Literature DB >> 12650874

Genetic control of sodium channel function.

Hanno L Tan1, Connie R Bezzina, Jeroen P P Smits, Arie O Verkerk, Arthur A M Wilde.   

Abstract

Sodium ion (Na) influx through cardiac Na channels triggers the action potential in cells of the working myocardium and the specialized conduction system. Na channels thus act as key molecular determinants of cardiac excitability and impulse propagation. Na channel dysfunction may cause life-threatening arrhythmias. Here, we review the ways in which Na channel function can be aberrant due to genetic changes. We discuss how biophysical studies of mutant Na channels combined with precise clinical phenotyping may improve our understanding of Na channel function in health and disease and may be useful as a model from which to derive improved treatment strategies for common disease.

Entities:  

Mesh:

Substances:

Year:  2003        PMID: 12650874     DOI: 10.1016/s0008-6363(02)00714-9

Source DB:  PubMed          Journal:  Cardiovasc Res        ISSN: 0008-6363            Impact factor:   10.787


  35 in total

1.  Characterization of the cardiac sodium channel SCN5A mutation, N1325S, in single murine ventricular myocytes.

Authors:  Sandro L Yong; Ying Ni; Teng Zhang; David J Tester; Michael J Ackerman; Qing K Wang
Journal:  Biochem Biophys Res Commun       Date:  2006-11-14       Impact factor: 3.575

Review 2.  Genetics of cardiac arrhythmias.

Authors:  Arthur A M Wilde; Connie R Bezzina
Journal:  Heart       Date:  2005-10       Impact factor: 5.994

3.  Sodium channel genes and the evolution of diversity in communication signals of electric fishes: convergent molecular evolution.

Authors:  Harold H Zakon; Ying Lu; Derrick J Zwickl; David M Hillis
Journal:  Proc Natl Acad Sci U S A       Date:  2006-02-27       Impact factor: 11.205

4.  Sodium channel Scn1b null mice exhibit prolonged QT and RR intervals.

Authors:  Luis F Lopez-Santiago; Laurence S Meadows; Sara J Ernst; Chunling Chen; Jyoti Dhar Malhotra; Dyke P McEwen; Audrey Speelman; Jeffrey L Noebels; Sebastian K G Maier; Anatoli N Lopatin; Lori L Isom
Journal:  J Mol Cell Cardiol       Date:  2007-08-10       Impact factor: 5.000

5.  Diversity in cardiac sodium channel disease phenotype in transgenic mice carrying a single SCN5A mutation.

Authors:  C A Remme; A O Verkerk; A A M Wilde; M W Veldkamp; J M T de Bakker; C R Bezzina
Journal:  Neth Heart J       Date:  2007       Impact factor: 2.380

Review 6.  Subtype-selective targeting of voltage-gated sodium channels.

Authors:  Steve England; Marcel J de Groot
Journal:  Br J Pharmacol       Date:  2009-10-20       Impact factor: 8.739

Review 7.  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

8.  Variable Na(v)1.5 protein expression from the wild-type allele correlates with the penetrance of cardiac conduction disease in the Scn5a(+/-) mouse model.

Authors:  Anne-Laure Leoni; Bruno Gavillet; Jean-Sébastien Rougier; Céline Marionneau; Vincent Probst; Solena Le Scouarnec; Jean-Jacques Schott; Sophie Demolombe; Patrick Bruneval; Christopher L H Huang; William H Colledge; Andrew A Grace; Hervé Le Marec; Arthur A Wilde; Peter J Mohler; Denis Escande; Hugues Abriel; Flavien Charpentier
Journal:  PLoS One       Date:  2010-02-19       Impact factor: 3.240

9.  Correlations between clinical and physiological consequences of the novel mutation R878C in a highly conserved pore residue in the cardiac Na+ channel.

Authors:  Y Zhang; T Wang; A Ma; X Zhou; J Gui; H Wan; R Shi; C Huang; A A Grace; C L-H Huang; D Trump; H Zhang; T Zimmer; M Lei
Journal:  Acta Physiol (Oxf)       Date:  2008-07-24       Impact factor: 6.311

10.  Characterization of a novel Nav1.5 channel mutation, A551T, associated with Brugada syndrome.

Authors:  Kun-Chi Chiang; Ling-Ping Lai; Ru-Chi Shieh
Journal:  J Biomed Sci       Date:  2009-08-25       Impact factor: 8.410

View more

北京卡尤迪生物科技股份有限公司 © 2022-2023.