photo of Dr James McNamara

Dr James McNamara

Dr James McNamara

Details

Role Team Leader / Senior Research Officer
Research area Stem Cell Medicine

Contact

Available for student supervision
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

  • Ng, Y-K, Blazev, R, McNamara, JW, Dutt, M, Molendijk, J, Porrello, ER, Elliott, DA, Parker, BL. Affinity Purification-Mass Spectrometry and Single Fiber Physiology/Proteomics Reveals Mechanistic Insights of C18ORF25.. J Proteome Res 23(4) : 1285 -1297 2024
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  • Austin, R, Brown, JS, Casauria, S, Madelli, EO, Mattiske, T, Boughtwood, T, Metke, A, Davis, A, Horton, AE, Winlaw, D, et al. A multi-tiered analysis platform for genome sequencing: design and initial findings of the Australian Genomics Cardiovascular Disorders Flagship. Genetics in Medicine Open 101842 2024
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  • dos Remedios, CG, Law, KYC, McNamara, JW, Kraft, T, Peckham, M, van der Velden, J, Linke, WA, Ackerman, M, Sequeira, V, Lal, S, et al. The Molecular Basis of the Frank-Starling Law of the Heart: A Possible Role for PIEZO1?. 25: 99 -124 2024
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  • Song, T, McNamara, JW, Baby, A, Ma, W, Landim-Vieira, M, Natesan, S, Pinto, JR, Lorenz, JN, Irving, TC, Sadayappan, S. Unlocking the Role of sMyBP-C: A Key Player in Skeletal Muscle Development and Growth.. 2023
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  • McNamara, JW, Parker, B, Voges, H, Mehdiabadi, N, Bolk, F, Ahmad, F, Zech, A, Watt, K, Porrello, ER, Ellliott, D. Abstract P1030: Alpha Kinase 3 Signaling At The M-band Regulates Sarcomeric Protein Quality Networks. Circulation Research 133(Suppl_1) : 2023
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