Mitochondrial permeability transition and oxidative stress
By A. Kowaltowski, R. F. Castilho, A. Vercesi. FEBS Letters, 2001
809 citations recorded by the source corpus.
Subfields: Clinical Biochemistry, Infectious Diseases, Molecular Biology
View Paper: https://www.semanticscholar.org/paper/b9addd3f8dc0ddba7eb815597b857cf7792b765d
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In Infectious Diseases
In Molecular Biology
- Guido Kroemer
- L. Galluzzi
- C. Brenner
- S. Cadenas
- Pier Giuseppe Pelicci
- Douglas R. Green
- Beth Levine
- Thomas G. Cotter
Citations in the corpus
- Glycogen synthase kinase-3β mediates convergence of protection signaling to inhibit the mitochondrial permeability transition pore (2004, neutral): “Mostly based on the results of experiments on isolated mitochondrial suspension, it was suggested that Ca 2+ is an important factor in MPT induction (11, 35).”
- Hydrogen peroxide: a metabolic by-product or a common mediator of ageing signals? (2007, background): “Whereas the ability of ROS to trigger senescence is thought to be secondary to their ability to induce hyperproliferation and the activation of a p53-dependent checkpoint, H 2 O 2 itself is instead a direct and potent inducer of apoptosi”
- The chemistry and biological activities of N-acetylcysteine. (2013, background): “, formation of aqueous pores (leaks), permeable to both non-electrolytes and ions [109-111].”
- Mitochondrial membrane permeabilization in cell death. (2007, background): “1) Kinetic analyses suggest that IM permeabilization can precede Bax/Bak/Bid activation (400, 897).”
- Antioxidant responses and cellular adjustments to oxidative stress (2015, background): “ever, this increases the oxidative state in the cell [77,78], resulting”
- Loss of PINK1 causes mitochondrial functional defects and increased sensitivity to oxidative stress (2008, neutral): “It has been shown that under conditions of stress, cysteines of the mitochondrial permeability transition pore (MPT pore) undergo oxidation, thus increasing the probability for the pore to open and collapse the transmembrane potential (28).”
- Redox Regulation of Cell Survival (2008, neutral): “10, the released cytochrome c forms a complex (apoptosome) with procaspase-9, Apaf-1, and ATP or dATP, leading to activation of caspase-9 and the downstream caspase cascade (168).”