Genetic basis and molecular mechanism for idiopathic ventricular fibrillation.

Chen, Q; Kirsch, G E; Zhang, D; Brugada, R; Brugada, J; Brugada, P; Potenza, D; Moya, A; Borggrefe, M; Breithardt, G; Ortiz-Lopez, R; Wang, Z; Antzelevitch, C; O'Brien, R E; Schulze-Bahr, E; Keating, M T; Towbin, J A; Wang, Q

Chen, Q; Kirsch, G E; Zhang, D; Brugada, R; Brugada, J; Brugada, P; Potenza, D; Moya, A; Borggrefe, M; Breithardt, G; Ortiz-Lopez, R; Wang, Z; Antzelevitch, C; O'Brien, R E; Schulze-Bahr, E; Keating, M T; Towbin, J A; Wang, Q.

Affiliation

Chen Q; Department of Pediatrics (Cardiology), Baylor College of Medicine, Houston, Texas 77030, USA.

Nature ; 392(6673): 293-6, 1998 Mar 19.

Article in En | MEDLINE | ID: mdl-9521325

Subject(s)

Mutation; Sodium Channels/genetics; Ventricular Fibrillation/genetics; Action Potentials; Animals; DNA Mutational Analysis; Electrocardiography; Electrophysiology; Female; Frameshift Mutation; Humans; Ion Channel Gating/genetics; Kinetics; Male; NAV1.5 Voltage-Gated Sodium Channel; Pedigree; Polymorphism, Single-Stranded Conformational; Protein Structure, Secondary; Recombinant Proteins/genetics; Recombinant Proteins/metabolism; Sodium Channels/chemistry; Sodium Channels/metabolism; Ventricular Fibrillation/etiology; Ventricular Fibrillation/metabolism; Xenopus

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Collection: 01-internacional Database: MEDLINE Main subject: Ventricular Fibrillation / Sodium Channels / Mutation Type of study: Etiology_studies / Prognostic_studies Limits: Animals / Female / Humans / Male Language: En Journal: Nature Year: 1998 Document type: Article Affiliation country: United States Country of publication: United kingdom

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