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Understanding The Role Of DNMT1 SUMOylation In Acute Myeloid Leukaemia
Funder
National Health and Medical Research Council
Funding Amount
$639,290.00
Summary
Most cancers have abnormally high levels of DNA methylation, which turns off cell death genes, making cancer cells immortal. We have a new drug, called DNMT1i, that targets this feature of cancer cells and we recently found a new drug target that enhances the activity of DNMT1i. Our research will determine how these two drugs synergise to effectively kill cancer cells and will justify their use in clinical trials, which we believe will improve outcomes for patients with cancer.
In this project we aim to define the role of the Siah proteins in tumour angiogenesis and inflammatory responses. Hypoxia, a decrease in oxygen tension, places constrains on tumour growth where access to oxygen is yet to be established via new blood vessel formation. In addition hypoxia is common in areas of inflammation and wound healing, where blood vessels have been shut down to help in recovery. With the use of our Siah knockout mice we have a unique model that allows us, for the first time, ....In this project we aim to define the role of the Siah proteins in tumour angiogenesis and inflammatory responses. Hypoxia, a decrease in oxygen tension, places constrains on tumour growth where access to oxygen is yet to be established via new blood vessel formation. In addition hypoxia is common in areas of inflammation and wound healing, where blood vessels have been shut down to help in recovery. With the use of our Siah knockout mice we have a unique model that allows us, for the first time, to investigate the role of Siah in the hypoxia signalling cascade. How cells sense and react to low oxygen levels is complex and involves several proteins. A key protein is called Hypoxia induced factor, Hif-1. It accumulates under hypoxia and is responsible for the expression of genes enabling the cell to tolerate and function under hypoxic conditions. tolerate and function under hypoxic conditions, which is involved in new blood vessel formation. PHD protein directs the degradation of Hif1, while Siah directs the degradation of PHD, when oxygen is limiting. Loss of Siah proteins (eg in our knockout models) leads to an increase in PHD proteins under hypoxia thus no stabilisation of Hif-1 and impaired response to hypoxia. Thus, sitting on the top of a cascade, which controls the trashing of proteins in the cell (focus of this year's Nobel price for medicine), Siah has primary control on the response to oxygen deprivation. The relative immunity of multicellular organisms to acquired defects is through redundancy. Oxygen is a unique case, for which organisms can not bypass the defect via redundancy, making it an attractive target for future therapy. Therefore, understanding the molecular and cellular response to hypoxia may allow us to identify key molecules which could be targeted for the development of novel anti inflammatory and cancer drugs. The scope of this study is to understand the key role of Siah utilising our knockout mice in models of inflammation and cancer.Read moreRead less
Exploring The Role Of Arrcd4 In Extracellular Vesicle Biogenesis And Its Implications In Tissue Homeostasis
Funder
National Health and Medical Research Council
Funding Amount
$678,742.00
Summary
Most cells in the body release small packages known as extracellular vesicles (or EVs in short), which carry proteins and other cellular material. EVs transport important cellular messages required for the everyday function of cells and play crucial roles both in normal wellbeing and disease. This proposal will investigate how EVs are formed, how they select their protein content and how they contribute to the maturation of some cell types in the body.
Characterising An Important Control Point In Cholesterol Synthesis Beyond HMG-CoA Reductase
Funder
National Health and Medical Research Council
Funding Amount
$480,739.00
Summary
The statins are the ‘go-to’ drugs for treating heart disease; blocking a very early, highly-controlled step in the pathway producing cholesterol. However, they inhibit the production of other vital molecules which explains why some patients do not tolerate them. We have identified that a later enzyme in this pathway is also highly controlled and here aim to characterise the molecular mechanisms involved. This work could translate into the development of even safer drugs for treating cholesterol- ....The statins are the ‘go-to’ drugs for treating heart disease; blocking a very early, highly-controlled step in the pathway producing cholesterol. However, they inhibit the production of other vital molecules which explains why some patients do not tolerate them. We have identified that a later enzyme in this pathway is also highly controlled and here aim to characterise the molecular mechanisms involved. This work could translate into the development of even safer drugs for treating cholesterol-related diseases.Read moreRead less
Identification Of Orphan F-box Helicase Substrates And Their Role In Genomic Stability And Life Extension.
Funder
National Health and Medical Research Council
Funding Amount
$281,684.00
Summary
Within each cell proteins are synthesised and destroyed with delicate control to ensure the cell functions appropriately. Excess proteins are removed by specific degradation pathways, which are often misregulated in cancer. This project aims to further our understanding of misregulated protein degradation in cancer. The knowledge gained will assist with the development of cancer targeting drugs specific to protein degradation pathways that become misregulated in tumour formation.
A Novel Mechanism For Regulating Membrane Proteins By Ubiquitin Ligases And Their Adaptors
Funder
National Health and Medical Research Council
Funding Amount
$627,897.00
Summary
Many membrane proteins act as ion channels, transporters or receptors for extracellular ligands and are critical to normal functioning of the cell. These proteins are generally regulated by transport to or from the membrane to ensure that correct levels are maintained at the membrane. This proposal is to study a novel way of regulating membrane proteins. The successful completion of the work will provide important knowledge relevant to many human diseases.
Molecular Basis Of Artemisinin Action And Resistance In Plasmodium Falciparum
Funder
National Health and Medical Research Council
Funding Amount
$758,464.00
Summary
The malaria parasite, P. falciparum causes ~450,000 deaths each year. Resistance to the front-line antimalarial drug, artemisinin, is increasing, threatening at least another 100,000 lives per year, and potentially causing an additional ~A$500M in lost productivity. This project will identify the components of the parasite's cellular defence system that underpin resistance and will point to strategies for overcoming resistance to this important drug class.
Mutations In Ubiquitin Proteasome Pathway Genes As A Cause Of Frontotemporal Dementia And Motor Neuron Disease
Funder
National Health and Medical Research Council
Funding Amount
$639,860.00
Summary
This project aims to identify genes that are mutated in families affected with dementia and motor neuron disease, and to determine whether the same genes are responsible for disease in large collections of patients with similar disorders. Identifying these genes will reveal what biological processes can lead to brain and nerve cell degeneration, providing knowledge important for development of new treatments for the many people worldwide affected with these disorders.
Determining The Role Of Parkin And PACRG In Protein Turnover
Funder
National Health and Medical Research Council
Funding Amount
$555,780.00
Summary
Alterations in the parkin gene are associated with neurodegenerative disorders such as Parkinson's disease (PD). The aim of this proposal is to characterise the function of parkin and the role it plays in disease development. We will determine the role of parkin in the brain and how loss of this function causes specific nerve cells to die. These studies will provide the means to develop novel therapeutic approaches to alleviate or prevent these disorders.
Regulation Of PML By E6AP: Implications For Tumour Development.
Funder
National Health and Medical Research Council
Funding Amount
$537,829.00
Summary
PML is a vital tumour suppressor, but little is known about its regulation. We established that PML levels are affected by another cellular protein E6AP. This study will define the mechanism by which E6AP influences PML. Human cancers will be screened for the involvement of these proteins, to gain new insights into cancer onset. The intended practical outcome of these studies is to aid cancer diagnosis and provide new anti-cancer drugs.