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Role of Mitochondria in Apoptosis
Author(s) -
Gulbins Erich,
Dreschers Stephan,
Bock Jürgen
Publication year - 2003
Publication title -
experimental physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.925
H-Index - 101
eISSN - 1469-445X
pISSN - 0958-0670
DOI - 10.1113/eph8802503
Subject(s) - microbiology and biotechnology , cytosol , mitochondrion , apoptosis , biology , organelle , caspase , cytoplasm , mitochondrial fission , intracellular , mitochondrial membrane transport protein , programmed cell death , biochemistry , inner mitochondrial membrane , enzyme
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.