Project description:Enhancer of Zeste Homolog 2 (EZH2) is a histone methyltransferase that catalyzes the trimethylation of histone H3 lysine 27 (H3K27me3). EZH2 expression is significantly upregulated in MPNST. In our study, we investigated the function of EZH2 and the molecular mechanisms that are regulated by EZH2 in MPNST pathogenesis. Our findings enhance the knowledge of EZH2’s function and biology, and have the potential to provide a novel therapeutic approach for MPNST patients in the clinic.
Project description:Enhancer of Zeste Homolog 2 (EZH2) is a histone methyltransferase that catalyzes the trimethylation of histone H3 lysine 27 (H3K27me3). EZH2 expression is significantly upregulated in MPNST. In our study, we investigated the function of EZH2 and the molecular mechanisms that are regulated by EZH2 in MPNST pathogenesis. Our findings enhance the knowledge of EZH2’s function and biology, and have the potential to provide a novel therapeutic approach for MPNST patients in the clinic.
Project description:The histone methyl transferase EZH2, a member of PRC2, is a master epigenetic regulator involved in histone H3 lysine 27 trimethylation and gene transcription repression. Here, we reported the K307 dimethylation of EZH2 could regulate its protein stability. Thus, to further investigate the biological significance of the K307 dimethylation of EZH2 and to explore its downstream regulated genes, we subsequently analyzed the genome-wide transcriptional targets of Ezh2K307R using an RNA sequencing (RNA-seq) approach in the livers of Ezh2K307R and WT mice.
Project description:Enhancer of Zeste Homolog 2 (EZH2) is a histone methyltransferase that catalyzes the trimethylation of histone H3 lysine 27 (H3K27me3). EZH2 expression is significantly upregulated in MPNST. In our study, we investigated the function of EZH2 and the molecular mechanisms that are regulated by EZH2 in MPNST pathogenesis. Our findings enhance the knowledge of EZH2’s function and biology, and have the potential to provide a novel therapeutic approach for MPNST patients in the clinic. An EZH2 knockdown experiment was carried out in MPNST cells. There are one control and one siEZH2 samples for three cell lines (724,462,26T) and two repeats for each cell line, so in total there are 8 samples. Two group comparison Two group comparison
Project description:Enhancer of Zeste Homolog 2 (EZH2) is a histone methyltransferase that catalyzes the trimethylation of histone H3 lysine 27 (H3K27me3). EZH2 expression is significantly upregulated in MPNST. In our study, we investigated the function of EZH2 and the molecular mechanisms that are regulated by EZH2 in MPNST pathogenesis. Our findings enhance the knowledge of EZH2’s function and biology, and have the potential to provide a novel therapeutic approach for MPNST patients in the clinic. An EZH2 knockdown experiment was carried out in MPNST cells. There are one control and one siEZH2 samples for two cell lines (724 and 462) and two repeats for each cell line, so in total there are 8 samples. Two group comparison
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.
Project description:Atherosclerosis is a focal disease that preferentially develop in the regions of atheroprone disturbed flow, but less in regions of atheroprotective laminar flow. The mechanisms by which atheroprotective laminar flow prevents atherosclerosis at the epigenetic level remain largely unknown. In this study, we observed that laminar flow decreased histone methyltransferase EZH2, which imposes a repressive epigenetic mark of histone 3 lysine 27 trimethylation (H3K27me3) onto target gene promoters, leading to transcriptional silencing. To evaluate the effect of atheroprotective flow on EZH2 and H3K27me3 dependent genome-wide transcriptional profile, we performed RNA-sequencing study on laminar flow and EZH2 siRNA treated human endothelial cells. Venn diagram was used to compare the common regulated genes by both laminar flow and EZH2 depletion. We found atheroprotective flow and EZH2 depletion altere endothelial gene landscape, which include upregulating atheroprotective genes while downregulating pro-atherosclerotic genes.
Project description:Normal cell type specific histone H3 lysine 27 trimethylation of miRNA genes. HMEC and HMF represent two distinct differentiated cell type present in mammary gland each with a distinct phenotype, a distinct epigenotype as well as distinct miRNA expression pattern. The aim of the study was to determine how epigenetic modifications including histone H3 lysine 27 trimethylation affect miRNA expression. Two cell types HMEC vs. HMF. Biological replicates: 3 pairs of HMEC-HMF of 3 distinct genotypes. Immunoprecipitation using anti-histone H3 trimethylated at lysine 27 (07-449, Millipore).