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

Maria Berndtsson, Yoshiyuki Konishi, Azad Bonni, Maria Hägg, Maria Shoshan, Stig Linder, Aleksandra Mandic Havelka

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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.

Original languageEnglish
Pages (from-to)3090-3094
Number of pages5
JournalFEBS Letters
Issue number14
StatePublished - Jun 6 2005


  • Apoptosis
  • BAD
  • Cell cycle
  • Taxol

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    Berndtsson, M., Konishi, Y., Bonni, A., Hägg, M., Shoshan, M., Linder, S., & Havelka, A. M. (2005). Phosphorylation of BAD at Ser-128 during mitosis and paclitaxel-induced apoptosis. FEBS Letters, 579(14), 3090-3094.