certain terminal residues: a five-cytosine tetrameric i-motif can bear ten-base flanking r

280 enase (Tet)-dependent decrease in methylated cytosines that act at imprinting control regions (ICRs)

281 The conversion of cytosine to 5-methylcystosine (5mC) is an important regu

282 ing an NPPY catalytic motif IV and modifying cytosine to m4C.

283 ces of these samples showed a high degree of cytosine to thymine mismatches, typical of post-mortem d

284 equence (73.33%), which was not observed for cytosine to uracil (17.86%) editing.

285 (TET) hydroxylases, which oxidize methylated cytosines to 5-hydroxymethylcytosine (5hmC), are essenti

286 ur (m5)C, while one enzyme requires all four cytosines to be modified for cleavage.

287 ivity factor (Vif) by deaminating viral cDNA cytosines to uracils.

288 quences, with varying numbers of consecutive cytosines, to gain insights into i-motif DNA sequence an

289 We also show that the predominant cytosine-to-thymine mutations observed in single-cell ge

290 as prompted by the earlier discovery of tRNA cytosine-to-uridine editing in eukaryotes, a reaction th

291 We found that increasing cytosine tract lengths resulted in increased thermal sta

292 Changes in the formylation profile of cytosine upon depletion of TDG suggest TET/TDG-mediated

293 We map three cytosine variants and two adenine variants.

294 significant retention of bisulfite-resistant cytosines was corroborated by reanalysis of previously p

295 ius plots for the uncatalyzed deamination of cytosine were linear over the temperature range from 90

296 Many cytosines were methylated in all replicates (on average

297 Finally, many cytosines were methylated in one sample only, due to eit

298 THYLASES (CMTs), which methylate CHH and CHG cytosines (where H is A, T, or C), and METHYLTRANSFERASE

299 d (ii) transposon-derived, methylated at all cytosines, which may or may not form epialleles.

300 By contrast, when cytosine within an UNCG tetraloop motif was replaced by