Redox regulation of mitochondrial ATP synthase: implications for cardiac resynchronization therapy. - Wikidata - awgldk - TriplyDB

Redox regulation of mitochondrial ATP synthase: implications for cardiac resynchronization therapy.

Redox regulation of mitochondrial ATP synthase: implications for cardiac resynchronization therapy.

http://www.wikidata.org/entity/Q36406423

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The Dual Function of Reactive Oxygen/Nitrogen Species in Bioenergetics and Cell Death: The Role of ATP Synthase Novel Perspectives in Redox Biology and Pathophysiology of Failing Myocytes: Modulation of the Intramyocardial Redox Milieu for Therapeutic Interventions-A Review Article from the Working Group of Cardiac Cell Biology, Italian Society of Cardiology The Measurement of Reversible Redox Dependent Post-translational Modifications and Their Regulation of Mitochondrial and Skeletal Muscle Function Redox signaling, Nox5 and vascular remodeling in hypertension Cysteine oxidative posttranslational modifications: emerging regulation in the cardiovascular system Focus on mitochondria dysfunction and dysregulation in heart failure: towards new therapeutic strategies to improve heart function From ATP to PTP and Back: A Dual Function for the Mitochondrial ATP Synthase Protein glutathionylation in cardiovascular diseases Recent advances in mitochondrial research Regulation of mitochondrial ATP synthase in cardiac pathophysiology Integration of cardiac proteome biology and medicine by a specialized knowledgebase Redox regulation of mitochondrial ATP synthase Electromechanical dyssynchrony and resynchronization of the failing heart Activation of transsulfuration pathway by salvianolic acid a treatment: a homocysteine-lowering approach with beneficial effects on redox homeostasis in high-fat diet-induced hyperlipidemic rats.Glutaredoxin-2 is required to control oxidative phosphorylation in cardiac muscle by mediating deglutathionylation reactions.Nitroalkenes confer acute cardioprotection via adenine nucleotide translocase 1.Glyceraldehyde-3-phosphate dehydrogenase acts as a mitochondrial trans-S-nitrosylase in the heart High fat, high sucrose diet causes cardiac mitochondrial dysfunction due in part to oxidative post-translational modification of mitochondrial complex II.Protein kinase C-α interaction with F0F1-ATPase promotes F0F1-ATPase activity and reduces energy deficits in injured renal cells.Redox signalling and cardioprotection: translatability and mechanism Ischaemic preconditioning preferentially increases protein S-nitrosylation in subsarcolemmal mitochondria Cardiac resynchronization therapy induces adaptive metabolic transitions in the metabolomic profile of heart failure.Cardiac mitochondrial network excitability: insights from computational analysis.The Mitochondrial Permeability Transition Pore: Channel Formation by F-ATP Synthase, Integration in Signal Transduction, and Role in Pathophysiology.Drug-induced mitochondrial dysfunction and cardiotoxicity.O-GlcNAcomic Profiling Identifies Widespread O-Linked β-N-Acetylglucosamine Modification (O-GlcNAcylation) in Oxidative Phosphorylation System Regulating Cardiac Mitochondrial Function OXPHOS mutations and neurodegeneration Additive cardioprotection by pharmacological postconditioning with hydrogen sulfide and nitric oxide donors in mouse heart: S-sulfhydration vs. S-nitrosylation.Pacemaker-induced transient asynchrony suppresses heart failure progression Mitochondrial Reactive Oxygen Species Mediate Cardiac Structural, Functional, and Mitochondrial Consequences of Diet-Induced Metabolic Heart Disease Dual Labeling Biotin Switch Assay to Reduce Bias Derived From Different Cysteine Subpopulations: A Method to Maximize S-Nitrosylation Detection.Cardiac resynchronization sensitizes the sarcomere to calcium by reactivating GSK-3β.Assessing Cardiac Metabolism: A Scientific Statement From the American Heart Association.Postconditioning leads to an increase in protein S-nitrosylation.Mitochondrial protein phosphorylation as a regulatory modality: implications for mitochondrial dysfunction in heart failure.Transcriptome, proteome, and metabolome in dyssynchronous heart failure and CRT.Novel aspects of ROS signalling in heart failure.Signaling by S-nitrosylation in the heart.Oxidative stress in muscular dystrophy: from generic evidence to specific sources and targets.Protein S-glutathionylation: from current basics to targeted modifications.

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Redox regulation of mitochondrial ATP synthase: implications for cardiac resynchronization therapy.

http://www.wikidata.org/entity/Q36406423

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Redox regulation of mitochondr ...... iac resynchronization therapy.

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Redox regulation of mitochondr ...... iac resynchronization therapy.

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Circulation Research

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Redox regulation of mitochondr ...... diac resynchronization therapy

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Brian O'Rourke

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David A Kass

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Jasma Rucker

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Jennifer E Van Eyk

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Sheng-Bing Wang

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P2860

The structure of the central stalk in bovine F(1)-ATPase at 2.4 A resolution

Mitochondrial membrane potential is dependent on the oligomeric state of F1F0-ATP synthase supracomplexes.

Oxidative modification of mitochondrial respiratory complexes in response to the stress of Trypanosoma cruzi infection

Characterization of potential S-nitrosylation sites in the myocardium

Blue native electrophoresis for isolation of membrane protein complexes in enzymatically active form

Introduction of the chloroplast redox regulatory region in the yeast ATP synthase impairs cytochrome c oxidase.

Oxygen, oxidative stress, hypoxia, and heart failure.

Preparation of proteins and peptides for mass spectrometry analysis in a bottom-up proteomics workflow.

Modulation of mitochondrial proteome and improved mitochondrial function by biventricular pacing of dyssynchronous failing hearts.

Regulation of mitochondrial glutathione redox status and protein glutathionylation by respiratory substrates

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