ライフサイエンスコーパス: DNA methyltransferase

1 ain 26695, encodes a N(6)-adenosine type III DNA methyltransferase.

2 in heme biogenesis or to function as adenine DNA methyltransferase.

3 DNMT3B is known as a de novo DNA methyltransferase.

4 erevisiae genome via restriction enzymes and DNA methyltransferases.

5 RNAs as the genome does not encode any other DNA methyltransferases.

6 modeling, nucleosomes are strong barriers to DNA methyltransferases.

7 independent of the CHROMOMETHYLASE (CMT)2/3 DNA methyltransferases.

8 f MLL2 is relieved by inhibition of PRC2 and DNA methyltransferases.

9 lights the substrate diversity of vertebrate DNA methyltransferases.

10 ding histone modifications and disruption of DNA methyltransferases.

11 und in defense islands, often also featuring DNA methyltransferases.

12 s study has demonstrated an up-regulation of DNA methyltransferase 1 (DNMT1) and a global hypermethyl

13 on-determining region [G1MDR]) that recruits DNA methyltransferase 1 (Dnmt1) and provokes methylation

14 tical for gene expression, are replicated by DNA methyltransferase 1 (DNMT1) and ubiquitin-like conta

15 gies, we define not only a dominant role for DNA methyltransferase 1 (DNMT1) but also distinct roles

16 cation foci targeting sequence (RFTS) of the DNA methyltransferase 1 (DNMT1) gene.

17 ith PHD and ring finger domains 1 (uhrf1) or DNA methyltransferase 1 (dnmt1) genes exhibit a robust i

18 ation and acetylation of STAT3 that targeted DNA methyltransferase 1 (DNMT1) in a sequential manner.

19 DNA methyltransferase 1 (DNMT1) is an essential regulato

20 -T cells displayed altered expression of the DNA methyltransferase 1 (DNMT1) isoform.

21 Human DNA methyltransferase 1 (DNMT1) maintains the epigenetic

22 The decreased hippocampal expression of DNA methyltransferase 1 (Dnmt1) that maintains the impri

23 chanistically, Naa10p facilitates binding of DNA methyltransferase 1 (Dnmt1) to DNA substrates, inclu

24 ied according to genotype for 11 SNPs within DNA methyltransferase 1 (DNMT1), DNA methyltransferase 3

25 iting the DNA methylation maintenance enzyme DNA methyltransferase 1 (DNMT1).

26 igenetically silenced from infancy onward by DNA methyltransferase 1 (DNMT1).

27 exts ((m) = methylated) and is maintained by DNA METHYLTRANSFERASE 1 (MET1) and CHROMOMETHYLASE (CMT)

28 Both oxidants inhibited DNA methyltransferase 1 activity, but only chloramine de

29 by site-alpha and TATA box, reversible after DNA methyltransferase 1 depletion.

30 Decitabine, a DNA methyltransferase 1 inhibitor or DNA hypomethylating

31 DNMT1 (DNA methyltransferase 1) is responsible for propagating

32 in conjunction with CG methylation by MET1 (DNA METHYLTRANSFERASE 1), CHG methylation by CMT3 (CHROM

33 isplayed improved inhibitory potency against DNA methyltransferase 1, improved selectivity against ot

34 oma HCT116 cells, which were hypomorphic for DNA methyltransferase 1, therefore showing a lower globa

35 ted with reduced activity of the E2F target, DNA methyltransferase 1.

36 cetylation of histones and downregulation of DNA methyltransferase 1.

37 talyse CpG methylation in DNA, including the DNA methyltransferases 1 (DNMT1), 3A (DNMT3A) and 3B (DN

38 f our dual G9a histone-methyltransferase and DNA-methyltransferase 1 (DNMT1) inhibitor in human HCC c

39 ation in MCT-RVfib reflected increased DNMT (DNA methyltransferase) 1 expression, which was associate

40 ine, a demethylation agent, and knockdown of DNA methyltransferase-1 partially rescued miR-184 level.

41 egative feedback loop in which SET9 controls DNA methyltransferase-1 protein stability, which repress

42 In addition, DNA methyltransferase-1 was recruited to the promoter re

43 We also show that knocking down DNA methyltransferase 1a (Dnmt1a), Dnmt3, or blocking DN

44 embryo are dependent on the oocyte-specific DNA methyltransferase 1o (DNMT1o), levels of which are d

45 DNA methyltransferase 2 (DNMT2), known to efficiently ca

46 al epigenetic regulatory molecules including DNA methyltransferase 3 alpha (DNMT3A) are commonly asso

47 SNPs within DNA methyltransferase 1 (DNMT1), DNA methyltransferase 3 Beta (DNMT3B), Tet methylcytosin

48 ng multiple copies of antibody-fused de novo DNA methyltransferase 3A (DNMT3A) (dCas9-SunTag-DNMT3A)

49 In addition, DNA methyltransferase 3A (DNMT3A) activity is modulated

50 Mutations in DNA methyltransferase 3A (DNMT3A) are common in acute my

51 DNA methyltransferase 3A (DNMT3A) catalyzes cytosine met

52 Mutations in the DNA methyltransferase 3A (DNMT3A) gene are the most comm

53 Despite a recognized role of DNA methyltransferase 3a (DNMT3a) in human cancer, the n

54 Here, we demonstrate that DNA methyltransferase 3a (Dnmt3a) is both necessary and

55 The gene that encodes de novo DNA methyltransferase 3A (DNMT3A) is frequently mutated

56 DNA methyltransferase 3A (DNMT3A) is frequently mutated

57 DNA methyltransferase 3A (DNMT3A) is the most commonly m

58 reduction in medial prefrontal cortex (mPFC)-DNA methyltransferase 3a (Dnmt3a) mRNA levels and a subs

59 ke behavior is accompanied by a reduction in DNA methyltransferase 3a (Dnmt3a) mRNA levels and global

60 Recurrent somatic mutations in DNA methyltransferase 3A (DNMT3A), most frequently at ar

61 which is then followed by the recruitment of DNA methyltransferase 3a (DNMT3a), ultimately resulting

62 partners modulate the activity of the human DNA methyltransferase 3A (DNMT3A), whose interactions wi

63 Knockdown of DNA methyltransferase 3a alters gene expression and inhi

64 DNA methyltransferase 3a and 3b are the enzymes capable

65 ion were apparent in decreased expression of DNA methyltransferase 3a and methyl-5'-cytosine-phosphod

66 Mutation of DNA methyltransferase 3A at arginine 882 (DNMT3A(R882mut

67 periments on mice show that an enzyme called DNA methyltransferase 3a is involved in insulin resistan

68 hematopoiesis driven by mutations of DNMT3A (DNA methyltransferase 3a) is associated with increased i

69 DNMT3A, the gene encoding the de novo DNA methyltransferase 3A, is among the most frequently m

70 expression in mice inhibits lipogenesis in a DNA methyltransferase-3a (DNMT3A)-dependent manner.

71 ns in the de novo DNA methyltransferase gene DNA methyltransferase 3alpha (DNMT3A) and poor prognoses

72 This process is dependent on DNA methyltransferase 3B (DNMT3B) and leads to suppressi

73 Here, we show that heterozygous mutations in DNA methyltransferase 3B (DNMT3B) are a likely cause of

74 erstanding the extent to which the effect of DNA methyltransferase 3b (DNMT3b) genotype on mortality

75 Here we report that DNA methyltransferase 3B (DNMT3B) is induced at distant

76 DNA methyltransferase 3B (DNMT3B) is the major DNMT that

77 In turn, MUC1-C/ZEB1 complexes recruit DNA methyltransferase 3b (DNMT3b) to the CpG island in t

78 on through the transcription factor PU.1 and DNA methyltransferase 3b (Dnmt3b).

79 xplained by mutations in the known ICF genes DNA methyltransferase 3B or zinc-finger and BTB domain c

80 The resulting hyperactivity of DNA methyltransferase 3b produces concurrent DNA methyla

81 H19 knockdown activates SAHH, enabling DNA methyltransferase 3B to methylate a subset of genes.

82 Moreover, we identify DNA methyltransferase 3ba (Dnmt3ba) as the primary enzym

83 Here, we show that DNA methyltransferase 3bb.1 (dnmt3bb.1) is essential for

84 affects DNA methylation by reducing de novo DNA methyltransferase activity at increasing PBB153 conc

85 ncentrations as well as reducing maintenance DNA methyltransferase activity at the lowest tested PBB1

86 -like), a member of the DNMT3 family, has no DNA methyltransferase activity but regulates de novo DNA

87 cells can be altered by oxidants that target DNA methyltransferase activity or deplete its substrate,

88 we explore the novel approach of inhibiting DNA methyltransferase activity using 5-azacytidine (Aza;

89 sm appears to occur with the Type II M.HinfI DNA methyltransferase and an ortholog of CcrM, BabI, but

90 ro-2'-deoxycytidine (FdCyd), an inhibitor of DNA methyltransferase and DNA hypermethylation, has show

91 MPNST(LOSS) were also highly sensitive to DNA methyltransferase and histone deacetylase (HDAC) inh

92 el of EOC, that clinically relevant doses of DNA methyltransferase and histone deacetylase inhibitors

93 mechanisms of action have been proposed for DNA methyltransferase and histone deacetylase inhibitors

94 juvant epigenetic therapy that uses low-dose DNA methyltransferase and histone deacetylase inhibitors

95 Temporally controlled synthesis of the CcrM DNA methyltransferase and Lon-mediated proteolysis restr

96 ation of a single gene (modA) that encodes a DNA methyltransferase and results in two phenotypically

97 known how the dynamic activities of cytosine DNA methyltransferases and 5-methylcytosine DNA glycosyl

98 ethylation is antagonistically controlled by DNA methyltransferases and DNA demethylases.

99 DNA methyltransferases and erythropoietin hypermethylati

100 etic studies of epigenetic modifiers such as DNA methyltransferases and histone acetyltransferases ha

101 how self-reinforcing feedback loops between DNA methyltransferases and histone modifications charact

102 hat extra-coding RNAs (ecRNAs) interact with DNA methyltransferases and regulate neuronal DNA methyla

103 Cytosine DNA bases can be methylated by DNA methyltransferases and subsequently oxidized by TET

104 fects, in part through the downregulation of DNA methyltransferases and their cofactors.

105 methylation is driven by the balance between DNA methyltransferases and transcription factor binding

106 NA methyltransferase, the Mettl4 (adenine-6) DNA methyltransferase, and the Tet DNA demethylase.

107 At the same time, DNA methyltransferases are upregulated, leading to eleva

108 reciprocal targeting of protein kinases and DNA methyltransferases as an essential strategy for dura

109 te that the two Notch repeat modules and the DNA methyltransferase-associated protein interaction dom

110 ptococcus neoformans, the loss of a cytosine DNA methyltransferase at least 50 million years ago has

111 This failed to reveal any known (cytosine-5) DNA methyltransferases, but identified homologues for th

112 ered a distinct mechanism regulating de novo DNA methyltransferase by CFK1 to control DNA methylation

113 lls exploits cooperative functions among the DNA methyltransferases, CAF-1, and histone-modifying enz

114 Caulobacter crescentus cell cycle-regulated DNA methyltransferase (CcrM) methylates the adenine of h

115 Caulobacter crescentus cell cycle-regulated DNA methyltransferase (CcrM), the MTA1-MTA9 complex from

116 JMJ24 directly targets a DNA methyltransferase, CHROMOMETHYLASE 3 (CMT3), for pro

117 ikely involves a feedback loop involving the DNA methyltransferase, CHROMOMETHYLASE 3 (CMT3), H3K9me2

118 coding the histone methyltransferase KYP and DNA methyltransferase CMT3.

119 plant species naturally without gbM lack the DNA methyltransferase, CMT3, which maintains CHG (H = A,

120 DNA methyltransferase MET1 and chromodomain DNA methyltransferases (CMTs).

121 l lines to small-molecule inhibitors against DNA methyltransferases (DAC), histone deacetylases (Deps

122 transcriptional repressors (dCas9-KRAB) and DNA methyltransferases (dCas9-DNMT3A, dCas9-DNMT3A3L) ca

123 enetic modifiers, including the inhibitor of DNA methyltransferase decitabine as well as the inhibito

124 e localization and catalytic activity of the DNA methyltransferase DIM-2.

125 eting KLRG1, or small-molecule inhibitors of DNA methyltransferases (DMNT) each reduced colony format

126 PAF suppressed the expression of DNA methyltransferase (DNMT) 1 and 3b.

127 decreased global methylation and attenuated DNA methyltransferase (DNMT) activity.

128 Therapeutic strategies based on DNA methyltransferase (DNMT) and histone deacetylase (HD

129 preoptic area (POA) is to reduce activity of DNA methyltransferase (Dnmt) enzymes, thereby decreasing

130 This study aims to evaluate the ability of DNA methyltransferase (Dnmt) inhibitor 5-azacytidine (5-

131 ed if combined treatment with broad spectrum DNA methyltransferase (DNMT) inhibitor hydralazine and h

132 he presence or absence of the non-nucleoside DNA methyltransferase (DNMT) inhibitors RG108, (-) epiga

133 ere to determine whether (1) TDCIPP inhibits DNA methyltransferase (DNMT) within embryonic nuclear ex

134 Furthermore, we find that inhibition of DNA methyltransferase (DNMT), whether during training or

135 hallmark of melanoma, but the expression of DNA methyltransferase (Dnmt)-1 in melanocytic tumors is

136 DNA methyltransferase (DNMT)-triggered DNA methylation s

137 n in its promoter region and upregulation of DNA methyltransferase (Dnmt)1.

138 and PKC412(R) displayed the up-regulation of DNA methyltransferase DNMT1 and tyrosine-protein kinase

139 ast in part from increased expression of the DNA methyltransferase DNMT1 in WDLS/DDLS.

140 models, we found that downregulation of the DNA methyltransferase DNMT1 induced by the brain microen

141 geting sequence (RFTS) domain of maintenance DNA methyltransferase DNMT1, a module known to bind the

142 yltransferase Dnmt3a but not the maintenance DNA methyltransferase Dnmt1.

143 moted autophagy-dependent degradation of the DNA methyltransferase DNMT1.

144 h restriction in vitro and in vivo, and that DNA methyltransferases Dnmt1 and Dnmt3a are highly enric

145 ion of DNA methylation through disruption of DNA methyltransferases DNMT1 and DNMT3B and pharmacologi

146 We used mouse models, including DNA methyltransferase (Dnmt1, Dnmt3a, and Dnmt3b) knocko

147 novo DNA methylation by catalytically active DNA methyltransferases (DNMT1 and DNMT3A/B) require acce

148 ofiling, and systematic genetic targeting of DNA methyltransferases (Dnmt1, Dnmt3a, and Dnmt3b) and T

149 we discover aptamers against the maintenance DNA methyltransferase, DNMT1, by coupling Asymmetrical F

150 he H3K9 methyltransferases, G9a/GLP, and the DNA methyltransferase, DNMT1, which both control keratin

151 ally increased the expression of the de novo DNA methyltransferase Dnmt3a [DNA (cytosine-5-)-methyltr

152 kedly enhanced in the absence of the de novo DNA methyltransferase Dnmt3a but not the maintenance DNA

153 Among these, the de novo DNA methyltransferase DNMT3A has emerged as one of the m

154 The DNA methyltransferase Dnmt3a has high expression in term

155 , we show that deletion of the gene encoding DNA methyltransferase Dnmt3a in hypothalamic AgRP neuron

156 ral nerve injury increases expression of the DNA methyltransferase DNMT3a in the injured DRG neurons

157 DNA methyltransferase DNMT3A is essential for establishm

158 The DNA methyltransferase Dnmt3a suppresses tumorigenesis in

159 (dCas9) nuclease and catalytic domain of the DNA methyltransferase DNMT3A targeted by co-expression o

160 how that in the brain during early life, the DNA methyltransferase DNMT3A transiently binds across tr

161 In this work, we employed a DNA methyltransferase Dnmt3a-Dnmt3L construct fused to t

162 sense mutations in DNMT3A, which encodes the DNA methyltransferase DNMT3A.

163 y in myeloid diseases, including the de novo DNA methyltransferase DNMT3A.

164 The de novo DNA methyltransferases Dnmt3a and Dnmt3b are of crucial

165 The DNA methyltransferases DNMT3A and DNMT3B are primarily r

166 016) find an unexpected role for the de novo DNA methyltransferases Dnmt3a and Dnmt3b in the regulati

167 The de novo DNA methyltransferases Dnmt3a and Dnmt3b play crucial ro

168 p53 restricts the expression of the de novo DNA methyltransferases Dnmt3a and Dnmt3b while up-regula

169 lly mediated by direct repression of de novo DNA methyltransferases Dnmt3a and Dnmt3b, leading to tra

170 rrelated with an upregulation of the de novo DNA methyltransferases DNMT3A and DNMT3B, the subsequent

171 tion patterns are established by two de novo DNA methyltransferases, DNMT3A and DNMT3B, which exhibit

172 CpG dinucleotide, is installed by two denovo DNA methyltransferases, DNMT3A and DNMT3B.

173 moter coincident with the recruitment of the DNA methyltransferase DNMT3B and histone methyltransfera

174 When the function of the de novo DNA methyltransferase DNMT3B is disrupted, as in ICF1 sy

175 Recent evidence associating the de novo DNA methyltransferase Dnmt3b with H3K36me3-rich chromati

176 licase DNA-binding protein 8 (CHD8), and the DNA methyltransferase DNMT3B, resulting in hypermethylat

177 ession of miR-203 is mediated by the de novo DNA methyltransferase DNMT3B, the recruitment of which t

178 Hypomorphic mutations in DNA-methyltransferase DNMT3B cause majority of the rare

179 in transposon-rich repeats and requires the DNA methyltransferase Dnmt5.

180 CpG methylation by de novo DNA methyltransferases (DNMTs) 3A and 3B is essential fo

181 lytically active enzymes function in mice as DNA methyltransferases (Dnmts) and as transcriptional re

182 Aberrant expression of the DNA methyltransferases (DNMTs) and disruption of DNA met

183 based on DNA damage-related binding between DNA methyltransferases (DNMTs) and PARP1.

184 DNA methyltransferases (DNMTs) are enzymes responsible f

185 DNA methyltransferases (DNMTs) are thought to be involve

186 establishment and maintenance activities of DNA methyltransferases (DNMTs) can help in the developme

187 DNA methyltransferases (DNMTs) deposit DNA methylation,

188 rant DNAm during OS through interacting with DNA methyltransferases (DNMTs) in a "Yin-Yang" complex t

189 caffeine exposure causes down-regulation of DNA methyltransferases (DNMTs) in embryonic heart and re

190 Despite the abundance of DNA methyltransferases (Dnmts) in the brain, which are r

191 ssociated gene silencing, through inhibiting DNA methyltransferases (DNMTs) is an important potential

192 lian DNA generated and maintained by several DNA methyltransferases (DNMTs) with partially overlappin

193 DNA methylation is catalyzed by DNA methyltransferases (DNMTs), and the two DNMT familie

194 on marks relies on the catalytic activity of DNA methyltransferases (DNMTs), and their active removal

195 ed drug screen, we report that inhibitors of DNA methyltransferases (DNMTs), decitabine and FdCyd, bl

196 inhibitors of histone deacetylases (HDACs), DNA methyltransferases (DNMTs), enhancer of zeste homolo

197 rentiation and is mediated by the actions of DNA methyltransferases (DNMTs).

198 fications, including cytosine methylation by DNA methyltransferases (DNMTs).

199 t-specific RNA polymerase V with the de novo DNA methyltransferase DRM2.

200 ion of SDCpro-GFP, redundantly controlled by DNA methyltransferases DRM2 and CMT3.

201 , where an inactive form of Cas9 is fused to DNA methyltransferase effectors.

202 DNA methylation and specifically the DNA methyltransferase enzyme DNMT3A are involved in the

203 hed at the exit from pluripotency by de novo DNA methyltransferases enzymes, DNMT3A and DNMT3B, which

204 DNMT3a is a de novo DNA methyltransferase expressed robustly after T-cell ac

205 DAC CSC, and we determined the importance of DNA methyltransferases for CSC maintenance and tumorigen

206 The maintenance DNA methyltransferase from Zea mays, ZMET2, recognizes d

207 probe that reported the localization of the DNA methyltransferase G9a in cells.

208 correlation between mutations in the de novo DNA methyltransferase gene DNA methyltransferase 3alpha

209 d further yielded a novel association in the DNA methyltransferase gene DNMT3B.

210 UHRF1) and its DNA methyltransferase partner DNA methyltransferase I (DNMT1) are critical for the res

211 Thus, we knocked out the main de novo DNA methyltransferase in cardiomyocytes, DNMT3A, in huma

212 which is not correlated with recruitment of DNA methyltransferases in gametes and suggestive of unex

213 CMTs are evolutionary conserved DNA methyltransferases in Viridiplantae.

214 that protein levels of the principal de novo DNA-methyltransferase in neurons, DNMT3A1, are tightly c

215 ance: These findings describe the effects of DNA methyltransferase inhibition on ERalpha and its pote

216 1 pathway as a determinant of sensitivity to DNA methyltransferase inhibition, specifically implicati

217 egulation of lung cancer, experiment using a DNA methyltransferase inhibitor (5-azacytidine, AZA), me

218 at reverse epigenetic silencing, such as the DNA methyltransferase inhibitor (DNMTi) 5-azacytidine (A

219 rate that treatment of rhabdomyosarcoma with DNA methyltransferase inhibitor (DNMTi) upregulates Hipp

220 and function of regulatory T cells using the DNA methyltransferase inhibitor 5-azacytidine (Aza).

221 Treatment with the DNA methyltransferase inhibitor azacitidine restored DPH

222 lored the effects of 5-fluorouracil plus the DNA methyltransferase inhibitor decitabine or the histon

223 ian cancer who received carboplatin plus the DNA methyltransferase inhibitor guadecitabine or a stand

224 Azacitidine (AZA) is a DNA methyltransferase inhibitor widely used to treat MDS

225 Treatment with the DNA methyltransferase inhibitor Zebularine increases miR

226 aser-stimulated mice with one dose of RG108 (DNA methyltransferase inhibitor), lead to marked symptom

227 on of cycloheximide but was disrupted by the DNA methyltransferase inhibitor, 5-AZA, when S1 had been

228 tized the screen by "priming" cells with the DNA methyltransferase inhibitor, 5-aza-2'-deoxycytidine

229 utcomes of patients who are coadministered a DNA methyltransferase inhibitor.

230 DNA methyltransferase inhibitors (DMTis) are used to tre

231 The DNA methyltransferase inhibitors (DNMTi) 5-azacytidine a

232 DNA methyltransferase inhibitors (DNMTi) increase PARP t

233 w stroma in regulating clinical responses to DNA methyltransferase inhibitors (DNMTi) is also poorly

234 chemotherapeutic regimens with low doses of DNA methyltransferase inhibitors (DNMTi, hypomethylating

235 how this deficiency may influence the use of DNA methyltransferase inhibitors (DNMTis) for treatment

236 Recent reports that low doses of DNA methyltransferase inhibitors (DNMTis) plus PARPis en

237 Combining DNA-demethylating agents (DNA methyltransferase inhibitors [DNMTis]) with histone

238 work showed that epigenetic drugs including DNA methyltransferase inhibitors and histone deacetylase

239 Overall, our results demonstrated that DNA methyltransferase inhibitors preferentially target c

240 as shown that epigenetic drugs, specifically DNA methyltransferase inhibitors, can upregulate immune

241 re-expression after treatment with EZH2 and DNA methyltransferase inhibitors.

242 ines, and this is reversed by treatment with DNA methyltransferase inhibitors.

243 nes, and could be reversed by treatment with DNA methyltransferase inhibitors.

244 DNA methyltransferases interact with their CpG target si

245 We observed that O (6)-methylguanine DNA methyltransferase is effective in removing the small

246 RANSFERASE 2 (DRM2), the de novo Arabidopsis DNA methyltransferase, is crucial to maintain DNA methyl

247 cells, Endo-T cells differentially expressed DNA methyltransferase isoforms and had increased levels

248 tones are involved in specifying patterns of DNA methyltransferase localization and DNA methylation a

249 nces SMRT sequencing was used to investigate DNA methyltransferases M.BceJIII and M.EcoGIX, using art

250 th factor or unmethylated O(6)-methylguanine-DNA methyltransferase may benefit from Ona + Bev.

251 on patterns are dynamically maintained, with DNA methyltransferases mediating inheritance of methyl m

252 dDM and RNA-independent mechanisms involving DNA methyltransferase MET1 and chromodomain DNA methyltr

253 elements hypomethylated through mutation of DNA methyltransferase MET1.

254 or size, resection extent, O-6-methylguanine-DNA methyltransferase-methylation, and isocitrate dehydr

255 O-6-methylguanine-DNA methyltransferase (MGMT) activity is directly correl

256 in addition to changes in O(6)-methylguanine DNA methyltransferase (MGMT) activity, small changes in

257 TMZ-induced DNA damage by O-6-methylguanine-DNA methyltransferase (MGMT) confers one mechanism of TM

258 O(6)-methylguanine-DNA methyltransferase (MGMT) is an enzyme that removes a

259 The O-6-methylguanine-DNA methyltransferase (MGMT) is responsible for the dire

260 mes, even in patients with O-6-Methylguanine-DNA Methyltransferase (MGMT) methylation.

261 , but only in patients with O6-methylguanine-DNA methyltransferase (MGMT) promoter methylated tumors.

262 While O(6)-methylguanine (O(6)-MeG)-DNA methyltransferase (MGMT) promoter methylation status

263 promoter methylation of O (6)-methylguanine-DNA methyltransferase (MGMT) remains controversial for b

264 status of the promoter of O(6)-methylguanine-DNA methyltransferase (MGMT) was assessed.

265 the cytotoxic response of O(6)-methylguanine-DNA methyltransferase (MGMT)-deficient mammalian cells a

266 to the DNA repair protein O(6)-methylguanine-DNA-methyltransferase (MGMT).

267 Three phase variable DNA methyltransferases (ModA, ModB and ModD), which medi

268 Cas9 (dCas9) with an engineered prokaryotic DNA methyltransferase MQ1.

269 Bio sequencing, the recognition sequences of DNA methyltransferases (MTases) are appearing rapidly.

270 on article, we propose that highly conserved DNA methyltransferases (MTases) represent a unique oppor

271 The advent of engineered DNA methyltransferases (MTases) to target DNA methylatio

272 H. pylori has an unusually large number of DNA methyltransferases (MTases), prompting speculation t

273 pigenetic mark in vertebrates established by DNA methyltransferases (MTases); the methylation mark ca

274 It is catalyzed by DNA methyltransferases, one of which -DNMT3A- is frequen

275 Of all known DNA methyltransferases, only CHROMOMETHYLASE 3 (CMT3) is

276 n containing endonucleases were not close to DNA methyltransferase ORFs, strongly supporting modifica

277 domain-containing protein 1 (UHRF1) and its DNA methyltransferase partner DNA methyltransferase I (D

278 hepatocyte growth factor, O(6)-methylguanine-DNA methyltransferase promoter methylation, and glioblas

279 P = 0.005) independent of O(6)-methylguanine-DNA-methyltransferase promoter methylation and other str

280 t harbors a nonmethylated O(6)-methylguanine-DNA methyltransferase promotor, standard temozolomide (T

281 ANSFERASE 1 (MET1) and CHROMOMETHYLASE (CMT) DNA methyltransferase protein families, respectively.

282 ort altered DNA methylation markers (altered DNA methyltransferase protein levels and increased globa

283 ably targets CTCF binding at the promoter of DNA methyltransferases, regulating their expression.

284 f chromatin folding that restricts access to DNA methyltransferases responsible for gene body methyla

285 of covalent attachment to O(6)-methylguanine DNA methyltransferase (SNAP-tag) fusion proteins.

286 al segment is found broadly in N4/N6-adenine DNA methyltransferases, some of which are human pathogen

287 rious epigenetic regulator families, such as DNA methyltransferases, ten-eleven translocation protein

288 Plants encode a diverse repertoire of DNA methyltransferases that have specialized to target c

289 and an ortholog of CcrM, BabI, but not with DNA methyltransferases that lack the conserved C-termina

290 cytidine) to alter the catalytic activity of DNA methyltransferases, the enzymes that methylate DNA.

291 e findings reveal how CTCF binding regulates DNA methyltransferase to reprogram the methylome in resp

292 ntrolled by the phase-variable expression of DNA methyltransferases via epigenetic mechanisms.

293 On the basis of similarities with a DNA methyltransferase, we propose that METTL5-TRMT112 ac

294 Our results show that mRNA levels of DNA methyltransferase were increased in demyelinated MS

295 ins to sites of DNA damage repair, including DNA methyltransferases where it imposes de novo DNA meth

296 rget base into the active-site pocket of the DNA methyltransferase, which is partially compatible wit

297 We have identified a highly conserved DNA methyltransferase, which we term Campylobacter trans

298 We discovered an orphan DNA methyltransferase with a well-defined specificity, t

299 ial methylation of open chromatin regions by DNA methyltransferases with low sequence specificity, in

300 picua (CIC), facilitates the interactions of DNA methyltransferases with the CIC promoter, and promot