ATP-sensitive K+ channel knockout compromises the metabolic benefit of exercise training, resulting in cardiac deficits. - Wikidata - wikimedia - TriplyDB

ATP-sensitive K+ channel knockout compromises the metabolic benefit of exercise training, resulting in cardiac deficits.

ATP-sensitive K+ channel knockout compromises the metabolic benefit of exercise training, resulting in cardiac deficits.

http://www.wikidata.org/entity/Q45161240

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ATP Sensitive Potassium Channels in the Skeletal Muscle Function: Involvement of the KCNJ11(Kir6.2) Gene in the Determination of Mechanical Warner Bratzer Shear Force Ocular Hypotensive Effects of the ATP-Sensitive Potassium Channel Opener Cromakalim in Human and Murine Experimental Model Systems Angiotensin II and tumour necrosis factor alpha as mediators of ATP-dependent potassium channel remodelling in post-infarction heart failure Early aging-associated phenotypes in Bub3/Rae1 haploinsufficient mice.Stem cell transplant into preimplantation embryo yields myocardial infarction-resistant adult phenotype.ATP-sensitive K+ channel knockout induces cardiac proteome remodeling predictive of heart disease susceptibility.Disruption of sarcolemmal ATP-sensitive potassium channel activity impairs the cardiac response to systolic overload.Human K(ATP) channelopathies: diseases of metabolic homeostasis.Deficiency of heme oxygenase-1 impairs renal hemodynamics and exaggerates systemic inflammatory responses to renal ischemia.Consequences of cardiac myocyte-specific ablation of KATP channels in transgenic mice expressing dominant negative Kir6 subunits.Exercise-induced expression of cardiac ATP-sensitive potassium channels promotes action potential shortening and energy conservation.Muscle KATP channels: recent insights to energy sensing and myoprotection Advances in cardiac ATP-sensitive K+ channelopathies from molecules to populations.Nicotinamide-rich diet improves physical endurance by up-regulating SUR2A in the heart ATP-sensitive potassium (KATP) channel activation decreases intraocular pressure in the anterior chamber of the eye Antiobesity strategy targets energy economy safeguards.Mice expressing a human K(ATP) channel mutation have altered channel ATP sensitivity but no cardiac abnormalities.Dynamic phosphometabolomic profiling of human tissues and transgenic models by 18O-assisted ³¹P NMR and mass spectrometry Decline of Phosphotransfer and Substrate Supply Metabolic Circuits Hinders ATP Cycling in Aging Myocardium.ATP-sensitive K+ channel channel/enzyme multimer: metabolic gating in the heart.Cardiac KATP channels in health and disease.K(ATP) channel therapeutics at the bedside.Cardiac system bioenergetics: metabolic basis of the Frank-Starling law.Current and future approaches using genetically modified mice in endocrine research.Systems biology approaches to metabolic and cardiovascular disorders: network perspectives of cardiovascular metabolism.Perspectives in innate and acquired cardioprotection: cardioprotection acquired through exercise.ATP-sensitive potassium channels: metabolic sensing and cardioprotection.Aging and cardioprotection.Kir6.2 is not the mitochondrial KATP channel but is required for cardioprotection by ischemic preconditioning Opposing roles for p16Ink4a and p19Arf in senescence and ageing caused by BubR1 insufficiency.ATP-sensitive potassium (K(ATP)) channel openers diazoxide and nicorandil lower intraocular pressure in vivo KATP channel Kir6.2 E23K variant overrepresented in human heart failure is associated with impaired exercise stress response.KCNJ11 knockout morula re-engineered by stem cell diploid aggregation.Proteomic profiling of KATP channel-deficient hypertensive heart maps risk for maladaptive cardiomyopathic outcome.Mice lacking sulfonylurea receptor 2 (SUR2) ATP-sensitive potassium channels are resistant to acute cardiovascular stress.Modeling cardiac action potential shortening driven by oxidative stress-induced mitochondrial oscillations in guinea pig cardiomyocytes.Impaired exercise tolerance and skeletal muscle myopathy in sulfonylurea receptor-2 mutant mice.Mechanical dyssynchrony precedes QRS widening in ATP-sensitive K⁺ channel-deficient dilated cardiomyopathy.Transgenic overexpression of human DMPK accumulates into hypertrophic cardiomyopathy, myotonic myopathy and hypotension traits of myotonic dystrophy.ATP sensitive potassium channel openers: A new class of ocular hypotensive agents.

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P2860

ATP-sensitive K+ channel knockout compromises the metabolic benefit of exercise training, resulting in cardiac deficits.

http://www.wikidata.org/entity/Q45161240

description

2004 nî lūn-bûn

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2004年の論文

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2004年学术文章

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2004年学术文章

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2004年学术文章

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2004年学术文章

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2004年学术文章

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2004年学术文章

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2004年學術文章

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2004年學術文章

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name

ATP-sensitive K+ channel knock ...... resulting in cardiac deficits.

@en

ATP-sensitive K+ channel knock ...... resulting in cardiac deficits.

@nl

type

label

ATP-sensitive K+ channel knock ...... resulting in cardiac deficits.

@en

ATP-sensitive K+ channel knock ...... resulting in cardiac deficits.

@nl

prefLabel

ATP-sensitive K+ channel knock ...... resulting in cardiac deficits.

@en

ATP-sensitive K+ channel knock ...... resulting in cardiac deficits.

@nl

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DIABETES.53.SUPPL_3.S169

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ATP-sensitive K+ channel knock ...... resulting in cardiac deficits.

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Andre Terzic

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

Atta Behfar

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

Carmen Perez-Terzic

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

Fearghas O'Cochlain

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

Garvan C Kane

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

Petras P Dzeja

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

Santiago Reyes

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

Satsuki Yamada

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

Susumu Seino

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

Takashi Miki

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

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S169-75

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scholarly article

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10.2337/DIABETES.53.SUPPL_3.S169

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53 Suppl 3

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2004-12-01T00:00:00Z

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15561907

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