ライフサイエンスコーパス: EZH2

1 r of zeste 1 (EZH1) and enhancer of zeste 2 (EZH2).

2 thyltransferase enhancer of zeste homolog 2 (EZH2).

3 the lower activity towards unphosphorylated EZH2.

4 and attaches poly-ADP-ribose (PAR) chains to EZH2.

5 richment of gene targets shared by FOXP3 and EZH2.

6 ed neuroblastomas expressed higher levels of EZH2.

7 h recruitment of the H3K27 methyltransferase EZH2.

8 show that WT1 also suppresses translation of EZH2.

9 2 function) and enhancer of zeste homolog 2 (EZH2) (a histone methyltransferase).

10 Purpose Enhancer of zeste homolog 2 (EZH2), a chromatin remodeler, is implicated in the patho

11 d on functional enhancer of zeste homolog 2 (EZH2), a component of polycomb repressive complex 2 (PRC

12 EZH2, a histone methyl transferase subunit of a Polycomb

13 ylation at Ser-96 resulted in recruitment of EZH2 across the ERG-cistrome and a genome-wide loss of E

14 EZH2 activated the Notch pathway by suppressing Notch re

15 Ezh2 activates Id3 while silencing Id2, Prdm1 and Eomes,

16 ct with EZH2 and subsequently inhibit HOTAIR-EZH2 activity and resensitize resistant ovarian tumors t

17 ationale for the pharmacologic inhibition of EZH2 activity in large-cell transformed cutaneous T-cell

18 and ARPC5) and stem cell molecules CD44 and EZH2, all of which are validated as direct and functiona

19 tations in both wild-type (WT) and GOF Y641N EZH2 alleles.

20 ping event in Enhancer of Zeste Homologue 2 (EZH2) along with expression changes showed significant d

21 Ezh2, although enriched in the embryonic retina, was not

22 tween Snail and enhancer of zeste homolog 2 (EZH2), an enzymatic subunit of the polycomb-repressive c

23 Here, we show enhancer of zeste homolog 2 (EZH2), an enzyme that catalyzes H3 lysine trimethylation

24 polycomb group proteins like RING1A, RING1B, EZH2 and also altered the expression of proteins associa

25 r mutations in epigenetic regulators such as EZH2 and ASXL1 also play a role in disease initiation an

26 Our study reveals that EZH2 and B2 together control activation of a large netwo

27 DDB2 recruited EZH2 and beta-catenin at an upstream site in the Rnf43 g

28 oth proneural and mesenchymal GSCs, combined EZH2 and BMI1 targeting proved more effective than eithe

29 Akt activation phosphorylates Ezh2 and decreases its control of these transcriptional

30 34a expression is silenced epigenetically by EZH2 and DNA methylation, which promotes CCA cell growth

31 eby recruiting the histone methyltransferase EZH2 and elevating H3K27me3 levels, thus conferring a re

32 potentially through modulation of the eIF4E, EZH2 and ERK pathways.

33 Recent studies have shown that EZH2 and EZH1 are not functionally redundant and inhibit

34 unctionally redundant and inhibition of both EZH2 and EZH1 is necessary to block the progression of c

35 as well as the first targetable versions of Ezh2 and Friend of GATA-1 (FOG1)).

36 uced EZH2 ubiquitination with an increase of EZH2 and H3K27me3 levels in PCa cells.

37 63-linked ubiquitination of EZH2 to decrease EZH2 and H3K27me3 levels in PCa cells.

38 We observed aberrant upregulation of Skp2, Ezh2 and histone H3 lysine 27 trimethylation (H3K27me3)

39 A role for MUC1-C in regulating EZH2 and histone methylation is not known.

40 ion of mutation status of 7 genes, including EZH2 and MEF2B, improves risk stratification.

41 diverse human carcinoma cells downregulates EZH2 and other PRC2 components.

42 fic interaction between the polycomb protein EZH2 and RNA made from B2 SINE retrotransposons controls

43 gulates plasticity and that miR302 regulates EZH2 and Snail independently.

44 of epigenetic reprogramming factors such as Ezh2 and Sox2.

45 tified loss of the histone methyltransferase EZH2 and subsequent reduction of histone H3K27 trimethyl

46 block the ability of HOTAIR to interact with EZH2 and subsequently inhibit HOTAIR-EZH2 activity and r

47 phosphorylation resulted in dissociation of EZH2 and SUZ12, components of polycomb repressive comple

48 y disrupted association of the PRC2 subunits EZH2 and SUZ12, thereby inhibiting PRC2 assembly.

49 complexed with the histone methyltransferase EZH2 and transcription factors YY1 and IKZF3.

50 esults support PRC2-independent functions of EZH2 and TRIM28 in activation of gene expression that pr

51 (H3K27me3) at the DPYD promoter regulated by Ezh2 and UTX suppresses DPYD expression by inhibiting tr

52 thyltransferase enhancer of zeste homolog 2 (Ezh2) and its trimethylation of histone H3 on Lysine 27

53 frequently mutated CMGs (KMT2D, CREBBP, and EZH2) and point to a role for these events in modifying

54 netic regulator enhancer of zeste homolog 2 (EZH2) and that EZH2 controls histone H3 lysine 27 trimet

55 P1 to be significantly downregulated in both EZH2- and MEF2B-mutated cases.

56 r genes that are differentially expressed in EZH2- and MEF2B-mutated cases.

57 ing of each component suggest that Smad3 and EZH2 are part of a complex that regulates plasticity and

58 gs establish Akt-mediated phosphorylation of Ezh2 as a critical target to potentiate antitumor immuno

59 ltiple diseases and led to identification of Ezh2 as a drug target.

60 cancer arises from disruption of the role of EZH2 as a master regulator of transcription.

61 way that governs GNA-mediated destruction of EZH2 as a promising anti-cancer strategy.

62 Overall, our results highlight EZH2 as a rational target for therapeutic intervention i

63 o suggests that the noncanonical function of EZH2 as a transcriptional activator upregulates a set of

64 Here we review the spectrum of EZH2-associated mutations, discuss the mechanisms underl

65 m enhanced CDK1-dependent phosphorylation of EZH2 at Thr487.

66 Pharmacologic or genetic depletion of EZH2 augmented TxnIP expression and oxidative stress in

67 ation at potential histone methyltransferase EZH2-binding sites.

68 letion, was rescued by ectopic expression of EZH2 but not by TRIM28 expression or by EZH2 mutated at

69 The pattern of high EZH2, but low H3K27me3 mark, is also prevalent in human

70 ease model, we found that phosphorylation of EZH2 by JAK3 promotes the dissociation of the PRC2 compl

71 PARylation of EZH2 by PARP1 then induces PRC2 complex dissociation and

72 Inhibition of EZH2 by RNA interference or pharmacological treatment wi

73 Knockdown of EZH2 by shRNA or siRNA resulted in inhibition of cell gr

74 methyltransferase activity and reconcile how EZH2 can be associated with both gene repression and act

75 Here, we investigated whether inhibition of Ezh2 can be leveraged for bone stimulatory applications.

76 Histone methyltransferases EZH1 and EZH2 catalyse the trimethylation of histone H3 at lysine

77 cells also exhibited enhanced expression of EZH2 coincident with Snail upregulation.

78 n the formation of a tripartite Snail/HOTAIR/EZH2 complex.

79 , we show that the histone methyltransferase Ezh2 controls CD8(+) T memory precursor formation and an

80 s defining a positive feedback loop in which EZH2 controls GC B cell proliferation by suppressing CDK

81 enhancer of zeste homolog 2 (EZH2) and that EZH2 controls histone H3 lysine 27 trimethylation on the

82 Moreover, oncogenic BCL6 and EZH2 cooperate to accelerate diffuse large B cell lympho

83 Overall, our results suggest that loss of Ezh2 cooperates with Jak2V617F in the development of MF

84 also show that MUC1-C binds directly to the EZH2 CXC region adjacent to the catalytic SET domain and

85 We find that EZH2 deficiency in FOXP3(+) T cells results in lethal mu

86 In a murine model of lymphoid-specific EZH2 deficiency we found that EZH2 was required for prop

87 RNA sequencing in Ezh2-deficient hematopoietic stem cells (HSCs) and megak

88 nd expansion of megakaryocytic precursors in Ezh2-deficient Jak2V617F mice.

89 Deletion of Cdkn2a in EZH2-deficient lymphocytes prevented p53 stabilization,

90 Here, we show that p38alpha kinase promotes EZH2 degradation in differentiating muscle cells through

91 ys668 within the EZH2-SET domain, triggering EZH2 degradation through COOH terminus of Hsp70-interact

92 of HSP90, CDK1 and the proteasome prevented EZH2 degradation, decreased HOX gene expression and rest

93 Of special interest, EZH2(Delta/Delta)FOXP3(+) mice develop spontaneous infla

94 We further demonstrate that EZH2(Delta/Delta)FOXP3(+) T cells lack a regulatory phen

95 e that lack EZH2 specifically in Treg cells (EZH2(Delta/Delta)FOXP3(+)).

96 Small-molecule inhibitors against EZH2 demonstrated anti-tumor activity in EZH2-mutated ly

97 significantly suppressed tumor growth in an EZH2-dependent manner, and tumors bearing a non-GNA-inte

98 Mammosphere formation, inhibited by EZH2 depletion, was rescued by ectopic expression of EZH

99 Loss of Ezh2 derepresses expression of myocardin and Tbx18, whic

100 ession of CCN3 by the Polycomb group protein EZH2 disrupted this negative feedback loop in both CRPC

101 oneural GSCs are preferentially sensitive to EZH2 disruption, whereas mesenchymal GSCs are more sensi

102 plex and TRIM28, which formed a complex with EZH2 distinct from PRC2.

103 ons in six epigenetic regulation genes-NSD1, EZH2, DNMT3A, CHD8, HIST1H1E, and EED-accounted for 44%

104 Unexpectedly, Eed and Eed/Ezh2 double mutants exhibit delayed superficial cell dif

105 RPi attenuates alkylating DNA damage-induced EZH2 downregulation, thereby promoting EZH2-mediated gen

106 1 then induces PRC2 complex dissociation and EZH2 downregulation, which in turn reduces EZH2-mediated

107 eover, the transcription factor E2F1 induces EZH2 during the GC reaction.

108 ycomb repressive complex 2 (PRC2) components EZH2, EED, and SUZ12.

109 lead to or result from deregulation of FOXP3/EZH2-enforced T cell gene networks contributing to the u

110 Histone methyl transferase EZH2 (Enhancer of Zeste Homolog 2) is generally associat

111 Previous work has demonstrated that Ezh2 (enhancer of zeste homolog 2), a histone 3 lysine 2

112 expression include histone methyltransferase EZH2 (enhancer of zeste homolog 2), COX2 (cyclooxygenase

113 plex also sequesters a core subunit of PRC2 (Ezh2 [enhancer of zeste homolog 2]) at the cell membrane

114 Pharmacological inhibition of EZH2 erased those marks and restored IRE1 expression and

115 Conclusion EZH2 expression accurately predicts risk of RCC death be

116 ne, concomitant with the re-establishment of EZH2 expression and blast clearance.

117 sly unreported role for MUC1-C in activating EZH2 expression and function in cancer cells.

118 Accordingly, MEK-ERK depletion decreased EZH2 expression in cells harboring the KRAS(G12C) mutati

119 g and Western blot analyses showed increased EZH2 expression in human CCA tissues and cell lines.

120 The endogenous loss of EZH2 expression in resistant cells and primary blasts fr

121 udy, we investigated the mechanisms by which EZH2 expression is regulated in non-small cell lung carc

122 Modulating EZH2 expression or activity suppressed phosphorylation o

123 tation, whereas PI3K/AKT depletion decreased EZH2 expression, EZH2 phosphorylation, and STAT3 activit

124 GC responses, which is rescued by restoring EZH2 expression, thus defining a positive feedback loop

125 s lack key NHRS (Nr2e3, RORA) or epigenetic (Ezh2) factors.

126 mbryonic stem cells with deletion of EZH1 or EZH2 fail to differentiate into ectoderm lineages.

127 ed and lysine(K) 63-linked ubiquitination of EZH2 for degradation.

128 ste 2 polycomb repressive complex 2 subunit (EZH2), forming repressive H3K27(me3) marks.

129 etion of the histone methyltransferase (HMT) Ezh2 from all retinal progenitors resulted in progressiv

130 t deletion of the histone methylating enzyme EZH2 from podocytes decreased H3K27me3 levels and sensit

131 hese results, targeting MUC1-C downregulates EZH2 function as evidenced by (i) global and promoter-sp

132 mutations, discuss the mechanisms underlying EZH2 function, and synthesize a unifying perspective tha

133 mouse model in which the most common somatic Ezh2 gain-of-function mutation (EZH2(Y646F) in human; Ez

134 n to evaluate the association of tumor-based EZH2 gene and protein expression with survival in three

135 by these results, we assessed the FOXP3 and EZH2 gene networks by RNA sequencing in isolated intesti

136 an important signaling network of SKP2-TRAF6-EZH2/H3K27me3, and targeting SKP2-EZH2 pathway may be a

137 Enhancer of zeste homolog 2 (EZH2) has been characterized as a critical oncogene and

138 ients in The Cancer Genome Atlas cohort with EZH2-high gene expression were 1.5 times more likely to

139 rly, patients in the Mayo Clinic cohort with EZH2-high protein expression were 1.4 times more likely

140 Patients in the Mayo Clinic cohort with EZH2-high protein expression were nearly two times more

141 exas Southwestern Medical Center cohort with EZH2-high protein expression were two times more likely

142 The EZH2 histone methyltransferase is a member of the polyco

143 The EZH2 histone methyltransferase is required for B cells t

144 Our results uncover a crucial role for EZH2 in adaptive lymphocytes to control the developmenta

145 lso additional strategies to combat roles of EZH2 in cancer.

146 e we show that the combined loss of Ezh1 and Ezh2 in chondrocytes severely impairs skeletal growth in

147 ) and followed by proteasomal degradation of EZH2 in drug-resistant cells.

148 ucer genes through H3K27me3, and deletion of Ezh2 in early pubertal mice results in premature cellula

149 s study, we show that JAK2-V617F and loss of Ezh2 in hematopoietic cells contribute synergistically t

150 igenetic reader protein EED, associated with Ezh2 in PRC2, has an additional function to stimulate th

151 veals a mesothelial cell-autonomous role for Ezh2 in repression of the smooth muscle differentiation

152 ss the enhanced enzymatic function of mutant EZH2 in some lymphomas.

153 most localized contributions, we identified EZH2 in the cerebellum, NR3C1 in the cerebral cortex and

154 ons in epigenetic regulator genes, including EZH2 In this study, we show that JAK2-V617F and loss of

155 To further address the role for EZH2 in Treg cellular function, we have now generated mi

156 ated polyubiquitination of recombinant human EZH2 in vitro.

157 nsferase enzyme enhancer of zeste homolog 2 (EZH2) in attenuating oxidative injury in podocytes, focu

158 2- and methyltransferase-independent role of EZH2 indicates that a complete suppression of all oncoge

159 Genetic and pharmacological suppression of EZH2 inhibited neuroblastoma growth in vitro and in vivo

160 Furthermore, Ezh2 inhibition also alleviated bone loss in an estrogen

161 y provide a rationale for combining PARP and EZH2 inhibition as a therapeutic strategy for BRCA-mutat

162 EZH2 inhibition decreased the looping at the CDKN2A/B lo

163 Ezh2 inhibition enhanced expression of Wnt10b and Pth1r

164 was associated with cellular sensitivity to EZH2 inhibition in SMARCA4 mutant cancer models, indepen

165 The induction of SMARCA2 in response to EZH2 inhibition is required for apoptosis, but not for g

166 g1 in podocytes, and derepression of Jag1 by EZH2 inhibition or knockdown facilitated podocyte dediff

167 EZH2 inhibition results in a heterogenous phenotypic res

168 the SWI/SNF ATPase, SMARCA4, is sensitive to EZH2 inhibition.

169 rmacological depletion of H3K27me3 using the EZH2 inhibitor GSK343 in HepG2 cells suppressed cell gro

170 tone methylases (EHMT2 inhibitor UNC0638 and EZH2 inhibitor GSK343).

171 Expression of SMARCA2 also delineates EZH2 inhibitor sensitivity for other SWI/SNF complex sub

172 Moreover, the addition of an EZH2 inhibitor sensitizes the BRCA-mutant breast cells t

173 JAK2-V617F-expressing mice treated with an Ezh2 inhibitor showed higher platelet counts than vehicl

174 Reversal of enhancer inactivation using an EZH2 inhibitor upregulates BCL2L11 and induces apoptosis

175 Inclusion of an EZH2 inhibitor with standard cytotoxic therapies prevent

176 Accordingly, treatment with the EZH2 inhibitor, selective S-adenosyl-methionine-competit

177 A new enhancer of zeste homolog 2 (EZH2) inhibitor series comprising a substituted phenyl r

178 rogram in neuroblastoma, and support testing EZH2 inhibitors in patients with MYCN-amplified neurobla

179 We show here that EZH2 inhibitors increased FMR1 expression and significan

180 Clinically relevant Ezh2 inhibitors restore androgen receptor expression and

181 The current EZH2 inhibitors strongly suppress the enhanced enzymatic

182 We further discuss EZH2 inhibitors that are now showing early signs of prom

183 came refractory to biochemical inhibition by EZH2 inhibitors.

184 y between histone deacetylase inhibitors and EZH2 inhibitors.

185 e, breast cancer-derived MCF7 cells revealed EZH2 interactions with subunits of chromatin remodeler S

186 ent discoveries, including ours, have placed EZH2 into the category of transcriptional coactivators a

187 EZH2 is a component of the multi-subunit polycomb repres

188 ndicate that signal-dependent degradation of EZH2 is a prerequisite for satellite cells differentiati

189 EZH2 is crucial for the progression of prostate cancer (

190 The histone methyl transferase EZH2 is frequently altered in many cancers, including cc

191 Our results suggest that EZH2 is involved in regulating ZIC2 and SHANK1 which hav

192 te suppression of all oncogenic functions of EZH2 is needed.

193 Here we report that EZH2 is post-transcriptionally regulated by SKP2 in vitr

194 We and others have shown previously that EZH2 is recruited to the FOXP3 promoter and its targets

195 However, the mechanisms by which EZH2 is regulated in PCa and CRPC remain elusive.

196 The histone methyltransferase EZH2 is required for B and T cell development; however,

197 We show in mouse that the PRC2 component Ezh2 is required to restrict smooth muscle differentiati

198 servations demonstrate that MYCN upregulates EZH2, leading to inactivation of a tumor suppressor prog

199 anism that reduced histone methyltransferase EZH2 leads to a lower trimethylation of histone H3 lysin

200 Finally, patients with reduced EZH2 levels at progression to standard therapy responded

201 SKP2 knockdown decreased EZH2 levels in human PCa cells through upregulation of T

202 s of Skp2 resulted in a striking decrease of Ezh2 levels in Pten/Trp53 double-null MEFs and in prosta

203 Low EZH2 levels resulted in derepression of HOX genes, and k

204 gase Praja1 (PJA1) is involved in regulating EZH2 levels upon p38alpha activation.

205 experience overall death than patients with EZH2-low expression (95% CI, 1.1 to 2.3; P = .028).

206 experience overall death than patients with EZH2-low expression (95% CI, 1.1 to 4.4; P = .034).

207 Ezh2 maintains the repression of key cell senescence ind

208 4a is caused by Enhancer of zeste homolog 2 (EZH2)-mediated H3 lysine 27 trimethylation as well as DN

209 t in the mature retina; these data reveal an Ezh2-mediated feed-forward pathway that is required for

210 duced EZH2 downregulation, thereby promoting EZH2-mediated gene silencing and cancer stem cell proper

211 d EZH2 downregulation, which in turn reduces EZH2-mediated H3 trimethylation.

212 te cancer by a combination of AR binding and EZH2-mediated repression at the GR locus, but is restore

213 Here we show that EZH2 mediates GC formation through repression of cyclin-

214 re the authors use a 3D GC organoid and show EZH2 mediates germinal centre (GC) formation through epi

215 Enhancer of Zeste homologue 2 (EZH2) methylates histone 3 at lysine 27 (H3K27) and abno

216 Polycomb repressive complex 2 (PRC2-EZH2) methylates histone H3 at lysine 27 (H3K27) and is

217 ious compounds recently developed to inhibit EZH2 methyltransferase activity have no such effect.

218 A 'direct tethering' strategy attaching the Ezh2 methyltransferase enzyme to dCas9, as well as a 're

219 GC B cells of Cdkn1a (-/-) Ezh2 (-/-) mice have high levels of phospho-Rb, indicati

220 eletion of Cdkn1a rescues the GC reaction in Ezh2 (-/-) mice.

221 by JAK2-V617F was accentuated in JAK2-V617F;Ezh2(-/-) mice, resulting in very high platelet and neut

222 Engineering T cells with an Akt-insensitive Ezh2 mutant markedly improves their memory potential and

223 These EZH2 mutants retained the substrate specificity of their

224 n of EZH2 but not by TRIM28 expression or by EZH2 mutated at the region (pre-SET domain) of TRIM28 in

225 nst EZH2 demonstrated anti-tumor activity in EZH2-mutated lymphomas and entered clinical trials.

226 d tumors bearing a non-GNA-interacting C668S-EZH2 mutation exhibited resistance to the inhibitors.

227 MDM2 physically associated with EZH2 on chromatin, enhancing the trimethylation of histo

228 However, the effect of EZH2 on outcomes in localized ccRCC is unclear, and mole

229 the catalytic SET domain and associates with EZH2 on the CDH1 and BRCA1 promoters.

230 Silencing EZH2 or inhibiting its histone methyltransferase activit

231 Modulation of PRC2 by either Ezh2 overexpression or Eed deletion enhances KRAS-driven

232 SKP2-TRAF6-EZH2/H3K27me3, and targeting SKP2-EZH2 pathway may be a promising therapeutic strategy for

233 I3K/AKT depletion decreased EZH2 expression, EZH2 phosphorylation, and STAT3 activity in KRAS(G12D)-m

234 antly reduce the growth of NKTL cells, in an EZH2 phosphorylation-dependent manner, whereas various c

235 ression data suggest that DPYD repression by Ezh2 predicts poor survival in 5-FU-treated cancers.

236 EZH2 premature degradation in proliferating myoblasts is

237 In adaptive lymphoid cells EZH2 prevented the premature expression of Cdkn2a and th

238 ectedly, transcriptome profiling showed that EZH2 primarily activates, rather than represses, transcr

239 MUC1-C activates (i) the EZH2 promoter through induction of the pRB-->E2F pathway

240 ChIP analysis showed that MYCN binds at the EZH2 promoter, thereby directly driving expression.

241 ing dedifferentiation and that inhibition of Ezh2 promotes multipotent progenitor expansion.

242 or TxnIP, and in diabetes, downregulation of EZH2 promotes oxidative stress.

243 These data suggest restoration of EZH2 protein as a viable approach to overcome treatment

244 Suppression of EZH2 protein expression induced chemoresistance of AML c

245 ecific death (95% CI, 1.5 to 2.6; P < .001); EZH2 protein expression was particularly prognostic amon

246 Low EZH2 protein levels correlated with poor prognosis in AM

247 noprecipitation and mass spectrometry of the EZH2-protein interactome in estrogen receptor positive,

248 TRIM28 depletion repressed EZH2 recruitment to chromatin and expression of this gen

249 Inhibition of Ezh2/VEC association increases Ezh2 recruitment to claudin-5, VE-PTP, and vWf promoters

250 susceptibility to lymphoma suggests that pRB-EZH2 recruitment to repetitive elements may be cancer re

251 neuroblastoma exhibited strong repression of EZH2-regulated genes.

252 n the polycomb repressive complex (PRC2) and EZH2 represents one such vulnerability in tumors with mu

253 as genetic rescue experiments, revealed that EZH2 represses neuronal differentiation in neuroblastoma

254 Thus, EZH2 represses the transcription factor Pax6, which cont

255 ly and covalently bound to Cys668 within the EZH2-SET domain, triggering EZH2 degradation through COO

256 hemia vera-like disease, concomitant loss of Ezh2 significantly reduced the red blood cell and hemato

257 elease of E2F1.The histone methyltransferase EZH2 silences genes by generating H3K27me3 marks.

258 tion of miR-22 in AML is caused by TET1/GFI1/EZH2/SIN3A-mediated epigenetic repression and/or DNA cop

259 Together, our study uncovers a TET1/GFI1/EZH2/SIN3A/miR-22/CREB-MYC signalling circuit and thereb

260 Loss of Ezh2 specifically in the developing mesothelium reveals

261 nction, we have now generated mice that lack EZH2 specifically in Treg cells (EZH2(Delta/Delta)FOXP3(

262 of high-molecular risk mutation (ie, ASXL1, EZH2, SRSF2, IDH1/ 2), and presence of two or more high-

263 ated reactive oxygen species accumulation in EZH2 suppressed cells and rescued cell growth disadvanta

264 s the GC reaction, we show that depletion of EZH2 suppresses G1 to S phase transition of GC B cells i

265 Moreover, EZH2 suppression de-repressed C-X-C motif chemokine liga

266 However, it remains unclear how EZH2 switches to this catalytic independent function.

267 Jak2V617F mice, indicating a role for these Ezh2 target genes in altered megakaryopoiesis involved i

268 tionally, overexpression of IGFBP3, a direct EZH2 target, suppressed neuroblastoma growth in vitro an

269 CA2 expression as a predictive biomarker for EZH2-targeted therapies in the context of SWI/SNF mutant

270 Here, we report a unique EZH2-targeting strategy by identifying a gambogenic acid

271 pon HBx expression requires methyltrasferase EZH2, TET2 a key factor in cytosine demethylation and in

272 higher levels of the H3K27 methyltransferase EZH2 than the ADC lesions, but there is a clear lack of

273 These data attribute a new function to EZH2 that is independent of its histone methyltransferas

274 e progenitors Enhancer of zeste homologue 2 (EZH2), the catalytic subunit of Polycomb Repressive Comp

275 we report that enhancer of zeste homolog 2 (EZH2), the catalytic subunit of polycomb repressive comp

276 atypical meningiomas exhibit upregulation of EZH2, the catalytic subunit of the PRC2 complex, as well

277 Deletion of Ezh2, the major enzymatic component of PRC2, causes upre

278 (AZA) leads to the transient recruitment of EZH2, the polycomb repressive complex 2 (PRC2) component

279 ed global H3K27me3 levels, while it switches EZH2 to a transcriptional activator, conferring higher p

280 F6 promoted the K63-linked ubiquitination of EZH2 to decrease EZH2 and H3K27me3 levels in PCa cells.

281 te for binding of the PRC2 methyltransferase Ezh2 to Suz12 and reduce PRC2 chromatin engagement.

282 , our findings revealed a novel mechanism on EZH2 ubiquitination and an important signaling network o

283 trast, TRAF6 knockdown resulted in a reduced EZH2 ubiquitination with an increase of EZH2 and H3K27me

284 ilis et al. report that the polycomb protein EZH2, upon heat shock, facilitates transcription of stre

285 Inhibition of Ezh2/VEC association increases Ezh2 recruitment to claud

286 ortantly, a concurrent elevation of Skp2 and Ezh2 was found in CRPC tumors of Pten/Trp53 mutant mice,

287 Mechanistically, EZH2 was recruited to the IRF8 promoter after RANKL stim

288 phoid-specific EZH2 deficiency we found that EZH2 was required for proper development of adaptive, bu

289 h of 17 residues in the N-terminal region of EZH2, we call the activation loop, in the stimulation of

290 tant mice, and expression levels of SKP2 and EZH2 were positively correlated in human PCa specimens.

291 gory (any mutations in ASXL1, SRSF2, IDH1/2, EZH2) were more represented in overt PMF.

292 Proneural, perivascular GSCs activated EZH2, whereas mesenchymal GSCs in hypoxic regions expres

293 g event may lead to the regain of functional EZH2 which was consistent with our previous finding that

294 residues are spread out along the surface of EZH2, with other subunits including EED also contributin

295 f H3K27me3, a histone modification placed by EZH2, within the gene body of SLFN11, inducing local chr

296 erentiation at least partly by targeting the EZH2/Wnt/beta-Catenin signaling pathway.

297 Interestingly, mutation of EZH2 WT alone generated an intermediate resistance pheno

298 iously proposed model of cooperation between EZH2 WT and Y641N mutants to promote tumorigenesis.

299 Although expression of Ezh2(Y641F) globally increased the abundance of trimethy

300 Expression of Ezh2(Y641F) in mouse B cells or melanocytes caused high-

301 -of-function mutation (EZH2(Y646F) in human; Ezh2(Y641F) in mouse) is conditionally expressed.

302 mmon somatic Ezh2 gain-of-function mutation (EZH2(Y646F) in human; Ezh2(Y641F) in mouse) is condition