Hwang Mi-Na, Kim Kwang Soo, Choi Yo-Woo, Jou Ilo, Yoon Sungpil
Research Institute, National Cancer Center, Goyang 411-764, Korea.
Mol Cells. 2007 Feb 28;23(1):94-9.
Suppressors of cytokine signaling (SOCS) family members are negative feedback regulators of the Jak/Stat pathway, which is an essential inflammatory signaling pathway. We investigated expression of eight members of the SOCS family in rat astrocytes, using two inflammatory stimulants, PMA and IFN-gamma. Only a few SOCS genes were induced by both stimulants, and we detected an increase in SOCS5 protein with PMA. PMA activated the Jnk, Erk, p38, and Jak/Stat signal pathways. In addition, it increased the level of activated-Stat3 resulting from tyrosine phosphorylation. A gel-shift assay showed that a protein in nuclear extracts from PMA-treated cells was able to bind to Stat binding elements. These results suggest that activated Stat3 binds to SOCS promoters and leads to their transcriptional induction.
细胞因子信号转导抑制因子（SOCS）家族成员是Jak/Stat信号通路的负反馈调节因子，而Jak/Stat信号通路是一条重要的炎症信号通路。我们使用两种炎症刺激物佛波酯（PMA）和γ干扰素（IFN-γ），研究了SOCS家族八个成员在大鼠星形胶质细胞中的表达情况。两种刺激物仅诱导了少数SOCS基因，并且我们检测到用PMA处理后SOCS5蛋白增加。PMA激活了Jnk、Erk、p38和Jak/Stat信号通路。此外，它还增加了酪氨酸磷酸化导致的活化Stat3水平。凝胶迁移试验表明，来自PMA处理细胞的核提取物中的一种蛋白质能够结合Stat结合元件。这些结果表明，活化的Stat3与SOCS启动子结合并导致其转录诱导。
