Directed Molecular Evolution Of G Protein-coupled Receptors For Stable And Functional Expression In Escherichia Coli
Funder
National Health and Medical Research Council
Funding Amount
$383,479.00
Summary
Approximately half of all prescription drugs on the market act on G protein coupled receptors (GPCRs). The mechanisms underlying GPCR function are mainly unknown due to a lack of structural information. No solved structures exist for any of the estimated 800 human GPCRs, making it difficult to design new drugs. By applying advanced protein engineering techniques I aim to produce human GPCRs in bacteria to ultimately acquire structural information, which will enable novel drug development.
Peptide Toxins From Animal Venoms Specifically Targeting Voltage-gated Sodium Channels As Novel Analgesics And Pesticides
Funder
National Health and Medical Research Council
Funding Amount
$316,449.00
Summary
This project aims to understand how certain animal toxins that cause analgesic and pesticidal effects in model animals interact with biological ion channels in atomistic detail using computational techniques. By understanding the detailed molecular interactions involved in the binding of the toxins to channels, toxin variants with improved potency and specificity may be designed as promising templates for novel analgesics and pesticides.
Alzheimer's, Huntington's and Parkinson's diseases involve the formation of protein aggregates, termed amyloid. The formation of amyloid leads to cell death and neurodegeneration. The most important cellular events perturbed by the formation of amyloid aggregates are unclear. Recent evidence suggests that sterols (including cholesterol) have an important role in cellular toxicity. This study will examine the molecular basis for this, enhancing our understanding of the amyloid diseases and could ....Alzheimer's, Huntington's and Parkinson's diseases involve the formation of protein aggregates, termed amyloid. The formation of amyloid leads to cell death and neurodegeneration. The most important cellular events perturbed by the formation of amyloid aggregates are unclear. Recent evidence suggests that sterols (including cholesterol) have an important role in cellular toxicity. This study will examine the molecular basis for this, enhancing our understanding of the amyloid diseases and could suggest novel therapeutic avenues.Read moreRead less
Structural Investigation Into The Regulation Of The Colony Stimulating Factor Receptor, C-FMS.
Funder
National Health and Medical Research Council
Funding Amount
$287,321.00
Summary
The colony stimulating factor receptor, c-FMS is a member of a family of protein signalling molecules expressed on the cell surface that are implicated in the development of serious diseases in humans, such as inflammatory diseases and cancer. A number of important proteins bind to and regulate c-FMS in different ways. I intend to visualise these interactions to further understand how c-FMS activity is controlled by alternative means.
Oligomers Of The Alzheimer's Amyloid-? Peptide: Structure, Mechanism Of Toxicity And Small Molecule Interactions
Funder
National Health and Medical Research Council
Funding Amount
$356,324.00
Summary
Alzheimer’s disease is a devastating neurodegenerative disease that currently affects 240 000 Australians. The protein called amyloid-? is found in deposits in the brains of Alzheimer’s patients. The toxic form of this protein is thought to be small aggregated particles called ‘oligomers’. This work aims to investigate the structure of these particles, the reason why they are toxic, as well as their interaction with the neuroprotective compound EGCG, which is found in green tea.
The Proteomics Of The Von Hippel-Lindau (VHL) Tumour Suppressor Protein
Funder
National Health and Medical Research Council
Funding Amount
$292,639.00
Summary
This project primarily intends to identify novel modifications to the von Hippel-Lindau (VHL) protein which plays a role in tumour suppression and blood vessel growth. It is the purpose of this project to characterise these changes to VHL and ultimately, understand what these changes mean to the function of VHL protein, and modulate them to ameliorate VHL disease.