Correction: “Ryanopathies” and RyR2 dysfunctions: can we further decipher them using in vitro human disease models?
Author:
Publisher
Springer Science and Business Media LLC
Subject
Cancer Research,Cell Biology,Cellular and Molecular Neuroscience,Immunology
Link
https://www.nature.com/articles/s41419-022-05468-3.pdf
Reference74 articles.
1. Jiang D, Jones PP, Davis DR, Gow R, Green MS, Birnie DH, et al. Characterization of a novel mutation in the cardiac ryanodine receptor that results in catecholaminergic polymorphic ventricular tachycardia. Channels. 2010;4:302–10.
2. Meli AC, Refaat MM, Dura M, Reiken S, Wronska A, Wojciak J, et al. A novel ryanodine receptor mutation linked to sudden death increases sensitivity to cytosolic calcium. Circ Res. 2011;109:281–90.
3. Lobo PA, Kimlicka L, Tung CC, Van, Petegem F. The deletion of exon 3 in the cardiac ryanodine receptor is rescued by beta strand switching. Structure. 2011;19:790–8.
4. Liu Y, Wei J, Wong King Yuen SM, Sun B, Tang Y, Wang R, et al. CPVT-associated cardiac ryanodine receptor mutation G357S with reduced penetrance impairs Ca2+ release termination and diminishes protein expression. PloS ONE. 2017;12:e0184177-e.
5. Xiong J, Liu X, Gong Y, Zhang P, Qiang S, Zhao Q, et al. Pathogenic mechanism of a catecholaminergic polymorphic ventricular tachycardia causing-mutation in cardiac calcium release channel RyR2. J Mol Cell Cardiol. 2018;117:26–35.
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