Abstract
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.
Original language | English |
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Pages (from-to) | 489-493 |
Number of pages | 5 |
Journal | FEBS Letters |
Volume | 554 |
Issue number | 3 |
DOIs | |
Publication status | Published - 2003 Nov 20 |
Keywords
- Dexamethasone
- Glucocorticoid receptor
- Interleukin 13
- RBL-2H3 cell line
- c-Jun
- c-Jun N-terminal kinase
ASJC Scopus subject areas
- Biophysics
- Structural Biology
- Biochemistry
- Molecular Biology
- Genetics
- Cell Biology