Studying the proteins that make platelets stick together in a blood clot
Structural and functional dissection of the role of kindlin-3 in platelet aggregation
Robert Gilbert (lead researcher)
Oxford, University of
Start date: 10 November 2014 (Duration 2 years)
Coronary heart disease is the UK’s single biggest killer. Research to unravel the intricacies of blood clotting may reveal new ways to stop thrombosis, reducing the chance of severe illnesses such as heart attacks and strokes.
Blood clotting is essential for our bodies to recover from injury. But formation of blood clots, or thrombosis, inside our arteries can be dangerous, slowing down or stopping blood flow and leading to a stroke or a heart attack. Blood clots are made up of tiny cells called platelets, bound into a meshwork of proteins such as fibrin and collagen. For platelets to stick together, proteins called integrins are needed, which in turn are activated by another protein called kindlin-3.
Dr Robert Gilbert has been awarded a grant to understand the detailed structure of kindlin-3 when it is bound to integrins. This should explain why it binds some integrins and not others, and how kindlin-3 interacts with the membrane forming the outside of the platelet. They will also develop new tests to measure kindlin activity to trial it as a measure of anticlotting drug effectiveness.
||10 November 2014
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