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Cambridge Cardiovascular



My research group focuses on how platelets and other cells are controlled during thrombosis. We are particularly interested in procoagulant platelets, a subpopulation of activated platelets that promote thrombin generation and release microparticles. We are also developing new models of arterial, venous and microvascular thrombosis so that we can understand these diseases in greater detail.


Key publications: 

Chloride channels are necessary for full platelet phosphatidylserine exposure and procoagulant activity. Harper MT, Poole AW. Cell Death Dis. 2013 Dec 19;4:e969.

Transient receptor potential channels function as a coincidence signal detector mediating phosphatidylserine exposure. Harper MT, Londoño JE, Quick K, Londoño JC, Flockerzi V, Philipp SE, Birnbaumer L, Freichel M, Poole AW. Sci Signal. 2013 Jun 25;6(281):ra50.

Bcl-xL-inhibitory BH3 mimetic ABT-737 depletes platelet calcium stores. Harper MT, Poole AW. Blood. 2012 May 3;119(18):4337-8.

Store-operated calcium entry and non-capacitative calcium entry have distinct roles in thrombin-induced calcium signalling in human platelets. Harper MT, Poole AW. Cell Calcium. 2011 Oct;50(4):351-8.

PKC inhibition markedly enhances Ca2+ signaling and phosphatidylserine exposure downstream of protease-activated receptor-1 but not protease-activated receptor-4 in human platelets. Harper MT, Poole AW. J Thromb Haemost. 2011 Aug;9(8):1599-607.

Most recent publications are available through PubMed.

Fellow in Pharmacology Jesus College
University Lecturer in Pharmacology


Person keywords: 
phosphatidylserine exposure
cell death
anti-platelet drugs
coagulation factors