JNK3通过与RelA/p65相互作用抑制NF-κB信号通路减弱Bel-7402细胞的黏附能力(英文)  

JNK3 Cooperates With RelA/p65 to Decrease Bel-7402 Cell Adhesion Upon The Inhibition of NF-κB Pathway

作　　者：李强[1] 韩卿[1] 虞东辉[1,2] 唐留军[1,2] 王建[1,2] 王晓辉[1,2] 许望翔[1,2] 詹轶群[1,2] 李长燕[1,2] 葛常辉[1,2] 于淼[1,2] 杨晓明[1,2] 

机构地区：[1]北京放射医学研究所,北京100850 [2]蛋白质组学国家重点实验室,北京100850

出　　处：《生物化学与生物物理进展》2012年第9期877-886,共10页Progress In Biochemistry and Biophysics

基　　金：supported by a grant from The Chinese National Science Fund General Program(30570682)~~

摘　　要：JNK信号通路在细胞的炎症、增殖与凋亡等生物学过程中发挥了重要的作用.我们采用酵母双杂交技术发现转录因子p65是JNK3的相互作用蛋白质.体内体外实验均证实JNK3与p65存在蛋白质相互作用.报告基因实验结果表明过表达JNK3抑制TNFα诱导NF-κB介导的转录激活.EMSA结果证明JNK3减弱NF-κB的DNA结合能力.实时定量PCR结果表明JNF3减少NF-κB靶基因的表达.综上所述,我们的研究结果表明JNK3做为一个调节分子在体内发挥了抑制p65转录活性的功能.The c-Jun amino-terminal kinase （JNK） is an important player in inflammation, proliferation, and apoptosis. Here, by using a yeast two-hybrid technology, p65 subunit of NF-κB transcription factor was identified as a partner of JNK3. We show that JNK3 physically associated with p65 in vivo and in vitro. Overexpression of JNK3 inhibited NF-κB- dependent transcription induced by TNFα. It was demonstrated that JNK3 decreased NF-κB binding to its cognate DNA sequences and NF-κB target genes expression. Taken together, these data suggest that JNK3 may function in vivo as a modulator in suppressing the transcriptional activity of p65.

关 键 词：JNK3 NF-ΚB P65 细胞黏附 蛋白质相互作用 

分 类 号：Q257[生物学—细胞生物学]