Cardioprotective effects of thioredoxin in myocardial ischemia and reperfusion: role of S-nitrosation [corrected]. - Wikidata - awgldk - TriplyDB

Cardioprotective effects of thioredoxin in myocardial ischemia and reperfusion: role of S-nitrosation [corrected].

Cardioprotective effects of thioredoxin in myocardial ischemia and reperfusion: role of S-nitrosation [corrected].

http://www.wikidata.org/entity/Q37388923

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Histone deacetylase signaling in cardioprotection S-nitrosylation in cardiovascular signaling Gene therapy for ischemic heart disease Thioredoxin and ventricular remodeling Crystal structure of human thioredoxin revealing an unraveled helix and exposedS-nitrosation site Thioredoxins, glutaredoxins, and peroxiredoxins--molecular mechanisms and health significance: from cofactors to antioxidants to redox signaling Tumor necrosis factor-α and lymphotoxin-α mediate myocardial ischemic injury via TNF receptor 1, but are cardioprotective when activating TNF receptor 2 Nuclear Factor (Erythroid-Derived 2)-Like 2 and Thioredoxin-1 in Atherosclerosis and Ischemia/Reperfusion Injury in the Heart.Protein S-nitrosylation and cardioprotection A common carcinogen benzo[a]pyrene causes neuronal death in mouse via microglial activation.Adiponectin: an indispensable molecule in rosiglitazone cardioprotection following myocardial infarction.Redox regulation of cell survival by the thioredoxin superfamily: an implication of redox gene therapy in the heart.Structure-function studies of an engineered scaffold protein derived from Stefin A. II: Development and applications of the SQT variant.Thioredoxin glycation: A novel posttranslational modification that inhibits its antioxidant and organ protective actions Apple pectin, a dietary fiber, ameliorates myocardial injury by inhibiting apoptosis in a rat model of ischemia/reperfusion.Methylglyoxal increases cardiomyocyte ischemia-reperfusion injury via glycative inhibition of thioredoxin activity.Structure-function studies of an engineered scaffold protein derived from stefin A. I: Development of the SQM variant.A redox-dependent mechanism for regulation of AMPK activation by Thioredoxin1 during energy starvation.A novel and efficient model of coronary artery ligation and myocardial infarction in the mouse.Modulation of signaling mechanisms in the heart by thioredoxin 1.Simultaneous measurement of protein oxidation and S-nitrosylation during preconditioning and ischemia/reperfusion injury with resin-assisted capture Inhibition of Fas-associated death domain-containing protein (FADD) protects against myocardial ischemia/reperfusion injury in a heart failure mouse model Thioredoxin-2 inhibits mitochondrial reactive oxygen species generation and apoptosis stress kinase-1 activity to maintain cardiac function.Thioredoxin 1-mediated post-translational modifications: reduction, transnitrosylation, denitrosylation, and related proteomics methodologies.Mechanisms underlying acute protection from cardiac ischemia-reperfusion injury Thioredoxin Activates MKK4-NFκB Pathway in a Redox-dependent Manner to Control Manganese Superoxide Dismutase Gene Expression in Endothelial Cells.Thioredoxin is required for S-nitrosation of procaspase-3 and the inhibition of apoptosis in Jurkat cells.AdipoRon, the first orally active adiponectin receptor activator, attenuates postischemic myocardial apoptosis through both AMPK-mediated and AMPK-independent signalings.A tutorial on oxidative stress and redox signaling with application to exercise and sedentariness.Nitrative thioredoxin inactivation as a cause of enhanced myocardial ischemia/reperfusion injury in the aging heart.Thioredoxin reduces post-ischemic myocardial apoptosis by reducing oxidative/nitrative stress.Reactive aldehyde modification of thioredoxin-1 activates early steps of inflammation and cell adhesion Molecular biology of apoptosis in ischemia and reperfusion.Female infertility and free radicals: potential role in adhesions and endometriosis.Loss of myocardial protection against myocardial infarction in middle-aged transgenic mice overexpressing cardiac thioredoxin-1 The role of thioredoxin 1 in the mycophenolic acid-induced apoptosis of insulin-producing cells AMP-activated protein kinase deficiency enhances myocardial ischemia/reperfusion injury but has minimal effect on the antioxidant/antinitrative protection of adiponectin.INO-4885 [5,10,15,20-tetra[N-(benzyl-4'-carboxylate)-2-pyridinium]-21H,23H-porphine iron(III) chloride], a peroxynitrite decomposition catalyst, protects the heart against reperfusion injury in mice.Up-regulation of thioredoxin interacting protein (Txnip) by p38 MAPK and FOXO1 contributes to the impaired thioredoxin activity and increased ROS in glucose-treated endothelial cells C1q/tumor necrosis factor-related protein-9, a novel adipocyte-derived cytokine, attenuates adverse remodeling in the ischemic mouse heart via protein kinase A activation.

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P2860

Cardioprotective effects of thioredoxin in myocardial ischemia and reperfusion: role of S-nitrosation [corrected].

http://www.wikidata.org/entity/Q37388923

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bilimsel makale

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scientific article published on 26 July 2004

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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

Cardioprotective effects of th ...... of S-nitrosation [corrected].

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Cardioprotective effects of th ...... of S-nitrosation [corrected].

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Cardioprotective effects of th ...... of S-nitrosation [corrected].

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PNAS.0402941101

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Proceedings of the National Academy of Sciences of the United States of America

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Cardioprotective effects of th ...... of S-nitrosation [corrected].

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Aihua Hu

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

Bernard L Lopez

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Hui-Rong Liu

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Junji Yodoi

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Ling Tao

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Martin Feelisch

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Nathan S Bryan

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Theodore A Christopher

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Walter J Koch

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Xin L Ma

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P2860

Nitric oxide down-regulates MKP-3 mRNA levels: involvement in endothelial cell protection from apoptosis

Mammalian thioredoxin is a direct inhibitor of apoptosis signal-regulating kinase (ASK) 1.

Active and inactive protein kinases: structural basis for regulation

S-Nitrosylation of mitochondrial caspases

Glutathionylation of human thioredoxin: a possible crosstalk between the glutathione and thioredoxin systems

c-Jun N-terminal kinase (JNK) repression during the inflammatory response? Just say NO.

Thioredoxin promotes ASK1 ubiquitination and degradation to inhibit ASK1-mediated apoptosis in a redox activity-independent manner.

Inhibition of endogenous thioredoxin in the heart increases oxidative stress and cardiac hypertrophy.

Nitrosylation. the prototypic redox-based signaling mechanism.

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