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A study from the Department of Cancer Biology, Dana-Farber Cancer Institute;  Department of Cell Biology, Harvard Medical SchoolBoston, 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 >35] 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 GBMD, reports here that: Anti-miRNA based therapy for NIDDM: Increased expression of Stress-responsive miRNA-195 promotes gluconeogenesis and hyperglycemia via down regulation of Cyclin D1.  This study may suggest that miRNA-206, by down regulating its target gene, it may promote  gluconeogenesis and hyperglycemia. Together, this study suggests that pharmacological formulations containing “antagomiR-206 or small molecule inhibitors of miRNA-206″  can be used in the treatment of NIDDM.

Idea Proposed/Formulated byDr L Boominathan PhD

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To citeBoominathan, L., Anti-miRNA based therapy for NIDDM: Increased expression of Stress-responsive miRNA-206 promotes gluconeogenesis and hyperglycemia via down regulation of Cyclin D1, 2/July/2014, 6.13 am,   Genome-2-Bio-Medicine Discovery center (GBMD), http://genomediscovery.org

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