English   español  
Please use this identifier to cite or link to this item: http://hdl.handle.net/10261/156721
Share/Impact:
Statistics
logo share SHARE logo core CORE   Add this article to your Mendeley library MendeleyBASE

Visualizar otros formatos: MARC | Dublin Core | RDF | ORE | MODS | METS | DIDL
Exportar a otros formatos:

Title

Role of the cellular prion protein in oligodendrocyte precursor cell proliferation and differentiation in the developing and adult mouse CNS

AuthorsBribián, Ana; Fontana, X.; Llorens, Franc; Gavín, Rosalina; Reina, M.; García-Verdugo, J.M.; Torres, J. M.; Castro Soubriet, Fernando de ; del Río, J.A.
Issue Date2012
PublisherPublic Library of Science
CitationPLoS ONE 7 (2012)
AbstractThere are numerous studies describing the signaling mechanisms that mediate oligodendrocyte precursor cell (OPC) proliferation and differentiation, although the contribution of the cellular prion protein (PrP c) to this process remains unclear. PrP c is a glycosyl-phosphatidylinositol (GPI)-anchored glycoprotein involved in diverse cellular processes during the development and maturation of the mammalian central nervous system (CNS). Here we describe how PrP c influences oligodendrocyte proliferation in the developing and adult CNS. OPCs that lack PrP c proliferate more vigorously at the expense of a delay in differentiation, which correlates with changes in the expression of oligodendrocyte lineage markers. In addition, numerous NG2-positive cells were observed in cortical regions of adult PrP c knockout mice, although no significant changes in myelination can be seen, probably due to the death of surplus cells. © 2012 Bribián et al.
URIhttp://hdl.handle.net/10261/156721
DOI10.1371/journal.pone.0033872
Identifiersdoi: 10.1371/journal.pone.0033872
issn: 1932-6203
Appears in Collections:(IC) Artículos
Files in This Item:
File Description SizeFormat 
Plos One 2012.pdf1,16 MBAdobe PDFThumbnail
View/Open
Show full item record
Review this work
 

Related articles:


WARNING: Items in Digital.CSIC are protected by copyright, with all rights reserved, unless otherwise indicated.