The 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.
| Identifer | oai:union.ndltd.org:arizona.edu/oai:arizona.openrepository.com:10150/624576 |
| Date | January 2017 |
| Creators | McConnell, Mark, McConnell, Mark |
| Contributors | Tardiff, Jil C., Tardiff, Jil C., Granzier, Hendrikus, Romanowski, Marek, Schwartz, Steven D. |
| Publisher | The University of Arizona. |
| Source Sets | University of Arizona |
| Language | en_US |
| Detected Language | English |
| Type | text, Electronic Dissertation |
| Rights | Copyright © 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. |
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