{"product_id":"cst-6891s","title":"CST,  6891S, Menin (D45B1) Rabbit Monoclonal Antibody","description":"Monoclonal Antibody for studying MEN1. Validated for Western Blotting,Immunofluorescence (Immunocytochemistry). Available in 2 sizes. Highly specific and rigorously validated in-house, Menin (D45B1) Rabbit Monoclonal Antibody (CST #6891) is ready to ship.\n\n\u003cb\u003eProduct Usage Information\u003c\/b\u003e\nWestern Blotting: 1:1000\nImmunofluorescence (Immunocytochemistry): 1:50 - 1:200\n\u003cb\u003eStorage\u003c\/b\u003e\nSupplied in 10 mM sodium HEPES (pH 7.5), 150 mM NaCl, 100 µg\/ml BSA, 50% glycerol and less than 0.02% sodium azide. Store at -20°C. Do not aliquot the antibody.\n\u003cb\u003eProtocol\u003c\/b\u003e\nAvailable protocols: Western Blotting, Immunofluorescence (Immunocytochemistry)\n\u003cb\u003eSpecificity \/ Sensitivity\u003c\/b\u003e\nMenin (D45B1) Rabbit Monoclonal Antibody recognizes total endogenous levels of all 3 isoforms of Menin protein.\nSpecies Reactivity: Human, Mouse, Rat, Monkey\n\u003cb\u003eSource \/ Purification\u003c\/b\u003e\nMonoclonal antibody is produced by immunizing animals with a synthetic peptide corresponding to residues surrounding Val597 of human Menin protein.\n\u003cb\u003eBackground\u003c\/b\u003e\nMutations in the tumor suppressor gene cause multiple endocrine neoplasia type 1 (MEN1), an autosomal dominant familial tumor syndrome typified by tumors of the pituitary, parathyroid, lung, and enteropancreatic endocrine tissues (1,2). Patients with this tumor syndrome have inherited either missense or truncation mutations in one allele of the gene, while the other allele is subject to loss of heterozygosity in tumors from these patients (1,2). Menin, the protein product of the gene, is a component of the mixed-lineage leukemia protein (MLL)-containing histone methyltransferase complex that facilitates methylation of histone H3 Lys4 to promote transcriptional activation (3,4). Menin functions to suppress proliferation of pancreatic islet cells, at least in part through MLL-mediated activation of the and cyclin-dependent kinase inhibitor genes (5,6). Loss of Menin leads to a decrease in methylation of histone H3 Lys4 and decreased expression of the and genes, leading to hyperplasia (5,6). In contrast to its role as a tumor suppressor in endocrine cells, Menin has been shown to promote proliferation in leukemia cells driven by MLL-fusion proteins. Menin is essential for oncogenic MLL-fusion-protein-mediated transformation of bone marrow cells and is required for histone H3 Lys4 methylation and expression of the gene (7,8). Menin interacts with a wide range of proteins, including JunD, SMAD family members, estrogen receptor, vitamin D receptor, PEM, NFκB, FANCD2, RPA2, NMMHC II-A, GFAP, vimentin, and HSP70, suggesting additional roles in transcriptional regulation, DNA processing and repair, cytoskeleton organization, and protein degradation (9,10).\n\u003cb\u003eAlternate Names\u003c\/b\u003e\nendocrine adenomatosis, multiple; MEAI; MEN1; Menin; menin 1; multiple endocrine neoplasia I; SCG2\n\n\u003cb\u003eSpecification\u003c\/b\u003e\n\nREACTIVITY: H M R Mk\nSENSITIVITY: Endogenous\nMW (kDa): 76\nSource\/Isotype: Rabbit IgG","brand":"CST","offers":[{"title":"Default Title","offer_id":46799857451177,"sku":"6891S","price":0.99,"currency_code":"USD","in_stock":true}],"url":"https:\/\/iright.com\/products\/cst-6891s","provider":"Iright","version":"1.0","type":"link"}