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
McNamara, JW, Schuckman, M, Becker, RC, Sadayappan, S.
A Novel Homozygous Intronic Variant in TNNT2 Associates With Feline Cardiomyopathy..
Front Physiol
11:
608473
2020
view publication
Li, A, Nelson, SR, Rahmanseresht, S, Braet, F, Cornachione, AS, Previs, SB, O'Leary, TS, McNamara, JW, Rassier, DE, Sadayappan, S, et al.
Skeletal MyBP-C isoforms tune the molecular contractility of divergent skeletal muscle systems..
Proc Natl Acad Sci U S A
116(43)
:
21882 -21892
2019
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Ge, Z, Li, A, McNamara, J, dos Remedios, C, Lal, S.
Pathogenesis and pathophysiology of heart failure with reduced ejection fraction: translation to human studies.
Heart Failure Reviews
24(5)
:
743 -758
2019
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Singh, RR, McNamara, JW, Sadayappan, S.
Abstract 915: Dysregulation of the Myosin and Myosin Binding Protein-C interaction in Hypertrophic Cardiomyopathy.
Circulation Research
125(Suppl_1)
:
2019
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McNamara, JW, Schwanekamp, JA, Patel, PN, Viswanathan, SK, Bohlooly, M, Madeyski-Bengtson, K, Knöll, R, Seidman, JG, Seidman, CE, Sadayappan, S.
Abstract 772: The Highly Prevalent 25bp Intronic Deletion in MYBPC3 is Benign Under Baseline Conditions.
Circulation Research
125(Suppl_1)
:
2019
view publication