Molecular therapy for DM: Ars2 (arsenite-resistance protein 2/Serrate RNA effector molecule homolog) inhibits gluconeogenesis and hyperglycemia via up regulation of Cyclin D1, 2/April/2015, 12.01 pm

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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 DM: Ars2 (arsenite-resistance protein 2/Serrate RNA effector molecule homolog)  inhibits gluconeogenesis and hyperglycemia via up regulation of Cyclin D1. This study suggests that Ars2 by down regulating its target gene, it may inhibit  gluconeogenesis and hyperglycemia. Together, this study suggests that pharmacological formulations encompassing Ars2  activators may be used in the treatment of DM.

Idea Proposed/Formulated byDr L Boominathan Ph.D.

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To citeBoominathan, L., Molecular therapy for DM: Ars2 (arsenite-resistance protein 2/Serrate RNA effector molecule homolog)  inhibits gluconeogenesis and hyperglycemia via up regulation of Cyclin D1, 2/April/2015, 12.01 pm, Genome-2-Bio-Medicine Discovery center (GBMD), http://genomediscovery.org

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Undisclosed information: How Ars2 increases the expression of CyclinD1

* Research cooperation

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