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

Rachel Pass, Karen Frudd, James P. Barnett, Claudia A. Blindauer, David R. Brown

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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 PrPSc in cells and resistance to prion infection. These studies strengthen the link between manganese and prion disease.
Original languageEnglish
Pages (from-to)186-193
Number of pages8
JournalMolecular and Cellular Neuroscience
Volume68
Early online date5 Aug 2015
DOIs
Publication statusPublished - Sep 2015

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Prions
Manganese
Zinc
Infection
Homeostasis
Metalloproteins
Prion Diseases
Prion Proteins
Copper
Cell Line

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Prion infection in cells is abolished by a mutated manganese transporter but shows no relation to zinc. / Pass, Rachel; Frudd, Karen; Barnett, James P.; Blindauer, Claudia A.; Brown, David R.

In: Molecular and Cellular Neuroscience, Vol. 68, 09.2015, p. 186-193.

Research output: Contribution to journalArticle

Pass, Rachel ; Frudd, Karen ; Barnett, James P. ; Blindauer, Claudia A. ; Brown, David R. / Prion infection in cells is abolished by a mutated manganese transporter but shows no relation to zinc. In: Molecular and Cellular Neuroscience. 2015 ; Vol. 68. pp. 186-193.
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