Reference - Detail
|Author||Hirasawa N, Izumi S, Linwong W, Ohuchi K.|
|Title||Inhibition by dexamethasone of interleukin 13 production via glucocorticoid receptor-mediated inhibition of c-Jun phosphorylation.|
The antigen stimulation of RBL-2H3 cells induced interleukin 13 (IL-13) production, which was inhibited by the steroidal anti-inflammatory drug dexamethasone and by the c-Jun N-terminal kinase (JNK) inhibitor SP600125. Dexamethasone did not inhibit the antigen-induced phosphorylation of JNK but inhibited that of c-Jun. In a cell-free system, the phosphorylation of glutathione S-transferase-fused c-Jun by recombinant JNK was not inhibited by dexamethasone but was inhibited by the addition of recombinant glucocorticoid receptor (GR). These findings suggest that the inhibition of antigen-induced IL-13 production by dexamethasone is due to the GR-mediated inhibition of c-Jun phosphorylation induced by JNK.
|MeSH||Animals Anthracenes / pharmacology Cell Line, Tumor Dexamethasone / pharmacology* Dinitrophenols / chemistry Dinitrophenols / pharmacology Humans Immunoblotting Immunoglobulin E / pharmacology Interleukin-13 / antagonists & inhibitors Interleukin-13 / biosynthesis* JNK Mitogen-Activated Protein Kinases Mitogen-Activated Protein Kinases / antagonists & inhibitors* Mitogen-Activated Protein Kinases / metabolism Phosphorylation Rats Receptors, Glucocorticoid / metabolism* Recombinant Fusion Proteins / genetics Recombinant Fusion Proteins / metabolism Serum Albumin / chemistry Serum Albumin / pharmacology Transcription Factor AP-1 / drug effects Transcription Factor AP-1 / metabolism|
|WOS Category||BIOPHYSICS BIOCHEMISTRY & MOLECULAR BIOLOGY CELL BIOLOGY|
|DNA material||pBS rcjun-1 Rat c-Jun protooncogene (RDB1130)|