LIF- and IL-6-induced acetylation of STAT3 at Lys-685 through PI3K/Akt activation

Norihiko Ohbayashi, Osamu Ikeda, Naohisa Taira, Yu Yamamoto, Ryuta Muromoto, Yuichi Sekine, Kenji Sugiyama, Tsutomu Honjoh, Tadashi Matsuda

研究成果: Article査読

43 被引用数 (Scopus)

抄録

Signal transducer and activator of transcription 3 (STAT3), which mediates biological actions in many physiological processes, is activated by cytokines and growth factors via specific tyrosine or serine phosphorylation, dimerization and nuclear translocation. A recent study has demonstrated, by using antibody to acetylated lysine, and a STAT3 mutant with Lys-685-to-Arg substitution, that STAT3 is acetylated at Lys-685 by histone acetyltransferase p300, and that acetylation at Lys-685 is critical for STAT3 activation. In the present study, we created an acetyl-specific antibody against STAT3 acetylated at Lys-685, and found that leukemia inhibitory factor (LIF) or interleukin (IL)-6 induced acetylation of STAT3 at Lys-685 in 293T and Hep3B cells. Moreover, acetylation of STAT3 at Lys-685 was suppressed by PI3K inhibitor LY294002, or a dominant negative Akt. Taken together, our findings demonstrate that endogenous STAT3 is acetylated at Lys-685 by LIF or IL-6 through PI3K/Akt activation.

本文言語English
ページ(範囲)1860-1864
ページ数5
ジャーナルBiological and Pharmaceutical Bulletin
30
10
DOI
出版ステータスPublished - 2007 10月
外部発表はい

ASJC Scopus subject areas

  • 薬理学
  • 薬科学

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