Bax, Bid and the permeabilization of the mitochondrial outer membrane in apoptosis.
Mitochondria provide a key amplification step in the apoptotic pathway of many cells by releasing apoptogenic proteins into the cytosol. Recent studies have provided insights into how Bax and Bid may operate synergistically to recruit mitochondria into the pathway and how GD3 ganglioside, a metabolite of the sphingomyelin pathway, may also be used. In ischaemic disease, activation of the mitochondrial permeability transition pore may bypass the requirement for these factors.
Crompton
M
M
Department of Biochemistry and Molecular Biology, University College London, London, WC1E 6BT, UK. m.crompton@biochemistry.ucl.ac.uk.
D000818:Animals; D017209:Apoptosis; D051023:BH3 Interacting Domain Death Agonist Protein; D002352:Carrier Proteins / Q000378:metabolism*; D005732:Gangliosides / Q000378:metabolism; D006801:Humans; D007425:Intracellular Membranes / Q000502:physiology; D008928:Mitochondria / Q000378:metabolism*; D010539:Permeability; D011518:Proto-Oncogene Proteins / Q000378:metabolism*; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000378:metabolism*; D051028:bcl-2-Associated X Protein
C494826:BAX protein, human; D051023:BH3 Interacting Domain Death Agonist Protein; C494814:BID protein, human; D002352:Carrier Proteins; D005732:Gangliosides; D011518:Proto-Oncogene Proteins; D019253:Proto-Oncogene Proteins c-bcl-2; D051028:bcl-2-Associated X Protein; C026226:ganglioside, GD3