Macromolecular Structure Laboratory - Honours in 2010
An Honours project undertaken in this lab would be administered by the Discipline of Pathology.
Focuses on understanding mechanisms underlying cardiovascular disease. Our group uses biochemical techniques (protein preparation, spectroscopic measurements), molecular techniques (PCR, in situ hybridization, real time PCR) and histopathology in our research.
- Recent interesting publications
- Oakley, CE, Chamoun, J, Brown, LJ, Hambly, BD. (2007) Myosin binding protein-C: enigmatic regulator of cardiac contraction. Int J Biochem Cell Biol 39: 2161-6.
- Harris, AK, Shen, J, Radford, J, Bao, S and Hambly, BD. (2009) GM-CSF deficiency delays neointima formation in a normolipidemic mouse model of endoluminal endothelial damage. Immunol Cell Biol 87(2):122-30.
Protein defects causing familial hypertrophic cardiomyopathy
Supervisor + contact details:
The commonest form of inherited heart disease is familial hypertrophic cardiomyopathy (FHC). We know that about 30% of all families with this disease have a mutation in a gene expressing the heart protein myosin binding protein-C (MyBP-C). This protein is an important protein in the heart that is responsible for adjusting the contraction of the heart in response to stress (adrenergic stimulation). MyBP-C does this by modifying the interaction between the key contractile proteins actin and myosin within the cardiomyocytes. Mutations that occur in FHC in MyBP-C interfere with this modulatory function, but the structural basis for these abnormalities is very poorly understood. These studies involve the use of DNA coding for MyBP-C to express parts of the MyBP-C protein, to allow us to study the protein, mainly using spectroscopic techniques, especially fluorescence spectroscopy.





