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The role of the prion protein in copper metabolism
Reference
BS410549
Principal Investigator / Supervisor
Professor Nigel Hooper
Co-Investigators /
Co-Supervisors
Professor David Coates
Institution
University of Leeds
Department
Inst of Molecular & Cellular Biology
Funding type
Research
Value (£)
177,116
Status
Completed
Type
Research Grant
Start date
01/03/1999
End date
01/03/2002
Duration
36 months
Abstract
Prion diseases are characterised by the conversion of the normal form of prion protein (PrPC) into an insoluble abnormal form (PrPSc). The prion protein is the causative agent of the transmissible spongiform encephalopathies. The role of PrPC in normal cellular function is unclear, although recent studies have implicated PrPC in cellular copper metabolism. The aim of this project is to investigate the biological role of PrPC, particularly its potential role in copper metabolism. To this end we will investigate how PrPC binds copper and whether disrupting this binding affects cellular functions or alters the conversion of PrPC to PrPSc. We will also examine whether PrPC through interaction of its GPI anchor with caveolae is involved in the cellular uptake of copper, an initiate the characterisation of prion-like proteins in C. elegans.
Summary
unavailable
Committee
Closed Committee - Agri-food (AF)
Research Topics
X – not assigned to a current Research Topic
Research Priority
X – Research Priority information not available
Research Initiative
Biology of Spongiform Encephalopathies - Phase 4 (BS4) [1998]
Funding Scheme
X – not Funded via a specific Funding Scheme
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