Rac is activated by tumor necrosis factor α and is involved in activation of Erk

Yurika Nosaka, Ayako Arai, Eiichiro Kanda, Takashi Akasaki, Hideki Sumimoto, Nobuyuki Miyasaka, Osamu Miura

研究成果: Contribution to journalArticle査読

29 被引用数 (Scopus)

抄録

Tumor necrosis factor α (TNFα) activates various signal transduction pathways including those involving phosphatidylinositol 3-kinase (PI3K), extracellular signal-regulated kinases (Erk), c-Jun N-terminal protein kinases (JNK), and p38 kinases. Using the Rac binding domain of PAK (PAK-RBD) as an activation-specific probe, here we demonstrate that TNFα very rapidly and transiently activates the Rho family GTPase Rac in L929 cells. The PI3K inhibitor LY294002 significantly inhibited TNFα activation of Rac as well as Erk and abolished that of the PI3K target Akt, without showing any inhibitory effects on JNK and p38 activation. Furthermore, TNFα activation of Erk was abolished by a dominant negative Rac mutant, Rac17N, or by an activated Rac mutant, Rac12V. These findings suggest that Rac is activated by a mechanism that is at least partly dependent on PI3K in TNFα stimulated cells and plays a critical role in activation of the Erk signaling pathway.

本文言語英語
ページ(範囲)675-679
ページ数5
ジャーナルBiochemical and Biophysical Research Communications
285
3
DOI
出版ステータス出版済み - 1 1 2001
外部発表はい

All Science Journal Classification (ASJC) codes

  • Biophysics
  • Biochemistry
  • Molecular Biology
  • Cell Biology

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