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PLoS One. 2016 Jan 8;11(1):e0145780. doi: 10.1371/journal.pone.0145780. eCollection 2016.

BAD, a Proapoptotic Protein, Escapes ERK/RSK Phosphorylation in Deguelin and siRNA-Treated HeLa Cells.

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Institute of Molecular Biology and Biotechnology and Center for Research in Molecular Medicine, the University of Lahore, Lahore, Pakistan.
Center of Excellence in Genomic Medicine Research, King Abdulaziz University, Jeddah, Saudi Arabia.
College of Applied Medical Sciences, King Saud Bin Abdulaziz University for Health Sciences, National Guards Health Affairs, Riyadh, Saudi Arabia.
King Fahd Medical Research Center, King Abdulaziz University, Jeddah, Saudi Arabia.
Department of Biotechnology, BUITEMS, Quetta, Pakistan.
College of Applied Medical Science, Al Majmaah University, Majmaah City, Saudi Arabia.


This study has been undertaken to explore the therapeutic effects of deguelin and specific siRNAs in HeLa cells. The data provided clearly show the silencing of ERK 1/2 with siRNAs and inhibition of ERK1/2 with deguelin treatment in HeLa cells. Additionally, we are providing information that deguelin binds directly to anti-apoptotic Bcl-2, Bcl-xl and Mcl-1 in the hydrophobic grooves, thereby releasing BAD and BAX from dimerization with these proteins. This results in increased apoptotic activity through the intrinsic pathway involved in rupture of mitochondrial membrane and release of cytochrome C. Evidence for inhibition of ERK1/2 by deguelin and escape of BAD phosphorylation at serine 112 through ERK/RSK pathway has been further fortified by obtaining similar results by silencing ERK 1/2 each with specific siRNAs. Increase in BAD after treatment with deguelin or siRNAs has been interpreted to mean that deguelin acts through several alternative pathways and therefore can be used as effective therapeutic agent.

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