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Bax, Bid and the permeabilization of the mitochondrial outer membrane in apoptosis

M Crompton1

  • 1Department of Biochemistry and Molecular Biology, University College London, London, WC1E 6BT, UK. m.crompton@biochemistry.ucl.ac.uk.

Current Opinion in Cell Biology
|June 30, 2000
PubMed

Insights

Mitochondria amplify cell death by releasing proteins. Bax, Bid, and GD3 ganglioside are involved, but ischaemic disease may bypass these factors via mitochondrial pores.

Area of Science:

  • Cell biology
  • Biochemistry
  • Pathology

Background:

  • Mitochondria play a crucial role in amplifying apoptosis by releasing proteins.
  • The proteins Bax and Bid are known to recruit mitochondria into the apoptotic pathway.
  • GD3 ganglioside, a sphingomyelin metabolite, is also implicated in this process.

Purpose of the Study:

  • To elucidate the mechanisms by which mitochondria are recruited into the apoptotic pathway.
  • To investigate the synergistic roles of Bax and Bid in mitochondrial apoptosis.
  • To explore the involvement of GD3 ganglioside in apoptosis.

Main Methods:

  • Investigating the synergistic action of Bax and Bid.
  • Analyzing the role of GD3 ganglioside.
  • Studying the mitochondrial permeability transition pore in ischaemic conditions.

Main Results:

  • Bax and Bid may work together to recruit mitochondria for apoptosis.
  • GD3 ganglioside is identified as a potential factor in mitochondrial apoptosis.
  • Ischaemic disease can activate the mitochondrial permeability transition pore, potentially bypassing other apoptotic factors.

Conclusions:

  • Mitochondrial recruitment is a key amplification step in apoptosis.
  • Bax, Bid, and GD3 ganglioside are significant players in this process.
  • The mitochondrial permeability transition pore offers an alternative apoptotic route in ischaemia.

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