ライフサイエンスコーパス: CpG island

1 ges in a DNA molecule with the sequence of a CpG island.

2 methylation of the truncated DLGAP4 promoter CpG island.

3 inks between circRNA biogenesis and flanking CpG island.

4 ver gene regions and location in relation to CpG islands.

5 aling pathway and lateralized methylation of CpG islands.

6 ulated by SOX2 and EZH2, which colocalize at CpG islands.

7 of the well-understood methylation-switch at CpG islands.

8 role for TDG in shaping 5fC distribution at CpG islands.

9 h the exception of genes that do not contain CpG islands.

10 rase II-enriched regions, and hypomethylated CpG islands.

11 iate the demethylation of DNA within genomic CpG islands.

12 pG rich while H3K27me3-only promoters lacked CpG islands.

13 rt of a mechanism that blocks methylation of CpG islands.

14 ications for polycomb-mediated repression at CpG islands.

15 c genes repressed by FGF19, have overlapping CpG islands.

16 nd generates paradoxical hypermethylation of CpG islands.

17 e and thus the transcriptional competence of CpG islands.

18 lated changes in DNA methylation at specific CpG islands.

19 moters, regardless of their association with CpG islands.

20 me methylation occurred in sequences outside CpG islands.

21 eases with age, corresponding with a loss of CpG islands.

22 aling pathway, and widespread methylation of CpG islands.

23 K27me3 domains, but retention of H3K27me3 at CpG islands.

24 equent acquisition of new DNA methylation in CpG islands.

25 compared with controls and were enriched for CpG islands.

26 methylation occurring preferentially outside CpG islands.

27 IC array targeting 866,562 methylation site (CpG) islands.

28 we demonstrated that hypermethylation of the CpG-island 5'of the G(4)C(2)-repeat is expansion-specifi

29 was associated with hypermethylation of the CpG-island (5'of the repeat) in DNA samples obtained fro

30 over-represented in CpG islands, comparative CpG island analysis using conventional sequence analysis

31 DNMT3b thereby decreases methylation of the CpG island and derepresses RASSF1A transcription.

32 ncing revealed that miR-210 is embedded in a CpG island and miR-210 gene has 2 CpG sites with lower m

33 induced obese (DIO) mice, methylation of the CpG island and the binding of methyl-CpG-binding domain

34 d by overwhelming age-related methylation in CpG islands and demethylation at shore/shelf and open se

35 DMRs found overlapping CpG islands and exons of imprinted genes such as MEST an

36 d in group H were more frequently located in CpG islands and marked for polycomb occupancy.

37 he MBD4MBD4 targets the intact protein to (m)CpG islands and promotes scanning by rapidly exchanging

38 ation and a CxxC zinc-finger that recognizes CpG islands and recruits the polycomb repressive complex

39 from the meta-analysis were enriched in non-CpG islands and shores ([Formula: see text]) and deplete

40 ng in eQTLs in blood and the frontal cortex, CpG islands and shores, and exons.

41 ylation signals in promoters located outside CpG islands and shores.

42 re preferentially located in areas distal to CpG islands and shores.

43 transcription factors and are distinct from CpG islands and shores.

44 ylated DMRs were more likely to overlap with CpG islands and shores.

45 osed method on eight independent assays (two CpG islands and six imprinting DMRs) and demonstrated it

46 Variants were collapsed across CpG islands and their flanking regions to identify varia

47 h recombination hot spots, are enriched near CpG islands and transcription start sites (P<2.2 x 10(-1

48 to normal plasma cells, were located outside CpG islands and were unexpectedly associated with intron

49 d in hypomethylation of positions outside of CpG islands and within intragenic (exon) regions of the

50 Absence of 5hmC was observed in CpG islands and, to a greater extent, in non-CpG island-

51 ers 96% of known cytosine-phosphate-guanine (CpG) islands and 485,000 CpG, and transcriptome profilin

52 d at transcription start sites (TSSs) and in CpG islands, and depleted in transcriptional enhancers.

53 proteins are crucial for PRC2 recruitment to CpG islands, and further clarifies the roles of these pr

54 ctivity, induces complete methylation of P16 CpG islands, and inactivates P16 transcription in the HE

55 CpG islands are GC-rich regions often located in the 5'

56 hes revealed that the majority of methylated CpG islands are intragenic and gene bodies are hypermeth

57 lling into question the prevailing view that CpG islands are not subject to selection.

58 Promoter CpG islands are typically unmethylated in normal cells,

59 ding their internal tandem repeat-associated CpG island, are near-universally methylated.

60 ed in lone intergenic CpGs and depleted from CpG islands around genes.

61 cipitation (MCIp) combined with whole-genome CpG island arrays.

62 tors revealed significant hypomethylation of CpG islands associated with the promoters of genes invol

63 Together these discoveries demonstrate that CpG-island associated gene promoters can prime genes for

64 uman and regulates DNA methylation status of CpG island-associated promoters in trans.

65 CpG islands and, to a greater extent, in non-CpG island-associated regions.

66 dation in cells triggers PRC2 recruitment to CpG islands at active genes.

67 Selective methylation of CpG islands at imprinting control regions (ICR) determin

68 Most genes with hypermethylated CpG islands at promoters are suppressed in malignant and

69 PRC2 is primarily associated with CpG islands at repressed genes and also possesses RNA bi

70 oters are primed for activation by FBXL19, a CpG island binding protein, through its capacity to recr

71 concordant alterations in H3K4me1 levels and CpG island border DNA methylation encroachment.

72 We show that the pattern of H3K4me1 at CpG island borders in normal cells predicts the differen

73 methylation encroachment across the 5' or 3' CpG island borders.

74 ed to individual regulatory elements such as CpG islands, but can extend across entire chromosomal do

75 en transcription and chromatin remodeling at CpG islands by histone demethylases.

76 stigated the methylation profile of the same CpG-island by bisulfite sequencing of DNA obtained from

77 sequence bias, such as those often found in CpG islands, can obscure the enrichment of biologically

78 nes lack a conventional TATA box but contain CpG islands, cCpG-I and cCpG-II for Cosmc and tCpG for T

79 w that the degrees of overall methylation in CpG island (CGI) and demethylation in intergenic regions

80 t of polycomb repressive complex 2 (PRC2) to CpG island (CGI) chromatin.

81 Global loss of DNA methylation and CpG island (CGI) hypermethylation are key epigenomic abe

82 ometabolite d-2-hydroxyglutarate (2HG) and a CpG island (CGI) hypermethylation phenotype (G-CIMP).

83 nscription is initiated by a distal upstream CpG island (CGI) located several kilobases away that fun

84 ere we report a novel method for genome-wide CpG island (CGI) methylation sequencing for single cells

85 alysis revealed hypermethylation at a distal CpG island (CGI) near the HLA-E gene in NIKS-16 cells co

86 which can analyse jointly all CpGs within a CpG island (CGI) or a Differentially Methylated Region (

87 t GC skew is prevalent at thousands of human CpG island (CGI) promoters and transcription termination

88 revealed that de novo DNA methylation of non-CpG island (CGI) promoters was more often associated wit

89 shed this phasing primarily at enhancers and CpG island (CGI) promoters, with little effect on insula

90 ically distinct subsets, which correspond to CpG island (CGI) proximal or distal regions, respectivel

91 found that 5hmC is significantly enriched in CpG island (CGI) shores while depleted in CGIs themselve

92 of nearly all genes under the control of the CpG island (CGI)-containing promoters.

93 e analyzed 85,134 CpG sites [28,114 sites in CpG islands (CGI) and 57,020 in non-CpG islands (NCGI)].

94 Aberrant hypermethylation of CpG islands (CGI) in human tumors occurs predominantly a

95 but not directly shown, to protect promoter CpG islands (CGIs) against abnormal DNA methylation (DNA

96 ay occur in vivo for DNA methylation outside CpG islands (CGIs) and could facilitate localization of

97 CpG islands (CGIs) are associated with over half of huma

98 CpG islands (CGIs) are associated with the majority of m

99 CpG islands (CGIs) are one of the most widely studied re

100 CpG islands (CGIs) are primarily promoter-associated gen

101 at postnatal DNA methylation increases at 3' CpG islands (CGIs) correlate with transcriptional activa

102 Specific CpG islands (CGIs) displayed characteristics indicating

103 we identify hundreds of genes and associated CpG islands (CGIs) for which the nearby presence of a so

104 DNA hypermethylation of promoter-associated CpG islands (CGIs) in cancer, hypermethylated sites in M

105 ell as increased methylation in the promoter CpG islands (CGIs) of a number of cell cycle related gen

106 methylation fidelity is lost at a number of CpG islands (CGIs) resulting in CGI hypermethylation at

107 owever, residual peaks of H3K27me3 remain at CpG islands (CGIs) through an unknown mechanism.

108 ferential binding of TET1-FL to unmethylated CpG islands (CGIs) through its CXXC domain.

109 , a DNA-binding module that often recognizes CpG islands (CGIs) where TET1 predominantly occupies.

110 stance, co-localization with coding regions, CpG islands (CGIs), and regulatory elements from the ENC

111 ion in the germline, especially at imprinted CpG islands (CGIs), is crucial to embryogenesis in mamma

112 half of human promoters are associated with CpG islands (CGIs), relatively CpG-rich stretches of gen

113 Regions known as CpG islands (CGIs), which are refractory to DNA methylat

114 The mammalian genome is punctuated by CpG islands (CGIs), which differ sharply from the bulk g

115 to CpG sites outside of genes, promoters and CpG islands (CGIs), while trans-meQTLs are over-represen

116 3 bivalent domains underlying methylated DNA CpG islands (CGIs).

117 One consequence is the creation of new CpG islands (CGIs).

118 has a CXXC domain that binds to unmethylated CpG islands (CGIs).

119 y demonstrates that Fn14 promoter contains a CpG island close to transcription start site.

120 as CpG dinucleotides are over-represented in CpG islands, comparative CpG island analysis using conve

121 protein, promotes H2Bub1 at the promoters of CpG island-containing genes by interacting with Rnf20.

122 equired for efficient recruitment of PRC2 to CpG island-containing promoters in mouse embryonic stem

123 eils the preferential occupancy of Fbxl19 on CpG island-containing promoters, and we further discover

124 The DM sites were depleted within CpG-island-containing promoters but enriched in predicte

125 This CpG-island contains binding sites for the methylation-se

126 Regulatory regions such as promoter CpG islands, CpG shores and enhancers show changes in me

127 Methylation of a Pax3 CpG island decreased upon neurulation of embryos and for

128 also correlated with the degree of aberrant CpG island DNA methylation in normal cells.

129 This NF-kappaB/RelA site is in a CpG island downstream from EpCAM transcriptional start s

130 terestingly, the human EpCAM gene also has a CpG island downstream from its TSS, and a NF-kappaB-bind

131 gion of high GC content (76%) derived from a CpG island embedded in such a long DNA substrate.

132 demonstrated that a 1.5 kb methylation-free CpG island from the human HNRPA2B1-CBX3 housekeeping gen

133 ions and methylation at loci concentrated in CpG islands genome wide in 95 nuclear pedigrees, using D

134 the genomic CpGs outside gene promoters and CpG islands has not been extensively characterized.

135 Although promoter-associated CpG islands have been established as targets of DNA meth

136 regions show enhanced de novo activity, and CpG islands have both poor maintenance and de novo activ

137 pigenetic repression occurs concomitant with CpG island hypermethylation and loss of nucleosomes at p

138 t EBV infection of oral keratinocytes led to CpG island hypermethylation as an epigenetic scar of pri

139 wide patterns of aberrant hypomethylation or CpG island hypermethylation in specific cancer types.

140 thesized that LTF expression is silenced via CpG island hypermethylation in the early stages of prost

141 Ls with DNMT3A(R882), while DNMT3A-dependent CpG island hypermethylation is a consequence of AML prog

142 Additionally, we observe that promoter CpG island hypermethylation is not restricted solely to

143 to EBV compared to uninfected controls, with CpG island hypermethylation observed at several cellular

144 non-cancer tissue, and identifying a cancer CpG island hypermethylation phenotype.

145 DNA CpG island hypermethylation was detected at promoters of

146 lly all AMLs with wild-type DNMT3A displayed CpG island hypermethylation, this change was not associa

147 Here we demonstrate the presence of promoter CpG island hypermethylation-linked inactivation of DERL3

148 cells predicts the different modes of cancer CpG island hypermethylation.

149 Intragenic CpG islands (iCGIs) and their corresponding host genes e

150 hat integration of genomic features, such as CpG islands improves TFBS prediction in some TFCT.

151 rum of methylated genomic DNA from the AGTR1 CpG island in metastatic melanoma implying that AGTR1 en

152 ing the changes in methylation patterns in a CpG island in the first exon of the promoter during lung

153 GATA2-dependent demethylation of a putative CpG island in the miR-221 promoter.

154 We find that a CpG island in the promoter of the dual-specificity phosp

155 Unexpectedly, a CpG island in the promoter region of the FoxA2 gene disp

156 uit DNA methyltransferase 3b (DNMT3b) to the CpG island in the RASSF1A promoter.

157 Although methylation of CpG islands in Nrf2 or NQO1 promoters was unaltered by G

158 defined as DNA hypermethylation at specific CpG islands in subsets of tumors, show high concordance

159 Aberrant hypermethylation of CpG islands in the promoter region of tumor suppressor g

160 Hypermethylation of CpG islands in the RASSF1A promoter region contribute to

161 ultiple SPRY3 transcripts originating at two CpG islands in the X-linked F8A3-TMLHE region, suggestin

162 ding pTreg displayed hypermethylation of the CpG islands in Treg-specific demethylated region, CTLA-4

163 Methylation-induced silencing of promoter CpG islands in tumor suppressor genes plays an important

164 high-level methylation in discrete promoter CpG islands, in a pattern clearly distinct from other lu

165 2235312 polymorphisms and methylation of the CpG island influence the expression of apelin in HAPE.

166 ilter always selected more features from non-CpG island intergenic regions.

167 We report that the LTF CpG island is frequently and densely methylated in high-

168 To determine whether the same CpG island is hypermethylated in the cerebella of cases

169 Likewise, the frequency at which the LTF CpG island is methylated across samples suggests it is a

170 5-Methylcytosine (5mC) in DNA CpG islands is an important epigenetic biomarker for mam

171 owever, the mechanism of PRC2 recruitment to CpG islands is not fully understood.

172 DNA-methylation at CpG islands is one of the prevalent epigenetic alteratio

173 f the variant PCGF1/PRC1 complex by KDM2B to CpG islands is required for normal polycomb domain forma

174 sults demonstrate that Fbxl19 recruitment to CpG islands is required for Rnf20-mediated H2B mono-ubiq

175 De novo methylation of CpG islands is seen in many cancers, but the general rul

176 A hallmark of CpG islands is their unmethylated state, and determining

177 the link between FTLD and methylation of the CpG-island is unknown.

178 of c9ALS cases show hypermethylation of the CpG island located at the 5' end of the repeat expansion

179 ing cells, and examined DNA methylation of a CpG island located downstream from SALL4 transcriptional

180 pigenetic changes such as DNA methylation of CpG islands located in the promoter region of some tumor

181 Hypermethylation was enriched at CpG islands marked with bivalent activating and repressi

182 we provide evidence that methylation beyond CpG islands may be related to regulation of gene express

183 f age-related changes in promoter-associated CpG islands may contribute to the increased cancer risk

184 ells due to DNA hypermethylation of promoter CpG islands may offer new cancer prevention or therapeut

185 est a role for H3K4me1 in the demarcation of CpG island methylation borders in normal cells, which be

186 CpG island methylation encroachment is widespread in pro

187 published data from a study of differential CpG island methylation in lung cancer and a dataset we g

188 melanomas expressing this receptor and AGTR1 CpG island methylation in serum may serve as a novel bio

189 report decreasing expression and increasing CpG island methylation of AGTR1 in metastatic versus pri

190 ed with the TCGA 'microsatellite instability/CpG island methylation phenotype' transcriptomic subtype

191 sis, which is associated with BRAF mutation, CpG island methylation phenotype, and MLH1 methylation.

192 utations, microsatellite instability status, CpG island methylation status, PTEN loss, EGFR expressio

193 or microsatellite instability, MLH1 promoter CpG island methylation, and KRAS and BRAF mutations in c

194 on differentiation, DNMT activation leads to CpG island methylation, causing loss of repressor protei

195 , a master kinase of the AMPK subfamily, via CpG island methylation.

196 re LTF mRNA has presumably been silenced via CpG island methylation.

197 terized by extensive, abnormal gene-promoter CpG-island methylation, or the methylator phenotype (CIM

198 epigenetic clusters, including a clear cell CpG island methylator phenotype (C-CIMP) subgroup associ

199 ocitrate dehydrogenase 1/2 (IDH1/2) have the CpG island methylator phenotype (CIMP) and significantly

200 ntaining activated BRAF (BRAF[V600E]) have a CpG island methylator phenotype (CIMP) characterized by

201 AS-positive colorectal cancers (CRCs) have a CpG island methylator phenotype (CIMP) characterized by

202 In colorectal cancer, the CpG island methylator phenotype (CIMP) is defined as wid

203 Colorectal cancer (CRC) with CpG island methylator phenotype (CIMP) is recognized as

204 dification recapitulated the hypermethylated CpG island methylator phenotype (CIMP) observed in EBV-a

205 ) but not with microsatellite instability or CpG island methylator phenotype (CIMP) positivity.

206 A CpG island methylator phenotype (CIMP) was observed in a

207 ellite instability (MSI), genetic mutations, CpG island methylator phenotype (CIMP), and immunostaini

208 rmation on microsatellite instability (MSI), CpG island methylator phenotype (CIMP), and mutations in

209 btypes for microsatellite instability (MSI), CpG island methylator phenotype (CIMP), and somatic muta

210 features: microsatellite instability (MSI), CpG island methylator phenotype (CIMP), B-Raf proto-onco

211 regulated colon cancers characterized by the CpG island methylator phenotype (CIMP).

212 IDH mutant gliomas thus manifest a CpG island methylator phenotype (G-CIMP), although the f

213 er differences, in a small set of non-glioma CpG island methylator phenotype (non-G-CIMP) primary tum

214 gnificantly enriched for those harboring the CpG island methylator phenotype (p = 0.036, Chi square t

215 pe 1 (microsatellite instability [MSI]-high, CpG island methylator phenotype [CIMP] -positive, positi

216 suppressor genes, such as APC and TP53; (3) CpG island methylator phenotype CRCs in approximately 20

217 y unmethylated CpGs, a characteristic of the CpG island methylator phenotype in cancer, a novel filte

218 tion status, microsatellite instability, and CpG island methylator phenotype were also evaluated.

219 ldtype] or BRAF [BRAF wildtype], no or a low CpG island methylator phenotype, and microsatellite stab

220 AS wildtype, BRAF wildtype, have no or a low CpG island methylator phenotype, and microsatellite stab

221 stics (including microsatellite instability, CpG island methylator phenotype, KRAS, BRAF, and PIK3CA

222 correlated tumor molecular characteristics (CpG island methylator phenotype, microsatellite instabil

223 way expression patterns, the hypermethylated CpG island methylator phenotype-associated (CIMP) RCCs a

224 CpG island methylator phenotype-positive hindbrain epend

225 or-prognosis hindbrain ependymomas exhibit a CpG island methylator phenotype.

226 roup showing some features consistent with a CpG island methylator phenotype.

227 Two AD subtypes manifested a CpG island methylator phenotype.

228 CRC tumors displaying CpG island methylator phenotypes (CIMPs), defined as DNA

229 c pancreatitis (CP) and normal tissues using CpG island microarrays and identified WNK2 as a prominen

230 nomic mC modification at the characteristic "CpG" island motif.

231 sites in CpG islands (CGI) and 57,020 in non-CpG islands (NCGI)].

232 Moreover, two CpG islands near the transcription start site of MYBL1 w

233 Many CpG islands not associated with imprinting also inherit

234 Aberrant DNA methylation in the promoter CpG island of Wnt inhibitory factor 1 (WIF1) has been ob

235 Specific site of CpG islands of adenomatous polyposis coli (APC), a well

236 ted the function of Gadd45b in demethylating CpG islands of representative gene targets, which have b

237 hile early studies were mostly restricted to CpG islands or promoter regions, recent findings indicat

238 that the degree of methylation of the entire CpG-island or contribution of specific CpGs (n = 26) is

239 observed rapid methylation increases at the CpG-island overlapping the first 5'-untranslated region

240 CpG-dense loci, called "CpG islands", play a particularly important role in modu

241 ed hypermethylation of positively correlated CpG islands potentiates ANO1 expression.

242 be explained by differential methylation of CpG islands present in the TERRA-expressing murine subte

243 Tet2 has a CpG island promoter with pluripotency-independent activi

244 c landscape the FXN gene promoter, a typical CpG island promoter, was found to be in a transcriptiona

245 pression for only those genes that contain a CpG island promoter.

246 el filter always selected more features from CpG island promoters and the standard deviation filter a

247 widespread formation has been detected over CpG island promoters in human genes.

248 Methylation of CpG island promoters is an epigenetic event that can eff

249 rgently targeted to species-specific sets of CpG island promoters that extend beyond known imprint co

250 ation at hundreds of embryonically protected CpG island promoters, particularly those that are associ

251 essible state characteristic of unmethylated CpG island promoters.

252 is associated with increased methylation of CpG islands proximal to the promoters of these genes; fu

253 We used the Methylated CpG Island Recovery Assay chip to survey DNA methylation

254 umulating evidence supports a model in which CpG islands recruit Polycomb group (PcG) complexes; howe

255 tion status of a miR-494 promoter-associated CpG island region (-186 to -20), which was confirmed by

256 This CpG island region was found to repress reporter gene exp

257 her levels of methylation in gene-regulatory CpG island regions (Deltamethylation = 4.1%, P < 0.0001)

258 The majority of mammalian promoters are CpG islands; regions of high CG density that require pro

259 rtion of RGM proximal to promoter-associated CpG islands reports the gain or loss of DNA methylation.

260 ng abnormal DNA hypermethylation of promoter CpG islands, repressive chromatin modifications and enha

261 , we conducted a comparative analysis of all CpG island sequences in 10 mammalian genomes.

262 b expression due to hyper-methylation in the CpG island shore region of mmu-miR-15b in both the sperm

263 Its genomic location, a CpG island shore within an H3K27ac enhancer mark, and th

264 hed in flanking regions of active promoters, CpG island shores, binding sites of the transcription fa

265 ferential methylation was overrepresented in CpG island shores, enriched within gene bodies but not i

266 ficantly overrepresented in regions flanking CpG islands (shores and shelves) and gene bodies.

267 1500 and TSS200), 1st exons, 5'UTRs, 3'UTRs, CpG islands, shores, shelves, open seas and FANTOM5 enha

268 ion-induced tumors gained DNA methylation at CpG islands, some of which are associated with putative

269 or epigenetically in various cancers, and a CpG island spanning the transcriptional start site of LT

270 The CpG islands surrounding miR-433 were hypermethylated, an

271 The CpG islands surrounding the PGC7-binding motifs are hype

272 bisulfite amplicon sequencing on a range of CpG island targets across a panel of human cell lines an

273 Importantly, MBD2 functions within CpG islands that contain 100s to 1000s of potential bind

274 We found three CpG islands that correlated with ANO1 expression, includ

275 nriched in CG content, which correlates with CpG islands that display a low level of DNA methylation.

276 Using methylome sequencing we identified CpG islands that display partial methylation encroachmen

277 onjunction with hypermethylation of promoter CpG islands that presumably lead to genome instability a

278 validate a set of 67 CpG dinucleotides in 51 CpG islands that undergo age-related methylomic drift.

279 e1 being the most variable and promoters and CpG islands the most stable.

280 n frequency at transcription start sites and CpG islands, thereby reducing the potential for insertio

281 onjunction with hypermethylation of promoter CpG islands; these changes are often correlated with pro

282 that mutant PPM1D drives hypermethylation of CpG islands throughout the genome and promotes epigeneti

283 d breaks enriched at Ssb-binding regions and CpG islands, together with the accumulation of R-loops a

284 iption start site, chromosome fragile sites, CpG islands, viral sequences and target sequences were i

285 Methylation of the apelin CpG island was significantly higher in HAPE-p at 11.92%

286 men while methylation of introns, exons and CpG islands was similar in the two groups.

287 Upon detailed analysis of the TLR2 promoter CpG Island, we noted higher CpG methylation in this dysr

288 whereas unmethylated and nucleosome-depleted CpG islands were enriched for CTCF sites that remained o

289 We found 44% promoter regions and 75% CpG islands were T-47D cell type-specific methylated.

290 2 targets NuRD to unmethylated or methylated CpG islands where its distinct dynamic binding modes hel

291 nding site in BCL6 exon1A within a potential CpG island, which is unmethylated both in cell lines and

292 lated regions (DMRs) such as hypermethylated CpG islands, which may account for epigenetic instabilit

293 lled by epigenetic modifications at critical CpG islands, which were mapped.

294 is unable to spread from large unmethylated CpG islands, while H3K27me2 can be deposited outside the

295 Genbank), which shares the first exon and a CpG island with STL but is transcribed in the opposite d

296 variable methylation of promoter-associated CpG islands with levels ranging from 4% to 35%, even at

297 cts on cytosine methylation are localized to CpG islands within intergenic regions.

298 hains, RNA binding protein binding sites and CpG islands within the flanking regions of the circular

299 In vitro, DF increased DNA methylation of CpG islands within the KLF4 promoter that significantly

300 hypermethylation of a positively correlated CpG island without a change in ANO1 expression.