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Inhibition of TNF-induced apoptosis by NF-kappa B

D J Van Antwerp1, S J Martin, I M Verma

  • 1Laboratory of Genetics, Salk Institute for Biological Studies, La Jolla, CA 92037, USA.

Trends in Cell Biology
|August 8, 1998
PubMed

Insights

Tumour necrosis factor (TNF) can trigger cell death (apoptosis). Protein synthesis inhibitors enhance TNF-induced apoptosis, revealing a regulatory role for NF-kappa B in controlling this cell death pathway.

Area of Science:

  • Immunology
  • Cell Biology
  • Molecular Biology

Background:

  • Tumour necrosis factor (TNF) is a key inflammatory cytokine.
  • TNF induces apoptosis (programmed cell death) in various cell types.
  • Cellular sensitivity to TNF-induced apoptosis is highly variable.

Purpose of the Study:

  • To investigate the mechanisms regulating TNF-induced apoptosis.
  • To identify genes involved in downregulating the apoptosis signal upon TNF receptor activation.
  • To elucidate the role of NF-kappa B in apoptosis regulation.

Main Methods:

  • Utilized TNF treatment in cell cultures.
  • Employed protein synthesis inhibitors to modulate apoptosis sensitivity.
  • Investigated the activation of NF-kappa B signaling pathway.

Main Results:

  • Most cells become highly sensitive to TNF-induced apoptosis when protein synthesis is inhibited.
  • TNF receptor activation induces genes that downregulate apoptosis.
  • NF-kappa B, activated by TNF signaling, plays a significant role in this downregulation.

Conclusions:

  • NF-kappa B is a crucial regulator of apoptosis.
  • The role of NF-kappa B extends beyond immune and inflammatory responses to include apoptosis control.
  • Understanding TNF and NF-kappa B interactions is vital for cancer and autoimmune disease research.

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