ライフサイエンスコーパス: PRC2

1 itment of the polycomb repressive complex 2 (PRC2).

2 olycomb repressive complex 1 and 2 (PRC1 and PRC2).

3 c subunits of Polycomb Repressive Complex 2 (PRC2).

4 ponent of the Polycomb repressive complex-2 (PRC2).

5 regions of the Hi-C A compartment marked by PRC2.

6 tify and develop small molecules that target PRC2.

7 RMT5 abrogates its subsequent methylation by PRC2.

8 repressed by the Polycomb complexes PRC1 and PRC2.

9 hat H3K27M impairs the intrinsic activity of PRC2.

10 tic activity of PRC2-EED-I363M over wildtype-PRC2.

11 istically regulate the enzymatic activity of PRC2.

12 HNRNPK, compromises recruitment of PRC1 and PRC2.

13 ith PRC2 or repressing them independently of PRC2.

14 r cells in a context distinct from canonical PRC2.

15 genes, di- and tri-methylated H3K36 inhibit PRC2.

16 Both holo-PRC2.1 and holo-PRC2.2 bind RNA, providing a unified mod

17 Two mutually exclusive subcomplexes, PRC2.1 and PRC2.2, are defined by the set of accessory p

18 on and define two major holo-PRC2 complexes: PRC2.1 and PRC2.2.

19 the SUZ12 subunit of PRC2 to drive it into a PRC2.1 or 2.2 subcomplex in human induced pluripotent st

20 isease or development by tuning the ratio of PRC2.1 to PRC2.2.

21 ssociated mutations also coerce formation of PRC2.1.

22 reases drastically when it is forced to form PRC2.1.

23 Both holo-PRC2.1 and holo-PRC2.2 bind RNA, providing a unified model to explain ho

24 We find that PRC2.2 occupies polycomb target genes at low levels and

25 mutually exclusive subcomplexes, PRC2.1 and PRC2.2, are defined by the set of accessory proteins bou

26 development by tuning the ratio of PRC2.1 to PRC2.2.

27 ne two major holo-PRC2 complexes: PRC2.1 and PRC2.2.

28 lterations in polycomb-repressive complex 2 (PRC2), a histone-modifying complex involved in transcrip

29 n analyses of Polycomb repressive complex 2 (PRC2), a key inducer of transcriptional gene silencing,

30 tment to chromatin, automethylation promotes PRC2 accessibility to the histone H3 tail.

31 les of a gene, NCU04278, encoding an unknown PRC2 accessory subunit (PAS).

32 27me3 and H3K27me2 are normally deposited by PRC2 across broad regions, their deposition is severely

33 Our findings suggest that Ybx1 fine-tunes PRC2 activities to regulate spatiotemporal gene expressi

34 GSCs have a non-canonical distribution of PRC2 activity and lack silenced chromatin like embryonic

35 at H3.3 G34 oncohistones selectively promote PRC2 activity by interfering with SETD2-mediated H3K36 m

36 PRC2 activity is regulated by a number of different inpu

37 However, it remains to be determined how PRC2 activity is regulated in normal and diseased settin

38 declines and newly induced Scm concentrates PRC2 activity on traditional Polycomb domains.

39 complexes, and RNA-DNA strand exchange as a PRC2 activity that could contribute to R-loop formation.

40 arising from these primitive tissues exploit PRC2 activity to enable immune evasion.

41 ells, that they each contribute to directing PRC2 activity to target sites.

42 understanding of the mechanisms that govern PRC2 activity, and highlight a role for JARID2 in de nov

43 t of PRC2 to chromatin and/or stimulation of PRC2 activity, are unclear.

44 partially regulate its ability to stimulate PRC2 activity.

45 R-155 enhances Polycomb repressor complex 2 (PRC2) activity indirectly by promoting the expression of

46 rry either EZH2 or EED mutants that abrogate PRC2 allosteric activation, indicating that H3K27M impai

47 Polycomb repressive complexes 1 and 2 (PRC1/PRC2) along the inactive X (Xi).

48 bition of the Polycomb Repressive Complex 2 (PRC2), an H3K27 tri-methyltransferase, exacerbated the i

49 We find that PHF19 interacts with PRC2 and binds to PRC2 targets on chromatin.

50 w that these genes are directly repressed by PRC2 and constitute a significant proportion of direct P

51 tors, repressive chromatin-modifiers such as PRC2 and DNA methyl-transferases, and proteins governing

52 opmental genes from repression via repelling PRC2 and DNA methylation machineries.

53 absence of MLL2 is relieved by inhibition of PRC2 and DNA methyltransferases.

54 nteracting with chromatin remodeling complex PRC2 and downregulation of cell migration-regulating gen

55 he latest advances toward exposing mammalian PRC2 and its high maintenance.

56 comb-like protein PHF19/PCL3 associates with PRC2 and mediates its recruitment to chromatin in embryo

57 r just over half of the genes corepressed by PRC2 and miRNAs, PRC2 promotes their miRNA-mediated repr

58 ally activates a transcriptome, enriched for PRC2 and SOX10 targets, that overrides developmental and

59 nscription repression through recruitment of PRC2 and that HIV Tat alleviates repression through disr

60 ar due to the context-dependent functions of PRC2 and the heterogeneity of breast cancer.

61 We found that Polycomb repressive complex 2 (PRC2) and its associated histone mark, H3K27me3, is enri

62 ulated by the polycomb repressive complex 2 (PRC2) and others previously implicated in known Bap1-rel

63 onents of the Polycomb Repressing Complex 2 (PRC2), and they are expressed higher in JIMT1 cells.

64 2, which encode two other core components of PRC2, and predict the presence of pathogenic variants in

65 Polycomb-repressive complex 1 (PRC1) and PRC2 are critical chromatin regulators of gene expressio

66 interferes with PRC2 function, thus FBP1 and PRC2 are part of a novel negative feedback loop that is

67 ndirectly by promoting the expression of the PRC2-associated factor Phf19 through downregulation of t

68 hat first PRC1-associated H2AK119Ub and then PRC2-associated H3K27me3 accumulate initially at large i

69 MTF2 and PHF19 associate with PRC2 at around the dimer interface and stabilize the dim

70 lated regions for PRC2 recruitment, diluting PRC2 at Polycomb-repressed genes.

71 ns that either increase the concentration of PRC2 at target sites or inhibit the rate that PRC2 sampl

72 lts reveal the hitherto unknown c-Src/mTORC1/PRC2 axis, which is essential for ErbB2-driven carcinoge

73 H3K27M inhibitor and support a model wherein PRC2 becomes trapped at H3K27M-H3K27me3 boundaries.

74 reveal an unexpectedly diverse repertoire of PRC2 binding configurations on chromatin.

75 Mechanistically, Ybx1 highly overlaps PRC2 binding genome-wide, controls PRC2 distribution, an

76 Additionally, PRC2 binding led to a 3-fold increase in the local bendi

77 Neither oncohistone interferes with PRC2 binding.

78 PRC2 binds RNAs broadly in vivo and in vitro.

79 We found that PRC2 binds to a bivalent inhibitor unit consisting of an

80 PRC2 binds to RNA, which inhibits its enzymatic activity

81 ne-regulatory functions, lending support for PRC2 blockade as a means for MM therapeutics.

82 While some PRC2-bound elements function as silencers in pluripotent

83 Deletion of certain PRC2-bound silencers in mice results in transcriptional

84 PRC2 is relieved by allosteric activation of PRC2 by H3K27me3 and JARID2-K116me3 peptides.

85 ometry that permits allosteric inhibition of PRC2 by methylated H3K36 in transcriptionally active chr

86 , our data also provide direct evidence that PRC2 can bridge pairs of distal nucleosomes.

87 In vitro, both PRC1 and PRC2 can recognize R-loops and open DNA bubbles.

88 The Polycomb Repressive Complexes PRC1 and PRC2 catalyse distinct chromatin modifications to enforc

89 The dysregulation of PRC2 catalytic activity by mutations has been implicated

90 EZHIP is necessary and sufficient to inhibit PRC2 catalytic activity in vitro and in vivo.

91 uencing PRC2 residence time on chromatin and PRC2 catalytic activity with a focus on the mechanisms g

92 G-quadruplex RNA evicts the PRC2 catalytic core from the substrate nucleosome.

93 Polycomb repressive complex 2 (PRC2) catalyzes methylation of histone H3 at lysine 27 (

94 Polycomb Repressive Complex 2 (PRC2) catalyzes mono-, di-, and trimethylation of lysine

95 n RNA-binding-defective mutant all disrupted PRC2 chromatin occupancy and localization genome wide.

96 We suggest that PRC2 chromatin occupancy can be altered in the context o

97 the distribution and stability of different PRC2-chromatin interaction modes are modulated by access

98 At higher concentrations, PRC2 compacted DNA by forming DNA loops typically anchor

99 mportance, the molecular mechanisms by which PRC2 compacts chromatin are relatively understudied.

100 vidual PRC2 core proteins, the disruption of PRC2 complex formation, and the degradation of its subun

101 single and multiple non-core subunits of the PRC2 complex in mouse embryonic stem cells, that they ea

102 During cold, a PHD-PRC2 complex metastably and digitally nucleates H3K27me3

103 Taken together, we show that JARID2 and the PRC2 complex regulate skeletal muscle proliferation in a

104 Brain TF expression is promoted by the PRC2 complex, acting to keep the brain free of anti-prol

105 rs have been developed to target EZH2 or the PRC2 complex, with some of these inhibitors now in early

106 th ripening regulator MSI1, a subunit of the PRC2 complex.

107 n (RB1) is a direct target of JARID2 and the PRC2 complex.

108 iscovered that HMGA2-EZH2 interacts with the PRC2 complex.

109 olocalized with Fie1, a component of the FIS-PRC2 complex.

110 ted through EZH2, a functional member of the PRC2 complex.

111 0313 bound to polycomb repressive complex 2 (PRC2) complex components, and this interaction was disru

112 ar differentiation and define two major holo-PRC2 complexes: PRC2.1 and PRC2.2.

113 In addition to four core subunits, PRC2 comprises multiple accessory subunits that vary in

114 Analysis of the resulting images showed PRC2, consisting of five subunits (EZH2, EED, SUZ12, AEB

115 es protein oligomerization in a noncanonical PRC2 context and is entirely sequestered.

116 that propagation of H3K27 methylation by the PRC2 core complex has geometrically defined preferences

117 U11 robustly immunoprecipitated in vivo with PRC2 core components and the accessory proteins, EMBRYON

118 the inhibition of the function of individual PRC2 core proteins, the disruption of PRC2 complex forma

119 te H3K27me3 by 50% each time DNA replicates, PRC2-deficient ISCs initially retain sufficient H3K27me3

120 eltaN-JARID2 suggesting that, in contrast to PRC2, DeltaN-JARID2 promotes activation of differentiati

121 pression in a Polycomb Repressive Complex 2 (PRC2)-dependent manner.

122 In GSCs, abundant Pcl inhibits PRC2-dependent silencing globally, while in nurse cells

123 Our results suggest that PRC2-dependent silencing is developmentally regulated by

124 One of these, Polycomb repressive complex 2 (PRC2), deposits the H3K27me3 mark of facultative heteroc

125 Stable removal of PRC2 derepresses R-loop-negative genes, as expected, but

126 PRC2 did not show sequence-specific binding to a region

127 The intrinsic PRC2 dimer is formed via domain swapping involving RBBP4

128 t of the C2 domain, disrupting the intrinsic PRC2 dimer.

129 PRC2 dimerization enhances CGI DNA binding by PCLs in pa

130 Loss of PRC2 dimerization impairs histone H3K27 trimethylation (

131 overlaps PRC2 binding genome-wide, controls PRC2 distribution, and inhibits H3K27me3 levels.

132 nt stem cells during mitosis and reveal that PRC2, DNA methylation and Mecp2 are required to maintain

133 Deletion of PRC2, Dnmt1/3a/3b or Mecp2 in ESCs leads to an increase

134 ification during skin morphogenesis, whereas PRC2 does.

135 Unexpectedly, we find that PRC2 drives formation of RNA-DNA hybrids, the key compon

136 ectively stimulate the catalytic activity of PRC2-EED-I363M over wildtype-PRC2.

137 lity of developing targeted therapeutics for PRC2-EED-I363M that act as allosteric agonists, potentia

138 bitors to probe the geometric constraints of PRC2 engagement of H3K27M and H3K27me3 in a biochemical

139 articular, the "1-3" bridging mode, in which PRC2 engages two nucleosomes separated by one spacer nuc

140 Nonetheless, the mechanism by which PRC2 engages with native-like chromatin remains incomple

141 Although PRMT5 does not directly affect PRC2 enzymatic activity, methylation of histone H3 by PR

142 In Ybx1-knockout NPCs, H3K27me3 reduction by PRC2 enzymatic inhibitor or genetic depletion partially

143 Automethylated EZH2/PRC2 exhibits a higher level of histone methyltransferas

144 TER (DME) is upregulated, which can activate PRC2 family members FIS2 and MEA, and may suppress the e

145 e show that G-tract RNA specifically removes PRC2 from genes in human and mouse cells.

146 LINC00313 contributed to the dissociation of PRC2 from LINC00313 and the disinhibition of LINC00313-i

147 en made to develop small molecules targeting PRC2 function for potential use as anticancer therapeuti

148 Aberrant PRC2 function has been extensively studied and proven to

149 PRC2 function is often deregulated in disease and is a p

150 glycolysis but also directly interferes with PRC2 function, thus FBP1 and PRC2 are part of a novel ne

151 ker of heterochromatin formation produced by PRC2, had minimal effects on the CBX2 condensate formati

152 In addition, PRC2 has been shown to automethylate its core subunits,

153 hile H3K27me2 can be deposited outside these PRC2 high-affinity sites but to levels corresponding to

154 The effectiveness of PRC2 hinges on its being recruited to the proper chromat

155 Methylation of these lysines increases PRC2 histone methyltransferase activity, whereas their m

156 In turn, ablating PRC1 or PRC2 impairs Xist spreading.

157 Thus, K219T-LMNA cooperates with PRC2 in downregulating SCN5A, leading to decreased sodiu

158 and functional interaction between BAP1 and PRC2 in embryonic stem cells.

159 ivity, but distinguishes a dominant role for PRC2 in restricting the germline.

160 orted frequent overexpression or mutation of PRC2 in various cancers including prostate cancer and ly

161 studies, we find that chromatin occupancy of PRC2 increases drastically when it is forced to form PRC

162 ggest that the bending and looping of DNA by PRC2, independent of PRC2's methylation activity, may co

163 sence of EZH2 mutations in MPNST is due to a PRC2-independent (i.e., noncanonical) function of the en

164 Our findings reveal a non-catalytic and PRC2-independent function for EZH2 in promoting NER thro

165 y inert in this context, thereby excluding a PRC2-independent function.

166 e, we show that EZH2 has a non-catalytic and PRC2-independent role in stabilizing DDB2 to promote nuc

167 These findings have implications for PRC2 inhibition in cancer therapy.

168 In this work, we used PRC2 inhibitor treatments in a transgenic H3K27M cell li

169 are driven in part by the action of peptidyl PRC2 inhibitors, the K27M oncohistone and the EZHIP 'onc

170 how that MM cells are generally sensitive to PRC2 inhibitors.

171 Polycomb repressive complex 2 (PRC2) installs and spreads repressive histone methylatio

172 ession of two Polycomb repressive complex 2 (PRC2)-interacting proteins, Pcl and Scm, initiate silenc

173 HF19-mediated oncogenic effect relies on its PRC2-interacting and chromatin-binding functions.

174 Perturbation of RNA-PRC2 interaction by RNase A, by a chemical inhibitor of

175 des reproducing known binding modes in which PRC2 interacts with bare DNA, mononucleosomes, and adjac

176 Here, we find that PRC2 interacts with the nucleic acid-binding protein Ybx

177 PRC2 is a histone-modifying complex that catalyses methy

178 The histone methyltransferase activity of PRC2 is central to the formation of H3K27me3-decorated f

179 PRC2 is critical for epigenetic gene silencing, cellular

180 s essential for epidermal integrity, whereas PRC2 is dispensable.

181 mechanism of RNA-mediated inhibition of holo-PRC2 is poorly understood.

182 RNA-mediated inhibition of holo-PRC2 is relieved by allosteric activation of PRC2 by H3K

183 While it is currently unknown how PRC2 is removed from genes, such knowledge would be usef

184 The Polycomb repressive complex 2 (PRC2) is a crucial chromatin modifier in executing neuro

185 Polycomb-repressive complex 2 (PRC2) is a histone methyltransferase that is critical fo

186 Polycomb repressive complex 2 (PRC2) is a histone methyltransferase that methylates his

187 The polycomb repressive complex 2 (PRC2) is composed of three core subunits, enhancer of ze

188 ubunit of the polycomb repressive complex 2 (PRC2), is an oxygen (O(2) )-regulated target of the PCO

189 7, induced by polycomb repressive complex 2 (PRC2), is responsible for downregulating FBP1 in liver a

190 and chromatin-associated G-tract RNA removes PRC2, leading to H3K27me3 depletion from genes.

191 role for ATRX-RNA interactions in regulating PRC2 localization to a subset of polycomb target genes.

192 embedded (FFPE) human MPNST with and without PRC2 loss (MPNST(LOSS) vs. MPNST(RET)).

193 To understand the role of PRC2 loss in pathogenesis and identify therapeutic targe

194 sion in archival human MPNST illustrates how PRC2 loss promotes oncogenesis but renders tumors vulner

195 inhibitors of Polycomb Repressive Complex 2 (PRC2) lysine methyltransferase activity.

196 Polycomb repressive complex 2 (PRC2) maintains repression of cell-type-specific genes b

197 sion as an important downstream mechanism of PRC2-mediated carcinogenesis.

198 In vitro, H1 promotes PRC2-mediated H3K27 methylation and inhibits NSD2-mediat

199 and cyclin E1, both of which are targets of PRC2-mediated H3K27 methylation.

200 y G34 mutations promotes an aberrant gain of PRC2-mediated H3K27me2/3 and loss of H3K27ac at active e

201 stained by cis-acting histone modifications, PRC2-mediated H3K27me3 and cPRC1-mediated H2AK119ub1, pr

202 al epidermal adhesion genes independently of PRC2-mediated H3K27me3.

203 f progenitor and daughter cells, promoted by PRC2-mediated repression of Hox activity.

204 ntributing to tumorigenesis by circumventing PRC2-mediated repression of oncogenic target genes.

205 es to tumor development, in part, by loss of PRC2-mediated repression of tumorigenic target genes and

206 rall, these data suggest that global loss of PRC2-mediated repression renders MPNST differentially de

207 We propose that PRC2-mediated silencing of enhancers involved in cell di

208 igated the role of two PRC proteins, StMSI1 (PRC2 member) and StBMI1-1, in potato development.

209 PRC2 methylation activity is abundant and dispersed thro

210 epression of genes by Polycomb requires that PRC2 modifies their chromatin by trimethylating lysine 2

211 DNA loops typically anchored by two or more PRC2 molecules.

212 Recent evidence suggests that PRC2 must simultaneously bind both H3K27M and H3K27me3 t

213 We identified a PRC2-NSD2/3-mediated MYC regulatory axis as a drug-induc

214 These genes, derepressed in PRC2-null villus cells, remain silent in intestinal stem

215 atin recruitment, with a genome-wide gain in PRC2 occupancy and H3K27me3 deposition.

216 ubunit of the Polycomb Repressive Complex 2 (PRC2), of unknown function.

217 ic subunit of polycomb repressive complex 2 (PRC2), often occurs in cancer.

218 Here, the cryo-EM structure of PRC2 on dinucleosomes reveals how binding of its catalyt

219 ine or alanine inhibits H3K27 methylation by PRC2 on nucleosomes in vitro.

220 amics simulations to dissect the behavior of PRC2 on polynucleosome arrays.

221 rming a feed-forward regulatory network with PRC2 or repressing them independently of PRC2.

222 Moreover, the mechanisms underlying PRC2 overexpression in cancer are obscure.

223 e kinase c-Src links energy sufficiency with PRC2 overexpression via control of mRNA translation.

224 Polycomb repressive complex 2 (PRC2) places H3K27me3 at developmental genes and is caus

225 ssue of Cancer Cell, Burr et al. report that PRC2 plays a conserved role in silencing antigen present

226 Because of the key roles that PRC2 plays in development and disease, how this epigenet

227 PRC2 preferentially binds G tracts within nascent precur

228 of the genes corepressed by PRC2 and miRNAs, PRC2 promotes their miRNA-mediated repression by increas

229 regulation of polycomb repressive complex 2 (PRC2) promotes oncogenesis partly through its enzymatic

230 abidopsis polycomb-group repressor complex2 (PRC2) protein MEDEA (MEA) suppresses both pattern-trigge

231 inding of the Polycomb Repressive Complex 2 (PRC2) protein SUZ12 and deposition of the repressive his

232 , R-loop removal leads to decreased PRC1 and PRC2 recruitment and Pol II activation into a productive

233 Our findings indicate that PRC2 recruitment and propagation on chromatin are seemin

234 chanisms proposed to take part in modulating PRC2 recruitment and shaping H3K27 methylation patterns

235 ful for the targeted reversal of deleterious PRC2 recruitment events.

236 While occurring independently of PRC2 recruitment to chromatin, automethylation promotes

237 ression of the RET proto-oncogene by loss of PRC2 recruitment, and activation of the RET/p38 signalin

238 ing up previously CpG methylated regions for PRC2 recruitment, diluting PRC2 at Polycomb-repressed ge

239 Polycomb Repressive Complexes (PRC1 and PRC2) regulate developmental transitions in plants.

240 ost-transcriptionally reinforce silencing of PRC2-repressed genes that are inefficiently repressed at

241 We conclude that PRC2 requires RNA binding for chromatin localization in

242 ncludes consideration of factors influencing PRC2 residence time on chromatin and PRC2 catalytic acti

243 on pathway expression in a manner similar to PRC2 restoration.

244 Loss of PRC2 resulted in increased histone posttranslational mod

245 The physiological relevance of PRC2-RNA interactions is further underscored by a cardio

246 is through enhancing H3K27me3 deposition and PRC2's gene-regulatory functions, lending support for PR

247 f zeste 12 homolog (SUZ12), but mutations in PRC2's main catalytic subunit enhancer of zeste homolog

248 g and looping of DNA by PRC2, independent of PRC2's methylation activity, may contribute to heterochr

249 RC2 at target sites or inhibit the rate that PRC2 samples chromatin.

250 eric structural architecture, accounting for PRC2 self-association that has long been implicated.

251 Our study demonstrates a PRC2 self-regulatory mechanism through its EZH1/2-mediat

252 eir importance, the molecular details of how PRC2 "senses" H3K36 methylation are unclear.

253 Polycomb repressive complex 2 (PRC2) silences expression of developmental transcription

254 we show that Polycomb Repressive Complex 2 (PRC2) silencing is genetically required by FCA to repres

255 nct phases of Polycomb repressive complex 2 (PRC2) silencing.

256 s H3K27me3 within FLC On return to warm, PHD-PRC2 spreads across the locus delivering H3K27me3 to mai

257 have implications for the mechanism by which PRC2 spreads histone modifications and compacts chromati

258 In contrast, the PRC2 subunit Eed binds an intragenic Tbx3 enhancer to op

259 oncomitant cold-triggered increases in other PRC2 subunits and cofactors.

260 lobal H3K27 methylation levels, the non-core PRC2 subunits are collectively required for focusing H3K

261 tinct mechanistic roles for specific BAF and PRC2 subunits during ESC differentiation.

262 reases the translation of mRNAs encoding the PRC2 subunits Ezh2 and Suz12.

263 eciprocal interactions between PAS and known PRC2 subunits, and sequence similarity searches demonstr

264 rious Polycomb Repressive Complex (PRC)1 and PRC2 subunits, including CBX proteins, but also other ch

265 nteraction with all other core and accessory PRC2 subunits.

266 set of accessory proteins bound to the core PRC2 subunits.

267 erase reduce H3K27me3 proportionately at all PRC2 target sites, but ~40% uniform residual levels keep

268 Furthermore, PRC2-targeted therapeutics overcome gene silencing and p

269 that PHF19 interacts with PRC2 and binds to PRC2 targets on chromatin.

270 equirement of PHF19 for optimal silencing of PRC2 targets, which include cell cycle inhibitors and in

271 onstitute a significant proportion of direct PRC2 targets.

272 HIP and H3 K27M preferentially interact with PRC2 that is allosterically activated by H3K27me3 at CGI

273 ubunit of the polycomb-repressive complex 2 (PRC2) that can alter gene expression by trimethylating l

274 d function of polycomb repressive complex 2 (PRC2) that mediates coordinated transcriptional silencin

275 ponent of the Polycomb Repressive complex 2 (PRC2) that methylates H3K27, switches the gene into an a

276 tic subunit of Polycomb Repressor Complex 2 (PRC2), the enzyme that catalyzes monomethylation, dimeth

277 by inhibiting the histone methyltransferase PRC2, the details of this proposed mechanism nevertheles

278 independent of methyltransferase activity or PRC2, thereby facilitating DDB2 localization to cyclobut

279 mplex (NuRD) and polycomb-related complex 2 (PRC2) through the invariant proteins RBBP4 and RBBP7.

280 PRC2 thus plays essential roles in maintaining embryonic

281 of H3K27 methylation, such as recruitment of PRC2 to chromatin and/or stimulation of PRC2 activity, a

282 function mutations into the SUZ12 subunit of PRC2 to drive it into a PRC2.1 or 2.2 subcomplex in huma

283 We propose that EZH2 automethylation allows PRC2 to modulate its histone methyltransferase activity

284 Here, we visualized the binding of PRC2 to naked DNA in liquid at the single-molecule level

285 ection demonstrated that PRC1 functions with PRC2 to silence/dampen expression of adhesion genes.

286 ty, which is critical for the recruitment of PRC2 to the target chromatin.

287 recruits the polycomb repressive complex 2 (PRC2) to alter the H3K27me3 landscape and repress genes

288 ecruitment of polycomb repressive complex 2 (PRC2) to CpG island (CGI) chromatin.

289 e activity of Polycomb-repressive complex 2 (PRC2) to maintain these repressed gene profiles.

290 component of polycomb-repressive-complex 2 (PRC2), to repress the transcriptional program associated

291 r targets EZH2, the enzymatic subunit of the PRC2 transcriptional silencing complex.

292 In cells, PRC2 transfers from chromatin to pre-mRNA upon gene acti

293 s spectrometry analysis of recombinant human PRC2, we identified three methylated lysine residues (K5

294 R-DUB was previously shown to cooperate with PRC2, we observed minimal overlap and functional interac

295 member of the polycomb repressive complex 2 (PRC2) which methylates of histone 3 lysine 27 (H3K27).

296 ic subunit of Polycomb Repressive Complex 2 (PRC2), which minimally requires two other subunits, EED

297 ors (MPNSTs), Polycomb repressive complex 2 (PRC2), which plays a crucial role in gene silencing, is

298 ic subunit of polycomb repressive complex 2 (PRC2), which silences transcription through trimethylati

299 C10, largely due to unappreciated defects in PRC2, which confers sensitivity to combined BET/MEK inhi

300 ic subunit of polycomb repressive complex 2 (PRC2), with a focus on EZH2 inhibition as a potentially