Apoptotic cell death can be induced via one of two main signaling pathways (Figure 1). One is activated upon interaction of certain ligands of the tumor necrosis factor (TNF) family with their cognate receptors, often referred to as death receptors, such as Fas/CD95 or the TNF-receptor itself. Death receptor and ligand mediated cell death fulfills critical roles e.g. in immune cell homeostasis and during responses to infectious agents. A second, more prevalent signaling pathway is controlled by members of the Bcl-2 family and involves mitochondria, hence often also referred to as the mitochondrial pathway to apoptosis. A large variety of developmental signals or cell-stress inducing agents or treatments can activate this cell death pathway, e.g. DNA damage, growth factor deprivation or oncogenic stress, that is of major interest to several groups within the MCBO program.
Fig. 1Apoptosis pathways. The intrinsic pathway (a) is activated by cellular stress and regulated by the Bcl-2 family. The extrinsic pathway (b) requires death-ligand-receptor interaction for its activation. Figure adopted from Tait, S.W.G. and D.R. Green,Nat Rev Mol Cell Biol, 2010
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