Reactive oxygen species mediate crosstalk between NF-kappaB and JNK |
| |
Authors: | Nakano H Nakajima A Sakon-Komazawa S Piao J-H Xue X Okumura K |
| |
Institution: | Department of Immunology, Juntendo University School of Medicine, Tokyo, Japan. hnakano@med.juntendo.ac.jp |
| |
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. |
| |
Keywords: | |
本文献已被 PubMed 等数据库收录! |
|