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- W2136624465 endingPage "4884" @default.
- W2136624465 startingPage "4871" @default.
- W2136624465 abstract "In apoptosis, mitochondrial outer membrane permeabilization (MOMP) triggers caspase-dependent death. However, cells undergo clonogenic death even if caspases are blocked. One proposed mechanism involved the release of cytotoxic proteins (e.g., AIF and endoG) from mitochondria. To initiate MOMP directly without side effects, we created a tamoxifen-switchable BimS fusion protein. Surprisingly, even after MOMP, caspase-inhibited cells replicated DNA and divided for ∼48 h before undergoing proliferation arrest. AIF and endoG remained in mitochondria. However, cells gradually lost mitochondrial membrane potential and ATP content, and DNA synthesis slowed to a halt by 72 h. These defects resulted from a partial loss of respiratory function, occurring 4–8 h after MOMP, that was not merely due to dispersion of cytochrome c. In particular, Complex I activity was completely lost, and Complex IV activity was reduced by ∼70%, whereas Complex II was unaffected. Later, cells exhibited a more profound loss of mitochondrial protein constituents. Thus, under caspase inhibition, MOMP-induced clonogenic death results from a progressive loss of mitochondrial function, rather than the release of cytotoxic proteins from mitochondria." @default.
- W2136624465 created "2016-06-24" @default.
- W2136624465 creator A5010282104 @default.
- W2136624465 creator A5024617546 @default.
- W2136624465 creator A5048228645 @default.
- W2136624465 creator A5067978666 @default.
- W2136624465 creator A5083877990 @default.
- W2136624465 creator A5086130862 @default.
- W2136624465 date "2009-12-01" @default.
- W2136624465 modified "2023-10-17" @default.
- W2136624465 title "Caspase-independent Mitochondrial Cell Death Results from Loss of Respiration, Not Cytotoxic Protein Release" @default.
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