|Other Names||Histone-lysine N-methyltransferase 2E, Lysine N-methyltransferase 2E, Myeloid/lymphoid or mixed-lineage leukemia protein 5, KMT2E, MLL5|
|Format||Synthetic peptide was lyophilized with 100% acetonitrile and is supplied as a powder. Reconstitute with 0.1 ml DI water for a final concentration of 1 mg/ml.|
|Storage||Maintain refrigerated at 2-8°C for up to 6 months. For long term storage store at -20°C.|
|Precautions||This product is for research use only. Not for use in diagnostic or therapeutic procedures.|
|Function||Histone methyltransferase that specifically mono- and dimethylates 'Lys-4' of histone H3 (H3K4me1 and H3K4me2). H3 'Lys- 4' methylation represents a specific tag for epigenetic transcriptional activation. Key regulator of hematopoiesis involved in terminal myeloid differentiation and in the regulation of hematopoietic stem cell (HSCs) self-renewal by a mechanism that involves DNA methylation. Plays an essential role in retinoic- acid-induced granulopoiesis by acting as a coactivator of RAR- alpha (RARA) in target gene promoters. Also acts as an important cell cycle regulator, participating in cell cycle regulatory network machinery at multiple cell cycle stages. Required to suppress inappropriate expression of S-phase-promoting genes and maintain expression of determination genes in quiescent cells. Overexpression inhibits cell cycle progression, while knockdown induces cell cycle arrest at both the G1 and G2/M phases.|
|Cellular Location||Nucleus speckle. Note=Absent from the nucleolus|
|Tissue Location||Widely expressed in both adult and fetal tissues. Highest levels of expression observed in fetal thymus and kidney and in adult hematopoietic tissues, jejunum and cerebellum Isoform NKp44L is not detected on circulating cells from healthy individuals, but it is expressed on a large panel of the tumor and transformed cells.|
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This gene is a member of the myeloid/lymphoid ormixed-lineage leukemia (MLL) family and encodes a protein with anN-terminal PHD zinc finger and a central SET domain. Overexpressionof the protein inhibits cell cycle progression. Alternatetranscriptional splice variants have been characterized. [providedby RefSeq].
Liu, J., et al. J. Biol. Chem. 285(27):20904-20914(2010)Fujiki, R., et al. Nature 459(7245):455-459(2009)Cheng, F., et al. Int. J. Biochem. Cell Biol. 40(11):2472-2481(2008)Sun, X.J., et al. PLoS ONE 3 (1), E1499 (2008) :Olsen, J.V., et al. Cell 127(3):635-648(2006)
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