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Dr Wayne Roberts

PositionLecturer in Medical Sciences
LocationL28b, Richmond building
DepartmentSchool of Medical Sciences
Telephone+44 (0) 1274 232131

Research Interests (key words only)

Platelets, thrombosis, diabetes, cancer

Teaching and Supervisory Responsibilities

Clinical Sciences Foundation Year

  • Biology
  • Special Studies
  • Personal and Professional development

Clinical Sciences First Year

  • Nutrition and Energy
  • Special Studies
  • Personal and Professional development

Clinical Sciences Second Year

  • Special Studies & Personal and Professional Development

Clinical Sciences Final Year

  • Special Studies Dissertation module

Biomedical Sciences Final Year

  • Research project module
  • Research Topics 2

Biomedical Sciences

  • MSc Research projects

Administrative Responsibilities

Module leader Clinical Sciences Foundation Year Biology.

Study History

2001-2005: Degree: 1st class BSc (Hons) Biomedical Sciences from The University of Bradford

2005-2008: PhD: ‘The regulation of platelet-extracellular matrix interactions by Nitric oxide’ from The University of Bradford

2008-2011: British Heart Foundation funded postdoctoral position looking at the regulation of platelet-nitric oxide interactions by Thrombospondin-1 at Hull-York Medical School

2011-2013: PGCE from The University of Leeds and teaching experience within secondary school

2013-current: Lecturer in Medical Sciences at The University of Bradford

Research Areas

Inappropriate platelet activation leading to thrombosis is the biggest killer in the western world. Diabetic patients are at a particularly high risk of developing thrombosis. Our current work is looking at how platelets are hyper-activated in diabetes.

Thrombotic episodes are also a big killer of cancer patients, yet relatively little is known about the interactions between platelets and tumour cells. Platelets release many factors which may promote or reduce cancer progression. Current projects are investigating how platelets aid cancer cell adhesion, migration, invasion and proliferation and how this may be altered in disease conditions such as diabetes.

Current Projects

Investigating the regulation of hepatocellular carcinoma by platelets.

Identifying how advanced glycation end products regulate platelet function.


  • Liverani E, Banerjee S, Roberts W, Naseem KM, Perretti M. Prednisolone exerts exquisite inhibitory properties on platelet functions. Biochem Pharmacol. 2012 May 15;83(10):1364-73
  • Naseem KM, Roberts W. Nitric oxide at a glance. Platelets. 2011;22(2):148-52
  • Roberts W, Magwenzi S, Aburima A, Naseem KM. Thrombospondin-1 induces platelet activation through CD36-dependent inhibition of the cAMP/protein kinase A signaling cascade. Blood. 2010 Nov 18;116(20):4297-306
  • Irwin C, Roberts W, Naseem KM. Nitric oxide inhibits platelet adhesion to collagen through cGMP-dependent and independent mechanisms: the potential role for S-nitrosylation. Platelets. 2009 Nov;20(7):478-86
  • Roberts W, Michno A, Aburima A, Naseem KM. Nitric oxide inhibits von Willebrand factor-mediated platelet adhesion and spreading through regulation of integrin alpha(IIb)beta(3) and myosin light chain. J Thromb Haemost. 2009 Dec;7(12):2106-15
  • Roberts W, Riba R, Homer-Vanniasinkam S, Farndale RW, Naseem KM. Nitric oxide specifically inhibits integrin-mediated platelet adhesion and spreading on collagen. J Thromb Haemost. 2008 Dec;6(12):2175-85
  • Oberprieler NG, Roberts W, Riba R, Graham AM, Homer-Vanniasinkam S, Naseem KM. cGMP-independent inhibition of integrin alphaIIbbeta3-mediated platelet adhesion and outside-in signalling by nitric oxide. FEBS Lett. 2007 Apr 3;581(7):1529-34
  • Oberprieler NG, Roberts W, Graham AM, Homer-Vanniasinkam S, Naseem KM. Inhibition of ADP-induced platelet adhesion to immobilised fibrinogen by nitric oxide: evidence for cGMP-independent mechanisms. Biochem Pharmacol. 2007 May 15;73(10):1593-601
  • Riba R, Oberprieler NG, Roberts W, Naseem KM. Von Willebrand factor activates endothelial nitric oxide synthase in blood platelets by a glycoprotein Ib-dependent mechanism. J Thromb Haemost. 2006 Dec;4(12)






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