Cardiology
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Nicole

Assistant Professor in Cardiac Physiology
health
University of Canberra
Australia

Biography

Dr Beard and her research team investigate how intracellular calcium signaling pathways initiate muscle contraction. We explore and define the mechanisms which lead to control of calcium signalling and the way in which these are disrupted in skeletal myopathies, cardiomyopathy and heart failure. Muscle contraction occurs due to a cascade of events and relies on calcium release from intracellular stores. The four main cogs in the intracellular calcium signalling pathway are the calcium binding protein calsequestrin (CSQ), the ryanodine receptor (RyR) calcium release channel, and two linking proteins - triadin and junctin - which bind CSQ to the RyR. Control of calcium release in muscle is vital; disturbances in the process can lead to potentially fatal skeletal and cardiac conditions. Despite their essential role in skeletal muscle and the heart, the functional and structural interactions between the proteins that drive calcium signalling are poorly understood and form the broad aims of our research. Currently funded projects include: Calcium signalling by intracellular calcium stores: implications for muscle performance and athletic ability Calcium homeostatis disturbances and human heart failure Understanding how chemotherapy agents cause cardiotoxicity Dr Beard and her research team investigate how intracellular calcium signaling pathways initiate muscle contraction. We explore and define the mechanisms which lead to control of calcium signalling and the way in which these are disrupted in skeletal myopathies, cardiomyopathy and heart failure. Muscle contraction occurs due to a cascade of events and relies on calcium release from intracellular stores. The four main cogs in the intracellular calcium signalling pathway are the calcium binding protein calsequestrin (CSQ), the ryanodine receptor (RyR) calcium release channel, and two linking proteins - triadin and junctin - which bind CSQ to the RyR. Control of calcium release in muscle is vital; disturbances in the process can lead to potentially fatal skeletal and cardiac conditions. Despite their essential role in skeletal muscle and the heart, the functional and structural interactions between the proteins that drive calcium signalling are poorly understood and form the broad aims of our research. Currently funded projects include: Calcium signalling by intracellular calcium stores: implications for muscle performance and athletic ability Calcium homeostatis disturbances and human heart failure Understanding how chemotherapy agents cause cardiotoxicity

Research Interest

Heart failure Cardiomyopathy Skeletal muscle ageing and myopathy

Publications

  • Walweel K, Li, L, Molenaar, P, Imtiaz, MS, dos Remedios, CG, Beard, NA, Dulhunty, AF, van Helden, DF and Laver, DR. (accepted 28/06/14) Regulation of human RyR2 by Ca2+ and Mg2+ in the cytoplasm and in the lumen of the sarcoplasmic reticulum. J Gen Physiol

  • Hanna AD, Lam, A, Thekkedam, C, Gallant, EM, Beard, NA and Dulhunty, AF. (accepted 27/07/14) Cardiac ryanodine receptor activation by high Ca2+ store load is reversed in a reducing cytoplasmic redox environment. J Cell Sci

  • Hanna AD, Lam, A, Tham, S, Dulhunty, AF and Beard, NA. (2014) Adverse Effects of Doxorubicin and its Metabolic Product on Cardiac RyR2 and SERCA2A. Mol Pharmacol

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