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First published online October 13, 2004
doi: 10.1242/10.1242/jcs.01483

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Linking JNK signaling to NF-B: a key to survival

Salvatore Papa, Francesca Zazzeroni^*, Can G. Pham, Concetta Bubici and Guido Franzoso

The Ben May Institute for Cancer Research, The University of Chicago, 924 East 57th Street, Chicago, IL 60637, USA

Author for correspondence (e-mail: gfranzos{at}midway.uchicago.edu)

In addition to marshalling immune and inflammatory responses, transcription factors of the NF-B family control cell survival. This control is crucial to a wide range of biological processes, including B and T lymphopoiesis, adaptive immunity, oncogenesis and cancer chemoresistance. During an inflammatory response, NF-B activation antagonizes apoptosis induced by tumor necrosis factor (TNF)-, a protective activity that involves suppression of the Jun N-terminal kinase (JNK) cascade. This suppression can involve upregulation of the Gadd45-family member Gadd45ß/Myd118, which associates with the JNK kinase MKK7/JNKK2 and blocks its catalytic activity. Upregulation of XIAP, A20 and blockers of reactive oxygen species (ROS) appear to be important additional means by which NF-B blunts JNK signaling. These recent findings might open up entirely new avenues for therapeutic intervention in chronic inflammatory diseases and certain cancers; indeed, the Gadd45ß-MKK7 interaction might be a key target for such intervention.

Key words: NF-B, JNK, Gadd45ß, TNF-, Apoptosis

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