1. Reactive oxygen species mediate crosstalk between NF-kappaB and JNK.
- Author
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Nakano H, Nakajima A, Sakon-Komazawa S, Piao JH, Xue X, and Okumura K
- Subjects
- Animals, Apoptosis, Down-Regulation, Drosophila, Mice, Models, Biological, Tumor Necrosis Factor-alpha pharmacology, JNK Mitogen-Activated Protein Kinases metabolism, NF-kappa B physiology, Reactive Oxygen Species metabolism, Signal Transduction
- Abstract
The activation of NF-kappaB inhibits apoptosis via a mechanism involving upregulation of various antiapoptotic genes, such as cellular FLICE-inhibitory protein (c-FLIP), Bcl-xL, A1/Bfl-1, and X chromosome-liked inhibitor of apoptosis (XIAP). In contrast, the activation of c-Jun N-terminal kinase (JNK) promotes apoptosis in a manner that is dependent on the cell type and the context of the stimulus. Recent studies have indicated that one of the antiapoptotic functions of NF-kappaB is to downregulate JNK activation. Further studies have also revealed that NF-kappaB inhibits JNK activation by suppressing accumulation of reactive oxygen species (ROS). In this review, we will focus on the signaling crosstalk between the NF-kappaB and JNK cascades via ROS.
- Published
- 2006
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