Mechanisms of arsenic-induced prolongation of cardiac repolarization. - Wikidata - wikimedia - TriplyDB

Mechanisms of arsenic-induced prolongation of cardiac repolarization.

Mechanisms of arsenic-induced prolongation of cardiac repolarization.

http://www.wikidata.org/entity/Q44949018

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Cell surface expression of human ether-a-go-go-related gene (hERG) channels is regulated by caveolin-3 protein via the ubiquitin ligase Nedd4-2 Cardiac applications for human pluripotent stem cells Translational toxicology and rescue strategies of the hERG channel dysfunction: biochemical and molecular mechanistic aspects Molecular pathogenesis of long QT syndrome type 2 Pentamidine reduces hERG expression to prolong the QT interval.Antidepressant-induced ubiquitination and degradation of the cardiac potassium channel hERG.Choline-modulated arsenic trioxide-induced prolongation of cardiac repolarization in Guinea pig.Iatrogenic QT Abnormalities and Fatal Arrhythmias: Mechanisms and Clinical Significance Hsp40 chaperones promote degradation of the HERG potassium channel.L-type calcium current (ICa,L) and inward rectifier potassium current (IK1) are involved in QT prolongation induced by arsenic trioxide in rat.hERG-related drug toxicity and models for predicting hERG liability and QT prolongation.Screening for acute IKr block is insufficient to detect torsades de pointes liability: role of late sodium current.HERG1 channelopathies R-type calcium channels are crucial for semaphorin 3A-induced DRG axon growth cone collapse Drug-induced QT interval prolongation: mechanisms and clinical management Drug-induced long QT syndrome Oxidative inactivation of the lipid phosphatase phosphatase and tensin homolog on chromosome ten (PTEN) as a novel mechanism of acquired long QT syndrome.Cardiac and cardiovascular toxicity of nonanthracycline anticancer drugs.Arsenic trioxide: safety issues and their management.Cellular basis of drug-induced torsades de pointes Protein trafficking abnormalities: a new mechanism in drug-induced long QT syndrome.Endocytosis of HERG is clathrin-independent and involves arf6.Cardiovascular disease and arsenic exposure in Inner Mongolia, China: a case control study QTc prolongation assessment in anticancer drug development: clinical and methodological issues Molecular determinants of pentamidine-induced hERG trafficking inhibition.High Throughput Measurement of Ca++ Dynamics in Human Stem Cell-Derived Cardiomyocytes by Kinetic Image Cytometery: A Cardiac Risk Assessment Characterization Using a Large Panel of Cardioactive and Inactive Compounds.Chronic arsenic exposure and cardiac repolarization abnormalities with QT interval prolongation in a population-based study.Impaired Inactivation of L-Type Ca2+ Current as a Potential Mechanism for Variable Arrhythmogenic Liability of HERG K+ Channel Blocking Drugs.In vitro cardiovascular effects of dihydroartemisin-piperaquine combination compared with other antimalarials Drug-induced long QT syndrome: hERG K+ channel block and disruption of protein trafficking by fluoxetine and norfluoxetine.Combined hERG channel inhibition and disruption of trafficking in drug-induced long QT syndrome by fluoxetine: a case-study in cardiac safety pharmacology.Antimalarial drugs: QT prolongation and cardiac arrhythmias.ICH S7B draft guideline on the non-clinical strategy for testing delayed cardiac repolarisation risk of drugs: a critical analysis.Mechanism and pharmacological rescue of berberine-induced hERG channel deficiency Arsenic trioxide induces the apoptosis of human breast cancer MCF-7 cells through activation of caspase-3 and inhibition of HERG channels.Long QT syndrome: reduced repolarization reserve and the genetic link.Suppression of phosphoinositide 3-kinase signaling and alteration of multiple ion currents in drug-induced long QT syndrome A search to predict potential for drug-induced cardiovascular toxicity.Molecular mechanisms for drug interactions with hERG that cause long QT syndrome.Mechanisms of zolpidem-induced long QT syndrome: acute inhibition of recombinant hERG K(+) channels and action potential prolongation in human cardiomyocytes derived from induced pluripotent stem cells

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Mechanisms of arsenic-induced prolongation of cardiac repolarization.

http://www.wikidata.org/entity/Q44949018

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年學術文章

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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

Mechanisms of arsenic-induced prolongation of cardiac repolarization.

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Mechanisms of arsenic-induced prolongation of cardiac repolarization.

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type

label

Mechanisms of arsenic-induced prolongation of cardiac repolarization.

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Mechanisms of arsenic-induced prolongation of cardiac repolarization.

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prefLabel

Mechanisms of arsenic-induced prolongation of cardiac repolarization.

@en

Mechanisms of arsenic-induced prolongation of cardiac repolarization.

@nl

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Molecular Pharmacology

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Mechanisms of arsenic-induced prolongation of cardiac repolarization.

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Adrienne T Dennis

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Arthur M Brown

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Barbara A Wible

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Carlos Obejero-Paz

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Eckhard Ficker

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Lu Wang

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Peter Hawryluk

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Yuri A Kuryshev

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33-44

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10.1124/MOL.66.1.33

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15213294

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