ライフサイエンスコーパス: CpG methylation

1 subtype-specific gene expression compared to CpG methylation.

2 cleotide variants, structural variations and CpG methylation.

3 gion, and identifies relevant differences in CpG methylation.

4 tudy the strand-specific distribution of non-CpG methylation.

5 r design of sequence-specific antagonists of CpG methylation.

6 ated by the neural master regulator REST and CpG methylation.

7 e analyses of microRNA expression levels and CpG methylation.

8 ided little or no relevant information about CpG methylation.

9 the structure of a nucleosome is affected by CpG methylation.

10 chanisms of gene repression and silencing by CpG methylation.

11 fection on MGMT RNA, protein expression, and CpG methylation.

12 in differential locus-specific propensity of CpG methylation.

13 sferase Dnmt3a/b and an increase in promoter CpG methylation.

14 ase in HP1 and Dnmt3a/b binding and promoter CpG methylation.

15 1) in leukemia cells revealed the absence of CpG methylation.

16 mitochondrial DNA failed to show meaningful CpG methylation.

17 s, while displaying a contrasting pattern to CpG methylation.

18 RE1 sequences is temporally regulated by non-CpG methylation.

19 different spacer lengths, and the effect of CpG methylation.

20 subset of body-methylated genes acquires non-CpG methylation.

21 regulators of cytosine guanine dinucleotide (CpG) methylation.

22 Here, we demonstrate that erasure of CpG methylation (5mC) in PGCs occurs via conversion to 5

23 Evaluation of non-CpG methylation, a marker of de novo methylation, furthe

24 Most of these elements remain protected from CpG methylation, a prevalent epigenetic modification ass

25 on, while somatic copy-number alteration and CpG methylation accounted for 7.3% and 3.3%, respectivel

26 ly, our results demonstrate the stability of CpG methylation across generations, clarify the interpla

27 of the brain; (ii) there was an increase in CpG methylation after neural differentiation that resemb

28 er and in principle it can differentiate any CpG methylation alterations and can be adapted to analyz

29 n of these putative piRNAs, single-base pair CpG methylation analyses across the genome of Mili/piRNA

30 pression analyses and genomic DNA (gDNA) for CpG methylation analyses.

31 utarate, which is associated with higher DNA CpG methylation and altered histone methylation that acc

32 tudy, we use nanopore sequencing to evaluate CpG methylation and chromatin accessibility simultaneous

33 chromosome-level allele-specific profiles of CpG methylation and chromatin accessibility.

34 corresponds to parental allele-specific DNA CpG methylation and chromatin composition.

35 lencing of Vbeta10 correlated with increased CpG methylation and decreased histone acetylation over t

36 -eMS), identified by integrating genome-wide CpG methylation and gene expression profiles collected e

37 ted DCM in association with markedly altered CpG methylation and gene expression.

38 egulatory activity in terms of resistance to CpG methylation and gene silencing in murine P19 embryon

39 DNA CpG methylation and histone H3 lysine 9 (H3K9) methylati

40 chanisms involving histone modifications and CpG methylation and hydroxymethylation as well as by the

41 of two alternative forms of methylation, non-CpG methylation and hydroxymethylation.

42 r S-adenosyl methionine (SAM) did not affect CpG methylation and IEG gene expression at baseline.

43 at the foxp3 locus, which leads to increased CpG methylation and inhibits foxp3 transcription.

44 ntergenic region exhibited constitutive high CpG methylation and low histone acetylation.

45 advanced glycation end-products, as well as CpG methylation and microRNAs, are reviewed.

46 nsplants, including through an evaluation of CpG methylation and mutation of critical CpG residues.

47 The overall genome CpG methylation and promoter methylation of PTEN and CDK

48 e dynamic interaction of DNMT3B-mediated non-CpG methylation and REST binding.

49 Correlations of CpG methylation and RNA expression are found for 34 gene

50 TORC1 signaling during development prevented CpG methylation and silencing of the Dlk1-Dio3 locus, th

51 nd also investigated the correlation between CpG methylation and single nucleotide polymorphisms (SNP

52 LADs were associated with increased CpG methylation and suppressed gene expression.

53 Here we describe a link between CpG methylation and the establishment of methylation in

54 at loss of PTEN drives global changes in DNA CpG methylation and transcriptomic gene expression and h

55 , very low changes in the Mat1A:Mat2A ratio, CpG methylation, and histone H4 acetylation occurred.

56 etween epigenetic modifications-in our case, CpG methylation-and educational attainment (EA), a biolo

57 Changes in CpG methylation are essential to cellular differentiatio

58 e to non-genetic effects, genetic effects of CpG methylation are shared across tissues and thus limit

59 including histone modifications and promoter CpG methylation, as a component of leukemia progression

60 (PHD(UHRF1)), an important regulator of DNA CpG methylation, as a histone H3 unmodified arginine 2 (

61 We conducted a study to assess differential CpG methylation at 1,500 genic loci during MM progressio

62 CpG methylation at 1505 CpG sites across 807 genes in 68

63 We found no evidence of CpG methylation at a biologically significant level in t

64 ase I sensitivity, H3ac, and H3K4me2 but not CpG methylation at both sites.

65 Platform technologies for measurement of CpG methylation at multiple loci across the genome have

66 DNA methylation, especially CpG methylation at promoter regions, has been generally

67 r that has previously been shown to regulate CpG methylation at repetitive sequences.

68 Up-regulation of FoxD3 and loss of CpG methylation at the Alb1 enhancer accompanied the rep

69 on activity was correlated with differential CpG methylation at the heterologous promoter: the promot

70 t dCas9-SunTag-DNMT3A dramatically increases CpG methylation at the HOXA5 locus in human embryonic ki

71 ore the FS challenge resulted in an enhanced CpG methylation at the IEG loci and suppression of IEG i

72 2(-/-) NK cells correlated with an increased CpG methylation at the Ifng locus.

73 An increase in CpG methylation at the Poxmc promoter enables binding of

74 xpression in HIV/HPs, there was an increased CpG methylation at the VDR promoter.

75 Cytosine guanine dinucleotide (CpG) methylation at approximately 470,000 CpG sites was

76 by histone chaperone Nap1 and the effects of CpG methylation based on three-color single molecule FRE

77 Methods for quantifying the imbalance in CpG methylation between alleles genome-wide have been de

78 In a locus-by-locus comparison of CpG methylation between tumor types, 1266 CpG loci had s

79 enhance the enzyme's ability to perform non-CpG methylation by 2-8-fold.

80 nuclear cells by >75% and repetitive element CpG methylation by approximately 10%, and increased HbF

81 CpG methylation by de novo DNA methyltransferases (DNMTs

82 omoters upon differentiation suggesting that CpG methylation can localize C/EBPalpha.

83 results suggest a general mechanism by which CpG methylation can modulate protein-DNA interaction str

84 d pronounced differences in both CpG and non-CpG methylation (CG-DMRs and CH-DMRs) only in neuronal c

85 disappeared upon B cell commitment, whereas CpG methylation changed extensively during B cell matura

86 Most CpG methylation changes associated with Crohn's disease

87 ons in human macrophages are associated with CpG methylation, chromatin compaction, and histone modif

88 ortance of cell type-specific differences in CpG methylation, claiming these are restricted to locali

89 Although CpG methylation clearly distributes genome-wide in verte

90 eveloped software, Cluster-Based analysis of CpG methylation (CluBCpG), and explored variation in rea

91 ate (2-HG), longer survival time, and higher CpG methylation compared with wtIDH1.

92 Transcriptional silencing driven by CpG methylation converges exclusively on targets of the

93 In this study, we asked whether CpG methylation could influence the DNA binding affinity

94 Unlike most CpG methylation, CpH methylation is established de novo

95 NAm data; expand on the relationship between CpG methylation, CpH methylation, and gene expression; a

96 dimensional data, such as the mRNA seq data, CpG methylation data etc.

97 native start site (39%), MBD-seq genome-wide CpG methylation data were analyzed for methylation alter

98 ons of high sequence complexity, and derived CpG-methylation data from 31 178 Alu elements and their

99 ional neural networks trained on genome-wide CpG-methylation data learned distinct sequence preferenc

100 48% of cases, P = .039), and mean levels of CpG methylation decreased from 12.6% to 5.7% (P = .025),

101 of CBX3 was associated with reduced promoter CpG-methylation, decreased levels of repressive and incr

102 al approaches enabled us to demonstrate that CpG methylation decreases I-CreI DNA binding affinity an

103 We find that at the chromosome level high CpG methylation density is correlated with subtelomeric

104 human cancer, suggesting that AID-mediated, CpG-methylation dependent mutagenesis is a common featur

105 e found that gene-associated neuron vs. glia CpG methylation differences are highly conserved across

106 imary study as exhibiting cell type-specific CpG methylation differences were misclassified.

107 We observed that non-CpG methylation disappeared upon B cell commitment, wher

108 read and highly conserved differences in non-CpG methylation distinguish neurons and glia.

109 de-methylation, despite the fact that global CpG methylation drops to 10% in primordial germ cells an

110 cancers, which also forms a feedback loop of CpG methylation during tumorigenesis.

111 cer units within SEs typified by distinctive CpG methylation dynamics in embryonic stem cells (ESCs).

112 nships into account and enables inference of CpG methylation dynamics.

113 d SOCS alignment tool, and was used to align CpG methylation-enriched Arabidopsis thaliana bisulfite

114 According to the results, CpG methylation expedites nucleosome assembly in the pre

115 cell line revealed a significant decrease in CpG methylation for the DNMT1 knockout and DNMT1, 3B dou

116 Upon CpG methylation, (H3-H4)2 tetramer incorporation and DNA

117 DNA CpG methylation has been associated with chromatin compa

118 tion occurs at CpG sites, and asymmetric non-CpG methylation has only been detected at appreciable le

119 Aberrant cytosine-phosphate-guanine (CpG) methylation has been discussed in the context of di

120 nt excess of quantitative trait loci for DNA CpG methylation, hereafter referred to as methylation qu

121 ent advances in our understanding of altered CpG methylation, hydroxymethylation, and active DNA deme

122 analyses of school-age asthma in relation to CpG methylation (Illumina450K) in blood measured either

123 We highlighted that altered intragenic CpG-methylation impairs multiple aspects of transcriptio

124 This Tet1-mediated antagonism of CpG methylation imparts differential maintenance of DNA

125 We demonstrated targeted CpG methylation in a approximately 35 bp wide region by

126 nome-wide methylation screening, we assessed CpG methylation in a diverse set of 89 primary invasive

127 Sparse profiling of CpG methylation in blood by microarrays has identified e

128 equences that may be susceptible to aberrant CpG methylation in both cancer and normal cells.

129 expressed in T cells increased Ifng promoter CpG methylation in both effector and memory Th2 cells.

130 Remarkably, dynamic CpG and non-CpG methylation in cardiac myocytes is confined to A com

131 disease-associated DNA variants regulate cis-CpG methylation in CD4(+) T and/or B cells at 37% RA loc

132 We measured D4Z4 CpG methylation in control, FSHD1 and FSHD2 individuals

133 fore reviewing what is currently known about CpG methylation in DNA viruses.

134 Enzymes that catalyse CpG methylation in DNA, including the DNA methyltransfer

135 Here, we profile CpG methylation in DS and control cerebral and cerebella

136 MGMT protein and RNA levels and induced MGMT CpG methylation in gastric AGS cells.

137 on of MGMT and its epigenetic regulation via CpG methylation in gastric tissue from patients with H p

138 sulfite genomic sequencing method to examine CpG methylation in HCT116 human cells and primary human

139 ns with strand-specific distributions of non-CpG methylation in humans.

140 that display significantly higher levels of CpG methylation in immortalized cell lines as compared t

141 non-CpG sites, we show that the skew of non-CpG methylation in introns is mainly guided by sequence

142 CpG methylation in isolated B lymphocytes was assayed on

143 we demonstrate our tool can induce targeted CpG methylation in mice by zygote microinjection, thereb

144 other DNA sources confirmed this absence of CpG methylation in mtDNA.

145 ays to test peripheral blood DNA to quantify CpG methylation in peripheral blood leukocytes at DMRs o

146 ut not cortisol, was associated with altered CpG methylation in placentas.

147 CpG methylation in promoters is an epigenetic modificati

148 , we describe a genome-wide study of altered CpG methylation in psoriatic skin.

149 en reported for large-scale ascertainment of CpG methylation in repeats.

150 phthamide pathway enzyme, was reduced by DNA CpG methylation in resistant cells.

151 only certain body-methylated genes gain non-CpG methylation in the absence of IBM1 and others do not

152 The latter correlated with increased CpG methylation in the distal gene 50 promoter, which wa

153 analyses showed a decrease in the degree of CpG methylation in the EcSOD promoter in the 3D versus 2

154 A. fumigatus was associated with changes in CpG methylation in the IFN-gamma and IL-4 promoters that

155 iPSCs correlates with an overall decrease in CpG methylation in the L1 promoter region.

156 bject to epigenetic regulation, specifically CpG methylation in the promoter region, by determining l

157 Herein, we firstly determined the role of CpG methylation in the regulation of ocular tissue-speci

158 Placental CpG methylation in the three genes was analyzed using 45

159 der positive selection, as well as increased CpG methylation in these regions.

160 he TLR2 promoter CpG Island, we noted higher CpG methylation in this dysregulated cell type.

161 pproach to studying the epigenetic mechanism CpG methylation in tissue samples is to identify regions

162 antly more long interspersed nuclear element CpG methylations in individuals at birth who were later

163 ound predominantly in CpGs but in plants non-CpG methylation (in the CpHpG or CpHpH contexts, where H

164 The results indicate that CpG methylation induces tighter wrapping of DNA around t

165 B was identified as an upstream viral genome CpG methylation initiator.

166 COR1 and H3K9me3 ChIP-Seq, FAIRE-seq and DNA CpG methylation interactions were related to gene expres

167 Promoter CpG methylation is a fundamental regulatory process of g

168 l sources, we can definitively conclude that CpG methylation is absent in mtDNA.

169 l packing unit of the eukaryotic genome, and CpG methylation is an epigenetic modification associated

170 changes in the structure of nucleosomes upon CpG methylation is an essential step toward the understa

171 Because CpG methylation is coupled to intake of essential nutrie

172 ransposable elements, we also found that non-CpG methylation is distributed in a strand-specific mann

173 In addition, CpG methylation is found in coding regions of active gen

174 tep epigenetic inhibitory mechanism in which CpG methylation is linked with histone posttranslational

175 H Genotype-Tissue Expression (GTEx) program, CpG methylation is measured by deep whole-genome bisulfi

176 We also find that non-CpG methylation is skewed between the two strands in int

177 In eukaryotes, CpG methylation is thought to account for CpG underrepre

178 e significance of the genome distribution of CpG methylation is unclear.

179 ion maps that revealed a strand-specific non-CpG methylation, its dynamic regulation, and its impact

180 e resolution, we quantitatively compared the CpG methylation landscape of adult mouse dentate granule

181 activity by Casilio-ME1 robustly alters the CpG methylation landscape of promoter regions and activa

182 This work provides a comprehensive CpG methylation landscape of the different layers of the

183 pting to different correlation structures in CpG methylation levels across the genome while taking in

184 of Nanog and, overall, had decreased genomic CpG methylation levels, which included the promoters of

185 l and nuclear level of MAT1A protein, global CpG methylation, lin-28 homolog B (Caenorhabditis elegan

186 nscriptome, epigenome H3K4me3, H3K27me3, and CpG methylation maps of trophoblast progenitors, purifie

187 ding the functional significance of specific CpG methylation marks in the context of endogenous gene

188 sical properties of nucleosomes induced upon CpG methylation may contribute directly to the formation

189 tics with genetics and sex, and suggest that CpG methylation may serve as an epigenetic record of lif

190 Dnmt3a is the sole 'writer' of atypical non-CpG methylation (mCH), and MeCP2 is the only known 'read

191 a responsiveness is associated with promoter CpG methylation nearby site-alpha and TATA box, reversib

192 Here we analyzed the basal CpG methylation of 11 KRAS-mutant and dependent pancreat

193 CpG methylation of DNA is an epigenetic modification ass

194 as overexpressed and associated with loss of CpG methylation of H3K4me1-associated enhancer regions.

195 CpG methylation of involved skin differed from normal sk

196 CpG methylation of MGMT was more frequent in the gastric

197 g-read nanopore sequencing to directly infer CpG methylation of novel and extant TE insertions in hip

198 egulation of DNMT3B results in decreased non-CpG methylation of RE1 sequences, reduced REST occupancy

199 rate that DNMT3B preferentially mediates non-CpG methylation of REST-targeted genes in the developing

200 ells in vitro and in vivo is associated with CpG methylation of several regions of the Cd8a locus.

201 E and airway eosinophilia and alterations in CpG methylation of T-helper genes in third-generation mi

202 Here we show that CpG methylation of the CRE sequence (TGACGTCA) enhances

203 CpG methylation of the EGFR HRE prevented induction unde

204 s also associated with a modest reduction in CpG methylation of the INS gene in cord blood mononuclea

205 configuration was required, because in vitro CpG methylation of the MOR promoter abolished MSK1 activ

206 cell lines through histone deacetylation and CpG methylation of the promoter region and can be re-act

207 Second, CpG methylation of the promoter region correlated with a

208 yltransferases (Dnmt1 and Dnmt3a) and lowers CpG methylation of the survival gene promoters, leading

209 ngineered meganucleases can be diminished by CpG methylation of the targeted endogenous site, and we

210 y in cancer cells, being able to inhibit the CpG methylation of tumor suppressor gene (TSG) promoters

211 Random forests classification of CpG methylation of tumors--which splits the data into tr

212 indings report that DNMT3B shapes intragenic CpG-methylation of highly-transcribed genes.

213 In vitro DNA CpG-methylation of the promoter partially blocked bindin

214 We studied the effects of CpG methylation on DNA recognition by the tumour suppres

215 The effect of CpG methylation on iNOS promoter and enhancer activities

216 a genomewide method for detecting regions of CpG methylation on the basis of the increased melting te

217 CTCF-binding region, is completely devoid of CpG methylation on the Xi.

218 whose expressions were regulated by LADs or CpG methylation, or by both, the latter pertained to gen

219 in utero exposure to BPA altered the global CpG methylation pattern of the uterine genome, subsequen

220 ries of pregnancy within our study reveals a CpG methylation pattern that is restricted to female ani

221 ethod was further validated by comparing the CpG methylation pattern, methylation profile of CGIs/pro

222 In addition, great tit neuronal non-CpG methylation patterns are very similar to those obser

223 effects of changes in leukocyte fractions on CpG methylation patterns as well as the potential import

224 vide a valuable resource for the analysis of CpG methylation patterns in a differentiated human cell

225 lation microarrays to analyze differences in CpG methylation patterns in cells relevant to the pathog

226 ces of DNMT3B are highly correlated with non-CpG methylation patterns in human cells.

227 rather than stochastic variation, read-level CpG methylation patterns in tissue whole genome bisulfit

228 uBCpG), and explored variation in read-level CpG methylation patterns in whole genome bisulfite seque

229 show 381 genes with significantly different CpG methylation patterns, with the vast majority being m

230 epigenetic analyses, our data indicate that CpG methylation plays a major role in neuroepigenetics,

231 It is highly unlikely that CpG methylation plays any role in direct control of mito

232 erase Dnmt1, which preserves the patterns of CpG methylation, plays a key role in CAG repeat instabil

233 l DNA (mtDNA) has much more than the 2 to 5% CpG methylation previously estimated.

234 and unmethylated compartments and estimates CpG methylation probabilities at single base resolution.

235 In utero BPA exposure altered the global CpG methylation profile of the uterine genome and subseq

236 Classifying samples based on CpG methylation profile with a mixture model approach, m

237 Therefore, CpG methylation profiles of TSGs may be used as a progno

238 Here we use, based on genome-wide CpG methylation profiling, a LASSO model to develop a fi

239 rgeted DNA, mRNA and microRNA sequencing and CpG methylation profiling.

240 These results suggest that in vitro CpG methylation protects exogenous DNA from degradation

241 our data demonstrate that IGSF4 silencing by CpG methylation provides an anti-apoptotic signal to HRS

242 While CpG methylation regulates TE activity, the locus-specifi

243 iations between cumulative lead exposure and CpG methylation remained unaltered from 30 to 78 months.

244 n from sequencing reads to a fully annotated CpG methylation report to biological interpretation.

245 s], SNPs, single nucleotide variants [SNVs], CpG methylation).RESULTSWe documented greater than 100-f

246 muscle cells was validated by the pattern of CpG methylation revealed by bisulfite sequencing.

247 In this study, we performed genome-wide CpG methylation sequencing of chondrosarcoma biopsies an

248 were silent, 65 cellular genes that acquired CpG methylation showed altered transcript levels.

249 leosomal H3K9me3 modification in addition to CpG methylation signals.

250 s the epigenetic state of DNA by replicating CpG methylation signatures from parent to daughter stran

251 Induced Deaminase (AID), which overlaps the CpG methylation site.

252 We identify cis-meQTLs at 14,118 CpG methylation sites and cis-eQTLs for 302 3'-mRNA tran

253 Here, we perform GWAS of >415 thousand CpG methylation sites in whole blood from 4170 individua

254 d for the presence of potentially functional CpG-methylation sites in enhancer and insulator regions

255 ated genes do not harbor more age-associated CpG-methylation sites than other genes, but are instead

256 ive smoking dose) with blood DNAm in 790,026 CpGs (methylation sites) measured with the Illumina Infi

257 Furthermore, for DNA CpG methylation state prediction, DeepSignal achieves 90

258 Our model can successfully infer unobserved CpG methylation states from observations at the same sit

259 ers in conjunction with the determination of CpG methylation states in the repeat expansion and in ad

260 me bisulfite sequencing datasets by imputing CpG methylation states on individual sequencing reads.

261 erent epi-allelic haplotypes, annotated with CpG methylation status and DNA polymorphisms, from whole

262 s enabled quantitative measurement of single CpG methylation status at relatively low cost and sample

263 study, we investigated gene copy number and CpG methylation status in CRPC to gain insight into spec

264 CpG methylation status in normal cells points to locally

265 The global CpG methylation status of eel liver was determined by me

266 nd miR-200b) and pyrosequencing to determine CpG methylation status of selected genes (Aph1a and Dkk4

267 ular memory and imprinting by regulating the CpG methylation status of specific promoter regions.

268 isulfite sequencing (scRRBS), to measure the CpG methylation status on the same cell for cell type in

269 ility in other assay formats used to analyze CpG methylation status.

270 d strategy for parallel determination of the CpG-methylation status of thousands of Alu repeats, and

271 Extensive DNA CpG methylation, surprisingly, does not help to restrain

272 1) this is the first report to indicate that CpG methylation susceptible "segments" exist; 2) our mod

273 n carriers, have a greater reduction of D4Z4 CpG methylation than can be expected based on the size o

274 nomic copy of the promoter element showed no CpG methylation, the same sequence carried by the transg

275 ry pathway that connects aberrant intergenic CpG methylation to human neoplastic and developmental ov

276 ional organization, and possesses a complete CpG methylation toolkit, its predicted genomic CpG conte

277 ed Infinium(R) Assay is used for analysis of CpG methylation using bisulfite-converted genomic DNA.

278 CpG methylation variation is involved in human trait for

279 identified in GLU and GABA neurons, and non-CpG methylation was a better predictor of subtype-specif

280 The percentage CpG methylation was decreased by 5-aza-dC treatment but

281 y for drug repositioning, while for 36 genes CpG methylation was found to influence transcription ind

282 wide in controls and DCM hearts, but overall CpG methylation was increased in DCM.

283 However, CpG methylation was significantly increased by dietary f

284 Finally, non-CpG methylation was substantially more prevalent in neur

285 Cytosine-phosphate-guanine (CpG) methylation was assayed on the HumanMethylation450k

286 Using penalised regression on genome-wide CpG methylation, we tested whether DNAm risk scores (MRS

287 ss associations between arsenic exposure and CpG methylation, we used linear regression models adjust

288 are strongly biased to light (L)-strand non-CpG methylation with conserved peak loci preferentially

289 tor-2 inhibition mechanisms of KLF4 promoter CpG methylation with regional consequences for atherosus

290 triking convergence of both CpG and CpH (non-CpG) methylation with pluripotent states; the pluripoten

291 widespread cell type-specific differences in CpG methylation, with a genome-wide tendency for neurona

292 evel of global methylation and extent of non-CpG methylation, with hESC highest, fibroblasts intermed

293 r did knockdown of DNMTs significantly alter CpG methylation within Cp.

294 arch to date for allele-specific patterns of CpG methylation within CpG isochores or CpG enriched seg

295 ion, protein expression, gene expression and CpG methylation within Forkhead box P3 (FOXP3) and inter

296 that was associated with increased levels of CpG methylation within the FOXP3 locus when compared to

297 In addition, there is an increase in CpG methylation within the promoter and the imprinting c

298 Site-specific CpG methylation within the proximal promoter regions of

299 ntroduce an age clock built exclusively with CpG methylation within the rDNA.

300 ng of YY1 to DXZ4 in vitro is not blocked by CpG methylation, yet in vivo both proteins are restricte