Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA235192 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Polycomb group (PcG) proteins including EZH2, SUZ12 ,BMI1,CBX8 and so on, which specifically catalyze trimethylation of histone 3 lysine 27 (H3K27me3), and methylated H3K27 can be recognized by other specific binding proteins to compress chromatin structure, leading to the transcriptional repression of the target genes. To explore a potential functional implication of PcG components in HCC, we stably transfected HepG2 cells with either vectors or constructs expressing shRNA that specifically targets EZH2, SUZ12, BMI1, or CBX8. A cDNA microarray analysis was performed on shRNA KDs of EZH2, SUZ12, BMI1, or CBX8 HepG2 cells. To obtain a broader understanding of the molecular network of PcG in HCC, the whole genome microarray expression profiling was performed on shRNA KDs of EZH2, SUZ12, BMI1, or CBX8 HepG2 cells. Comparison of gene expression results from shRNA KDs of EZH2, SUZ12, BMI1 or CBX8 HepG2 cells.
2014-01-16 | E-GEOD-54108 | biostudies-arrayexpress
Project description:Polycomb group (PcG) proteins including EZH2, SUZ12 ,BMI1,CBX8 and so on, which specifically catalyze trimethylation of histone 3 lysine 27 (H3K27me3), and methylated H3K27 can be recognized by other specific binding proteins to compress chromatin structure, leading to the transcriptional repression of the target genes. To explore a potential functional implication of PcG components in HCC, we stably transfected HepG2 cells with either vectors or constructs expressing shRNA that specifically targets EZH2, SUZ12, BMI1, or CBX8. A cDNA microarray analysis was performed on shRNA KDs of EZH2, SUZ12, BMI1, or CBX8 HepG2 cells. To obtain a broader understanding of the molecular network of PcG in HCC, the whole genome microarray expression profiling was performed on shRNA KDs of EZH2, SUZ12, BMI1, or CBX8 HepG2 cells.
2014-01-16 | GSE54108 | GEO
Project description:Polycomb group (PcG) proteins including EZH2, SUZ12 and so on, which specifically catalyze trimethylation of histone 3 lysine 27 (H3K27me3), and methylated H3K27 can be recognized by other specific binding proteins to compress chromatin structure, leading to the transcriptional repression of the target genes. To completely understand the epigenetic profile and molecular network of PcG in HCC, we performed ChIP-on-chip screens with EZH2, SUZ12 and H3K27me3 antibodies in HepG2 cells. Comparison of ChIP-on-chip results from EZH2, SUZ12 and H3K27me3.
2013-11-13 | E-GEOD-52300 | biostudies-arrayexpress
Project description:We sequenced mRNA from F9 cells after knockdown of EZH2, SUZ12 and EED by shRNA. EZH2, SUZ12 and EED are the core componnets of PRC2 which repress its target genes by H3K27me3.
2018-02-27 | GSE111145 | GEO
Project description:Suz12 in hematopoiesis II. Retroviral Infection and shRNA-mediated knock-down of Suz12 and Ezh2 in mouse G1ME cells.
2008-07-03 | E-TABM-396 | biostudies-arrayexpress
Project description:EBV proteins EBNA3A, EBNA3B and EBNA3C control hundreds of host genes after infection. Changes in epigenetic marks around EBNA3-regulated genes suggest they exert transcriptional control in collaboration with epigenetic factors. The roles of PRC2 subunit SUZ12 and of PRC1 subunit BMI1 were assessed for their importance in EBNA3-mediated repression and activation. ChIP-seq experiments for SUZ12 and BMI1 were performed to determine their global localization on chromatin and analysis offered further insight into polycomb protein distribution in differentiated cells. Their localization was compared to that of each EBNA3, to resolve longstanding questions about the EBNA3-polycomb relationship. SUZ12 did not co-localize with any EBNA3, whereas EBNA3C co-localized significantly and co-immunoprecipitated with BMI1. In cells expressing a conditional EBNA3C, BMI1 was sequestered to EBNA3C binding sites after EBNA3C activation. When SUZ12 or BMI1 was knocked down in the same cells, SUZ12 did not contribute to EBNA3C-mediated regulation. Surprisingly, after BMI1 knock down, EBNA3C repressed equally efficiently, but host gene activation by EBNA3C was impaired. This overturns previous assumptions about BMI1/PRC1 functions during EBNA3C-mediated regulation, for the first time identifies directly a host factor involved in EBNA3-mediated activation and provides a new insight of how PRC1 can be involved in gene activation.
2018-10-14 | GSE119823 | GEO
Project description:Polycomb group (PcG) proteins including EZH2, SUZ12 and so on, which specifically catalyze trimethylation of histone 3 lysine 27 (H3K27me3), and methylated H3K27 can be recognized by other specific binding proteins to compress chromatin structure, leading to the transcriptional repression of the target genes. To completely understand the epigenetic profile and molecular network of PcG in HCC, we performed ChIP-on-chip screens with EZH2, SUZ12 and H3K27me3 antibodies in HepG2 cells.
2013-11-13 | GSE52300 | GEO
Project description:We report that these features are associated with distinct transcriptional programs, with vascular regions showing a proneural profile and hypoxic regions a mesenchymal pattern. As these regions harbor glioma stem cells (GSCs), we investigated the epigenetic regulation of these two niches. Proneural, perivascular GSCs activated EZH2, whereas mesenchymal GSCs in hypoxic regions expressed BMI1 protein. To determine the differential regional activation of EZH2 and BMI1 function, we performed chromatin immunoprecipitation followed by deep sequencing (ChIP-seq) with H3K27me3 (histone modification by EZH2) or H2AK119Ub (histone modification by BMI1) antibodies in CD15-postive GSCs from enhancing and necrotic regions of two GBM specimens, and found over 80% of regional specific target genes displayed distinct H3K27me3 or H2AK119Ub marks, indicating distinct PRC function in GSCs residing in different regions. H3K27me3, generally associated with inhibition of transcription, marked neuronal and cellular development targets in both the enhancing and necrotic regions, albeit without substantial overlap in gene identity, with EZH2/SUZ12/H3K27me3 targets most significantly in the enhancing regions. In contrast, H2AK119Ub marked very different targets in the enhancing and necrotic regions, with H2AK119Ub in CD15-positive GSCs from the hypoxia (necrotic) regions marking genes strongly associated with mesenchymal subtype signaling pathways, such as TGFb, NFkB, and WNT, indicating probable microenvironment-specific functions of EZH2 and BMI1.
2017-10-01 | GSE103274 | GEO
Project description:Chip-chip from HepG2 cells with EZH2, SUZ12 and H3K27me3
| PRJNA227365 | ENA
Project description:Polycomb Repressive Complex 2 (PRC2) plays crucial roles in transcriptional regulation and stem cell development. However, the context-specific functions associated with alternative subunits remain largely unexplored. Here we show that the related enzymatic subunits EZH1 and EZH2 undergo an expression switch during hematopoiesis. We examine the in vivo stoichiometry of the PRC2 complexes by quantitative proteomics and reveal the existence of an EZH1-SUZ12 sub-complex lacking EED. We provide evidence that EZH1 together with SUZ12 form a non-canonical PRC2 complex, occupy active chromatin domains in the absence of H3K27me3, and positively regulate gene expression. Loss of EZH2 expression leads to global repositioning of EZH1 chromatin occupancy to EZH2 targets. Moreover, we demonstrate that an erythroid-specific enhancer mediates transcriptional activation of EZH1, and a switch from GATA2 to GATA1 controls the developmental EZH1/2 switch by differential association with EZH1 enhancers during erythropoiesis. Thus, the lineage- and developmental stage-specific regulation of PRC2 expression and subunit composition leads to a switch from canonical silencing to non-canonical PRC2 functions during blood stem cell specification. Transcriptional profiling in primary human fetal liver proerythroblasts upon lentiviral shRNA-mediated knockdown of EZH1, EZH2, EED, or SUZ12 by RNA-seq analysis.
2015-01-01 | E-GEOD-59089 | biostudies-arrayexpress