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Functional Importance Of Oxidative Post-Translational Modifications Of Ryanodine Receptor In Cardiac Sarcoplasmic Reticulum Ca2+ Handling During Oxidative Stress, Stefan R. Mazurek
Functional Importance Of Oxidative Post-Translational Modifications Of Ryanodine Receptor In Cardiac Sarcoplasmic Reticulum Ca2+ Handling During Oxidative Stress, Stefan R. Mazurek
Dissertations
Free ionic calcium (Ca2+) plays an essential role as a second messenger that initiates muscle contraction in the heart. Ryanodine receptor (RyR2) acts as the primary Sarcoplasmic Reticulum (SR) Ca2+ release channel in the heart. In the event that intracellular SR Ca2+ handling is compromised, both the contractility and electrical excitability of the heart can be altered. As a consequence, heart function may not be able to maintain the necessary cardiac output to meet the metabolic demand of the body.
Increased oxidation of RyR2 has been implicated in abnormal Ca2+ handling that promotes the onset and progression of cardiovascular disease. …
Haploinsufficiency Of Cardiac Myosin Binding Protein-C In The Development Of Hypertrophic Cardiomyopathy, David Barefield
Haploinsufficiency Of Cardiac Myosin Binding Protein-C In The Development Of Hypertrophic Cardiomyopathy, David Barefield
Dissertations
Heart Failure is one of the leading causes of morbidity and mortality in the human population and represents a common endpoint for several diseases including inherited cardiomyopathies. Hypertrophic Cardiomyopathy (HCM) is characterized by left ventricular wall thickening, diastolic dysfunction, and sarcomere disarray. Mutations in sarcomeric protein encoding genes have been established as causative for HCM.
The gene MYBPC3, encoding cardiac myosin binding protein-C (cMyBP-C), is the second most commonly mutated gene in HCM cases. As a majority of these mutations have been determined to result in a null allele which does not produce any protein, it is thought that haploinsufficiency …