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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.
BRD4 (show BRD4 ELISA Kits) positively regulates EZH2 transcription through upregulation of C-MYC (show MYC ELISA Kits), and is a novel promising target for pharmacologic treatment in transcriptional program intervention against this intractable disease.
findings suggest that EZH2 possesses anti-apoptotic activity in gastric tumorigenesis following STAT3 (show STAT3 ELISA Kits) activation
Inhibition of EZH2 (by GSK-343 or EPZ-6438) or inhibition of EHMT2 (show EHMT2 ELISA Kits) (by UNC-0638) in the Th17 primary cell model of HIV latency or resting memory T cells isolated from HIV-1-infected patients receiving highly active antiretroviral therapy, was sufficient to induce the reactivation of latent proviruses.
Data indicate that enhancer of zeste homolog 2 (Drosophila) protein (EZH2) is a direct target of microRNA miR (show MLXIP ELISA Kits)-126 and restoration of EZH2 expression blocks the suppressive roles of miR (show MLXIP ELISA Kits)-126.
the functional association between EZH2 expression and silencing of key tumor suppressor loci , was investigated.
H19 (show NCKAP1 ELISA Kits) inhibited E-cadherin (show CDH1 ELISA Kits) expression and promoted cell invasion of NPC (show NPC1 ELISA Kits) cells via the miR (show MLXIP ELISA Kits)-630/EZH2 pathway
We also showed that knockdown of urothelial carcinoma-associated 1 increased the p21 protein (show NRAS ELISA Kits) expression through regulating enhancer of zeste homolog 2. In addition, bioinformatics analysis and dual-luciferase reporter assays confirmed that miR (show MLXIP ELISA Kits)-495 was a target of urothelial carcinoma-associated 1 in renal cell carcinoma, and urothelial carcinoma-associated 1 promoted cell proliferation by negatively regulating miR (show MLXIP ELISA Kits)-495
EZH2, through a methyltransferase-independent mechanism, promotes the transcriptional activation of the non-canonical NF-kappaB (show NFKB1 ELISA Kits) subunit RelB (show RELB ELISA Kits)
enhancer of zeste homolog 2 (EZH2) accounts for the silence of 11beta-HSD2 (show HSD11B2 ELISA Kits) expression via trimethylation of histone H3 (show HIST3H3 ELISA Kits) lysine 27 at the promoter of the 11beta-HSD2 (show HSD11B2 ELISA Kits) gene.
In vivo silencing of SLFN11 was associated with marked deposition of H3K27me3, a histone modification placed by EZH2, within the gene body of SLFN11, inducing local chromatin condensation and gene silencing.
Menin (show MEN1 ELISA Kits) binds on the promoter of Inhbb (show INHBB ELISA Kits) gene where it favours the recruitment of Ezh2 via an indirect mechanism involving Akt (show AKT1 ELISA Kits)-phosphorylation.
EZH2 directly interacted with and stabilized BubR1 (show BUB1B ELISA Kits), an effect driving EZH2 into the concert of meiosis regulation.
A long noncoding RNA, lnc-beta-Catm, elicits EZH2-dependent beta-catenin (show CTNNB1 ELISA Kits) stabilization and sustains liver cancer stem cells self-renewal.
these results suggest that the inflammatory milieu found in Crohn's disease could lead to or result from deregulation of FOXP3 (show FOXP3 ELISA Kits)/EZH2-enforced T cell gene networks contributing to the underlying intestinal inflammation.
Data show that enhancer of zeste 2 polycomb (show CBX2 ELISA Kits) repressive complex 2 subunit (EZH2-containing PRC2) is required for differentiation of terminal effector CD8 (show CD8A ELISA Kits)+ T cells.
these data suggest that inhibition of Ezh2 promotes paracrine signaling in osteoblasts a
demonstrate that a specific interaction between the polycomb protein EZH2 and RNA made from B2 SINE retrotransposons controls stress-responsive genes in mouse cells. In the heat-shock model, B2 RNA binds stress genes and suppresses their transcription. Upon stress, EZH2 is recruited and triggers cleavage of B2 RNA. B2 degradation in turn upregulates stress genes.
The Ezh2 expression could be clearly seen in outer and inner hair cells, supporting cells, the stria vascularis, and spiral ganglion cells. Ezh2 continued to be expressed in the cochlear epithelium of adult mice.
Genetic inactivation of Ezh2 or Eed (show EED ELISA Kits) cooperates with NRASQ61K in leukemogenesis.
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