Dr. James McNamara is a researcher in the Heart Disease and Regeneration Group at The Murdoch Children’s Research Institute. His research has focused on molecular mechanisms of hypertrophic cardiomyopathy, a common form of genetic heart disease. This research led to the discovery that mutations linked to hypertrophic cardiomyopathy increased the number of active myosin motors in mouse and human hearts, providing a mechanism for how these mutations impair contraction, relaxation, and energy utilisation. He received his PhD in Medicine from the University of Sydney in 2017. He then undertook undertake postdoctoral training at the University of Cincinnati, supported by an American Heart Association Postdoctoral Fellowship for this period and continued to focus on the function of MYBPC3, establishing a mechanism for its role in adrenergic signaling in the heart. In 2020 he joined Prof. Enzo Porrello and A/Prof David Elliott’s groups at MCRI. Here, he continues to study molecular mechanisms of genetic heart diseases, now utilising human pluripotent stem cells as a human model of disease. James’ research is currently supported by multiple early career fellowships.
Dr. James McNamara is a researcher in the Heart Disease and Regeneration Group at The Murdoch Children’s Research Institute. His research has focused on molecular mechanisms of hypertrophic cardiomyopathy, a common form of genetic heart disease. ...
Dr. James McNamara is a researcher in the Heart Disease and Regeneration Group at The Murdoch Children’s Research Institute. His research has focused on molecular mechanisms of hypertrophic cardiomyopathy, a common form of genetic heart disease. This research led to the discovery that mutations linked to hypertrophic cardiomyopathy increased the number of active myosin motors in mouse and human hearts, providing a mechanism for how these mutations impair contraction, relaxation, and energy utilisation. He received his PhD in Medicine from the University of Sydney in 2017. He then undertook undertake postdoctoral training at the University of Cincinnati, supported by an American Heart Association Postdoctoral Fellowship for this period and continued to focus on the function of MYBPC3, establishing a mechanism for its role in adrenergic signaling in the heart. In 2020 he joined Prof. Enzo Porrello and A/Prof David Elliott’s groups at MCRI. Here, he continues to study molecular mechanisms of genetic heart diseases, now utilising human pluripotent stem cells as a human model of disease. James’ research is currently supported by multiple early career fellowships.
Top Publications
Robbins, N, Gilbert, M, Kumar, M, McNamara, JW, Daly, P, Koch, SE, Conway, G, Effat, M, Woo, JG, Sadayappan, S, et al.
Probenecid Improves Cardiac Function in Patients With Heart Failure With Reduced Ejection Fraction In Vivo and Cardiomyocyte Calcium Sensitivity In Vitro..
J Am Heart Assoc
7(2)
:
2018
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Grimes, KM, Barefield, DY, Kumar, M, McNamara, JW, Weintraub, ST, de Tombe, PP, Sadayappan, S, Buffenstein, R.
The naked mole-rat exhibits an unusual cardiac myofilament protein profile providing new insights into heart function of this naturally subterranean rodent..
Pflugers Arch
469(12)
:
1603 -1613
2017
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Dos Remedios, CG, Lal, SP, Li, A, McNamara, J, Keogh, A, Macdonald, PS, Cooke, R, Ehler, E, Knöll, R, Marston, SB, et al.
The Sydney Heart Bank: improving translational research while eliminating or reducing the use of animal models of human heart disease..
Biophys Rev
9(4)
:
431 -441
2017
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Nguyen, L, McNamara, J, Dos Remedios, C, Li, A, Lal, S.
Increased Phosphorylation of Cardiac Myosin Binding Protein C and Increased Expression of Troponin I in Normal Human Ageing.
Biophysical Journal
112(3)
:
557a
2017
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Viswanathan, SK, Sanders, HK, McNamara, JW, Jagadeesan, A, Jahangir, A, Tajik, AJ, Sadayappan, S.
Hypertrophic cardiomyopathy clinical phenotype is independent of gene mutation and mutation dosage..
PLoS One
12(11)
:
e0187948
2017
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