Opposite and tissue-specific effects of coenzyme Q2 on mPTP opening and ROS production between heart and liver mitochondria: role of complex I. (Q42502933)

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English	Opposite and tissue-specific effects of coenzyme Q2 on mPTP opening and ROS production between heart and liver mitochondria: role of complex I.	scientific article

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24 January 2020

Opposite and tissue-specific effects of coenzyme Q2 on mPTP opening and ROS production between heart and liver mitochondria: role of complex I (English)

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24 January 2020

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Denis Angoulvant

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24 January 2020

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Lionel Augeul

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24 January 2020

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Michel Ovize

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24 January 2020

Elisabeth Couture-Lepetit

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24 January 2020

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Ludovic Gomez

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24 January 2020

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Abdallah Gharib

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24 January 2020

Damien De Paulis

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24 January 2020

Bo Li

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24 February 2012

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24 January 2020

Journal of Molecular and Cellular Cardiology

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24 January 2020

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24 January 2020

1091-1095

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24 January 2020

Oxidative phosphorylation: structure, function, and intermediary metabolism

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7 January 2021

Metabolism and function of coenzyme Q.

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Mitochondria and cell death. Mechanistic aspects and methodological issues

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The mitochondrial permeability transition.

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Ubiquinone analogs: a mitochondrial permeability transition pore-dependent pathway to selective cell death

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Regulation of the permeability transition pore in skeletal muscle mitochondria. Modulation By electron flow through the respiratory chain complex i.

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Three classes of ubiquinone analogs regulate the mitochondrial permeability transition pore through a common site

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Recent progress on regulation of the mitochondrial permeability transition pore; a cyclosporin-sensitive pore in the inner mitochondrial membrane

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Inhibitors of the quinone-binding site allow rapid superoxide production from mitochondrial NADH:ubiquinone oxidoreductase (complex I).

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Mechanism of O2- generation in reduction and oxidation cycle of ubiquinones in a model of mitochondrial electron transport systems

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Desflurane-induced preconditioning alters calcium-induced mitochondrial permeability transition.

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Calcium-binding properties of the mitochondrial channel-forming hydrophobic component

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Preconditioning delays Ca2+-induced mitochondrial permeability transition

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A Ubiquinone-binding Site Regulates the Mitochondrial Permeability Transition Pore

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7 January 2021

Opening of the mitochondrial permeability transition pore induces reactive oxygen species production at the level of the respiratory chain complex I.

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7 January 2021

Steady-state kinetics of the reduction of coenzyme Q analogs by complex I (NADH:ubiquinone oxidoreductase) in bovine heart mitochondria and submitochondrial particles.

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On the virtual existence of superoxide anions in mitochondria: thoughts regarding its role in pathophysiology.

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Estimation of H2O2 gradients across biomembranes.

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Mitochondrial production of superoxide anions and its relationship to the antimycin insensitive respiration

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Superoxide radicals as precursors of mitochondrial hydrogen peroxide

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The permeability transition pore signals apoptosis by directing Bax translocation and multimerization.

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Mitochondria as the central control point of apoptosis

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Coenzyme Q is an obligatory cofactor for uncoupling protein function

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Role of the mitochondrial permeability transition in myocardial disease

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Properties of the permeability transition pore in mitochondria devoid of Cyclophilin D.

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Two protons are pumped from the mitochondrial matrix per electron transferred between NADH and ubiquinone

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