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Reactive oxygen species mediate crosstalk between NF-kappaB and JNK Nakano H; Nakajima A; Sakon-Komazawa S; Piao JH; Xue X; Okumura KCell Death Differ 2006[May]; 13 (5): 730-7The 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.|*Signal Transduction[MESH]|Animals[MESH]|Apoptosis[MESH]|Down-Regulation[MESH]|Drosophila[MESH]|JNK Mitogen-Activated Protein Kinases/*metabolism[MESH]|Mice[MESH]|Models, Biological[MESH]|NF-kappa B/*physiology[MESH]|Reactive Oxygen Species/*metabolism[MESH]|Tumor Necrosis Factor-alpha/pharmacology[MESH] |
