Molecular therapy for T2DM: β-catenin promotes gluconeogenesis and hyperglycemia via up regulation of Cyclin D1, 11/February/2014, 23.19

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A study from the Department of Cancer Biology, Dana-Farber Cancer Institute;  Department of Cell Biology, Harvard Medical School, Boston, Massachusetts, USA; and others shows that Cyclin D1–Cdk4 controls glucose metabolism independently of cell cycle progression.”

This study was published in the June 26, 2014 Nature [I.F >42] by Prof. Puigserver and others from the Department of Cancer Biology, Dana-Farber Cancer Institute;  Department of Cell Biology, Harvard Medical School, Boston, Massachusetts, USA.

On the foundation of this interesting finding, Dr L Boominathan, Director-cum-chief Scientist of GBMDreports here that: Molecular therapy for T2DM: β-catenin inhibits gluconeogenesis and hyperglycemia via up regulation of Cyclin D1. This study may suggest that β-catenin by up regulating its target gene, it may inhibit  gluconeogenesis and hyperglycemia. Together, this study suggests that pharmacological formulations encompassing β-catenin activators”  can be used in the treatment of NIDDM.

Idea Proposed/Formulated byDr L Boominathan Ph.D.

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To citeBoominathan, L., Molecular therapy for DM: β-catenin promotes gluconeogenesis and hyperglycemia via up regulation of Cyclin D1, 11/February/2014, 23.19, Genome-2-Bio-Medicine Discovery center (GBMD), http://genomediscovery.org

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