Calpain-mediated cleavage of Atg5 switches autophagy to apoptosis

By S. Yousefi, R. Perozzo, Inès Schmid, A. Ziemiecki, T. Schaffner, L. Scapozza, T. Brunner, H. Simon. Nature Cell Biology, 2006

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Connecting endoplasmic reticulum stress to autophagy by unfolded protein response and calcium (2007, positive): “In addition to activating the UPR by the pathways discussed above, ER-stress leads to a release of Ca2þ from the ER into the cytosol, which, in turn, can activate various kinases and proteases possibly involved in autophagy signaling.(24,38,39)”
Cannabinoid action induces autophagy-mediated cell death through stimulation of ER stress in human glioma cells. (2009, background): “Autophagy has been proposed to protect from apoptosis, act as an apoptosis-alternative pathway to induce cell death, or act together with apoptosis as a combined mechanism for cell death (6, 33).”
Cardiac autophagy is a maladaptive response to hemodynamic stress. (2007, background): “Recent studies have uncovered significant interactions between autophagic and apoptotic signaling pathways (19, 22).”
Autophagic cell death: the story of a misnomer (2008, background): “51 )) and to ATG5 (which can translocate to mitochondria and induce MOMP after calpain-mediated cleavag”
Novel targets for Huntington’s disease in an mTOR-independent autophagy pathway (2008, background): “Another candidate we considered was Atg5, which may be cleaved by calpains in certain cell death context”