NF-κB and Its Role in Health and Disease

A special issue of Biology (ISSN 2079-7737). This special issue belongs to the section "Biochemistry and Molecular Biology".

Deadline for manuscript submissions: closed (30 June 2024) | Viewed by 1769

Special Issue Editor

UQ Centre for Clinical Research, The University of Queensland, Brisbane, QLD 4029, Australia
Interests: NF-κB-related proteins and genes; NF-κB regulators and biomarkers; disease-related NF-κB activity; function of N-κB in health; dysregulations of NF-κB activity; constitutive activation of NF-κB

Special Issue Information

Dear Colleagues,

Nuclear factor-kappa B (NF-κB) is a transcription factor that plays a pivotal role in immune responses, inflammation, cell survival, and various physiological processes. The activity of NF-κB is tightly regulated and essential for maintaining homeostasis in the body. However, the dysregulation of NF-κB signaling has been implicated in the pathogenesis of numerous diseases.

In normal physiological conditions, NF-κB is maintained in an inactive state in the cytoplasm through its interaction with inhibitory proteins called IκBs (inhibitor of κB). Upon activation by various stimuli, such as pro-inflammatory cytokines or pathogens, the IκB proteins are phosphorylated and degraded, allowing NF-κB to translocate into the nucleus. Once in the nucleus, NF-κB binds to specific DNA sequences, known as κB sites, and regulates the transcription of target genes, which are involved in inflammation, chemokines, cell survival, and so on. These functions are important for maintaining healthy immune homeostasis, wound healing, and tissue development.

However, aberrant NF-κB activation is implicated in the pathogenesis of numerous diseases such as neurodegenerative disorders, autoimmune diseases, and metabolic disorders. In these diseases, abnormal NF-κB activation contributes to tissue damage, oxidative stress, and chronic inflammation.

Given the prominent role of NF-κB in disease pathogenesis, targeting NF-κB signaling has emerged as a therapeutic strategy. The goal is to restore the balance of NF-κB activation, alleviate inflammation, and potentially mitigate the progression of various diseases.

There are several unsolved issues in NF-κB-related diseases, such as the specificity of targeting NF-κB, as it is involved in numerous cellular processes and regulates a wide range of genes. Additionally, achieving the selective inhibition of pathological NF-κB activity without disrupting its physiological functions remains a challenge. The complexity of NF-κB signaling networks and the crosstalk with other pathways make it challenging to unravel the specific contributions of NF-κB in disease pathogenesis. Therefore, this Special Issue provides a platform where you can publish your research on any aspect of NF-κB-related health and diseases, including the pathophysiologic mechanisms, diagnosis, and treatment of inflammatory disease, or experimental, translational, and clinical research. We accept reviews, short communications, methodology papers, and full-size research papers with a focus on understanding the mechanisms of NF-κB signaling in health and diseases and provide valuable insights for developing targeted therapies and interventions to manage inflammatory and immune-related disorders.

Dr. Jun Yan
Guest Editor

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Keywords

  • NF-κB
  • κB
  • IKKs
  • inflammation
  • pro-inflammation
  • immune system
  • disease
  • biomarker
  • gene

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Published Papers (1 paper)

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Research

18 pages, 3557 KiB  
Article
A Novel Quinoline Inhibitor of the Canonical NF-κB Transcription Factor Pathway
by Panagiotis Ntavaroukas, Konstantinos Michail, Rafaela Tsiakalidou, Eleni Stampouloglou, Aikaterini Tsingene, Dimitrios Komiotis, Nikitas Georgiou, Thomas Mavromoustakos, Stella Manta, Danielle Aje, Panagiotis Michael, Barry J. Campbell and Stamatia Papoutsopoulou
Biology 2024, 13(11), 910; https://doi.org/10.3390/biology13110910 - 7 Nov 2024
Viewed by 1345
Abstract
The NF-κB family of transcription factors is a master regulator of cellular responses during inflammation, and its dysregulation has been linked to chronic inflammatory diseases, such as inflammatory bowel disease. It is therefore of vital importance to design and test new effective NF-κB [...] Read more.
The NF-κB family of transcription factors is a master regulator of cellular responses during inflammation, and its dysregulation has been linked to chronic inflammatory diseases, such as inflammatory bowel disease. It is therefore of vital importance to design and test new effective NF-κB inhibitors that have the potential to be utilized in clinical practice. In this study, we used a commercial transgenic HeLa cell line as an NF-κB activation reporter to test a novel quinoline molecule, Q3, as a potential inhibitor of the canonical NF-κB pathway. Q3 inhibited NF-κB-induced luciferase in concentrations as low as 5 μM and did not interfere with cell survival or induced cell death. A real-time PCR analysis revealed that Q3 could inhibit the TNF-induced transcription of the luciferase gene, as well as the TNF gene, a known downstream target gene. Immunocytochemistry studies revealed that Q3 moderately interferes with TNF-induced NF-κB nuclear translocation. Moreover, docking and molecular dynamics analyses confirmed that Q3 could potentially modulate transcriptional activity by inhibiting the interaction of NF-κB and DNA. Therefore, Q3 could be potentially developed for further in vivo studies as an NF-κB inhibitor. Full article
(This article belongs to the Special Issue NF-κB and Its Role in Health and Disease)
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