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The role of the prion protein in copper metabolism

ReferenceBS410549
Principal Investigator / Supervisor Professor Nigel Hooper
Co-Investigators /
Co-Supervisors
Professor David Coates
Institution University of Leeds
DepartmentInst of Molecular & Cellular Biology
Funding typeResearch
Value (£) 177,116
StatusCompleted
TypeResearch Grant
Start date 01/03/1999
End date 01/03/2002
Duration36 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 TopicsX – not assigned to a current Research Topic
Research PriorityX – Research Priority information not available
Research Initiative Biology of Spongiform Encephalopathies - Phase 4 (BS4) [1998]
Funding SchemeX – not Funded via a specific Funding Scheme
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