Figure 3.

A peptide that blocks the interaction of NF-κB p65 subunit with Smad4 enhances BMP2-induced bone formation. Inhibitors of the classical NF-κB pathway have been reported to promote bone formation, but mice deficient in p65, the main subunit of NF-κB, are embryonic lethal and must be considered for possible side effects. Therefore, we investigated the molecular mechanism by which NF-κB suppresses BMP signaling and revealed that p65 and the BMP-signaling molecule Smad4 are associated. We suggested the possibility of enhancing the effect of BMP without impairing the function of NF-κB by using a peptide that specifically inhibits the association site.