This paper was published as Oncogene, 2008, 27 (31), pp. 4363-4372. It is available from http://www.nature.com/onc/journal/v27/n31/index.html. Doi: 10.1038/onc.2008.64Metadata only entryThe p73 protein, a member of the p53 family, has both\ud developmental and tumorigenic functions. Here we show\ud that p73 is cleaved by caspase-3 and -8 both in vitro and in\ud vivo during apoptosis elicited by DNA-damaging drugs\ud and tumor necrosis factor-related apoptosis-inducing\ud ligand (TRAIL) receptor ligation. TAp73 and some of\ud its cleavage products are localized to mitochondria.\ud siRNA-mediated downregulation of p73 expression induced\ud a small but significant change in the susceptibility of\ud HCT116 cells to TRAIL-induced apoptosis. A transcription-\ud deficient mutant of TAp73 enhanced TRAIL-induced\ud apoptosis suggesting that p73 protein has transcriptionindependent\ud functions during death receptor-mediated\ud apoptosis. Additionally, recombinant p73 protein induced\ud cytochrome c release from isolated mitochondria providing\ud evidence that nonnuclear p73 may have additional\ud functions in the progression of apoptosi
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