DNMT3A Antibody (64B1446) [Alexa Fluor® 594]

Alexa Fluor (R) products are provided under an intellectual property license from Life Technologies Corporation. The purchase of this product conveys to the buyer the non-transferable right to use the purchased product and components of the product only in research conducted by the buyer (whether the buyer is an academic or for-profit entity). The sale of this product is expressly conditioned on the buyer not using the product or its components, or any materials made using the product or its components, in any activity to generate revenue, which may include, but is not limited to use of the product or its components: (i) in manufacturing; (ii) to provide a service, information, or data in return for payment; (iii) for therapeutic, diagnostic or prophylactic purposes; or (iv) for resale, regardless of whether they are resold for use in research. For information on purchasing a license to this product for purposes other than as described above, contact Life Technologies Corporation, 5791 Van Allen Way, Carlsbad, CA 92008 USA or outlicensing@lifetech.com. This conjugate is made on demand. Actual recovery may vary from the stated volume of this product. The volume will be greater than or equal to the unit size stated on the datasheet.

Methylation of cytosine residues is essential for mammalian development by regulating gene expression, gene silencing and genomic imprinting (1). This process is controlled by the enzyme DNA (cytosine-5)-methyltransferase 3A (DNMt3a), which is encoded by the DNMT3A gene and has a predicted molecular weight of 102 kDa. DNA methyltransferases including DNMt3a are involved in de novo cytosine methylation and maintenance of embryonic and somatic cells through the transfer of methyl groups to specific CpG structures in DNA (2). Somatic mutations in DNMT3A are responsible for cytogenetically normal acute myeloid leukemia (CN-AML). Hypermethylation of CpG islands in tumor suppressor genes or hypomethylation of bulk genomic DNA are linked with cancer (3,4). Mutations in the DNMT3A gene have also been found to cause DNMT3A overgrowth syndrome and myelodysplastic syndromes.

References

1. Thakur, A., Mackin, S. J., Irwin, R. E., O'Neill, K. M., Pollin, G., & Walsh, C. (2016). Widespread recovery of methylation at gametic imprints in hypomethylated mouse stem cells following rescue with DNMT3A2. Epigenetics Chromatin, 9, 53. doi:10.1186/s13072-016-0104-2

2. Ravichandran, M., Lei, R., Tang, Q., Zhao, Y., Lee, J., Ma, L., . . . Dawlaty, M. M. (2019). Rinf Regulates Pluripotency Network Genes and Tet Enzymes in Embryonic Stem Cells. Cell Rep, 28(8), 1993-2003.e1995. doi:10.1016/j.celrep.2019.07.080

3. Pang, Y., Liu, J., Li, X., Xiao, G., Wang, H., Yang, G., . . . Ren, H. (2018). MYC and DNMT3A-mediated DNA methylation represses microRNA-200b in triple negative breast cancer. J Cell Mol Med, 22(12), 6262-6274. doi:10.1111/jcmm.13916

4. Xia, L., Huang, W., Bellani, M., Seidman, M. M., Wu, K., Fan, D., . . . Baylin, S. B. (2017). CHD4 Has Oncogenic Functions in Initiating and Maintaining Epigenetic Suppression of Multiple Tumor Suppressor Genes. Cancer Cell, 31(5), 653-668.e657. doi:10.1016/j.ccell.2017.04.005

This product is for research use only and is not approved for use in humans or in clinical diagnosis. Primary Antibodies are guaranteed for 1 year from date of receipt.

Array NB120-13888AF594

• DNMT3A Antibodies
• DNMT3A ELISA Kits
• DNMT3A Kit
• DNMT3A Lysate
• DNMT3A Proteins