EZH2 deficiency induced gene expression change in CRCs
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ABSTRACT:
PROVIDER: PRJNA668530 | ENA |
REPOSITORIES: ENA
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Project description:Knockdown of EZH2 in colorectal cancer cells by lentivirus-mediated shRNA, and use total RNA for sequencing analysis after determining the efficiency of EZH2 knockdown in order to analyze the gene expression affected by EZH2.
2021-05-01 | GSE159352 | GEO
Project description:To identify genes whose expression was suppressed by EZH2, we performed gene expression microarray analysis in control and EZH2 knockdown human SKOV3 EOC cells. Two individual short hairpin RNAs to the human EZH2 gene (shEZH2) were used to limit potential off-target effects. Two individual short hairpin RNAs to the human EZH2 gene (shEZH2) were used to limit potential off-target effects. Three technical replicates per group were used.
2011-12-12 | E-GEOD-31433 | biostudies-arrayexpress
Project description:To identify genes whose expression was suppressed by EZH2, we performed gene expression microarray analysis in control and EZH2 knockdown human SKOV3 EOC cells. Two individual short hairpin RNAs to the human EZH2 gene (shEZH2) were used to limit potential off-target effects.
2011-12-12 | GSE31433 | GEO
Project description:Overexpression of EZH2 in estrogen receptor negative (ER-) breast cancer promotes metastasis. EZH2 has been mainly studied as the catalytic component of the Polycomb Repressive Complex 2 (PRC2) that mediates gene repression by trimethylating histone H3 at lysine 27 (H3K27me3). However, how EZH2 drives metastasis despite the low H3K27me3 levels observed in ER- breast cancer is unknown. We have shown that in human invasive carcinomas and distant metastases, cytoplasmic EZH2 phosphorylated at T367 is significantly associated with ER- disease and low H3K27me3 levels. Here, we explore the interactome of EZH2 and of a phosphodeficient mutant EZH2_T367A. We identified novel interactors of EZH2, and identified interactions that are dependent on the phosphorylation and cellular localization of EZH2 that may play a role in EZH2 dependent metastatic progression.
2018-07-03 | PXD010073 | Pride
Project description:The symptoms of ataxia-telangiectasia (A-T) include a progressive neurodegeneration caused by ATM protein deficiency. We previously found that nuclear accumulation of histone deacetylase-4, HDAC4, contributes to this degeneration; we now report that increased histone H3K27 trimethylation (H3K27me3) mediated by polycomb repressive complex 2 (PRC2) also plays an important role in the A-T phenotype. Enhancer of zeste homolog 2 (EZH2), a core catalytic component of PRC2, is identified as a new ATM kinase target, and its S734 phosphorylation reduces protein stability. Thus, PRC2 formation is elevated along with H3K27me3in ATM deficiency. ChIP-sequencing shows a significant increase in H3K27me3 ‘marks’ and a dramatic shift in their location. The change of H3K27me3 chromatin-binding pattern is directly related to cell cycle re-entry and cell death of ATM-deficient neurons. Lentiviral knockdown of EZH2 rescues Purkinje cell degeneration and behavioral abnormalities in Atm / mice, demonstrating that EZH2-mediated H3K27me3 is another key factor in A-T neurodegeneration. Two samples each were run of brain total RNA from Atm+/+ and Atm-/- mice.
2013-10-25 | E-GEOD-50951 | biostudies-arrayexpress
Project description:The responses of macrophages to lipopolysaccharide (LPS) might determine the direction of clinical manifestations of sepsis, which is the immune response against severe infection. Meanwhile, the enhancer of zeste homologue 2 (Ezh2), a histone lysine methyltransferase of epigenetic regulation, might interfere with LPS response. With a single LPS stimulation, Ezh2 null(Ezh2flox/flox; LysM-Crecre/−) macrophages demonstrated lower supernatant TNF-α than Ezh2 control (Ezh2fl/fl; LysM-Cre−/−), perhaps due to an upregulation of Socs3, which is a suppressor of cytokine signaling 3, due to the loss of the Ezh2 gene. In LPS tolerance, Ezh2 null macrophages indicated higher supernatant TNF-α and IL-6 than the control, supporting an impact of the loss of the Ezh2 inhibitory gene. In parallel, Ezh2 null mice demonstrated lower serum TNF-α and IL-6 than the control mice after an LPS injection, indicating a less severe LPS-induced hyper-inflammation in Ezh2 null mice. In conclusion, an absence of Ezh2 in macrophages resulted in less severe LPS-induced inflammation, as indicated by low serum cytokines, with less severe LPS tolerance, as demonstrated by higher cytokine production, partly through the upregulated Socs3.
2023-07-20 | PXD041265 | Pride
Project description:Cold induced transcriptome change in skeletal muscle
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Project description:Expression profiles from Rag1 mutant and Rag1/Ezh2 double mutant double negative thymocytes Keywords = Rag1 Keywords = Ezh2 Keywords = Thymocyte Keywords: repeat sample
2005-09-01 | GSE1565 | GEO
Project description:EZH2 is shown to be involved in regulation of DNA damage repair which may contribute to development of breast tumor initiating cells. To identify genomic aberrations regulated by EZH2 expression, we performed genome wide copy number variation analysis in breast tumor initiating cells expressing EZH2 compared to the vector control. This finding suggests EZH2 contributes to oncogenic amplification in breast tumor initiating cells. Affymetrix SNP arrays were performed according to the manufacturer's directions on DNA extracted from primary breast tumor initiating cells infected with EZH2 or Vector control constructs Copy number variation analysis of Affymetrix SNP 6.0 arrays was performed and compared between EZH2 and Vector control infected groups
2010-09-17 | E-GEOD-24144 | biostudies-arrayexpress
Project description:Microarray experiments were performed to elucidate the transcriptome changes due to EZH2 deficiency in follicular T helper (TFH) cells. These data suggest TFH-lineage associated genes are down-regulated in EZH2-null TFH cells, indicating that EZH2 primes TFH differentiation by regulating canonical genes of TFH cells.
2018-12-25 | GSE110458 | GEO