Molecular therapy for NIDDM: Tumor necrosis factor-like weak inducer of apoptosis (TWEAK) inhibits gluconeogenesis and hyperglycemia via up regulation of Cyclin D1, 14/February/2014, 12.51 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 GBMD, reports here that: Molecular therapy for NIDDM: Tumor necrosis factor-like weak inducer of apoptosis (TWEAK) inhibits gluconeogenesis and hyperglycemia via up regulation of Cyclin D1.  This study may suggest that TWEAK, by down regulating its target gene, it may inhibit gluconeogenesis and hyperglycemia. Together, this study suggests that pharmacological formulations encompassing “TWEAK activators”  can be used in the treatment of NIDDM.

Idea Proposed/Formulated byDr L Boominathan PhD

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To citeBoominathan, L., Molecular based therapy for NIDDM: Tumor necrosis factor-like weak inducer of apoptosis (TWEAK) inhibits gluconeogenesis and hyperglycemia via up regulation of CyclinD1, 14/February/2014, 12.51 pm,   Genome-2-Bio-Medicine Discovery center (GBMD), http://genomediscovery.org

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* Research cooperation

Undisclosed information: How TWEAK increases the expression of CyclinD1

Amount: $ 500*

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