|Reactivity||Human, Mouse, Rat|
|Calculated MW||68023 Da|
|Application & Usage||Western blotting (1:500 – 1:2000). However, the optimal concentrations should be determined individually. 293T cell lysate can be used as a positive control. The antibody recognizes the Menin of human, mouse, and rat origins. Reactivity to other species has not been tested.|
|Other Names||MEAI, Multiple Endocrine Adenomatosis 1; ZES, Zollinger-Ellison Syndrome; SCG2, Suppressor Candidate Gene 2|
|Formulation||100 µl affinity purified rabbit polyclonal antibody in phosphate-buffered saline (PBS) containing 30% glycerol, 0.5% BSA and 0.01% thimerosal.|
|Handling||The antibody solution should be gently mixed before use.|
|Reconstitution & Storage||-20 °C|
|Precautions||Menin Antibody is for research use only and 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 (multiple endocrine neoplasia I, MEN1, MEAI, SCG2) is a nuclear tumor suppressor that is mutated in patients with multiple endocrine neoplasia type I (MEN1). Menin can activate the transcription of differentiation-regulating genes by covalent histone modification. In osteoblasts, the interaction of menin and the TGFβ/Smad3 pathway negatively regulates BMP2/Smad1/5- and Runx2-dependent transcription activities leading to inhibition of late-stage differentiation. Menin regulates the expression of IGFBP-2 by influencing the IGFBP-2 promoter. Ectopic overexpression of menin via adenoviruses induces apoptosis in murine embryonic fibroblasts in a Bax/Bak-dependent manner. Two mRNA exist and two variants of the shorter mRNA have alternative splicing that changes the CDS. Five variants where alternative splicing takes place in the 5' UTR have been identified.
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