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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 issue of Nature [the number 1 journal in General science with an I.F of >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 GBMD, reports here that: Molecular therapy for NIDDM: Lin28 inhibits gluconeogenesis and hyperglycemia via up regulation of Cyclin D1.  This study may suggest that Lin28, by down regulating its target gene, it may inhibit  gluconeogenesis and hyperglycemia. Together, this study suggests that pharmacological formulations encompassing “Lin-28 activators”  can be used  treat NIDDM.

Idea Proposed/Formulated byDr L Boominathan Ph.D.

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To citeBoominathan, L., Molecular therapy for NIDDM: Lin28 inhibits gluconeogenesis and hyperglycemia via up regulation of Cyclin D1, 10/June/2015, 6.55 am, Genome-2-Bio-Medicine Discovery center (GBMD), http://genomediscovery.org

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