Insulin receptor substrates are essential for the bioenergetic and hypertrophic response of the heart to exercise training. - Wikidata - awgldk - TriplyDB

Insulin receptor substrates are essential for the bioenergetic and hypertrophic response of the heart to exercise training.

Insulin receptor substrates are essential for the bioenergetic and hypertrophic response of the heart to exercise training.

http://www.wikidata.org/entity/Q34056611

about

New Molecular Insights of Insulin in Diabetic Cardiomyopathy Exercise for the heart: signaling pathways How exercise may amend metabolic disturbances in diabetic cardiomyopathy Insulin Signaling and Heart Failure.Evidence for distinct effects of exercise in different cardiac hypertrophic disorders.Phosphoinositide dependent protein kinase 1 is required for exercise-induced cardiac hypertrophy but not the associated mitochondrial adaptations.Exercise training improves vascular mitochondrial function.FVB/NJ Mice Are a Useful Model for Examining Cardiac Adaptations to Treadmill Exercise.Insulin regulation of myocardial autophagy.Recent advances of adapter proteins in the regulation of heart diseases.Insulin and β Adrenergic Receptor Signaling: Crosstalk in Heart.Molecular Mechanisms Underlying Cardiac Adaptation to Exercise.Engineered Substrate-Specific Delta PKC Antagonists to Enhance Cardiac Therapeutics.Exercise-Induced Changes in Glucose Metabolism Promote Physiological Cardiac Growth.Physical Exercise Can Spur Beneficial Neoangiogenesis and Microvasculature Remodeling Within the Heart - Our Salvation?Glucose transporter 4-deficient hearts develop maladaptive hypertrophy in response to physiological or pathological stresses.OPA1 deficiency promotes secretion of FGF21 from muscle that prevents obesity and insulin resistance.Understanding Key Mechanisms of Exercise-Induced Cardiac Protection to Mitigate Disease: Current Knowledge and Emerging Concepts.Peroxisome proliferator-activated receptor-γ coactivator 1 α1 induces a cardiac excitation-contraction coupling phenotype without metabolic remodelling.The IGF1-PI3K-Akt Signaling Pathway in Mediating Exercise-Induced Cardiac Hypertrophy and Protection.Moderate Modulation of Cardiac PGC-1α Expression Partially Affects Age-Associated Transcriptional Remodeling of the Heart.An "Exercise" in Cardiac Metabolism.Cardiovascular Effects and Benefits of Exercise Metabolic Mechanisms of Exercise-Induced Cardiac Remodeling

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Insulin receptor substrates are essential for the bioenergetic and hypertrophic response of the heart to exercise training.

http://www.wikidata.org/entity/Q34056611

description

2014 nî lūn-bûn

@nan

2014 թուականի Յուլիսին հրատարակուած գիտական յօդուած

@hyw

2014 թվականի հուլիսին հրատարակված գիտական հոդված

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2014年の論文

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2014年学术文章

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2014年学术文章

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2014年学术文章

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2014年学术文章

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2014年学术文章

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2014年學術文章

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name

Insulin receptor substrates ar ...... he heart to exercise training.

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Insulin receptor substrates ar ...... he heart to exercise training.

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Insulin receptor substrates ar ...... he heart to exercise training.

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type

label

Insulin receptor substrates ar ...... he heart to exercise training.

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Insulin receptor substrates ar ...... he heart to exercise training.

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Insulin receptor substrates ar ...... he heart to exercise training.

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prefLabel

Insulin receptor substrates ar ...... he heart to exercise training.

@ast

Insulin receptor substrates ar ...... he heart to exercise training.

@en

Insulin receptor substrates ar ...... he heart to exercise training.

@nl

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Insulin receptor substrates ar ...... the heart to exercise training

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Adam R Wende

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Annie Bello Moreira

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Bum Jun Kim

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Christian Riehle

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Jack Bevins

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Junghyun Noh

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Karen J Oliveira

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Monika Rech

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Morris F White

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Rajkumar Manivel

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P2860

Disruption of IRS-2 causes type 2 diabetes in mice

Cardiac hypertrophy with preserved contractile function after selective deletion of GLUT4 from the heart

Dysregulation of insulin receptor substrate 2 in beta cells and brain causes obesity and diabetes

Regulation of 4E-BP1 phosphorylation: a novel two-step mechanism

PGC-1alpha deficiency causes multi-system energy metabolic derangements: muscle dysfunction, abnormal weight control and hepatic steatosis

Autophosphorylation of JAK2 on tyrosines 221 and 570 regulates its activity

Regulation of STAT3 by direct binding to the Rac1 GTPase

Reduced expression of the murine p85alpha subunit of phosphoinositide 3-kinase improves insulin signaling and ameliorates diabetes

Regulation of protein serine-threonine phosphatase type-2A by tyrosine phosphorylation

Inactivation of hepatic Foxo1 by insulin signaling is required for adaptive nutrient homeostasis and endocrine growth regulation

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3450-3460

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10.1128/MCB.00426-14

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18

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34

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Eric T Weatherford

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2014-07-07T00:00:00Z

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25002528

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