Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA227365 | ENA |
REPOSITORIES: ENA
Similar Datasets
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: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: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:This experiment sought to determine the chromatin structure and PRC2 occupancy at the promoters of all genes in mouse ESCs ChIP-seq for EZH2, SUZ12, and H3K27me3 were performed on WT E14 cells in 2 biological replicates each. In addition H3K27me3 ChIP-seq was also performed on a clone of E14 cells expressing a tagged version of EZH2, which for the purpose of this study was used as replicate #3.
2013-10-19 | E-GEOD-49431 | biostudies-arrayexpress
Project description:Ezh2 and EZH1 are histone H3 lysine 27 (H3K27)-specific methyltransferases. Their hyperactive mutations and overexpression were found in cancer including various hematological malignancies. UNC1999 is a highly selective inhibitor for both enzymes. It suppresses H3K27 tri- and di-methylation globally and inhibits growth of MLL-rearranged acute leukemia. Here we performed ChIP-Seq to profile how UNC1999 affects distribution of H3K27me3 and its antagonizing H3K27ac in MLL-AF9-immortalized leukemia cells. We also performed ChIP-seq of SUZ12, an essential common cofactor of EZH2 and EZH1 following compound treatments. We treated MLL-AF9 transformed murine leukemia cells with DMSO, UNC1999 or UNC2400 (an inactive analog compound of UNC1999). Cells were then collected and used for ChIP-Sequencing of Input, H3K27me3, SUZ12, and H3K27ac.
2014-10-30 | E-GEOD-62437 | biostudies-arrayexpress
Project description:Upon EZH2 inhibitor treatment, PRC2 components EZH2 and SUZ12 are redistributed across the genome towards a small number of genomic loci that are refractory to H3K27me3 loss. Focal PRC2 accumulation and H3K27me3 retention occur primarily at CpG islands and transcription start sites of genes, with enrichment at canonical PRC2 nucleation sites. EZH2 and SUZ12 are present at low levels at actively transcribed TSSs, and this signal is lost with EZH2 inhibition.
2019-08-09 | GSE134136 | GEO
Project description:H3K27me3, H3K79me2, and Suz12 ChIP-Seq in Human Embryonic Stem Cells (BG03).
| PRJNA132757 | ENA
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:A cDNA microarray analysis was performed on shRNA KDs of EZH2, SUZ12, BMI1, or CBX8 HepG2 cells.
| PRJNA235192 | ENA