Molecular Modeling of Human BAD, a Pro-Apoptotic Bcl-2 Family Member, Integrating Glycolysis and Apoptosis

Jie      Yang

Abstract

Comparison between the BAD complexes indicated that BAD all docks a hydrophobic surface of PKAc regardless of its phosphorylation. PKAc may prevent Bcl-xL from rebinding to BAD by phosphorylating human BAD at Ser118; whereas human BAD is phosphorylated on Ser75 in a BAD-Bcl-xL complex, resulting in the dissociation of BAD.

Keywords: Computational modeling, protein-protein interaction, sequence alignment

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