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Updated: Jul 20, 2026

Comparative Strategies for Ubiquitination Detection in Mammalian Cell Lysates Using SMAD2/SMURF2 as a Model
Published on: April 17, 2026
Ubiquitin: tool and target for intracellular NF-kappaB inhibitors
Andy Wullaert1, Karen Heyninck, Sophie Janssens
1Unit of Molecular Signal Transduction in Inflammation, Department for Molecular Biomedical Research, Flanders Interuniversity Institute for Biotechnology (VIB) - Ghent University, Technologiepark 927, B-9052 Ghent (Zwijnaarde), Belgium.
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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