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

Journal of Cell Science 117, 5197-5208 (2004)
Published by The Company of Biologists 2004
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Linking JNK signaling to NF-{kappa}B: a key to survival

Salvatore Papa, Francesca Zazzeroni*, Can G. Pham, Concetta Bubici and Guido Franzoso{ddagger}

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



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  		Fig. 1. TNFR1-induced pathways modulating apoptosis. Formation of complex I leads to NF-{kappa}B activation, Gadd45ß induction, JNK inhibition and cell survival. Formation of complex II leads to caspase-8/10-mediated cleavage of Bid into tBid, which then targets mitochondria to induce cytochrome c release and, ultimately, cell death. The figure also depicts JNK activation, which results in formation of jBid; this promotes PCD by triggering release of Smac/Diablo into the cytosol, inhibiting the TRAF2-IAP1 complex and consequently activating caspase-8. The Gadd45ß-MKK7 interaction linking the JNK and NF-{kappa}B pathways is also shown.

 


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  		Fig. 2. The various mediators of the NF-{kappa}B suppression of JNK signaling and their potential modes of action.

 


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  		Fig. 3. Potential therapeutic implications of the NF-{kappa}B-mediated blockade of TNF-{alpha}-induced JNK signaling. A positive-feedback loop between TNF-{alpha} and NF-{kappa}B drives chronic inflammatory states; several pharmacological agents can be used to treat these states. The effects of MKK7-mimicking peptides are also shown (Papa et al., 2004Go), which support the therapeutic feasibility of blocking the NF-{kappa}B anti-apoptotic activity without significantly affecting the immune system.

 

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© The Company of Biologists Ltd 2004