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

dc.creatorLowe, John Stewart
dc.date.accessioned2020-08-23T16:00:43Z
dc.date.available2010-12-01
dc.date.issued2008-12-01
dc.identifier.urihttps://etd.library.vanderbilt.edu/etd-12012008-163706
dc.identifier.urihttp://hdl.handle.net/1803/14960
dc.description.abstractThe 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.mimetypeapplication/pdf
dc.subjectankyrin-G
dc.subjectNav1.5
dc.subjectSodium channels -- Pathophysiology
dc.subjectHeart -- Pathophysiology
dc.subjectArrhythmia -- Pathophysiology
dc.titleTargeting of the cardiac voltage-gated sodium channel 1.5 requires an ankyrin-G-dependent pathway
dc.typedissertation
dc.type.materialtext
thesis.degree.namePHD
thesis.degree.leveldissertation
thesis.degree.disciplinePathology
thesis.degree.grantorVanderbilt University
local.embargo.terms2010-12-01
local.embargo.lift2010-12-01
dc.contributor.committeeChairRichard Hoover


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