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

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Please use this identifier to cite or link to this item:http://hdl.handle.net/2115/28115

Title: Daxx enhances Fas-mediated apoptosis in a murine pro-B cell line, BAF3.
Authors: Muromoto, Ryuta Browse this author
Yamamoto, Tetsuya Browse this author
Yumioka, Taro Browse this author
Sekine, Yuichi Browse this author
Sugiyama, Kenji Browse this author
Shimoda, Kazuya Browse this author
Oritani, Kenji Browse this author
Matsuda, Tadashi Browse this author →KAKEN DB
Keywords: Daxx
Fas
Apoptosis
B lymphocyte
Jun N-terminal kinase
Interferon
Issue Date: 10-Apr-2003
Publisher: Elsevier
Journal Title: FEBS Letters
Volume: 540
Issue: 1-3
Start Page: 223
End Page: 228
Publisher DOI: 10.1016/S0014-5793(03)00269-2
PMID: 12681512
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.
Relation: http://www.sciencedirect.com/science/journal/00145793
Type: article (author version)
URI: http://hdl.handle.net/2115/28115
Appears in Collections:薬学研究院 (Faculty of Pharmaceutical Sciences) > 雑誌発表論文等 (Peer-reviewed Journal Articles, etc)

Submitter: 松田 正

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