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Prion infection in cells is abolished by a mutated manganese transporter but shows no relation to zinc.

Abstract
The cellular prion protein has been identified as a metalloprotein that binds copper. There have been some suggestions that prion protein also influences zinc and manganese homeostasis. In this study we used a series of cell lines to study the levels of zinc and manganese under different conditions. We overexpressed either the prion protein or known transporters for zinc and manganese to determine relations between the prion protein and both manganese and zinc homeostasis. Our observations supported neither a link between the prion protein and zinc metabolism nor any effect of altered zinc levels on prion protein expression or cellular infection with prions. In contrast we found that a gain of function mutant of a manganese transporter caused reduction of manganese levels in prion infected cells, loss of observable PrP(Sc) in cells and resistance to prion infection. These studies strengthen the link between manganese and prion disease.
AuthorsRachel Pass, Karen Frudd, James P Barnett, Claudia A Blindauer, David R Brown
JournalMolecular and cellular neurosciences (Mol Cell Neurosci) Vol. 68 Pg. 186-93 (Sep 2015) ISSN: 1095-9327 [Electronic] United States
PMID26253862 (Publication Type: Journal Article)
CopyrightCopyright © 2015 Elsevier Inc. All rights reserved.
Chemical References
  • Cation Transport Proteins
  • DNA-Binding Proteins
  • Membrane Transport Proteins
  • Prions
  • Receptors, AMPA
  • Slc30a1 protein, mouse
  • Transcription Factors
  • transcription factor MTF-1
  • Manganese
  • Endopeptidase K
  • Atp2c1 protein, mouse
  • Calcium-Transporting ATPases
  • Zinc
  • glutamate receptor ionotropic, AMPA 1
Topics
  • Animals
  • Calcium-Transporting ATPases (genetics, metabolism)
  • Cation Transport Proteins (genetics, metabolism)
  • Cell Line
  • DNA-Binding Proteins (genetics, metabolism)
  • Endopeptidase K (pharmacology)
  • Manganese (metabolism)
  • Membrane Transport Proteins (genetics, metabolism)
  • Mice
  • Mutation (genetics)
  • Prions (metabolism)
  • Receptors, AMPA (genetics, metabolism)
  • Transcription Factors (genetics, metabolism)
  • Transfection
  • Zinc (metabolism)

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