ライフサイエンスコーパス: PRC2

1 n mediated by Polycomb repressive complex 2 (PRC2).

2 tic subunit of polycomb repressor complex 2 (PRC2).

3 ing recruitment of other PRC1 complexes, and PRC2.

4 ficantly rescued in intestinal cells lacking PRC2.

5 Wnt signaling was regulated directly by PRC2.

6 in Drosophila ovaries, likely via inhibiting PRC2.

7 s of the inhibitor-bound wild-type and Y641N PRC2.

8 ability of RBFox2 to directly interact with PRC2.

9 at leverages interactions between lncRNA and PRC2.

10 h2), which encode the enzymatic component of PRC2.

11 ich formed a complex with EZH2 distinct from PRC2.

12 tin contexts and set a ground state to allow PRC2 activation by other cellular mechanisms as well.

13 ed the target recognition specificity of the PRC2 active site and used the resultant data to screen f

14 rating a functional balance between MLL1 and PRC2 activities at these sites.

15 has an additional function to stimulate the PRC2 activity after binding to H3K27me3.

16 we obtained evidence for cooperation between PRC2 activity and DNA methylation in blocking tumor-supp

17 complicated by early embryonic dependence on PRC2 activity and the partial functional redundancy of e

18 Several inhibitors of the PRC2 activity have shown efficacy in EZH2-mutated lympho

19 ructural platform that may enable control of PRC2 activity in response to diverse transcriptional sta

20 Residual PRC2 activity is required to maintain DIPG proliferative

21 Despite a major loss of H3K27me3, PRC2 activity is still detected in DIPG cells positive f

22 Aberrant PRC2 activity produces gene repressive epigenetic marks

23 ass transcription factor known to antagonize PRC2 activity.

24 ells thought to be mediated by inhibition of PRC2 activity.

25 which, in vitro, has been shown to stimulate PRC2 activity.

26 genes in WT and Eed (-/-) TSCs suggests that PRC2 acts as a brake to prevent induction of transcribed

27 Intriguingly, HOTAIR interacts with PRC2 and also binds RNA-binding E3 ligases, serving as a

28 gonizing formation of the chromatin modifier PRC2 and by epigenetically activating NOTCH signals in h

29 combination treatments, which targeted both PRC2 and DNA methylation.

30 some but not other PRC2 target genes require PRC2 and H3K27me3 for silencing.

31 SMN-AS1 and PRC2 inhibit the recruitment of PRC2 and increase SMN2 expression in primary neuronal cu

32 non-catalytic but an essential component of PRC2 and its mutations were identified in hematopoietic

33 nctional co-dependence between LINC-PINT and PRC2 and lead us to propose a new mechanism where the ln

34 fications of the EpCAM promoter, a target of PRC2 and LSD1/Co-REST/HDAC1 complexes.

35 nd DNA, and indirectly via interactions with PRC2 and RNA PolII.

36 PRC2 and Xist foci are not randomly distributed but show

37 pendency on the polycomb repressive complex (PRC2) and EZH2 represents one such vulnerability in tumo

38 lysis connects RBFox2 to Polycomb complex 2 (PRC2) and H3K27me3, and biochemical experiments demonstr

39 1A interacts with histone methyltransferase (PRC2) and histone deacetylase (NuRD and SIN3A) complexes

40 meodomain-Polycomb repressive complex 2 (PHD-PRC2) and indicates a role for the transcriptional repre

41 ivation of the Polycomb Repressor Complex 2 (PRC2) and its catalytic component EZH2.

42 s silenced by polycomb repressive complex 2 (PRC2) and ZNF198/LSD1/Co-REST/HDAC1 chromatin-modifying

43 activity of three PcG repressive complex 2s (PRC2s) and the participation of a yet poorly defined PRC

44 lenced by the Polycomb repressive complex 2 (PRC2), and identify the conserved histone demethylase UT

45 ractions with Polycomb repressive complex 2 (PRC2), and systematically investigated the sequence feat

46 to H3K27me3, the histone modification set by PRC2, and also associates genome-wide with trimethylatio

47 omatin, physically interact with and recruit PRC2, and are required for PRC2-mediated gene silencing

48 he multi-subunit polycomb repressive complex PRC2, and the down-regulation of exon-skipping event may

49 rationalizes the promiscuous RNA binding of PRC2, and their enrichment at Polycomb target genes prov

50 that Scm is a key mediator connecting PRC1, PRC2, and transcriptional silencing.

51 thermore, this colocalization requires PRC1, PRC2, and TrxG complexes, which are essential regulatory

52 However, the recent identification of a PRC2- and methyltransferase-independent role of EZH2 ind

53 ey form multiple complexes of which PRC1 and PRC2 are evolutionary conserved and obligatory for repre

54 The Polycomb repressive complexes PRC1 and PRC2 are key mediators of heritable gene silencing in mu

55 subunits EZH2 and SUZ12, thereby inhibiting PRC2 assembly.

56 te, which represents a novel conformation of PRC2 associated with enzyme regulation in light of the b

57 in mESCs, the Polycomb repressive complex 2 (PRC2)-associated protein EPOP (Elongin BC and Polycomb R

58 proteins, such as PHF1, MTF2 and PHF19, are PRC2-associated factors that form sub-complexes with PRC

59 Of particular novelty, we identified the PRC2-associated protein, ASXL3, which was markedly upreg

60 We also show divergence patterns of the PRC2-associated VERNALIZATION5/VIN3-LIKE2 that are simil

61 he lncRNA regulates the availability of free PRC2 at the proximity of co-regulated genomic loci.

62 ates with the Polycomb repressive complex 2 (PRC2) at a subset of developmental promoters, including

63 e hypothesize that Piwi negatively regulates PRC2 binding by sequestering PRC2 in the nucleoplasm, th

64 t with this, RNA and nucleosomes compete for PRC2 binding in vitro.

65 Although interacting with RNA promiscuously, PRC2 binding is enriched at specific locations within RN

66 approximately 72 genomic sites and inhibits PRC2 binding to many non-Piwi-binding genomic targets an

67 ering PRC2 in the nucleoplasm, thus reducing PRC2 binding to many targets and influencing transcripti

68 occupying the polycomb repressive complex 2 (PRC2) binding sites in human embryonic stem cells, there

69 We further identified fragments of PRC2-binding lncRNAs that are enriched with these sequen

70 Through that, PRC2-binding lncRNAs were found to be associated with a

71 DNA sequences coding for PRC2-binding RNA motifs are enriched at PRC2-binding sit

72 Collectively, the abundance of PRC2-binding RNA motifs rationalizes the promiscuous RNA

73 equence features, and found they show strong PRC2-binding signals and are more highly conserved acros

74 Mammalian PRC2-binding sites are enriched in CG content, which cor

75 for PRC2-binding RNA motifs are enriched at PRC2-binding sites on chromatin and H3K27me3-modified nu

76 ract motifs are significantly enriched among PRC2-binding transcripts in vivo.

77 ther RNA binding proteins, we show here that PRC2 binds nascent RNA at essentially all active genes.

78 Mammalian PRC2 binds RNA promiscuously, with thousands of target t

79 nd that PRC1 can bind PREs in the absence of PRC2 but at many PREs PRC2 requires PRC1 to be targeted.

80 Modulation of PRC2 by either Ezh2 overexpression or Eed deletion enhan

81 f the Polycomb repressive complexes PRC1 and PRC2 by Xist RNA is an important paradigm for chromatin

82 ession is targeted and suggest that PRC1 and PRC2 can communicate independently of histone modificati

83 mplify the complex outcomes that the lack of PRC2 can have in a somatic stem cell system.

84 Polycomb repressive complex 2 (PRC2) catalyzes histone H3K27me3, which marks many trans

85 Polycomb Repressive Complex 2 (PRC2) catalyzes the trimethylation of lysine 27 of histo

86 on of Ezh2, the major enzymatic component of PRC2, causes upregulation of Upk3a(+) superficial cells.

87 n RNA and chromatin underlies the pattern of PRC2 chromatin association across the genome.

88 2 methyltransferase Ezh2 to Suz12 and reduce PRC2 chromatin engagement.

89 Here, we characterise AEBP2, a known PRC2 co-factor which, in vitro, has been shown to stimul

90 Here we demonstrate a critical role for the PRC2 cofactor Jarid2 in mediating the interaction of PRC

91 EZH2 is the catalytic engine of the PRC2 complex and thus represents a key candidate oncolog

92 as Bim), by promoting the enrichment of the PRC2 complex at the Bcl2l11 promoter to maintain this ge

93 ecific genes by regulating the expression of PRC2 complex components.

94 The VERNALIZATION (VRN)-PRC2 complex contains VRN2 and SWINGER (SWN), and both g

95 PARylation of EZH2 by PARP1 then induces PRC2 complex dissociation and EZH2 downregulation, which

96 erous human cancers, therefore inhibition of PRC2 complex has emerged as a promising therapeutic appr

97 ZH2 by JAK3 promotes the dissociation of the PRC2 complex leading to decreased global H3K27me3 levels

98 In addition, the Brassicaceae-specific FIS-PRC2 complex modified the regulatory pathways in female

99 ch function in the Brassicaceae-specific FIS-PRC2 complex that regulates seed development.

100 lation of EZH2, the catalytic subunit of the PRC2 complex, as well as the E2F2 and FOXM1 transcriptio

101 f Ezh2, the methyltransferase subunit of the PRC2 complex, results in reduced H3K27me3 and profound t

102 2 subunits may function independently of the PRC2 complex.

103 e of our inhibitor series bound to the human PRC2 complex.

104 d Ezh1/2 function largely as subunits of the PRC2 complex.

105 ng, as a member of the polycomb repressor 2 (PRC2) complex.

106 We propose that EOL1 interacts with LHP1-PRC2 complexes during replication and thereby participat

107 t, resulting in functional divergence of the PRC2 complexes in Brassicaceae.

108 omb group (PcG) proteins within the PRC1 and PRC2 complexes, and the Trithorax group (TrxG) proteins

109 trithorax group proteins, but not of PRC1 or PRC2 complexes, suggesting that Pcgf6 functions atypical

110 firms that AEBP2 associates exclusively with PRC2 complexes.

111 We show in mouse that the PRC2 component Ezh2 is required to restrict smooth muscl

112 of EZH2, the polycomb repressive complex 2 (PRC2) component responsible for H3K27 trimethylation, an

113 Loss-of-function studies of PRC2 components have been complicated by early embryonic

114 carcinoma cells downregulates EZH2 and other PRC2 components.

115 encoding the polycomb repressive complex 2 (PRC2) components EZH2, EED, and SUZ12.

116 ic subunit of Polycomb Repressive Complex 2 (PRC2), contributes to maintain the chromatin of muscle g

117 PRC2 controls gene expression in multiple signaling path

118 gs uncover the epigenetic mechanism by which PRC2 controls urothelial progenitor cell fate and the ti

119 Polycomb repressive complex 2 (PRC2) controls maintenance and lineage determination of

120 cidating the first crystal structures of the PRC2 core complex, yielding seminal insights into its ca

121 ify critical residues for RNA interaction in PRC2 core complexes from Homo sapiens and Chaetomium the

122 ociated factors that form sub-complexes with PRC2 core components, and have been proposed to modulate

123 In ESCs, Spt6 interacted with the PRC2 core subunit Suz12 and prevented H3K27me3 accumulat

124 We show that PRC2 deficiency in striatal neurons leads to the de-repr

125 se are the predominant genes de-repressed in PRC2-deficient adult cells, where aberrant expression is

126 The transcriptional changes in PRC2-deficient neurons lead to progressive and fatal neu

127 By inhibiting PRC2-dependent H3K27me3 in the absence of MLL1, we can r

128 uronal differentiation in neuroblastoma in a PRC2-dependent manner.

129 proteins that would otherwise interfere with PRC2-dependent reprogramming of PGC chromatin.

130 Without Eed, the obligatory subunit of PRC2, embryonic urothelial progenitors demonstrate reduc

131 Chromatin coimmunoprecipitation of Piwi, the PRC2 enzymatic subunit E(z), histone H3 trimethylated at

132 Here, we report the stage-specific roles of PRC2 epigenetic regulators in embryonic and adult urothe

133 in complex also sequesters a core subunit of PRC2 (Ezh2 [enhancer of zeste homolog 2]) at the cell me

134 Polycomb repressive complex 2 (PRC2-EZH2) methylates histone H3 at lysine 27 (H3K27) an

135 Furthermore, some PRC2 family genes and DNA methylation-related genes incl

136 Correspondingly, the release of PRC2 from chromatin in cells increases RNA binding.

137 e determined the crystal structure of an apo-PRC2 from the fungus Chaetomium thermophilum captured in

138 Dysregulation of PRC2 function correlates with certain malignancies and p

139 Although there have been numerous studies on PRC2 function in somatic tissue development and stem cel

140 trates of PRC2 that might also contribute to PRC2 function is not known.

141 enes on the inactive X chromosome, a mode of PRC2 function that may apply broadly.

142 rm development (EED) (a subunit required for PRC2 function) and enhancer of zeste homolog 2 (EZH2) (a

143 To abrogate PRC2 function, we delete the core PRC2 protein EED in F1

144 Here, the authors show that ablation of PRC2 genes in human embryonic stem cells and in mice res

145 that predict which PRC2 target genes require PRC2/H3K27me3 for silencing by interrogating imprinted m

146 Thus, our study demonstrates that PRC2 has an important regulatory role in lineage-committ

147 PRC2 has been shown to interact with thousands of RNA sp

148 Polycomb repressive complex 2 (PRC2) has been shown to play a major role in transcripti

149 reader protein EED, associated with Ezh2 in PRC2, has an additional function to stimulate the PRC2 a

150 oint mutations in the individual subunits of PRC2 have been shown to contribute to tumorigenesis.

151 PRC2 helps to maintain adult stem cell populations, but

152 ex that exhibited Ras-mediated dependence on PRC2 histone methyltransferase activity, a finding that

153 A missense mutation in the substrate of PRC2, histone H3K27M, is associated with certain pediatr

154 PRC2 hyperactivity and/or hypertrimethylation of H3K27 a

155 However, the RNAs that bind PRC2 in cells, the subunits that mediate these interacti

156 By performing iCLIP for PRC2 in comparison with other RNA binding proteins, we s

157 present here the crystal structure of human PRC2 in complex with the inhibitory H3K27M peptide bound

158 nding that demethylation may cause regain of PRC2 in demethylated regions.

159 vestigate the functional roles of H3K27M and PRC2 in DIPG pathogenesis, we profiled the epigenome of

160 However, the role of PRC2 in lineage-committed somatic cells is mostly unknow

161 racts with Polycomb group complexes PRC1 and PRC2 in niche and germline cells to regulate ovarian ger

162 Our results point to a key role of PRC2 in protecting neurons against degeneration.

163 mplex initiates recruitment of both PRC1 and PRC2 in response to Xist RNA expression.

164 SMARCA2 is suppressed by PRC2 in sensitive models, and induced SMARCA2 expression

165 Comparison of PRC2 in the basal and stimulated states reveals a mobile

166 To investigate the function of PRC2 in the control of skin development, we generated an

167 d define a key mechanism that links PRC1 and PRC2 in the establishment of Polycomb domains.

168 The strikingly different roles of PRC2 in the formation of three lineages exemplify the co

169 ively regulates PRC2 binding by sequestering PRC2 in the nucleoplasm, thus reducing PRC2 binding to m

170 n factor, Elongin A (EloA), is methylated by PRC2 in vivo.

171 We studied POLYCOMB REPRESSIVE COMPLEX2 (PRC2) in Brassicaceae.

172 Importantly, PRC2 inactivation results in context-dependent phenotypi

173 ls, a mark of Polycomb repressive complex 2 (PRC2), increase at these loci.

174 id2 has also been shown to exert pleiotropic PRC2-independent actions during embryogenesis.

175 These results support PRC2-independent functions of EZH2 and TRIM28 in activat

176 ecific mouse knock-out of the Eed subunit of PRC2 indicate that demethylation is a rate-limiting step

177 disrupt the interaction between SMN-AS1 and PRC2 inhibit the recruitment of PRC2 and increase SMN2 e

178 he design and development of next-generation PRC2 inhibitors through establishment of a structure-bas

179 Here, we show that PRC2 is a critical regulator of KRAS-driven non-small ce

180 ochemical, and structural data indicate that PRC2 is broadly conserved from yeast to human in many as

181 loci of actively transcribed genes, whereas PRC2 is excluded from these regions; this suggests that

182 Misregulation of PRC2 is linked to a range of neoplastic malignancies, wh

183 The targeting of PRC1 and PRC2 is poorly understood and was proposed to be hierarc

184 PRC2 is primarily associated with CpG islands at repress

185 PRC2 is required for chromatin reprogramming in the germ

186 The interaction between Chaer and PRC2 is transiently induced after hormone or stress stim

187 Polycomb repressive complex 2 (PRC2) is a histone methyltransferase that trimethylates

188 Polycomb repressive complex 2 (PRC2) is a key chromatin modifier responsible for methyl

189 Polycomb repressive complex 2 (PRC2) is an essential regulator of cell physiology.

190 Polycomb repressive complex 2 (PRC2) is responsible for methylation of histone H3 lysin

191 ponent of the Polycomb repression complex 2 (PRC2), is required to maintain a stable pool of germline

192 t RNAs, including bacterial mRNAs, also bind PRC2; Kds depend to some extent on the experimental cond

193 Simultaneous disruption of Tsix and PRC2 leads to derepression of Xist and in turn silencing

194 and demonstrate that this domain facilitates PRC2 localization to H2AK119u1 both in vivo and in vitro

195 The Polycomb repressive complex 2 (PRC2) mainly mediates transcriptional repression and has

196 In intestinal tissues of mice, PRC2 maintains small intestinal stem cells by promoting

197 on is through polycomb repressive complex 2 (PRC2)-mediated gene repression, which requires its histo

198 the levels of polycomb repressive complex 2 (PRC2)-mediated H3K27 trimethylation (H3K27me3), and this

199 s function in polycomb repressive complex 2 (PRC2)-mediated transcriptional regulation, suggesting it

200 DDX5), as a regulator of SUZ12 stability and PRC2-mediated gene repression, acting by regulating RNA-

201 with and recruit PRC2, and are required for PRC2-mediated gene silencing in vivo.

202 icase activity of DDX5 stabilized SUZ12- and PRC2-mediated gene silencing, by displacing the RNA-bind

203 ent with this, we observe elevated levels of PRC2-mediated histone H3K27 methylation at target loci i

204 Polycomb repressive complex 2 (PRC2) mediates gene silencing through chromatin reorgani

205 Polycomb repressive complex 2 (PRC2) methylates lysine 27 in histone H3, a modification

206 PHF1 relies on this interaction to regulate PRC2 methyltransferase activity, localize to DNA double

207 d that Spt6 could compete for binding of the PRC2 methyltransferase Ezh2 to Suz12 and reduce PRC2 chr

208 omplex inhibition of the polycomb complex 2 (PRC2) methyltransferase Enhancer of Zeste Homologue 2 (E

209 Polycomb repressive complex 2 (PRC2) modifies chromatin to maintain genes in a represse

210 PRC1 and PRC2 modify chromatin by catalysing histone H2A lysine 1

211 We propose that PRC2 modulates transcription of a subset of low expressi

212 equence mediates a specific interaction with PRC2, necessary for the LINC-PINT-dependent repression o

213 pressors thus recruits the machinery for PHD-PRC2 nucleation and epigenetic silencing.

214 Molecular defects in various PRC2 null adult tissues lack a unifying explanation.

215 s down RBBP4, RBBP7, and other components of PRC2, NuRD, and SIN3A from the cell lysate of the TNBC c

216 ies that bind to these PREs, colocalize with PRC2 on chromatin, physically interact with and recruit

217 this suggests that H3K27M does not sequester PRC2 on chromatin.

218 ntagonists through the direct recruitment of PRC2 on these targets.

219 oposed to modulate the enzymatic activity of PRC2 or the recruitment of PRC2 to specific genomic loci

220 ellular differentiation and development, and PRC2 overexpression and mutations have been implicated i

221 Polycomb repressive complex 2 (PRC2) participates in transcriptional repression through

222 , that direct Polycomb repressive complex 2 (PRC2) placement at developmental genes regulated by sile

223 cription, and Polycomb Repressive Complex 2 (PRC2) places K27me3, which is erased at lineage-restrict

224 Polycomb repressor complex 2 (PRC2) places the histone mark H3K27me3 predominantly at

225 The Polycomb repressive complexes PRC1 and PRC2 play a central role in developmental gene regulatio

226 The Polycomb-repressive complexes PRC1 and PRC2 play a key role in chromosome silencing induced by

227 These findings indicate Ezh2/PRC2 plays crucial roles in regulating neurogenesis from

228 ate decisions.Polycomb repressive complex 2 (PRC2) plays an essential role in development by modifyin

229 bition of H3K27 methyltransferases or of the PRC2 (Polycomb Repressive Complex 2) by pharmaceutical i

230 in O1) and beta-catenin, which contribute to PRC2 (polycomb repressive complex-2) binding to promoter

231 s a domain of Polycomb repressive complex 2 (PRC2), promoting the methylation of H3K27 and the silenc

232 o abrogate PRC2 function, we delete the core PRC2 protein EED in F1 hybrid trophoblast stem cells (TS

233 mice with intestine-specific deletion of the PRC2 proteins embryonic ectoderm development (EED) (a su

234 But what does PRC2 recognize in these RNAs?

235 Here we show that purified human PRC2 recognizes G > C,U >> A in single-stranded RNA and

236 Thus PRC2 recruitment in Arabidopsis relies in large part on

237 e these interactions, and the role of RNA in PRC2 recruitment to chromatin all remain unclear.

238 We propose that RNA prevents PRC2 recruitment to chromatin at active genes and that m

239 RNA degradation in cells triggers PRC2 recruitment to CpG islands at active genes.

240 However, the mechanism of PRC2 recruitment to CpG islands is not fully understood.

241 emonstrate that PCL proteins are crucial for PRC2 recruitment to CpG islands, and further clarifies t

242 of ITD-positive CCSKs reveals enrichment for PRC2-regulated genes and similarity to undifferentiated

243 The polycomb repressive complex 2 (PRC2) regulates differentiation by contributing to repre

244 Our data support a model in which PRC1 and PRC2 reinforce each other's binding but suggest that the

245 ms, Polycomb Repressive Complex 1 (PRC1) and PRC2 repress target genes through histone modification a

246 f DDX5 and/or HOTAIR enabled reexpression of PRC2-repressed genes epithelial cell adhesion molecule (

247 ion-dependent communication between PRC1 and PRC2, repressive Polycomb chromatin domains can erode, r

248 PREs in the absence of PRC2 but at many PREs PRC2 requires PRC1 to be targeted.

249 mline, and the transcriptome of PGCs lacking PRC2 resembles that of nos-1nos-2 PGCs.

250 Interestingly, the absence of PRC2 results in dramatically different phenotypes across

251 depletion disrupted the interactions between PRC2, RNA PolII S5P, H3K4me3 and H3K27me3 and resulted i

252 ly reactivated polycomb repressor complex 2 (PRC2)-silenced tumor suppressor genes.

253 Polycomb repressive complex 2 (PRC2) silences gene expression through trimethylation of

254 Thus, in adult animals, PRC2 specifically represses genes with acquired, tissue-

255 carrying a mutation in the catalytic core of PRC2, strongly enhanced the clf phenotype; furthermore,

256 and future directions for inquiry regarding PRC2 structure and function.

257 te that mutant ESCs assemble atypical hybrid PRC2 subcomplexes, potentially accounting for enhancemen

258 fining the mutually exclusive composition of PRC2 subcomplexes.

259 PRC2 subunit genes and several prosurvival lymphoma gene

260 with stable knockdown of SUZ12, an essential PRC2 subunit, upon HBx expression demethylate a CpG dinu

261 , these have focused on the loss of a single PRC2 subunit.

262 the essential Polycomb Repressive Complex 2 (PRC2) subunit EED in the SCC lesions.

263 knockout mouse lines, in which the essential PRC2 subunits embryonic ectoderm development (EED), supp

264 P competitively disrupted association of the PRC2 subunits EZH2 and SUZ12, thereby inhibiting PRC2 as

265 Recent studies, however, have shown that PRC2 subunits may function independently of the PRC2 com

266 Deletion of other PRC2 subunits reveals that SUZ12 is sufficient to establ

267 Piwi physically interacts with the PRC2 subunits Su(z)12 and Esc in the ovary and in vitro.

268 , namely, the polycomb repressive complex 2 (PRC2) subunits enhancer of zeste 1 (EZH1) and enhancer o

269 DLK1, another PRC2 target gene, also upregulated in HBV-mediated HCCs,

270 residue decreased repression of a subset of PRC2 target genes as measured by both steady-state and n

271 y, it remains unclear why some but not other PRC2 target genes require PRC2 and H3K27me3 for silencin

272 al and chromatin features that predict which PRC2 target genes require PRC2/H3K27me3 for silencing by

273 pression of selected, predominantly bivalent PRC2 target genes that are dominated by self-regulating

274 We show that AEBP2 localises specifically to PRC2 target loci, including the inactive X chromosome.

275 Strikingly, RBFox2 inactivation eradicates PRC2 targeting on the majority of bivalent gene promoter

276 by a 66-mer motif in Chaer, interferes with PRC2 targeting to genomic loci, thereby inhibiting histo

277 By contrast, PRC2 targets that remain repressed in Eed (-/-) TSCs are

278 but not DDX5, resulting in de-repression of PRC2 targets, including EpCAM and pluripotency genes.

279 on can compensate for SMARCA4 and antagonize PRC2 targets.

280 e full spectrum of non-histone substrates of PRC2 that might also contribute to PRC2 function is not

281 ic subunit of polycomb repressive complex 2 (PRC2) that catalyzes methylation of histone H3 lysine 27

282 member of the polycomb repressive complex 2 (PRC2) that is highly expressed in diverse human cancers

283 of other noncanonical PRC1 complexes and of PRC2, the latter leading to deposition of histone H3 lys

284 or that SS18-SSX is able to directly recruit PRC2 to aberrantly silence target genes.

285 ns are required for efficient recruitment of PRC2 to CpG island-containing promoters in mouse embryon

286 matic activity of PRC2 or the recruitment of PRC2 to specific genomic loci.

287 ssociated with an increase in the binding of PRC2 to these genes and is mediated redundantly by the E

288 acts with the Polycomb-repressive complex 2 (PRC2) to enable H3K27me3-mediated epigenetic repression.

289 ecruiting the Polycomb Repressive Complex 2 (PRC2) to its locus.

290 component of polycomb repressive complex 2 (PRC2), to inhibit c-Met expression.

291 components of polycomb repressive complex 2 (PRC2), transcriptional activation of ERG target genes, a

292 ore subunit of Polycomb repressive complex2 (PRC2), undergoes proteasomal degradation.

293 ween PRC1 and Polycomb repressive complex 2 (PRC2) which is required for normal histone H3 lysine 27

294 mponent of the Polycomb Repressor complex 2 (PRC2), which is responsible for genome-wide H3K27me3 dep

295 we show that polycomb repressive complex 2 (PRC2), which supports neuron specification during differ

296 RepA RNA is a good binding partner for PRC2, while multiple non-relevant RNAs, including bacter

297 by PRC1 is well defined, the interaction of PRC2 with H2AK119u1 is poorly understood.

298 actor Jarid2 in mediating the interaction of PRC2 with H2AK119u1.

299 nism underlying the enigmatic association of PRC2 with numerous active genes, highlight the importanc

300 we also demonstrate that the interaction of PRC2 with RNA or chromatin is mutually antagonistic in c