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Related Experiment Videos

Adding facets to TNF signaling. The JNK angle.

Zheng-gang Liu1

  • 1Cell and Cancer Biology Branch, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA.

Molecular Cell
|October 29, 2003
PubMed
Summary
This summary is machine-generated.

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Tumor necrosis factor (TNF) triggers apoptosis through a JNK-dependent mitochondrial pathway. This pathway involves Smac/DIABLO release and a processed Bid protein, essential for caspase 8 activation.

Area of Science:

  • Cell biology
  • Molecular biology
  • Biochemistry

Background:

  • Tumor necrosis factor (TNF) is a key cytokine involved in inflammation and apoptosis.
  • Caspase 8 activation is a critical step in the extrinsic apoptosis pathway.
  • Mitochondrial pathways play a significant role in regulating programmed cell death.

Purpose of the Study:

  • To investigate the role of mitochondrial signaling in TNF-induced apoptosis.
  • To elucidate the mechanism of caspase 8 activation downstream of TNF.
  • To identify novel proteins involved in the apoptotic cascade.

Main Methods:

  • Western blotting to detect protein processing and activation.
  • Mitochondrial fractionation to assess protein localization.

Related Experiment Videos

  • Caspase activity assays to measure apoptosis.
  • Use of specific inhibitors for JNK and caspases.

    • Main Results:

    • TNF-induced apoptosis requires a JNK-dependent signal originating from mitochondria.
    • The release of Smac/DIABLO from mitochondria is essential for TNF-induced caspase 8 activation.
    • A novel processed form of the BH3-only protein Bid mediates this mitochondrial signal.

    Conclusions:

    • Smac/DIABLO release acts as a crucial mitochondrial checkpoint for TNF-induced apoptosis.
    • Processed Bid is a key mediator linking JNK signaling to mitochondrial events and caspase activation.
    • This study reveals a novel crosstalk between JNK, mitochondria, and the caspase cascade in apoptosis.