Novel Mediators in NF-κB Activation
A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Genetics and Genomics".
Deadline for manuscript submissions: closed (20 January 2023) | Viewed by 11176
Special Issue Editor
Interests: NEMO/IKKgamma; IKK complex; NF-κB signaling; NF-κB mutation in rare inflammatory disease; mechanism regulating programmed cell death; TNF signaling; genetic basis of rare immunological/autoimmune disease
Special Issue Information
Dear Colleagues,
In mammals, the canonical NF-κB is activated by a diversity of external stimuli, transducing a rapid but transient transcriptional activity to regulate the expression of various genes involved in immune response, cell proliferation, differentiation and inflammation. NF-κB is a collective name for an evolutionarily conserved family of five different transcription factors (p65, RelB, c-Rel, p50 and p52) that can form homodimers or heterodimers to reprogram gene expression. The five members of the NF-κB family are typically sequestered in the cytosol in inactive complexes with the inhibitory IκB proteins. The activation of the canonical NF-κB is triggered by phosphorylation-dependent activation of the IKK complex composed of IKKα/β kinases and NEMO, which function as a regulatory component that mediates the recruitment of the IKK complex to receptor. This event enables IκBs phosphorylation, proteasomal degradation, translocation of NF-κB to the nucleus and activation of target genes.
Most NF-κB components undergo several post-translational modifications that regulate their function. Moreover, while the upstream cytoplasmic regulatory events for the activation of NF-κB are well known, less is known about the nuclear regulation of NF-κB. Emerging evidence suggests novel actors also regulate NF-κB signaling in cellular organelles (such as mitochondria and peroxisomes).
NF-κB is better known for its pro-survival role, and in fact it has become increasingly clear that the alteration of NF-κB determines a pathological outcome due to uncontrolled programmed cell death induced by pro-inflammatory cytokines such as TNF-α, IL-1, and LPS. Regulators of the NF-κB cascade can act by both directly modulating upstream components of the cell death machinery or downstream by inducing pro-survival gene expression.
Authors are welcome to contribute original research articles, current review articles, and commentaries, focusing on novel mediators or on novel roles of known components of the NF-κB pathway, the post-translational modifications that regulate their activity and their influence on transcriptional output and in life/death decisions of the cell.
Prof. Dr. Matilde Valeria Ursini
Guest Editor
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Keywords
- NF-κB signaling
- NEMO (NF-κB Essential MOdulator)
- NF-κB mutations in inflammatory human diseases
- programmed cell death machinery
- post-translational modification of NF-κB components
- IKK complex regulation
