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Published online
doi:10.1083/jcb.200712098
The Journal of Cell Biology, Vol. 180, No. 1, 13-15
The Rockefeller University Press, 0021-9525 $30.00
© Bennett et al.
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Being there: cellular targeting of voltage-gated sodium channels in the heart



Vann Bennett1,2,3 and Jane Healy1,2,3

1 Howard Hughes Medical Institute, 2 Department of Cell Biology, and 3 Department of Biochemistry, Duke University Medical Center, Durham, NC 27710

Correspondence to Vann Bennett: v.bennett{at}cellbio.duke.edu

Voltage-gated sodium (Nav) channels in cardiomyocytes are localized in specialized membrane domains that optimize their functions in propagating action potentials across cell junctions and in stimulating voltage-gated calcium channels located in T tubules. Mutation of the ankyrin-binding site of Nav1.5, the principal Nav channel in the heart, was previously known to cause cardiac arrhythmia and the retention of Nav1.5 in an intracellular compartment in cardiomyocytes. Conclusive evidence is now provided that direct interaction between Nav1.5 and ankyrin-G is necessary for the expression of Nav1.5 at the cardiomyocyte cell surface.


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