Thesis: Identifying the site/s of modification on human L-type calcium channel protein isoforms during oxidative stress
The L-type calcium channel (LTCC) is the major route for calcium influx into cardiac myocytes. Reactive oxygen species and calcium contribute to the development of cardiac hypertrophy. The oxidative redox modification of the L-type calcium channel is associated with an increase in protein synthesis leading to an onset of cardiac myocyte hypertrophy. This provides a direct evidence for the role of L-type calcium channel in development of pathology. As the cysteines in the channel respond to the redox modification we intend to identify the reactive cysteines on the channel protein that respond well to the oxidative stress. This would facilitate the development of a therapeutic target that will modify the channel’s response to the oxidative stress with the aim of reducing the development of cardiac hypertrophy.
Why my research is important
Cardiovascular disease is the leading cause of death in Australia. It kills one Australian every 12 minutes. Thus, this research aims to identify the therapeutic target for cardiac hypertrophy.