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
Toepfer, CN, Wakimoto, H, Garfinkel, AC, McDonough, B, Liao, D, Jiang, J, Tai, AC, Gorham, JM, Lunde, IG, Lun, M, et al.
Hypertrophic cardiomyopathy mutations in MYBPC3 dysregulate myosin.
Science Translational Medicine
11(476)
:
2019
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McNamara, JW, Sadayappan, S.
Skeletal myosin binding protein-C: An increasingly important regulator of striated muscle physiology.
Archives of Biochemistry and Biophysics
660:
121 -128
2018
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McNamara, JW, Grimes, KM, Sadayappan, S.
Basic Cardiovascular Sciences Scientific Sessions 2018.
Circulation Research
123(9)
:
1024 -1029
2018
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McNamara, JW, Lynch, TL, Song, T, Rubinstein, JL, Sadayappan, S.
Abstract 303: Fast Skeletal Myosin Binding Protein-c Expression in Heart Failure.
Circulation Research
123(Suppl_1)
:
2018
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Meng, Q, Bhandary, B, Osinska, H, James, J, Shay-Winkler, K, Gulick, J, McNamara, J, Bhuiyan, MS, Sadayappan, S, Robbins, J.
Abstract 265: TGF Beta Signaling and Fibrosis in cMyBP-C-dependent Cardiac Disease.
Circulation Research
123(Suppl_1)
:
2018
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