Literature DB >> 15192037

Biology of cardiac arrhythmias: ion channel protein trafficking.

Brian P Delisle1, Blake D Anson, Sridharan Rajamani, Craig T January.   

Abstract

The mechanisms underlying normal and abnormal cardiac rhythms are complex and incompletely understood. Through the study of uncommon inheritable arrhythmia syndromes, including the long QT and Brugada syndromes, new insights are emerging. At the cellular and tissue levels, we now recognize that ion channel current is the sum of biophysical (gating, permeation), biochemical (phosphorylation, etc), and biogenic (biosynthesis, processing, trafficking, and degradation) properties. This review focuses on how heart cells process ion channel proteins and how this protein trafficking may be altered in some cardiac arrhythmia diseases. In this review, we honor Dr Harry A. Fozzard, a modern pioneer in cardiac arrhythmias, cell biology, and molecular electrophysiology. As a scientist and physician, his writings and mentorship have served to foster a generation of investigators who continue to bring this complex field toward greater scientific understanding and impact on humankind.

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Year:  2004        PMID: 15192037     DOI: 10.1161/01.RES.0000128561.28701.ea

Source DB:  PubMed          Journal:  Circ Res        ISSN: 0009-7330            Impact factor:   17.367


  82 in total

1.  Electrophysiological study of V535M hERG mutation of LQT2.

Authors:  Chunyan Shao; Yan Lu; Mohan Liu; Qi Chen; Yunfeng Lan; Yan Liu; Min Lin; Yang Li
Journal:  J Huazhong Univ Sci Technolog Med Sci       Date:  2011-12-16

Review 2.  Cardiac KATP channels in health and disease.

Authors:  Garvan C Kane; Xiao-Ke Liu; Satsuki Yamada; Timothy M Olson; Andre Terzic
Journal:  J Mol Cell Cardiol       Date:  2005-04-25       Impact factor: 5.000

3.  Total chemical synthesis and biophysical characterization of the minimal isoform of the KChIP2 potassium channel regulatory subunit.

Authors:  Sudarshan Rajagopal; Stephen B H Kent
Journal:  Protein Sci       Date:  2007-07-27       Impact factor: 6.725

4.  Protein trafficking abnormalities: a new mechanism in drug-induced long QT syndrome.

Authors:  Lee L Eckhardt; Sridharan Rajamani; Craig T January
Journal:  Br J Pharmacol       Date:  2005-05       Impact factor: 8.739

5.  Mechanisms of pharmacological rescue of trafficking-defective hERG mutant channels in human long QT syndrome.

Authors:  Qiuming Gong; Melanie A Jones; Zhengfeng Zhou
Journal:  J Biol Chem       Date:  2005-12-16       Impact factor: 5.157

6.  A highly conserved motif at the COOH terminus dictates endoplasmic reticulum exit and cell surface expression of NKCC2.

Authors:  Nancy Zaarour; Sylvie Demaretz; Nadia Defontaine; David Mordasini; Kamel Laghmani
Journal:  J Biol Chem       Date:  2009-06-17       Impact factor: 5.157

7.  Nonsense mutations in hERG cause a decrease in mutant mRNA transcripts by nonsense-mediated mRNA decay in human long-QT syndrome.

Authors:  Qiuming Gong; Li Zhang; G Michael Vincent; Benjamin D Horne; Zhengfeng Zhou
Journal:  Circulation       Date:  2007-06-18       Impact factor: 29.690

Review 8.  Sudden cardiac death without structural heart disease: update on the long QT and Brugada syndromes.

Authors:  Ilan Goldenberg; Arthur J Moss; Wojciech Zareba
Journal:  Curr Cardiol Rep       Date:  2005-09       Impact factor: 2.931

9.  The ever-shrinking world of cardiac ion channel remodeling: the role of microRNAs in heart disease.

Authors:  Heather S Duffy
Journal:  Heart Rhythm       Date:  2009-09-18       Impact factor: 6.343

10.  Rescue of protein expression defects may not be enough to abolish the pro-arrhythmic phenotype of long QT type 2 mutations.

Authors:  Matthew D Perry; Chai Ann Ng; Kevin Phan; Erikka David; Kieran Steer; Mark J Hunter; Stefan A Mann; Mohammad Imtiaz; Adam P Hill; Ying Ke; Jamie I Vandenberg
Journal:  J Physiol       Date:  2016-05-27       Impact factor: 5.182

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