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The BH3-only protein Bad is dispensable for TNF-mediated cell death

E Ottina1, M Sochalska1, R Sgonc2

  • 1Division of Developmental Immunology, Biocenter, Medical University Innsbruck, Innsbruck, Austria.

Cell Death & Disease
|January 23, 2015
PubMed

Insights

Tumor necrosis factor (TNF) triggers cell death pathways. While Bad protein was thought to be crucial for TNF-mediated apoptosis, genetic studies show it is not essential for this process.

Area of Science:

  • Cellular biology
  • Immunology
  • Molecular mechanisms of cell death

Background:

  • Tumor necrosis factor (TNF) is a critical mediator of immune and inflammatory responses.
  • TNF signaling can induce both apoptosis and necroptosis.
  • TNF-induced apoptosis involves pro-apoptotic Bcl-2 family proteins, including Bid, a substrate of caspase-8.

Purpose of the Study:

  • To investigate the role of the BH3 domain-containing protein Bad in TNF-mediated cell death.
  • To determine if Bad is rate-limiting or synergistic with Bid in TNF-induced apoptosis.

Main Methods:

  • Genetic analyses of TNF-mediated cell death pathways.
  • Examination of the involvement of Bcl-2 family proteins.

Main Results:

  • The BH3 domain-containing protein Bad is not essential for TNF-mediated cell death.
  • Genetic analyses demonstrate Bad's dispensability in this process, contrary to recent suggestions of it being rate-limiting.

Conclusions:

  • Bad is dispensable for TNF-mediated apoptotic cell death.
  • The role of Bad in TNF signaling requires further clarification, as it does not appear to be rate-limiting.

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