The Australian Research Data Commons (ARDC) invites you to participate in a short survey about your
interaction with the ARDC and use of our national research infrastructure and services. The survey will take
approximately 5 minutes and is anonymous. It’s open to anyone who uses our digital research infrastructure
services including Reasearch Link Australia.
We will use the information you provide to improve the national research infrastructure and services we
deliver and to report on user satisfaction to the Australian Government’s National Collaborative Research
Infrastructure Strategy (NCRIS) program.
Please take a few minutes to provide your input. The survey closes COB Friday 29 May 2026.
Complete the 5 min survey now by clicking on the link below.
A unified model of amino acid homeostasis. This project aims to develop a unified model of amino acid homeostasis in mammalian cells and apply it to brain cells. The model will be underpinned by a mathematical algorithm that allows predicting amino acid levels in the cytosol based on fundamental parameters such as transport and metabolism. This project should provide the significant benefit of enabling the prediction of essential functions such as cell growth and survival.
Dynamic Trafficking Of Amino Acid Transporters At Synapses And Their Role In Regulating Neurotransmission
Funder
National Health and Medical Research Council
Funding Amount
$421,219.00
Summary
Brain cells release chemical neurotransmitters to activate their neighbours. The most abundant neurotransmitter is glutamate, which mediates most of the communication in the brain. Following release, this neurotransmitter must be rapidly recycled to prevent levels being depleted and neurotransmission failing. The subject of this grant is to understand what molecules and pathways are used to recycle glutamate in the brain, and how its supply is controlled to sustain continual brain activation.
Epigenetic Programming Of Immune Development In Utero: Role Of The Maternal Environment In The Allergy Epidemic
Funder
National Health and Medical Research Council
Funding Amount
$764,463.00
Summary
This study will provide new insights into the development of allergic disease. Specifically, we will explore the hypothesis that allergic disease and other disorders or immune dysregulation occur as a result of gene-environmental interactions in early life, and that these events begin in pregnancy when the developing fetus is still developing and most susceptible to these effects.
Examination Of The Molecular Pharmacology Of Anthracyclines Induced Via Their Interaction With Iron
Funder
National Health and Medical Research Council
Funding Amount
$618,401.00
Summary
Anthracyclines are highly effective anti-cancer drugs, but their use is limited by toxic effects on the heart. This is thought to be due to these drugs directly binding iron (Fe). Indeed, we showed that anthracyclines induced marked changes in the way heart cells utilise Fe (DR1-3, 38; Mol. Pharmacol. 2002, 2003, 2004, 2005). We were the first to show that anthracyclines prevent Fe release from the criticial Fe storage protein ferritin. This prevents the use of Fe for vital processes eg. DNA and ....Anthracyclines are highly effective anti-cancer drugs, but their use is limited by toxic effects on the heart. This is thought to be due to these drugs directly binding iron (Fe). Indeed, we showed that anthracyclines induced marked changes in the way heart cells utilise Fe (DR1-3, 38; Mol. Pharmacol. 2002, 2003, 2004, 2005). We were the first to show that anthracyclines prevent Fe release from the criticial Fe storage protein ferritin. This prevents the use of Fe for vital processes eg. DNA and haem synthesis. Hence, this effect probably contributes to the cytotoxic activity of anthracyclines on the heart. We showed that novel drugs developed in my lab that bind Fe called chelators show high activity in animals (DR4) and prevent anthracycline-mediated Fe accumulation in ferritin. Importantly, Fe chelators have been shown to inhibit anthracycline-mediated cardiotoxicity. Indeed, the clinically used cardioprotective agent, ICRF-187, is actually an Fe chelator (5, DR6). However, ICRF-187 is not totally successful in terms of its cardioprotective effects and can cause myelosuppression (5, DR6). While the clinically used chelator, desferrioxamine (DFO), can prevent anthracycline-mediated cardiotoxicity, its poor membrane permeability limits its effectiveness. Our chelators are highly permeable and overcome the disadvantages of DFO (DR4). Thus, they are vital to examine for preventing anthracycline-mediated cardiotoxicity. In this proposal we will examine the changes in Fe metabolism induced by anthracyclines and test the hypothesis that novel Fe chelators may prevent the cardiotoxicity of these agents. We also aim to be the first to assess if preparation of anthracyclines which cannot bind iron prevents their cardiotoxicity. This will be done by preparing metal complexes of these drugs which prevent Fe-binding eg. anthracycline-zinc complexes. These studies are important for the development of less cardiotoxic forms of these very useful anti-tumour agents.Read moreRead less
Understanding The Acute And Cumulative Metabolic Effects Of Prolonged Sitting In Adults
Funder
National Health and Medical Research Council
Funding Amount
$416,597.00
Summary
Sedentary behaviour (sitting time) has been linked to an increased risk of chronic illnesses, including type 2 diabetes and obesity, but recent evidence suggests that light-intensity activity (non-exercise activities of daily living) is associated with reduced risk. These studies will examine whether breaking up sitting time with frequent short periods of activity can overcome the negative effects of prolonged sitting on blood glucose and blood fats in overweight older adults.
How do apicomplexan parasites steal amino acids from their hosts? The single-celled parasites that cause malaria and toxoplasmosis are adept at stealing nutrients from the host animals that they infect. How they do this is, however, poorly understood. This project seeks to identify the processes by which these parasites scavenge amino acids, an essential class of nutrient, from their hosts. Using innovative experimental approaches, the project aims to identify and characterise the parasite prote ....How do apicomplexan parasites steal amino acids from their hosts? The single-celled parasites that cause malaria and toxoplasmosis are adept at stealing nutrients from the host animals that they infect. How they do this is, however, poorly understood. This project seeks to identify the processes by which these parasites scavenge amino acids, an essential class of nutrient, from their hosts. Using innovative experimental approaches, the project aims to identify and characterise the parasite proteins that mediate the uptake of different amino acids into the parasite. The intended outcomes of the project are to provide comprehensive insights into a fundamental aspect of parasite biology, and inform strategies to treat the diseases caused by these parasites by cutting off their nutrient supply.Read moreRead less
Role of a novel zinc-binding motif in the structure-function of deubiquitinating enzymes. The ubiquitin pathway destroys many proteins that control cell function and growth, by attaching ubiquitin to them and marking them for degradation. Deubiquitinating enzymes (DUBs) regulate protein destruction by controlling the amount of ubiquitin attached. DUBs and the ubiquitin pathway can also be manipulated in biotechnology applications. However, very little is known about the structure/function of DUB ....Role of a novel zinc-binding motif in the structure-function of deubiquitinating enzymes. The ubiquitin pathway destroys many proteins that control cell function and growth, by attaching ubiquitin to them and marking them for degradation. Deubiquitinating enzymes (DUBs) regulate protein destruction by controlling the amount of ubiquitin attached. DUBs and the ubiquitin pathway can also be manipulated in biotechnology applications. However, very little is known about the structure/function of DUBs. We have identified a new zinc-binding motif in DUBs, and we will explore how this contributes to their structure, and interactions with other proteins. This will significantly enhance our knowledge of how DUBs function in both biotechnology and in controlling cell function.Read moreRead less
Protein degradation in mammals. One mechanism by which the regulation of protein turnover occurs is the balance between the activity of enzymes responsible for the ubiquitination and deubiquitination of target proteins. The majority of targets of this second family of enzymes are unknown. This project proposes a method for the identification of the targets of two specific mammalian deubiquitinating enzymes in order to understand their function and to begin to explore this new research field. ....Protein degradation in mammals. One mechanism by which the regulation of protein turnover occurs is the balance between the activity of enzymes responsible for the ubiquitination and deubiquitination of target proteins. The majority of targets of this second family of enzymes are unknown. This project proposes a method for the identification of the targets of two specific mammalian deubiquitinating enzymes in order to understand their function and to begin to explore this new research field. Knowledge about this new aspect of protein degradation could provide a powerful tool to test the effect of the stabilisation or removal of specific proteins in the cell and also to develop new technologies in protein production.Read moreRead less
Regulating nutrient uptake in intracellular parasites. Parasites impose a major economic and medical burden on human societies. In order to grow and reproduce, parasites scavenge nutrients from their animal or human hosts. As they move within and between hosts they encounter different levels of nutrients; how they adapt to these differences is poorly understood. This project aims to investigate the mechanisms by which the model parasite Toxoplasma senses and responds to the nutrients in its envi ....Regulating nutrient uptake in intracellular parasites. Parasites impose a major economic and medical burden on human societies. In order to grow and reproduce, parasites scavenge nutrients from their animal or human hosts. As they move within and between hosts they encounter different levels of nutrients; how they adapt to these differences is poorly understood. This project aims to investigate the mechanisms by which the model parasite Toxoplasma senses and responds to the nutrients in its environment, thereby shedding light on how they adapt to the different environments that they inhabit and, in the longer term, informing novel treatment strategies that aim to limit the parasites’ nutrient supply.Read moreRead less
Mitochondrial Iron Overload And Friedreich's Ataxia: The Role Of Frataxin In Iron And Haem Metabolism
Funder
National Health and Medical Research Council
Funding Amount
$285,990.00
Summary
Friedreich's ataxia (FA) is due to the lack of a protein known as frataxin. Recent studies using Baker's yeast have shown that the deletion of frataxin results in the accumulation of toxic iron in the mitochondrion. More recently, a variety of studies have shown that FA patients have iron loading within their cells. The iron build-up may cause severe damage. At present, the role of frataxin in mammalian mitochondrial iron metabolism is unknown. Our preliminary studies demonstrate that frataxin i ....Friedreich's ataxia (FA) is due to the lack of a protein known as frataxin. Recent studies using Baker's yeast have shown that the deletion of frataxin results in the accumulation of toxic iron in the mitochondrion. More recently, a variety of studies have shown that FA patients have iron loading within their cells. The iron build-up may cause severe damage. At present, the role of frataxin in mammalian mitochondrial iron metabolism is unknown. Our preliminary studies demonstrate that frataxin is down-regulated by either erythroid differentiation or the haem precursor protoporphyrin IX (Becker and Richardson, submitted). These data strongly suggest a role for frataxin in iron metabolism. In the present study we will continue to assess if frataxin plays a role in the way cells handle iron. Using a unique model of mitochondrial iron overload developed in my lab (Richardson et al. (1996) BLOOD 87:3477), we will extensively investigate the iron metabolism of the mitochondrion in order to determine the function of frataxin and its role in Friedreich's ataxia. In addition, we have developed a series of new drugs known as iron chelators that can enter the mitochondrion due to their high lipid solubility (Becker and Richardson 1999 J. Lab. Clin. Med. 134:510). These latter drugs are far more effective than the chelator currently used to treat iron overload, desferrioxamine (DFO). Indeed, our chelators have been designed to result in high iron chelation efficacy but low toxicity (see Becker and Richardson, 1999). This exciting research may be crucial in understanding the development of FA and in creating new therapies such as the use of iron chelators.Read moreRead less