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Abstract:
AIMS:Pathogenic variants of the SCN5A gene can cause Brugada syndrome (BrS) and long QT syndrome (LQTS), which predispose individuals to potentially fatal ventricular arrhythmias and sudden cardiac death. SCN5A encodes the NaV 1.5 protein, the pore forming α-subunit of the voltage-dependent cardiac Na+ channel. Using a WW domain, the E3 ubiquitin ligase Nedd4-2 binds to the PY-motif ([L/P]PxY) within the C-terminus of NaV 1.5, which results in decreased protein expression and current through NaV 1.5 ubiquitination. Here, we investigate the role of E3 ubiquitin ligase Nedd4-2-mediated NaV 1.5 degradation in the pathological mechanisms of the BrS-associated variant SCN5A-p.L1239P and LQTS-associated variant SCN5A-p.Y1977N. METHODS AND RESULTS:Using a combination of molecular biology, biochemical and electrophysiological approaches, we examined the expression, function and Nedd4-2 interactions of SCN5A-p.L1239P and SCN5A-p.Y1977N. SCN5A-p.L1239P is characterized as a loss-of-function, whereas SCN5A-p.Y1977N is a gain-of-function variant of the NaV 1.5 channel. Sequence alignment shows that BrS-associated SCN5A-p.L1239P has a new Nedd4-2-binding site (from LLxY to LPxY). This new Nedd4-2-binding site increases the interaction between NaV 1.5 and Nedd4-2, enhancing ubiquitination and degradation of the NaV 1.5 channel. Disruption of the new Nedd4-2-binding site of SCN5A-p.L1239P restores NaV 1.5 expression and function. However, the LQTS-associated SCN5A-p.Y1977N disrupts the usual Nedd4-2-binding site (from PPxY to PPxN). This decreases NaV 1.5-Nedd4-2 interaction, preventing ubiquitination and degradation of NaV 1.5 channels. CONCLUSIONS:Our data suggest that the PY-motif plays an essential role in modifying the expression/function of NaV 1.5 channels through Nedd4-2-mediated ubiquitination. Alterations of NaV 1.5-Nedd4-2 interaction represent a novel pathological mechanism for NaV 1.5 channel diseases caused by SCN5A variants.
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最新影响因子:7.523 | 期刊ISSN:1748-1708 | CiteScore:3.42 |
出版周期:Monthly | 是否OA:YES | 出版年份:2006 |
期刊官方网址:http://onlinelibrary.wiley.com/journal/10.1111/(ISSN)1748-1716
自引率:28.20% | 研究方向:医学-生理学 |
出版地区:ENGLAND |
SCI期刊coverage:Science Citation Index Expanded(科学引文索引扩展)
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Published by John Wiley and Sons. ISSN (printed): 1748-1708. ISSN (electronic): 1748-1716. Acta Physiologica plays an important part in advancing effective communication among physiologists.
由John Wiley and Sons出版。ISSN(印刷):1748 - 1708。ISSN(电子):1748 - 1716。 生理学行为在促进生理学家之间的有效沟通中起着重要的作用。
大类(学科) | 小类(学科) | 学科排名 |
医学 |
PHYSIOLOGY (生理学) 2区 |
5/83 |
年度总发文量 | 年度论文发表量 | 年度综述发表量 |
100 | 67 | 33 |
引文计数(2018)
文献(2015-2017)
1632次引用
477篇文献
序号 | 类别 | 排名 | 百分位 |
1 |
大类(学科):Biochemistry, Genetics and Molecular Biology
小类(学科):Physiology
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研究方向:生命科学 生理学 整合生物学 系统生理学
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影响因子:0.704
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研究方向:医学-内分泌学与代谢
发表一篇学和医学成像类SCI论文
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