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Targeting of the cardiac voltage-gated sodium channel 1.5 requires an ankyrin-G-dependent pathway

The focus of this project is determining if an ankyrin-G-dependent pathway controls the membrnae expression of the voltage-gated sodium channel 1.5 in cardiomyocytes. Disruption of the normal localization of Nav1.5 can result in Brugada syndrome and has been linked to myopathic disease.
This project defines that an ankyrin-G-based pathway is required for the expression, localization and function of Nav1.5 at the cariomyocyte plasma membrane.

Identiferoai:union.ndltd.org:VANDERBILT/oai:VANDERBILTETD:etd-12012008-163706
Date01 December 2008
CreatorsLowe, John Stewart
ContributorsRichard Hoover
PublisherVANDERBILT
Source SetsVanderbilt University Theses
LanguageEnglish
Detected LanguageEnglish
Typetext
Formatapplication/pdf
Sourcehttp://etd.library.vanderbilt.edu/available/etd-12012008-163706/
Rightsunrestricted, I hereby certify that, if appropriate, I have obtained and attached hereto a written permission statement from the owner(s) of each third party copyrighted matter to be included in my thesis, dissertation, or project report, allowing distribution as specified below. I certify that the version I submitted is the same as that approved by my advisory committee. I hereby grant to Vanderbilt University or its agents the non-exclusive license to archive and make accessible, under the conditions specified below, my thesis, dissertation, or project report in whole or in part in all forms of media, now or hereafter known. I retain all other ownership rights to the copyright of the thesis, dissertation or project report. I also retain the right to use in future works (such as articles or books) all or part of this thesis, dissertation, or project report.

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