ライフサイエンスコーパス: CpG methylation

1 gion, and identifies relevant differences in CpG methylation.

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

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

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

5 e analyses of microRNA expression levels and CpG methylation.

6 ided little or no relevant information about CpG methylation.

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

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

9 different spacer lengths, and the effect of 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 which include H3 K27 trimethylation and DNA CpG methylation.

17 rter provided a sequence-specific readout of CpG methylation.

18 erates robust activity for measuring de novo CpG methylation.

19 and for cytological detection of chromosomal CpG methylation.

20 criptional silencing via promoter-associated CpG methylation.

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

22 ing, spread of heterochromatin, and regional CpG methylation.

23 subtype-specific gene expression compared to CpG methylation.

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

25 regulators of cytosine guanine dinucleotide (CpG) methylation.

26 MD can attract some paternal-allele-specific CpG methylation 5' of H19 in preimplantation embryos, al

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

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

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

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

31 e distinct patterns consisted of 5' promoter CpG methylation alone, 5' and 3' promoter CpG methylatio

32 CpG methylation also was decreased at another metastable

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

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

35 CpG methylation analyses in resting neonatal cells revea

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

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

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

39 ack of imprinting is independent of promoter CpG methylation and correlates with the absence of the a

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

41 bladder samples, the combination of promoter CpG methylation and EGR1 expression regulated heparanase

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

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

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

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

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

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

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

49 principal enzyme responsible for maintaining CpG methylation and is required for embryonic developmen

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

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

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

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

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

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

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

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

58 ome-wide promoter analysis of MeCP2 binding, CpG methylation, and gene expression revealed that 63% o

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

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

61 Changes in CpG methylation are essential to cellular differentiatio

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

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

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

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

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

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

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

69 ed Bob1 promoter showed one pattern of dense CpG methylation at essentially all sites.

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

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

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

73 n1c allele correlates closely with a loss of CpG methylation at the 5' DMR at the Cdkn1c promoter, wh

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

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

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

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

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

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

80 Promoter analysis revealed CpG methylations at -25 and -140 that correlated with th

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

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

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

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

85 DNA CpG methylation can cooperate with histone H3 lysine 9 (

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

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

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

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

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

91 Although CpG methylation clearly distributes genome-wide in verte

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

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

94 The 14-3-3sigma gene silencing because of CpG methylation correlates with binding of MBD2.

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

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

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

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

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

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 However, how the CpG methylation-dependent silencing mechanism works in r

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

107 ication, the intertissue and interindividual CpG methylation differences in promoter sequence for two

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

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

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

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

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 development of tolerance in macrophages and CpG methylation for T regulatory cell development and fu

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

117 of the human genome and contain much of the CpG methylation found in normal human postnatal somatic

118 results lend support to the hypothesis that CpG methylation functions to suppress spurious transcrip

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

120 DNA CpG methylation has been associated with chromatin compa

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

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

123 Among animals, variable patterns of genomic CpG methylation have been described, ranging from undete

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

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

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

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

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

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

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

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

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

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

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

137 Recent research highlights the role of CpG methylation in genomic imprinting, histone and chrom

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

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

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

153 In contrast, no detectable CpG methylation in the endogenous mouse ROSA26 counterpa

154 up differences in overall or allele-specific CpG methylation in the H19 differentially methylated reg

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

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

157 Analysis of CpG methylation in the MAOA promoter region revealed sub

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

159 revealed that the silencing was coupled with CpG methylation in the promoter, as well as a global his

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

161 adduction, we examined whether the extent of CpG methylation in the supF gene can determine acrolein-

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

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

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

165 re is little evidence addressing the role of CpG methylation in transcriptional control of genes that

166 quence in the SB Tn exhibited high levels of CpG methylation in transgenic mouse lines, irrespective

167 l region and X chromosome, is insensitive to CpG methylation in vitro.

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

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

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

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

172 Promoter CpG methylation is a fundamental regulatory process of g

173 ples and 73 matched normal tissues indicated CpG methylation is a gene-specific and nonrandom event i

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

175 We further demonstrate that local CpG methylation is altered by the presence of the mutati

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

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

178 Because CpG methylation is coupled to intake of essential nutrie

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

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

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

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

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

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

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

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

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

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

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

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

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

192 otentially more labile epigenetic changes in CpG methylation may also record somatic cell ancestry.

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

194 that the loss of 14-3-3sigma expression via CpG methylation may contribute to malignant transformati

195 Because CpG methylation may intensify acrolein-DNA adduction, we

196 eflected in the ongoing debate about whether CpG methylation merely suppresses retroelements or if it

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

198 We investigated the CpG methylation of 19 specific members of Alu sub-famili

199 In this study, we demonstrate that CpG methylation of a minimal KIR promoter inhibited tran

200 Furthermore, CpG methylation of Betaig-h3 promoter was also shown in

201 CpG methylation of DNA is an epigenetic modification ass

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

203 diet of mice affects allelic expression and CpG methylation of Igf2.

204 CpG methylation of involved skin differed from normal sk

205 CpG methylation of MGMT was more frequent in the gastric

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

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

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

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

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

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

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

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

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

215 CpG methylation of the transgene correlated inversely wi

216 Furthermore, CpG methylation of TIMP-2 promoter was also shown in pri

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

218 Aberrant CpG methylation of tumor suppressor gene regulatory elem

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

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

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

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

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

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

225 roach can be used to quantify the effects of CpG methylation on the DNA recognition by other DNA-bind

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

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

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

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

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

231 Comprehensive analysis of CpG methylation patterns at a single DNA molecule level

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

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

234 mammalian enzyme responsible for maintaining CpG methylation patterns in the cell following replicati

235 nt cell types also have primarily concordant CpG methylation patterns on complementary strands, and (

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

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

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

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

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

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

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

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

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

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

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

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

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

249 .5 and 0.7 at two CpG loci), indicating that CpG methylation regulates gene expression.

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

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

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

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

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

255 leosomal H3K9me3 modification in addition to CpG methylation signals.

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

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

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

259 es that occur at cytosine-phosphate-guanine (CpG) methylation sites due to spontaneous deamination of

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

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

262 er CpG methylation alone, 5' and 3' promoter CpG methylation sparing sites in the central cores, and

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

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

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

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

267 CpG methylation status in normal cells points to locally

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

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

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

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

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

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

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

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

276 Here we propose a mathematical model of CpG methylation that is consistent with the cooperative

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

278 te gene silencing, in some cases of complete CpG methylation throughout entire promoters both the act

279 ing sites in the central cores, and complete CpG methylation throughout the promoter regions.

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

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

282 CpG methylation variation is involved in human trait for

283 Non-CpG methylation was >250-fold reduced compared with wild

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

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

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

287 However, CpG methylation was significantly increased by dietary f

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

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

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

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

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

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

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

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

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

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

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

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

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