Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
2540937 | International Immunopharmacology | 2013 | 6 Pages |
Abstract
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.
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Authors
Jee Youn Kim, Hyung Sook Kim, Yeon Jin Kim, Hong Kyung Lee, Ji Sung Kim, Jong Soon Kang, Jin Tae Hong, Youngsoo Kim, Bang Yeon Hwang, Sang-Bae Han,