ライフサイエンスコーパス: CpG site

1 alue for each CpG site (or aggregated across CpG sites).

2 assembly of sMTase fragments at the targeted CpG site.

3 HCCs correlated with demethylation of these CpG sites.

4 gnostic performance of the optimal subset of CpG sites.

5 s into account the correlations among nearby CpG sites.

6 ciated with 7 SNPs and with methylation at 5 CpG sites.

7 of biased gene conversion and methylation at CpG sites.

8 plication propagates demethylation to nearby CpG sites.

9 highly disrupted methylation levels at many CpG sites.

10 vealed an optimized library comprised of 300 CpG sites.

11 population studies, in 998 promoter-located CpG sites.

12 ted by flanking sequences at non-CpG than at CpG sites.

13 ed by biased gene conversion or hypermutable CpG sites.

14 icantly increased methylation levels at four CpG sites.

15 methylation are correlated among neighboring CpG sites.

16 igenetic changes, such as DNA methylation at CpG sites.

17 ractions on birth weight were observed for 5 CpG sites.

18 damage formation at hypomethylated promoter CpG sites.

19 ylation at 5,458 cytosine-phosphate-guanine (CpG) sites.

20 LS, we successfully expanded the coverage of CpG sites 18.5-fold and accounts for about 30% of all th

21 ll-scale changes affecting 5% of the studied CpG sites (22,272 out of studied 437,022 CpGs, FDR < 0.0

22 cestry and replicated (P < 2.29 x 10(-4)) 58 CpG sites (45 unique loci) among African Americans.

23 -related methylation differences at specific CpG sites [5].

24 nd opposing methylated and hydroxymethylated CpG sites (5hmC/5mCpGs) in mouse genomic DNA across mult

25 Of the 71 CpG sites, 7 mediated the association between prenatal s

26 nome Atlas, we show that of 365,092 analyzed CpG sites, 70,591 (19%) were hypermethylated in IDH(mut)

27 as quantified using Sanger sequencing of the CpG sites 74-98 within the MGMT promotor region.

28 An additive weighted score of replicated CpG sites accounted for up to 6% inter-individual variat

29 n recurrent aberrant methylation at specific CpG sites across different studies.

30 tration with methylation beta-values of each CpG site, adjusting for estimated cell count using a cor

31 lls, identifying 26 expression probes and 92 CpG sites, almost all of which are affected only in fema

32 e number of the genes identified in both the CpG site and DMR approaches were located in the MHC regi

33 od, we examined the association between each CpG site and PTSD diagnosis using linear models that adj

34 richment of key features such as TSSs, TTSs, CpG sites and DNA replication timing around 4C sites.

35 itiated by the recognition of hemimethylated CpG sites and further flipping of methylated cytosines (

36 ines the kinetic information for neighboring CpG sites and increases the confidence in identifying th

37 ere observed between birth weight-associated CpG sites and phenotypic characteristics in childhood.

38 o determine both the level of methylation of CpG sites and the haplotype from which each read arises.

39 ues, the methylation information of flanking CpG sites and the methylation tendency of flanking DNA s

40 cusing on single cytosine-phosphate-guanine (CpG) sites and another on differentially methylated regi

41 tify significant Cytosine-phosphate-Guanine (CpG) sites and differentially methylated regions (DMRs)

42 DNAm) at 720,077 cytosine-phosphate-guanine (CpG) sites and prenatal maternal smoking among 441 mothe

43 sthma-associated cytosine-phosphate-guanine (CpG) sites and such an association was sex-specific.

44 A methylation in cytosine-phosphate-guanine (CpG) sites and surrounding regions was obtained.

45 r data therefore highlight the importance of CpG-sites and transcriptional activity for UCOE function

46 quent recurrence of mutations at polymorphic CpG sites, and an increase in C to T mutations in a 5' C

47 it demethylation of these NF-kappaB-flanking CpG sites, and HBV replication propagates demethylation

48 containing combinations of mRNA transcripts, CpG sites, and SNPs by jointly testing for genotypic eff

49 ly correlated with methylation at 2 out of 8 CpG sites, and was lower in hard foraging conditions, de

50 induced DNA methylation occurred in a GHRE-, CpG site-, and sex-specific manner.

51 Using an individual CpG site approach, we found 1,309 differentially-methyla

52 variants; (iii) 22% and 3% of the autosomal CpG sites are associated with age and sex, respectively;

53 Finally, we found that the Horvath clock CpG sites are characterized by a higher Shannon methylat

54 Since <2% of CpG sites are covered by the Illumina 450K array and who

55 detection (i) methylation statuses of nearby CpG sites are highly correlated, but this fact has seldo

56 As neighboring CpG sites are highly correlated, here, we present a new

57 reover, as methylation levels of neighboring CpG sites are known to be strongly correlated, methods t

58 es when the DNA methylation states of single CpG sites are representative of the methylation status o

59 These CpG sites are subjected to the influences of environment

60 uman and mouse MIOX promoters, enriched with CpG sites, are hypomethylated and unmethylated under HG

61 ng genotype at sites close to the methylated CpG site as a proxy for DNA methylation in ALSPAC and in

62 ile taking into account the distance between CpG sites as a covariate.

63 p RNA-programmed DNA methylation to targeted CpG sites as a function of distance and orientation from

64 e UPM models the rates of change of multiple CpG sites, as well as their starting methylation levels,

65 Swift achieved the highest proportion of CpG sites assayed and effective coverage at 26x (P < 0.0

66 epigenome-wide association study we explored CpG sites associated with a breast cancer diagnosis in t

67 Nearly all CpG sites associated with a breast cancer diagnosis were

68 We identified 58 differentially methylated CpG sites associated with a subsequent breast cancer dia

69 CpG sites associated with asthma severity and environmen

70 ements and Main Results: We identified seven CpG sites associated with mortality (false discovery rat

71 CI-associated DNA methylation states at 12 CpG sites associated with neuropsychological testing per

72 To search for CpG sites associated with PrCa risk, here we establish g

73 and variance signals but only examining one CpG site at a time.

74 (coexposure) led to significant changes in 7 CpG sites at 48 hours.

75 For CpG sites at genes of the dopaminergic (COMT, ANKK1) and

76 f associations between previously identified CpG sites at HIF3A and adiposity in approximately 1,000

77 the E2F1 pathway and hypermethylation of the CpG sites at miR-184 promoter, resulting in downregulati

78 methylation analysis demonstrates that nine CpG sites at the Ido1 promoter constitute a differential

79 ensitive pyrosequencing analysis showed that CpG sites at the Thy1 locus have increased methylation d

80 d to the promoter region of miR-184, and the CpG sites at the upstream region of miR-184 were hyperme

81 We aimed to identify CpG sites at which DNA methylation levels are associated

82 CpG modules, specifically those enriched in CpG sites belonging to genes that mediate T-cell activat

83 e found 1,309 differentially-methylated (DM) CpG sites between groups, including 1,271 CpG sites that

84 Inference of differentially methylated (DM) CpG sites between two groups of tumor samples with diffe

85 We defined 147,888 blocks of tightly coupled CpG sites, called methylation haplotype blocks, after an

86 with 48.5% increased methylation at a single CpG site (cg12701571) located in the promoter of the gen

87 However, the three CpG sites (cg21926276, cg27042065 and cg26387355) have n

88 Methylation status in individual CpG sites correlated with FCGRT mRNA expression.

89 Three CpG sites (CpG11 and CpG12 + 13) showed lower methylatio

90 /radiotherapy identified one hypermethylated CpG site (CpG6882469) in the VAV1 gene body that was cor

91 of Ankrd26 promoter at the -436 and -431 bp CpG sites (CpGs) and impaired its expression.

92 ewborn blood DNA methylation at over 450,000 CpG sites (CpGs) by using the Illumina 450K BeadChip.

93 on patterns, and show that correlation among CpG sites decays rapidly, making predictions solely base

94 rates from less than 1 to well over 10 % per CpG site, dependent on preservation of the methylated or

95 chnique and linear regression identified 111 CpG sites differentially methylated between isolation te

96 t differential methylation spanning multiple CpG sites (differentially methylated regions).

97 We identified 2 219 CpG sites differently-methylated in BCVY vs. BCO (FDR <

98 ion was measured from whole blood at 421,695 CpG sites distributed throughout the genome and analysed

99 , there were 2,332 differentially methylated CpG sites (DMSs) between sexes, which were enriched with

100 the impact of sequence variation on proximal CpG site DNA methylation.

101 ed SALL4 exhibited demethylation of specific CpG sites downstream of SALL4 TSS.

102 ularization for data imputation on unassayed CpG sites, enabling transfer of information between indi

103 tion of cytosine (C) at C-phosphate-guanine (CpG) sites enhances reactivity of DNA towards electrophi

104 n DNA methylation at some smoking-responsive CpG sites, even among individuals with a short smoking h

105 arly, however; in particular, transitions at CpG sites exhibit a more clocklike behavior than do othe

106 We identified and replicated 16 CpG-sites (false discovery rate [FDR] < 0.05), at 11 ind

107 S profile had differential methylation at 29 CpG sites (FDR < 10%).

108 We found moderate conservation of CpG sites for which methylation is altered with age, wit

109 urodevelopmental disorders, particularly for CpG sites found differentially methylated in brain tissu

110 tional analysis of differentially methylated CpG sites found genes involved in transcription factor a

111 t penalized regression was used to select 94 CpG sites from a training dataset (n = 1,032), with perf

112 characteristic elevated C>T mutation rate in CpG sites has been related to 5-methylcytosine (5mC), an

113 s age based on DNA methylation at 329 unique CpG sites, has a median absolute error of 3.33 weeks and

114 er wild-type DNA or DNA methylated at all 26 CpG sites highlight the utility of NMR in investigating

115 lated to newborn DNA methylation of specific CpG sites, highlighting the importance of examining nutr

116 Genetic variants and CpG sites identified in this study were enriched for his

117 revealed that the location of the methylated CpG site in a gene determined which isoform was used.

118 hylation of the COMT promoter at a conserved CpG site in exon II.

119 Modeling of the methylation levels for a CpG site in the AHRR gene indicates that MS modifies the

120 Methylation at a CpG site in the exon 1 area was positively related to so

121 Loss of methylation at a single CpG site in the TET1 promoter (cg23602092) and increased

122 ned the DNA methylation profiles of >450,000 CpG sites in 3 macrodissected regions of 79 colorectal t

123 nificant SNPs with DNA methylation (DNAm) at CpG sites in 40 Saguenay-Lac-Saint-Jean asthma study fam

124 DNA methylation pattern of more than 450 000 CpG sites in 44 SRS patients.

125 od identifies eQTLs by leveraging methylated CpG sites in a LIM homeobox member gene (LHX9), which ma

126 Patterns of methylation over multiple CpG sites in a region are often complex and cell type sp

127 Furthermore, differentially methylated CpG sites in ASXL1 mutated MF cases are found in regulat

128 ration stage, methylation also occurs at non-CpG sites in both lineages.

129 rast, neither SNPs nor methylation levels at CpG sites in CHI3L1 were associated with asthma.

130 s, we also identify an association with four CpG sites in chromosome 16p11.2.

131 in the equalization of methylation rates of CpG sites in favored and disfavored sequence contexts by

132 espective of their mode of conception) at 96 CpG sites in genes we have found previously to be relate

133 amatically greater number of undermethylated CpG sites in GLU versus GABA neurons were identified.

134 te genes or a very small fraction of genomic CpG sites in human pancreatic islets, the tissue of prim

135 Klotho experiences increased methylation of CpG sites in its promoter region, which is associated wi

136 Adjacent CpG sites in mammalian genomes can be co-methylated owin

137 CpG sites in multiple genes, including novel findings an

138 en also upregulated the number of methylated CpG sites in the AIRE promoter.

139 It predicts age quite well from 353 CpG sites in the DNA methylation profile in unknown samp

140 itochondrial 5-methylcytosine in CpG and non-CpG sites in the entorhinal cortex and substantia nigra

141 rection, PTSD associated with methylation of CpG sites in the HDAC4 gene, which encodes histone deace

142 es in host cell DNA methylation, at multiple CpG sites in the host cell genome, following infection.

143 nally, we found that methylation at multiple CpG sites in the HOXA4 promoter region was associated wi

144 , only cover a small proportion of the total CpG sites in the human genome, which considerably limite

145 robes that target methylated or unmethylated CpG sites in the MSP amplicon, and measures the differen

146 ulated by the methylation status of specific CpG sites in the promoter and may determine RUNX2 availa

147 ocytes and the percentage methylation of the CpG sites in the RUNX2 P1 promoter.

148 luence of the methylation status of specific CpG sites in the RUNX2 promoter on RUNX2-driven MMP13 ge

149 ing mean correlation with far fewer genes or CpG sites in the signature set.

150 arby genes, and on DNA methylation of nearby CpG sites in whole blood and in the fetal brain.

151 Herein, we typed over 450,000 CpG sites in whole blood of 573 individuals of diverse H

152 CHI3L1 SNPs, methylation levels at 14 CHI3L1 CpG sites in whole-blood DNA, and circulating YKL-40 lev

153 of cytosine-phosphate-guanine dinucleotide (CpG) sites in relation to alcohol intake in 13 populatio

154 findings, we examined the methylation at 12 CpGs sites in the bace-1 promoter, using genome-wide DNA

155 ed blood DNA methylomes (~483,000 individual CpG sites) in 168 subjects across two generations, inclu

156 undertaken DNA methylome analysis (850,000 + CpG sites) in human skeletal muscle after acute and chro

157 plicated previously reported eGFR-associated CpG sites including cg17944885 (P = 2.5 x 10-5) located

158 tion in prefrontal cortex tissue at multiple CpG sites, including one just upstream of ATPB81 (cg1959

159 ignificantly (p < 10(-7)) associated with 33 CpG sites, including the HTT gene (p = 6.5 x 10(-26)).

160 yesian Gaussian mixture modeling to classify CpG sites into fully methylated, partially methylated, a

161 ingly, methylation studies revealed that the CpG site is fully methylated in leukocytes of GG carrier

162 e digestion of SacII when the hemimethylated CpG site is methylated, which inhibits Sau96I cleavage.

163 lity of 0.14; (ii) DNA methylation at 14% of CpG sites is associated with nearby sequence variants; (

164 hese biomarkers, the methylation of multiple CpG sites is typically linearly combined to predict chro

165 OR), a 433-bp genomic region encompassing 52 CpG sites located immediately upstream of the TERT core

166 Fourteen CpG sites located in nine genes (SREBF1, SREBF2, PHOSPHO

167 Eleven CpG sites located in seven gene regions were differentia

168 ols (N = 15) validated the association of 10 CpG sites located on 8 genes CD1C, TNFSF10, PARVG, NID1,

169 MT3B permits both enzymes to comethylate two CpG sites located on the same DNA substrates.

170 We found that differentially methylated CpG sites located to genes involved in 'cancer' and 'emb

171 The most significant CpG sites, located at MAD1L1, TSNARE1/BAI1, and LTV1, we

172 ew candidates identified in blood cells, 655 CpG sites, located in 99 genes, were differentially meth

173 cant increase in DNA methylation at specific CpG sites (loci 2) of Bdnf promoter IV in the hippocampu

174 The 21 CpG sites mapped to relevant genes, including ACOT7, LMA

175 Furthermore, CpG sites mapping to genes with known genetic or functio

176 e-wide significant differentially methylated CpG sites mapping to the PARG, RERE, and CFAP77 genes.

177 sistance; (v) DNA methylation levels at five CpG sites, mapping to three well-characterized genes (TX

178 e meta-analysis revealed that two individual CpG-sites, mapping to DNAJC16 and TTC17, were differenti

179 Differentially methylated CpG sites may act as mediators between genetic variation

180 PrCa, and our findings suggest that specific CpG sites may influence PrCa via regulating expression o

181 sociations and that hypomethylation of these CpG sites may mediate the effect of tobacco on lung canc

182 data from bisulfite sequencing approaches to CpG sites measured with the widely used Illumina methyla

183 than 400 000 cytosine guanine dinucleotide (CpG) sites measured from peripheral blood mononuclear ce

184 ine (1) whether methylation levels at CHI3L1 CpG sites mediate the association of CHI3L1 single nucle

185 n that the propagation of DNA methylation at CpG sites, mediated in Arabidopsis by MET1, plays a cent

186 CpG sites meeting nominal significance (P < 0.05) for ea

187 tin immunoprecipitation assays indicate that CpG site methylation impacts the binding of the methylat

188 ntribute to prediction accuracy: neighboring CpG site methylation, CGIs, co-localized DNase I hyperse

189 d and bisulfite sequencing, and for 92.0% of CpG sites, methylation levels ranging over [0,1] were in

190 Among those 759 CpG sites, methylation of 42 is associated with expressi

191 expression and found that DNA methylation at CpG sites near the primary transcription start site and

192 Most CpG sites of ANKRD30B in blood were significantly correl

193 genome but reduces that in promoter regions CpG sites of CYP2B6 and CYP3A4 genes under the presence

194 es in the DNA methylation status of specific CpG sites of the proximal promoter, as well as by the ac

195 DNMT3b methylates CpG sites of the SHP-1 phosphatase promoter, which abrog

196 on in four 5'-cytosine-phosphate-guanine-3' (CpG) sites of long interspersed nuclear element-1 repeti

197 nce of the DNA sequences flanking the target CpG site on DNMT1 activity.

198 roups, including 28 regions encompassing 686 CpG sites on chromosome 6.

199 comparing the methylation status of adjacent CpG sites on long sequencing reads.

200 Mutations at CpG sites on the p53 tumor suppressor gene that can resu

201 of non-coding regions of DNA (in this case, CpG sites) on mapping eQTLs.

202 use either single differentially methylated CpG sites or differentially methylated regions that map

203 ised as an average percentage value for each CpG site (or aggregated across CpG sites).

204 nied by active demethylation of thousands of CpG sites overlapping distal enhancer elements.

205 well as decreased methylation in 2 out of 4 CpG sites (P < 0.05 for all), respectively.

206 ferential DNA methylation levels at multiple CpG sites (P<5 x 10(-8)), and differential DNA methylati

207 covery phase, of which 21 (including 5 novel CpG sites) passed genome-wide significance after meta-an

208 variation in the methylation of cytosines at CpG sites plays a critical role in early development of

209 erns at specific cytosine-phosphate-guanine (CpG) sites predictably change with age and can be used t

210 Using 2620 CpG sites previously associated with cigarette smoking,

211 ted with loss of hypermethylation at several CpG sites primarily localized in the intergenic regions

212 cal analysis of methylation patterns at four CpG sites producing unreliable statistical evidence.

213 Differential methylation was observed in 64 CpG sites (q < 0.05).

214 We identified 67,604 age-associated CpG sites reaching genome-wide significance of FWER <0.0

215 We assessed whether CpG sites related to smoking in blood from newborns and

216 hylation in the blood and are located nearby CpG sites reported to be associated with exposure to tob

217 to interrogate methylation status at single CpG site resolution epigenome-wide, is a powerful techni

218 also a scrambled CBX3 version with preserved CpG-sites retained the anti-silencing activity despite t

219 a DNA methylation gestational age using 148 CpG sites selected through elastic net regression in six

220 Overall, 25 CpG sites show consistent association directions for the

221 Many CpG sites show significant tissue-independent correlatio

222 h, age 7 and 17 years demonstrated that some CpG sites showed reversibility of methylation (GFI1, KLF

223 e and HDMCs, we identified a small number of CpG sites showing a hypermethylated state with age, in b

224 We identify 759 CpG sites showing an association, including 15 located a

225 between the two placenta cohorts, with most CpG sites showing increased percent of methylation in mi

226 es RelA, propagating demethylation to nearby CpG sites, shown by sodium bisulfite sequencing.

227 Of 19 CpG sites significantly associated (P < 1e-07) with eGFR

228 tion with DNA methylation at multiple nearby CpG sites, suggesting that, at some of the loci identifi

229 Furthermore, the risk allele disrupts a CpG site that undergoes differential methylation in CD8(

230 pecies, strains or individuals can result in CpG sites that are exclusive to a subset of samples, and

231 , if-then rules that identify all individual CpG sites that are hypermethylated in the presence of a

232 n skin cancers occur primarily at methylated CpG sites that coincide with sites of UV-induced cyclobu

233 By focusing on promoter CpG sites that localize to Polycomb group target genes t

234 We identified methylation changes at 3 CpG sites that might contribute to the development of Cr

235 associated with DNA methylation at numerous CpG sites that replicate across studies despite variatio

236 We identified 80 differentially methylated CpG sites that showed a 1% to 3% methylation difference

237 Moreover, the baseline DNA methylation of 12 CpG sites that was annotated to 9 genes [e.g., mitogen-a

238 ultiple testing correction, we identified 38 CpG sites that were differentially methylated at 7 years

239 M) CpG sites between groups, including 1,271 CpG sites that were hyper-methylated in the HIV-infected

240 -methylated in the HIV-infected group and 38 CpG sites that were hypo-methylated in the HIV-infected

241 ied 1189 5'-cytosine-phosphate-guanosine-3' (CpG) sites that were differentially methylated between p

242 ne observation of the 450K data is that many CpG sites the beadchip interrogates have very large meas

243 d SNP were each associated with at least one CpG site; the most significant association was rs6490029

244 is at individual cytosine-phosphate-guanine (CpG) sites, thus ignoring correlations in the methylatio

245 We found differential methylation at 218 CpG sites to be associated with CRP (P < 1.15 x 10(-7))

246 r, we can easily model micro-RNAs instead of CpG sites to study the effects of post-transcriptional e

247 pute the methylation value at the unmeasured CpG sites using the mixture of regression model (MRM) of

248 DNA methylation at nine (16%) CpG sites was associated with whole blood gene expressio

249 Hypermethylation of selected CpG sites was confirmed in a separate validation cohort

250 e same animals, methylation of four intronic CpG sites was decreased, amplifying glucose-induced tran

251 DNAm at these 94 CpG sites was highly predictive of age in the test cohor

252 Methylation of surrounding CpG sites was lower in the variant compared to the wild-

253 Reduced whole blood DNA methylation at 21 CpG sites was significantly associated with childhood al

254 hylation of 4875 Cytosine-phosphate-guanine (CpG) sites was affected differently between the 2 diets.

255 To identify differentially methylated CpG sites, we performed an association analysis adjustin

256 Normalized beta values for each CpG site were tested (t test) for differential methylati

257 All 21 CpG sites were also significantly differentially methyla

258 ty and precision of our method on individual CpG sites were approximately 93.7%.

259 ession in cis (P < 8.47 x 10(-5)), ten (17%) CpG sites were associated with a nearby genetic variant

260 entire cohort, larger numbers of methylated CpG sites were associated with favourable outcome.

261 Individual CpG sites were clustered in coherent modules without a p

262 Only few differentially methylated CpG sites were common among the three cell populations.

263 ylation changes at BRCA1 and CRISP2 specific CpG sites were consistently associated with subclinical

264 highest power when methylation levels across CpG sites were correlated.

265 Eighteen CpG sites were differentially methylated by treatment re

266 s wild-type cases, differentially methylated CpG sites were enriched in regions marked by histone H3K

267 Highest numbers of methylated CpG sites were found for oligodendroglioma, IDH-mutant a

268 o-deletion was absent, numbers of methylated CpG sites were higher in the presence of IDH-mutation.

269 IDH(wt)) gliomas, and only 3%, 2%, and 4% of CpG sites were hypermethylated in IDH(mut) AML, melanoma

270 , a comparable number of undermethylated non-CpG sites were identified in GLU and GABA neurons, and n

271 Six hyper-methylated CpG sites were in EBF4, which codes for a transcription

272 particularly rs10399931 and rs4950928) and 5 CpG sites were observed.

273 CpG sites were predominantly hypomethylated genome-wide

274 ated with age and sex, respectively; (iv) 53 CpG sites were significantly associated with liability t

275 Two CpG sites were significantly associated with prevalent A

276 Most importantly, hypomethylated CpG sites were strongly enriched in the active chromatin

277 DNA methylation of HDAC4 CpG sites were tagged by a nearby single-nucleotide poly

278 of 473,921 5'-cytosine-phosphate-guanine-3' (CpG) sites were hypomethylated, 3.2% showed marked enric

279 +)) WJ MSCs found 67 genes with at least one CpG site where the methylation difference was >/=0.2 in

280 stational age at delivery, we identified 188 CpG sites where placental DNA methylation was associated

281 with one hemimethylated and two unmethylated CpG sites, which are also recognition sites for Sau96I a

282 ented variability in C-to-T substitutions at CpG sites, which is not immediately explained by differe

283 ving a preponderance of C>T substitutions at CpG sites, which is the case for most spontaneous cancer

284 to regulatory effects of genetic variants on CpG sites, which may further influence expression of PrC

285 ect on DNA methylation in offspring at three CpG sites, which was replicated for one of the sites.

286 thylation at 605 cytosine-phosphate-guanine (CpG) sites, which were associated with future T2D.

287 Epigenetic clocks comprise a set of CpG sites whose DNA methylation levels measure subject a

288 nally, the Wnt10a 5'-region is enriched with CpG sites, whose methylation levels were markedly reduce

289 oreover, the DMS had an overlap of 890 (38%) CpG sites with a cohort submitted to toxic exposition du

290 n associated with reaction severity, and 203 CpG sites with differential DNA methylation associated w

291 ered DNA demethylation is more pronounced at CpG sites with flanks disfavored by DNMT1.

292 edded in a CpG island and miR-210 gene has 2 CpG sites with lower methylation percentage in ONs compa

293 Of differentially methylated CpG sites with the largest absolute changes in methylati

294 identified that a differentially methylated CpG site within the melatonin receptor 1A (MTNR1A) gene

295 A CpG site within the VNN1 promoter was differentially met

296 Four CpG sites within the aryl-hydrocarbon receptor repressor

297 correlated the mean methylation level of 12 CpG sites within the L1 gene, to the histological grade

298 enrichment and selection for hypermethylated CpG sites within the proximal region of gene promoters,

299 ts model that models both variations between CpG sites within the region and differential methylation

300 ion, and DNA methylation was quantified at 7 CpG sites within the SFRP1 promoter region by pyrosequen