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目的 :探讨鼻咽癌细胞中JIP抑制激活蛋白 1(AP - 1)信号转导途径的分子机制。方法 :用Dox诱导L7(Tet-on -LMP1-HNE2 )细胞表达LMP1,观察AP - 1活性的动力学变化 ,然后用不同浓度的JIP质粒转染L7细胞后 ,观察JIP的表达对LMP1诱导的AP - 1活性的影响 ,并用荧光免疫组化方法观察JIP抑制JNK核移位引起磷酸化的JNK在胞浆中的滞留。结果 :在转染JIP表达质粒 2 4h之后 ,抑制了活化的JNK核移位 ,下调了AP - 1的生物活性。结论 :JIP能够通过抑制磷酸化的JNK核移位 ,从而下调AP - 1活性。
Objective: To investigate the molecular mechanism of JIP inhibitory activator - 1 (AP - 1) signal transduction pathway in nasopharyngeal carcinoma cells. Methods: LMP1 was induced by Dox in L7 (Tet-on-LMP1-HNE2) cells and the dynamic changes of AP-1 activity were observed. After L7 cells were transfected with different concentrations of JIP plasmid, the expression of LMP1 AP - 1 activity, and observed by fluorescence immunohistochemistry JIP JNK nuclear translocation caused phosphorylation of JNK retention in the cytoplasm. Results: After transfection with JIP expression plasmid for 24 h, the nuclear translocation of activated JNK was inhibited and the biological activity of AP - 1 was down - regulated. Conclusion: JIP can down - regulate AP - 1 activity by inhibiting the phosphorylation of JNK nuclear translocation.