Quick Search:

uzh logo
Browse by:
bullet
bullet
bullet
bullet

Zurich Open Repository and Archive 

Permanent URL to this publication: http://dx.doi.org/10.5167/uzh-2711

Julius, C; Heikenwalder, M; Schwarz, P; Marcel, A; Karin, M; Prinz, M; Pasparakis, M; Aguzzi, A (2008). Prion propagation in mice lacking central nervous system NF-kappaB signalling. Journal of General Virology, 89(6):1545-1550.

[img] PDF - Registered users only
1MB

Abstract

Prions induce highly typical histopathological changes including cell death, spongiosis and activation of glia, yet the molecular pathways leading to neurodegeneration remain elusive. Following prion infection, enhanced nuclear factor-kappaB (NF-kappaB) activity in the brain parallels the first pathological changes. The NF-kappaB pathway is essential for proliferation, regulation of apoptosis and immune responses involving induction of inflammation. The IkappaB kinase (IKK) signalosome is crucial for NF-kappaB signalling, consisting of the catalytic IKKalpha/IKKbeta subunits and the regulatory IKKgamma subunit. This study investigated the impact of NF-kappaB signalling on prion disease in mouse models with a central nervous system (CNS)-restricted elimination of IKKbeta or IKKgamma in nearly all neuroectodermal cells, including neurons, astrocytes and oligodendrocytes, and in mice containing a non-phosphorylatable IKKalpha subunit (IKKalpha AA/AA). In contrast to previously published data, the observed results showed no evidence supporting the hypothesis that impaired NF-kappaB signalling in the CNS impacts on prion pathogenesis.

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
Language:English
Date:2008
Deposited On:09 Jul 2008 08:51
Last Modified:27 Nov 2013 23:51
Publisher:Society for General Microbiology
ISSN:0022-1317
Publisher DOI:10.1099/vir.0.83622-0
PubMed ID:18474572
Citations:Web of Science®. Times Cited: 9
Google Scholar™
Scopus®. Citation Count: 10

Users (please log in): suggest update or correction for this item

Repository Staff Only: item control page