A recent study from the Department of Cell Biology, Beth Israel Deaconess Medical Center, Boston, MA 02115, USA shows that “Metabolic regulation of protein N-alpha-acetylation by Bcl-xL promotes cell survival.” This study was published in the 19 August 2011 issue of the Journal “Cell”[I.F: 33] by Prof. Yuan J. and Dr. Yi CH and others.
On the foundation of this interesting finding, Dr L Boominathan PhD, Director-cum-chief Scientist of GBMD, reports that: Mechanistic insight into apoptosis: TAp63γ increases the levels of acetyl-CoA and N-alpha-acetylated proteins and suppresses the expression of Bcl-xL via up regulation of its target gene. This study suggests, for the first time, that TAp63γ, by increasing the expression of its target gene, it may (1) decrease the expression of Bcl-xL; (2) increase the levels of acetyl-CoA and N-alpha-acetylated proteins; and (3) promote apoptosis.
Idea Proposed/Formulated by: Dr L Boominathan Ph.D.
Citation: Boominathan, L., Mechanistic insight into apoptosis: TAp63γ increases the levels of acetyl-CoA and N-alpha-acetylated proteins and suppresses the expression of Bcl-xL via up regulation of its target gene, 15/November/2015, 7.48 am, Genome-2-Bio-Medicine Discovery center (GBMD), http://genomediscovery.org
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Undisclosed information: How TAp63γ increases the levels of acetyl-CoA and N-alpha-acetylated proteins and suppresses the expression of Bcl-xL
