Control of mitochondrial permeability by Bcl-2 family members

Control of mitochondrial permeability by Bcl-2 family members Programmed cell death (apoptosis) is regulated by the Bcl-2 family of proteins. Although it remains unclear how these family members control apoptosis, they clearly have the capacity to regulate the permeability of intracellular membranes to ions and proteins. Proapoptotic members of the Bcl-2 family, especially Bax and Bid, have been extensively analyzed for the ability to form channels in membranes and to regulate preexisting channels. Anti-apoptotic members of the family tend to have the opposing effects on membrane channel formation. The molecular mechanisms of the different models for the permeabilization of membranes by the Bcl-2 family members and the regulation of Bcl-2 family member subcellular localizations are discussed. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Biochimica et Biophysica Acta (BBA) - Molecular Cell Research Elsevier

Control of mitochondrial permeability by Bcl-2 family members

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Publisher
Elsevier
Copyright
Copyright © 2003 Elsevier B.V.
ISSN
0167-4889
D.O.I.
10.1016/j.bbamcr.2003.10.016
Publisher site
See Article on Publisher Site

Abstract

Programmed cell death (apoptosis) is regulated by the Bcl-2 family of proteins. Although it remains unclear how these family members control apoptosis, they clearly have the capacity to regulate the permeability of intracellular membranes to ions and proteins. Proapoptotic members of the Bcl-2 family, especially Bax and Bid, have been extensively analyzed for the ability to form channels in membranes and to regulate preexisting channels. Anti-apoptotic members of the family tend to have the opposing effects on membrane channel formation. The molecular mechanisms of the different models for the permeabilization of membranes by the Bcl-2 family members and the regulation of Bcl-2 family member subcellular localizations are discussed.

Journal

Biochimica et Biophysica Acta (BBA) - Molecular Cell ResearchElsevier

Published: Mar 1, 2004

References

  • Movement of Bax from the cytosol to mitochondria
    Wolter, K.G.
  • Regulated targeting of BAX to mitochondria
    Goping, I.S.
  • Conformation of the Bax C-terminus regulates subcellular location and cell death
    Nechushtan, A.
  • Bax and Bak coalesce into novel mitochondria-associated clusters during apoptosis
    Nechushtan, A.
  • Bid-induced conformational change of Bax is responsible for mitochondrial cytochrome c release during apoptosis
    Desagher, S.
  • Cell damage-induced conformational changes of the pro-apoptotic protein Bak in vivo precede the onset of apoptosis
    Griffiths, G.J.
  • Mitochondrial release of AIF and EndoG requires caspase activation downstream of Bax/Bak-mediated permeabilization
    Arnoult, D.
  • Mitochondrial release of apoptosis-inducing factor occurs downstream of cytochrome c release in response to several proapoptotic stimuli
    Arnoult, D.
  • Direct evidence for membrane pore formation by the apoptotic protein Bax
    Epand, R.F.
  • A novel, high conductance channel of mitochondria linked to apoptosis in mammalian cells and Bax expression in yeast
    Pavlov, E.V.
  • Mitochondrial membrane permeabilisation by Bax/Bak
    Degli Esposti, M.; Dive, C.
  • Sequence and functional similarities between pro-apoptotic Bid and plant lipid transfer proteins
    Degli Esposti, M.
  • The role of cytochrome c in caspase activation in Drosophila melanogaster cells
    Dorstyn, L.

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