Role of mitochondria in apoptosis.
Apoptosis is an evolutionary-conserved physiological mechanism to remove cells from an organism. Cellular apoptosis is mediated via an intracellular signalling programme that involves a variety of signalling molecules and cellular organelles including caspases, sphingomyelinases, Bcl-2-like proteins and proteins to cleave the DNA and mitochondria. Mitochondria contain several pro-apoptotic molecules that activate cytosolic proteins to execute apoptosis, block anti-apoptotic proteins in the cytosol and directly cleave nuclear DNA. Mitochondria trap these pro-apoptotic proteins and physically separate pro-apoptotic proteins from their cytoplasmic targets. Apoptosis is then initiated by the release of mitochondrial pro-apoptotic proteins into the cytosol. This process seems to be regulated by Bcl-2-like proteins and several ion channels, in particular the permeability transition pore (PTP) that is activated by almost all pro-apoptotic stimuli.
Gulbins
Erich
E
Department of Molecular Biology, University of Essen, Hufelandstrase 55, 45122 Essen, Germany. erich.gulbins@uni-essen.de
Dreschers
Stephan
S
Bock
Jürgen
J
D000818:Animals; D017209:Apoptosis / Q000235:genetics / Q000502:physiology*; D020169:Caspases / Q000502:physiology; D006801:Humans; D007425:Intracellular Membranes / Q000502:physiology; D008565:Membrane Proteins / Q000502:physiology*; D008928:Mitochondria / Q000378:metabolism / Q000502:physiology*; D024101:Mitochondrial Proteins / Q000502:physiology*; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000378:metabolism / Q000502:physiology*; D015398:Signal Transduction / Q000502:physiology*
D008565:Membrane Proteins; D024101:Mitochondrial Proteins; D019253:Proto-Oncogene Proteins c-bcl-2; D020169:Caspases