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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 

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IKK{beta} programs to turn on the GADD45{alpha}-MKK4-JNK apoptotic cascade specifically via p50 NF-{kappa}B in arsenite response.

Cross talk between NF-kappaB and c-Jun N-terminal kinases (JNKs) has been implicated in the cell life and death decision under various stresses. Functional suppression of JNK activation by NF-kappaB has recently been proposed as a key cellular survival mechanism and contributes to cancer cells escaping from apoptosis. We provide a novel scenario of the proapoptotic role of IkappaB kinase beta (IKKbeta)-NF-kappaB, which can act as the activator of the JNK pathway through the induction of GADD45alpha for triggering MKK4/JNK activation, in response to the stimulation of arsenite, a cancer therapeutic reagent. This effect of IKKbeta-NF-kappaB is dependent on p50 but not the p65/relA NF-kappaB subunit, which can increase the stability of GADD45alpha protein through suppressing its ubiquitination and proteasome-dependent degradation. IKKbeta-NF-kappaB can therefore either activate or suppress the JNK cascade and consequently mediate pro- or antiapoptotic effects, depending on the manner of its induction. Furthermore, the NF-kappaB p50 subunit can exert a novel regulatory function on protein modification independent of the classical NF-kappaB transcriptional activity.[1]

References

  1. IKK{beta} programs to turn on the GADD45{alpha}-MKK4-JNK apoptotic cascade specifically via p50 NF-{kappa}B in arsenite response. Song, L., Li, J., Zhang, D., Liu, Z.G., Ye, J., Zhan, Q., Shen, H.M., Whiteman, M., Huang, C. J. Cell Biol. (2006) [Pubmed]
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