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 MicroRNA-545 promotes gluconeogenesis and hyperglycemia via down regulation of Cyclin D1. This study may suggest that miRNA-545, by down regulating its target gene, it may promote gluconeogenesis and hyperglycemia. Together, this study suggests that pharmacological formulations encompassing “anti-miRNA-545 or small molecule inhibitors of miRNA-545″ can be used in the treatment of NIDDM.
Idea Proposed/Formulated by: Dr L Boominathan Ph.D.
Web: http://genomediscovery.org
Terms & Conditions apply http://genomediscovery.org/registration/terms-and-conditions/
To cite: Boominathan, L., Anti-miRNA based therapy for NIDDM: Increased expression of Stress-responsive miRNA-545 promotes gluconeogenesis and hyperglycemia via down regulation of Cyclin D1, 02/September/2014, 10.45 am, Genome-2-Bio-Medicine Discovery center (GBMD), http://genomediscovery.org
Courtesy: When you cite drop us a line at info@genomediscovery.org
* Research cooperation
