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J Biol Chem, Vol. 273, Issue 5, 2505-2508, January 30, 1998
Is a Mediator of
G
-dependent Jun Kinase Activation
, and
From the Max Planck Research Unit "Molecular Cell Biology,"
Medical Faculty, University of Jena, 07747 Jena, Germany and the
Jun kinases (JNK) are involved in the stress
response of mammalian cells. Stimulation of JNK can be induced by
stress factors and by agonists of tyrosine kinase and G protein-coupled
receptors. G protein-dependent receptors stimulate JNK via
G Molecular Signaling Unit, Laboratory of Cellular
Development and Oncology, NIDR, National Institutes of Health,
Bethesda, Maryland 20892
subunits of heterotrimeric G proteins, but the subsequent
signaling reaction has been undefined. Here we demonstrate JNK
activation in COS-7 cells by G-stimulated phosphoinositide
3-kinase (PI3K). Signal transduction from PI3K to JNK can be
suppressed by dominant negative mutants of Ras, Rac, and the protein
kinase PAK. These results identify PI3K as a mediator of
G-dependent regulation of JNK activity.
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