MOG1 Rescues Defective Trafficking of Nav1.5 Mutations in Brugada Syndrome and Sick Sinus Syndrome-Reference-Cited by-同舟云学术

MOG1 Rescues Defective Trafficking of Nav1.5 Mutations in Brugada Syndrome and Sick Sinus Syndrome

Published:2013-04 Issue:2 Volume:6 Page:392-401
ISSN:1941-3149
Container-title:Circulation: Arrhythmia and Electrophysiology
language:en
Short-container-title:Circ Arrhythm Electrophysiol

Author:

Chakrabarti Susmita¹,Wu Xiaofen¹,Yang Zhaogang¹,Wu Ling¹,Yong Sandro L.¹,Zhang Cuntai¹,Hu Keli¹,Wang Qing K.¹,Chen Qiuyun¹

Affiliation:

1. From the Department of Molecular Cardiology, Center for Cardiovascular Genetics, Lerner Research Institute, Cleveland Clinic, Cleveland, OH (S.C., X.W., L.W., S.L.Y., Q.K.W., Q.C.); Department of Molecular Medicine, Lerner College of Medicine of Case Western Reserve University, Cleveland Clinic, Cleveland, OH (S.C., Q.K.W., Q.C.); Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China (X.W., C.Z.); Division of Pharmacology, College of Pharmacy, Ohio...

Publisher

Ovid Technologies (Wolters Kluwer Health)

Subject

Physiology (medical),Cardiology and Cardiovascular Medicine

Reference14 articles.

1. Genetic basis and molecular mechanism for idiopathic ventricular fibrillation

2. Multiple Loss-of-Function Mechanisms Contribute to SCN5A-Related Familial Sick Sinus Syndrome

3. Identification of a New Co-factor, MOG1, Required for the Full Function of Cardiac Sodium Channel Nav1.5

4. Identification of a Conserved Loop in Mog1 that Releases GTP from Ran

5. MOG1

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