Disruption of mitochondrial function during apoptosis is mediated by caspase cleavage of the p75 subunit of complex I of the electron transport chain.
By J. Ricci, C. Muñoz-Pinedo, Patrick Fitzgerald, B. Bailly-maitre, G. Perkins, N. Yadava, I. Scheffler, Mark Ellisman, Douglas R. Green. Cell, 2004
612 citations recorded by the source corpus.
Subfields: Molecular Biology
View Paper: https://www.semanticscholar.org/paper/133cb366c1836dc20c940d1268253b8ed01e66c3
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Citations in the corpus
- Mitochondrial outer membrane permeabilization during apoptosis: the innocent bystander scenario (2006, background): “caspase-dependent cleavage of a subunit of complex I of the respiratory chain and hence can be a byproduct of MOMP rather than causative.(34,35) Otherwise, there is no”
- Cell Death Signaling. (2015, background): “For example, caspase cleavage of the p75 subunit of complex I of the electron transport chain disrupts the mitochondrial transmembrane potential, electron transport, and ATP production during apoptosis (Ricci et al. 2004).”
- Nitric oxide‐induced mitochondrial fission is regulated by dynamin‐related GTPases in neurons (2006, methodology): “Sample preparation and conventional EM were carried out as described before (Ricci et al, 2004).”
- Mitochondria and cell death: outer membrane permeabilization and beyond (2010, background): “Caspase-dependent dissipation of ΔΨ m is mediated, at least in part, through caspase cleavage of NADH–ubiquinone oxidoreductase 75 kDa subunit ( NDUFS1 ), an essential component of respiratory chain complex”
- Apoptosis: controlled demolition at the cellular level (2008, background): “Caspase-mediated proteolysis of the p75 subunit of complex I of the electron transport chain was found to be partially required for the swelling and destructive morphological changes that are suffered by mitochondria during apoptosi”
- Extrinsic versus intrinsic apoptosis pathways in anticancer chemotherapy (2006, background): “In addition, caspase activity further damages the function of permeabilized mitochondria by affecting the activity of complexes I and II, inevitably leading to the loss of MMP and the generation of reactive oxygen species (Ricci et al., 2004).”