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Comment
. 2008 Jan 14;180(1):13-5.
doi: 10.1083/jcb.200712098. Epub 2008 Jan 7.

Being there: cellular targeting of voltage-gated sodium channels in the heart

Vann Bennett  1 , Jane Healy
Affiliations
Comment

Being there: cellular targeting of voltage-gated sodium channels in the heart

Vann Bennett et al. J Cell Biol. .

Abstract

Voltage-gated sodium (Na(v)) 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 Na(v)1.5, the principal Na(v) channel in the heart, was previously known to cause cardiac arrhythmia and the retention of Na(v)1.5 in an intracellular compartment in cardiomyocytes. Conclusive evidence is now provided that direct interaction between Na(v)1.5 and ankyrin-G is necessary for the expression of Na(v)1.5 at the cardiomyocyte cell surface.

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Figures

Figure 1.
Figure 1.
Schematic model depicting the association of Nav channels with ankyrin-G/spectrin at intercalated discs and T tubules in cardiomyocytes. Evidence for this scheme is that Nav1.5, the predominant Nav channel in the heart, binds to ankyrin-G, requires ankyrin-G for cell surface expression, and, at steady state, colocalizes with ankyrin-G.
See this image and copyright information in PMC

Comment on

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