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Merck

Role of STAT3 in glucocorticoid-induced expression of the human IL-10 gene.

Molecular immunology (2008-04-12)
Claudia Unterberger, Karl J Staples, Timothy Smallie, Lynn Williams, Brian Foxwell, Annette Schaefer, Bettina Kempkes, T P J Hofer, Max Koeppel, Marion Lohrum, Henk Stunnenberg, Marion Frankenberger, Loems Ziegler-Heitbrock
要旨

In the present report we have determined the molecular mechanisms, which govern the expression of the human IL-10 gene when induced by the glucocorticoid Methyl-Prednisolone (MP). Treatment of cells with MP at 10(-6) M will readily induce IL-10 in CD19+ primary B cells and in a human B cell line. Analysis of the IL-10 promoter showed a robust 18-fold induction and demonstrated that a potential GRE motif was not required, while mutation of the -120 STAT-motif strongly reduced MP-induced trans-activation. A strong induction was also seen with a trimeric STAT-motif and over-expression of dominant-negative STAT3 could block MP induction of IL-10 mRNA. Finally, MP treatment induced binding of STAT3 to the promoter as shown by gelshift, supershift and by chromatin-immunoprecipitation. These data show that glucocorticoid-induced expression of the IL-10 gene is mediated by the transcription factor STAT3.

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抗ウサギIgG (全分子)-ペルオキシダーゼ ヤギ宿主抗体, affinity isolated antibody
Sigma-Aldrich
抗アクチン ウサギ宿主抗体, affinity isolated antibody, buffered aqueous solution
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アンチパイン 二塩酸塩 微生物由来, protease inhibitor
Sigma-Aldrich
ロイペプチン トリフルオロアセタート塩, ≥90% (HPLC), microbial