Putative partners in Bax mediated cytochrome-c release: ANT, CypD, VDAC or none of them?

Mitochondrion. 2009 Feb;9(1):1-8. doi: 10.1016/j.mito.2008.10.003. Epub 2008 Nov 1.

Abstract

Release of cytochrome-c from mitochondria is a key regulatory event in the intrinsic pathway of apoptosis, and its mechanism has been the subject of extensive debate with investigators proposing different and contrasting models. While some models suggest that cytochrome-c release can occur in absence of permeability transition and is mediated by the pro-apoptotic protein Bax, some suggest involvement of various components of permeability transition pore with or without cooperative action of Bax. Various models of PTP-dependent or -independent cytochrome-c release are discussed in this review with special emphasis on all the independent/cooperative roles of Bax evidenced so far.

Publication types

  • Review

MeSH terms

  • Animals
  • Apoptosis*
  • Cell Membrane Permeability
  • Cyclophilins / metabolism*
  • Cytochromes c / metabolism*
  • Humans
  • Mitochondria / metabolism
  • Mitochondrial Proteins / metabolism
  • Models, Biological
  • Peptidyl-Prolyl Isomerase F
  • Permeability
  • Voltage-Dependent Anion Channels / metabolism*
  • bcl-2-Associated X Protein / metabolism*

Substances

  • Peptidyl-Prolyl Isomerase F
  • Mitochondrial Proteins
  • Voltage-Dependent Anion Channels
  • bcl-2-Associated X Protein
  • Cytochromes c
  • Cyclophilins