Lack of Contribution of p66shc and Its Mitochondrial Translocation to Ischemia-Reperfusion Injury and Cardioprotection by Ischemic Preconditioning
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Title
Lack of Contribution of p66shc and Its Mitochondrial Translocation to Ischemia-Reperfusion Injury and Cardioprotection by Ischemic Preconditioning
Authors
Keywords
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Journal
Frontiers in Physiology
Volume 8, Issue -, Pages -
Publisher
Frontiers Media SA
Online
2017-10-05
DOI
10.3389/fphys.2017.00733
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Note: Only part of the references are listed.- Sirtuin1-regulated lysine acetylation of p66Shc governs diabetes-induced vascular oxidative stress and endothelial dysfunction
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- Sirtuin 1-Mediated Inhibition of p66shc Expression Alleviates Liver Ischemia/Reperfusion Injury
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- Targeting prolyl-isomerase Pin1 prevents mitochondrial oxidative stress and vascular dysfunction: insights in patients with diabetes
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- Mitochondrial oxidative metabolism and uncoupling proteins in the failing heart
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- Redox regulation of cardiac hypertrophy
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- Essential Role of the Redox-Sensitive Kinase p66shc in Determining Energetic and Oxidative Status and Cell Fate in Neuronal Preconditioning
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