Cardiac O-GlcNAcylation blunts autophagic signaling in the diabetic heart - Wikidata - wikimedia - TriplyDB

Cardiac O-GlcNAcylation blunts autophagic signaling in the diabetic heart

Cardiac O-GlcNAcylation blunts autophagic signaling in the diabetic heart

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Metabolic, autophagic, and mitophagic activities in cancer initiation and progression How exercise may amend metabolic disturbances in diabetic cardiomyopathy Myocardial autophagic energy stress responses--macroautophagy, mitophagy, and glycophagy Functional O-GlcNAc modifications: implications in molecular regulation and pathophysiology Redox signaling in cardiovascular pathophysiology: A focus on hydrogen peroxide and vascular smooth muscle cells Teaching the basics of autophagy and mitophagy to redox biologists--mechanisms and experimental approaches Redox biology and the interface between bioenergetics, autophagy and circadian control of metabolism O-GlcNAc cycling mutants modulate proteotoxicity in Caenorhabditis elegans models of human neurodegenerative diseases.Activation of AKT by O-linked N-acetylglucosamine induces vascular calcification in diabetes mellitus Decreased O-linked GlcNAcylation protects from cytotoxicity mediated by huntingtin exon1 protein fragment Consuming a Western diet for two weeks suppresses fetal genes in mouse hearts.Protein O-GlcNAcylation and cardiovascular (patho)physiology.Macrophage migration inhibitory factor (MIF) knockout preserves cardiac homeostasis through alleviating Akt-mediated myocardial autophagy suppression in high-fat diet-induced obesity.A little sugar goes a long way: the cell biology of O-GlcNAc.Muscle ring finger-3 protects against diabetic cardiomyopathy induced by a high fat diet.MuRF2 regulates PPARγ1 activity to protect against diabetic cardiomyopathy and enhance weight gain induced by a high fat diet.Mechanisms of lipotoxicity in the cardiovascular system.Post-translational protein modification by O-linked N-acetyl-glucosamine: its role in mediating the adverse effects of diabetes on the heart.O-Linked β-N-acetylglucosamine (O-GlcNAc) Acts as a Glucose Sensor to Epigenetically Regulate the Insulin Gene in Pancreatic Beta Cells.O-GlcNAcylation of ATG4B positively regulates autophagy by increasing its hydroxylase activity Stromal interaction molecule 1 is essential for normal cardiac homeostasis through modulation of ER and mitochondrial function.Regulation of autophagy by protein post-translational modification.Molecular Functions of Glycoconjugates in Autophagy.Fine-tuning autophagy: from transcriptional to posttranslational regulation.O-GlcNAc modification is essential for the regulation of autophagy in Drosophila melanogaster.SNARE-mediated membrane fusion in autophagy.O-GlcNAcylation and neurodegeneration.Myocardial stress and autophagy: mechanisms and potential therapies.Diabetes-Related Cardiac Dysfunction.O-GlcNAcase deficiency suppresses skeletal myogenesis and insulin sensitivity in mice through the modulation of mitochondrial homeostasis.O-GlcNAc regulation of autophagy and α-synuclein homeostasis; implications for Parkinson's disease.O-GlcNAc-modification of SNAP-29 regulates autophagosome maturation.O-GlcNAcylation of 8-Oxoguanine DNA Glycosylase (Ogg1) Impairs Oxidative Mitochondrial DNA Lesion Repair in Diabetic Hearts.Myocyte membrane and microdomain modifications in diabetes: determinants of ischemic tolerance and cardioprotection.Nutrient-driven O-GlcNAc in proteostasis and neurodegeneration.Roles of Glycoproteins in the Diagnosis and Differential Diagnosis of Chronic and Latent Keshan Disease.Moderate mammalian target of rapamycin inhibition induces autophagy in HTR8/SVneo cells via O-linked β-N-acetylglucosamine signaling.AMPK activation counteracts cardiac hypertrophy by reducing O-GlcNAcylation.Protective effects of desacyl ghrelin on diabetic cardiomyopathy.Sugar modification inhibits autophagosome-lysosome fusion.

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Cardiac O-GlcNAcylation blunts autophagic signaling in the diabetic heart

http://www.wikidata.org/entity/Q36336533

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2012 nî lūn-bûn

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2012年の論文

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2012年学术文章

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2012年学术文章

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2012年学术文章

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2012年学术文章

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2012年學術文章

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2012年學術文章

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name

Cardiac O-GlcNAcylation blunts autophagic signaling in the diabetic heart

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Cardiac O-GlcNAcylation blunts autophagic signaling in the diabetic heart

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Cardiac O-GlcNAcylation blunts autophagic signaling in the diabetic heart

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Cardiac O-GlcNAcylation blunts autophagic signaling in the diabetic heart

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Cardiac O-GlcNAcylation blunts autophagic signaling in the diabetic heart

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Cardiac O-GlcNAcylation blunts autophagic signaling in the diabetic heart

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J.LFS.2012.06.011

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Cardiac O-GlcNAcylation blunts autophagic signaling in the diabetic heart

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Louis J Dell'italia

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Pamela C Powell

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P2860

Guidelines for the use and interpretation of assays for monitoring autophagy in higher eukaryotes

LC3, GABARAP and GATE16 localize to autophagosomal membrane depending on form-II formation

Bad, a heterodimeric partner for Bcl-XL and Bcl-2, displaces Bax and promotes cell death

DAP-kinase-mediated phosphorylation on the BH3 domain of beclin 1 promotes dissociation of beclin 1 from Bcl-XL and induction of autophagy

Bcl-2 antiapoptotic proteins inhibit Beclin 1-dependent autophagy

Impact of Type 2 diabetes and aging on cardiomyocyte function and O-linked N-acetylglucosamine levels in the heart

Glucosamine protects neonatal cardiomyocytes from ischemia-reperfusion injury via increased protein-associated O-GlcNAc

Self-eating and self-killing: crosstalk between autophagy and apoptosis

Glucosamine protects neonatal cardiomyocytes from ischemia-reperfusion injury via increased protein O-GlcNAc and increased mitochondrial Bcl-2

Overexpression of TRPC3 increases apoptosis but not necrosis in response to ischemia-reperfusion in adult mouse cardiomyocytes.

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