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

  • 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, 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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  • Ng, Y-K, Blazev, R, McNamara, J, Dutt, M, Molendijk, J, Porrello, E, Elliott, D, Parker, B. Affinity purification-mass spectrometry and single fiber physiology/proteomics reveals mechanistic insights of C18ORF25. 2023
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  • Blazev, R, Carl, CS, Ng, Y-K, Molendijk, J, Voldstedlund, CT, Zhao, Y, Xiao, D, Kueh, AJ, Miotto, PM, Haynes, VR, et al. Phosphoproteomics of three exercise modalities identifies canonical signaling and C18ORF25 as an AMPK substrate regulating skeletal muscle function. Cell Metabolism 34(10) : 1561 -1577.e9 2022
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  • McNamara, J, Parker, B, Voges, H, Mehdiabadi, N, Bolk, F, Chung, J, Charitakis, N, Molendijk, J, Lal, S, Ramialison, M, et al. Alpha kinase 3 signaling at the M-band maintains sarcomere integrity and proteostasis in striated muscle. 2022
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