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The molecular mechanisms of thrombosis and haemostasis

  • Full or part time
  • Application Deadline
    Applications accepted all year round
  • Self-Funded PhD Students Only
    Self-Funded PhD Students Only

About This PhD Project

Project Description

A healthy cardiovascular system relies on the cells lining the blood vessels (endothelial cells) and heart cells (cardiomyocytes) to function normally. In cardiovascular disease the blood vessels narrow due to the formation of an atherosclerotic plaque. If the plaque ruptures, platelets, whose job it is to prevent bleeding under normal conditions, become activated and form a thrombus. This thrombus can block the blood vessel, or break away (embolise), causing a blockage elsewhere. This can cause a heart attack or stroke.

Tyrosine kinases play an essential role in the activation of many cell types, including platelets. This project will investigate how some of these kinases are regulated, and which signalling networks they play roles in. Drugs which target these kinases are already an area of interest to the pharmaceutical industry for treatment of some cancers and some autoimmune diseases. What application these drugs may have in the treatment of cardiovascular disease remains to be discovered.

Based in the Institute for Cardiovascular and Metabolic Research, School of Biological Sciences, which provides a multidisciplinary interactive research environment for over 30 research groups, this project will provide an excellent opportunity for training in a wide range of basic molecular and cell biology methods including flow cytometry, immunoprecipitation, functional assays such as platelet aggregometry and real-time flow-adhesion, as well as specialist training in microscopy techniques such as confocal.

References

‘Fibrin activates GPVI in human and mouse platelets’ Alshehri OM*, Hughes CE*, Montague S, Watson SK, Frampton J, Bender M, Watson SP (*joint first authors). Blood 2015 126(13) 1601-8.

‘The N-terminal SH2 domain of Syk is required for (hem)ITAM but not integrin signalling in mouse platelets’ Hughes CE, Finney BA, Koentgen F, Lowe KL, Watson SP. Blood 2015 125(1) 144-54.

‘Critical role for an acidic amino acid region in platelet signalling by the hemITAM (hemi-Immunoreceptor Tyrosine-based Activation Motif) containing receptor CLEC-2 (C-type Lectin receptor-2)’ Hughes CE, Sinha U, Pandey A, Eble JA, O'Callaghan CA, Watson SP. JBC 2013 288(7) 5127-35

‘G6f-like is an ITAM-containing collagen receptor in thrombocytes’ Hughes CE, Radhakrishnan UP, Egginton S, Dijkstra JM, Jagadeeswaran P, Watson SP. PLOS ONE 2012 7(12) e52622

‘CLEC-2 is not required for platelet aggregation at arteriolar shear’ Hughes CE, Navarro-Núñez L, Finney BA, Mourão-Sá D, Pollitt AY, Watson SP. JTH 2010 8(10) 2328-32

‘CLEC-2 activates Syk through dimerisation’ Hughes CE, Pollitt AY, Mori J, Eble JA, Tomlinson MG, Hartwig JH, O’Callaghan CA, Fütterer K, Watson SP. Blood 2010 115(14) 2947-55

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