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Conformational change of mitochondrial complex I increases ROS sensitivity during ischemia.

Conformational change of mitochondrial complex I increases ROS sensitivity during ischemia.

http://www.wikidata.org/entity/Q37231724

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Pivotal Importance of STAT3 in Protecting the Heart from Acute and Chronic Stress: New Advancement and Unresolved Issues Ischemic A/D transition of mitochondrial complex I and its role in ROS generation Understanding and preventing mitochondrial oxidative damage Cardioprotection by S-nitrosation of a cysteine switch on mitochondrial complex I.Mitochondrial complex I deactivation is related to superoxide production in acute hypoxia.European contribution to the study of ROS: A summary of the findings and prospects for the future from the COST action BM1203 (EU-ROS).Reversible blockade of complex I or inhibition of PKCβ reduces activation and mitochondria translocation of p66Shc to preserve cardiac function after ischemia Reduction of infarct size by the therapeutic protein TAT-Ndi1 in vivo Characterisation of the active/de-active transition of mitochondrial complex I.Molecular mechanism and physiological role of active-deactive transition of mitochondrial complex I.Modulation of the conformational state of mitochondrial complex I as a target for therapeutic intervention.A LON-ClpP Proteolytic Axis Degrades Complex I to Extinguish ROS Production in Depolarized Mitochondria.Differential susceptibility of mitochondrial complex II to inhibition by oxaloacetate in brain and heart.ND3, ND1 and 39kDa subunits are more exposed in the de-active form of bovine mitochondrial complex I.Natural thermal adaptation increases heat shock protein levels and decreases oxidative stress.Effect of monovalent cations on the kinetics of hypoxic conformational change of mitochondrial complex I.Alterations in mitochondrial respiration and reactive oxygen species in patients poisoned with carbon monoxide treated with hyperbaric oxygen.Structure of the Deactive State of Mammalian Respiratory Complex I.Mitochondrial complex I dysfunction and altered NAD(P)H kinetics in rat myocardium in cardiac right ventricular hypertrophy and failure.Critical Role of Flavin and Glutathione in Complex I-Mediated Bioenergetic Failure in Brain Ischemia/Reperfusion Injury.OGG1-initiated base excision repair exacerbates oxidative stress-induced parthanatos.

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Conformational change of mitochondrial complex I increases ROS sensitivity during ischemia.

http://www.wikidata.org/entity/Q37231724

description

article científic

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article scientifique

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articolo scientifico

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artigo científico

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bilimsel makale

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scientific article published on 29 March 2013

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vedecký článok

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vetenskaplig artikel

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videnskabelig artikel

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vědecký článek

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name

Conformational change of mitoc ...... S sensitivity during ischemia.

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Conformational change of mitoc ...... S sensitivity during ischemia.

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Conformational change of mitoc ...... S sensitivity during ischemia.

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Conformational change of mitoc ...... S sensitivity during ischemia.

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Conformational change of mitoc ...... S sensitivity during ischemia.

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Conformational change of mitoc ...... S sensitivity during ischemia.

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Antioxidants & Redox Signaling

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Conformational change of mitoc ...... S sensitivity during ischemia.

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Alexander Galkin

http://www.w3.org/2001/XMLSchema#string

David J Grieve

http://www.w3.org/2001/XMLSchema#string

Emma Robinson

http://www.w3.org/2001/XMLSchema#string

Natalia Gorenkova

http://www.w3.org/2001/XMLSchema#string

P2860

Structure of the membrane domain of respiratory complex I

Proximity-based protein thiol oxidation by H2O2-scavenging peroxidases.

Mitochondrial dysfunction in cardiac ischemia-reperfusion injury: ROS from complex I, without inhibition.

Direct evidence that oxygen-derived free radicals contribute to postischemic myocardial dysfunction in the intact dog.

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

Tricine-SDS-PAGE.

S-nitrosation of mitochondrial complex I depends on its structural conformation.

Identification of the mitochondrial ND3 subunit as a structural component involved in the active/deactive enzyme transition of respiratory complex I.

Damage to mitochondrial complex I during cardiac ischemia reperfusion injury is reduced indirectly by anti-anginal drug ranolazine.

Early mitochondrial dysfunction in electron transfer activity and reactive oxygen species generation after cardiac arrest

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1459-1468

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scholarly article

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10.1089/ARS.2012.4698

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13

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19

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2013-03-29T00:00:00Z

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235657851

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23419200

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3797456

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