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Physical and functional interactions between Daxx and STAT3.

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Title: Physical and functional interactions between Daxx and STAT3.
Authors: Muromoto, R. Browse this author
Nakao, K. Browse this author
Watanabe, T. Browse this author
Sato, N. Browse this author
Sekine, Y. Browse this author
Sugiyama, K. Browse this author
Oritani, K. Browse this author
Shimoda, K. Browse this author
Matsuda, T. Browse this author →KAKEN DB
Keywords: IL-6
transcriptional regulation
Issue Date: 30-Mar-2006
Publisher: Nature Publishing Group
Journal Title: Oncogene
Volume: 25
Issue: 14
Start Page: 2131
End Page: 2136
Publisher DOI: 10.1038/sj.onc.1209235
PMID: 16331268
Abstract: 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.
Type: article (author version)
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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