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1                                              DNMT activity was measured with a functional assay, and
2                                              DNMT inhibition or ISL1 expression in breast cancer cell
3                                              DNMT inhibition prevents the PP1 methylation increase, r
4                                              DNMT mRNA levels decreased rapidly, with significant sup
5                                              DNMT-1 has a direct suppressive role in 15-LOX-1 transcr
6                                              DNMT-1 protein hypomorphism impaired DNMT-1 recruitment
7                                              DNMT-1 up-regulation occurs in hepatobiliary cancers and
8                                              DNMTs are important epigenetic targets.
9 s and ERK-regulated DNA methyltransferase 1 (DNMT-1) levels.
10  methyltransferase, DNA methyltransferase 1 (DNMT-1), has been shown in carcinomas of the colon, lung
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 Treatment of HCT116 cells with Decitabine (a DNMT inhibitor) or trichostatin A (a histone deacetylase
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 and restored expression in response to acute DNMT suppression were assayed for methylation changes us
22 ibited zebrafish DNMT, TDCIPP did not affect DNMT activity in vitro at concentrations as high as 500
23 oylanilide hydroxamic acid (SAHA) only after DNMT-1 dissociation from the 15-LOX-1 promoter and witho
24 eviously described in RA FLS through altered DNMT expression.
25 gene hypermethylation in cancer with altered DNMT RNA levels, and that this hypermethylation is neith
26                                     Although DNMTs associate with both methylated and unmethylated rD
27 am(Akita) mice showed the highest DNMT-1 and DNMT-3a levels compared with the other groups.
28                              Both DNMT-1 and DNMT-3a were detected at the U6-1 locus by chromatin imm
29 he forced diminution of DNMT-1, DNMT-3a, and DNMT-3b by siRNA targeting resulted in increased U6 leve
30 igenetic feedback loop between miR-17~92 and DNMT-1 in lung fibrosis.
31 lationship between the miR-17~92 cluster and DNMT-1 expression was examined in vitro.
32          Importantly, changes in ERalpha and DNMT expression in the cortex (males) and hypothalamus (
33 reasing DNMT1 and DNMT3a mRNA expression and DNMT enzyme activity similar to mitogen-activated protei
34 ary fibrosis model reduced fibrotic gene and DNMT-1 expression, enhanced miR-17~92 cluster expression
35 reover, in addition to the reported HDAC and DNMT dual epigenetic inhibitory profile of the parent co
36            The results suggest that HDAC and DNMT inhibitors activate reelin and GAD67 expression thr
37 MTG8 and support the combination of HDAC and DNMT inhibitors as a novel therapeutic approach for t(8;
38 on, resulting in global DNA methylation- and DNMT-dependent downregulation of multiple microRNAs (miR
39 ose uptake, and elevated levels of HDACs and DNMTs.
40 ad increased expression of GLUTs, HDACs, and DNMTs.
41    Several molecules have been identified as DNMT inhibitors and, among the non-nucleoside inhibitors
42 pied the same regions of its own promoter as DNMT corepressors, and ectopic overexpression of SALL4 l
43 istent with this idea, only nucleoside-based DNMT inhibitors that form covalent DNA adducts induce p5
44 alysis to probe for the interactions between DNMTs and native nucleosomes.
45 MT inhibitors (DNMTis) alone covalently bind DNMTs into DNA and increase PARP1 tightly bound into chr
46                                         Both DNMT-1 and DNMT-3a were detected at the U6-1 locus by ch
47                                However, both DNMT occupancy and low frequency methylation were correl
48 ncer cell line, HCT116, in which one or both DNMT genes were disrupted by homologous recombination.
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 nalysis of the promoter region after chronic DNMT suppression.
53 warranting further investigation of combined DNMT and HDAC inhibition in refractory or drug-resistant
54        Using luciferase reporter constructs, DNMT-1 was verified as a target for miR-148a and miR-152
55 hold with patient-tolerable doses of current DNMT inhibitors (DNMTIs).
56 Precursors to miR-148a and miR-152 decreased DNMT-1 protein expression, increased Rassf1a and p16INK4
57        Dose responses demonstrated decreased DNMT expression at concentrations as low as 1 pg/ml of I
58  alters DNA methylation in FLS by decreasing DNMT expression and function.
59 tterns in a DNA methyltransferase-dependent (DNMT-dependent) manner.
60 udy the effect of interactions between diet, DNMT-1 levels, and genetic predisposition on the develop
61              Our data suggest that different DNMT domains are responsible for targeting DNA methylati
62 stably transfected with each of 13 different DNMTs (DNMT1, two DNMT3A isoforms, nine DNMT3B isoforms
63 tically engineered deficiencies in different DNMTs and find that the major activity against these sub
64                                The different DNMTs display a wide spectrum of genomic DNA-directed ac
65 lycomb group proteins; upon differentiation, DNMT activation leads to CpG island methylation, causing
66 ed BAG-1 expression in the single and double DNMT knockout cells.
67                              Similarly, dual DNMT knockout caused dramatic hypomethylation of the MAG
68  the DNA methylation changes induced by each DNMT.
69 -dC-containing DNA suggests that the engaged DNMT is catalytically active in the cell.
70 n of the DNA maintenance methylation enzyme, DNMT-1.
71 ght all postmitotic neurons and glia express DNMTs at comparable levels, the coexpression of selected
72 tern at CG-X promoters was altered following DNMT knockout.
73 roughput screening of chemical libraries for DNMT inhibition activity.
74 ty, together demonstrating a requirement for DNMTs in mutant Htt-triggered neuronal death and suggest
75 cells is DNMT1, with minor contribution from DNMT 3b and none from DNMT3a, the only known bona fide d
76                                 Furthermore, DNMTs and histone deacetylase repressors synergistically
77 nce and will help to develop next-generation DNMT inhibitors.
78 ression of host DNA methyltransferase genes (DNMTs) was measured.
79                                       Global DNMT-dependent epigenetic modifications lead to changes
80 ance of regional DNA methylation, and global DNMT activity in CD133- Huh7 cells was inhibited by TGFb
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         DNMT-1 protein hypomorphism impaired DNMT-1 recruitment to the 15-LOX-1 promoter, which allow
84  The induction of chromosomal alterations in DNMT-deficient cells was evidenced both by aneuploidy an
85 onclusion, DAC upregulates p21(WAF1/CIP1) in DNMT-independent manner via the DNA damage/ATM/p53 axis.
86                           Thus, reduction in DNMT and histone deacetylase activities that likely bloc
87 nd the magnitude of methylation reduction in DNMT knockout cells.
88 3a negated the ability of PGE(2) to increase DNMT activity.
89 reased levels of HDAC2 protein and increased DNMT expression in the dorsal hippocampus.
90 ore, PP2Ac suppression resulted in increased DNMT enzyme activity, DNA hypermethylation, and decrease
91    siRNAs were used to knock down individual DNMT expression in primary cultures of mouse embryonic c
92      This study demonstrates that individual DNMTs can be tracked and that their binding to genomic D
93                              DF also induced DNMT-sensitive propathological expression of downstream
94        In vitro, hydralazine did not inhibit DNMT activity.
95 hat this class of chemical compounds inhibit DNMTs by interacting with the DNA substrate.
96 e substrate, EGCG dose-dependently inhibited DNMT activity, showing competitive inhibition with a K(i
97                               Interestingly, DNMT activity is required for protein kinase C-induced i
98                            However, isolated DNMTs are weak catalysts and are difficult to assay.
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 the role DNA (cytosine-5) methyltransferase (DNMT) activity might play in regulating the induction of
103          DNA (cytosine-5)-methyltransferase (DNMT) 1 participates in transcriptional repression of ge
104 cytidine, or siRNA to DNA Methyltransferase (DNMT) 1 and 3b in HCC cells.
105 sed the expression of DNA methyltransferase (DNMT) 1 and 3b.
106 epigenetic regulators DNA methyltransferase (DNMT) 1 and DNMT3A in the juvenile cortex and hypothalam
107 gnant T cells express DNA methyltransferase (DNMT) 1 and that constantly activated signal transducer
108 on of the maintenance DNA methyltransferase (DNMT) 1 by a proteasomal pathway.
109 gh the recruitment of DNA methyltransferase (DNMT) 3a and histone methyltransferase G9a.
110 aused by mutations in DNA methyltransferase (DNMT) 3B, a de novo DNA methyltransferase.
111 logical inhibition of DNA methyltransferase (DNMT) activity and the forced diminution of DNMT-1, DNMT
112  of ERK activation or DNA methyltransferase (DNMT) activity blocked the memory-enhancing effects of E
113  compounds to inhibit DNA methyltransferase (DNMT) activity.
114 lasts was reversed by DNA methyltransferase (DNMT) and histone deacetylase (HDAC) inhibitors, and MLL
115 d by prokaryotic SssI DNA methyltransferase (DNMT) and human DNMT1.
116 e function of two key DNA methyltransferase (DNMT) enzymes in epigenetic regulation of X-linked cance
117  able to complex with DNA methyltransferase (DNMT) enzymes, leading us to explore a role for CBX7 in
118 y in the reduction of DNA methyltransferase (DNMT) expression, hence inducing the transcription of me
119  to each other and to DNA methyltransferase (DNMT) gene expression is ill defined.
120    Here, we show that DNA methyltransferase (DNMT) inhibition in hippocampal neurons results in activ
121 ergistically with the DNA methyltransferase (DNMT) inhibitor 5-aza-2'-deoxycytidine (ADC) to reactiva
122 essing cells with the DNA methyltransferase (DNMT) inhibitor 5-aza-2'-deoxycytidine reduces cytosine
123                       DNA methyltransferase (DNMT) inhibitor and small-interfering RNA depletion of D
124 ld be reversed with a DNA methyltransferase (DNMT) inhibitor in vitro and in vivo with beneficial eff
125 ial administration of DNA methyltransferase (DNMT) inhibitors and histone deacetylase (HDAC) inhibito
126 cts were mitigated by DNA methyltransferase (DNMT) inhibitors and knockdown of DNMT3A.
127 eacetylase (HDAC) and DNA methyltransferase (DNMT) inhibitors.
128 resence or absence of DNA methyltransferase (DNMT) inhibitors.
129 e sequencing of three DNA methyltransferase (DNMT) knockout cell lines and the wild-type HCT116 colon
130    The DNMT3B de novo DNA methyltransferase (DNMT) plays a major role in establishing DNA methylation
131 r (1) TDCIPP inhibits DNA methyltransferase (DNMT) within embryonic nuclear extracts; (2) uptake of T
132 -dC), an inhibitor of DNA methyltransferase (DNMT), induces a senescence-like state.
133 nd that inhibition of DNA methyltransferase (DNMT), whether during training or shortly afterwards, bl
134 et fibrotic genes and DNA methyltransferase (DNMT)-1 expression.
135 d as a consequence of DNA methyltransferase (DNMT)-mediated hypermethylation.
136  strand by 5-cytosine DNA methyltransferase (DNMT).
137 ies to the 3'-UTRs of DNA methyltransferase (DNMT)3A and -3B (de novo methyltransferases), two key en
138 acetylase (HDAC)1 and DNA methyltransferase (DNMT)3a to the CRE site (-111/-104) probably accounts fo
139 protein SUZ12 and the DNA methyltransferase (DNMT)3b preferentially in undifferentiated hESCs as comp
140 c analysis, using somatic methyltransferase (DNMT) knockout cells, we showed that hypomethylation dec
141 pression of HDACs and DNA methyltransferase (DNMTs) also was increased.
142 ed the expression of DNA methyltransferases (DNMT) 1 and DNMT3beta, which are critical in the mainten
143  explore the role of DNA methyltransferases (DNMT) and ten eleven translocation (Tet) proteins in per
144                      DNA methyltransferases (DNMT) are promising drug targets in cancer provided that
145  using inhibitors of DNA methyltransferases (DNMT) or/and histone deacetylases (HDACs) has shown prom
146 lation activities of DNA methyltransferases (DNMT) thought to catalyze these reactions.
147 nes here defined as: DNA methyltransferases (DNMT), methyl-CpG-binding domain (MBD) proteins, histone
148 ed that BRCA1, EZH2, DNA methyltransferases (DNMT)1/3a/3b and H3K27me3 are recruited to the endogenou
149  maintained by three DNA methyltransferases (DNMT): DNMT1, DNMT3A, and DNMT3B.
150 ., depsipeptide) and DNA methyltransferases (DNMT; i.e., decitabine) in RUNX1/MTG8-positive Kasumi-1
151         DNA (cytosine-5)-methyltransferases (DNMTs) catalyze the transfer of a methyl group from S-ad
152 s-link to DNA cytosine-5-methyltransferases (DNMTs) through the active Cys residue, which provides a
153 nt expression of the DNA methyltransferases (DNMTs) and disruption of DNA methylation patterns are as
154 ated binding between DNA methyltransferases (DNMTs) and PARP1.
155 acted with different DNA methyltransferases (DNMTs) and purified DNMT enzymatic activities from nucle
156 on levels of several DNA methyltransferases (DNMTs) and their interacting proteins by TaqMan qPCR and
157                      DNA methyltransferases (DNMTs) are a family of related proteins that both cataly
158                      DNA methyltransferases (DNMTs) are critical enzymes that establish and maintain
159             Although DNA methyltransferases (DNMTs) are dispensable for embryonic stem cell maintenan
160                      DNA methyltransferases (DNMTs) are important enzymes involved in epigenetic cont
161 protein 2 (MBD2) and DNA methyltransferases (DNMTs) at the leptin promoter are increased and RNA Pol
162 enance activities of DNA methyltransferases (DNMTs) can help in the development of predictive biomark
163                      DNA methyltransferases (DNMTs) catalyze methylation of cytosines in CGs.
164 ugh interacting with DNA methyltransferases (DNMTs) in a "Yin-Yang" complex targeted to chromatin and
165 s down-regulation of DNA methyltransferases (DNMTs) in embryonic heart and results in impaired cardia
166 catalytically active DNA methyltransferases (DNMTs) in human embryonic stem cells (ESCs) using CRISPR
167 functional mammalian DNA methyltransferases (DNMTs) in regulating the rDNA promoters activity.
168 , through inhibiting DNA methyltransferases (DNMTs) is an important potential cancer therapy paradigm
169                      DNA methyltransferases (DNMTs) play an important role in establishing and mainta
170                      DNA methyltransferases (DNMTs) primarily establish and maintain global DNA methy
171 ity as inhibitors of DNA methyltransferases (DNMTs) require further investigation.
172 catalytic domains of DNA methyltransferases (DNMTs) to engineered transcription activator-like effect
173 disruption models of DNA methyltransferases (DNMTs) to study the effects of this methylation on 15-LO
174  enhances binding of DNA methyltransferases (DNMTs) to the promoter.
175 expression levels of DNA methyltransferases (DNMTs), 1, 3A and 3B in CSE-treated cells.
176 t that inhibitors of DNA methyltransferases (DNMTs), decitabine and FdCyd, block mutant huntingtin (H
177 ated action of three DNA methyltransferases (DNMTs), DNMT1, DNMT3A and DNMT3B.
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 ed by the actions of DNA methyltransferases (DNMTs).
182 nine, a substrate of DNA methyltransferases (DNMTs).
183  of DNA catalyzed by DNA methyltransferases (DNMTs).
184 osine methylation by DNA methyltransferases (DNMTs).
185 cing the activity of DNA methyltransferases (DNMTs).
186 h both viral DNA and 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         The binding efficiency of the mutant DNMT proteins at the replication foci and heterochromati
190 ots might be under control of SetDB1 and not DNMT for silencing.
191                     Among the non-nucleoside DNMT inhibitors, N-phthaloyl-l-tryptophan 1 (RG108) was
192                       A number of nucleoside DNMT inhibitors (DNMTi) have been studied in cancer, inc
193 ncing excitatory activity, in the absence of DNMT inhibitors, also produces similar decreases in DNA
194             We show the concerted actions of DNMT enzymes in the establishment and maintenance of met
195 icate that IL-6 can regulate the activity of DNMT-1 and expression of methylation-dependent tumor sup
196  provide a comprehensive characterization of DNMT-mutant ESCs, including single-base genome-wide maps
197 bitor and small-interfering RNA depletion of DNMT genes were used to reverse KLF10 expression in the
198 (DNMT) activity and the forced diminution of DNMT-1, DNMT-3a, and DNMT-3b by siRNA targeting resulted
199                       The specific effect of DNMT inhibition on spontaneous excitatory neurotransmiss
200 s that genetic factors affecting function of DNMT genes may underlie the propensity of tumors to acqu
201 hts for the design of the next-generation of DNMT inhibitors.
202                       Combined inhibition of DNMT activities and JAK signalling, in vitro and in vivo
203 ated training; moreover, later inhibition of DNMT eliminates consolidated LTM.
204 ine and 5-aza-2-deoxycytidine, inhibitors of DNMT activity, blocked the induction of long term potent
205 ot accounted for by changes in the levels of DNMT proteins.
206 65-DNMT-1 interactions, chromatin loading of DNMT-1 and subsequent BRMS1 promoter methylation and tra
207 9), and Arg(1309) in the catalytic pocket of DNMT.
208 ssor gene promoter via direct recruitment of DNMT-1 (DNA (cytosine-5)-methyltransferase 1) to chromat
209 illatory shear stress (OS), and reduction of DNMT with either the inhibitor 5-aza-2'-deoxycytidine (5
210 lementarity to the 3'-untranslated region of DNMT-1, namely miR-148a, miR-152, and miR-301.
211    To understand the potential regulation of DNMT-1 by IL-6-dependent miRNAs, we examined the express
212 se-resolution DNA methylomes for a series of DNMT knockout embryonic stem cells, with deep coverage a
213 expression after RNAi-induced suppression of DNMT in a glioblastoma multiforme (GBM) cell line.
214  and time dependence comparable with that of DNMT inhibitors.
215                      Short-term treatment of DNMT wild-type female mice with low doses of the demethy
216 may be warranted when considering the use of DNMT inhibitors in development of Treg-based cellular th
217  and transcriptional repressor activities of DNMTs and HDACs.
218  provide a new assay for de novo activity of DNMTs and data suggesting a potential role for DNMT1 in
219 thermore, we are able to observe assembly of DNMTs at CBX7 target gene promoters.
220                       Aberrant expression of DNMTs and their isoforms has been found in many types of
221 gnificantly down-regulated the expression of DNMTs, a reaction normally elicited by demethylation age
222                                Inhibition of DNMTs in HD model primary cortical or striatal neurons r
223       In vivo, pharmacological inhibition of DNMTs in HD mouse brains restored the mRNA levels of key
224 steine (a potent noncompetitive inhibitor of DNMTs) during the catechol-O-methyltransferase-mediated
225 BNA gene transcription, nor did knockdown of DNMTs significantly alter CpG methylation within Cp.
226               Robust nuclear localization of DNMTs in cones compared to rods suggests a potential rol
227    These results demonstrate localization of DNMTs with the inactive rDNA in the nucleolus, the speci
228     However, virus-induced overexpression of DNMTs also leads to methylation of host CpG islands.
229                        To assess the role of DNMTs in these events, we investigated the effects of re
230   To investigate whether the upregulation of DNMTs could also have an effect on the methylation of ho
231 way signaling abnormality and its effects on DNMT expression, and inhibiting this pathway induces aut
232 son, the strong inhibitory effect of EGCG on DNMT-mediated DNA methylation was independent of its own
233                 The effect of hydralazine on DNMT was tested in vitro using enzyme inhibition studies
234                                     Overall, DNMT mRNA levels reached their highest point in the firs
235 minimal interacting domains between RelA/p65-DNMT-1 and RelA/p65-BRMS1 promoter abrogates BRMS1 methy
236 of S276 on RelA/p65 is required for RelA/p65-DNMT-1 interactions, chromatin loading of DNMT-1 and sub
237  DNA methyltransferases (DNMTs) and purified DNMT enzymatic activities from nuclear extracts.
238  The ability of RelA/p65 to directly recruit DNMT-1 to chromatin, resulting in promoter-specific meth
239 DNMT3A, and DNMT3B protein levels and reduce DNMT enzyme activity.
240 ents, we investigated the effects of reduced DNMT expression on embryonic cardiomyocytes.
241 that the COX2 inhibitor NS398 down-regulated DNMTs and increased expression of SPARC, which led to tu
242                        As mice age, residual DNMT activity declines further, and the probability of s
243 parable levels, the coexpression of selected DNMTs with markers of distinct neurotransmitter phenotyp
244 lyses indicated that double, but not single, DNMT knock-out cells display two specific alterations in
245 on failed, supporting the notion of specific DNMT-histone methyltransferase networks.
246          We propose a model wherein specific DNMT-histone methyltransferase networks are utilized to
247 dy-based tracking method will allow specific DNMTs and their DNA targets to be recovered and analyzed
248 etin, fisetin, and myricetin) inhibited SssI DNMT- and DNMT1-mediated DNA methylation in a concentrat
249 ed that directed DNA methylation with a TALE-DNMT targeting the CDKN2A locus, which encodes the cycli
250  Together, our results demonstrate that TALE-DNMTs can selectively target specific genes and suggest
251              We demonstrated that these TALE-DNMTs direct DNA methylation specifically to the targete
252 l miRNAs from the miR-17~92 cluster targeted DNMT-1 expression resulting in a negative feedback loop.
253  DNA hypomethylation, and RNA levels for ten DNMT isoforms.
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 r, spectral karyotype analyses revealed that DNMT-deficient HCT116 cells are highly unstable with res
259                     In summary, we show that DNMT deficiency in human cancer cells results in constit
260 sidered together, these results suggest that DNMT activity is dynamically regulated in the adult nerv
261 in regional DNA copy number, suggesting that DNMT deficiency and genomic DNA hypomethylation are not
262 n but does not induce p53R2, suggesting that DNMT/DNA adduct formation is the molecular trigger for p
263                          We demonstrate that DNMTs and NuRD cooperate to maintain the silencing of se
264                           We discovered that DNMTs and the core components of the NuRD (Mi-2/nucleoso
265                                We found that DNMTs have specific and overlapping target sites and the
266                            We speculate that DNMTs and MBD proteins allow RNA molecules to participat
267 how that new approaches, like decreasing the DNMT targeting protein, UHRF1, can augment the DNA demet
268 tion target profiles are a reflection of the DNMT domains.
269                         A combination of the DNMT inhibitor 5-azacytidine and the HDAC inhibitor buty
270  was turned off following treatment with the DNMT inhibitor, decitabine.
271                                          The DNMTs methylate viral DNA, leading to decreased viral ge
272                 We show that a subset of the DNMTs and MBD proteins can form RNA.protein complexes.
273                                       Of the DNMTs, DNMT1 and DNMT3a are most highly expressed in pos
274  largely due to its direct inhibition of the DNMTs.
275  repression complexes (PRC1 and PRC2) to the DNMTs have begun to shed light on how methylation is tar
276 ion of the structures and functions of these DNMTs, in particular their roles in Ca(2+) ion-dependent
277 chemical fractionation showed that all three DNMTs (DNMT1, DNMT3A, and DNMT3B) are associated with th
278  of repressor complexes containing all three DNMTs, MeCP2, and HDAC1 from the corresponding promoters
279 ete understanding of precisely how the three DNMTs, 1, 3A, and 3B, interact for maintaining DNA methy
280 nfluence endothelial KLF4 expression through DNMT enrichment/myocyte enhancer factor-2 inhibition mec
281 ism involving direct DNA methyl transferase (DNMT) promoter transactivation, resulting in global DNA
282                      DNA methyl transferase (DNMT)1, DNMT3a and two proteins that regulate methylatio
283 ncreased binding of DNA methyl-transferases (DNMTs) 3a and 3b and methyl-CpG-binding domain protein 2
284 which provides a new tool to covalently trap DNMT-DNA complexes.
285 tes respond to HBV infection by upregulating DNMTs.
286 -beta1 to modulate the expression of various DNMTs in primary lung fibroblasts (CCL210).
287  mammalian DNMTs, and likely the vertebrates DNMTs in general, can also act as Ca(2+) ion- and redox
288 ramatic changes in cytosine methylation when DNMT activity was inhibited.
289  fibroblasts from patients with IPF, whereas DNMT-1 expression and methylation of the miR-17~92 promo
290 rect and active antiviral mechanism by which DNMTs can be recruited to retroviral DNA.
291  of Foxp3 can be predictably controlled with DNMT inhibitors to generate functional, stable, and spec
292                Finally, as 5 interacted with DNMT only when the DNA duplex was present, we hypothesiz
293 nthesized to understand its interaction with DNMT.
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

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