Journal
ONCOGENE
Volume 27, Issue 31, Pages 4363-4372Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/onc.2008.64
Keywords
p73; mitochondria; p53; transcription independent; apoptosis; TRAIL
Funding
- Medical Research Council [MC_U132670600] Funding Source: researchfish
- Medical Research Council [MC_U132670600] Funding Source: Medline
- MRC [MC_U132670600] Funding Source: UKRI
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The p73 protein, a member of the p53 family, has both developmental and tumorigenic functions. Here we show that p73 is cleaved by caspase-3 and -8 both in vitro and in vivo during apoptosis elicited by DNA-damaging drugs and tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) receptor ligation. TAp73 and some of its cleavage products are localized to mitochondria. siRNA-mediated downregulation of p73 expression induced a small but significant change in the susceptibility of HCT116 cells to TRAIL-induced apoptosis. A transcription-deficient mutant of TAp73 enhanced TRAIL-induced apoptosis suggesting that p73 protein has transcriptionin-dependent functions during death receptor-mediated apoptosis. Additionally, recombinant p73 protein induced cytochrome c release from isolated mitochondria providing evidence that nonnuclear p73 may have additional functions in the progression of apoptosis.
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