JCB logo
  Home | Help | Feedback | Subscriptions | Archive | Search | Table of Contents
Published online January 7, 2008
doi:10.1083/jcb.200712098
The Journal of Cell Biology, Vol. 180, No. 1, 13-15
The Rockefeller University Press, 0021-9525 $30.00
© 2008 Bennett et al.
This Article
Right arrow Full Text
Right arrow Full Text (PDF, 1076K)
Right arrow PPT slides of all figures
Right arrow Alert me when this article is cited
Right arrow Citation Map
Services
Right arrow Email this article
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new content in the JCB
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via CrossRef
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Bennett, V.
Right arrow Articles by Healy, J.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Bennett, V.
Right arrow Articles by Healy, J.
Related Collections
Right arrowRelated Article
Social Bookmarking
Add to CiteULike   Add to Complore   Add to Connotea   Add to Del.icio.us   Add to Digg   Add to Reddit   Add to Technorati  
What's this?

Comment

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.


Add to CiteULike CiteULike   Add to Complore Complore   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us   Add to Digg Digg   Add to Reddit Reddit   Add to Technorati Technorati    What's this?

Related Article

Voltage-gated Nav channel targeting in the heart requires an ankyrin-G–dependent cellular pathway
John S. Lowe, Oleg Palygin, Naina Bhasin, Thomas J. Hund, Penelope A. Boyden, Erwin Shibata, Mark E. Anderson, and Peter J. Mohler
J. Cell Biol. 2008 180: 173-186. [Abstract] [Full Text] [PDF]





  Home | Help | Feedback | Subscriptions | Archive | Search | Table of Contents