How is Bam32 regulated in platelets and does it contribute to platelet function and thrombosis?

Contribution of the PI(3,4,5)P3 binding adaptor protein Bam32 to PI3 kinase-mediated platelet function and arterial thrombosis

Thrombosis is a serious condition that can develop when a blood vessel becomes damaged and small blood cells called platelets stick to the damaged area, forming a clot. If the clot breaks away from the vessel wall, it can block an artery leading to the heart or brain, causing heart attack or stroke. Medications that are currently used to control clotting can cause unwanted side-effects, and this research could lead to new, safer treatments. Dr Ingeborg Hers has been awarded a three-year grant to study platelets which important in controlling bleeding, but also contribute to life-threatening thrombosis. When platelets become activated, they clump together to form a blood clot. Dr Hers has identified a key molecule that acts on a protein called Bam32 to cause platelet activation. Platelets contain lots of Bam32 protein and it may be a key factor in platelet clot formation. Dr Hers plans to find out how Bam32 is controlled in platelets and how it contributes to platelet activation and thrombosis. The results of this study will help scientists better understand how platelets are activated, so they can devise new ways to prevent dangerous clots from forming.