Glucose phosphorylation is required for insulin-dependent mTOR signalling in the heart. - Wikidata - awgldk - TriplyDB

Glucose phosphorylation is required for insulin-dependent mTOR signalling in the heart.

Glucose phosphorylation is required for insulin-dependent mTOR signalling in the heart.

http://www.wikidata.org/entity/Q34635114

about

Remodeling of glucose metabolism precedes pressure overload-induced left ventricular hypertrophy: review of a hypothesis.The two faces of miR-29 Glucose regulation of load-induced mTOR signaling and ER stress in mammalian heart.Quantitative PET imaging detects early metabolic remodeling in a mouse model of pressure-overload left ventricular hypertrophy in vivo Deficiency of cardiac Acyl-CoA synthetase-1 induces diastolic dysfunction, but pathologic hypertrophy is reversed by rapamycin Interrogating functional integration between injected pluripotent stem cell-derived cells and surrogate cardiac tissue.Mouse cardiac acyl coenzyme a synthetase 1 deficiency impairs Fatty Acid oxidation and induces cardiac hypertrophy.Hexokinase II integrates energy metabolism and cellular protection: Akting on mitochondria and TORCing to autophagy.Mitochondrial dysfunction in some triple-negative breast cancer cell lines: role of mTOR pathway and therapeutic potential Glucose-6-phosphate isomerase deficiency results in mTOR activation, failed translocation of lipin 1α to the nucleus and hypersensitivity to glucose: Implications for the inherited glycolytic disease Loss of long-chain acyl-CoA synthetase isoform 1 impairs cardiac autophagy and mitochondrial structure through mechanistic target of rapamycin complex 1 activation.Cardiomyocyte-specific deletion of leptin receptors causes lethal heart failure in Cre-recombinase-mediated cardiotoxicity.Nonischemic heart failure in diabetes mellitus.Nutrient-sensing mTORC1: Integration of metabolic and autophagic signals Insulin signalling in the heart.Insulin stimulates mitochondrial fusion and function in cardiomyocytes via the Akt-mTOR-NFκB-Opa-1 signaling pathway Cardiac metabolism and its interactions with contraction, growth, and survival of cardiomyocytes.Amino acids and derivatives, a new treatment of chronic heart failure?Rethinking cardiac metabolism: metabolic cycles to refuel and rebuild the failing heart.Fuel availability and fate in cardiac metabolism: A tale of two substrates.Metabolism in cardiomyopathy: every substrate matters.Mammalian target of rapamycin (mTOR) as a potential therapeutic target in various diseases.The combination of the novel glycolysis inhibitor 3-BrOP and rapamycin is effective against neuroblastoma Cardiac energy dependence on glucose increases metabolites related to glutathione and activates metabolic genes controlled by mechanistic target of rapamycin.Insulin resistance: marker or mediator?SH003 suppresses breast cancer growth by accumulating p62 in autolysosomes.Cardiac Metabolism in Perspective.Functionally redundant control of cardiac hypertrophic signaling by inositol 1,4,5-trisphosphate receptors.Exercise training reduces insulin resistance and upregulates the mTOR/p70S6k pathway in cardiac muscle of diet-induced obesity rats.

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P2860

Glucose phosphorylation is required for insulin-dependent mTOR signalling in the heart.

http://www.wikidata.org/entity/Q34635114

description

2007 nî lūn-bûn

@nan

2007 թուականի Մայիսին հրատարակուած գիտական յօդուած

@hyw

2007 թվականի մայիսին հրատարակված գիտական հոդված

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2007年の論文

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2007年学术文章

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2007年学术文章

@zh-cn

2007年学术文章

@zh-hans

2007年学术文章

@zh-my

2007年学术文章

@zh-sg

2007年學術文章

@yue

name

Glucose phosphorylation is required for insulin-dependent mTOR signalling in the heart.

@ast

Glucose phosphorylation is required for insulin-dependent mTOR signalling in the heart.

@en

Glucose phosphorylation is required for insulin-dependent mTOR signalling in the heart.

@nl

type

label

Glucose phosphorylation is required for insulin-dependent mTOR signalling in the heart.

@ast

Glucose phosphorylation is required for insulin-dependent mTOR signalling in the heart.

@en

Glucose phosphorylation is required for insulin-dependent mTOR signalling in the heart.

@nl

prefLabel

Glucose phosphorylation is required for insulin-dependent mTOR signalling in the heart.

@ast

Glucose phosphorylation is required for insulin-dependent mTOR signalling in the heart.

@en

Glucose phosphorylation is required for insulin-dependent mTOR signalling in the heart.

@nl

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P356

J.CARDIORES.2007.05.004

P1433

Cardiovascular Research

P1476

Glucose phosphorylation is required for insulin-dependent mTOR signalling in the heart.

@en

P2093

Heinrich Taegtmeyer

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

Patrick H Guthrie

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

Saumya Sharma

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

Suzanne S Chan

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

Syed Haq

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

P2860

Elucidating TOR signaling and rapamycin action: lessons from Saccharomyces cerevisiae.

TOR, a central controller of cell growth.

Amino acid-induced stimulation of translation initiation in rat skeletal muscle

The glucose fatty-acid cycle. Its role in insulin sensitivity and the metabolic disturbances of diabetes mellitus

Thr2446 is a novel mammalian target of rapamycin (mTOR) phosphorylation site regulated by nutrient status

[5-3H]glucose overestimates glycolytic flux in isolated working rat heart: role of the pentose phosphate pathway.

The TOR kinases link nutrient sensing to cell growth.

Akt/protein kinase B promotes organ growth in transgenic mice.

Control of protein synthesis by amino acid availability.

Hexosamines as mediators of nutrient sensing and regulation in diabetes.

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71-80

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10.1016/J.CARDIORES.2007.05.004

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1

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76

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2007-05-10T00:00:00Z

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6284203

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17553476

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phosphorylation

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2257479

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