CST, 87298SF, Menin (E5P1R) Rabbit Monoclonal Antibody (BSA and Azide Free)

Monoclonal Antibody for studying MEN1. Validated for Western Blotting,Immunohistochemistry (Paraffin). Highly specific and rigorously validated in-house, Menin (E5P1R) Rabbit Monoclonal Antibody (BSA and Azide Free) (CST #87298) is ready to ship. Product Usage Information This product is the carrier free version of product #19893. All data were generated using the same antibody clone in the standard formulation which contains BSA and glycerol. This formulation is ideal for use with technologies requiring specialized or custom antibody labeling, including fluorophores, metals, lanthanides, and oligonucleotides. It is not recommended for ChIP, ChIP-seq, CUT&RUN or CUT&Tag assays. If you require a carrier free formulation for chromatin profiling, please contact us . Optimal dilutions/concentrations should be determined by the end user. BSA and Azide Free antibodies are quality control tested by size exclusion chromatography (SEC) to determine antibody integrity. Formulation Supplied in 1X PBS (10 mM Na 2 HPO 4 , 3 mM KCl, 2 mM KH 2 PO 4 , and 140 mM NaCl (pH 7.8)). BSA and Azide Free. For standard formulation of this product see product # 19893 Storage Store at -20°C. This product will freeze at -20°C so it is recommended to aliquot into single-use vials to avoid multiple freeze/thaw cycles. A slight precipitate may be present and can be dissolved by gently vortexing. This will not interfere with antibody performance. Specificity / Sensitivity Menin (E5P1R) Rabbit Monoclonal Antibody (BSA and Azide Free) recognizes endogenous levels of total Menin protein. Species cross-reactivity for IHC-P is human only. Species Reactivity: Human, Mouse, Rat, Monkey Source / Purification Monoclonal antibody is produced by immunizing animals with a synthetic peptide corresponding to residues surrounding Pro600 of human Menin protein. Background Mutations 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). Alternate Names endocrine adenomatosis, multiple; MEAI; MEN1; Menin; menin 1; multiple endocrine neoplasia I; SCG2 Specification REACTIVITY: H M R Mk SENSITIVITY: Endogenous MW (kDa): 76 Source/Isotype: Rabbit IgG