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Human EZH2 Protein expressed in Human - ABIN2720645
Pedram Fatemi, Salah-Uddin, Modarresi, Khoury, Wahlestedt, Faghihi: Screening for Small-Molecule Modulators of Long Noncoding RNA-Protein Interactions Using AlphaScreen. in Journal of biomolecular screening 2015
Show all 2 references for ABIN2720645
Human EZH2 Protein expressed in Wheat germ - ABIN1353283
Guil, Soler, Portela, Carrère, Fonalleras, Gómez, Villanueva, Esteller: Intronic RNAs mediate EZH2 regulation of epigenetic targets. in Nature structural & molecular biology 2012
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.
The function of hsa (show CD24 Proteins)-miR (show MLXIP Proteins)-138-5p and its target EZH2 was involved in hippocampus in Down syndrome patients
PVT1 binds to EZH2, recruits EZH2 to the miR (show MLXIP Proteins)-200b promoter, increases histone H3K27 trimethylation level on the miR (show MLXIP Proteins)-200b promoter, and inhibits miR (show MLXIP Proteins)-200b expression.
The aurora kinase A (show AURKA Proteins) inhibited by MLN (show MLN Proteins) 8054 are both implicated in cell cycle progression and, thus, in cellular proliferation.Epigenetic regulators were targeted by SAHA inhibiting HDACs and by DZNep inhibiting the histone methyltransferase EZH2, which silences genes by trimethylating histone H3K27.Combinations of small molecular inhibitors act synergistically in rhabdoid tumor
MiR (show MLXIP Proteins)-203 may contribute to the metastasis and enhance apoptosis of hepatocellular carcinoma cells by regulating EZH2 and Bmi-1 (show BMI1 Proteins) expression.
We found a novel heterozygous EZH2 mutation within exon 5 that caused an amino acid change from proline to leucine at position 132 (p.Pro132Leu) within the catalytic D1 domain. Analysis of a remission sample also showed this mutation, indicating a germline mutation.
Suppression of EHZ2 using lentiviral small hairpin RNA inhibited hepatoblastoma cell proliferation, induced cell cycle arrest in G1 phase and enhanced the expression of G1/Sphase checkpoint protein p27 (show PAK2 Proteins).
Notch1 (show NOTCH1 Proteins) and EZH2 coexpression contributes to the progression and prognosis of breast invasive ductal carcinoma.
Mutating or deleting EZH2 can have both oncogenic and tumor suppressive functions by increasing or decreasing H3K27me3. (Review)
Loss of EZH2 expression is associated with increased transformation of myelodysplastic syndrome into acute myeloid leukemia (show BCL11A Proteins).
miR (show MLXIP Proteins)-214 was able to prevent cell death by targeting EZH2, the catalytic core component of PRC2 complex that is responsible for tri (show VANGL2 Proteins)-methylation reaction at lysine 27 (K27 (show KRT27 Proteins)) of histone 3 (H3 (show HIST3H3 Proteins)) (H3K27me3), by which As-induced miR (show MLXIP Proteins)-214 reduction
Genetic inactivation of Ezh2 or Eed (show EED Proteins) cooperates with NRASQ61K in leukemogenesis.
Study demonstrated that redundant EZH2 shifted mesenchymal stem cell lineage commitment to adipocyte, which contributed to the development of osteoporosis.
Data indicate increased natural killer (NK) lineage cells in Ezh2 (enhancer of zeste homolog 2)-deficient mice.
Ezh2 cooperates with let-7 microRNAs in silencing the fetal gene signature in BM HSPCs and restricts their transformation.
Conditional deletion of Ezh2 in the developing midbrain resulted in decreased neural progenitor proliferation, which is associated with derepression of cell cycle inhibitors and negative regulation of Wnt (show WNT2 Proteins)/beta-catenin (show CTNNB1 Proteins) signaling.
The dichotomous function of EZH2 in regulating differentiation and senescence in effector and regulatory T cells helps to explain the apparent existing contradictions in literature.
Modulation of Polycomb repressive complexes by either Ezh2 overexpression or Eed deletion enhances KRAS-driven adenomagenesis and inflammation
Study used Ezh2 conditional knockout mice to clarify the role of histone H3K27me3 modification in the retina
The presence of EZH2 is required to control progressive differentiation of milk secreting epithelium during pregnancy.
These results clearly demonstrated an essential role of Ezh1 (show EZH1 Proteins) in the pathogenesis of hematopoietic malignancies induced by Ezh2 insufficiency, and highlighted the differential functions of Ezh1 (show EZH1 Proteins) and Ezh2 in hematopoiesis.
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