|Other Names||Menin, MEN1, SCG2|
|Target/Specificity||The synthetic peptide sequence used to generate the antibody AP7415b was selected from the T594 region of human MEN1. A 10 to 100 fold molar excess to antibody is recommended. Precise conditions should be optimized for a particular assay.|
|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||Essential component of a MLL/SET1 histone methyltransferase (HMT) complex, a complex that specifically methylates 'Lys-4' of histone H3 (H3K4). Functions as a transcriptional regulator. Binds to the TERT promoter and represses telomerase expression. Plays a role in TGFB1-mediated inhibition of cell-proliferation, possibly regulating SMAD3 transcriptional activity. Represses JUND-mediated transcriptional activation on AP1 sites, as well as that mediated by NFKB subunit RELA. Positively regulates HOXC8 and HOXC6 gene expression. May be involved in normal hematopoiesis through the activation of HOXA9 expression (By similarity). May be involved in DNA repair.|
|Cellular Location||Nucleus. Note=Concentrated in nuclear body-like structures. Relocates to the nuclear matrix upon gamma irradiation|
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Provided below are standard protocols that you may find useful for product applications.
Menin (MEN1) is a putative tumor suppressor associated with a syndrome known as multiple endocrine neoplasia type 1. In vitro studies have shown menin is localized to the nucleus, possesses two functional nuclear localization signals, and inhibits transcriptional activation by JunD, however, the function of this protein is not known.
Hashimoto,M., Int. J. Oncol. 33 (2), 333-340 (2008)Vidal,A., J Eur Acad Dermatol Venereol 22 (7), 835-838 (2008)Pieterman,C.R., Clin. Endocrinol. (Oxf) (2008)
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