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NF-κB-dependent Signaling Pathway02:26

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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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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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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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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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The orderly progression of the cell cycle depends on the activation of Cdk protein by binding to its cyclin partner. However, the cell cycle must be restricted when undergoing abnormal changes. Most cancers correlate to the deregulated cell cycle, and since Cdks are a central component of the cell cycle, Cdk inhibitors are extensively studied to develop anticancer agents. For instance, cyclin D associates with several Cdks, such as Cdk 4/6, to form an active complex. The cyclin D-Cdk4/6 complex...
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A Guide to Production, Crystallization, and Structure Determination of Human IKK1/α
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NF-κB and Its Role in Checkpoint Control.

Annika C Betzler1, Marie-Nicole Theodoraki1, Patrick J Schuler1

  • 1Department of Oto-Rhino-Laryngology, Head and Neck Surgery, Ulm University Medical Center, 89075 Ulm, Germany.

International Journal of Molecular Sciences
|June 4, 2020
PubMed
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Nuclear factor-kappa B (NF-κB) links inflammation and cancer, and regulates immune checkpoints. Targeting NF-κB with immune checkpoint blockade offers promising cancer therapy strategies.

Keywords:
NF-κBPD-L1immune checkpoint expression

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Area of Science:

  • Oncology
  • Immunology
  • Molecular Biology

Background:

  • Nuclear factor-kappa B (NF-κB) is a key mediator connecting inflammation and cancer development.
  • Emerging evidence highlights NF-κB's role in regulating immune checkpoint expression on tumor cells.
  • Immune checkpoint inhibitors represent a significant advancement in cancer immunotherapy.

Purpose of the Study:

  • To review the association between NF-κB and immune checkpoint expression.
  • To explore the therapeutic potential of targeting NF-κB in combination with immune checkpoint blockade for cancer treatment.

Main Methods:

  • Literature review of recent scientific evidence.
  • Analysis of studies investigating NF-κB signaling pathways.
  • Examination of therapeutic strategies involving NF-κB inhibitors and immune checkpoint blockade.

Main Results:

  • NF-κB signaling is implicated in the expression of critical immune checkpoint molecules.
  • Inhibiting NF-κB directly or its regulatory pathways may enhance anti-tumor immune responses.
  • Combination therapies targeting both NF-κB and immune checkpoints show therapeutic promise.

Conclusions:

  • NF-κB plays a crucial role in immune evasion by modulating immune checkpoints.
  • Targeting NF-κB in conjunction with immune checkpoint blockade presents a viable strategy for improving cancer immunotherapy outcomes.