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Updated: Sep 22, 2026

Lighting Up the Pathways to Caspase Activation Using Bimolecular Fluorescence Complementation
08:47

Lighting Up the Pathways to Caspase Activation Using Bimolecular Fluorescence Complementation

Published on: March 5, 2018

Cell stress-associated caspase activation: intrinsically complex?

Emma M Creagh1, Seamus J Martin

  • 1Molecular Cell Biology Laboratory, Department of Genetics, The Smurfit Institute, Trinity College, Dublin 2, Ireland.

Science'S STKE : Signal Transduction Knowledge Environment
|March 27, 2003
PubMed

Insights

Programmed cell death involves caspases. Emerging evidence suggests caspases activate before mitochondrial cytochrome c release, with the apoptosome amplifying apoptosis, challenging the established intrinsic pathway model.

Area of Science:

  • Cellular biology
  • Biochemistry
  • Molecular biology

Background:

  • Apoptosis, or programmed cell death, is a crucial biological process.
  • Caspases, a family of cysteine proteases, execute cellular demolition during apoptosis.
  • The intrinsic pathway of apoptosis is initiated by cell stress and involves mitochondria.

Purpose of the Study:

  • To critically discuss recent research challenging the established model of the intrinsic pathway of apoptosis.
  • To evaluate the role of the apoptosome in caspase activation during apoptosis.
  • To propose a revised understanding of the sequence of events in mitochondrial-mediated apoptosis.

Main Methods:

  • Literature review and critical analysis of existing studies on apoptosis.
  • Examination of experimental evidence regarding caspase activation and cytochrome c release.
  • Discussion of the proposed role of the apoptosome as an amplifier versus initiator.

Main Results:

  • The prevailing view holds that caspases activate within the apoptosome after mitochondrial cytochrome c release.
  • Recent research indicates that caspase activation may precede cytochrome c release.
  • The apoptosome might function as an amplifier of apoptosis-associated caspase activation, not the primary initiator.

Conclusions:

  • The established model of the intrinsic pathway of apoptosis requires re-evaluation.
  • The role of the apoptosome in initiating apoptosis is questioned.
  • Further research is needed to fully elucidate the precise mechanisms of caspase activation in programmed cell death.

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