EZH2 Antibodies

Histone-lysine N-methyltransferase EZH2 (EZH2)

Polycomb group (PcG) protein. Catalytic subunit of the PRC2/EED-EZHtwo complex, which methylates'Lys-9' (H3K9me) and'Lys- 27' (H3K27me) of histone H3, leading to transcriptional repression of the affected target gene.

Willing to mono-, di- and trimethylate'Lys-27' of histone H3 to form H3K27me1, H3K27me2 and H3K27me3, respectively. Displays a preference for substrates with less methylation, loses action when increasingly more methyl groups are incorporated into H3K27, H3K27me0 > H3K27me1 > H3K27me2 (PubMed:22323599).

Gene Information

Human
Gene Name:	EZH2
Uniprot:	Q15910
Entrez:	2146

Family

Belongs to:
class V-like SAM-binding methyltransferase superfamily

Alternative Names

EC 2.1.1; EC 2.1.1.43; enhancer of zeste (Drosophila) homolog 2; enhancer of zeste 2; enhancer of zeste homolog 2 (Drosophila); Enhancer of zeste homolog 2; ENX1; ENX-1KMT6EZH1KMT6A; EZH2; histone-lysine N-methyltransferase EZH2; KMT6; Lysine N-methyltransferase 6; MGC9169

Molecular Weight

Mass (kDA):
85.363 kDA

Genomic Context

Human
Location:	7q36.1
Sequence:	7; NC_000007.14 (148807374..148884344, complement)

Tissue Specificity

Expressed in many tissues. Overexpressed in numerous tumor types including carcinomas of the breast, colon, larynx, lymphoma and testis.

Subcellular Localizations

Nucleus.

Diseases

• Malignant Neoplasms
• Neoplasms
• Carcinoma
• Cell Transformation, Neoplastic
• Malignant Neoplasm Of Prostate
• Neoplasm Metastasis
• Prostatic Neoplasms
• Malignant Paraganglionic Neoplasm
• Malignant Neoplasm Of Breast
• Leukemia
• Mammary Neoplasms
• Cell Invasion

• Lymphoma
• Myeloid Leukemia
• Neoplasm Invasiveness
• Leukemia, Myelocytic, Acute
• Adenocarcinoma
• Carcinogenesis

Interacting Proteins

• ASXL1
• ATRX
• CEP63
• DNMT1
• DNMT3A

• DNMT3B
• Dnmt3l
• EED
• PHF1
• RARA

• STAT3
• SUV39H1
• SUZ12

Pathways

• Methylation
• Cell Cycle
• Gene Silencing
• Cell Proliferation
• Dna Methylation
• Histone Methylation
• Pathogenesis
• Cell Growth
• Rna Interference
• Cell Differentiation
• Oncogenesis
• Histone Modification
• Senescence

• Cell Cycle Arrest
• Demethylation
• Chromatin Remodeling
• Angiogenesis
• Cell Migration
• Stem Cell Maintenance
• Dna Repair

PTMs

• Methylation
• Phosphorylation
• Acetylation
• Demethylation
• Ubiquitination
• Deacetylation

• Reduction
• Cleavage
• Sumoylation
• Hydroxylation
• Dephosphorylation
• Myristoylation

Research Areas

• Breast Cancer
• Cancer
• Chromatin Research
• Phospho-Specific
• Prostate Cancer

For details, visit:
bosterbio.com/bosterbio-gene-info-cards/EZH2

Boster Bio - What Are the Best Uses of the EZH2 Marker?

What Are The Best Uses Of The EZH2Marker? The EZH2 histone methyltransferase plays a key role in cell growth regulation and regulates miR-139 expression in OC cells. Inhibition of this gene inhibits the proliferation of OC cells and promotes apoptosis. Here are some examples of its uses in research.

EZH2 is a histone methyltransferase

EZH2 regulates H3K27me3 in chondrocytes. In early mesenchymal progenitors, knockdown of Ezh2 does not result in skeletal defects. Loss of Ezh2 does, however, promote osteogenic gene expression. This suggests that Ezh2 may suppress bone formation in distinct mesenchymal lineages.

The EZH2 gene product is a critical regulator of epigenetics and is a key component of the polycomb repressive complex 2. EZH2 inhibits transcription by catalyzing trimethylation of H3K27 on target genes. Moreover, EZH2 plays a role in cancer progression by promoting cell proliferation, invasion, and drug resistance. In addition, it suppresses proapoptotic genes and increases tumor cell survival. In the present study, we analyzed the molecular status of EZH2 in different pediatric leukemia cells and assessed its effect on the occurrence of cancer cells.

EZH2 overexpression affects cellular response to DNA damage. Inhibiting EZH2 may improve the effects of conventional chemotherapy on cancer cells. Furthermore, it is associated with an epigenetic mechanism, which affects DNA damage checkpoints and apoptosis. Hence, therapeutic inhibition of EZH2 is a promising approach to combat cancer cells.

Moreover, EZH2 inhibition suppresses the proliferation of ovarian cancer cells. In vitro and in vivo studies have shown that inhibition of EZH2 inhibits cancer cell growth. Further studies are necessary to determine whether EZH2 depletion also suppresses the growth and spread of endometrial cancer. While these findings are encouraging, further research is necessary to determine if EZH2 is a causal factor in endometrial cancer.

Recent studies have revealed that EZH2 is overexpressed in B-cell lymphomas. In addition, it is implicated in some types of breast cancers. Because of these roles, therapeutic targeting of EZH2 is expected to produce selective sensitization of tumor cells while minimally affecting normal cells. Further, EZH2 knockdown inhibits cell proliferation and apoptosis, a potential mechanism for anti-tumor treatment.

A gene-specific shRNA (si-EZH2) targeting EZH2 is synthesized using an EZH2 sequence obtained from GenBank. After synthesis, complementary DNA fragments were dissolved in annealing buffer, placed in a 90-degree water bath for 15 min, and cooled at room temperature. After this, the fragments were cloned into a shRNA expression vector and packaged for lentiviral transduction of A2780 and SKOV3 cells.

It regulates miR-139 expression

The EZH2 marker, which is an important regulator of miR-139 expression, was recently discovered in human colon cancer cells. These cells have the ability to invade collagen-coated membranes. Moreover, silencing EZH2 inhibited cancer cell invasion and proliferation. These results suggest that miR-139 is a therapeutic target for NSCLC. Further, this discovery may help in the development of a better understanding of the mechanism of miR-139 in cancer.

Overexpression of EZH2 increased miR-139 expression in lung cancer cells. EZH2 regulates miR-139 expression by promoting methylation of miR-139 promoter. Moreover, silencing of EZH2 inhibited OC cell proliferation, migration, and invasion. The silencing of EZH2 also suppressed tumor xenograft growth in mice. The miR-139-silencing inhibited tumor growth by regulating LPA1-mediated TGF-b signaling pathway.

RNAi inhibitors inhibit miR-139 expression by targeting EZH2. Moreover, silencing EZH2 decreases p-Smad2 and LPA1 protein expression. Further, shRNA-EZH2-expressing mice displayed reduced tumor growth and significantly reduced weight and volume. Further, p-Genesil-1 containing EZH2-targeting shRNAs inhibited miR-139 expression in glioma cells.

Previous studies have indicated that the EZH2 gene regulates miR-139 expression in pancreatic cancer. However, the EZH2 gene is also important for the development of OC in people. This gene is involved in the regulation of miR-139 expression by EZH2.

EZH2 is part of the polycomb group of genes. Expression levels of EZH2 are associated with aggressive behavior of tumor cells. This is in line with the association of EZH2 expression with poor prognosis in gastric cancer. The EZH2 gene is present in non-neoplastic brain tissues. The EZH2 gene is required for embryonic development and is associated with various cancer subgroups.

Interestingly, tumors with high EZH2 protein expression expressed higher EZH2 mRNA than did tumors with low EZH2 protein levels. The findings suggest that EZH2 depletion inhibits cell proliferation, inhibits migration and invasion, and stimulates cell apoptosis. Although these results have been reported previously, it is still unclear exactly how miR-139 functions in cancer cells.

It inhibits OC cell proliferation

The effects of Boster Bio EZH2 inhibitors on OC cell proliferation have been demonstrated in mouse models. In fact, the compounds inhibited glioma cell proliferation by inhibiting the synthesis of IL-22, a key molecule for glioma development. Additionally, the compounds inhibited the polarization of M2 macrophages. These results indicate that EZH2 may serve as a new target for glioma treatment.

The antibodies for EZH2 are validated on several platforms, including flow cytometry and immunohistochemistry. Additionally, they are validated using known positive and negative samples. In addition, these antibodies exhibit high specificity and high affinity, and Boster will reward scientists who review their products first. To further support their research, Boster offers a bounty to first reviewers. Interestingly, this award is extended to scientists from around the world.

The EZH2 inhibitors target a number of pathways that regulate OC cell proliferation, including the Wnt/b-catenin signalling pathway. Furthermore, they target c-myc and a-SMA, two essential molecules in HSC activation. Inhibitors of EZH2 inhibit the cyclinD1 and Dkk1 signalling pathways.

Dkk1 was also downregulated in HSC-T6 cells treated with TGF-b1. This suggests that the inhibition of EZH2 may promote hepatic fibrosis. Moreover, a-SMA is downregulated by Dkk1 in HSC-T6 cells. Thus, it is important to consider the potential role of EZH2 in OC cell proliferation.

Ezh2 is an important epigenetic inhibitor that suppresses myogenic differentiation by inhibiting expression of myogenic markers. Knockout of Ezh2 in SCs decreased muscle regeneration and reduced Pax7+ cells. Neat1 knockdown also increased myofiber cross-sectional area and impaired muscle regeneration. Neat1 physically interacts with Ezh2 through its core binding region.

It promotes apoptosis

The EZH2 marker is involved in many different cancer-related processes, including gene expression regulation through epigenetic mechanisms. In addition, it can function as a PRC2-independent transcriptional activator. The precise role of EZH2 in cancer progression varies by tumor type and cellular context. Here, we provide an overview of its role in cancer development and progression.

EZH2 is recruited to the promoter regions of Traf2 and Traf5 in IECs. In IECs containing mutant EZH2 levels, expression levels of these two factors increased. In contrast, the EZH2-deficient cells showed a reduced expression of TRAF2 and TRAF5. This suggests that the EZH2 marker is involved in regulating TNFa signaling and apoptosis.

EZH2 overexpression may result from gene amplification and alterations in signaling pathways. According to Fujii et al., a breast cancer cell line expressed EZH2 and showed upregulation of the MEK-ERK-Elk-1 pathway. Furthermore, knockout mice exhibit abnormal cellular behaviors and were more resistant to apoptosis.

Recent research indicates that the EZH2 locus is amplified in approximately 15% of breast cancer tissues. Its high expression may result from a decreased level of miR-26a, but re-expression of the EZH2 protein is capable of partially reversing this effect. MiR-26a is a potent tumor suppressor, but its role in carcinogenesis is a mystery.

Moreover, the EZH2 marker is involved in regulating the expression of FBP1 and c-Myc. These two proteins are known to be physically associated and inhibit each other's expression. Hence, they may be mutually beneficial in the regulation of apoptosis. This study reveals the molecular mechanisms underlying this relationship. This study reveals the first direct evidence supporting the hypothesis that EZH2 promotes apoptosis in human cancer cells.

Using the CRISPR/Cas9 system, researchers knocked out SKOV3 cells in vitro and in vivo assays. Furthermore, mRNA-seq and ChIP-seq were used to study the molecular mechanism of EZH2 in ovarian cancer cells. Further, the researchers used immunohistochemical staining to analyze the correlation between EZH2 expression and CYP27B1 expression.