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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 

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Menin and MLL cooperatively regulate expression of cyclin-dependent kinase inhibitors.

Mutations in the MEN1 gene are associated with the multiple endocrine neoplasia syndrome type 1 (MEN1), which is characterized by parathyroid hyperplasia and tumors of the pituitary and pancreatic islets. The mechanism by which MEN1 acts as a tumor suppressor is unclear. We have recently shown that menin, the MEN1 protein product, interacts with mixed lineage leukemia (MLL) family proteins in a histone methyltransferase complex including Ash2, Rbbp5, and WDR5. Here, we show that menin directly regulates expression of the cyclin-dependent kinase inhibitors p27Kip1 and p18Ink4c. Menin activates transcription by means of a mechanism involving recruitment of MLL to the p27Kip1 and p18Ink4c promoters and coding regions. Loss of function of either MLL or menin results in down-regulation of p27Kip1 and p18Ink4c expression and deregulated cell growth. These findings suggest that regulation of cyclin-dependent kinase inhibitor transcription by cooperative interaction between menin and MLL plays a central role in menin's activity as a tumor suppressor.[1]

References

  1. Menin and MLL cooperatively regulate expression of cyclin-dependent kinase inhibitors. Milne, T.A., Hughes, C.M., Lloyd, R., Yang, Z., Rozenblatt-Rosen, O., Dou, Y., Schnepp, R.W., Krankel, C., Livolsi, V.A., Gibbs, D., Hua, X., Roeder, R.G., Meyerson, M., Hess, J.L. Proc. Natl. Acad. Sci. U.S.A. (2005) [Pubmed]
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