spacer gif spacer gif spacer gif spacer gif spacer gif
 QUICK SEARCH:   [advanced]


spacer gif
     Home     Help     Feedback     Subscriptions     Archive     Search    

The fully linked HTML version of this article has now been published.
JCS ePress online publication date 19 Oct 2004
doi: 10.1242/jcs.01484


This Article
Right arrow Full Text (PDF)
Right arrow All Versions of this Article:
jcs.01484v1
117/23/5591    most recent
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Crozet, C.
Right arrow Articles by Perrier, V.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Crozet, C.
Right arrow Articles by Perrier, V.
Social Bookmarking
 Add to CiteULike   Add to Complore   Add to Connotea   Add to Del.icio.us   Add to Digg   Add to Reddit   Add to Technorati   Add to Twitter  
What's this?

Research Article

Inhibition of PrPSc formation by lentiviral gene transfer of PrP containing dominant negative mutations


Carole Crozet, Yea-Lih Lin, Clément Mettling, Chantal Mourton-Gilles, Pierre Corbeau, Sylvain Lehmann, and Véronique Perrier*
* Author for correspondence (e-mail: vperrier{at}igh.cnrs.fr)

Currently, there is no treatment to cure transmissible spongiform encephalopathies. By taking advantage of the 'prion-resistant' polymorphisms Q171R and E219K that naturally exist in sheep and humans, respectively, we have evaluated a therapeutic approach of lentiviral gene transfer. Here, we show that VSV-G (vesicular stomatitis virus G glycoprotein) pseudotyped FIV- (feline immunodeficiency virus) derived vectors carrying the mouse Prnp gene in which these mutations have been inserted, are able to inhibit prion replication in chronically prion-infected cells. Because lentiviral tools are able to transduce post-mitotic cells such as neurons or cells of the lymphoreticular system, this result might help the development of gene- or cell-therapy approaches to prion disease.


Add to CiteULike CiteULike   Add to Complore Complore   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us   Add to Digg Digg   Add to Reddit Reddit   Add to Technorati Technorati   Add to Twitter Twitter    What's this?


This article has been cited by other articles:


Home page
J. Gen. Virol.Home page
H. Pflanz, K. Vana, G. Mitteregger, C. Pace, D. Messow, C. Sedlaczek, D. Nikles, H. A. Kretzschmar, and S. F. T. Weiss
Microinjection of lentiviral vectors expressing small interfering RNAs directed against laminin receptor precursor mRNA prolongs the pre-clinical phase in scrapie-infected mice
J. Gen. Virol., January 1, 2009; 90(1): 269 - 274.
[Abstract] [Full Text] [PDF]


Home page
Protein Eng Des SelHome page
D. Ott, C. Taraborrelli, and A. Aguzzi
Novel dominant-negative prion protein mutants identified from a randomized library
Protein Eng. Des. Sel., October 1, 2008; 21(10): 623 - 629.
[Abstract] [Full Text] [PDF]


Home page
BrainHome page
C. R Trevitt and J. Collinge
A systematic review of prion therapeutics in experimental models
Brain, September 1, 2006; 129(9): 2241 - 2265.
[Abstract] [Full Text] [PDF]




© The Company of Biologists Ltd 2004