ライフサイエンスコーパス: EZH2

1 omplex member enhancer of zeste homologue 2 (EZH2).

2 ste 2 polycomb repressive complex 2 subunit (EZH2).

3 dependence on the transcriptional repressor EZH2.

4 es at A and C nucleotides can substitute for EZH2.

5 g from loss of the histone methyltransferase EZH2.

6 rogram requires cooperation of both EZH1 and EZH2.

7 on a disordered but highly conserved loop of EZH2.

8 ing a novel mechanism of lipid regulation by EZH2.

9 omplex 2 histone methyltransferases EZH1 and EZH2.

10 arbor frequent loss-of-function mutations in EZH2.

11 activation function of EZH1, the paralog of EZH2.

12 isplatin resistance in SCLC cells, including EZH2.

13 ression by the methyltransferase activity of EZH2.

14 s positively correlated with that of TET2 or EZH2.

15 uced histone methylation is mediated through EZH2, a functional member of the PRC2 complex.

16 cological or genetic inhibition of CDK4/6 or EZH2 abrogated psoriasis-related proinflammatory gene ex

17 However, contact with EZH2 accelerates cleavage rate by >100-fold, suggesting

18 rgets EZH2 mRNA, and increased expression of EZH2 activates cellular survival pathways, resulting in

19 Here we report that suppressing EZH2 activity ameliorates experimental intestinal inflam

20 ions in TFBS of over-represented TFs such as EZH2 affected MCF2L and ADP-ribosylhydrolase like 1 expr

21 pecifically interacted with EZH2 to increase EZH2 affinity to FOXM1 without binding the latter.

22 Emerging evidence indicates that EZH2 also activates gene expression in cancer cells in a

23 Loss of Ezh1 and Ezh2 also resulted in liver fibrosis.

24 ste 2 polycomb-repressive complex 2 subunit (Ezh2) also bound to this region; however, its methyltran

25 Activating mutations of EZH2, an epigenetic regulator, are present in approximat

26 by their re-expression after treatment with EZH2 and DNA methyltransferase inhibitors.

27 Mechanistically, mutant p53 interacts with EZH2 and enhances its association with the chromatin, th

28 lysine methyltransferases Ash1l, Smyd2, and Ezh2 and histone lysine demethylases Kdm5b and Kdm6b in

29 ontext and disease phase for the function of Ezh2 and its potential therapeutic implications.

30 and also accompanied by specific changes in EZH2 and its targets.

31 thway in association with induction of MYCN, EZH2 and NE differentiation markers (ASCL1, AURKA and SY

32 enes, FOXM1 was absent and SCIRT antagonized EZH2 and SOX2 activity, balancing toward repression.

33 pheres but colocalized with and counteracted EZH2 and SOX2 during cell-cycle and self-renewal regulat

34 own to automethylate its core subunits, EZH1/EZH2 and SUZ12.

35 nslation of mRNAs encoding the PRC2 subunits Ezh2 and Suz12.

36 We down-regulated EZH2 and TET2 in AML cell lines and assessed the effect

37 , the expression, methylation or mutation of EZH2 and TET2 was determined and further correlated with

38 negative regulators of antigen presentation, EZH2 and thymidylate synthase, enhanced DLBCL MHC-I pres

39 ethyltransferase enhancer of zest homolog 2 (EZH2) and specifically causes EZH2 degradation via lysos

40 omplex components (G9A, Enhancer of Zeste 2 (EZH2) and Suppressor of Zeste 12 (SUZ12)).

41 showing strong association between H3K27me3, Ezh2, and SATB2 in cells from rats and humans.

42 e identify the lysine residues at which EZH1/EZH2 are automethylated with EZH2-K510 and EZH2-K514 bei

43 Instead, we show that EZH1 and EZH2 are functionally redundant in the slowly proliferat

44 tant cells, the expressions of both KDM8 and EZH2 are further elevated, so are neuroendocrine markers

45 the Polycomb-group histone methyltransferase EZH2 as a p53 mRNA-binding protein.

46 4 (CDK4) and CDK6 and the methyltransferase EZH2 as a valid target for psoriasis therapy.

47 cs identified enhancer of zeste homologue 2 (EZH2) as an epigenetic regulator of the cholangiocyte TG

48 deubiquitinating enzyme that deubiquitinates EZH2 at K222.

49 fic and diametrically opposite functions for Ezh2 at the early and late stages of disease.

50 EZH2 augmented p53 GOF mutant-mediated cancer growth and

51 We propose that EZH2 automethylation allows PRC2 to modulate its histone

52 Intriguingly, EZH2 automethylation is significantly reduced in diffuse

53 al., demonstrated that the CD38/NAD/Sirtuin1/EZH2 axis reduces cytolytic CD8(+) T cell function and m

54 a novel role of miR-137 in regulating c-Myc-EZH2 axis that is crucial to the regulation of cisplatin

55 n vitro, suggesting FN as a direct target of EZH2-based repression.

56 zation, suggesting a rationale for targeting EZH2 beyond its catalytic activity for overcoming cispla

57 ive Snail-binding domain but depleted of the EZH2-binding domain.

58 including the oncogenic chromatin repressors EZH2, BMI1 and LSD1, which are functionally interdepende

59 EZH2 bound to an internal ribosome entry site (IRES) in

60 ases (DNMTs), enhancer of zeste homologue 2 (EZH2), bromodomain and extra-terminal domain proteins (B

61 stant cells c-Myc enhances the expression of EZH2 by directly suppressing miR-137 that targets EZH2 m

62 ggest that the interaction of an lncRNA with EZH2 can alter the affinity of EZH2 for its protein-bind

63 uence and structural similarities with human EZH2, catalyzes methylation of histone H3 in vitro and i

64 EZH2 complexes with DDB1-DDB2 and promotes DDB2 stabilit

65 Thus, the Ezh2 conditional knockout mouse model may be useful to e

66 Therefore, Ezh2 coordinates the repression of multiple gene program

67 These results reveal that DSCR6 and Ezh2 critically and post-translationally regulate Stat3

68 Targeting the EZH2/DAB2IP/C-JUN axis therefore presents a promising st

69 e, genetic and pharmacological inhibition of EZH2 decreases the repopulating potential of p53 mutant

70 However, adult Ezh2-deficient B lymphocytes expressed Lin28b, which enc

71 Thus, the interaction between ARID1A and EZH2 defines cancer IFN responsiveness and immune evasio

72 l domain, abrogates both TGF-beta-stimulated EZH2 degradation and FN release.

73 est homolog 2 (EZH2) and specifically causes EZH2 degradation via lysosomes, reducing the cellular H3

74 cular bone mass from pre-osteoblast specific Ezh2 deletion (Ezh2(flox/flox) Osx-Cre(+) cko) mice comp

75 Further gain and loss of AOX1 confirm the EZH2-dependent activation, metabolic deregulation, and t

76 r epigenetic control of SATB2 expression via Ezh2-dependent mechanisms.

77 EZH2 depletion causes cellular cisplatin and UV hypersen

78 Mechanistically, both HMGA2 and EZH2 displaced Groucho/TLE1 from TCF-4 and served as gat

79 ed H3K36 occupies a critical position in the EZH2-DNA interface.

80 This is consistent with EZH2-driven dedifferentiated invasive states associated

81 ostic classification of sequence variants in EZH2, EED, and SUZ12 supports the emerging paradigm shif

82 es showed PRC2, consisting of five subunits (EZH2, EED, SUZ12, AEBP2 and RBBP4), bound to a 2.5-kb DN

83 The crystal structure of an EZH2-EED binary complex indicates that the EZH2 TAD medi

84 of three core subunits, enhancer of zeste 2 (EZH2), embryonic ectoderm development (EED), and suppres

85 cent studies also suggest that inhibition of EZH2 enhances the response to tumor immunotherapy.

86 However, inhibitors of EZH2 enzymatic activity have not shown the expected effi

87 In vivo, cholangiocyte-selective knockout of EZH2 exacerbates bile duct ligation-induced fibrosis whe

88 SUMOylation regulated EZH2 expression by enhancing binding of the E2F1 transcr

89 We found that EZH2 expression correlates with NPC growth potential and

90 EZH2 expression results in the silencing of genes that s

91 dm5b and Kdm6b expression, whereas Ash1l and Ezh2 expression were induced by transcription factor MeC

92 correlating with higher levels of c-Myc and EZH2 expression.

93 To determine the role of uterine EZH2, Ezh2 was conditionally deleted using progesterone

94 from pre-osteoblast specific Ezh2 deletion (Ezh2(flox/flox) Osx-Cre(+) cko) mice compared with those

95 specific EZH2 KO mice, generated by crossing EZH2 floxed mice with adiponectin-Cre mice, displayed si

96 Furthermore, targeting EZH2 for depletion with DZNep strongly sensitizes SCLC c

97 n lncRNA with EZH2 can alter the affinity of EZH2 for its protein-binding partners to regulate cancer

98 nism underlying the functional conversion of EZH2 from a gene repressor to an activator is unclear.

99 androgen-response-elements, which switch the EZH2 function from histone-methyltransferase to non-hist

100 ediction that drug-induced interference with EZH2 function increases the proportion of pro-memory/pro

101 dendritic cell (FDC) networks and recurrent EZH2 gain-of-function mutations.

102 ubjects, we show that pathogenic variants in EZH2 generate a highly specific and sensitive DNAm signa

103 Here, we show that EZH2 harbors a hidden, partially disordered transactivat

104 Here, we show that EZH2 has a non-catalytic and PRC2-independent role in st

105 EZH2 has been involved in epithelial-mesenchymal transit

106 EZH2 has been traditionally known to mediate histone H3K

107 talytic subunit enhancer of zeste homolog 2 (EZH2) have never been found.

108 studies have uncovered an important role for EZH2 in cancer progression and have suggested that it ma

109 ings demonstrate that manipulation of T-cell EZH2 in cellular therapies may yield cellular products a

110 Knockdown of Ezh2 in EOCCs and ST2 cells increased SATB2 expression;

111 pathway revealed that CDK4/6 phosphorylated EZH2 in keratinocytes, thereby triggering a methylation-

112 Disruption of Ezh1 and Ezh2 in livers caused perinatal hepatocytes to different

113 01, resulting in the upregulation of OGT and EZH2 in metastatic CRC, thus forming a vicious cycle.

114 ltransferases EZH1 (enhancer of zeste 1) and EZH2 in NPC maintenance.

115 C-JUN and can be epigenetically silenced by EZH2 in OCSC.

116 al proof-of-principle evidence for targeting EZH2 in patients with MB.

117 -catalytic and PRC2-independent function for EZH2 in promoting NER through DDB2 stabilization, sugges

118 ed ubiquitin linkage and chain elongation on EZH2 in response to TGF-beta.

119 t EZH1 could partially safeguard the role of EZH2 in the formation of H3K27me2.

120 However, the role of EZH2 in this setting is unclear due to the context-depen

121 However, inhibition of EZH2 induced lipid accumulation in certain cancer and he

122 repressive complex 2 (PRC2), with a focus on EZH2 inhibition as a potentially promising approach to e

123 Pharmacological EZH2 inhibition diminished H3K27me3 histone markers, inc

124 mediated, p53-independent mechanism by which EZH2 inhibition leads to mitochondrial dysfunction and t

125 in adipocytes was lipoprotein-dependent, and EZH2 inhibition or gene deletion promoted lipoprotein-de

126 Collectively, these results indicate that EZH2 inhibition promotes lipoprotein-dependent lipid acc

127 Here we show that EZH2 inhibition upregulates MAD2L2 and sensitizes HR-pro

128 EZH2 inhibition upregulates MAD2L2 to decrease DNA end r

129 ID1A, KDM6, and BAP1 are highly sensitive to EZH2 inhibition, thus increasing its potential as a ther

130 most epithelioid sarcomas, are sensitive to EZH2 inhibition.

131 MDSCs in the colons, which are essential for EZH2 inhibitor activity.

132 tudies using the PDX mouse model proved that EZH2 inhibitor could block the Enz-induced NED.

133 Coadministration of EZH2 inhibitor GSK126 and RAC1 inhibitor NSC23766 suppre

134 also partially rescued by treatment with an EZH2 inhibitor in several leukemia cell lines.

135 Treating AML cells with an EZH2 inhibitor partially restored the expression of appr

136 Significantly, EZH2 inhibitor sensitizes CARM1-high, but not CARM-low,

137 titative scale, we examine the impacts of an EZH2 inhibitor through the lens of ChIP-Seq.

138 the Polycomb complex and are diminished upon EZH2 inhibitor treatment.

139 rthermore, the combination of either CDK2 or EZH2 inhibitor with tamoxifen effectively suppresses tum

140 nd safety of tazemetostat, an oral selective EZH2 inhibitor, in patients with epithelioid sarcoma.

141 fety of tazemetostat, a first-in-class, oral EZH2 inhibitor, in patients with follicular lymphoma.

142 zemetostat), an enhancer of zeste homolog 2 (EZH2) inhibitor approved for clinical trials, blocks MB

143 t also proposes the repurposing of CDK4/6 or EZH2 inhibitors as a new therapeutic option for patients

144 These results suggest that EZH2 inhibitors may be most effectively targeted to immu

145 mportantly, topical application of CDK4/6 or EZH2 inhibitors on the skin was sufficient to fully prev

146 Consequently, EZH2 inhibitors or KDM8 knockdown both resensitize the c

147 inhibitors, BET bromodomain inhibitors, and EZH2 inhibitors, as mutations in SWI/SNF complex compone

148 To determine correlates of response to EZH2 inhibitors, we screened a panel of 53 melanoma cell

149 natures that were reversed by treatment with EZH2 inhibitors.

150 athways that are known to abnormally convert EZH2 into a gene activator in cancer cells can now be un

151 e show that the first SANT domain (SANT1) of EZH2 is a histone binding domain with specificity for th

152 EZH2 is commonly overexpressed in cancer and shows activ

153 The histone methylase EZH2 is frequently dysregulated in melanoma and is assoc

154 issue of Cancer Cell, it is shown that, when EZH2 is functionally silenced, HR+, CARM1-high, high-gra

155 EZH2 is involved in global transcriptional repression, m

156 nding protein and histone methyltransferase, EZH2 is not known to be a nuclease.

157 Oncogenic EZH2 is overexpressed and extensively involved in the pa

158 in primary cells, and that elevated soluble EZH2 is part of an error-prone mechanism by which modify

159 We conclude that EZH2 is required for NPC renewal potential and that temp

160 using a multi-omics approach, we found that Ezh2 is required for the deposition of H3K27me3 and is e

161 Here we show that maternal EZH2 is required for the establishment of H3K27me3 in mo

162 Among them, Ezh2 is responsible for catalyzing the epigenetic repres

163 orrelates with NPC growth potential and that EZH2 is the dominant H3K27 methyltransferase in NPCs and

164 Enhancer of Zeste Homolog 2 (EZH2) is the catalytic subunit of Polycomb Repressive Co

165 Enhancer of zeste homolog 2 (EZH2) is the catalytic subunit of polycomb repressive co

166 Enhancer of Zeste Homolog 2 (EZH2) is the catalytic subunit of Polycomb Repressor Com

167 thyltransferase enhancer of zeste homolog 2 (EZH2) is the enzymatic catalytic subunit of the polycomb

168 e highlight the recent advances in targeting EZH2, its successes, and potential limitations, and we d

169 phorylation along with a concomitant loss of EZH2 K222 ubiquitination, suggesting a phosphorylation-d

170 s at which EZH1/EZH2 are automethylated with EZH2-K510 and EZH2-K514 being the major such sites in vi

171 1/EZH2 are automethylated with EZH2-K510 and EZH2-K514 being the major such sites in vivo.

172 Knockdown of Ash1l, Ezh2, Kdm5b, and Kdm6b by specific small interfering RNA

173 helium-specific enhancer of zeste homolog 2 (EZH2) knockout mice to show the general applicability of

174 Moreover, adipocyte-specific EZH2 KO mice, generated by crossing EZH2 floxed mice wit

175 A deletion mutant of EZH2, lacking its N-terminal domain, abrogates both TGF-

176 During disease induction, Ezh2 loss derepresses a subset of bivalent promoters tha

177 mined the importance of cellular context for Ezh2 loss during the evolution of acute myeloid leukemia

178 Unlike Ezh2 loss of function, dual inactivation of Ezh1 and Ezh

179 h as Plag1, whose overexpression phenocopies Ezh2 loss to accelerate AML induction in mouse models.

180 g a specific O-GlcNAcylation that determines EZH2 lysosomal degradation, rather than the traditional

181 Our results showed that TET2, EZH2, MAD2 and CDC20 were aberrantly expressed in AML pa

182 Enhancer of zeste homolog 2 (EZH2)-mediated trimethylation of histone 3 lysine 27 (H3

183 recruiting FOXM1 through EZH2 to antagonize EZH2-mediated effects at target genes.

184 ation and overexpression of LRRC16A explains EZH2-mediated fibroblast migration in SSc.

185 -interacting protein (DAB2IP) is silenced by EZH2-mediated H3K27 trimethylation of the DAB2IP promote

186 H2 via its carboxyl terminal and antagonized EZH2-mediated IFN responsiveness.

187 mpanied by increased Polycomb repression and EZH2-mediated redistribution of H3K27me3 toward promoter

188 to bind Snail and, in turn, trigger H3K27me3/EZH2-mediated repression of Snail epithelial target gene

189 Mouse intestinal cells lacking EZH2 methyltransferase reduce H3K27me3 proportionately a

190 SUMOylation resulted in decreased levels of EZH2 mRNA and protein as well as reduced H3K27me3 levels

191 of SUMOylation not only resulted in reduced EZH2 mRNA and protein levels but also increased expressi

192 by directly suppressing miR-137 that targets EZH2 mRNA, and increased expression of EZH2 activates ce

193 onths (95% CI 7.2-not estimable [NE]) in the EZH2(mut) cohort and 13.0 months (5.6-NE) in the EZH2(WT

194 69% (95% CI 53-82; 31 of 45 patients) in the EZH2(mut) cohort and 35% (23-49; 19 of 54 patients) in t

195 w-up was 22.0 months (IQR 12.0-26.7) for the EZH2(mut) cohort and 35.9 months (24.9-40.5) for the EZH

196 15, and May 24, 2019, 99 patients (45 in the EZH2(mut) cohort and 54 in the EZH2(WT) cohort) were enr

197 nts were categorised by EZH2 status: mutant (EZH2(mut)) or wild-type (EZH2(WT)).

198 t transgenic expression of phospho-mimicking EZH2 mutant EZH2(T416D) in mammary glands leads to tumor

199 EZH2 mutant human lymphoma cells also require multiple d

200 amming T cells to express a gain-of-function EZH2 mutant resulted in an enhanced ability of T cells t

201 Thus, EZH2 mutation fosters malignant transformation by epigen

202 ficient tumour tissue for central testing of EZH2 mutation status.

203 Herein, we show that EZH2 mutations initiate FL by attenuating GC B cell requ

204 vidence showing enhancer of zeste homolog 2 (EZH2) negatively regulated CBX6 expression in a Polycomb

205 r inducer of EMT, requires HOTAIR to recruit EZH2 on specific epithelial target genes (i.e., HNF4alph

206 YAP colocalized with YY1 and EZH2 on the genome to transcriptionally repress a broad

207 (H3K27M), but not in cells that carry either EZH2 or EED mutants that abrogate PRC2 allosteric activa

208 Down-regulation of EZH2 or TET2 expression inhibited apoptosis, affected MA

209 ule inhibitors have been developed to target EZH2 or the PRC2 complex, with some of these inhibitors

210 We show that Ezh2 overexpression and activity are pivotal in ErbB2-me

211 may serve as a potential strategy to address EZH2 overexpression and improve current cancer therapeut

212 nt biological insights into the mechanism of EZH2 overexpression in cancers and suggest that inhibiti

213 ST2 cells increased SATB2 expression; while Ezh2 overexpression in EOCCs and ST2 cells decreased SAT

214 EZH2 overexpression suppressed TGF-beta-induced FN prote

215 sting a need for other strategies to address EZH2 overexpression.

216 er, we found a hyperactivation of the CDK4/6-EZH2 pathway in human and mouse psoriatic skin lesions.

217 further confirm the activated c-Myc-miR-137-EZH2 pathway in platinum drug-resistant or recurrent ova

218 Inhibition of c-Myc-miR-137-EZH2 pathway re-sensitizes resistant cells to cisplatin.

219 Furthermore, interference with Ezh2 phosphorylation also prevented Stat3 lysine methyla

220 EZH2 TAD can be unlocked by cancer-specific EZH2 phosphorylation events to undergo structural transi

221 Thus, inhibition of either Ezh2 phosphorylation or Stat3 lysine methylation compens

222 Therefore, TET2 and EZH2 play a tumor-inhibiting role in AML that affects CI

223 TET2 and EZH2 play important roles in the epigenetic regulation i

224 By impairing T cell help, mutant EZH2 prevents induction of proliferative MYC programs.

225 Loss of EZH2 promoted stratification of uterine epithelium, an u

226 of the E2F1 transcriptional activator to the EZH2 promoter.

227 cleavage rate by >100-fold, suggesting that EZH2 promotes a cleavage-competent RNA conformation.

228 Ezh2 promotes Stat3 activation in ventral mesoderm forma

229 Mechanistically, targeting EZH2 promotes transition from H3K27me3 to H3K27ac at the

230 Proteasome inhibition rescued EZH2 protein and led to reduced FN production.

231 in NKTL, and its expression correlates with EZH2 protein expression as determined by tissue microarr

232 , which likely promoted the EMT by enhancing EZH2 protein stability and function.

233 likely promotes CRC metastasis by enhancing EZH2 protein stability and function.

234 In this study, we examine EZH2 protein turnover in NKTL and identify MELK kinase a

235 led to ubiquitination and destabilization of EZH2 protein.

236 We show that, in the absence of SUZ12, EZH2 remains bound to EED but loses its interaction with

237 At the chromatin level, EZH1 and EZH2 restricted accessibility to AP-1-binding motifs, an

238 Inhibition of EZH2 resulted in de-repression of IHH, decreased self-re

239 Loss of Ezh2 resulted in dorsalization of ventral mesoderm and f

240 ion between B2 RNA and the Polycomb protein, EZH2, results in cleavage of B2 RNA, release of B2 RNA f

241 FOXM1), DNA replication regulators (CDKN1A, EZH2, RRM2), G1/S-transition regulators (CCNB1, CCND1, R

242 sis, we observed a MELK-mediated increase of EZH2 S220 phosphorylation along with a concomitant loss

243 We found that the EZH2-selective inhibitor GSK126 induced lipid accumulati

244 ltransferase, enhancer of zeste homologue 2 [Ezh2]) showed that this phenotype was associated with in

245 -dependent biomarkers for beta-CATENIN/HMGA2/EZH2 signaling predictive of reduced relapse-free surviv

246 tion of Star and Cyp11b1 and upregulation of Ezh2, similar to ACC patients with a poor prognosis.

247 8-nt helix-loop intimately contacts multiple EZH2 sites surrounding T309, a known O-GlcNAcylation sit

248 mportant role of MELK and USP36 in mediating EZH2 stability in NKTL.

249 ults suggest targeting the Enz/AR/lncRNA-p21/EZH2/STAT3 signaling may help urologists to develop a tr

250 Patients were categorised by EZH2 status: mutant (EZH2(mut)) or wild-type (EZH2(WT)).

251 so increased expression of genes silenced by EZH2, such as E-cadherin, which suppresses epithelial-me

252 b repressive complex 2, with core components EZH2, SUZ12, and EED, is responsible for writing histone

253 are enriched in polycomb repressive complex (EZH2/SUZ12) recognizing regions.

254 Coexpression of EZH2(T416D) in mammary epithelia of HER2/Neu transgenic

255 expression of phospho-mimicking EZH2 mutant EZH2(T416D) in mammary glands leads to tumors with TNBC

256 The EZH2 TAD can be unlocked by cancer-specific EZH2 phospho

257 The EZH2 TAD comprises the SRM (Stimulation-Responsive Motif

258 The EZH2 TAD directly interacts with the transcriptional coa

259 n EZH2-EED binary complex indicates that the EZH2 TAD mediates protein oligomerization in a noncanoni

260 rstood in a common structural context of the EZH2 TAD.

261 The expression of putative EZH2 target genes was shown to be highly relevant to the

262 s reveal a non-methyltransferase function of EZH2 that controls protein translation of p53 GOF mutant

263 immune cells of enhancer of zeste homolog 2 (EZH2), the catalytic subunit of polycomb repressive comp

264 are two SANT domains in Enhancer of Zeste 2 (EZH2), the catalytic subunit of the Polycomb Repressive

265 nt at the ADGRB1 promoter, and inhibition of EZH2, the catalytic component of the Polycomb Repressive

266 Elevated expression of EZH2, the enzymatic subunit of polycomb repressive compl

267 s lysine methyltransferase inhibitor targets EZH2, the enzymatic subunit of the PRC2 transcriptional

268 The relay of interactions between EZH2, the nucleosomal DNA and the H3 N-terminus therefor

269 EZH1 and EZH2 thereby promote liver homeostasis and prevent liver

270 h represses CDKN1A expression indirectly via EZH2, thereby accelerating cell-cycle transit.

271 induced in hepatocytes with loss of Ezh1 and Ezh2-these genes included those that regulate hepatocyte

272 iving the switch from the SWI/SNF complex to EZH2 through methylating the BAF155 subunit of the SWI/S

273 GF-beta regulates proteasomal degradation of EZH2 through N-terminal, K63-linked ubiquitination in ch

274 e gene promoters by recruiting FOXM1 through EZH2 to antagonize EZH2-mediated effects at target genes

275 SCIRT specifically interacted with EZH2 to increase EZH2 affinity to FOXM1 without binding

276 reveals how binding of its catalytic subunit EZH2 to nucleosomal DNA orients the H3 N-terminus via an

277 ylation at inducible NO synthase promoter by Ezh2 to suppress their expression in macrophages.

278 bine treatment restored TET2 methylation and EZH2 transcription and ameliorated CIN in AML.

279 e (Lys) residue on target proteins, enhances EZH2 transcription.

280 s of function, dual inactivation of Ezh1 and Ezh2 triggered overexpression of the transcriptional rep

281 L and identify MELK kinase as a regulator of EZH2 ubiquitination and turnover.

282 Therefore, modulation of EZH2 ubiquitination status by targeting MELK may be a ne

283 ib treatment in NKTL based on deprivation of EZH2 ubiquitination.

284 ng a phosphorylation-dependent regulation of EZH2 ubiquitination.

285 However, the mechanisms regarding EZH2 upregulation is poorly understood, and it still rem

286 Mechanistically, ARID1A interacted with EZH2 via its carboxyl terminal and antagonized EZH2-medi

287 To determine the role of uterine EZH2, Ezh2 was conditionally deleted using progesterone recept

288 fferent cancer types, expression of UBA2 and EZH2 was positively correlated.

289 xes containing the histone methyltransferase EZH2 were detected in the genomic regions of the STB-spe

290 gene expression are coregulated by SOX2 and EZH2, which colocalize at CpG islands.

291 ic variants in the histone methyltransferase EZH2, which encodes a core component of the Polycomb rep

292 tion of the polycomb group proteins BMI1 and EZH2, which formed complexes with PARP1 during the DNA d

293 In this study, we demonstrate that Ezh2, which represses gene expression through methylatio

294 Our data suggest that manipulation of T-cell EZH2 within the context of cellular therapies may yield

295 rt and 35% (23-49; 19 of 54 patients) in the EZH2(WT cohort.) Median duration of response was 10.9 mo

296 ts (45 in the EZH2(mut) cohort and 54 in the EZH2(WT) cohort) were enrolled in the study.

297 ) cohort and 35.9 months (24.9-40.5) for the EZH2(WT) cohort.

298 (mut) cohort and 13.0 months (5.6-NE) in the EZH2(WT) cohort; median progression-free survival was 13

299 ZH2 status: mutant (EZH2(mut)) or wild-type (EZH2(WT)).

300 histone methylation in constitutively active EZH2((Y641)) mutant melanoma and assessed whether these