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

被引：0

作者：

Li Qiang ^{[1
]}

Han Qing ^{[1
]}

Yu Dong-Hui ^{[1
,2
]}

Tang Liu-Jun ^{[1
,2
]}

Wang Jian ^{[1
,2
]}

Wang Xiao-Hui ^{[1
,2
]}

Xu Wang-Xiang ^{[1
,2
]}

Zhan Yi-Qun ^{[1
,2
]}

Li Chang-Yan ^{[1
,2
]}

Ge Chang-Hui ^{[1
,2
]}

Yu Miao ^{[1
,2
]}

Yang Xiao-Ming ^{[1
,2
]}

机构：

[1] Beijing Inst Radiat Med, Beijing 100850, Peoples R China

[2] State Key Lab Proteom, Beijing 100850, Peoples R China

来源：

PROGRESS IN BIOCHEMISTRY AND BIOPHYSICS | 2012年 / 39卷 / 09期

关键词：

JNK3; NF-kappa B; p65; cell adhesion; protein-protein interaction; SIGNAL-TRANSDUCTION; TERMINAL KINASE; JUN; PHOSPHORYLATION; EXPRESSION; ACTIVATION; GROWTH; GENE; ISOFORM;

D O I：

10.3724/SP.J.1206.2012.00041

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

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-kappa B 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-kappa B- dependent transcription induced by TNF alpha. It was demonstrated that JNK3 decreased NF-kappa B binding to its cognate DNA sequences and NF-kappa B target genes expression. Taken together, these data suggest that JNK3 may function in vivo as a modulator in suppressing the transcriptional activity of p65.

引用

页码：877 / 886

页数：10

共 41 条

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