A recent study from the Department of Chemical and Systems Biology, Stanford University School of Medicine, Stanford, California, USA shows that “Aldehyde dehydrogenase-2 regulates nociception in rodent models of acute inflammatory pain.” This study was published in the August 27 2014 Sci Transl Med by Prof D. Mochly-Rosen, and others.
On the foundation of this interesting finding, Dr L Boominathan PhD, Director-cum-chief Scientist of GBMD, reports that: Insights into the development of cardiac-safe analgesics: Cell cycle regulated pro-proliferative protein E2F3 inhibits inflammatory pain stimuli via up regulation of aldehyde dehydrogenase 2. E2F3, by suppressing the expression of its target gene, it may decrease the accumulation of aldehyde (a pain-stimulating agent). Together, this study suggests that pharmacological formulations encompassing “E2F3 activators“ may be used to inhibit inflammatory pain stimuli.
Idea Proposed/Formulated by: Dr L Boominathan Ph.D.
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Citation: Boominathan, Insights into the development of cardiac-safe analgesics: Cell cycle regulated pro-proliferative protein E2F3 inhibits inflammatory pain stimuli via up regulation of aldehyde dehydrogenase 2, 3/September/2014, 9.29 am, Genome-2-Bio-Medicine Discovery center (GBMD), http://genomediscovery.org
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