photo of Dr James McNamara

Dr James McNamara

Dr James McNamara

Details

Role Team Leader / Senior Research Officer
Research area Stem cell biology

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

  • McNamara, JW, Parker, BL, Voges, HK, Mehdiabadi, NR, Bolk, F, Ahmad, F, Chung, JD, Charitakis, N, Molendijk, J, Zech, ATL, et al. Alpha kinase 3 signaling at the M-band maintains sarcomere integrity and proteostasis in striated muscle. Nature Cardiovascular Research 2(2) : 159 -173 2023
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  • McNamara, JW, Schuckman, M, Becker, RC, Sadayappan, S. A Novel Homozygous Intronic Variant in TNNT2 Associates With Feline Cardiomyopathy. Frontiers in Physiology 11: 608473 2023
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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 2023
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  • McNamara, JW, Li, A, Lal, S, Bos, JM, Harris, SP, van der Velden, J, Ackerman, MJ, Cooke, R, dos Remedios, CG. MYBPC3 mutations are associated with a reduced super-relaxed state in patients with hypertrophic cardiomyopathy. PLOS ONE 12(6) : e0180064 2023
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  • Yogeswaran, A, Troidl, C, McNamara, JW, Wilhelm, J, Truschel, T, Widmann, L, Aslam, M, Hamm, CW, Sadayappan, S, Lipps, C. The C0-C1f Region of Cardiac Myosin Binding Protein-C Induces Pro-Inflammatory Responses in Fibroblasts via TLR4 Signaling. Cells 10(6) : 1326 2023
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