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Enhancer of zeste homolog 2

EZH2, enhancer of zeste homolog 2
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. [provided by RefSeq, Feb 2011] (from NCBI)
Top mentioned proteins: Histone, Polycomb, CAN, V1a, miR
Papers using EZH2 antibodies
Fate tracing reveals the endothelial origin of hematopoietic stem cells
Nizetic D et al., In Oncogene, 2007
... Mouse monoclonal anti-hRUNX1 antibody and rabbit polyclonal anti-mouse EZH2 antibody were from Abcam (Cambridge, UK) ...
Endothelial barrier disruption by VEGF-mediated Src activity potentiates tumor cell extravasation and metastasis
Oshima Robert G. et al., In Oncogene, 2003
... (Covance, PRB-155P); CD31 (Pharmingen, 01951D, BD Bioscience), PCNA (Sigma, P8825), smooth muscle actin (Sigma, C6198), EZH2 (6A10, Novocastra and AC22, Cell Signaling).
Papers on EZH2
Mutations in epigenetic modifiers in acute myeloid leukemia and their clinical utility.
Tien et al., Taipei, Taiwan. In Expert Rev Hematol, Feb 2016
Somatic mutations in epigenetic modifiers, including IDH1, IDH2, TET2, DNAMT3A, ASXL1, MLL and EZH2 are enriched in patients with acute myeloid leukemia (AML), especially those with intermediate-risk cytogenetics.
An ornamental plant targets epigenetic signaling to block cancer stem cell-driven colon carcinogenesis.
Umar et al., Kansas City, United States. In Carcinogenesis, Feb 2016
Relative levels of β-catenin, Notch-ICD, Hes1 and EZH2 were also attenuated by AR extract.
A double-negative feedback loop between EZH2 and miR-26a regulates tumor cell growth in hepatocellular carcinoma.
Hu et al., Wuhan, China. In Int J Oncol, Feb 2016
In the present study, we performed western blot analysis, qRT-PCR, luciferase reporter assay and chromatin immunoprecipitation assay to investigate the relationship between miR-26a and the enhancer of zest homologue 2 (EZH2).
Osteogenic potential of human adipose-tissue derived mesenchymal stromal cells cultured on 3D-printed porous structured titanium.
van Wijnen et al., Rochester, United States. In Gene, Feb 2016
Compared to standard tissue culture plastic, AMSCs grown in the porous titanium microenvironment showed differences in temporal expression for genes involved in cell cycle progression (CCNB2, HIST2H4), extracellular matrix production (COL1A1, COL3A1), mesenchymal lineage identity (ACTA2, CD248, CD44), osteoblastic transcription factors (DLX3, DLX5, ID3) and epigenetic regulators (EZH1, EZH2).
Atypical teratoid/rhabdoid tumors-current concepts, advances in biology, and potential future therapies.
Chi et al., Boston, United States. In Neuro Oncol, Feb 2016
Among these are the pathways of cyclin D1/cyclin-dependent kinases 4 and 6, Hedgehog/GLI1, Wnt/ß-catenin, enhancer of zeste homolog 2, and aurora kinase A, among others.
MicroRNAs in CD4(+) T cell subsets are markers of disease risk and T cell dysfunction in individuals at risk for type 1 diabetes.
Harrison et al., Australia. In J Autoimmun, Feb 2016
For example, in pre-T1D, increased expression of miR-26a in nTreg activated in vivo or in vitro was associated with decreased expression of its target, the histone methyltransferase EZH2.
Cancer mediates effector T cell dysfunction by targeting microRNAs and EZH2 via glycolysis restriction.
Zou et al., Ann Arbor, United States. In Nat Immunol, Jan 2016
Here we found that ovarian cancers imposed glucose restriction on T cells and dampened their function via maintaining high expression of microRNAs miR-101 and miR-26a, which constrained expression of the methyltransferase EZH2.
Myelodysplastic syndromes: Contemporary review and how we treat.
Tefferi et al., Rochester, United States. In Am J Hematol, Jan 2016
With the advent of next generation sequencing, recurrent somatic mutations in genes involved in epigenetic regulation (TET2, ASXL1, EZH2, DNMT3A, IDH1/2), RNA splicing (SF3B1, SRSF2, U2AF1, ZRSR2), DNA damage response (TP53), transcriptional regulation (RUNX1, BCOR, ETV6) and signal transduction (CBL, NRAS, JAK2) have been identified in MDS.
SWI/SNF-mutant cancers depend on catalytic and non-catalytic activity of EZH2.
Roberts et al., Boston, United States. In Nat Med, Dec 2015
Here we show that EZH2, a catalytic subunit of the polycomb repressive complex 2 (PRC2), is essential in all tested cancer cell lines and xenografts harboring mutations of the SWI/SNF subunits ARID1A, PBRM1, and SMARCA4, which are several of the most frequently mutated SWI/SNF subunits in human cancer, but that co-occurrence of a Ras pathway mutation is correlated with abrogation of this dependence.
Myeloproliferative neoplasms: Current molecular biology and genetics.
Saeidi, Kermān, Iran. In Crit Rev Oncol Hematol, Dec 2015
Some other genes' location such as TET oncogene family member 2 (TET2), additional sex combs-like 1 (ASXL1), casitas B-lineage lymphoma proto-oncogene (CBL), isocitrate dehydrogenase 1/2 (IDH1/IDH2), IKAROS family zinc finger 1 (IKZF1), DNA methyltransferase 3A (DNMT3A), suppressor of cytokine signaling (SOCS), enhancer of zeste homolog 2 (EZH2), tumor protein p53 (TP53), runt-related transcription factor 1 (RUNX1) and high mobility group AT-hook 2 (HMGA2) have also identified to be involved in MPNs phenotypes.
Epigenetic silencing of TH1-type chemokines shapes tumour immunity and immunotherapy.
Zou et al., Ann Arbor, United States. In Nature, Dec 2015
Using human ovarian cancers as our model, here we show that enhancer of zeste homologue 2 (EZH2)-mediated histone H3 lysine 27 trimethylation (H3K27me3) and DNA methyltransferase 1 (DNMT1)-mediated DNA methylation repress the tumour production of T helper 1 (TH1)-type chemokines CXCL9 and CXCL10, and subsequently determine effector T-cell trafficking to the tumour microenvironment.
Challenges in profiling and lead optimization of drug discovery for methyltransferases.
Horiuchi, United States. In Drug Discov Today Technol, Nov 2015
Protein methyltransferases are one of the target classes which have gained attention as potential therapeutic targets after promising results of inhibitors for EZH2 and DOT1L in clinical trials.
Loss of BAP1 function leads to EZH2-dependent transformation.
Levine et al., New York City, United States. In Nat Med, Nov 2015
Here we demonstrate that Bap1 loss in mice results in increased trimethylated histone H3 lysine 27 (H3K27me3), elevated enhancer of zeste 2 polycomb repressive complex 2 subunit (Ezh2) expression, and enhanced repression of polycomb repressive complex 2 (PRC2) targets.
Ductal pancreatic cancer modeling and drug screening using human pluripotent stem cell- and patient-derived tumor organoids.
Muthuswamy et al., Toronto, Canada. In Nat Med, Nov 2015
Tumor organoids maintain the differentiation status, histoarchitecture and phenotypic heterogeneity of the primary tumor and retain patient-specific physiological changes, including hypoxia, oxygen consumption, epigenetic marks and differences in sensitivity to inhibition of the histone methyltransferase EZH2.
Identification of novel pathogenic gene mutations in pediatric acute myeloid leukemia by whole-exome resequencing.
Shiba, In Rinsho Ketsueki, 2014
A new class of gene mutations, identified in the pathogenesis of adult acute myeloid leukemia (AML), includes DNMT3A, IDH1/2, TET2 and EZH2.
Ezh2 augments leukemogenicity by reinforcing differentiation blockage in acute myeloid leukemia.
Iwama et al., Chiba, Japan. In Blood, 2012
Ezh2 inhibits differentiation programs in leukemic stem cells, thereby augmenting their leukemogenic activity.
Cancer angiogenesis induced by Kaposi sarcoma-associated herpesvirus is mediated by EZH2.
Gao et al., Minneapolis, United States. In Cancer Res, 2012
Taken together, our findings indicate that KSHV regulates the host epigenetic modifier EZH2 to promote angiogenesis.
Intronic RNAs mediate EZH2 regulation of epigenetic targets.
Esteller et al., Barcelona, Spain. In Nat Struct Mol Biol, 2012
Overexpression of EZH2-bound intronic RNA for the H3K4 methyltransferase gene SMYD3 is concomitant with an increase in EZH2 occupancy throughout the corresponding genomic fragment and is sufficient to reduce levels of the endogenous transcript and protein
The enhancer of zeste homolog 2 (EZH2), a potential therapeutic target, is regulated by miR-101 in renal cancer cells.
Tomita et al., Yamagata, Japan. In Biochem Biophys Res Commun, 2012
these results show nuclear EZH2 as a prognostic marker of worse survival in human RCC, and identify miR-101 as a negative regulator of EZH2 expression and renal cancer cell proliferation.
Notch1 intracellular domain increases cytoplasmic EZH2 levels during early megakaryopoiesis.
Banerjee et al., Calcutta, India. In Cell Death Dis, 2011
Interaction of EZH2 with LIMK1 changed the activity of cofilin (a downstream target of LIMK1) towards actin filaments, thereby leading to lower filamentous actin content within these cells.
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