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  • 标题:LIF- and IL-6-Induced Acetylation of STAT3 at Lys-685 through PI3K/Akt Activation
  • 本地全文:下载
  • 作者:Norihiko Ohbayashi ; Osamu Ikeda ; Naohisa Taira
  • 期刊名称:Biological and Pharmaceutical Bulletin
  • 印刷版ISSN:0918-6158
  • 电子版ISSN:1347-5215
  • 出版年度:2007
  • 卷号:30
  • 期号:10
  • 页码:1860-1864
  • DOI:10.1248/bpb.30.1860
  • 出版社:The Pharmaceutical Society of Japan
  • 摘要: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.
  • 关键词:signal transducer and activator of transcription 3;interleukin-6;acetylation;leukemia inhibitory factor;PI3K;Akt
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