[Mitochondrial control of apoptosis].
By Guido Kroemer. Bulletin de l'Académie Nationale de Médecine, 2001
1,250 citations recorded by the source corpus.
Subfields: Cellular and Molecular Neuroscience, Molecular Biology
View Paper: https://www.semanticscholar.org/paper/b21122e1c17a6aa97805bc797859150278f32017
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Citations in the corpus
- Oxidative stress and apoptosis. (2000, background): “[23] G.”
- Mitochondrial Dysfunction in Diabetes: From Molecular Mechanisms to Functional Significance and Therapeutic Opportunities (2010, neutral): “Conversely, transient opening may be physiologic, being involved in functions such as voltage, redox or pH sensing, divalent cation sensing, or regulation of adenine nucleotide concentrations (178).”
- Mitochondrial reactive oxygen species in cell death signaling. (2002, background): “In this model, the redox state of glutathione or other cellular antioxidants such as thioredoxine, would be in equilibrium with that of thiols resident in some redox sensitive crucial components of the execution machinery [80].”
- Cisplatin: The first metal based anticancer drug. (2019, background): “ROS together with Bax (Bcl2 associated X) and Ca2+ cause mtDNA damage and fall in MPT (Mitochondrial permeability transition) [53] which facilitate rupture of mitochondria [54].”
- NAD+/NADH and NADP+/NADPH in Cellular Functions and Cell Death: Regulation and Biological Consequences (2008, neutral): “Because the ratios of NAD /NADH and NADP /NADPH can affect numerous enzymatic activities and MPT (352) which play important roles in cell death under many conditions (69, 150, 165), it is warranted to further determine the changes of these ratios under both physiological and pathological conditions.”
- Bid Induces the Oligomerization and Insertion of Bax into the Outer Mitochondrial Membrane (2000, background): “As a result of PTP opening, mitochondria would swell, leading to rupture of the outer mitochondrial membrane and passive release of cytochrome c (23, 24).”
- BNIP3 and Genetic Control of Necrosis-Like Cell Death through the Mitochondrial Permeability Transition Pore (2000, background): “The loss of mitochondrial membrane potential and ROS production can be both an inducer and a consequence of PT pore opening depending on the death signal (8, 26, 65).”
- Mitochondrial membrane permeabilization in cell death. (2007, background): “Both routes to apoptotic death can be divided at least in three distinct phases: initiation, integration/decision, and execution/degradation (409).”
- Achieving the Balance between ROS and Antioxidants: When to Use the Synthetic Antioxidants (2013, background): “It is well documented that low levels of ROS are signaling molecules, modulating cell proliferation [55], apoptosis [56, 57], and gene expression through activation of transcription factors [58], like NFkappa-B and hypoxia-inducible-factor-1α (HIF) [59].”