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Journal of Cell Science, Vol 111, Issue 7 907-915, Copyright © 1998 by Company of Biologists
JOURNAL ARTICLES |
Y Kita, KD Kimura, M Kobayashi, S Ihara, K Kaibuchi, S Kuroda, M Ui, H Iba, H Konishi, U Kikkawa, S Nagata and Y Fukui
Department of Biological Chemistry, Faculty of Agricultural and Life Science, University of Tokyo, Tokyo, Japan.
We have previously shown that sustained phosphatidylinositol (PI)-3 kinase activity is necessary for neurite outgrowth of PC12 cells induced by nerve growth factor (NGF). Microinjection of a constitutively active mutant of PI-3 kinase induced process formation suggesting that PI-3 kinase is indeed involved in the neurite outgrowth. However, the processes appeared to be incomplete neurites as they had very poor organization of F-actin and GAP43 antigen. The microtubule network was enhanced in the process-bearing cells and process formation was inhibited by colchicine suggesting that microtubules play an important role in process formation downstream of PI-3 kinase. These cell responses were inhibited by dominant-negative mutants of Rac and Sek1/SAPK but not by a dominant-negative mutant Ras and PD98059, a MAP kinase kinase (MEK) inhibitor, suggesting that not the Ras-MAP kinase pathway but the Rac-Jun N-terminal kinase (JNK) pathway is involved in process formation.
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