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Rel/NF-kappa B transcription factors and the control of apoptosis

G E Sonenshein1

  • 1Department of Biochemistry, Boston University School of Medicine, MA 02118, USA.

Seminars in Cancer Biology
|April 1, 1997
PubMed

Insights

Rel/NF-kappa B transcription factors play a dual role in programmed cell death (apoptosis). These factors can protect cells from apoptosis, but also promote it under certain conditions, highlighting their complex regulation.

Area of Science:

  • Cell Biology
  • Molecular Biology
  • Genetics

Background:

  • Apoptosis, or programmed cell death, is a fundamental biological process essential for development and tissue homeostasis across many organisms.
  • Extracellular signals trigger apoptosis through diverse intracellular pathways, often exhibiting cell-type-specific responses.
  • Rel/NF-kappa B transcription factors are increasingly recognized for their involvement in regulating cellular fate, including apoptosis.

Purpose of the Study:

  • To investigate the multifaceted role of Rel/NF-kappa B transcription factors in the regulation of apoptosis.
  • To elucidate the conditions under which Rel/NF-kappa B promotes cell survival versus cell death.

Main Methods:

  • Analysis of gene expression data related to apoptosis and Rel/NF-kappa B.
  • Cellular assays to assess apoptosis induction and Rel/NF-kappa B activation.
  • Investigation of signaling pathways converging on Rel/NF-kappa B.

Main Results:

  • Rel/NF-kappa B transcription factors were found to be key regulators of apoptosis in numerous cell types.
  • In most cellular contexts, Rel/NF-kappa B activation mediates survival signals, conferring resistance to apoptosis.
  • Specific cellular circumstances were identified where Rel/NF-kappa B activation conversely promotes apoptosis.

Conclusions:

  • Rel/NF-kappa B transcription factors exhibit a context-dependent dual function in apoptosis, acting as both pro-survival and pro-apoptotic regulators.
  • Understanding this duality is crucial for deciphering cell fate decisions and developing targeted therapies.

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