Sodium channel haploinsufficiency and structural change in ventricular arrhythmogenesis-Reference-Cited by-同舟云学术

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Sodium channel haploinsufficiency and structural change in ventricular arrhythmogenesis

Published:2015-09-24 Issue:2 Volume:216 Page:186-202
ISSN:1748-1708
Container-title:Acta Physiologica
language:en
Short-container-title:Acta Physiol

Author:

Jeevaratnam K.¹²,Guzadhur L.³⁴,Goh Y. M.⁵,Grace A. A.³,Huang C. L.-H.³⁶

Affiliation:

1. Faculty of Health and Medical Science; University of Surrey; Guilford UK

2. Perdana University - Royal College of Surgeons Ireland; Serdang Selangor Darul Ehsan Malaysia

3. Division of Cardiovascular Biology; Department of Biochemistry; University of Cambridge; Cambridge UK

4. Niche Science & Technology; Richmond UK

5. Department of Preclinical Sciences; Faculty of Veterinary Medicine; University Putra Malaysia; Serdang Selangor Darul Ehsan Malaysia

6. Physiological Laboratory; University of Cambridge; Cambridge UK

Funder

Ministry of Higher Education, Malaysia

Fundamental Research Grant Scheme

McVeigh Benefaction

Medical Research Council

Wellcome Trust

Publisher

Wiley

Subject

Physiology

Reference124 articles.

1. Cardiac sodium channel Na(v)1.5 and interacting proteins: physiology and pathophysiology;Abriel;J Mol Cell Cardiol,2010

2. Channelopathies from mutations in the cardiac sodium channel protein complex;Adsit;J Mol Cell Cardiol,2013

3. The three human syntrophin genes are expressed in diverse tissues, have distinct chromosomal locations, and each bind to dystrophin and its relatives;Ahn;J Biol Chem,1996

4. Cellular basis for trigger and maintenance of ventricular fibrillation in the Brugada syndrome model: high-resolution optical mapping study;Aiba;J Am Coll Cardiol,2006

5. A novel SCN5A mutation associated with idiopathic ventricular fibrillation without typical ECG findings of Brugada syndrome;Akai;FEBS Lett,2000

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