Inherited human disease, Bone and cartillage development disease (Connective tissue research)
Professor John Bateman is the Director of the Cell Biology Theme at the Murdoch Childrens Research Institute, and Head of the Skeletal Biology and Disease Research Group and is a Professorial Fellow of the University of Melbourne. His research interests include the molecular mechanisms of extracellular matrix protein assembly in health and disease and molecular genetics of musculoskeletal disease. A major focus of current research involves using mouse models of bone and cartilage disease to explore the fundamental disease mechanisms. Recently his laboratory has developed proteomic and RNA expression profiling approaches to study cartilage development and disease including osteoarthritis.
He has over 160 peer-reviewed publication and is an NHMRC Senior Principal Research Fellow.
He has served on the Editorial Boards of several journals including The Journal of Biological Chemistry; The Biochemical Journal, Matrix Biology. He is a Past-President of International Society of Matrix Biology and Matrix Biology of Australia and New Zealand. He is a member of the NHMRC Academy (Cell Biology and Biochemistry).
Contact me on 03 8341 6422 or email@example.com
to discuss how projects could be tailored to your specific research interests and to arrange a visit to our laboratories.
BSc (Hons) and PhD scholarships are available.
The cell biology of protein misfolding (ER stress) in genetic cartilage and bone disease
Inherited cartilage disorders affecting growth and joint function are a significant disease burden. Gene mutations have been defined, but our knowledge of the molecular mechanisms of how these mutations cause the disorders, and ultimately how these mechanisms could be therapeutically manipulated, is only just beginning to be explored. We have a major laboratory research program exploring how protein misfolding mutations cause cartilage and bone disease. Our research so far has shown that these unfolded proteins can cause cellular stress and activate intracellular signalling and degradation pathways (proteasomal and autophagy) that have profound effects on gene expression and cellular pathology (see Bateman et al., Nature Reviews Genetics 2009 Mar;10(3):173-83). Several projects are available which will explore the molecular signalling pathways and disease mechanisms using cutting-edge biochemical, molecular biology, cell biology (eg confocal microscopy) and proteomic analysis on cells transfected with mutant genes, and cells and tissues from mouse models. These studies will also explore the use of new therapeutic agents in cell culture to overcome protein misfolding and cell stress.
microRNAs in arthritis
Arthritis is a major healthcare problem, costing A$24 billion pa in clinical care and disability. While the crucial pathology in arthritis is the progressive destruction of articular cartilage, the molecular mechanisms of the initiation and progression of cartilage destruction are not clear. microRNAs