Daxx enhances Fas-mediated apoptosis in a murine pro-B cell line, BAF3.

• Muromoto, Ryuta

• Yamamoto, Tetsuya

• Yumioka, Taro

• Sekine, Yuichi

• Sugiyama, Kenji

• Shimoda, Kazuya

• Oritani, Kenji

• Matsuda, Tadashi

Abstract

Daxx has been shown to play an essential in type I interferon (IFN-α/β)-mediated suppression of B cell development and apoptosis. Recently, we demonstrated that Tyk2 is directly involved in IFN signaling for the induction and nuclear translocation of Daxx, which may result in growth arrest and/or apoptosis of B lymphocyte progenitors. To clarify the mechanism of Daxx-mediated apoptosis signaling in B lymphocyte progenitors, here we introduced an efficient suicide switch in a murine pro-B cell line, BAF3, by expressing FK506-binding protein-fused Fas intracellular domain (FKBP-Fas) and Daxx. It allows us to monitor Fas/Daxx-mediated signal by induction of Fas dimerization with the dimerizer drug AP20187. AP20187-mediated Fas dimerization induced not only apoptosis but also Jun N-terminal kinase (JNK) activation. However, AP20187 had no effect on cells expressing either Fas or Daxx only. Furthermore, expression of a JNK inhibitor, the JNK-binding domain of JIP-1, resulted in resistance to AP20187-mediated apoptosis in cells expressing FKBP-Fas and Daxx. These results imply that our novel suicide switch system may provide a powerful tool to delineate or identify the signaling molecules for Daxx-mediated apoptotic machinery in B lymphocyte progenitors through JNK activation.

Journal

• FEBS Letters

  FEBS Letters 540 (1-3), 223-228, 2003-04-10

  Elsevier

Keywords

• Daxx
• Fas
• Apoptosis
• B lymphocyte
• Jun N-terminal kinase
• Interferon

Details

• CRID: 1050282813968220416
• NII Article ID: 120000973629
• HANDLE: 2115/28115
• ISSN: 00145793
• Text Lang: en
• Article Type: journal article
• Data Source:
  • IRDB
  • CiNii Articles