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Render Timestamp: 2024-12-20T11:31:30.037Z
Commit: f2d32940205a64f990b886d724ccee2c9935daff
XML generation date: 2024-09-30 01:59:07.969
Product last modified at: 2024-12-17T18:50:06.143Z
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PDP - Template Name: Monoclonal Antibody
PDP - Template ID: *******c5e4b77
  1. Products /
  2. Primary Antibodies /
  3. Menin (E5P1R) Rabbit mAb
R Recombinant
Recombinant: Superior lot-to-lot consistency, continuous supply, and animal-free manufacturing.

Menin (E5P1R) Rabbit mAb #19893

Filter:
  • WB
  • IP
  • IHC
  • ChIP

    Supporting Data

    REACTIVITY H M R Mk
    SENSITIVITY Endogenous
    MW (kDa) 76
    Source/Isotype Rabbit IgG
    Application Key:
    • WB-Western Blotting 
    • IP-Immunoprecipitation 
    • IHC-Immunohistochemistry 
    • ChIP-Chromatin Immunoprecipitation 
    Species Cross-Reactivity Key:
    • H-Human 
    • M-Mouse 
    • R-Rat 
    • Mk-Monkey 

    Product Information

    Product Usage Information

    For optimal ChIP and ChIP-seq results, use 10 μl of antibody and 10 μg of chromatin (approximately 4 x 106 cells) per IP. This antibody has been validated using SimpleChIP® Enzymatic Chromatin IP Kits.
    Application Dilution
    Western Blotting 1:1000
    Immunoprecipitation 1:200
    Immunohistochemistry (Paraffin) 1:1250 - 1:5000
    Chromatin IP 1:50
    Chromatin IP-seq 1:50

    Storage

    Supplied 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.

    Protocol

    Specificity / Sensitivity

    Menin (E5P1R) Rabbit mAb 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 MEN1 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 MEN1 gene, while the other allele is subject to loss of heterozygosity in tumors from these patients (1,2). Menin, the protein product of the MEN1 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 p18 and p27 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 p18 and p27 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 HoxA9 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).

    Database Links

    UniProt ID: O00255


    Entrez-Gene Id: 4221


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