Stephen S. Taylor, Ph.D.

Affiliations:	1992-1995	Biochemistry	University of Oxford, Oxford, United Kingdom
	1995-1998	Cell Biology	Harvard Medical School, Boston, MA, United States
	1998-2015	Faculty of Life Sciences	University of Manchester, Manchester, England, United Kingdom
	2015-	Manchester Cancer Research Centre	University of Manchester, Manchester, England, United Kingdom

Area:

Cell division, mitosis, spindle assembly checkpoint, anti-mitotic chemotherapeutics

Website:

http://www.bub1.com

Google:

"stephen taylor manchester"

Bio:

After completing his Bachelors degree in Biochemistry at the University of Manchester, Stephen moved to the Department of Biochemistry in Oxford to pursue his doctoral studies, working with Prof. Edwin Southern and Dr Chris Tyler-Smith. His graduate work focused on developing mammalian artificial chromosomes in order to define the DNA sequences required for human centromere function. After completing his PhD in 1995, Stephen moved to Harvard Medical School funded by a Wellcome Trust Traveling post-doctoral fellowship. There, he worked with Prof. Frank McKeon in the Department of Cell Biology, where he discovered several components of the mammalian spindle assembly checkpoint. In 1998, Stephen moved back to Manchester, funded by a BBSRC David Phillips Fellowship. In 2004 he was awarded a Senior Research Fellowship from Cancer Research UK. In 2009 Stephen renewed his CR-UK Senior Fellowship and was promoted to Professor of Cell Biology. He won the Translational Research Award from the British Association for Cancer Research in 2004, the University of Manchester’s Kilburn-Williams Medal in 2009, and was elected to Academia Europaea in 2010. In 2015, Stephen was awarded the Leech Chair of Pharmacology. During his time in Manchester, Stephen continued to be a pioneer in the spindle checkpoint field, and in collaboration with AstraZeneca described the first inhibitors targeting the Aurora B and Mps1 protein kinases. More recently his research has focused on understanding cell fate in response to anti-mitotic chemotherapy agents.
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