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

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Chen, F. et al.

Protective roles of NF-kappa B for chromium(VI)-induced cytotoxicity is revealed by expression of Ikappa B kinase-beta mutant.

To delineate the molecular mechanisms of NF-kappaB-mediated regulation of chromium(VI)-induced cell death, the signaling pathway leading to the activation of NF-kappaB was interrupted by stable transfection of a kinase-mutated form of IkappaB kinase beta (IKKbeta-KM). Here we demonstrate a novel role for the NF-kappaB transcription factor in inhibiting chromium(VI)-induced cell death. Inhibition of NF-kappaB by IKKbeta-KM or IKKbeta gene deficiency resulted in a spontaneous cleavage of Bcl-xL antiapoptotic protein due to the elevated caspase-3 activity. DNA microarray assay suggested a decreased expression of genes encoding antiapoptotic proteins, cIAP1 and cIAP2, in the cells overexpressing IKKbeta-KM. Chromium(VI) treatment of these NF-kappaB-inhibited cells induced necrotic-like cell death. Such chromium(VI)-induced cell killing could be partially inhibited by expression of exogenous cIAP1, an inhibitor of caspases, indicating that caspases along with others may be involved in chromium(VI)-induced cell death. These results suggest that NF-kappaB is essential for inhibiting toxic metal-induced cytotoxicity. Such inhibition may involve up-regulation of the expression of anti-death proteins including cIAP1 that prevents spontaneous caspase activation and subsequent cleavage of Bcl-xL protein.[1]

References

Protective roles of NF-kappa B for chromium(VI)-induced cytotoxicity is revealed by expression of Ikappa B kinase-beta mutant. Chen, F., Bower, J., Leonard, S.S., Ding, M., Lu, Y., Rojanasakul, Y., Kung, H.F., Vallyathan, V., Castranova, V., Shi, X. J. Biol. Chem. (2002) [Pubmed]

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