Cardiac remodeling and atrial fibrillation in transgenic miceoverexpressing junctin-Reference-Cited by-同舟云学术

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Cardiac remodeling and atrial fibrillation in transgenic miceoverexpressing junctin

Published:2002-06-21 Issue:10 Volume:16 Page:1310-1312
ISSN:0892-6638
Container-title:The FASEB Journal
language:en
Short-container-title:FASEB j.

Author:

Hong Chang‐Soo¹,Cho Myeong‐Chan²,Kwak Yong‐Geun³,Song Chang‐Ho⁴,Lee Young‐Hoon⁴,Lim Jung Su⁵,Kwon Yunhee Kim⁵,Chae Soo‐Wan³,Kim Do Han¹

Affiliation:

1. Department of Life ScienceKwangju Institute of Science and Technology (K‐JIST) Kwangju Korea

2. Department of Cardiology, College of MedicineChungbuk National University Cheongju Korea

3. Department of PharmacologyInstitute of Cardiovascular Research

4. Department of AnatomyChonbuk National University Medical School Chonju Korea

5. Department of BiologyKyunghee University Seoul Korea

Funder

Korea Science and Engineering Foundation

Ministry of Education

Publisher

Wiley

Subject

Genetics,Molecular Biology,Biochemistry,Biotechnology

Link

https://onlinelibrary.wiley.com/doi/pdf/10.1096/fj.01-0908fje

Reference50 articles.

1. A lethal mutation in mice eliminates the slow calcium current in skeletal muscle cells

2. Involvement of dihydropyridine receptors in excitation–contraction coupling in skeletal muscle

3. Structural evidence for direct interaction between the molecular components of the transverse tubule/sarcoplasmic reticulum junction in skeletal muscle.

4. Restoration of excitation—contraction coupling and slow calcium current in dysgenic muscle by dihydropyridine receptor complementary DNA

5. Voltage sensor of excitation-contraction coupling in skeletal muscle.

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