Dysferlin And The Emergency Vesicle Fusion Of Membrane Repair
Funder
National Health and Medical Research Council
Funding Amount
$481,496.00
Summary
Membrane repair is a vital cell survival mechanism of all eukaryotic cells, using calcium-triggered vesicle fusion to ‘patch’ membrane ruptures. The muscular dystrophy protein dysferlin is a key mediator of membrane repair, although, exactly how dysferlin mends membranes has been unclear. We show that the calcium that floods through membrane tears, activates a group of enzymes called calpains, that specifically cleave dysferlin to release a specialist vesicle-fusion module for membrane repair.
Investigation Of Novel Mechanisms Regulating Platelet Reactivity During Haemostasis And Thrombosis
Funder
National Health and Medical Research Council
Funding Amount
$221,210.00
Summary
Platelets are small specialised blood cells that are critical for normal blood clotting and blood vessel repair following injury. We are studying the processes that enable platelets to stick to the site of vessel injury and to each other to form a stable blood clot. These very processes, when unchecked, are responsible for the formation of harmful blood clots in the bloodstream that may block blood vessels in the heart or brain and result in a heart attack or stroke. Many factors control how big ....Platelets are small specialised blood cells that are critical for normal blood clotting and blood vessel repair following injury. We are studying the processes that enable platelets to stick to the site of vessel injury and to each other to form a stable blood clot. These very processes, when unchecked, are responsible for the formation of harmful blood clots in the bloodstream that may block blood vessels in the heart or brain and result in a heart attack or stroke. Many factors control how big and how rapidly a blood clot grows and whether it becomes harmful enough to lead to a heart attack or stroke. One of these factors is the level of platelet 'reactivity' or 'stickiness' . We are working towards a better understanding of how platelet reactivity is regulated and how this dictates the potential of a blood clot to become harmful. This knowledge will not only increase our knowledge of blood clot formation in health and disease, but also help in the development of new therapies for the prevention of heart attack and stroke.Read moreRead less
Investigate The Role Of Ectoenzymes In Regulating The Haemostatic Function Of Human Platelets
Funder
National Health and Medical Research Council
Funding Amount
$215,882.00
Summary
Platelets are cells found in the blood that are essential for stopping bleeding after injury. These cells stick to the blood vessel wall and initiate the formation of a blood clot which plugs the injured blood vessel. Similiar processes are involved in the formation of harmful blood clots that block blood vessels in the heart or brain, causing heart attacks and stroks, respectively. Platelets stick to the blood vessel wall through proteins called receptors, which are located on the platelet surf ....Platelets are cells found in the blood that are essential for stopping bleeding after injury. These cells stick to the blood vessel wall and initiate the formation of a blood clot which plugs the injured blood vessel. Similiar processes are involved in the formation of harmful blood clots that block blood vessels in the heart or brain, causing heart attacks and stroks, respectively. Platelets stick to the blood vessel wall through proteins called receptors, which are located on the platelet surface. We are investigating the processes that naturally regulate these receptors and therefore modulate the adhesive properties of platelets. We have found that a group of enzymes, also located on the platelet surface, remove these receptors, thereby limiting the ability of these cells to stick to blood vessels and form clots. Unravelling these processes will not only help with our understanding of clot formation in health and disease, but also with the potential development of new therapies for the prevention of heart disease and stroke.Read moreRead less
The Human Papilloma Virus Oncoprotein E7 Degrades The Retinoblastoma Protein By Enhancing Calpain Activity
Funder
National Health and Medical Research Council
Funding Amount
$258,067.00
Summary
Cervical cancer is the second most prevalent cancer worldwide and the fifth leading cause of cancer deaths in women. Approximately 470,000 new cases are diagnosed annually. In most cases cervical cancer is thought to be caused by certain types of the human papillomavirus. Human papillomavirus makes a seies of proteins that cause the destruction of key host proteins in the cells they infect. This destruction is central to the formation of cervical cancer. We have recently discovered that we can p ....Cervical cancer is the second most prevalent cancer worldwide and the fifth leading cause of cancer deaths in women. Approximately 470,000 new cases are diagnosed annually. In most cases cervical cancer is thought to be caused by certain types of the human papillomavirus. Human papillomavirus makes a seies of proteins that cause the destruction of key host proteins in the cells they infect. This destruction is central to the formation of cervical cancer. We have recently discovered that we can prevent this destruction and rescue the key host proteins using inhibitors of the enzyme calpain. Here we seek to determine whether calpain inhibitors could find application in the treatment of human papillomavirus associated cancer.Read moreRead less