The Journal of Immunology · 1998 · 59 citations · 22 references
Life SciencesCell BiologyImmunologyCell SignalingInnate ImmunitySignal TransductionCytokine Receptor SignalingInflammatory SignalingC-jun N-terminal Kinase SignalingJnk Pathway ActivationJnk Signaling PathwayJun N-terminal Kinase SignalingKinase InhibitorsPhosphatidylinositol 3-Kinase Pathway
Antigen stimulation of IgE-sensitized rat basophilic leukemia RBL-2H3 cells induced activation of c-Jun N-terminal kinase (JNK) within a few minutes with maximum activity attained 40 min later. The increase in JNK activity was accompanied with an increase in phosphorylation of c-Jun in the cells. The Ag-induced JNK activation was inhibited by the phosphatidylinositol 3-kinase inhibitors wortmannin (10-100 nM) and LY 294002 (100 microM) but not by the protein kinase C inhibitors calphostin C (1 and 3 microM) and Ro 31-8425 (1 and 3 microM). Pretreatment with dexamethasone (10 and 100 nM) for 18 h inhibited the Ag-induced increase in JNK activity in a concentration-dependent manner. At least 6 h of preincubation with dexamethasone was necessary to inhibit the Ag-induced JNK activation. The phosphorylation of c-Jun induced by the Ag stimulation was reduced by pretreatment with dexamethasone without reduction of the content of c-Jun protein. The Ag-induced activation of the JNK kinase kinase mitogen-activated protein kinase-extracellular signal-regulated kinase kinase-1 was also inhibited by pretreatment with dexamethasone at 10 and 100 nM. These findings indicate that dexamethasone reduces JNK protein level and inhibits the Ag-induced activation of JNK resulting in the inhibition of c-Jun phosphorylation.
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Phosphorylation of c-jun mediated by MAP kinases
Bernd Pulverer, John Kyriakis, Joseph Avruch et al. · Nature · 1991 · 1.5K citations
Functional antagonism between oncoprotein c-Jun and the glucocorticoid receptor
Roland Schüle, Steven A. Kliewer, Lynn J. Ransone et al. · Cell · 1990 · 1.3K citations