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 GBMD, reports here that: Interleukin-based therapy for DM: Interleukin-17B (IL-17B) inhibits gluconeogenesis and hyperglycemia via up regulation of Cyclin D1. Thus, pharmacological formulations encompassing “Interleukin-17B (IL-17B) activators“ may be used in the treatment of DM.
Idea Proposed/Formulated by: Dr L Boominathan Ph.D.
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To cite: Boominathan, L., Interleukin-based therapy for DM: Interleukin-17B (IL-17B) inhibits gluconeogenesis and hyperglycemia via up regulation of Cyclin D1, 30/April/2015, 18.27, Genome-2-Bio-Medicine Discovery center (GBMD), http://genomediscovery.org
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Undisclosed information: How Interleukin-17B (IL-17B) increases the expression of CyclinD1
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