FAK is the upstream signal protein of the phosphatidylinositol 3- kinase-Akt survival pathway in hydrogen peroxide-induced apoptosis of a human glioblastoma cell line

Yoshiko Sonoda, Shiro Watanabe, Yaeko Matsumoto, Eriko Aizu-Yokota, Tadashi Kasahara

研究成果: Article査読

220 被引用数 (Scopus)

抄録

Protein phosphorylation in a human glioblastoma cell line, T98G, was examined after exposure to oxidative stress in vitro. Hydrogen peroxide (1 mM) markedly induced tyrosine phosphorylation of focal adhesion kinase (FAK) and serine phosphorylation of Akt at 1 h after stimulation. Concommitantly, the association of FAK with phosphatidylinositide 3'-OH-kinase (PI 3-kinase) was also observed by the hydrogen peroxide stimulation. When T98G cells were incubated with wortmannin, a PI 3-kinase inhibitor, both PI 3-kinase activity and phosphorylation of Akt were inhibited, whereas apoptosis by oxidative stress was accelerated. Concomitant with apoptosis, elevated level of CPP32 protease activity (caspase-3) was observed, with decreases in Bcl-2 protein and increases in Bax protein. These results suggested that in the signal transduction pathway from FAK to PI 3-kinase, Akt promotes survival. Thus, it became apparent that FAK is the upstream signal protein of the PI 3-kinase- Akt survival pathway in hydrogen peroxide-induced apoptosis in T98G cells.

本文言語English
ページ(範囲)10566-10570
ページ数5
ジャーナルJournal of Biological Chemistry
274
15
DOI
出版ステータスPublished - 1999 4月 9

ASJC Scopus subject areas

  • 生化学
  • 分子生物学
  • 細胞生物学

フィンガープリント

「FAK is the upstream signal protein of the phosphatidylinositol 3- kinase-Akt survival pathway in hydrogen peroxide-induced apoptosis of a human glioblastoma cell line」の研究トピックを掘り下げます。これらがまとまってユニークなフィンガープリントを構成します。

引用スタイル