Keith Spriggs
Lecturer in Gene Regulation, Faculty of Science
Contact
Biography
I was awarded my PhD from the Division of Genetics, University of Nottingham in 2000, following which I held post-doctoral positions in the Department of Biochemistry, University of Leicester, where I developed my interest in post-transcriptional regulation of gene expression. After further post-doctoral work in the Department of Biochemistry and Molecular Medicine at UC Davis, California, and the School of Pharmacy, University of Nottingham, I was appointed as a Lecturer in Gene Regulation here in the School of Pharmacy in November 2006.
Summary of Academic Career
PhD Structure and evolution of the vertebrate transcription elongation factor TFIIS, with Dr Garry Morgan, University of Nottingham.
2001-2004 Postdoctoral Research Associate: Department of Biochemistry, University of Leicester, with Professor Anne Willis. Funded by BBSRC. Project aims were to investigate some of the mechanisms behind internal ribosome entry.
2004-2006 Postdoctoral Research Associate, University of Nottingham, UK & University of California, Davis, USA. Funded by the Wellcome Trust.
2006-Present Lecturer in Gene Regulation, School of Pharmacy, University of Nottingham.
Research Summary
Recently the focus of my research has been the RNA helicase eIF4A, the most abundant eukaryotic translation initiation factor. eIF4A is required for maximal expression of mRNAs with structured 5'… read more
Recent Publications
WADELIN, FRANCES, FULTON, JOEL, MCEWAN, PAUL A, SPRIGGS, KEITH A, EMSLEY, JONAS and HEERY, DAVID M, 2010. Leucine-rich repeat protein PRAME: expression, potential functions and clinical implications for leukaemia. Molecular cancer. 9, 226 LE QUESNE, JOHN P C, SPRIGGS, KEITH A, BUSHELL, MARTIN and WILLIS, ANNE E, 2010. Dysregulation of protein synthesis and disease. The Journal of pathology. 220(2), 140-51 COBBOLD, L C, WILSON, L A, SAWICKA, K, KING, H A, KONDRASHOV, A V, SPRIGGS, K A, BUSHELL, M and WILLIS, A E, 2010. Upregulated c-myc expression in multiple myeloma by internal ribosome entry results from increased interactions with and expression of PTB-1 and YB-1. Oncogene. 29(19), 2884-91 BOTTLEY, ANDREW, PHILLIPS, NICOLA M, WEBB, THOMAS E, WILLIS, ANNE E and SPRIGGS, KEITH A, 2010. eIF4A inhibition allows translational regulation of mRNAs encoding proteins involved in Alzheimer's disease. PloS one. 5(9),
Current Research
Recently the focus of my research has been the RNA helicase eIF4A, the most abundant eukaryotic translation initiation factor. eIF4A is required for maximal expression of mRNAs with structured 5' UTRs, yet there remains much to understand about its mechanisms of action and its effects on global gene regulation. The observation that genes involved in important cell regulatory processes tend to have long structured 5' UTRs provides a obvious though largely unexplored route through which eIF4A could coordinately regulate gene expression. We know that eIF4A expression, and expression of its inhibitor Pdcd4, are important in cell growth and differentiation but the specific targets are largely unknown.
By using translational profiling techniques in combination with multiple approaches to compromising eIF4A function, we can identify novel targets of eIF4A mediated gene control, and better understand the processes involved. As eIF4A is an important protein in cancer, we are also interested in the potential of eIF4A inhibitors as novel therapeutic agents.