Phosphorylation of BAD at Ser‐128 during mitosis and paclitaxel‐induced apoptosis

Abstract

Phosphorylation of BCL‐2 family member BAD at different residues triggers different physiological effects, either inhibiting or promoting apoptosis. The recently identified phosphorylation site at Ser‐128 enhances the apoptotic activity of BAD. We here show that BAD becomes phosphorylated at Ser‐128 in the mitotic phase of the cell cycle in NIH3T3 cells. We also show that BAD‐S128 is phosphorylated in taxol‐treated mouse fibroblasts and MDA‐MB‐231 human breast cancer cells. However, expression of a phosphorylation‐defective dominant negative BAD mutant did not block taxol‐induced apoptosis. These data support the view that the phosphorylation of BAD Serine 128 exerts cell‐specific effects on apoptosis. Whereas the BAD Serine 128 phosphorylation induces apoptosis in neuronal cells, it does not appear to promote apoptosis in proliferating non‐neural cells during mitosis or upon exposure to the antineoplastic agent taxol.