ライフサイエンスコーパス: CpG island

1 methylation of the truncated DLGAP4 promoter CpG island.

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

3 equent acquisition of new DNA methylation in CpG islands.

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

5 iate the demethylation of DNA within genomic CpG islands.

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

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

8 ications for polycomb-mediated repression at CpG islands.

9 nd generates paradoxical hypermethylation of CpG islands.

10 e and thus the transcriptional competence of CpG islands.

11 methylation occurring preferentially outside CpG islands.

12 lated changes in DNA methylation at specific CpG islands.

13 moters, regardless of their association with CpG islands.

14 me methylation occurred in sequences outside CpG islands.

15 igenetic regulatory elements than studies of CpG islands.

16 network show concomitant hypermethylation of CpG islands.

17 frequently in the shores than in the actual CpG islands.

18 otif significantly enriched in the effective CpG islands.

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

20 aling pathway and lateralized methylation of CpG islands.

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

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

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

24 Among the methylated CpG islands, 11,481 islands were found located in the pr

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

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

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

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

29 eins, MBD1, MBD2 and MeCP2 to the methylated CpG island and repression of transcription.

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

31 ead differences in methylation levels across CpG islands and a large number of differentially methyla

32 of myeloma occurred predominantly outside of CpG islands and affected distinct sets of gene pathways,

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

34 hat of RelA-AP1 and are enriched in introns, CpG islands and DNase accessible sites.

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

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

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

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

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

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

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

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

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

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

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

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

47 depending on the methylation status of this CpG island, and physically interacts with and up-regulat

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

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

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

51 tory regions, methylation levels in promoter CpG islands are actually higher for genes within placent

52 Several of these hypermethylated CpG islands are associated with genes involved in the ME

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

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

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

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

57 rential methylation patterns in the promoter CpG islands as well as in various less studied genomic r

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

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

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

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

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

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

64 cRNA genes, also a differentially methylated CpG island, binds GLI2 depending on the methylation stat

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

66 edominately enriched in promoter regions, or CpG islands, but rather in the 3' UTR, gene bodies, CpG

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

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

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

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

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

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

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

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

75 By exploiting a CpG island (CGI) point mutation causing a Mendelian dise

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

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

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

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

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

81 that this exon is imbedded in a well-defined CpG island (CGI) that is highly methylated in the human

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

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

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

85 n analysis of the pre-B ALL methylome beyond CpG-islands (CGI).

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

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

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

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

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

91 velopment, a small but significant number of CpG islands (CGIs) become methylated.

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

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

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

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

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

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

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

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

100 d with regions of non-methylated DNA, called CpG islands (CGIs), which counteract the repressive effe

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

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

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

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

105 3 bivalent domains underlying methylated DNA CpG islands (CGIs).

106 ared DNA methylation levels within promoter 'CpG islands' (CGIs) with 'CGI shores', recently describe

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

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

109 nct associations between DHSs and promoters, CpG islands, conserved elements, and transcription facto

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

111 in vertebrate cells, preferentially binds to CpG island-containing promoters and affects the organiza

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

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

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

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

116 Aberrant DNA methylation of CpG islands, CpG island shores and first exons is known

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

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

119 By using CpG island demethylation profiles, and by integrating th

120 a, we have determined genome-wide methylated CpG island distributions by next-generation sequencing.

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

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

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

124 Methylation of the CpG island encompassing the AP-2 regulatory region was i

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

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

127 Only a small fraction of the methylated CpG islands had any effect on RNA expression.

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

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

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

131 -based approach to monitor global changes in CpG island hypermethylation between HPV-negative and HPV

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

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

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

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

136 DNA CpG island hypermethylation was detected at promoters of

137 Regions of CpG island hypermethylation were enriched for genes impl

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

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

140 These domains involve aberrant CpG-island hypermethylation similar to that observed in

141 enomic regions such as those surrounding the CpG islands, i.e. shores and shelves.

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

143 errant DNA methylation of this MGMT promoter CpG island in lung tumours.

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

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

146 lung tumour-derived methylation data from a CpG island in the O6-methylguanine-DNA methyltransferase

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

148 The CpG island in the promoter region of LXN was almost univ

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

150 ion status at 12 CpGs near the 5' end of the CpG island in two lung tumour samples for both alleles o

151 The important role of CpG islands in gene transcription strongly suggests evol

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

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

154 The method is also used to classify CpG islands in the human genome.

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

156 CpG islands in the upstream regulatory regions of many c

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

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

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

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

161 2235312 polymorphisms and methylation of the CpG island influence the expression of apelin in HAPE.

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

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

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

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

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

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

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

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

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

171 es such as MMP13 and IL1B, which have sparse CpG islands, is poorly understood in the context of musc

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

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

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

175 omethylation in PMF was seen to occur in non-CpG island loci, showing further qualitative differences

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

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

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

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

180 s of CpG island methylation, suggesting that CpG island methylation alone might not be sufficient to

181 onally, we found that Smchd1 is required for CpG island methylation and silencing at a cluster of fou

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

183 known to exhibit widespread promoter region CpG island methylation leading to the inactivation of ke

184 ssays of melanoma patient tissue samples for CpG island methylation near the noncoding RNA gene SNORD

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

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

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

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

189 expression did not correlate with levels of CpG island methylation, suggesting that CpG island methy

190 Both intragene and promoter CpG island methylations negatively affected gene express

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

192 mismatch repair) system, the presence of the CpG island methylator phenotype (CIMP or CIMP-High) and

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

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

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

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

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

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

199 Although the CpG island methylator phenotype (CIMP) was first identif

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

201 nations of microsatellite instability (MSI), CpG island methylator phenotype (CIMP), and mutations in

202 hibit BRAF mutation, MLH1 methylation, and a CpG island methylator phenotype (CIMP), but precursors a

203 olorectal cancer risk according to status of CpG island methylator phenotype (CIMP), microsatellite i

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

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

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

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

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

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

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

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

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

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

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

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

216 CpG island methylator phenotype-positive hindbrain epend

217 Two AD subtypes manifested a CpG island methylator phenotype.

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

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

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

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

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

223 Of those in CpG islands (n = 44), most (75%) exhibited higher methyl

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

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

226 ns as compared to introns while unmethylated CpG islands near transcription start sites became enrich

227 Many CpG islands not associated with imprinting also inherit

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

229 Bisulfite sequencing revealed that promoter CpG islands of ABCC3 and SLCO2A1 were not hypermethylate

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

231 0(-15); effect size = 14-17%), an intergenic CpG island on 2q37.1 (cg21566642, P = 3.73 x 10(-13); ef

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

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

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

235 Methylation of the CpG-rich region (CpG island) overlapping a gene's promoter is a generally

236 ally significant enrichment of these loci in CpG islands (p = 0.009).

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

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

239 atedly used over the past decade to describe CpG island promoter methylation in other tumor types, in

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

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

242 focused on MagohB, which is controlled by a CpG island promoter.

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

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

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

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

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

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

249 essible state characteristic of unmethylated CpG island promoters.

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

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

252 ed methylation profiling with the methylated-CpG island recovery assay in combination with microarray

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

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

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

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

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

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

259 ficult to conduct, we used exact patterns in CpG island sequences and single character discrepancies

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

261 ter discrepancies to identify differences in CpG island sequences.

262 hine learning algorithms to demonstrate that CpG islands sequences can be characterized using k-mers.

263 Recently, other patterns such as CpG island shore methylation and long partially hypometh

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

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

266 Aberrant DNA methylation of CpG islands, CpG island shores and first exons is known to play a key

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

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

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

270 1500 and TSS200), 1st exons, 5'UTRs, 3'UTRs, CpG islands, shores, shelves, open seas and FANTOM5 enha

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

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

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

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

275 ysis of the human SAMHD1 promoter revealed a CpG island that is methylated in CD4(+) T cell lines (su

276 This region contained a CpG island that was hypermethylated in CD133-ve glioma s

277 gene expression data to identify a subset of CpG islands that are most likely to regulate downstream

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

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

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

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

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

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

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

285 er characterized 982 DM loci in the promoter CpG islands to evaluate their potential biological funct

286 the key regulatory sequences (promoters and CpG islands) to expression of their respective transcrip

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

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

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

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

291 2 targets NuRD to unmethylated or methylated CpG islands where its distinct dynamic binding modes hel

292 uncertain significance occurred primarily in CpG islands, whereas differentially methylated loci in c

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

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

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

296 generate lists of differentially methylated CpG islands with approximately 50% concordance with gene

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

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

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.