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Physical and functional interactions between Daxx and STAT3.

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タイトル: Physical and functional interactions between Daxx and STAT3.
著者: Muromoto, R. 著作を一覧する
Nakao, K. 著作を一覧する
Watanabe, T. 著作を一覧する
Sato, N. 著作を一覧する
Sekine, Y. 著作を一覧する
Sugiyama, K. 著作を一覧する
Oritani, K. 著作を一覧する
Shimoda, K. 著作を一覧する
Matsuda, T. 著作を一覧する
キーワード: IL-6
transcriptional regulation
発行日: 2006年 3月30日
出版者: Nature Publishing Group
誌名: Oncogene
巻: 25
号: 14
開始ページ: 2131
終了ページ: 2136
出版社 DOI: 10.1038/sj.onc.1209235
抄録: Signal transducer and activator of transcription 3 (STAT3) play key roles in the intracellular signaling pathways of the interleukin (IL)-6 family of cytokines, which exhibit a diverse set of cellular responses, including cell proliferation and differentiation. Dysregulated IL-6/STAT3 signaling is involved in the pathogenesis of several diseases, for example autoimmune diseases and tumors. Type I interferon (IFN) induces the expression of proapoptotic genes and has been used in the clinical treatment of several tumors. In the present study, we found that type I IFN suppressed IL-6/STAT3-mediated transcription and gene expression. Furthermore, a type I IFN-induced protein, Daxx, also suppressed STAT3-mediated transcriptional activation, while overexpression of Daxx inhibited IL-6/STAT3-mediated gene expression. Importantly, small-interfering RNA-mediated reduction of Daxx expression enhanced IL-6/leukemia inhibitory factor (LIF)-induced STAT3-dependent transcription. Co-immunoprecipitation studies revealed a physical interaction between Daxx and STAT3 in transiently transfected 293T cells. We further found that Daxx and STAT3 were co-localized in the nucleus. These results indicate that Daxx may serve as a transcriptional regulator of type I IFN-mediated suppression of the IL-6/STAT3 signaling pathway.
Rights: Nature Publishing Group, ONCOGENE, 25, 14, 2006, 2131-2136.
資料タイプ: article (author version)
出現コレクション:雑誌発表論文等 (Peer-reviewed Journal Articles, etc)

提供者: 松田 正


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