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.
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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
|Deposited On:||09 Jul 2008 08:51|
|Last Modified:||27 Nov 2013 23:51|
|Publisher:||Society for General Microbiology|
|Citations:||Web of Science®. Times Cited: 10|
Scopus®. Citation Count: 10
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