ライフサイエンスコーパス: hypermethylation

1 6) 2A) methylation than controls, so-called 'hypermethylation'.

2 nocortical tissues, which is a result of CpG hypermethylation.

3 correlated better with gene expression than hypermethylation.

4 histone demethylases, to cause broad histone hypermethylation.

5 factors that prevent gene repression and DNA hypermethylation.

6 utant WT1 to be causally associated with DNA hypermethylation.

7 % of the promoters of these genes displaying hypermethylation.

8 (NPC) and many other tumors due to promoter hypermethylation.

9 NK cell subsets correlated with promoter DNA hypermethylation.

10 hypomethylation to a much higher extent than hypermethylation.

11 nal repression of TSGs through engagement of hypermethylation.

12 d that silence of SOX30 was regulated by its hypermethylation.

13 lon primary tumors concomitant with promoter hypermethylation.

14 pressed genes (458) and miRNA (0) and genome hypermethylation.

15 ciates with normalization of Rasal1 promoter hypermethylation.

16 at derepress gene silencing by reversing DNA hypermethylation.

17 hose repressed by CNOT3 binding and promoter hypermethylation.

18 TGCTs show focal recurrent imprinted domain hypermethylation.

19 loss of GPC5 expression was regulated by its hypermethylation.

20 ation punctuated by regions of glia-specific hypermethylation.

21 in-7 expression, also exhibited promoter DNA hypermethylation, a modification associated with transcr

22 demonstrated that miR-34A was inactivated by hypermethylation across many histologic types of primary

23 ation-induced epigenetic alterations and DNA hypermethylation alterations observed in inflammation-in

24 Finally, promoter-associated hypermethylation analysis shows silencing of LED in huma

25 tral role for G9a- and EZH2-mediated histone hypermethylation and a model of bidirectional, mutually

26 Reversal of DNA hypermethylation and associated gene silencing is an eme

27 or maximally reversing abnormal promoter DNA hypermethylation and associated gene silencing to reexpr

28 scriptional activity resulting from promoter hypermethylation and binding with tumor suppressor menin

29 about the association between MGMT promoter hypermethylation and breast and gynecologic cancers.

30 etic landscape of cancer includes both focal hypermethylation and broader hypomethylation in a genome

31 B1 and RAB25 are downregulated with promoter hypermethylation and CA9 is upregulated with promoter hy

32 n of miR-217 coincided with DNMT3b-dependent hypermethylation and decreased occupancy of nuclear fact

33 hylome analyses of TKO EBs revealed promoter hypermethylation and deregulation of genes implicated in

34 and interdependent crosstalk between histone hypermethylation and DNA methylation in COX-2 epigenetic

35 se prevented maternal HFD-induced Pgc-1alpha hypermethylation and enhanced Pgc-1alpha and its target

36 enhancer-associated NDRs is associated with hypermethylation and epigenetic silencing marks, and con

37 esults in DNMT3b induction and MEG3 promoter hypermethylation and expression inhibition, further redu

38 a number of candidate drivers of cancer DNA hypermethylation and hypomethylation.

39 l application also inhibited UVB-induced DNA hypermethylation and its elevation of the levels of TET

40 These genes are silenced, predominantly by hypermethylation and less frequently by mutations, and d

41 epression occurs concomitant with CpG island hypermethylation and loss of nucleosomes at promoters, b

42 kdown of the Fos ecRNA locus results in gene hypermethylation and mRNA silencing, and hippocampal exp

43 ly, the profibrotic factor TGF-beta1 induced hypermethylation and repression of erythropoietin in per

44 IDM2 dysfunction causes DNA hypermethylation and silencing of reporter genes and som

45 Our results show that promoter hypermethylation and silencing of the DOC2B gene is an e

46 ese data suggest that BRCA1 suppresses FOXA1 hypermethylation and silencing.

47 profiles and are characteristic by increased hypermethylation and stroma-related genes.

48 Epigenetic changes such as aberrant hypermethylation and subsequent atypical gene expression

49 BRCA1 promoter hypermethylation and the BRCAness phenotype of BC cell l

50 strong association between RHOX gene cluster hypermethylation and three independent types of semen ab

51 enotype (CIMP) characterized by aberrant DNA hypermethylation and transcriptional silencing of many g

52 e DNA methyltransferase DNMT3B, resulting in hypermethylation and transcriptional silencing.

53 NA methyltransferase DNMT1, resulting in DNA hypermethylation and transcriptional silencing.

54 e DNA methyltransferase DNMT3B, resulting in hypermethylation and transcriptional silencing.

55 CBS(+/-) mice showed global hypermethylation and up-regulation of DNA methyltransfer

56 that cadmium exposure is associated with DNA hypermethylation and with a decrease in total RNA synthe

57 nch syndrome, 2 of 10 (20%) tumors with MLH1 hypermethylation, and 12 of 78 (15%) tumors with microsa

58 evels of H3K9Ac and H3K14Ac, reduced DNA CpG hypermethylation, and recovered D-CMSC proliferation and

59 an colorectal cancers (CRCs) due to promoter hypermethylation, and that the RSPO2 reduction correlate

60 evels of genome-wide DNA hypomethylation and hypermethylation are controlled by distinct processes.

61 tein-Barr virus (EBV) infection and cellular hypermethylation are hallmarks of undifferentiated nasop

62 DNA methyltransferases and erythropoietin hypermethylation are upregulated in myofibroblasts.

63 tion of oral keratinocytes led to CpG island hypermethylation as an epigenetic scar of prior EBV infe

64 Using promoter hypermethylation as an epigenetic signature of XCI, we h

65 (siRNA) was found to result in a global DNA hypermethylation as well as increased methylation in the

66 At TSGs, CHD4 retention helps maintain DNA hypermethylation-associated transcriptional silencing.

67 Hypermethylation associates with enhancer silencing.

68 Methylome analysis revealed hypermethylation at a distal CpG island (CGI) near the H

69 e show that human IDH mutant gliomas exhibit hypermethylation at cohesin and CCCTC-binding factor (CT

70 Several IMs exhibited hypermethylation at DNA methylation valleys; however, IM

71 poxia-induced loss of TET activity increases hypermethylation at gene promoters in vitro.

72 PSCs harboring abnormal hypermethylation at ICRs of the Dlk1-Gtl2-Dio3 imprintin

73 latin resistance was associated with loss of hypermethylation at several CpG sites primarily localize

74 ethylator phenotypes (CIMPs), defined as DNA hypermethylation at specific CpG islands in subsets of t

75 screens for Arabidopsis mutants showing DNA hypermethylation at specific loci and increased silencin

76 f DNMT3B in TKO hESCs partially reverses the hypermethylation at the PAX6 promoter and improves diffe

77 tin immunoprecipitation assay confirmed that hypermethylation at the promoter IV region of CIITA is m

78 sequencing, we identified an APL-associated hypermethylation at the upstream differentially methylat

79 y promoting EZH2 dephosphorylation and H3K27 hypermethylation both in vitro and in refractory murine

80 Canyon hypermethylation coincided with disturbed regulation of

81 WT1mut) into wild-type AML cells induced DNA hypermethylation, confirming mutant WT1 to be causally a

82 Deletions, mutations and promoter DNA hypermethylation convergently impacted Wnt signaling, Po

83 erasure, NSEs harbor a malignancy-associated hypermethylation core, akin to that of a diverse cancer

84 Here, we explored whether such causative hypermethylation could be reversed through endogenous me

85 owth factor beta treatment induced gene-body hypermethylation, dissociation of DNMT1 from the promote

86 negative breast cancers express aberrant DNA hypermethylation due to overexpression of DNA methyltran

87 gents; however, MGMT is silenced by promoter hypermethylation during carcinogenesis.

88 ttern globally characterized by regional DNA hypermethylation embedded in extensive hypomethylation.

89 Our data suggest that up to half of hypermethylation events are due to hypoxia, with these e

90 Age-associated hypo- and hypermethylation events occur at distinct regulatory fea

91 d its downstream targets may be regulated by hypermethylation has significant implications for unders

92 quently, Tet1 and Tet2 deletion led to Foxp3 hypermethylation, impaired Treg cell differentiation and

93 d carcinoma (n = 10) showed RASSF1A promoter hypermethylation in 14 (61%), 9 (90%), and 7 (70%), resp

94 trong association between mutant WT1 and DNA hypermethylation in AML and demonstrate that Boolean imp

95 IDH2, and CEBPA were strongly linked to DNA hypermethylation in AML using a novel integrative analys

96 DS fetal cortices and observed a significant hypermethylation in approximately 4% of probes in the DS

97 03 was frequently down-regulated by promoter hypermethylation in both RMS cell lines and RMS biopsies

98 This study is the first to report cerebellar hypermethylation in c9FTD/ALS, and the first to identify

99 on in peripheral and mucosal tissues and DNA hypermethylation in CD patients requiring surgical inter

100 ffect was mediated by BBP-induced global DNA hypermethylation in CD4(+) T cells of the offspring beca

101 and superenhancers, affected by histone H3K4 hypermethylation in disease cases.

102 is restored to wild-type levels, implicating hypermethylation in enhanced growth.

103 d the expression of CIITA/MHC-II by inducing hypermethylation in histone H3 lysine 9 (H3K9me2/3).

104 oxidative stress, suggesting the role of DNA hypermethylation in inactivation of MSH2 expression and

105 pressing histone modifications and resembled hypermethylation in liver cancer.

106 r of the Wnt pathway that is silenced by DNA hypermethylation in many colon cancers.

107 er Cell, Letouze and colleagues describe DNA hypermethylation in paragangliomas harboring mutations i

108 The NISCH promoter experiences hypermethylation in several cancers, whereas some highly

109 ns of aberrant hypomethylation or CpG island hypermethylation in specific cancer types.

110 genome-wide repetitive LINE-1 elements, and hypermethylation in specific promoter regions of single-

111 Hypermethylation in the 3'-protein-phosphatase-1G (PPM1G

112 the effect of a putative persistent Ddo gene hypermethylation in the brain, we used Ddo knock-out mic

113 ls owing to an increased DNA copy number and hypermethylation in the H19 promoter of the IGF2 gene.

114 We also found that the acquisition of DNA hypermethylation in the human lineage is frequently coup

115 -seq and DNase-seq further revealed that DNA hypermethylation in these regions is related to enhancer

116 DNA methyltransferase 1 (DNMT1) and a global hypermethylation in vascular endothelium subjected to di

117 ing type gametes followed by chloroplast DNA hypermethylation in zygotes.

118 Frequent hypermethylation including that of CDH1 in AM increased

119 isulfite sequencing confirmed dense promoter hypermethylation indicative of silencing in multiple mal

120 miR-199a-2 promoter hypermethylation inhibits miR-199a-5p expression and was

121 Stromal Tgfbr2 promoter hypermethylation, initiated by LNCaP cells, was found to

122 ced Dnmt3b expression induced widespread DNA hypermethylation inMyc-Bcl2-induced leukemias, preferent

123 T3A(R882), while DNMT3A-dependent CpG island hypermethylation is a consequence of AML progression.

124 nous mechanisms and whether such reversal of hypermethylation is a constituent of the antifibrotic ac

125 Aberrant promoter DNA hypermethylation is a hallmark of cancer; however, wheth

126 rmined that abrogation of drug-induced H3K27 hypermethylation is associated with cell adhesion-mediat

127 So, promoter hypermethylation is associated with down-regulation of C

128 itro reporter assays indicated that enhancer hypermethylation is globally associated with down-regula

129 differentiation, provide evidence that 14q32 hypermethylation is implicated in the pathogenesis of AP

130 This induced hypermethylation is maintained in somatic cells of carri

131 Specifically, histone hypermethylation is rapidly reversed within days, wherea

132 ur data indicate that TFB1M 12S m(6) 2A rRNA hypermethylation is unlikely to be a pathogenic mechanis

133 t HHcy causes renovascular remodeling by DNA hypermethylation, leading to glomerulosclerosis.

134 s melanomas the KIT promoter is a target for hypermethylation, leading to its downregulation.

135 ntly reported that HPV E7-dependent promoter hypermethylation leads to downregulation of the chemokin

136 Engineered p16(Ink4a) promoter hypermethylation led to transcriptional suppression in s

137 The overall hypermethylation level in FTH showed a statistically sig

138 cord blood surprisingly revealed comparable hypermethylation levels.

139 onstrate the presence of promoter CpG island hypermethylation-linked inactivation of DERL3 (Derlin-3)

140 Such hypermethylation may account for the diminished expressi

141 n a DNMT3A-dependent manner, suggesting that hypermethylation may be a response to, rather than a cau

142 miRNA silencing by promoter hypermethylation may represent a mechanism by which lung

143 In NPM-ALK(+) cell lines, DNA hypermethylation-mediated miR-150 repression required AL

144 Hypo- or hypermethylation-mediated oncogene activation, or tumor

145 ared to uninfected controls, with CpG island hypermethylation observed at several cellular genes.

146 A methylation changes, including significant hypermethylation, occur more frequently in early colonic

147 Hypermethylation occurred only in carriers of an allele

148 ts and observed widespread aberrant cytosine hypermethylation occurring preferentially outside CpG is

149 Downregulation of WNK2 by promoter hypermethylation occurs early in PDAC pathogenesis and m

150 Pericentromeric DNA hypermethylation occurs in a subset of msh1 mutants, ind

151 We show that DNA hypermethylation occurs predominantly at oestrogen-respo

152 Constitutional hypermethylation of 1 allele throughout the soma (consti

153 es with enhanced DCL4(NLS) expression, while hypermethylation of a DCL4 transgene causes a reduction

154 but not E6 transfection of NOK cells led to hypermethylation of a positively correlated CpG island w

155 typical for proinflammatory M1-Mvarphis and hypermethylation of anti-inflammatory, proangiogenic M2-

156 les, and demonstrate that the conjunction of hypermethylation of bivalent chromatin and up-regulation

157 that can identify cancer samples solely from hypermethylation of bivalent chromatin.

158 genomic-imprint and DPPA3 erasure, recurrent hypermethylation of cancer-associated targets, and subty

159 Aberrant hypermethylation of CpG islands (CGI) in human tumors oc

160 Hypermethylation of CpG islands in the RASSF1A promoter

161 me differentiation and generates paradoxical hypermethylation of CpG islands.

162 as a stronger effect, and it does so through hypermethylation of CpG sites in the regulatory sequence

163 Even though the hypermethylation of CpG-177 island located directly upst

164 Overall, we have identified DNA hypermethylation of developmentally regulated enhancers

165 Our results uncover the hypermethylation of DNA methylation canyons as the genom

166 epigenetic program that is characterized by hypermethylation of DNA methylation valleys that are cha

167 fferentiated cells, aging is associated with hypermethylation of DNA regions enriched in repressive h

168 ce and distribution of 5hmC, which prevented hypermethylation of DNA, and for regulation of the B cel

169 ssion and cell death functions, differential hypermethylation of genes associated with transcriptiona

170 SG-derived hepatocytes, also associated with hypermethylation of GH-response elements in the CYP2C11

171 dhesion counteracted anticancer drug-induced hypermethylation of H3K27 via inactivating phosphorylati

172 KD of Kdm5c resulted in hypermethylation of H3K4 and prevented the expression of

173 Moreover, hypermethylation of HES4 promoter sequences was striking

174 o act as an oncogenic metabolite by inducing hypermethylation of histones and DNA.

175 E methylation accumulate SAM, which leads to hypermethylation of histones and the major phosphatase P

176 tion of lncRNA HOTAIR in DCIS-C1 lesions and hypermethylation of HOXA5 and SOX genes.

177 a tumour-suppressor gene inactivated by DNA hypermethylation of its canonical CpG (cytidine-phosphat

178 found decreased expression of miR-125b-1 and hypermethylation of its promoter in HNSCC compared with

179 or gene was shown to be often inactivated by hypermethylation of its promoter region.

180 sues from children with UC was attributed to hypermethylation of its promoter region.

181 Rbeta1 down-regulation was not the result of hypermethylation of its promoter, but was associated wit

182 f TFF2 to be down-regulated in human PDAC by hypermethylation of its promoter.

183 ition of progesterone signaling is caused by hypermethylation of its receptor Pgr by Notch1 overexpre

184 Germline hypermethylation of KLLN, a gene uncovered well after th

185 r phenotype (CIMP) characterized by aberrant hypermethylation of many genes, including the mismatch r

186 a-analysis to assess the association between hypermethylation of MGMT promoter and the risk of breast

187 , but not in cancer cells because of the DNA hypermethylation of miR-148a and miR-152 gene promoters.

188 tion and gene expression data, we found that hypermethylation of MITF and its co-regulated differenti

189 dic type (6.8%) with BRAF mutation and/or or hypermethylation of MLH1 and the familial type (2.6%), w

190 ins in immunohistochemical analysis, without hypermethylation of MLH1), but no germline mutations in

191 ial type (2.6%), which lacked BRAF(V600E) or hypermethylation of MLH1.

192 in the level of histone H3 acetylation, and hypermethylation of MSH2 promoter were also observed in

193 We show that hypermethylation of p16/Ink4a and p19/Arf in CNT- and as

194 lation of the TP63N transcriptional network, hypermethylation of pancreatic endodermal cell-fate dete

195 h differential expression of ANO1, we showed hypermethylation of positively correlated CpG islands po

196 And small shift of hypermethylation of previously hypomethylated region was

197 TET2 reduction results in hypermethylation of promoter CGIs and enhancers in loci

198 al gene silencing in cancer cells due to DNA hypermethylation of promoter CpG islands may offer new c

199 y global hypomethylation in conjunction with hypermethylation of promoter CpG islands that presumably

200 epigenetic regulation including abnormal DNA hypermethylation of promoter CpG islands, repressive chr

201 Aberrant DNA hypermethylation of promoter of tumor suppressor genes i

202 CpG hypermethylation of promoter regions is often associated

203 In contrast to the widely reported DNA hypermethylation of promoter-associated CpG islands (CGI

204 e regulators of STAT3, including by promoter hypermethylation of PTPRT.

205 ast with NUC1, disruption of NUC2 induces CG hypermethylation of rDNA and NOR association with the nu

206 be repressed in human breast cancer cells by hypermethylation of regulatory promoter regions, leading

207 of ocular tissue-specification and described hypermethylation of retinal transcription factors (i.e.,

208 Hypermethylation of selected CpG sites was confirmed in

209 bundance of 24-nt siRNAs was associated with hypermethylation of TEs and gene promoters, with influen

210 Hypermethylation of the ANO1 promoter was strongly corre

211 oral keratinocytes (NOK) were used to induce hypermethylation of the ANO1 promoter.

212 Bisulfite sequencing confirmed hypermethylation of the APEX1 promoter region in HD cell

213 None of the studied BC cell lines presented hypermethylation of the BRCA1 promoter region.

214 Future studies will need to evaluate hypermethylation of the C9orf72 promoter in a larger coh

215 lated region (UTR) hypomethylation and 3'UTR hypermethylation of the cellular epitranscriptome, regul

216 AIE exposure was associated with hypermethylation of the COMT promoter at a conserved CpG

217 which harbor a silenced Cosmc, confirmed the hypermethylation of the Cosmc core promoter but not for

218 reported that about 40% of c9ALS cases show hypermethylation of the CpG island located at the 5' end

219 The expanding pTreg displayed hypermethylation of the CpG islands in Treg-specific dem

220 leads to suppression of the E2F1 pathway and hypermethylation of the CpG sites at miR-184 promoter, r

221 ealed that the expansion was associated with hypermethylation of the CpG-island (5'of the repeat) in

222 In conclusion, we demonstrated that hypermethylation of the CpG-island 5'of the G(4)C(2)-rep

223 omatal lineage cells, which is linked to DNA hypermethylation of the ERECTA family genes, including E

224 cumulation of 2-hydroxyglutarate resulted in hypermethylation of the Foxp3 gene locus and inhibited F

225 Hypermethylation of the miR-137 promoter and negative re

226 Hypermethylation of the Pgc-1alpha promoter caused by a

227 ; several lipid metabolism mRNAs; coincident hypermethylation of the PPARgamma2 proximal promoter; an

228 hromosome arm 10q, gain of chromosome 7, and hypermethylation of the promoter of MGMT were available

229 Hypermethylation of the promoter of the SLIT2 gene, whic

230 Hypermethylation of the promoters of tumour suppressor g

231 Hypermethylation of the Rasal1 promoter contributes to a

232 We propose that hypermethylation of the RHOX gene cluster serves as a ma

233 Persistent abnormal hypermethylation of the SRY gene was observed together w

234 displays a schizophrenia-like phenotype and hypermethylation of the transcription factor, Sp5.

235 Disruption of DLGAP4 results in monoallelic hypermethylation of the truncated DLGAP4 promoter CpG is

236 etic analysis displayed significant promoter hypermethylation of the tumor-suppressor gene RASSF1A in

237 Furthermore, a relative hypermethylation of the TYLCV V1 promoter region was obs

238 sis behind one such predictive model linking hypermethylation of the UBB ubiquitin gene to a dependen

239 e rugose begomovirus, where a similar genome hypermethylation of the V1 promoter region was discerned

240 Hypermethylation of these genes was associated with sign

241 hat in A. thaliana, which is associated with hypermethylation of this region in the allotetraploids.

242 We observed that hypermethylation of tumor suppressor genes is a frequent

243 Indeed, it has been shown that hypermethylation of tumor suppressor genes promoters is

244 Exposing cancer cells to metformin leads to hypermethylation of tumor-promoting pathway genes and co

245 howed that PSTVd infection promotes a strong hypermethylation of TYLCSV DNA, thus supporting a mechan

246 Promoter hypermethylation of ULK2 was confirmed by bisulfite sequ

247 f synaptotagmin 2 (Syt2) gene expression and hypermethylation on CpG#5 of its first exon.

248 tellite instability not attributable to MLH1 hypermethylation or germline mutations contain 2 or more

249 Lynch syndrome while 106 (9.0%) have somatic hypermethylation or mutations in the mismatch repair gen

250 es, but lymphoid malignancies also exhibited hypermethylation, particularly at promoter regions.

251 ydroxyglutarate (2HG) and a CpG island (CGI) hypermethylation phenotype (G-CIMP).

252 ls was independent of the well-described DNA hypermethylation phenotype in IDH1-mutated cancers.

253 (R)-2-hydroxyglutarate (2-HG), leading to a hypermethylation phenotype that dysregulates hematopoiet

254 tissue, and identifying a cancer CpG island hypermethylation phenotype.

255 leukemia (AML) and are associated with a DNA hypermethylation phenotype.

256 eversed within days, whereas reversal of DNA hypermethylation proceeds in a progressive manner over t

257 with a genome-wide tendency for neuronal CpG-hypermethylation punctuated by regions of glia-specific

258 f 5hmC at enhancers, accompanied by enhancer hypermethylation, reduction of enhancer activity, and de

259 he tumor suppressor gene RASSF1A by promoter hypermethylation represents a key event underlying the i

260 ements in cancer cells is accompanied by DNA hypermethylation susceptibility of enhancers and insulat

261 re associated with global shifts towards DNA hypermethylation, targeting cis-regulatory elements in p

262 mors harboring TERT promoter mutation and/or hypermethylation than those without either aberration (P

263 nephritis via a mechanism involving promoter hypermethylation that is associated with Ifitm3 repressi

264 ction and cannot accomplish the viral genome hypermethylation that is invariably observed in asymptom

265 s with wild-type DNMT3A displayed CpG island hypermethylation, this change was not associated with ge

266 on in tumors was 10 times more frequent than hypermethylation, three times more frequent in CLL than

267 ukemogenesis showed much less pronounced DNA hypermethylation upon Dnmt3b expression.

268 on was attributed to nickel-induced promoter hypermethylation via elevating DNMT3b expression, wherea

269 Furthermore, this reversal of pathologic hypermethylation was achieved specifically through Tet3-

270 mission paired patient samples, we show that hypermethylation was acquired in APL in a monoallelic ma

271 Moreover, a signature of hypermethylation was also detected in leukemic cells fro

272 Moreover, miR-34A tumor hypermethylation was associated with decreased overall s

273 Hypermethylation was detectable for all genes in maligna

274 DNA CpG island hypermethylation was detected at promoters of genes invo

275 SOX30 hypermethylation was detected in 100% of lung cancer cel

276 Hypermethylation was enriched at CpG islands marked with

277 Failure of SRY expression due to hypermethylation was further correlated with silencing o

278 WNK2 hypermethylation was higher in tumor than in surrounding

279 The promoter hypermethylation was inversely associated with mRNA expr

280 Further, significant hypermethylation was observed in promoter DNA region of

281 For the hormone receptor, this hypermethylation was positively correlated with the cont

282 Hypermethylation was restricted specifically to the RHOX

283 nalysis and functional relevance of promoter hypermethylation was shown in demethylation experiments

284 utaneous T-cell lymphoma cell line, promoter hypermethylation was shown to downregulate MTAP expressi

285 This meta-analysis indicated that MGMT hypermethylation was significantly associated with the r

286 Neuropathology-associated ANK1 hypermethylation was subsequently confirmed in cortical

287 gulated genes linked to promoter or enhancer hypermethylation were identified.

288 Escape genes showing CH hypermethylation were the only genes with CG-hypomethyla

289 i depicted hypomethylation, and 225 depicted hypermethylation, whereas in Monos, 155 hypomethylated l

290 ydroxyglutarate resulting in DNA and histone hypermethylation, which leads to blocked cellular differ

291 d DNMT3B binding is associated with promoter hypermethylation, which precipitates a neural differenti

292 ed hypoxia in mouse breast tumours increases hypermethylation, while restoration of tumour oxygenatio

293 s underwent hypo-hydroxymethylation prior to hypermethylation, while retaining H3K27me3.

294 ese, 42 showed hypomethylation and 28 showed hypermethylation with age.

295 The authors found association of PPM1G hypermethylation with early escalation of alcohol use an

296 They also observed association of PPM1G hypermethylation with increased blood-oxygen-level-depen

297 NAMPT promoter analysis revealed CpG hypermethylation within the dilated human thoracic aorta

298 hat d-flow in the carotid artery resulted in hypermethylation within the promoters of 11 mechanosensi

299 eparated cell data shows that IBD-associated hypermethylation within the TXK promoter region negative

300 (hESCs) exhibit prominent bivalent promoter hypermethylation without an overall corresponding decrea