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- W2024896191 abstract "In postmitotic sympathetic neurons, unlike most mitotic cells, death by apoptosis requires not only the release of cytochrome c from the mitochondria, but also an additional step to relieve X-linked inhibitor of apoptosis protein (XIAP)'s inhibition of caspases. Here, we examined the mechanism by which XIAP is inactivated following DNA damage and found that it is achieved by a mechanism completely different from that following apoptosis by nerve growth factor (NGF) deprivation. NGF deprivation relieves XIAP by selectively degrading it, whereas DNA damage overcomes XIAP via a p53-mediated induction of Apaf-1. Unlike wild-type neurons, p53-deficient neurons fail to overcome XIAP and remain resistant to cytochrome c after DNA damage. Restoring Apaf-1 induction in p53-deficient neurons is sufficient to overcome XIAP and sensitize cells to cytochrome c. Although a role for p53 in apoptosis upstream of cytochrome c release has been well established, this study uncovers an additional, essential role for p53 in regulating caspase activation downstream of mitochondria following DNA damage in neurons." @default.
- W2024896191 created "2016-06-24" @default.
- W2024896191 creator A5040585581 @default.
- W2024896191 creator A5073858666 @default.
- W2024896191 date "2007-01-12" @default.
- W2024896191 modified "2023-10-16" @default.
- W2024896191 title "Essential postmitochondrial function of p53 uncovered in DNA damage-induced apoptosis in neurons" @default.
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- W2024896191 doi "https://doi.org/10.1038/sj.cdd.4402084" @default.
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