Mechanisms Regulating Mitochondrial Outer Membrane Permeabilisation During Programmed Cell Death
Funder
National Health and Medical Research Council
Funding Amount
$306,562.00
Summary
Apoptosis is a form of cell suicide that is vital in human development and health by removing damaged or unwanted cells in a regulated manner. Disturbances in this pathway are known to be the cause of cancers and other diseases. This research will investigate how the pivotal step in cell death, termed mitochondrial outer membrane permeabilisation (MOMP) is regulated.
Unraveling The Dynamic Munc18a:Syntaxin1 Interaction Required For Neurotransmission
Funder
National Health and Medical Research Council
Funding Amount
$674,591.00
Summary
Membrane trafficking, the topic of the 2013 Nobel prize in Medicine, is required for delivery of cellular cargo. This research will investigate the interactions and structures of proteins from the neuronal membrane trafficking system. Understanding how this system operates will expand our knowledge of processes fundamental to learning and memory and may ultimately lead to development of selective therapeutics for treating a range of diseases.
Molecular Dissection Of The Munc18c:Syntaxin4 Complex Required For Insulin-regulated Exocytosis In Adipocytes
Funder
National Health and Medical Research Council
Funding Amount
$601,008.00
Summary
When blood glucose levels are high, insulin signals to fat and muscle cells to remove glucose from the blood. The uptake of glucose relies on membrane fusion events that deliver a specific glucose transporter protein to the cell surface in response to insulin signals. This process is affected in Type II diabetes. Our research will characterise the regulation of these membrane fusion events and will be important for understanding how insulin signals are communicated in health and disease.
The Role Of Intracellular Protein Trafficking In Alzheimer's Disease
Funder
National Health and Medical Research Council
Summary
Alzheimer’s disease (AD) is a progressive neurological disorder and is the most common cause of dementia. The development of therapies must be preceded by a thorough understanding of the molecular processes that underpin the disease. In this project we will examine the interactions between the Alzheimer’s precursor protein (APP) and the molecular machinery that controls its intracellular localization and breakdown to the toxic A? peptide that is central to disease pathology.
Understanding How Membrane Trafficking Controls The Levels Of Alzheimer's Disease Causing A? Peptides
Funder
National Health and Medical Research Council
Funding Amount
$478,905.00
Summary
Alzheimer’s disease is a progressive neurological disorder and is the most common cause of dementia. No effective treatments are currently available. The toxic amyloid peptide is central to disease pathology and is derived from breakdown of the Alzheimer’s amyloid precursor protein (APP). In this project we will examine the interactions between APP and the molecular machinery that controls its location in the cell and subsequent degradation.
The Role Of Protein Glycosylation In The Malaria Parasite
Funder
National Health and Medical Research Council
Funding Amount
$644,428.00
Summary
The parasites that cause malaria have unique proteins on their surface that are essential for infection of humans. These proteins are useful for making vaccines to train our immune system to recognize and block infection by the malaria parasite. Our latest research has shown that these proteins are modified with sugars that enhance parasite virulence. We are studying these modifications more closely to facilitate the development of improved malaria vaccines.
Investigations On Copper Regulated Trafficking Of Amyloid Precursor Protein Of Alzheimer's Disease
Funder
National Health and Medical Research Council
Funding Amount
$296,212.00
Summary
Sufferers of Alzheimer's disease have excessive levels of a particular protein (Abeta) as well as a copper imbalance in the brain. It is widely accepted that high Abeta content contributes to the onset of Alzheimer's disease. Copper imbalance in the brain also plays a major role in the pathology of the disease. This research aims to investigate the interplay between copper and the protein which gives rise to Abeta, with the view to developing targeted treatments for Alzheimer's patients.
Membrane Trafficking Of BACE1 And Amyloid Precursor Protein In Primary Neurons And The Production Of Abeta Amyloid Peptides
Funder
National Health and Medical Research Council
Funding Amount
$705,984.00
Summary
The development of Alzheimer’s disease results from the generation of toxic peptides by the cleavage of a membrane protein by an enzyme called BACE. A key feature of which regulates the generation of toxic peptides involves the movement of BACE between compartments in the cell by a process known as membrane transport. Our recent work has identified the itinerary of BACE in the cell. The studies here will reveal the molecular machinery of the BACE pathway in neurons. This fundamental informati
Effector Export In P. Falciparum Infected Human Erythrocytes
Funder
National Health and Medical Research Council
Funding Amount
$1,066,920.00
Summary
We will investigate malaria, a parasitic disease that kills over 450,000 people a year. We will explore how the parasite identifies, invades and remodels the host cells in which it lives, scavenging nutrients and hiding from the immune system. We will characterize the proteins involved in these critical events, as they are potential targets for drugs. We will study how parasites cause disease and how the host responds to infection.
Membrane Trafficking Of The ?-secretase, BACE1, And The Generation Of Alzheimer's Disease A? Amyloid Peptides
Funder
National Health and Medical Research Council
Funding Amount
$465,704.00
Summary
Alzheimer’s disease results from the production of toxic neuropeptides by the action of an enzyme called BACE. The generation of toxic peptides requires the movement or trafficking of BACE between different cell compartments. This research will reveal the molecular machinery of the BACE transport pathway. This new knowledge will provide a strategy to develop drugs to inhibit BACE activity and the production of the toxic peptide, which would be of significant benefit to patients and families.