Permanent URL to this publication: http://dx.doi.org/10.5167/uzh-4648
Julius, C; Hutter, G; Wagner, U; Seeger, H; Kana, V; Kranich, J; Klöhn, P C; Weissmann, C; Miele, G; Aguzzi, A (2008). Transcriptional stability of cultured cells upon prion infection. Journal of Molecular Biology, 375(5):1222-1233.
- Registered users only
View at publisher
Prion infections induce severe disruption of the central nervous system with neuronal vacuolation and extensive glial reactions, and invariably lead to death of affected individuals. The molecular underpinnings of these events are not well understood. To better define the molecular consequences of prion infections, we analyzed the transcriptional response to persistent prion infection in a panel of three murine neural cell lines in vitro. Colony spot immunochemistry assays indicated that 65-100% of cells were infected in each line. Only the Nav1 gene was marginally modulated in one cell line, whereas transcripts previously reported to be derailed in prion-infected cells were not confirmed in the present study. We attribute these discrepancies to the experimental stringency of the current study, which was performed under conditions designed to minimize potential genetic drifts. These findings are at striking variance with gene expression studies performed on whole brains upon prion infections in vivo, suggesting that many of the latter changes represent secondary reactions to infection. We conclude that, surprisingly, there are no universal transcriptional changes induced by prion infection of neural cells in vitro.
1 download since deposited on 11 Nov 2008
0 downloads since 12 months
|Item Type:||Journal Article, refereed, original work|
|Communities & Collections:||04 Faculty of Medicine > University Hospital Zurich > Institute of Neuropathology|
|DDC:||570 Life sciences; biology
610 Medicine & health
|Deposited On:||11 Nov 2008 15:18|
|Last Modified:||02 Dec 2013 16:37|
Users (please log in): suggest update or correction for this item
Repository Staff Only: item control page