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Arrhythmogenesis in a catecholaminergic polymorphic ventricular tachycardia mutation that depresses ryanodine receptor function
Current mechanisms of arrhythmogenesis in catecholaminergic polymorphic ventricular tachycardia (CPVT) require spontaneous Ca(2+) release via cardiac ryanodine receptor (RyR2) channels affected by gain-of-function mutations. Hence, hyperactive RyR2 channels eager to release Ca(2+) on their own appea...
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| Vydáno v: | Proc Natl Acad Sci U S A |
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| Hlavní autoři: | , , , , , , , |
| Médium: | Artigo |
| Jazyk: | Inglês |
| Vydáno: |
National Academy of Sciences
2015
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| Témata: | |
| On-line přístup: | https://ncbi.nlm.nih.gov/pmc/articles/PMC4386375/ https://ncbi.nlm.nih.gov/pubmed/25775566 https://ncbi.nlm.nih.govhttp://dx.doi.org/10.1073/pnas.1419795112 |
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