Navigation auf zora.uzh.ch

Search ZORA

ZORA (Zurich Open Repository and Archive)

Ectopic expression of prion protein (PrP) in T lymphocytes or hepatocytes of PrP knockout mice is insufficient to sustain prion replication.

Raeber, A J; Sailer, A; Hegyi, I; Klein, M A; Rülicke, T; Fischer, Marek; Brandner, S; Aguzzi, Adriano; Weissmann, C (1999). Ectopic expression of prion protein (PrP) in T lymphocytes or hepatocytes of PrP knockout mice is insufficient to sustain prion replication. Proceedings of the National Academy of Sciences of the United States of America (PNAS), 96(7):3987-3992.

Abstract

The cellular form of the Prion protein (PrPC) is necessary for prion replication in mice. To determine whether it is also sufficient, we expressed PrP under the control of various cell- or tissue-specific regulatory elements in PrP knockout mice. The interferon regulatory factor-1 promoter/Emu enhancer led to high PrP levels in the spleen and low PrP levels in the brain. Following i.p. scrapie inoculation, high prion titers were found in the spleen but not in the brain at 2 weeks and 6 months, showing that the lymphoreticular system by itself is competent to replicate prions. PrP expression directed by the Lck promoter resulted in high PrP levels on T lymphocytes only but, surprisingly, did not allow prion replication in the thymus, spleen, or brain following i.p. inoculation. A third transgenic line, which expressed PrP in the liver under the control of the albumin promoter/enhancer-albeit at low levels-also failed to replicate prions. These results show that expression of PrP alone is not sufficient to sustain prion replication and suggest that additional components are needed.

Additional indexing

Item Type:Journal Article, refereed, original work
Communities & Collections:04 Faculty of Medicine > University Hospital Zurich > Institute of Neuropathology
Dewey Decimal Classification:570 Life sciences; biology
610 Medicine & health
Scopus Subject Areas:Health Sciences > Multidisciplinary
Language:English
Date:30 March 1999
Deposited On:11 Feb 2008 12:25
Last Modified:01 Nov 2024 02:36
Publisher:National Academy of Sciences
ISSN:0027-8424
OA Status:Hybrid
Free access at:PubMed ID. An embargo period may apply.
Publisher DOI:https://doi.org/10.1073/pnas.96.7.3987
Related URLs:http://www.pnas.org/cgi/content/abstract/96/7/3987
PubMed ID:10097150

Metadata Export

Statistics

Citations

Dimensions.ai Metrics
93 citations in Web of Science®
98 citations in Scopus®
Google Scholar™

Altmetrics

Downloads

110 downloads since deposited on 11 Feb 2008
6 downloads since 12 months
Detailed statistics

Authors, Affiliations, Collaborations

Similar Publications