Ubiquitin: tool and target for intracellular NF-kappaB inhibitors.

Abstract

The transcription factor nuclear factor-kappaB (NF-kappaB) has a pivotal role in initiating inflammation and raising an effective immune response. Because NF-kappaB activation depends on ubiquitination, cells have developed ubiquitin (Ub)-mediated strategies for inhibiting NF-kappaB activation and preventing excessive inflammation. Recent findings concerning tumor necrosis factor (TNF) receptor and toll-like receptor (TLR)-interleukin-1 (IL-1) receptor signalling pathways show that Ub can be a tool as well as a target for NF-kappaB inhibitory proteins, either by labelling specific signalling proteins for proteasome-dependent degradation or by serving as a target for specific de-ubiquitinating enzymes that prevent the formation of pertinent signalling complexes. Interfering with ubiquitination therefore seems to be a versatile means for regulating NF-kappaB activity, indicating that studies of Ub-mediated signalling might hold the key for developing new therapeutic strategies for inflammatory disease.

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@article{Wullaert2006UbiquitinTA, title={Ubiquitin: tool and target for intracellular NF-kappaB inhibitors.}, author={Andy Wullaert and Karen Heyninck and Sophie Janssens and Rudi Beyaert}, journal={Trends in immunology}, year={2006}, volume={27 11}, pages={533-40} }