Expression of a constitutively active phosphatidylinositol 3-kinase induces process formation in rat PC12 cells

Michimoto Kobayashi, Satoshi Nagata, Yoshihiro Kita, Noriyuki Nakatsu, Sayoko Ihara, Kozo Kaibuchi, Shinya Kuroda, Motoyasu Ui, Hideo Iba, Hiroaki Konishi, Ushio Kikkawa, Izumu Saitoh, Yasuhisa Fukui

研究成果: Article査読

122 被引用数 (Scopus)


It has been shown that inhibition of phosphatidylinositol (PI) 3-kinase blocks neurite outgrowth of PC12 cells stimulated with nerve growth factor. To further assess the role of PI 3-kinase, the active form of PI 3-kinase was expressed in PC12 cells by the adenovirus mediated introduction of a site- specific recombinase, Cre. After expression of the active PI 3-kinase, elevation of the levels of PI 3,4-diphosphate and PI 3,4,5-trisphosphate as well as formation of neurite-like processes was observed. The process formation was inhibited by wort-mannin, a selective inhibitor of PI 3- kinase, which suggests that a high activity of PI 3-kinase was responsible for the formation of these processes. The processes lacked accumulation of F- actin and GAP43 at the growth cone, which suggests that the processes were incomplete compared with neurites. Instead, the bundling of microtubules was enhanced, which suggests that organization of the microtubules might be driving the process of elongation in the cells expressing the active PI 3- kinase. Induction of active PI 3-kinase resulted in activation of Jun N- terminal kinase but not of mitogen-activated protein kinase or protein kinase B/Rac protein kinase/Akt. These results suggest that PI 3-kinase is involved in neurite outgrowth in PC12 cells and that activation of Jun N-terminal kinase cascade may be involved in the cell response.

ジャーナルJournal of Biological Chemistry
出版ステータスPublished - 27-06-1997

All Science Journal Classification (ASJC) codes

  • 生化学
  • 分子生物学
  • 細胞生物学


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