ライフサイエンスコーパス: DNMT

1 DNMT activity was measured with a functional assay, and

2 DNMT inhibition is actively pursued in cancer treatment,

3 DNMT inhibition or ISL1 expression in breast cancer cell

4 DNMT inhibition prevents the PP1 methylation increase, r

5 DNMT mRNA levels decreased rapidly, with significant sup

6 DNMT-1 has a direct suppressive role in 15-LOX-1 transcr

7 DNMT-1 protein hypomorphism impaired DNMT-1 recruitment

8 DNMT-1 up-regulation occurs in hepatobiliary cancers and

9 DNMTs are important epigenetic targets.

10 s and ERK-regulated DNA methyltransferase 1 (DNMT-1) levels.

11 rease expression of DNA methyltransferase-1 (DNMT-1) and epigenetically regulate the expression of se

12 erase-3a [DNMT-3a]; DNA methyltransferase-1 [DNMT-1]; 5-methylcytosine [5-mC]; and 5-hydroxymethylcyt

13 ctivity and the forced diminution of DNMT-1, DNMT-3a, and DNMT-3b by siRNA targeting resulted in incr

14 netic alterations (DNA methyltransferase-3a [DNMT-3a]; DNA methyltransferase-1 [DNMT-1]; 5-methylcyto

15 e found no evidence for 11c functioning as a DNMT inhibitor.

16 Within this study, 5-azacytidine (5-azaC, a DNMT inhibitor) was used as a positive control.

17 It harbors a DNMT domain and SNF2 ATPase domain.

18 ols epigenomic DNA methylation patterns in a DNMT-dependent manner, which in turn alters endothelial

19 in congenic HCT 116 colon cancer cells in a DNMT-independent and p53-dependent fashion.

20 -1 stimulation also mimicked the effect of a DNMT inhibitor on FLS gene expression.

21 of depleting the three catalytically active DNMTs in human pluripotent stem cells.

22 and restored expression in response to acute DNMT suppression were assayed for methylation changes us

23 ibited zebrafish DNMT, TDCIPP did not affect DNMT activity in vitro at concentrations as high as 500

24 oylanilide hydroxamic acid (SAHA) only after DNMT-1 dissociation from the 15-LOX-1 promoter and witho

25 eviously described in RA FLS through altered DNMT expression.

26 am(Akita) mice showed the highest DNMT-1 and DNMT-3a levels compared with the other groups.

27 Both DNMT-1 and DNMT-3a were detected at the U6-1 locus by chromatin imm

28 he forced diminution of DNMT-1, DNMT-3a, and DNMT-3b by siRNA targeting resulted in increased U6 leve

29 igenetic feedback loop between miR-17~92 and DNMT-1 in lung fibrosis.

30 lationship between the miR-17~92 cluster and DNMT-1 expression was examined in vitro.

31 Importantly, changes in ERalpha and DNMT expression in the cortex (males) and hypothalamus (

32 ary fibrosis model reduced fibrotic gene and DNMT-1 expression, enhanced miR-17~92 cluster expression

33 reover, in addition to the reported HDAC and DNMT dual epigenetic inhibitory profile of the parent co

34 The results suggest that HDAC and DNMT inhibitors activate reelin and GAD67 expression thr

35 pachytene oocytes exhibit reduced HDAC2 and DNMT-1.

36 on, resulting in global DNA methylation- and DNMT-dependent downregulation of multiple microRNAs (miR

37 to a functional interaction between TET and DNMT proteins and providing a potential explanation for

38 plexes between small molecular compounds and DNMTs that suffers from low efficacy and high cytotoxici

39 ose uptake, and elevated levels of HDACs and DNMTs.

40 ad increased expression of GLUTs, HDACs, and DNMTs.

41 s the possibility of exploring the aptameric DNMT inhibitors being a new cancer therapeutic approach,

42 Several molecules have been identified as DNMT inhibitors and, among the non-nucleoside inhibitors

43 pied the same regions of its own promoter as DNMT corepressors, and ectopic overexpression of SALL4 l

44 istent with this idea, only nucleoside-based DNMT inhibitors that form covalent DNA adducts induce p5

45 alysis to probe for the interactions between DNMTs and native nucleosomes.

46 MT inhibitors (DNMTis) alone covalently bind DNMTs into DNA and increase PARP1 tightly bound into chr

47 Both DNMT-1 and DNMT-3a were detected at the U6-1 locus by ch

48 However, both DNMT occupancy and low frequency methylation were correl

49 ionine) rescues the suppression of mEPSCs by DNMT inhibitors in wild-type neurons, as well as the def

50 yltransferases 1 and 3B (DNMT1 and 3B) or by DNMT inhibitors (DNMTi).

51 loid leukemia (AML) and breast cancer cells, DNMT inhibitors (DNMTis) alone covalently bind DNMTs int

52 f flanking sequence preferences and cellular DNMT targets.

53 nalysis of the promoter region after chronic DNMT suppression.

54 warranting further investigation of combined DNMT and HDAC inhibition in refractory or drug-resistant

55 Using luciferase reporter constructs, DNMT-1 was verified as a target for miR-148a and miR-152

56 hold with patient-tolerable doses of current DNMT inhibitors (DNMTIs).

57 Precursors to miR-148a and miR-152 decreased DNMT-1 protein expression, increased Rassf1a and p16INK4

58 Dose responses demonstrated decreased DNMT expression at concentrations as low as 1 pg/ml of I

59 alters DNA methylation in FLS by decreasing DNMT expression and function.

60 tterns in a DNA methyltransferase-dependent (DNMT-dependent) manner.

61 udy the effect of interactions between diet, DNMT-1 levels, and genetic predisposition on the develop

62 Our data suggest that different DNMT domains are responsible for targeting DNA methylati

63 stably transfected with each of 13 different DNMTs (DNMT1, two DNMT3A isoforms, nine DNMT3B isoforms

64 tically engineered deficiencies in different DNMTs and find that the major activity against these sub

65 as well as no selectivity towards different DNMTs.

66 lycomb group proteins; upon differentiation, DNMT activation leads to CpG island methylation, causing

67 ed BAG-1 expression in the single and double DNMT knockout cells.

68 the DNA methylation changes induced by each DNMT.

69 atically dissect the factors specifying each DNMT's activity, we engineered combinatorial knock-in of

70 ght all postmitotic neurons and glia express DNMTs at comparable levels, the coexpression of selected

71 roughput screening of chemical libraries for DNMT inhibition activity.

72 thionine (SAM), the essential metabolite for DNMT-catalyzed methylation, is an evolutionarily conserv

73 ty, together demonstrating a requirement for DNMTs in mutant Htt-triggered neuronal death and suggest

74 cells is DNMT1, with minor contribution from DNMT 3b and none from DNMT3a, the only known bona fide d

75 Furthermore, DNMTs and histone deacetylase repressors synergistically

76 nce and will help to develop next-generation DNMT inhibitors.

77 ression of host DNA methyltransferase genes (DNMTs) was measured.

78 Global DNMT-dependent epigenetic modifications lead to changes

79 ance of regional DNA methylation, and global DNMT activity in CD133- Huh7 cells was inhibited by TGFb

80 reast cancer prevention strategies with HDAC/DNMT inhibitors need to be individually tailored.

81 ges induced by 29 compounds targeting HDACs, DNMTs, histone lysine methyltransferases (HKMTs), and pr

82 Sham(Akita) mice showed the highest DNMT-1 and DNMT-3a levels compared with the other groups

83 We then discuss how DNMTs are recruited to or excluded from certain genomic

84 e revealed the key mechanisms underlying how DNMTs catalyze de novo and maintenance DNA methylation.

85 e engineered combinatorial knock-in of human DNMT genes in Komagataella phaffii, a yeast species lack

86 DNMT-1 protein hypomorphism impaired DNMT-1 recruitment to the 15-LOX-1 promoter, which allow

87 onclusion, DAC upregulates p21(WAF1/CIP1) in DNMT-independent manner via the DNA damage/ATM/p53 axis.

88 nd the magnitude of methylation reduction in DNMT knockout cells.

89 3a negated the ability of PGE(2) to increase DNMT activity.

90 reased levels of HDAC2 protein and increased DNMT expression in the dorsal hippocampus.

91 ore, PP2Ac suppression resulted in increased DNMT enzyme activity, DNA hypermethylation, and decrease

92 activation in MCT-RVfib reflected increased DNMT (DNA methyltransferase) 1 expression, which was ass

93 siRNAs were used to knock down individual DNMT expression in primary cultures of mouse embryonic c

94 DF also induced DNMT-sensitive propathological expression of downstream

95 hat this class of chemical compounds inhibit DNMTs by interacting with the DNA substrate.

96 Interestingly, DNMT activity is required for protein kinase C-induced i

97 However, isolated DNMTs are weak catalysts and are difficult to assay.

98 A methyltransferase 3B (DNMT3B) is the major DNMT that methylates mammalian genomes during early deve

99 rprisingly, we have found that the mammalian DNMTs, and likely the vertebrates DNMTs in general, can

100 wnregulated expression) of epigenetic (5-mC, DNMTs), vascular (endothelial nitric oxide synthase), gl

101 n for the three major DNA methyltranserases (DNMTs)--DNMT1, DNMT3a and DNMT3b--in the developing rat

102 ific maintenance-type CpG methyltransferase (DNMT) that mediates long-term epigenome evolution.

103 cytidine, or siRNA to DNA Methyltransferase (DNMT) 1 and 3b in HCC cells.

104 sed the expression of DNA methyltransferase (DNMT) 1 and 3b.

105 epigenetic regulators DNA methyltransferase (DNMT) 1 and DNMT3A in the juvenile cortex and hypothalam

106 on of the maintenance DNA methyltransferase (DNMT) 1 by a proteasomal pathway.

107 gh the recruitment of DNA methyltransferase (DNMT) 3a and histone methyltransferase G9a.

108 aused by mutations in DNA methyltransferase (DNMT) 3B, a de novo DNA methyltransferase.

109 logical inhibition of DNA methyltransferase (DNMT) activity and the forced diminution of DNMT-1, DNMT

110 of ERK activation or DNA methyltransferase (DNMT) activity blocked the memory-enhancing effects of E

111 compounds to inhibit DNA methyltransferase (DNMT) activity.

112 lation and attenuated DNA methyltransferase (DNMT) activity.

113 c strategies based on DNA methyltransferase (DNMT) and histone deacetylase (HDAC) inhibitors are curr

114 able to complex with DNA methyltransferase (DNMT) enzymes, leading us to explore a role for CBX7 in

115 y in the reduction of DNA methyltransferase (DNMT) expression, hence inducing the transcription of me

116 Here, we show that DNA methyltransferase (DNMT) inhibition in hippocampal neurons results in activ

117 DNA methyltransferase (DNMT) inhibitor and small-interfering RNA depletion of D

118 t with broad spectrum DNA methyltransferase (DNMT) inhibitor hydralazine and histone deacetylase (HDA

119 ld be reversed with a DNA methyltransferase (DNMT) inhibitor in vitro and in vivo with beneficial eff

120 ial administration of DNA methyltransferase (DNMT) inhibitors and histone deacetylase (HDAC) inhibito

121 cts were mitigated by DNA methyltransferase (DNMT) inhibitors and knockdown of DNMT3A.

122 of the non-nucleoside DNA methyltransferase (DNMT) inhibitors RG108, (-) epigallocatechin-3-gallate (

123 eacetylase (HDAC) and DNA methyltransferase (DNMT) inhibitors.

124 resence or absence of DNA methyltransferase (DNMT) inhibitors.

125 e sequencing of three DNA methyltransferase (DNMT) knockout cell lines and the wild-type HCT116 colon

126 The DNMT3B de novo DNA methyltransferase (DNMT) plays a major role in establishing DNA methylation

127 r (1) TDCIPP inhibits DNA methyltransferase (DNMT) within embryonic nuclear extracts; (2) uptake of T

128 nd that inhibition of DNA methyltransferase (DNMT), whether during training or shortly afterwards, bl

129 et fibrotic genes and DNA methyltransferase (DNMT)-1 expression.

130 d as a consequence of DNA methyltransferase (DNMT)-mediated hypermethylation.

131 DNA methyltransferase (DNMT)-triggered DNA methylation silences gene expression

132 ies to the 3'-UTRs of DNA methyltransferase (DNMT)3A and -3B (de novo methyltransferases), two key en

133 acetylase (HDAC)1 and DNA methyltransferase (DNMT)3a to the CRE site (-111/-104) probably accounts fo

134 protein SUZ12 and the DNA methyltransferase (DNMT)3b preferentially in undifferentiated hESCs as comp

135 c analysis, using somatic methyltransferase (DNMT) knockout cells, we showed that hypomethylation dec

136 pression of HDACs and DNA methyltransferase (DNMTs) also was increased.

137 ed the expression of DNA methyltransferases (DNMT) 1 and DNMT3beta, which are critical in the mainten

138 explore the role of DNA methyltransferases (DNMT) and ten eleven translocation (Tet) proteins in per

139 DNA methyltransferases (DNMT) are promising drug targets in cancer provided that

140 using inhibitors of DNA methyltransferases (DNMT) or/and histone deacetylases (HDACs) has shown prom

141 lation activities of DNA methyltransferases (DNMT) thought to catalyze these reactions.

142 nes here defined as: DNA methyltransferases (DNMT), methyl-CpG-binding domain (MBD) proteins, histone

143 ed that BRCA1, EZH2, DNA methyltransferases (DNMT)1/3a/3b and H3K27me3 are recruited to the endogenou

144 maintained by three DNA methyltransferases (DNMT): DNMT1, DNMT3A, and DNMT3B.

145 DNA (cytosine-5)-methyltransferases (DNMTs) catalyze the transfer of a methyl group from S-ad

146 s-link to DNA cytosine-5-methyltransferases (DNMTs) through the active Cys residue, which provides a

147 thylation by de novo DNA methyltransferases (DNMTs) 3A and 3B is essential for mammalian development

148 nt expression of the DNA methyltransferases (DNMTs) and disruption of DNA methylation patterns are as

149 ated binding between DNA methyltransferases (DNMTs) and PARP1.

150 acted with different DNA methyltransferases (DNMTs) and purified DNMT enzymatic activities from nucle

151 on levels of several DNA methyltransferases (DNMTs) and their interacting proteins by TaqMan qPCR and

152 DNA methyltransferases (DNMTs) are a family of related proteins that both cataly

153 DNA methyltransferases (DNMTs) are critical enzymes that establish and maintain

154 Although DNA methyltransferases (DNMTs) are dispensable for embryonic stem cell maintenan

155 DNA methyltransferases (DNMTs) are enzymes responsible for establishing and main

156 DNA methyltransferases (DNMTs) are important enzymes involved in epigenetic cont

157 DNA methyltransferases (DNMTs) are thought to be involved in the cellular respon

158 protein 2 (MBD2) and DNA methyltransferases (DNMTs) at the leptin promoter are increased and RNA Pol

159 enance activities of DNA methyltransferases (DNMTs) can help in the development of predictive biomark

160 DNA methyltransferases (DNMTs) deposit DNA methylation, which regulates gene exp

161 ugh interacting with DNA methyltransferases (DNMTs) in a "Yin-Yang" complex targeted to chromatin and

162 s down-regulation of DNA methyltransferases (DNMTs) in embryonic heart and results in impaired cardia

163 catalytically active DNA methyltransferases (DNMTs) in human embryonic stem cells (ESCs) using CRISPR

164 , through inhibiting DNA methyltransferases (DNMTs) is an important potential cancer therapy paradigm

165 DNA methyltransferases (DNMTs) play an important role in establishing and mainta

166 DNA methyltransferases (DNMTs) primarily establish and maintain global DNA methy

167 ity as inhibitors of DNA methyltransferases (DNMTs) require further investigation.

168 catalytic domains of DNA methyltransferases (DNMTs) to engineered transcription activator-like effect

169 disruption models of DNA methyltransferases (DNMTs) to study the effects of this methylation on 15-LO

170 enhances binding of DNA methyltransferases (DNMTs) to the promoter.

171 aintained by several DNA methyltransferases (DNMTs) with partially overlapping functions and genomic

172 expression levels of DNA methyltransferases (DNMTs), 1, 3A and 3B in CSE-treated cells.

173 tion is catalyzed by DNA methyltransferases (DNMTs), and the two DNMT families, DNMT3 and DNMT1, are

174 atalytic activity of DNA methyltransferases (DNMTs), and their active removal relies on the activity

175 t that inhibitors of DNA methyltransferases (DNMTs), decitabine and FdCyd, block mutant huntingtin (H

176 ated action of three DNA methyltransferases (DNMTs), DNMT1, DNMT3A and DNMT3B.

177 eacetylases (HDACs), DNA methyltransferases (DNMTs), enhancer of zeste homologue 2 (EZH2), bromodomai

178 Among DNA methyltransferases (DNMTs), only DNMT1 was significantly up-regulated in GC

179 n is reversible, the DNA methyltransferases (DNMTs), responsible for this epigenetic mark, are consid

180 tic actions of three DNA methyltransferases (DNMTs), the de novo enzymes DNMT3A and DNMT3B and the ma

181 cing the activity of DNA methyltransferases (DNMTs).

182 h both viral DNA and DNA methyltransferases (DNMTs).

183 nine, a substrate of DNA methyltransferases (DNMTs).

184 of DNA catalyzed by DNA methyltransferases (DNMTs).

185 ed by the actions of DNA methyltransferases (DNMTs).

186 osine methylation by DNA methyltransferases (DNMTs).

187 uate the role of de novo methyltransferases (DNMTs) in the establishment of these methylation marks,

188 he involvement of miR-29, which can modulate DNMT 1 and 3.

189 w cancer therapeutic approach, by modulating DNMT activity selectively through reversible interaction

190 The binding efficiency of the mutant DNMT proteins at the replication foci and heterochromati

191 ots might be under control of SetDB1 and not DNMT for silencing.

192 nance methyltransferase, acts as the de novo DNMT and is required for neuropathic pain genesis likely

193 ion nor binding activity towards two de novo DNMTs, DNMT3A and DNMT3B.

194 Inhibition of these events by non-nucleoside DNMT inhibitors represents a potential strategy to treat

195 Among the non-nucleoside DNMT inhibitors, N-phthaloyl-l-tryptophan 1 (RG108) was

196 A number of nucleoside DNMT inhibitors (DNMTi) have been studied in cancer, inc

197 ncing excitatory activity, in the absence of DNMT inhibitors, also produces similar decreases in DNA

198 We show the concerted actions of DNMT enzymes in the establishment and maintenance of met

199 icate that IL-6 can regulate the activity of DNMT-1 and expression of methylation-dependent tumor sup

200 provide a comprehensive characterization of DNMT-mutant ESCs, including single-base genome-wide maps

201 Combinations of DNMT inhibitors with anti-TIGIT or anti-KLRG1 antibodies

202 bitor and small-interfering RNA depletion of DNMT genes were used to reverse KLF10 expression in the

203 (DNMT) activity and the forced diminution of DNMT-1, DNMT-3a, and DNMT-3b by siRNA targeting resulted

204 The specific effect of DNMT inhibition on spontaneous excitatory neurotransmiss

205 hts for the design of the next-generation of DNMT inhibitors.

206 Combined inhibition of DNMT activities and JAK signalling, in vitro and in vivo

207 ated training; moreover, later inhibition of DNMT eliminates consolidated LTM.

208 Inhibition of DNMT in HTR-8/SVneo cells resulted in reduced DNA methyl

209 or-bearing mice, pharmacologic inhibition of DNMT with the DNA methyltransferease inhibitor decitabin

210 ine and 5-aza-2-deoxycytidine, inhibitors of DNMT activity, blocked the induction of long term potent

211 ot accounted for by changes in the levels of DNMT proteins.

212 65-DNMT-1 interactions, chromatin loading of DNMT-1 and subsequent BRMS1 promoter methylation and tra

213 ssor gene promoter via direct recruitment of DNMT-1 (DNA (cytosine-5)-methyltransferase 1) to chromat

214 illatory shear stress (OS), and reduction of DNMT with either the inhibitor 5-aza-2'-deoxycytidine (5

215 lementarity to the 3'-untranslated region of DNMT-1, namely miR-148a, miR-152, and miR-301.

216 To understand the potential regulation of DNMT-1 by IL-6-dependent miRNAs, we examined the express

217 se-resolution DNA methylomes for a series of DNMT knockout embryonic stem cells, with deep coverage a

218 expression after RNAi-induced suppression of DNMT in a glioblastoma multiforme (GBM) cell line.

219 and time dependence comparable with that of DNMT inhibitors.

220 may be warranted when considering the use of DNMT inhibitors in development of Treg-based cellular th

221 and transcriptional repressor activities of DNMTs and HDACs.

222 ons modulate the recruitment and activity of DNMTs.

223 thermore, we are able to observe assembly of DNMTs at CBX7 target gene promoters.

224 his reaction resulted in the co-evolution of DNMTs and ALKB2 DNA repair enzymes, but its mechanism re

225 Aberrant expression of DNMTs and their isoforms has been found in many types of

226 gnificantly down-regulated the expression of DNMTs, a reaction normally elicited by demethylation age

227 valuable tools for study of the functions of DNMTs and the related epigenetic mechanisms.

228 Inhibition of DNMTs in HD model primary cortical or striatal neurons r

229 In vivo, pharmacological inhibition of DNMTs in HD mouse brains restored the mRNA levels of key

230 BNA gene transcription, nor did knockdown of DNMTs significantly alter CpG methylation within Cp.

231 Robust nuclear localization of DNMTs in cones compared to rods suggests a potential rol

232 These results demonstrate localization of DNMTs with the inactive rDNA in the nucleolus, the speci

233 However, virus-induced overexpression of DNMTs also leads to methylation of host CpG islands.

234 To assess the role of DNMTs in these events, we investigated the effects of re

235 To investigate whether the upregulation of DNMTs could also have an effect on the methylation of ho

236 Overall, DNMT mRNA levels reached their highest point in the firs

237 minimal interacting domains between RelA/p65-DNMT-1 and RelA/p65-BRMS1 promoter abrogates BRMS1 methy

238 of S276 on RelA/p65 is required for RelA/p65-DNMT-1 interactions, chromatin loading of DNMT-1 and sub

239 DNA methyltransferases (DNMTs) and purified DNMT enzymatic activities from nuclear extracts.

240 Direct addition of iron to purified DNMT in vitro decreased enzyme activity in a concentrati

241 The ability of RelA/p65 to directly recruit DNMT-1 to chromatin, resulting in promoter-specific meth

242 DNMT3A, and DNMT3B protein levels and reduce DNMT enzyme activity.

243 ents, we investigated the effects of reduced DNMT expression on embryonic cardiomyocytes.

244 that the COX2 inhibitor NS398 down-regulated DNMTs and increased expression of SPARC, which led to tu

245 As mice age, residual DNMT activity declines further, and the probability of s

246 parable levels, the coexpression of selected DNMTs with markers of distinct neurotransmitter phenotyp

247 on failed, supporting the notion of specific DNMT-histone methyltransferase networks.

248 We propose a model wherein specific DNMT-histone methyltransferase networks are utilized to

249 findings reveal that MDSCs establish a STAT3-DNMT epigenetic axis, regulated by autocrine IL6, to sil

250 ed that directed DNA methylation with a TALE-DNMT targeting the CDKN2A locus, which encodes the cycli

251 Together, our results demonstrate that TALE-DNMTs can selectively target specific genes and suggest

252 We demonstrated that these TALE-DNMTs direct DNA methylation specifically to the targete

253 l miRNAs from the miR-17~92 cluster targeted DNMT-1 expression resulting in a negative feedback loop.

254 lowing contextual fear conditioning and that DNMT inhibition blocks memory formation.

255 gulated in the adult nervous system and that DNMT may play a role in regulating the induction of syna

256 lation, we have previously demonstrated that DNMT inhibitors coordinately increase reelin and GAD67 m

257 Here we report that DNMT gene expression is upregulated in the adult rat hip

258 sidered together, these results suggest that DNMT activity is dynamically regulated in the adult nerv

259 n but does not induce p53R2, suggesting that DNMT/DNA adduct formation is the molecular trigger for p

260 We demonstrate that DNMTs and NuRD cooperate to maintain the silencing of se

261 We discovered that DNMTs and the core components of the NuRD (Mi-2/nucleoso

262 We found that DNMTs have specific and overlapping target sites and the

263 how that new approaches, like decreasing the DNMT targeting protein, UHRF1, can augment the DNA demet

264 tion target profiles are a reflection of the DNMT domains.

265 A combination of the DNMT inhibitor 5-azacytidine and the HDAC inhibitor buty

266 en used to monitor cellular responses to the DNMT and HDAC inhibitors 5-Aza-2'-deoxycytidine and sube

267 rolysis by the SNF2 domain is coupled to the DNMT domain conformational changes induced by preferred

268 was turned off following treatment with the DNMT inhibitor, decitabine.

269 The DNMTs methylate viral DNA, leading to decreased viral ge

270 ribe the methylation machinery including the DNMTs and their essential cofactors.

271 Of the DNMTs, DNMT1 and DNMT3a are most highly expressed in pos

272 repression complexes (PRC1 and PRC2) to the DNMTs have begun to shed light on how methylation is tar

273 ion of the structures and functions of these DNMTs, in particular their roles in Ca(2+) ion-dependent

274 of repressor complexes containing all three DNMTs, MeCP2, and HDAC1 from the corresponding promoters

275 ete understanding of precisely how the three DNMTs, 1, 3A, and 3B, interact for maintaining DNA methy

276 nfluence endothelial KLF4 expression through DNMT enrichment/myocyte enhancer factor-2 inhibition mec

277 ism involving direct DNA methyl transferase (DNMT) promoter transactivation, resulting in global DNA

278 DNA methyl transferase (DNMT)1, DNMT3a and two proteins that regulate methylatio

279 ncreased binding of DNA methyl-transferases (DNMTs) 3a and 3b and methyl-CpG-binding domain protein 2

280 which provides a new tool to covalently trap DNMT-DNA complexes.

281 DNA methyltransferases (DNMTs), and the two DNMT families, DNMT3 and DNMT1, are responsible for meth

282 These two DNMTs preferentially bind to nucleosomes, yet cannot met

283 T3A(R882mut) binding to endogenous wild-type DNMT proteins partially reversed the CpG hypomethylation

284 tes respond to HBV infection by upregulating DNMTs.

285 -beta1 to modulate the expression of various DNMTs in primary lung fibroblasts (CCL210).

286 mammalian DNMTs, and likely the vertebrates DNMTs in general, can also act as Ca(2+) ion- and redox

287 ramatic changes in cytosine methylation when DNMT activity was inhibited.

288 fibroblasts from patients with IPF, whereas DNMT-1 expression and methylation of the miR-17~92 promo

289 rect and active antiviral mechanism by which DNMTs can be recruited to retroviral DNA.

290 of Foxp3 can be predictably controlled with DNMT inhibitors to generate functional, stable, and spec

291 Finally, as 5 interacted with DNMT only when the DNA duplex was present, we hypothesiz

292 nthesized to understand its interaction with DNMT.

293 Pretreatment with DNMT inhibitors prevented these infection-induced change

294 d that depletion of CHD4 is synergistic with DNMT inhibition in reducing the viability of colon cance

295 Treatment with DNMT inhibitors increased TGF-beta pathway activity.

296 Treatment with DNMT inhibitors reveals an activity-driven demethylation

297 tify additional proteins that cooperate with DNMTs in silencing these key silenced TSGs in colon canc

298 ses gene expression through interaction with DNMTs.

299 experiences a concurrent transcription with DNMTs in cell cycle.

300 ugh 5-azaC significantly inhibited zebrafish DNMT, TDCIPP did not affect DNMT activity in vitro at co