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J Biol Chem, Vol. 273, Issue 32, 19929-19932, August 7, 1998
From the Dana-Farber Cancer Institute and the Department of
Pathology, Harvard Medical School, Boston, Massachusetts 02115
Growth factor-dependent survival of a
variety of mammalian cells is dependent on the activation of
phosphatidylinositol (PI) 3-kinase and its downstream effector, the
protein kinase Akt. Glycogen synthase kinase-3 (GSK-3) has been
previously identified as a physiological target of Akt, which is
inhibited by phosphorylation, so we have investigated the role of GSK-3
in cell survival. Overexpression of catalytically active GSK-3 induced
apoptosis of both Rat-1 and PC12 cells, whereas dominant-negative GSK-3
prevented apoptosis following inhibition of PI 3-kinase. GSK-3 thus
plays a critical role in regulation of apoptosis and represents a key
downstream target of the PI 3-kinase/Akt survival signaling
pathway.
COMMUNICATION
Role of Glycogen Synthase Kinase-3 in the Phosphatidylinositol
3-Kinase/Akt Cell Survival Pathway
Copyright © 1998 by The American Society for Biochemistry and Molecular Biology, Inc.
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S. Liu, S. Yu, Y. Hasegawa |
