Blog
About

9
views
0
recommends
+1 Recommend
0 collections
    0
    shares
      • Record: found
      • Abstract: found
      • Article: not found

      Reactive oxygen species mediate crosstalk between NF-kappaB and JNK.

      Cell Death and Differentiation

      pharmacology, Animals, Tumor Necrosis Factor-alpha, Signal Transduction, metabolism, Reactive Oxygen Species, physiology, NF-kappa B, Models, Biological, Mice, JNK Mitogen-Activated Protein Kinases, Drosophila, Down-Regulation, Apoptosis

      Read this article at

      ScienceOpenPublisherPubMed
      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          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.

          Related collections

          Author and article information

          Journal
          10.1038/sj.cdd.4401830
          16341124

          Comments

          Comment on this article