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 is developed for hypothesis testing at each CpG site.

3 assembly of sMTase fragments at the targeted CpG site.

4 of biased gene conversion and methylation at CpG sites.

5 plication propagates demethylation to nearby CpG sites.

6 highly disrupted methylation levels at many CpG sites.

7 vealed an optimized library comprised of 300 CpG sites.

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

9 erential methylation of tumor cell-intrinsic CpG sites.

10 ern and affecting around 30% of all measured CpG sites.

11 ucleotide level in the neighborhood of these CpG sites.

12 inomas acquire additional C > T mutations at CpG sites.

13 roves the number of mapped reads and covered CpG sites.

14 s into account the correlations among nearby CpG sites.

15 es for DNA methylation detection of specific CpG sites.

16 y of DNMT1 for methylation of hemimethylated CpG sites.

17 ly measure DNA methylation at up to 48.4% of CpG sites.

18 sis for information sharing across different CpG sites.

19 ions can be found associated with only a few CpG sites.

20 (5mC) is mostly symmetrically distributed in CpG sites.

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

22 HCCs correlated with demethylation of these CpG sites.

23 her frequency of transitions at CpG than non-CpGs sites.

24 thylation profiles of AHRR in monocytes (542 CpG sites +/- 150 kb of AHRR, using Illumina 450K array)

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

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

27 Methylation of the Pgc-1alpha promoter at CpG site -260 and expression of Pgc-1alpha mRNA were ass

28 We analyzed 85,134 CpG sites [28,114 sites in CpG islands (CGI) and 57,020

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

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

31 uence of the retrotransposed CGI on flanking CpG sites, a phenomenon that we described as "sloping sh

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

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

34 een arsenic exposure and methylation at each CpG site, adjusted for sex, age, and batch.

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

36 ognize and amplify a C to T base change at a CpG site and measuring the change electrochemically (eLC

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

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

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

40 d highly dependent on DNA methylation at the CpG sites and highly dependent on the AID enzyme to crea

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

42 of gBGC does not differ between hypermutable CpG sites and non-CpG sites, suggesting that in humans g

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

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

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

46 264), we characterized methylation (>485 000 CpG sites) and mRNA expression (>48K transcripts) and ca

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

48 In mammals, most DNA methylation occurs at CpG sites, and asymmetric non-CpG methylation has only b

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

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

51 based on ENCODE data, gene tracks, reference CpG-sites, and user-defined features.

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

53 Ten novel lipid-related CpG sites annotated to various genes including ABCG1, MI

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

55 iterature suggests that clusters of adjacent CpG sites are co-regulated.

56 748 individuals, methylation levels at 1,919 CpG sites are correlated with at least one distal (trans

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

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

59 Methylated CpG sites are involved in gene expression and are biomar

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

61 It is evident that neighboring CpG sites are often highly correlated with each other, a

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

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

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

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

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

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

68 ide association studies to identify specific CpG sites associated with a phenotype.

69 35 hypermethylated and 45,407 hypomethylated CpG sites associated with aging.

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

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

72 We report that demethylation of specific CpG sites at -110 bp and -299 bp of the proximal MMP13 a

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

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

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

76 This enrichment of mutations at CpG sites at hotspots could predominate in methylated re

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

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

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

80 We identified 65 gene promoters enriched for CpG sites at which methylation levels are associated wit

81 e length, and 36 gene promoters enriched for CpG sites at which methylation levels are associated wit

82 Higher M.SssI MTase activity leads to more CpG sites being methylated and consequently impedes more

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

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

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

86 stimated DNA methylation correlation between CpG sites (co-methylation), with further options to visu

87 ocal meQTLs encompass common SNPs that alter CpG sites (CpG-SNPs).

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

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

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

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

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

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

94 The demethylation of a specific CpG site (designated CpG 2), which is juxtaposed to a ke

95 iments with substrates containing one or two CpG sites did not provide evidence for a processive mech

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

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

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

99 aortic samples and a high-density (>450 000 CpG sites) DNA methylation microarray.

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

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

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

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

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

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

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

107 DNA methylation levels at individual CpG sites generated from dorsolateral prefrontal cortex

108 tion of BatMeth, all mappers covered >70% of CpG sites genome-wide and yielded highly concordant esti

109 at a large-effect allele at a highly mutable CpG site has promoted physiological differentiation in b

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

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

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

113 Methylation of a CpG site in ABCG1 on chromosome 21 was significantly ass

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

115 Once the CpG site in the 5'-CCGG-3' is methylated, HpaII recognit

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

117 We assessed methylation at a CpG site in the promoter of ADCYAP1R1 (cg11218385) using

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

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

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

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

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

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

124 ethylation of forkhead box protein 3 (FOXP3) CpG sites in antigen-induced regulatory T cells were sig

125 ty along with increased methylation of FOXP3 CpG sites in antigen-induced regulatory T cells.

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

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

128 5D, showed increased methylation at several CpG sites in both normal and HD cells, as well as in DNA

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 ation and causes hypomethylation at specific CpG sites in Fn14 promoter leading to the increased gene

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 ed global DNA methylation changes, including CpG sites in long interspersed nuclear elements (LINE-1)

137 tecture of cytosine modifications at 283,540 CpG sites in lymphoblastoid cell lines (LCLs) derived fr

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

139 CpG sites in multiple genes, including novel findings an

140 thylation (< or >/= median) at 26 individual CpG sites in nine candidate genes in a well-characterize

141 Methylation status of 17 CpG sites in PLAC8 negatively correlated with mRNA expre

142 ook a genome-wide analysis of methylation at CpG sites in relation to BMI.

143 In cord blood, methylation at 15 CpG sites in seven gene regions (AHRR, MYO1G, GFI1, CYP1

144 richment of positively associated methylated CpG sites in subtelomeric loci (within 4 Mb of the telom

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

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

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

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

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

150 DNA methylation of CpG sites in the leptin promoter was measured using pyro

151 Among the four CpG sites in the methylation assay, CpG4 and the other t

152 revealed significant demethylation of three CpG sites in the Ppargamma2 promoter after exposure to b

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

154 Multiple CpG sites in the promoter region of ADRB2 gene were anal

155 , and it does so through hypermethylation of CpG sites in the regulatory sequences of the gene.

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

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

158 xplains the lower-than-expected frequency of CpG sites in these genes.

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

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

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

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

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

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

165 The proportion of C>T transitions at CpG sites increased during tumor progression.

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

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

168 Methylation of DNA CpG sites is a major mechanism of epigenetic gene silenc

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

170 bled us to show that DNA sequence context of CpG sites is informative about methylation dynamics acro

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

172 that on the antisense strand of Alus, a non-CpG site just downstream of the A-box is highly methylat

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

174 Specifically, methylation of the CpG sites located in the central dyad and the major groo

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

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

177 The methylation status of 1,421 autosomal CpG sites located within 768 cancer-related genes was in

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

179 expression was associated with our candidate CpG sites, LRRN3 appeared to be particularly interesting

180 which were enriched by more than 9-fold for CpG sites mapped to population-specific mQTL.

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

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

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

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

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

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

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

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

189 olution using features including neighboring CpG site methylation levels and genomic distance, co-loc

190 Differential CpG site methylation was measured by methylation-specifi

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

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

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 ediated through hypomethylating the specific CpG sites on IL-1beta proximal promoter.

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

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

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

201 ial approach across biological samples for a CpG site or region, and identifies relevant differences

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

203 inct patterns: cis-meQTLs mostly localize to CpG sites outside of genes, promoters and CpG islands (C

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

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

206 of genome-wide methylation levels at single-CpG-site precision.

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

208 escc), to identify differentially methylated CpG sites prognostic of ESCC progression.

209 tion involved birth weight, methylation of a CpG site proximal to the NFIX locus and bone mineral den

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

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

212 d covariation in DNA methylation at the risk CpG sites relative to normal tissue, but lower levels re

213 classifier to predict methylation levels at CpG site resolution using features including neighboring

214 ssifier to predict DNA methylation levels at CpG site resolution with high accuracy.

215 the door to study DNA methylation at single CpG site resolution.

216 idual copies of epiallelic species at single-CpG-site resolution in fractions as low as 0.005%, provi

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

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

219 Many CpG sites show significant tissue-independent correlatio

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

221 regions in LTBP1, and DNA methylation of two CpG sites showed significant correlation with its RNA ex

222 Interestingly, two CpG sites showed significant correlation with TSC1 prote

223 For the CpG sites showing genome-wide significant association wi

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

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

226 Computational prediction of CpG site-specific methylation levels is critical to enab

227 iffer between hypermutable CpG sites and non-CpG sites, suggesting that in humans gBGC is not caused

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 ing) algorithm to detect sets of neighboring CpG sites that are correlated with each other.

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

232 prove accuracy of cross-tissue prediction at CpG sites that are variable in the target tissue [R(2) i

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

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

235 invasive cancer allows the identification of CpG sites that indicate the risk of neoplastic transform

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

237 proach, we discovered a DNAm signature of 96 CpG sites that predict clinical outcomes.

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

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

240 mited, but overlapping, subset of methylated CpG sites that were altered by HDAC inhibition in both n

241 CpG sites that were hypermethylated in group H were more

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

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

246 We further show that the identified risk CpG sites undergo preferential DNA methylation changes i

247 e (CpG) methylation at approximately 470,000 CpG sites was assayed in CD4(+) T cells using the Illumi

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 In cord blood, methylation at 224 CpG sites was found to be associated with GA and 23 CpG

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

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

254 For each CpG site, we calculated the intraclass correlation coeff

255 ontrolling for the proximal sequences of non-CpG sites, we show that the skew of non-CpG methylation

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

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

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

259 The CpG sites were clustered into low- and high-reliability

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

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

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

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

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

265 Two distinct classes of CpG sites were identified: sites whose methylation rever

266 t a high number (n = 85) of epigenetic clock CpG sites were located within glucocorticoid response el

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

268 omere length and DNA methylation at >450,000 CpG sites were obtained for both blood (N = 24) and EBV-

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

270 Two CpG sites were significantly associated with prevalent A

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

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

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

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

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

276 rm of epigenetic variation is methylation at CpG sites, which can be measured as methylation quantita

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

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

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

280 sis was detectable for a small proportion of CpG sites, which were enriched by more than 9-fold for C

281 Genetically dependent CpG sites whose modification levels negatively (repressi

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

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

284 es was found to be associated with GA and 23 CpG sites with birth weight.

285 ntration and three differentially methylated CpG sites with blood arsenic concentration, based on the

286 The CpG sites with greater modification levels in European d

287 We suggest that CpG sites with low ICC may be excluded from subsequent a

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

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

290 , we observed four differentially methylated CpG sites with urinary total arsenic concentration and t

291 tion of the ALPi promoter, particularly of a CpG site within a critical KLF/Sp regulatory element req

292 Our findings suggest that methylation of a CpG site within ABCG1 is associated with fasting insulin

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

294 A CpG site within the VNN1 promoter was differentially met

295 accuracy increases to 98% when restricted to CpG sites within CGIs and is robust across platform and

296 Methylation of CpG sites within promoter region is an important epigene

297 ified the extracted DNA and PCR-amplified 26 CpG sites within the C9orf72 promoter region.

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

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

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