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.
LI Qiang, HAN Qing, YU Dong-Hui, TANG Liu-Jun, WANG Jian, WANG Xiao-Hui, XU Wang-Xiang, ZHAN Yi-Qun, LI Chang-Yan, GE Chang-Hui, YU Miao, YANG Xiao-Ming. JNK3 Cooperates With RelA/p65 to Decrease Bel-7402 Cell Adhesion Upon The Inhibition of NF-κB Pathway[J]. Progress in Biochemistry and Biophysics,2012,39(9):877-886
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