Nakano H, Nakajima A, Sakon-Komazawa S, Piao J-H, Xue X, Okumura K
Department of Immunology, Juntendo University School of Medicine, Tokyo, Japan.
Cell Death Differ. 2006 May;13(5):730-7. doi: 10.1038/sj.cdd.4401830.
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.
核因子κB（NF-κB）的激活通过上调多种抗凋亡基因来抑制细胞凋亡，这些抗凋亡基因包括细胞FLICE抑制蛋白（c-FLIP）、Bcl-xL、A1/Bfl-1以及X染色体连锁凋亡抑制蛋白（XIAP）。相反，c-Jun氨基末端激酶（JNK）的激活以一种依赖于细胞类型和刺激背景的方式促进细胞凋亡。最近的研究表明，NF-κB的抗凋亡功能之一是下调JNK的激活。进一步的研究还揭示，NF-κB通过抑制活性氧（ROS）的积累来抑制JNK的激活。在这篇综述中，我们将重点关注NF-κB和JNK级联反应之间通过ROS进行的信号转导串扰。
