Cell models of arrhythmogenic cardiomyopathy: advances and opportunities.

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2017 nî lūn-bûn

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2017年の論文

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2017年学术文章

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2017年学术文章

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2017年学术文章

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2017年学术文章

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2017年学术文章

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2017年學術文章

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2017年學術文章

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2017年學術文章

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Cell models of arrhythmogenic cardiomyopathy: advances and opportunities.

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Cell models of arrhythmogenic cardiomyopathy: advances and opportunities.

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Cell models of arrhythmogenic cardiomyopathy: advances and opportunities.

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P1476

Cell models of arrhythmogenic cardiomyopathy: advances and opportunities.

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Claudio Tondo

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Giulio Pompilio

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Creative Commons Attribution

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Identification of mutations in the cardiac ryanodine receptor gene in families affected with arrhythmogenic right ventricular cardiomyopathy type 2 (ARVD2)

Molecular insights into arrhythmogenic right ventricular cardiomyopathy caused by plakophilin-2 missense mutations

Mutations in the area composita protein αT-catenin are associated with arrhythmogenic right ventricular cardiomyopathy

Mechanistic insights into arrhythmogenic right ventricular cardiomyopathy caused by desmocollin-2 mutations

Ryanodine receptor mutations associated with stress-induced ventricular tachycardia mediate increased calcium release in stimulated cardiomyocytes

Suppression of canonical Wnt/beta-catenin signaling by nuclear plakoglobin recapitulates phenotype of arrhythmogenic right ventricular cardiomyopathy

Arrhythmogenic right ventricular cardiomyopathy type 5 is a fully penetrant, lethal arrhythmic disorder caused by a missense mutation in the TMEM43 gene

Treatment of arrhythmogenic right ventricular cardiomyopathy/dysplasia: an international task force consensus statement

Sex differences in the mechanisms underlying long QT syndrome

Arrhythmogenic ventricular cardiomyopathy: A paradigm shift from right to biventricular disease

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scholarly article

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10.1242/DMM.029363

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Gianluca L Perrucci

Ilaria Stadiotti

Elena Sommariva

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2017-07-01T00:00:00Z

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28679668

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heart arrhythmia

biomedical investigative technique

cardiomyopathy

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5536909

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