¹Department of Immunology, Juntendo University School of Medicine, Tokyo, Japan

Correspondence: H Nakano, Department of Immunology, Juntendo University School of Medicine, 2-1-1 Hongo, Bunkyo-ku, Tokyo 113-8421, Japan. Tel: +81-3-5802-1045; Fax: +81-3-3813-0421; E-mail: hnakano@med.juntendo.ac.jp

Received 23 September 2005; Revised 28 October 2005; Accepted 3 November 2005; Published online 9 December 2005.

Abstract

The activation of NF-B inhibits apoptosis via a mechanism involving upregulation of various antiapoptotic genes, such as cellular FLICE-inhibitory protein (c-FLIP), Bcl-x_L, 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-B is to downregulate JNK activation. Further studies have also revealed that NF-B inhibits JNK activation by suppressing accumulation of reactive oxygen species (ROS). In this review, we will focus on the signaling crosstalk between the NF-B and JNK cascades via ROS.