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

dc.contributor.committeeChair	Richard Hoover
dc.creator	Lowe, John Stewart
dc.date.accessioned	2020-08-23T16:00:43Z
dc.date.available	2010-12-01
dc.date.issued	2008-12-01
dc.description.abstract	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.
dc.format.mimetype	application/pdf
dc.identifier.uri	https://etd.library.vanderbilt.edu/etd-12012008-163706
dc.identifier.uri	http://hdl.handle.net/1803/14960
dc.subject	ankyrin-G
dc.subject	Nav1.5
dc.subject	Sodium channels -- Pathophysiology
dc.subject	Heart -- Pathophysiology
dc.subject	Arrhythmia -- Pathophysiology
dc.title	Targeting of the cardiac voltage-gated sodium channel 1.5 requires an ankyrin-G-dependent pathway
dc.type	dissertation
dc.type.material	text
local.embargo.lift	2010-12-01
local.embargo.terms	2010-12-01
thesis.degree.discipline	Pathology
thesis.degree.grantor	Vanderbilt University
thesis.degree.level	dissertation
thesis.degree.name	PHD

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