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Related Concept Videos

NF-κB-dependent Signaling Pathway02:26

NF-κB-dependent Signaling Pathway

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.
NF-κB-dependent Signaling Mechanism
The heterodimer of NF-κB...
NF-kB-dependent Signaling Pathway02:26

NF-kB-dependent Signaling Pathway

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.
NF-κB-dependent Signaling Mechanism
The heterodimer of NF-κB...
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Inflammatory Bowel Disease II: Ulcerative Colitis

Ulcerative colitis is a chronic inflammatory disorder of the colon characterized by continuous mucosal inflammation that typically begins in the rectum and extends proximally in a uniform pattern. Its pathogenesis involves a complex interplay of genetic predisposition, immune dysregulation, and environmental influences. These factors converge to impair the colon’s epithelial defenses and promote an exaggerated inflammatory response against luminal contents.Breakdown of the Mucosal BarrierA...
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Crohn’s disease is a chronic, relapsing form of inflammatory bowel disease characterized by segmental, transmural inflammation that can affect any part of the gastrointestinal tract. Its pathogenesis arises from a combination of genetic susceptibility, environmental exposures, epithelial barrier dysfunction, and immune dysregulation. Together, these factors lead to an exaggerated immune response against components of the gut microbiome.Genetic and Environmental InfluencesMultiple genetic...
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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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Chronic inflammation is a prolonged, dysregulated immune response that persists for weeks to years when the inciting stimulus is difficult to eradicate or when self‑antigens drive ongoing reactivity. Morphologically, it is defined by mononuclear cell infiltration, progressive tissue destruction, and concurrent attempts at healing via angiogenesis and fibrosis. Compared with acute inflammation, edema is less prominent while cellular infiltration predominates; triggers include persistent...

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Blocking NF-κB: an inflammatory issue.

Arshad Rahman1, Fabeha Fazal

  • 1Department of Pediatrics, Box 850, Lung Biology and Disease Program, University of Rochester School of Medicine, Rochester, New York 14642, USA. Arshad_Rahman@URMC.Rochester.edu

Proceedings of the American Thoracic Society
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Nuclear factor kappa B (NF-κB) regulates inflammation but also aids tissue repair. Dampening NF-κB activation in endothelial cells may offer a safer treatment for inflammatory lung diseases.

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Area of Science:

  • Molecular Biology
  • Immunology
  • Cell Biology

Background:

  • Nuclear factor kappa B (NF-κB) is a key regulator of inflammatory responses.
  • NF-κB mediates inflammatory conditions, including acute lung injury and acute respiratory distress syndrome.
  • Endothelial cells are crucial in leukocyte migration during inflammation.

Purpose of the Study:

  • To review NF-κB regulation in endothelial cell signaling.
  • To explore the dual role of NF-κB in inflammation and tissue repair.
  • To propose a therapeutic strategy for inflammatory diseases.

Main Methods:

  • Review of existing literature on NF-κB signaling pathways.
  • Analysis of NF-κB's role in endothelial cells.
  • Examination of NF-κB's function in inflammation resolution and homeostasis.

Main Results:

  • NF-κB is a critical mediator in inflammatory diseases, particularly pulmonary conditions.
  • Endothelial NF-κB signaling is a potential therapeutic target.
  • Recent findings highlight NF-κB's role in inflammation resolution and tissue repair.

Conclusions:

  • Therapeutic inhibition of NF-κB is challenged by its role in repair.
  • "Dampening" NF-κB activation, not abolishing it, may be a safer strategy.
  • Targeting endothelial NF-κB offers a promising approach for treating inflammatory diseases.