Role Of Oxidative Stress In Activating ATM To Protect Against Neurodegeneration
Funder
National Health and Medical Research Council
Funding Amount
$570,334.00
Summary
ATM is the protein defective in the human genetic disorder ataxia-telangiectasia (A-T). This project is designed to investigate how this protein is activated by oxidative stress. The study is largely a mechanistic one, to investigate changes occurring in ATM as part of the activation process. There is evidence that ATM exists in the cytoplasm in neuronal cells and understanding its function in these cells may assist in understanding the basis for neurodegeneration in A-T.
The overall goal of the program is to develop novel approaches to slow the progress or prevent neurodegeneration in patients with rare human genetic disorders. The second program is designed to develop novel therapeutics from snake venom proteins. These include proteins with anti-bleeding activity and those with application in wound healing. The third program involves the development of novel biomarkers for the early detection and prognosis in prostate cancer.