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Mouse Anti-EZH1 (AA 1-110) Recombinant Antibody (CBFYE-1429) (CBMAB-E2054-FY)

This product is mouse antibody that recognizes EZH1. The antibody CBFYE-1429 can be used for immunoassay techniques such as: S-ELISA, ELISA.
See all EZH1 antibodies

Summary

Host Animal
Mouse
Specificity
Human
Clone
CBFYE-1429
Antibody Isotype
IgG1, κ
Application
S-ELISA, ELISA

Basic Information

Immunogen
EZH2 partial recombinant protein with GST tag. MW of the GST tag alone is 26 KDa
Specificity
Human
Antibody Isotype
IgG1, κ
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
Buffer
PBS, pH 7.2
Storage
Store at +4°C short term (1-2 weeks). Aliquot and store at -20°C long term. Avoid repeated freeze/thaw cycles.
Epitope
AA 1-110

Target

Full Name
Enhancer Of Zeste 1 Polycomb Repressive Complex 2 Subunit
Introduction
EZH1 is a component of a noncanonical Polycomb repressive complex-2 (PRC2) that mediates methylation of histone H3 (see MIM 602812) lys27 (H3K27) and functions in the maintenance of embryonic stem cell pluripotency and plasticity (Shen et al., 2008).
Entrez Gene ID
2145
UniProt ID
Q92800
Alternative Names
Enhancer Of Zeste 1 Polycomb Repressive Complex 2 Subunit; Enhancer Of Zeste Homolog 1; EC 2.1.1.43; ENX-2; Enhancer Of Zeste (Drosophila) Homolog 1; Enhancer Of Zeste Homolog 1 (Drosophila); Histone-Lysine N-Methyltransferase EZH1; KIAA0388; KMT6B
Research Area
Polycomb group (PcG) protein. Catalytic subunit of the PRC2/EED-EZH1 complex, which methylates 'Lys-27' 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. Required for embryonic stem cell derivation and self-renewal, suggesting that it is involved in safeguarding embryonic stem cell identity. Compared to EZH2-containing complexes, it is less abundant in embryonic stem cells, has weak methyltransferase activity and plays a less critical role in forming H3K27me3, which is required for embryonic stem cell identity and proper differentiation.
Biological Process
Anatomical structure morphogenesis Source: ProtInc
Chromatin remodeling Source: ARUK-UCL
Chromatin silencing at telomere Source: ARUK-UCL
Heterochromatin assembly Source: ARUK-UCL
Hippocampus development Source: Ensembl
Histone H3-K27 methylation Source: InterPro
Negative regulation of transcription by RNA polymerase II Source: ARUK-UCL
Positive regulation of transcription by RNA polymerase II Source: Ensembl
Cellular Location
Nucleus. Colocalizes with trimethylated 'Lys-27' of histone H3.

Jing, R., Scarfo, I., Najia, M. A., da Rocha, E. L., Han, A., Sanborn, M., ... & Daley, G. Q. (2022). EZH1 repression generates mature iPSC-derived CAR T cells with enhanced antitumor activity. Cell Stem Cell, 29(8), 1181-1196.

Grau, D., Zhang, Y., Lee, C. H., Valencia-Sánchez, M., Zhang, J., Wang, M., ... & Armache, K. J. (2021). Structures of monomeric and dimeric PRC2: EZH1 reveal flexible modules involved in chromatin compaction. Nature communications, 12(1), 1-12.

Kusakabe, Y., Chiba, T., Oshima, M., Koide, S., Rizq, O., Aoyama, K., ... & Kato, N. (2021). EZH1/2 inhibition augments the anti-tumor effects of sorafenib in hepatocellular carcinoma. Scientific reports, 11(1), 1-14.

El Said, N. H., Della Valle, F., Liu, P., Paytuví-Gallart, A., Adroub, S., Gimenez, J., & Orlando, V. (2021). Malat-1-PRC2-EZH1 interaction supports adaptive oxidative stress dependent epigenome remodeling in skeletal myotubes. Cell death & disease, 12(10), 1-10.

Kagiyama, Y., Fujita, S., Shima, Y., Yamagata, K., Katsumoto, T., Nakagawa, M., ... & Kitabayashi, I. (2021). CDKN1C‐mediated growth inhibition by an EZH1/2 dual inhibitor overcomes resistance of mantle cell lymphoma to ibrutinib. Cancer Science, 112(6), 2314-2324.

Lau-Corona, D., Bae, W. K., Hennighausen, L., & Waxman, D. J. (2020). Sex-biased genetic programs in liver metabolism and liver fibrosis are controlled by EZH1 and EZH2. PLoS genetics, 16(5), e1008796.

Wassef, M., Luscan, A., Aflaki, S., Zielinski, D., Jansen, P. W., Baymaz, H. I., ... & Margueron, R. (2019). EZH1/2 function mostly within canonical PRC2 and exhibit proliferation-dependent redundancy that shapes mutational signatures in cancer. Proceedings of the National Academy of Sciences, 116(13), 6075-6080.

Jung, C. K., Kim, Y., Jeon, S., Jo, K., Lee, S., & Bae, J. S. (2018). Clinical utility of EZH1 mutations in the diagnosis of follicular-patterned thyroid tumors. Human Pathology, 81, 9-17.

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

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