Point Mutation in the HCN4 Cardiac Ion Channel Pore Affecting Synthesis, Trafficking, and Functional Expression Is Associated With Familial Asymptomatic Sinus Bradycardia | Zendy

Eyal Nof | Zendy; David Luria | Zendy; Dovrat Brass | Zendy; Dina Marek | Zendy; Hadas Lahat | Zendy; Haya Reznik-Wolf | Zendy; Elon Pras | Zendy; Nathan Dascal | Zendy; Michael Eldar | Zendy; Michael Glikson | Zendy

Open Access

Point Mutation in the HCN4 Cardiac Ion Channel Pore Affecting Synthesis, Trafficking, and Functional Expression Is Associated With Familial Asymptomatic Sinus Bradycardia

Author(s) -

Eyal Nof,

David Luria,

Dovrat Brass,

Dina Marek,

Hadas Lahat,

Haya Reznik-Wolf,

Elon Pras,

Nathan Dascal,

Michael Eldar,

Michael Glikson

Publication year - 2007

Publication title -

circulation

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 7.795

H-Index - 607

eISSN - 1524-4539

pISSN - 0009-7322

DOI - 10.1161/circulationaha.107.706887

Subject(s) - missense mutation , sinus bradycardia , medicine , sick sinus syndrome , mutant , mutation , endocrinology , bradycardia , genetics , cardiology , biology , gene , heart rate , blood pressure

The hyperpolarization-activated nucleotide-gated channel--HCN4 plays a major role in the diastolic depolarization of sinus atrial node cells. Mutant HCN4 channels have been found to be associated with inherited sinus bradycardia.

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