TRAF6在NF-κB信号通路中的修饰与降解

Modification and Degradation of TRAF6 in the Activation of NF-κB Pathway

目的:研究肿瘤坏死因子受体相关因子6(TRAF6)在调节NF-κB通路中的作用机制。方法:利用转导了并稳定表达TRAF6基因的293RZC细胞株,用荧光素酶报告基因系统测定CoA1对293RZC细胞NF-κB通路的激活,WesternBlot分析在NF-κB通路激活过程中TRAF6和IκBα的降解。结果:CoA1可诱导293RZC细胞NF-κB通路的激活,在这一过程中,TRAF6被修饰并降解,IκBα也发生降解,二者的降解被蛋白酶抑制剂MG132抑制。结论:TRAF6介导NF-κB通路的激活需要蛋白酶复合体的作用。

Objective:To investigate the possible roles of TRAF6 on the ac tiva tion of NF-êB pathway. Methods:293 RZC stable cell line made by transfection w ith expressible TRAF6 gene, and luciferase reporter were applied for detecting t he activation of NF-êB pathway triggered by CoA1. The modification and degrada tion of TRAF6 as well as degradation of IêBáwere determined by Western Blot as say. Results:CoA1 was able to induce activation of NF-êB pathway in the 293RZ C cells. During the course of activation, TRAF6 was modified and degraded appare ntly. Furthermore, IêBádegradation was detected simultaneously. Proteasome inh ibitor MG132 inhibited the degradation both of TRAF6 and IêBá. Conclusion:Pro teasome might be involved in activation of NF-êB pathway mediated by TRAF6.