Inhibition of TAK1 by kamebakaurin in dendritic cells. 
Kamebakaurin (KA) has anti-cancer and anti-inflammatory activities through direct inhibition of DNA-binding activity of nuclear factor-kappa B (NF-κB) p50.  We suggest here another molecular target of KA by the use of lipopolysaccharide-treated dendritic cells.  In cell- and enzyme-based assays, KA directly inhibited autophosphorylation and kinase activity of TAK1, followed by the inhibition of TAK1-downstream signaling cascades, such as IKK phosphorylation-IκBα degradation-nuclear translocation of NF-κB, phosphorylation of MEK3/6-p38 mitogen activated protein kinase (MAPK), and MKK4/7-c-Jun N-terminal kinase MAPK.  These results demonstrated that TAK1 might be the direct molecular target of KA.