Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Experiment Videos

Nuclear factor-kappa B

P J Barnes1

  • 1Department of Thoracic Medicine, Imperial School of Medicine at National Heart and Lung Institute, London, U.K.

The International Journal of Biochemistry & Cell Biology
|June 1, 1997
PubMed
Summary
This summary is machine-generated.

Related Concept Videos

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Glucocorticoid resistance in asthma.

American journal of respiratory and critical care medicine·1995
Same author

Abnormal glucocorticoid receptor-activator protein 1 interaction in steroid-resistant asthma.

The Journal of experimental medicine·1995
Same author

Inhibition of macrophage inflammatory protein-1 alpha expression by IL-10. Differential sensitivities in human blood monocytes and alveolar macrophages.

Journal of immunology (Baltimore, Md. : 1950)·1995
Same author

Suppression of lipopolysaccharide-induced tumor necrosis factor-alpha generation from human peripheral blood monocytes by inhibitors of phosphodiesterase 4: interaction with stimulants of adenylyl cyclase.

Molecular pharmacology·1995
Same author

Corticosteroid inhibition of macrophage inflammatory protein-1 alpha in human monocytes and alveolar macrophages.

The American journal of physiology·1995
Same author

Cytokine expression in normal, atopic, and asthmatic subjects using the combination of sputum induction and the polymerase chain reaction.

Thorax·1995
Same journal

Corrigendum to "Sodium butyrate down-regulation of indoleamine 2, 3-dioxygenase at the transcriptional and post-transcriptional levels" [Int. J. Biochem. Cell Biol. 42 (2010) 1840-1846].

The international journal of biochemistry & cell biology·2026
Same journal

Whole-brain spatial metabolomics reveals metabolic gradient shifts in a murine glioma model following boron neutron capture therapy (130 characters).

The international journal of biochemistry & cell biology·2026
Same journal

LCN2 modulates Th17/Treg balance in vitro and is associated with an adaptive response to intestinal ischemia-reperfusion injury under Hmox1-deficient conditions.

The international journal of biochemistry & cell biology·2026
Same journal

Chloroquine modulates the redox-sensitive signalling via inhibiting the AMPK-ULK1 under LPS induced state in murine splenic macrophages.

The international journal of biochemistry & cell biology·2026
Same journal

The vicious cycle of hyperglycemia and oxidative stress: Novel mechanistic insights into a pathogenic alliance.

The international journal of biochemistry & cell biology·2026
Same journal

Fibroblast growth factors (FGF) in the pathogenesis and treatment of inflammatory bowel diseases (IBD): An overview.

The international journal of biochemistry & cell biology·2026
See all related articles

Nuclear factor-kappa B (NF-kappa B), a key regulator of inflammatory genes, becomes active upon various stimuli. Glucocorticoids inhibit NF-kappa B, and new inhibitors are being developed for inflammatory diseases.

Area of Science:

  • Molecular Biology
  • Immunology
  • Cell Biology

Background:

  • Nuclear factor-kappa B (NF-kappa B) is a crucial transcription factor regulating inflammatory and immune responses.
  • It exists as an inactive cytoplasmic complex with I kappa B, activated by diverse extracellular stimuli.
  • Dysregulation of NF-kappa B is implicated in chronic inflammatory diseases.

Purpose of the Study:

  • To elucidate the role of NF-kappa B in host defense and inflammatory diseases.
  • To understand the activation pathways and gene targets of NF-kappa B.
  • To highlight the therapeutic potential of targeting NF-kappa B.

Main Methods:

  • Review of existing literature on NF-kappa B.
  • Analysis of NF-kappa B's role in gene regulation.

Related Experiment Videos

  • Discussion of glucocorticoid inhibition and novel inhibitor development.

    • Main Results:

    • NF-kappa B activation leads to the expression of proinflammatory cytokines, chemokines, inflammatory enzymes, and adhesion molecules.
    • Glucocorticoids effectively inhibit activated NF-kappa B, contributing to their anti-inflammatory effects.
    • NF-kappa B is a validated therapeutic target for inflammatory conditions.

    Conclusions:

    • NF-kappa B is a central mediator in inflammatory and immune gene expression.
    • Targeting NF-kappa B presents a promising strategy for treating inflammatory diseases like asthma, rheumatoid arthritis, and inflammatory bowel disease.