Dataset Information


Expression data from pancreatic islets from Men1flf RIP-Cre mice, Rbp2flf RIP-Cre mice, Men1flf Rbp2flf RIP-Cre mice and matched control.

ABSTRACT: The menin tumor suppressor protein (Men1) is deficient in many endocrine tumors and forms an active complex with MLL family histone methyltransferases. This Men1 complex promotes histone H3 lysine 4 trimethylation at target loci including homeobox genes and cyclin-dependent kinase inhibitor genes. The loss of Men1 may be tumorigenic because it leads to decreased histone H3 lysine 4 trimethylation resulting in expressional changes of specific genes. Reversing tumorigenesis induced by a Men1 deficiency might be achieved by inhibition of histone H3 lysine 4 demethylase Rbp2 (Kdm5a). To this end, pancreatic islets from Men1f|f, Rbp2f|f and Men1f|f Rbp2f|f mice were expression profiled to determine what transcriptional changes induced by a Men1 deficiency are reversed by the loss of Rpb2. Pancreatic islets were isolated from Men1flf RIP-Cre mice, Rbp2flf RIP-Cre mice, Men1flf Rbp2flf RIP-Cre mice and two month old matched control mice. Total mRNA was extracted from islets and expression profiled on microarrays.

ORGANISM(S): Mus musculus  

SUBMITTER: Wenchu Lin   Andrew Cherniack  Matthew Meyerson 

PROVIDER: E-GEOD-26978 | ArrayExpress | 2011-07-25



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Aberrations in epigenetic processes, such as histone methylation, can cause cancer. Retinoblastoma binding protein 2 (RBP2; also called JARID1A or KDM5A) can demethylate tri- and dimethylated lysine 4 in histone H3, which are epigenetic marks for transcriptionally active chromatin, whereas the multiple endocrine neoplasia type 1 (MEN1) tumor suppressor promotes H3K4 methylation. Previous studies suggested that inhibition of RBP2 contributed to tumor suppression by the retinoblastoma protein (pRB  ...[more]

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