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Stengel, A. ; Bach, C. ; Vorberg, I.* ; Frank, O.* ; Gilch, S.* ; Lutzny, G.* ; Seifarth, W.* ; Erfle, V. ; Maas, E.* ; Schätzl, H.* ; Leib-Mösch, C. ; Greenwood, A.D.

Prion infection influences murine endogenous retrovirus expression in neuronal cells.

Biochem. Biophys. Res. Commun. 343, 825-831 (2006)
Open Access Green as soon as Postprint is submitted to ZB.
Prions as causative agents of transmissible spongiform encephalopathies have been well investigated in experimental and modelling work. However, little is known about the molecular pathogenesis of prion-induced encephalopathies, the role of co-factors, and the interaction of prions with cellular components. We investigated the influence of prion infection on expression of murine endogenous retroviruses (ERVs), which compose approximately 10% of the mouse genome. Hypothalamic neuronal cells (GT1) and neuroblastoma cells (N2a) were examined. Both cell lines can be persistently infected with mouse adapted prion strains, i.e., RML. Using a mammalian retrovirus-specific DNA microarray and quantitative PCR methods, we compared the expression profiles of ERVs in prion-infected, uninfected, and anti-prion compound-treated murine neuronal cell lines, including clonal cell populations. The results suggest that prion infection influences ERV expression in neuronal cell lines, that this influence is cell line-specific, ERV-specific, and responsive to anti-prion compound treatment.
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Publication type Article: Journal article
Document type Scientific Article
Keywords endogenous retrovirus; prions; neuron; DNA microarray; GT1
Language english
Publication Year 2006
HGF-reported in Year 0
ISSN (print) / ISBN 0006-291X
e-ISSN 1090-2104
Journal Biochemical and Biophysical Research Communications
Quellenangaben Volume: 343, Issue: , Pages: 825-831 Article Number: , Supplement: ,
Publisher Elsevier
Reviewing status Peer reviewed
Institute(s) Institute of Virology (VIRO)
POF-Topic(s) 30203 - Molecular Targets and Therapies
Research field(s) Immune Response and Infection
PSP Element(s) G-502700-001
Erfassungsdatum 2006-12-20
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