Cell Signaling Technology
XP Monoclonal Antibody

Product Pathways - Chromatin Regulation / Epigenetics

Menin (D45B1) XP® Rabbit mAb #6891

Applications Reactivity Sensitivity MW (kDa) Isotype
W IF-IC H M R Mk (B) (Pg) (Hr) Endogenous 68 Rabbit IgG

Applications Key:  W=Western Blotting  IF-IC=Immunofluorescence (Immunocytochemistry)
Reactivity Key:  H=Human  M=Mouse  R=Rat  Mk=Monkey  B=Bovine  Pg=Pig  Hr=Horse
Species cross-reactivity is determined by western blot. Species enclosed in parentheses are predicted to react based on 100% sequence homology.

Protocols

Specificity / Sensitivity

Menin (D45B1) XP® Rabbit mAb recognizes total endogenous levels of all 3 isoforms of Menin protein.

Source / Purification

Monoclonal antibody is produced by immunizing animals with a synthetic peptide corresponding to residues surrounding Val597 of human Menin protein.

Western Blotting

Western Blotting

Western blot analysis of extracts from various cell lines using Menin (D45B1) XP® Rabbit mAb.

IF-IC

IF-IC

Confocal immunofluorescent analysis of COS-7 cells using Menin (D45B1) XP® Rabbit mAb (green). Actin filaments were labeled with DY-554 phalloidin (red). Blue pseudocolor = DRAQ5® #4084 (fluorescent DNA dye).

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 p18INK4c (p18) and p27CIP/KIP (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).

  1. Chandrasekharappa, S.C. et al. (1997) Science 276, 404-7.
  2. Lemmens, I. et al. (1997) Hum Mol Genet 6, 1177-83.
  3. Hughes, C.M. et al. (2004) Mol Cell 13, 587-97.
  4. Yokoyama, A. et al. (2004) Mol Cell Biol 24, 5639-49.
  5. Karnik, S.K. et al. (2005) Proc Natl Acad Sci USA 102, 14659-64.
  6. Schnepp, R.W. et al. (2006) Cancer Res 66, 5707-15.
  7. Yokoyama, A. et al. (2005) Cell 123, 207-18.
  8. Chen, Y.X. et al. (2006) Proc Natl Acad Sci USA 103, 1018-23.
  9. Agarwal, S.K. et al. (2005) Horm Metab Res 37, 369-74.
  10. Wu, X. and Hua, X. (2008) Curr Mol Med 8, 805-15.

Application References

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Companion Products

For Research Use Only. Not For Use In Diagnostic Procedures.

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