Professor Nathan Subramaniam

Biography

Prof Nathan Subramaniam is an NHMRC Senior Research Fellow and Research Capacity Building Professor in the School of Biomedical Sciences, QUT. Prof Nathan Subramaniam received his PhD from Purdue University, W. Lafayette, Indiana, USA. He did his research at Purdue and at the Department of Biochemistry, University of California at Davis, USA with Prof Don Carlson. He then joined the group of Prof Wanjin Hong at the Institute of Molecular and Cell Biology, Singapore, where he completed his postdoctoral training on cell biology and protein trafficking. Prof Nathan Subramaniam established his own research group, the Membrane Transport Laboratory at the Queensland Institute of Medical Research, Brisbane, Australia in 1999. He has an Honorary Professor appointment in the Faculty of Medicine and Biochemical Sciences, University of Queensland. In 2016 he was appointed a Research Capacity Building Professor as Professor in Biomedical Sciences (Molecular Medicine) at the Queensland University of Technology. He  established his research group, the Hepatogenomics Research Group, at the School of Biomedical Sciences, Institute of Health and Biomedical Innovation in August 2016. Prof Subramaniam's interests lie in the study of liver injury and understanding how the liver regulates iron homeostasis. Prof Subramaniam has many years of experience in the research of iron overload disorders and was instrumental in defining many genetic mutations associated with the iron overload disorder hereditary haemochromatosis.  His basic science interests include defining the functional consequences of these disease-causing mutations and elucidating the molecules and mechanisms regulating iron homeostasis. His group has developed novel Next-Generation sequencing tools to examine the molecular basis of iron disorders and novel in vitro and in vivo models to investigate liver injury and iron metabolism. An important area of research in the group is the study of liver diseases associated with liver injury, co-toxicity associated increased fat and iron, and liver fibrosis.