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Mechanism Of Proteotoxic Stress Induced Type I Interferon Signalling And Implications For Human Disease
Funder
National Health and Medical Research Council
Funding Amount
$322,952.00
Summary
All cells have a proteasome system to degrade unwanted proteins. Proteasome dysfunction causes a build-up of proteins that triggers, through an unknown mechanism, activation of the immune system leading to inflammation. People with mutations in genes which code for proteasome activity experience a severe disease known as Proteasome-Associated Autoinflammatory Syndrome. We aim to elucidate the link between protein aggregation and immune activation and employ this knowledge in disease treatment.
Synthetic Approaches For Dissection Of The Signalling Response Heterogeneity And Targeted Therapeutic Use Of Type-1 Interferons
Funder
National Health and Medical Research Council
Funding Amount
$375,974.00
Summary
Type-1 interferons have been used to treat at least 14 diseases, including cancer, hepatitis and multiple sclerosis. Differing success of treatment and serious side effects felt by patients, however, have limited use of these otherwise powerful therapies. I aim to better understand the responses different cells have to interferons to improve their utility in the clinic. Also, I will develop approaches to target interferons to the site of disease, reducing the side effects felt by patients.
Identifying Novel Genome Instability Signatures In Cancer
Funder
National Health and Medical Research Council
Funding Amount
$320,891.00
Summary
Cancer is the single biggest clinical problem facing the world. An underlying hallmark of cancer is the accumulation of errors in the genetic information of a cell which arises through genomic instability. This research project aims to investigate novel molecules identified by our screening that function in response to genomic instability in cancer. This study is expected to define roles for each molecule in the maintenance of genomic stability and predict for patient diagnosis and outcome.
Investigating The Cellular Requirement For STIM1 Phosphorylation And Store-operated Calcium Entry Suppression During Mitosis: Roles In Development And Cancer
Funder
National Health and Medical Research Council
Funding Amount
$344,900.00
Summary
Cells are constantly interacting with and modifying their surrounding environment. The intracellular calcium signal is one mechanism cells use to translate signals from the microenvironment into cellular responses. This proposal seeks to explore why a key calcium signalling pathway, known as store-operated calcium entry, is specifically silenced during cell division, and to determine how reversing this inhibition affects cell division during normal development and in cancer.