Recombinant Mouse Histone-lysine N-methyltransferase EZH2 (Ezh2)

1. Exogenous RA signaling activation in the Ezh2 mutants leads to synergistic activation of the anti-osteogenic factors in the cranial mesenchyme in vivo. Thus, RA signaling and EZH2 can function in parallel to guide calvarial bone progenitor commitment by balancing the suppression of anti-osteogenic factors. PMID: 30222957
2. p38-mediated phosphorylation at threonine 367 induces EZH2 cytoplasmic localization to promote breast cancer metastasis. PMID: 30022044
3. Targeting EZH2 reactivates a breast cancer subtype-specific anti-metastatic transcriptional program driven by FOXC1. PMID: 29959321
4. Praja1 promotes skeletal myogenesis through degradation of EZH2 upon p38alpha activation. PMID: 28067271
5. the data demonstrate that EZH2 is essential in facilitating epigenetic changes that regulate antibody-secreting cell fate, function, and metabolism. PMID: 29288200
6. Data show that the histone methyltransferase Ezh2 controls CD8(+) T memory precursor formation and antitumor activity. PMID: 29242551
7. Ezh2 maintains the repression of key cell senescence inducer genes through H3K27me3, and deletion of Ezh2 in early pubertal mice results in premature cellular senescence, depleted MSPCs pool, and impaired osteogenesis as well as osteoporosis in later life. PMID: 29101351
8. Our data demonstrates that EZH2 participates in Glioblastoma multiforme-induced immune deficient and EZH2 suppression in Glioblastoma multiforme can remodel microglia immune functions PMID: 29132376
9. the induction of EZH2 led to beta-catenin signaling activation by increasing H3K27me3 on the promoter of SFRP1, while the inhibition of EZH2 silenced beta-catenin signaling. Finally, intraarticular injection of EPZ005687 delayed OA development in mice. These results implicated EZH2 activity in OA development. Pharmacological inhibition of EZH2 may be an effective therapeutic approach for osteoarthritis. PMID: 27539752
10. PRC2-mediated repression of SMARCA2 predicts EZH2 inhibitor activity in SWI/SNF mutant tumors. PMID: 29087303
11. EZH2 plays a nonclassical role in the regulation of spermatogonial differentiation and apoptosis in murine spermatogenesis. PMID: 28982932
12. macroH2A1.1 (mH2A1.1), a variant of histone H2A, was upregulated during adipocyte differentiation in 3T3-L1 cells and in the white adipose tissue of obese mice. mH2A1.1 regulated Wnt/beta-catenin signaling pathway by cooperating with EZH2, a histone H3K27 methyltransferase, thus led to accumulation of H3K27me2 and H3K27me3 on the promoters of Wnt genes. PMID: 28992292
13. findings highlight an epigenetic mechanism by which EZH2 integrates the multifaceted effects of TNFalpha signaling to promote the inflammatory response and apoptosis in colitis. PMID: 28439030
14. cardiomyocyte-specific loss of Ezh2 did not affect fibrotic scar size after MI or apical resection at P7, suggesting that it does not extend the regenerative time window. Our results demonstrate that Ezh2 is not required for innate neonatal cardiac regeneration PMID: 29466371
15. results, together with our previous report, support a cell lineage-specific mechanism of Ezh2-mediated gene repression, especially those critically involved in cellular function and homeostasis PMID: 29408885
16. CARM1 promotes EZH2-mediated silencing of EZH2/BAF155 target tumor suppressor genes by methylating BAF155. PMID: 29434212
17. EZH2 mediates germinal centre (GC) formation through epigenetic silencing of CDKN1A and release of cell cycle checkpoints. PMID: 29026085
18. It has been demonstrated that FAK depletion reduces hepatocellular carcinoma cell growth by affecting cancer-promoting genes including the pro-oncogene EZH2. PMID: 28338656
19. decline in HDAC9c expression over time was accompanied by increased EZH2 expression. PMID: 27250566
20. 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 via miR-31 PMID: 28963737
21. Gfi1 disruption antagonized the tumor-promoting effects of Ezh2 loss; conversely, Gfi1 overexpression collaborated with Myc to bypass effects of Trp53 inactivation in driving medulloblastoma progression in primary cerebellar neuronal progenitors. PMID: 28329683
22. 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. PMID: 27926872
23. 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 PMID: 27150236
24. High EZH2 expression is associated with Neuroblastoma. PMID: 28807939
25. 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. PMID: 29033324
26. These findings indicate that Ezh2 targets are the major targets of the epigenetic switch in MDS with Ezh2 insufficiency. PMID: 27694924
27. 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. PMID: 28666321
28. results uncover a crucial role for EZH2 in adaptive lymphocytes to control the developmental timing of effectors of the pre-Ag receptor checkpoints PMID: 28490575
29. These findings identify the Ezh2-Hsp90 interaction as a previously unrecognized mechanism essential for T-cell responses and an effective target for controlling graft-versus-host disease. PMID: 28246193
30. Eed and Ezh2 have distinct roles in urothelial differentiation PMID: 28049658
31. Findings uncover an Ezh2-dependent mechanism to restrict the smooth muscle gene expression program in the developing mesothelium and allow appropriate cell fate decisions to occur in this multipotent mesoderm lineage. PMID: 27578795
32. This study identified Ezh2 as enriched in melanoma cancer stem cells (MCS cells) and showed that Ezh2 knockdown or treatment with small molecule Ezh2 inhibitors reduces MCS cell spheroid formation, survival, invasion and migration. PMID: 26693692
33. Ezh2-/- deletion resulted in skeletal deformities, increased osteoclastogenic potential and upregulation of Rankl and M-csf expression by mesenchymal stem cells. PMID: 27934660
34. These findings indicate Ezh2/PRC2 plays crucial roles in regulating neurogenesis from both cerebellar germinal zones. PMID: 27068104
35. our results revealed a novel mechanism in which EZH2 stability is regulated by SKP2 through the TRAF6-mediated and K63-linked ubiquitination, which contributes to elevated levels of H3K27me3 during prostate tumorigenesis and CRPC growth. PMID: 27869166
36. N-Myc Induces an EZH2-Mediated Transcriptional Program Driving Neuroendocrine Prostate Cancer and redirects EZH2 activity and sensitizes cells to EZH2 inhibitors. PMID: 27728805
37. we propose that through its control of PLZF concentration, Ezh2 maintains NKT cell numbers at appropriate levels and facilitates immune homeostasis. We believe that our study establishes a paradigm for alternative roles of Ezh2 and non-histone methylation in the regulation of cell fate determination. PMID: 28223321
38. Residual PRC2 activity, via EZH2 binding to mutant H3K27M histones, is required for the proliferation of H3K27M-expressing diffuse intrinsic pontine gliomas. PMID: 28263309
39. EZH2 is part of the protein machinery that shapes the aging epigenome. PMID: 28249716
40. S6K1 phosphorylation of H2B mediates EZH2 trimethylation of H3 early in adipogenesis, contributing to the promotion of obesity. PMID: 27151441
41. results suggest that loss of Ezh2 cooperates with Jak2V617F in the development of myelofibrosis in Jak2V617F PMID: 27081096
42. JAK2-V617F-expressing mice treated with an Ezh2 inhibitor showed higher platelet counts than vehicle controls. Our data support the proposed tumor suppressor function of EZH2 PMID: 27401344
43. an EZH2 insufficiency not only cooperated with active JAK2 to induce MF, but also conferred an oncogenic addiction to the H3K27ac modification in primary myelofibrosis -initiating cells that was capable of being restored by bromodomain inhibition. PMID: 27401345
44. The findings obtained from apoE-/- mice provide epigenetic insights into how EZH2 increases the risk of atherosclerotic heart disease. One of the pathways by which EZH2 leads to lipid accumulation and foam cell formation is via epigenetic downregulation of ABCA1 expression. PMID: 27295295
45. Our data uncover a dual role of PRC2 in intestinal homeostasis highlighting the importance of this repressive layer in controlling cell plasticity and lineage choices in adult tissues PMID: 27585866
46. The levels of EZH2 and H3K27me3 were increased in the aorta of ApoE-/- mice fed a high-methionine diet for 16 weeks, whereas miR-92a expression was decreased. PMID: 27936205
47. the functional association between EZH2 expression and silencing of key tumor suppressor loci , was investigated. PMID: 27419533
48. Menin binds on the promoter of Inhbb gene where it favours the recruitment of Ezh2 via an indirect mechanism involving Akt-phosphorylation. PMID: 28215965
49. these results suggest that the inflammatory milieu found in Crohn's disease could lead to or result from deregulation of FOXP3/EZH2-enforced T cell gene networks contributing to the underlying intestinal inflammation. PMID: 27909059
50. Data show that enhancer of zeste 2 polycomb repressive complex 2 subunit (EZH2-containing PRC2) is required for differentiation of terminal effector CD8+ T cells. PMID: 28410989

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KEGG: mmu:14056

STRING: 10090.ENSMUSP00000080419

UniGene: Mm.246688