Prion infection in cells is abolished by a mutated manganese transporter but shows no relation to zinc
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- 作者：Rachel Passa ; Karen Frudda ; James P. Barnettb ; Claudia A. Blindauerb ; David R. Browna ; bssdrb@bath.ac.uk" class="auth_mail" title="E-mail the corresponding author
- 关键词：AMPA ; 伪-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid ; BSE ; bovine spongiform encephalopathy ; CJD ; Creutzfeldt-Jakob disease ; vCJD ; the variant of CJD ; F14 ; PrP knockout fusion cell line ; F21 ; wild-type fusion cell line ; ICP-MS ; inductively-coupled plasma mass spectrometry ; MTF-1 ; metal-regulatory transcription factor 1 ; N2a ; neuro 2a neuroblastoma cell line ; PK ; proteinase K ; PrP ; prion protein ; PrPSc ; abnormal isoform of PrP ; SPCA ; secretory pathway calcium ATPase-1 ; SPCA-Q746A ; mutant of
- 刊名：Molecular and Cellular Neuroscience
- 出版年：2015
- 出版时间：September 2015
- 年：2015
- 卷：68
- 期：Complete
- 页码：186-193
- 全文大小：790 K
文摘
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We studied the impact of PrP expression on levels of zinc and manganese in cells.
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10">We found no relation between the prion protein and zinc metabolism.
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15">Prion infected cells have higher levels of manganese.
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A mutant manganese transporter diminishes manganese in prion infected cells.
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Reduction of manganese in cells cures them of prion infection.