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 >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-503 promotes gluconeogenesis and hyperglycemia via down regulation of Cyclin D1. This study may suggest that miRNA-503, by down regulating its target gene, it may promote gluconeogenesis and hyperglycemia. Together, this study suggests that pharmacological formulations containing “antagomiR-503 or small molecule inhibitors of miRNA-503″ can be used in the treatment of NIDDM.
Idea Proposed/Formulated by: Dr L Boominathan Ph.D.
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To cite: Boominathan, L., Anti-miRNA based therapy for NIDDM: Increased expression of Stress-responsive MiRNA-503 promotes gluconeogenesis and hyperglycemia via down regulation of Cyclin D1, Genome-2-Bio-Medicine Discovery center (GBMD), 4/07/2014, 8.33 am., http://genomediscovery.org
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