O-linked β-N-acetylglucosamine transferase is indispensable in the failing heart. - Wikidata - awgldk - TriplyDB

O-linked β-N-acetylglucosamine transferase is indispensable in the failing heart.

O-linked β-N-acetylglucosamine transferase is indispensable in the failing heart.

http://www.wikidata.org/entity/Q34199818

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How exercise may amend metabolic disturbances in diabetic cardiomyopathy The role of O-GlcNAc transferase in regulating the gene transcription of developing and failing hearts Functional O-GlcNAc modifications: implications in molecular regulation and pathophysiology A Drosophila model of high sugar diet-induced cardiomyopathy A New Method to Stabilize C-Kit Expression in Reparative Cardiac Mesenchymal Cells.O-GlcNAcylation and oxidation of proteins: is signalling in the cardiovascular system becoming sweeter?Glucose Transporters in Cardiac Metabolism and Hypertrophy Protein quality control and metabolism: bidirectional control in the heart Interplay between troponin T phosphorylation and O-N-acetylglucosaminylation in ischaemic heart failure O-GlcNAc signaling entrains the circadian clock by inhibiting BMAL1/CLOCK ubiquitination O-linked β-N-acetylglucosamine supports p38 MAPK activation by high glucose in glomerular mesangial cells Cardiac-specific hexokinase 2 overexpression attenuates hypertrophy by increasing pentose phosphate pathway flux Glutathione depletion and acute exercise increase O-GlcNAc protein modification in rat skeletal muscle.Activation of AKT by O-linked N-acetylglucosamine induces vascular calcification in diabetes mellitus Responses of hypertrophied myocytes to reactive species: implications for glycolysis and electrophile metabolism Acute regulation of cardiac metabolism by the hexosamine biosynthesis pathway and protein O-GlcNAcylation.Metabolomic analysis of pressure-overloaded and infarcted mouse hearts.O-GlcNAc modification of NFκB p65 inhibits TNF-α-induced inflammatory mediator expression in rat aortic smooth muscle cells Finding the missing link between the unfolded protein response and O-GlcNAcylation in the heart.MicroRNA-539 is up-regulated in failing heart, and suppresses O-GlcNAcase expression.Z-band alternatively spliced PDZ motif protein (ZASP) is the major O-linked β-N-acetylglucosamine-substituted protein in human heart myofibrils Reduced cardiac fructose 2,6 bisphosphate increases hypertrophy and decreases glycolysis following aortic constriction Protein O-GlcNAcylation and cardiovascular (patho)physiology.Glucose metabolism and cardiac hypertrophy High fat feeding in mice is insufficient to induce cardiac dysfunction and does not exacerbate heart failure.Roles of glucose in photoreceptor survival.High glucose induces mitochondrial dysfunction independently of protein O-GlcNAcylation.Cardiac overexpression of 8-oxoguanine DNA glycosylase 1 protects mitochondrial DNA and reduces cardiac fibrosis following transaortic constriction O-GlcNAcylation Negatively Regulates Cardiomyogenic Fate in Adult Mouse Cardiac Mesenchymal Stromal Cells.The roles of O-linked β-N-acetylglucosamine in cardiovascular physiology and disease.O-GlcNAc signaling is essential for NFAT-mediated transcriptional reprogramming during cardiomyocyte hypertrophy.Removal of Abnormal Myofilament O-GlcNAcylation Restores Ca2+ Sensitivity in Diabetic Cardiac Muscle.Metabolic remodeling in the hypertrophic heart: fuel for thought.Glucose deprivation-induced increase in protein O-GlcNAcylation in cardiomyocytes is calcium-dependent Induction of activating transcription factor 3 limits survival following infarct-induced heart failure in mice.Overview: the maturing of proteomics in cardiovascular research.E2F1 Transcription Factor Regulates O-linked N-acetylglucosamine (O-GlcNAc) Transferase and O-GlcNAcase Expression.Post-translational protein modification by O-linked N-acetyl-glucosamine: its role in mediating the adverse effects of diabetes on the heart.Enhanced cardiac protein glycosylation (O-GlcNAc) of selected mitochondrial proteins in rats artificially selected for low running capacity.Proteomic analysis of physiological versus pathological cardiac remodeling in animal models expressing mutations in myosin essential light chains.

P2860

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P2860

O-linked β-N-acetylglucosamine transferase is indispensable in the failing heart.

http://www.wikidata.org/entity/Q34199818

description

2010 nî lūn-bûn

@nan

2010 թուականի Սեպտեմբերին հրատարակուած գիտական յօդուած

@hyw

2010 թվականի սեպտեմբերին հրատարակված գիտական հոդված

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2010年の論文

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2010年学术文章

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2010年学术文章

@zh-cn

2010年学术文章

@zh-hans

2010年学术文章

@zh-my

2010年学术文章

@zh-sg

2010年學術文章

@yue

name

O-linked β-N-acetylglucosamine transferase is indispensable in the failing heart.

@ast

O-linked β-N-acetylglucosamine transferase is indispensable in the failing heart.

@en

O-linked β-N-acetylglucosamine transferase is indispensable in the failing heart.

@nl

type

label

O-linked β-N-acetylglucosamine transferase is indispensable in the failing heart.

@ast

O-linked β-N-acetylglucosamine transferase is indispensable in the failing heart.

@en

O-linked β-N-acetylglucosamine transferase is indispensable in the failing heart.

@nl

prefLabel

O-linked β-N-acetylglucosamine transferase is indispensable in the failing heart.

@ast

O-linked β-N-acetylglucosamine transferase is indispensable in the failing heart.

@en

O-linked β-N-acetylglucosamine transferase is indispensable in the failing heart.

@nl

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PNAS.1001907107

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

P1476

O-linked β-N-acetylglucosamine transferase is indispensable in the failing heart

@en

P2093

Bethany W Long

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

Kewakebt M Lemma

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

Lewis J Watson

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

Mohamed Ameen

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

Robert E Brainard

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

Sumanth D Prabhu

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

Yu-Ting Xuan

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

P2860

Phosphoinositide signalling links O-GlcNAc transferase to insulin resistance

The O-GlcNAc transferase gene resides on the X chromosome and is essential for embryonic stem cell viability and mouse ontogeny

Analysis of Relative Gene Expression Data Using Real-Time Quantitative PCR and the 2−ΔΔCT Method

Cycling of O-linked beta-N-acetylglucosamine on nucleocytoplasmic proteins

Effects of diabetes and hyperglycemia on the hexosamine synthesis pathway in rat muscle and liver

Glycosylation of nucleocytoplasmic proteins: signal transduction and O-GlcNAc.

O-GlcNAc signaling in the cardiovascular system.

Transverse aortic constriction leads to accelerated heart failure in mice lacking PPAR-gamma coactivator 1alpha.

Endothelial nitric oxide synthase overexpression attenuates congestive heart failure in mice.

Hypothalamic malonyl-CoA triggers mitochondrial biogenesis and oxidative gene expression in skeletal muscle: Role of PGC-1alpha.

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10.1073/PNAS.1001907107

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107

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Heberty Facundo

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46578301

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