Publication Date
2023
Document Type
Thesis
Committee Members
Andrew Ednie, Ph.D. (Advisor); Mark Rich, M.D., Ph.D. (Committee Member); Eric Bennett, Ph.D. (Committee Member)
Degree Name
Master of Science (MS)
Abstract
Abnormal glycosylation can impact cardiac proteins, affecting signaling, contraction, and metabolism, which leads to compromised cardiac function. O-GlcNAcylation, the only form of intracellular glycosylation, involves adding a single GlcNAc molecule to proteins via enzymes: O-GlcNAc Transferase (OGT) for addition and O-GlcNAcase (OGA) for removal. The Ednie/Bennett lab has previously demonstrated that in both chronic (OGT KO) and acute (OGT inhibition) models of reduced cardiomyocyte O-GlcNAcylation, a disruption of Ca2+ homeostasis occurs. This study delved into the cardiac voltage-gated sodium channel (NaV 1.5) in these models. NaV 1.5 expression was analyzed through western blotting and immunocytochemistry, while its functional activity was gauged using whole cell voltage-clamping. We also investigated how the trafficking proteins LITAF and NEDD4-2 might influence NaV 1.5 expression in the OGT KO. Initial results highlight distinct regulatory mechanisms, warranting additional studies
Page Count
74
Department or Program
Department of Neuroscience, Cell Biology, and Physiology
Year Degree Awarded
2023
Copyright
Copyright 2023, some rights reserved. My ETD may be copied and distributed only for non-commercial purposes and may not be modified. All use must give me credit as the original author.
Creative Commons License
This work is licensed under a Creative Commons Attribution-NonCommercial-No Derivative Works 4.0 International License.
ORCID ID
0000-0003-0524-2810
