De Novo Mutation in the SCN5A Gene Associated with Brugada Syndrome | Zendy

Lumin Wang | Zendy; Xiangyun Meng | Zendy; Zhiguang Yuchi | Zendy; Zhenghang Zhao | Zendy; Dehui Xu | Zendy; David Fedida | Zendy; Zhuren Wang | Zendy; Chen Huang | Zendy

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De Novo Mutation in the SCN5A Gene Associated with Brugada Syndrome

Author(s) -

Lumin Wang,

Xiangyun Meng,

Zhiguang Yuchi,

Zhenghang Zhao,

Dehui Xu,

David Fedida,

Zhuren Wang,

Chen Huang

Publication year - 2015

Publication title -

cellular physiology and biochemistry

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 1.486

H-Index - 87

eISSN - 1421-9778

pISSN - 1015-8987

DOI - 10.1159/000430189

Subject(s) - missense mutation , brugada syndrome , sodium channel , nav1.5 , hek 293 cells , mutation , mutant , western blot , wild type , microbiology and biotechnology , patch clamp , biology , transfection , sudden death , chemistry , genetics , medicine , gene , electrophysiology , sodium , neuroscience , organic chemistry

Brugada syndrome (BrS) is a genetically determined cardiac electrical disorder, characterized by typical electrocardiography (ECG) alterations, and it is an arrhythmogenic syndrome that may lead to sudden cardiac death. The most common genotype found among BrS patients is caused by mutations in the SCN5A gene, which lead to a loss of function of the cardiac sodium (Na(+)) channel (Nav1.5) by different mechanisms.

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