Phosphoinositide 3-Kinase γ Is a Mediator of Gβγ-dependent Jun Kinase Activation

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 Gβγ subunits of heterotrimeric G proteins, but the subsequ...

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Αποθηκεύτηκε σε:
Λεπτομέρειες βιβλιογραφικής εγγραφής
Κύριοι συγγραφείς: Marco López-Ilasaca, J. Silvio Gutkind, Reinhard Wetzker
Μορφή: Artigo
Γλώσσα:Αγγλικά
Έκδοση: 1998
Διαθέσιμο Online:https://doi.org/10.1074/jbc.273.5.2505
http://www.jbc.org/article/S0021925818949240/pdf
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Περιγραφή
Περίληψη: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 Gβγ subunits of heterotrimeric G proteins, but the subsequent signaling reaction has been undefined. Here we demonstrate JNK activation in COS-7 cells by Gβγ-stimulated phosphoinositide 3-kinase γ (PI3Kγ). Signal transduction from PI3Kγ to JNK can be suppressed by dominant negative mutants of Ras, Rac, and the protein kinase PAK. These results identify PI3Kγ as a mediator of Gβγ-dependent regulation of JNK activity.