Our People

James Krycer

Dr | Senior Research Officer

Cardiac Bioengineering



I am fascinated by how cells balance nutrient supply with their bioenergetic demands. For instance, a surge of a nutrient will trigger transcription factors and/or kinases to modify the activity of enzymes required to metabolise this nutrient. Conversely, when a metabolite exceeds what is needed, signalling pathways reduce its synthesis or uptake. This interplay between signalling and metabolism was first observed mid last century with transcription operons in bacteria, and has since been shown to occur in many ways, with metabolites acting as signalling ligands or even substrates for post-translational modifications.

My passion for this area began with my PhD with Prof. Andrew Brown at the University of New South Wales (2009-2012), where I studied how the feedback from cholesterol metabolism to gene transcription is turned off in prostate cancer. This allows cells to accumulate cholesterol, an emerging pharmacological target for this disease. I then worked with Prof. David James at the University of Sydney (2013-2019), initially as a junior post-doc and subsequently funded by competitive fellowships. I examined how insulin regulates glucose metabolism, and the converse, in adipocytes.

These experiences allowed me to specialise in molecular metabolism, the intersection of molecular cell biology, systems biology, and metabolic biochemistry. For the latter, I use a combination of metabolomics, metabolic labelling (with stable and radioisotopes), and respirometry to comprehensively assess a cell’s metabolic phenotype. This will enable me to understand how cells balance metabolic supply and demand, which I believe is key to treating a range of complex diseases such as diabetes (nutrient oversupply) and cancer (high demand).


I joined the Cardiac Bioengineering laboratory to understand the role of metabolism in cardiac regeneration. The heart is a metabolic omnivore, capable of metabolising a range of nutrients such as glucose, fatty acids, and lactate. As the human heart matures in the first few weeks of life, the primary source of energy switches from the fermentation of glucose (glucose to lactate) to the oxidation of fatty acids (fatty acids to CO2). At the same time, cardiomyocytes (heart muscle cells) lose their ability to regenerate. Are the two connected and if so, how so? Solving this could be the key to heart regeneration, currently the holy grail for curing heart failure.


  • Senior Research Officer, QIMR Berghofer Medical Research Institute
  • Adjunct Associate Professor, School of Biomedical Sciences, Queensland University of Technology


  • 2014-2019: Research Fellow, Charles Perkins Centre and the University of Sydney
  • 2013: Research Officer, Garvin Institute of Medical Research
  • 2013: Research Associate, School of Biochemistry and Biomolecular Sciences, The University of New South Wales
  • 2008-2012: Casual academic, School of Biochemistry and Biomolecular Sciences, The University of New South Wales




  • 2018: Australian Diabetes Society Skip Martin Early Career Fellow
  • 2014-2017: NHMRC Early Career Fellow
  • 2011: UNSW Vice Chancellor’s Award for Teaching Excellence
  • 2010: Faculty of Science Award for Teaching Excellence


  • 2012: Doctor of Philosophy (Biochemistry & Molecular Genetics), The University of New South Wales, Sydney, Australia
  • 2008: Bachelor of Science (Hons I, University Medal), majoring in Molecular Biology, The University of New South Wales, Sydney, Australia