Review
Mitochondria as the target of the pro-apoptotic protein Bax

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Abstract

During apoptosis, engagement of the mitochondrial pathway involves the permeabilization of the outer mitochondrial membrane (OMM), which leads to the release of cytochrome c and other apoptogenic proteins such as Smac/DIABLO, AIF, EndoG, Omi/HtraA2 and DDP/TIMM8a. OMM permeabilization depends on activation, translocation and oligomerization of multidomain Bcl-2 family proteins such as Bax or Bak. Factors involved in Bax conformational change and the function(s) of the distinct domains controlling the addressing and the insertion of Bax into mitochondria are described in this review. We also discuss our current knowledge on Bax oligomerization and on the molecular mechanisms underlying the different models accounting for OMM permeabilization during apoptosis.

Abbreviations

ANT
adenosine nucleotide translocator
AIF
Apoptosis inducing factor
ART
Apoptosis Regulation of Targeting
BdGBM
Bax-deficient Glioblastoma Multiforme
Bif-1
Bax interacting factor 1
BH
Bcl-2 homology
BOPs
BH3-only proteins
BimEL
extra long isoform of Bim
GFP
green fluorescent protein
Hα, α helix;Hn
Humanin
MAC
Mitochondrial Apoptosis-induced Channel
Δψm
mitochondrial change in potential
mPTP
mitochondrial permeability Transition Pore
OMM
outer mitochondrial membrane
PI3
phosphatidylinositol 3
tBid
truncated form of Bid
VDAC
voltage dependent anionic channel

Keywords

Apoptosis
Bax
Activation
Conformational change
Addressing/targeting
Permeabilization
Mitochondrion

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