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Rabbit Anti-EZH2 Recombinant Antibody (CBFYE-0268) (CBMAB-E0547-FY)

This product is rabbit antibody that recognizes EZH2. The antibody CBFYE-0268 can be used for immunoassay techniques such as: WB, IP, IHC-P, IF, FC, ChIP.
See all EZH2 antibodies

Summary

Host Animal
Rabbit
Specificity
Human, Mouse, Rat, Monkey
Clone
CBFYE-0268
Antibody Isotype
IgG
Application
WB, IP, IHC-P, IF, FC, ChIP

Basic Information

Specificity
Human, Mouse, Rat, Monkey
Antibody Isotype
IgG
Clonality
Monoclonal
Application Notes
The COA includes recommended starting dilutions, optimal dilutions should be determined by the end user.

Formulations & Storage [For reference only, actual COA shall prevail!]

Format
Liquid
Storage
Store at +4°C short term (1-2 weeks). Aliquot and store at -20°C long term. Avoid repeated freeze/thaw cycles.

Target

Full Name
Enhancer Of Zeste 2 Polycomb Repressive Complex 2 Subunit
Introduction
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.
Entrez Gene ID
Human2145
Mouse14055
Rat303547
Monkey709075
UniProt ID
HumanQ92800
MouseP70351
RatF1LZH3
MonkeyA0A1D5RJQ2
Alternative Names
WVS; ENX1; KMT6; WVS2; ENX-1; EZH2b; KMT6A
Research Area
Polycomb group (PcG) protein. Catalytic subunit of the PRC2/EED-EZH2 complex, which methylates 'Lys-9' (H3K9me) and 'Lys-27' (H3K27me) of histone H3, leading to transcriptional repression of the affected target gene. Able 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 activity when progressively more methyl groups are incorporated into H3K27, H3K27me0> H3K27me1> H3K27me2 (PubMed:22323599, PubMed:30923826).

Compared to EZH1-containing complexes, it is more abundant in embryonic stem cells and plays a major role in forming H3K27me3, which is required for embryonic stem cell identity and proper differentiation. The PRC2/EED-EZH2 complex may also serve as a recruiting platform for DNA methyltransferases, thereby linking two epigenetic repression systems. Genes repressed by the PRC2/EED-EZH2 complex include HOXC8, HOXA9, MYT1, CDKN2A and retinoic acid target genes. EZH2 can also methylate non-histone proteins such as the transcription factor GATA4 and the nuclear receptor RORA. Regulates the circadian clock via histone methylation at the promoter of the circadian genes. Essential for the CRY1/2-mediated repression of the transcriptional activation of PER1/2 by the CLOCK-ARNTL/BMAL1 heterodimer; involved in the di and trimethylation of 'Lys-27' of histone H3 on PER1/2 promoters which is necessary for the CRY1/2 proteins to inhibit transcription.
Biological Process
B cell differentiation Source: Ensembl
Cardiac muscle hypertrophy in response to stress Source: Ensembl
Cell development Source: Ensembl
Cellular response to hydrogen peroxide Source: Ensembl
Cellular response to trichostatin A Source: Ensembl
Cerebellar cortex development Source: Ensembl
Chromatin organization Source: ProtInc
Chromatin silencing at telomere Source: ARUK-UCL
DNA methylation Source: Ensembl
G1 to G0 transition Source: Ensembl
Hepatocyte homeostasis Source: Ensembl
Hippocampus development Source: Ensembl
Histone H3-K27 methylation Source: UniProtKB
Histone H3-K27 trimethylation Source: Ensembl
Histone methylation Source: UniProtKB
Liver regeneration Source: Ensembl
Negative regulation of cytokine production involved in inflammatory response Source: Ensembl
Negative regulation of DNA-binding transcription factor activity Source: Ensembl
Negative regulation of epidermal cell differentiation Source: Ensembl
Negative regulation of G1/S transition of mitotic cell cycle Source: Ensembl
Negative regulation of gene expression, epigenetic Source: UniProtKB
Negative regulation of retinoic acid receptor signaling pathway Source: UniProtKB
Negative regulation of striated muscle cell differentiation Source: Ensembl
Negative regulation of transcription, DNA-templated Source: UniProtKB
Negative regulation of transcription by RNA polymerase II Source: UniProtKB
Negative regulation of transcription elongation from RNA polymerase II promoter Source: Ensembl
Positive regulation of cell cycle G1/S phase transition Source: BHF-UCL
Positive regulation of cell population proliferation Source: BHF-UCL
Positive regulation of dendrite development Source: Ensembl
Positive regulation of epithelial to mesenchymal transition Source: UniProtKB
Positive regulation of GTPase activity Source: UniProtKB
Positive regulation of MAP kinase activity Source: UniProtKB
Positive regulation of protein serine/threonine kinase activity Source: UniProtKB
Protein localization to chromatin Source: Ensembl
Regulation of circadian rhythm Source: UniProtKB
Regulation of gliogenesis Source: Ensembl
Regulation of transcription, DNA-templated Source: ProtInc
Response to estradiol Source: Ensembl
Response to tetrachloromethane Source: Ensembl
Rhythmic process Source: UniProtKB-KW
Skeletal muscle satellite cell maintenance involved in skeletal muscle regeneration Source: Ensembl
Synaptic transmission, GABAergic Source: Ensembl
Cellular Location
Nucleus. Localizes to the inactive X chromosome in trophoblast stem cells.
Involvement in disease
Weaver syndrome (WVS):
A syndrome of accelerated growth and osseous maturation, unusual craniofacial appearance, hoarse and low-pitched cry, and hypertonia with camptodactyly. Distinguishing features of Weaver syndrome include broad forehead and face, ocular hypertelorism, prominent wide philtrum, micrognathia, deep horizontal chin groove, and deep-set nails. In addition, carpal bone development is advanced over the rest of the hand.
PTM
Phosphorylated by AKT1. Phosphorylation by AKT1 reduces methyltransferase activity. Phosphorylation at Thr-345 by CDK1 and CDK2 promotes maintenance of H3K27me3 levels at EZH2-target loci, thus leading to epigenetic gene silencing.
Sumoylated.
Glycosylated: O-GlcNAcylation at Ser-75 by OGT increases stability of EZH2 and facilitates the formation of H3K27me3 by the PRC2/EED-EZH2 complex.

Zhong, J., Yang, X., Chen, J., He, K., Gao, X., Wu, X., ... & Zhang, N. (2022). Circular EZH2-encoded EZH2-92aa mediates immune evasion in glioblastoma via inhibition of surface NKG2D ligands. Nature communications, 13(1), 1-18.

Wang, J., Yu, X., Gong, W., Liu, X., Park, K. S., Ma, A., ... & Wang, G. G. (2022). EZH2 noncanonically binds cMyc and p300 through a cryptic transactivation domain to mediate gene activation and promote oncogenesis. Nature Cell Biology, 24(3), 384-399.

Liu, Z., Hu, X., Wang, Q., Wu, X., Zhang, Q., Wei, W., ... & Yu, L. (2021). Design and synthesis of EZH2-based PROTACs to degrade the PRC2 complex for targeting the noncatalytic activity of EZH2. Journal of Medicinal Chemistry, 64(5), 2829-2848.

Tu, Y., Sun, Y., Qiao, S., Luo, Y., Liu, P., Jiang, Z. X., ... & Wen, S. (2021). Design, synthesis, and evaluation of VHL-based EZH2 degraders to enhance therapeutic activity against lymphoma. Journal of Medicinal Chemistry, 64(14), 10167-10184.

Morel, K. L., Sheahan, A. V., Burkhart, D. L., Baca, S. C., Boufaied, N., Liu, Y., ... & Ellis, L. (2021). EZH2 inhibition activates a dsRNA–STING–interferon stress axis that potentiates response to PD-1 checkpoint blockade in prostate cancer. Nature cancer, 2(4), 444-456.

Ma, A., Stratikopoulos, E., Park, K. S., Wei, J., Martin, T. C., Yang, X., ... & Jin, J. (2020). Discovery of a first-in-class EZH2 selective degrader. Nature chemical biology, 16(2), 214-222.

Duan, R., Du, W., & Guo, W. (2020). EZH2: a novel target for cancer treatment. Journal of hematology & oncology, 13(1), 1-12.

Eich, M. L., Athar, M., Ferguson, J. E., & Varambally, S. (2020). EZH2-Targeted Therapies in Cancer: Hype or a RealityEZH2 as a Therapeutic Target. Cancer research, 80(24), 5449-5458.

Li, Z., Wang, D., Lu, J., Huang, B., Wang, Y., Dong, M., ... & Bai, J. (2020). Methylation of EZH2 by PRMT1 regulates its stability and promotes breast cancer metastasis. Cell Death & Differentiation, 27(12), 3226-3242.

Li, B., & Chng, W. J. (2019). EZH2 abnormalities in lymphoid malignancies: underlying mechanisms and therapeutic implications. Journal of Hematology & Oncology, 12(1), 1-13.

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For research use only. Not intended for any clinical use.

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