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Ligand-independent activation of the androgen receptor by insulin-like growth factor-i and the role of the MAPK pathway in skeletal muscle cells
- Ligand-independent activation of the androgen receptor by insulin-like growth factor-i and the role of the MAPK pathway in skeletal muscle cells
- Kim H.J.; Lee W.J.
- Ewha Authors
- SCOPUS Author ID
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- Journal Title
- Molecules and Cells
- Molecules and Cells vol. 28, no. 6, pp. 589 - 593
- SCI; SCIE; SCOPUS; KCI
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- In this study, the roles of the p38 MAPK, ERK1/2 and JNK signaling pathway in IGF-I-induced AR induction and activation were examined. C2C12 cells were treated with IGF-I in the absence or presence of various inhibitors of p38 MAPK (SB203580), ERK1/2 (PD98059), and JNK (SP600125). Inhibition of the MAPK pathway with SB203580, PD98059, or SP600125 significantly decreased IGF-I-induced AR phosphorylation and total AR protein expression. IGF-I-induced nuclear fraction of total AR and phosphorylated AR were significantly inhibited by SB203580, PD98059, or SP600125. Furthermore, IGF-I-induced AR mRNA and skeletal α-actin mRNA were blocked by those inhibitors in dose-dependent manner. Confocal images showed that IGF-I-induced AR nuclear translocation from cytosol was significantly blocked by SB203580, PD98059, or SP600125, suggesting that the MAPK pathway regulates IGF-I-induced AR nuclear localization in skeletal muscle cells. The present results suggest that the MAPK pathways are required for the ligand-independent activation of AR by IGF-I in C2C12 skeletal muscle cells. © 2009 The Korean Society for Molecular and Cellular Biology and Springer Netherlands.
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