The adenine nucleotide translocator in apoptosis.
Alteration of mitochondrial membrane permeability is a central mechanism leading invariably to cell death, which results, at least in part, from the opening of the permeability transition pore complex (PTPC). Indeed, extended PTPC opening is sufficient to trigger an increase in mitochondrial membrane permeability and apoptosis. Among the various PTPC components, the adenine nucleotide translocator (ANT) appears to act as a bi-functional protein which, on the one hand, contributes to a crucial step of aerobic energy metabolism, the ADP/ATP translocation, and on the other hand, can be converted into a pro-apoptotic pore under the control of onco- and anti-oncoproteins from the Bax/Bcl-2 family. In this review, we will discuss recent advances in the cooperation between ANT and Bax/Bcl-2 family members, the multiplicity of agents affecting ANT pore function and the putative role of ANT isoforms in apoptosis control.
Belzacq
Anne-Sophie
AS
Centre national de la recherche scientifique, UMR 6022, université de technologie de Compiègne, Royallieu, BP20529, 60205 Compiègne, France.
Vieira
Helena L A
HL
Kroemer
Guido
G
Brenner
Catherine
C
D000255:Adenosine Triphosphate / Q000378:metabolism; D000818:Animals; D017209:Apoptosis / Q000502:physiology*; D002463:Cell Membrane Permeability / Q000502:physiology; D006801:Humans; D008928:Mitochondria / Q000502:physiology*; D000226:Mitochondrial ADP, ATP Translocases / Q000502:physiology*; D011518:Proto-Oncogene Proteins / Q000378:metabolism; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000502:physiology*; D051028:bcl-2-Associated X Protein
C494826:BAX protein, human; D011518:Proto-Oncogene Proteins; D019253:Proto-Oncogene Proteins c-bcl-2; D051028:bcl-2-Associated X Protein; D000255:Adenosine Triphosphate; D000226:Mitochondrial ADP, ATP Translocases