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目的研究两条主要的 IL- 6信号转导途径—— JAK/STAT和 Ras/MAPK/NF- IL- 6在人骨髓瘤细胞系 KM-3中的诱导活化情况和调控机制。方法首先分别采用凝胶阻滞电泳 (EMSA)和免疫沉淀 (IP)方法检测参与 IL- 6信号转导功能的转录因子 (STAT3、NF- IL- 6 )和蛋白激酶 (JAK1、MAPK)在 KM- 3细胞中的诱导活化情况。然后采用特异性酪氨酸蛋白激酶抑制剂 Genistein作用于 KM- 3细胞 ,观察酪氨酸磷酸化作用对 KM- 3细胞中 IL- 6信号转导功能的影响。结果 IL- 6刺激后 ,KM- 3细胞中只出现了 Ras/MAPK/NF- IL- 6信号转导途径的诱导激活 ,而 JAK/STAT途径则不参与 IL- 6在 KM- 3细胞中的信号转导功能。Genistein的作用可明显抑制 Ras/MAPK/NF- IL- 6途径的活化。结论一种目前尚无法确定的非 JAK1酪氨酸蛋白激酶可参与并调节 Ras/MAPK/NF- IL- 6信号转导途径在 KM- 3细胞中的诱导活化。
Objective To investigate the induction and activation mechanisms of two major IL-6 signaling pathways, JAK/STAT and Ras/MAPK/NF-IL-6, in human myeloma cell line KM-3. METHODS: EMSA and IP were used to detect transcription factors (STAT3, NF-IL-6) and protein kinases (JAK1, MAPK) involved in IL-6 signaling in KM. - Induction of activation in 3 cells. The effect of tyrosine phosphorylation on IL-6 signal transduction in KM-3 cells was then investigated using tyrosine kinase inhibitor Genistein on KM-3 cells. Results After IL-6 stimulation, only activated Ras/MAPK/NF-IL-6 signaling pathway was induced in KM-3 cells, while JAK/STAT pathway was not involved in IL-6 in KM-3 cells. Signal transduction function. The effect of Genistein can significantly inhibit the activation of the Ras/MAPK/NF-IL-6 pathway. Conclusion A non-JK1 tyrosine protein kinase that is currently undefined can participate in and regulate the induction of Ras/MAPK/NF-IL-6 signal transduction pathway in KM-3 cells.