Abstract
The family of NF-κB transcription factors plays a key role in diverse biological processes, such as inflammatory and immune responses, cell survival and tumor development. Beyond the classical NF-κB activation pathway, a second NF-κB pathway has more recently been uncovered, the so-called alternative NF-κB activation pathway. It has been shown that this pathway mainly controls the activity of RelB, a member of the NF-κB family. Post-translational modifications, such as phosphorylation, acetylation, methylation, ubiquitination and SUMOylation, have recently emerged as a strategy for the fine-tuned regulation of NF-κB. Our review discusses recent progress in the understanding of RelB regulation by post-translational modifications and the associated functions in normal and pathological conditions.
Highlights
Nuclear factor κB (NF-κB) was first described in 1986 as nuclear factor binding the kappa light chain enhancer in B cells [1]
We have demonstrated that nuclear interaction with the inhibitory protein IκBα and binds to the promoter of critical migration-associated phosphorylated on serine 472 dissociates its interaction with the inhibitory
Phosphorylation, ubiquitinylation and SUMOylation have been reported to have an effect on RelB activity, either enhancing or weakening it
Summary
Nuclear factor κB (NF-κB) was first described in 1986 as nuclear factor binding the kappa light chain enhancer in B cells [1]. The first one is called the classical NF-κB pathway It involves activation of the IκB kinase (IKK) complex, leading to phosphorylation of IκB proteins and their subsequent ubiquitinylation and degradation by the proteasome [11] (Figure 1, left). The classical pathway usually regulates the activity of RelA and cRel containing dimers It is typically responsible for a strong and rapid NF-κB activating signal in response to stress situations and plays a crucial role in the regulation of inflammation and innate immunity. It is activated by a more restricted processes such as lymphoid organogenesis and B cell survival, as well as in the regulation of adaptive subset of TNF family members (e.g., lymphotoxin β (LTβ), B-cell activating factor (BAFF) and CD40 immunity It is activated by a more restricted subset of TNF family members (e.g., lymphotoxin β ligand).
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