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dc.contributor.advisorTardiff, Jil C.en
dc.contributor.authorMcConnell, Mark
dc.creatorMcConnell, Marken
dc.date.accessioned2017-06-30T16:56:50Z
dc.date.available2017-06-30T16:56:50Z
dc.date.issued2017
dc.identifier.urihttp://hdl.handle.net/10150/624576
dc.description.abstractThe progression of genetically inherited cardiomyopathies from an altered protein structure to the clinical presentation of the disease is not well understood. One of the main roadblocks to mechanistic insight remains a lack of high-resolution structural information of multiprotein complexes within the cardiac sarcomere. One example is the tropomyosin (Tm) overlap region of the thin filament that is crucial for the function of the cardiac sarcomere. To address this central question, we devised coupled experimental and computational methods to characterize the baseline function and structure of the Tm overlap, as well as the effects that mutations causing divergent patterns of ventricular remodeling have on both structure and function.
dc.language.isoen_USen
dc.publisherThe University of Arizona.en
dc.rightsCopyright © is held by the author. Digital access to this material is made possible by the University Libraries, University of Arizona. Further transmission, reproduction or presentation (such as public display or performance) of protected items is prohibited except with permission of the author.en
dc.subjectcardiomyopathiesen
dc.subjecttropomyosinen
dc.subjecttroponinen
dc.titleInvestigating the Effects of Tropomyosin D230N and cTnT R92L on the Tropomyosin Overlap Regionen_US
dc.typetexten
dc.typeElectronic Dissertationen
thesis.degree.grantorUniversity of Arizonaen
thesis.degree.leveldoctoralen
dc.contributor.committeememberTardiff, Jil C.en
dc.contributor.committeememberGranzier, Hendrikusen
dc.contributor.committeememberRomanowski, Mareken
dc.contributor.committeememberSchwartz, Steven D.en
thesis.degree.disciplineGraduate Collegeen
thesis.degree.disciplineBiomedical Engineeringen
thesis.degree.namePh.D.en
refterms.dateFOA2018-04-26T18:27:04Z
html.description.abstractThe progression of genetically inherited cardiomyopathies from an altered protein structure to the clinical presentation of the disease is not well understood. One of the main roadblocks to mechanistic insight remains a lack of high-resolution structural information of multiprotein complexes within the cardiac sarcomere. One example is the tropomyosin (Tm) overlap region of the thin filament that is crucial for the function of the cardiac sarcomere. To address this central question, we devised coupled experimental and computational methods to characterize the baseline function and structure of the Tm overlap, as well as the effects that mutations causing divergent patterns of ventricular remodeling have on both structure and function.


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