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

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.