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Study shows that the PRC2 core components are enriched in retinal progenitors and downregulated in differentiated cells. Knockdown of the PRC2 core component Ezh2 leads to reduced retinal progenitor proliferation.
Data show that embryonic stem cells with deletion of EZH1 (show EZH1 ELISA Kits) or EZH2 fail to differentiate into ectoderm lineages.
EZH2 directly binds to the Puma (show BBC3 ELISA Kits) promoter thus epigenetically repressing PUMA (show BBC3 ELISA Kits) expression in non-small cell lung cancer cells.
EZH2 was more highly expressed in the colorectal cancer stem (CCS (show CCS ELISA Kits))-like cell subpopulation than in the non-CCS (show CCS ELISA Kits)-like cell subpopulation. EZH2 knockdown significantly reduced the CD133+/CD44 (show CD44 ELISA Kits)+ subpopulation, suppressed mammosphere formation, and decreased the expression of self-renewal-related genes and strongly impaired tumor-initiating capacity in a re-implantation mouse model.
Results showed that EZH2 expression was significantly increased in metastatic lesions compared with primary lesions of breast cancer patients. High-level expression of EZH2 in metastatic lesions was associated with poorer overall survival outcomes after primary surgery and recurrence.
EZH2 can directly associate with ANCR, the ANCR-EZH2 binding is probably able to facilitate CDK1 interaction with EZH2 to promote phosphorylation of EZH2 at Thr-345 and Thr-487, and potentiate EZH2 ubiquitination degradation through ubiquitin-proteasome pathway.
Altered EZH2 splicing is associated with myelodysplastic syndrome.
Given that glioblastomas contain both proneural and mesenchymal GSCs, combined EZH2 and BMI1 (show BMI1 ELISA Kits) targeting proved more effective than either agent alone both in culture and in vivo, suggesting that strategies that simultaneously target multiple epigenetic regulators within glioblastomas may be effective in overcoming therapy resistance caused by intratumoral heterogeneity
The histone methyltransferase EZH2 is overexpressed in adverse-prognosis CLL and associated with increased cell survival and proliferation.
Enhancer of zeste homolog 2 (EZH2) expression is positively correlated with the expression of Wnt (show WNT2 ELISA Kits)/beta-catenin (show CTNNB1 ELISA Kits) signaling and negatively correlated with the expression of GSK-3beta (show GSK3b ELISA Kits) and TP53 (show TP53 ELISA Kits) in cervical cancer tissues.
Transwell invasion assay, wound healing assay and flow cytometry results showed that the inhibition of EZH2 or the up-regulation of miR (show MLXIP ELISA Kits)-101-3p inhibited the viability, migration, invasion and cell cycle but promoted cell apoptosis of lung squamous cell carcinoma.
ompounding a previously described Bmi1 (show BMI1 ELISA Kits)-transgene and Pten-deficiency prostate cancer mouse model with the Ezh2 transgene did not enhance tumour progression or drive metastasis formation. In conclusion, we here report the generation of a wildtype Ezh2 overexpression mouse model that allows for intravital surveillance of tissues with activated transgene
decline in HDAC9c expression over time was accompanied by increased EZH2 expression.
Long non-coding RNA LOC554202 may play an important role in the progression of chordoma by the direct upregulation of EZH2 and indirect promotion of RNF144B (show RNF144B ELISA Kits) via miR (show MLXIP ELISA Kits)-31
Gfi1 (show ZNF163 ELISA Kits) disruption antagonized the tumor-promoting effects of Ezh2 loss; conversely, Gfi1 (show ZNF163 ELISA Kits) overexpression collaborated with Myc (show MYC ELISA Kits) to bypass effects of Trp53 (show TP53 ELISA Kits) inactivation in driving medulloblastoma progression in primary cerebellar neuronal progenitors.
EZH2-deficient hESCs can initiate differentiation toward developmental lineages; however, they cannot fully differentiate into mature specialized tissues. Thus, EZH2 is required for stable ESC self-renewal, regulation of transcriptional programs, and for late-stage differentiation in this model of early human development.
we found that the miRNA biogenesis enzyme DICER was required for the binding of the PRC2 core components EZH2 and SUZ12, and for the presence of the PRC2-mediated histone modification H3K27me3 at many bivalent genes
High EZH2 expression is associated with Neuroblastoma (show ARHGEF16 ELISA Kits).
Biochemical as well as functional experiments revealed that Spt6 could compete for binding of the PRC2 methyltransferase Ezh2 to Suz12 and reduce PRC2 chromatin engagement.
These findings indicate that Ezh2 targets are the major targets of the epigenetic switch in MDS (show MECOM ELISA Kits) with Ezh2 insufficiency.
Insight regarding how androgen-induced extranuclear kinase signaling and intranuclear transcription through Ezh2 modifications may influence the expression pattern of genes, ultimately affecting various downstream physiological processes.
ezh2-deficient mutants fail to properly regenerate their spinal cord after caudal (show CAD ELISA Kits) fin transection suggesting that Ezh2 and H3K27me3 methylation might also be involved in the process of regeneration in zebrafish.
This gene encodes a member of the Polycomb-group (PcG) family. PcG family members form multimeric protein complexes, which are involved in maintaining the transcriptional repressive state of genes over successive cell generations. This protein associates with the embryonic ectoderm development protein, the VAV1 oncoprotein, and the X-linked nuclear protein. This protein may play a role in the hematopoietic and central nervous systems. Multiple alternatively splcied transcript variants encoding distinct isoforms have been identified for this gene.
enhancer of zeste 2
, enhancer of zeste homolog 2 (Drosophila)
, Polycomb protein EZH2
, histone-lysine N-methyltransferase EZH2
, histone-lysine N-methyltransferase EZH2-like
, Enhancer of zeste homolog 2-A
, Polycomb protein EZH2-A
, lysine N-methyltransferase 6
, enhancer of zeste homolog 2
, eyes absent homolog 2