Prof Nigel Pyne Seminar

Nigel Pyne

Prof Nigel Pyne, Ph.D,
Strathclyde Institute for Pharmacy and Biomedical Sciences,
University of Strathclyde,
Glasgow, UK.

Date: Thursday, 17 September, 2015
Time: 11:00 am – 12:00 pm
Venue: MD1-08-03E
Chairperson: Dr. Deron R. Herr

Role of Sphingosine 1-phosphate in disease.
Professor Nigel Pyne obtain his BSc in Biochemistry in 1982 from the University of Birmingham (UK) and his PhD in Biochemistry from the University of Manchester (UK) in 1985. He undertook his post-doctoral work at the University of Glasgow with Professor Miles Houslay on insulin signaling. Since, 1989, he has worked within the Strathclyde Institute of Pharmacy and Biomedical Sciences (SIPBS) at the University of Strathclyde. With Professor Susan Pyne he has studied the bioactive lipid, sphingosine-1 phosphate since 1994 and has published approx. 80 papers in this area (164 papers in total). Professor Nigel Pyne is a recipient of the Sandoz Prize (awarded by the British Pharmacological Society, 1995) for contributions to Pharmacology. He is an elected member of the Academy of Science of the Institute of Bologna (founded in 1690), Editor in Chief of the international scientific journal, Cellular Signalling and co-founder of Mironid Ltd (2014-present). The research on the bioactive lipid sphingosine 1-phosphate has focussed specifically on the role of sphingosine kinase 1 and 2 (the enzymes that catalyse formation of sphingosine 1-phosphate) and sphingosine 1-phosphate receptors in the control of cell biology in health and disease. Specific investigation has been on the functional interaction of S1P receptors with receptor tyrosine kinases and oncogenes and the role of sphingosine kinase in regulating cell survival, migration and growth. Sphingosine kinases and S1P receptors represent targets for a potential therapeutic intervention in the treatment of cancer, inflammation, cardiovascular diseases and infection. Their role in disease and opportunities for novel drug discovery in this area will be discussed.

 

Save