Identifying the site/s of modification on human L-type calcium channel protein isoforms during oxidative stress

Padmapriya Muralidharan

    Research output: ThesisDoctoral Thesis

    225 Downloads (Pure)

    Abstract

    Heart disease is the leading cause of death in Australia. Reactive oxygen species and calcium ions play a significant role in the onset of cardiac hypertrophy. It is recognized that the function of the cell can be affected by changes in the redox state of the native L-type calcium channel (LTCC) protein caused by an altered level of intracellular ROS. Previous studies undertaken in our laboratory strongly suggest a direct role of LTCC in the development of cardiac pathology. Cysteines in the channel are likely targets for redox modification. This thesis investigates the site/s of modification on the human long N-terminal (LNT) isoform of the a 1c subunit of the LTCC protein during oxidative stress. The function of the purified human LNT isoform of Ca,1.2 in proteoliposomes was directly assessed by patch clamping. Mutation of three cysteines in the AID region attenuate the
    sensitivity of Ca,1.2 to oxidative stress.
    Original languageEnglish
    QualificationDoctor of Philosophy
    Supervisors/Advisors
    • Ingley, Evan, Supervisor
    • Hool, Livia, Supervisor
    Publication statusUnpublished - 2015

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