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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.
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.
inactivating mutations of KDM6A (show KDM6A ELISA Kits), which are common in urothelial bladder carcinoma, are potentially targetable by inhibiting EZH2.
Loss of PRC2-mediated gene expression is accompanied by up-regulation of EZH2 and HIF1A (show HIF1A ELISA Kits) in breast cancer.
Combination of TPA (show PLAT ELISA Kits) with GSK126, an inhibitor of the catalytic activity of EZH2, has a synergic effect on the induction of muscle differentiation in embryonal rhabdomyosarcoma cells.
decline in HDAC9c expression over time was accompanied by increased EZH2 expression.
TT genotype of EZH2 (rs2072408) was associated with lymph node metastasis and the depth of gastric wall invasion in patients with gastric cancer.
Results show that EZH2 is a direct target of miR (show MLXIP ELISA Kits)-101 and an inverse relationship was found between lncRNA XIST and miR (show MLXIP ELISA Kits)-101 where lncRNA XIST exerted its tumor-suppressive effects at least in part through regulating miR (show MLXIP ELISA Kits)-101 to modulate EZH2 expression.
Overexpression of the wild-type TET1/2/3 3'UTR (show UTS2R ELISA Kits) caused a significant increase in EZH2 expression and tumor growth, whereas the mutation in miR (show MLXIP ELISA Kits)-26-binding sites abolished this effect.
The EZH2-mediated change in the epigenome of oral squamous cell carcinoma cells induces upregulation of ROS1 and its target genes, conferring greater invasiveness and plasticity to cope with the tumor microenvironment.
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.
results uncover a crucial role for EZH2 in adaptive lymphocytes to control the developmental timing of effectors of the pre-Ag receptor checkpoints
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