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The transcription factor NF-κB was discovered in 1986 in the lab of Nobel laureate Professor David Baltimore, for its interaction with the immunoglobulin light chain enhancer in B-cells. After more than three decades of study, it is now evident that NF-κB regulates the expression of over 100 genes. Most of these genes play an essential role in the innate and adaptive immune responses as well as the inflammatory responses of animals.
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Gene transcription is regulated by the synergistic action of several proteins that form a complex at a gene regulatory site. This is observed in eukaryotes, where the regulation of gene expression is a complex process. Regulatory proteins in eukaryotes can broadly be classified into two types – regulators that bind directly to specific DNA sequences and co-regulators that associate with regulatory proteins but cannot directly bind to the DNA. These co-regulators are further divided into...
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Internal cellular stress, such as cellular injury or hypoxia, triggers intrinsic apoptosis. The B-cell lymphoma 2 (Bcl-2) family of proteins are the primary regulators of the intrinsic apoptotic pathway. For example, during DNA damage, checkpoint proteins, such as Ataxia Telangiectasia Mutated (ATM protein) and Checkpoints Factor-2 (Chk2) proteins, are activated. These proteins phosphorylate p53 which further activates pro-apoptotic proteins, such as Bax, Bak, PUMA, and Noxa, and inhibits...
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Several cytokine receptors have tightly bound Janus kinase or JAK proteins attached at their cytosolic tail. Small signaling molecules such as cytokines, growth hormones, or prolactins bind to the cytokine receptors and initiate their dimerization. The dimerization brings the cytosolic JAKs together that trans-phosphorylate and activates each other. The activated JAKs now phosphorylate cytosolic tails of the cytokine receptors, which serve as binding sites for adaptor proteins such as  SH2...
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Tumor Necrosis Factor (TNF), a proinflammatory cytokine, contributes significantly to the inflammation seen in Crohn's disease. It exists as soluble TNF and membrane-bound TNF, with actions mediated through TNF receptors (TNFR). TNFR activation leads to the release of proinflammatory cytokines, T-cell activation, collagen production, and leukocyte migration, all contributing to inflammation in Crohn's disease. Anti-TNF monoclonal antibodies, namely infliximab (Remicade), adalimumab...
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NF-κB in inflammation and cancer.

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Nuclear factor-kappa B (NF-κB) plays a key role in inflammation and cancer. Targeting this pathway offers potential therapeutic strategies for inflammatory diseases and cancer, despite challenges.

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Area of Science:

  • Molecular Biology
  • Immunology
  • Oncology

Background:

  • Nuclear factor-kappa B (NF-κB) is a transcription factor family regulating immune responses, inflammation, cell growth, and survival.
  • Dysregulated NF-κB activation is implicated in inflammatory disorders, autoimmune diseases, and cancer development.
  • NF-κB's role in oncogenesis includes promoting tumor cell proliferation, survival, metabolism, metastasis, angiogenesis, and therapy resistance.

Purpose of the Study:

  • To review recent findings on the role of NF-κB in pathological processes.
  • To discuss the underlying mechanisms of NF-κB's involvement in disease.
  • To explore therapeutic strategies targeting the NF-κB pathway and analyze potential challenges.

Main Methods:

  • Literature review of recent scientific findings.
  • Analysis of molecular mechanisms.
  • Exploration of therapeutic strategies and challenges.

Main Results:

  • NF-κB dysregulation contributes to inflammatory and autoimmune diseases.
  • NF-κB is linked to cancer development and progression.
  • Targeting NF-κB presents therapeutic potential for inflammatory diseases and cancer.

Conclusions:

  • NF-κB is a critical mediator in inflammation and cancer.
  • Targeting the NF-κB pathway is a promising therapeutic avenue.
  • Further research is needed to overcome challenges in NF-κB-targeted therapies.