Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4
pubmed:dateCreated
2003-3-24
pubmed:abstractText
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.
pubmed:commentsCorrections
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Mar
pubmed:issn
0008-6363
pubmed:author
pubmed:issnType
Print
pubmed:day
15
pubmed:volume
57
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
961-73
pubmed:dateRevised
2007-11-15
pubmed:meshHeading
pubmed:year
2003
pubmed:articleTitle
Genetic control of sodium channel function.
pubmed:affiliation
Experimental and Molecular Cardiology Group, Department of Cardiology, Academic Medical Center, Room M0-052, P.O. Box 22700, 1100 DE, Amsterdam, The Netherlands. h.l.tan@amc.uva.nl <h.l.tan@amc.uva.nl>
pubmed:publicationType
Journal Article, Review, Research Support, Non-U.S. Gov't