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Species | C WeissmannSummaryAffiliation: University of Zurich Country: Switzerland Publications
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Publications
Bovine spongiform encephalopathy and early onset variant Creutzfeldt-Jakob diseaseC Weissmann
Institut für Molekularbiologie I, Universitat Zurich, Zurich, Switzerland
Curr Opin Neurobiol 7:695-700. 1997..Recent evidence links the appearance of new variant Creutzfeldt-Jakob disease in humans to consumption of BSE-contaminated cattle-derived products...- The Ninth Datta Lecture. Molecular biology of transmissible spongiform encephalopathiesC Weissmann
Institut für Molekularbiologie I, Universitat Zurich, Switzerland
FEBS Lett 389:3-11. 1996.... - Prion protein devoid of the octapeptide repeat region restores susceptibility to scrapie in PrP knockout miceE Flechsig
Institut fur Molekularbiologie, Abteilung I, Universitat Zurich, Switzerland
Neuron 27:399-408. 2000..Thus, while the region comprising the octarepeats is not essential for mediating pathogenesis and prion replication, it modulates the extent of these events and of disease presentation... 
Normal host prion protein (PrPC) is required for scrapie spread within the central nervous systemS Brandner
Institute of Neuropathology, University Hospital, Zurich, Switzerland
Proc Natl Acad Sci U S A 93:13148-51. 1996..Again, intraocular inoculation did not lead to disease in the PrP-producing graft. These results demonstrate that PrP is necessary for prion spread along neural pathways...- Induction of type I interferon genes and interferon-inducible genes in embryonal stem cells devoid of interferon regulatory factor 1H Ruffner
Institut für Molekularbiologie I, University of Zurich, Switzerland
Proc Natl Acad Sci U S A 90:11503-7. 1993.... - PrP-deficient mice are resistant to scrapieC Weissmann
Institut für Molekularbiologie I, Universitat Zurich, Switzerland
Ann N Y Acad Sci 724:235-40. 1994..These experiments show that PrPC, possibly at close to normal levels, is required for the usual susceptibility to scrapie and that lack of homology between incoming prions and the host's PrP genes retards disease... - High prion and PrPSc levels but delayed onset of disease in scrapie-inoculated mice heterozygous for a disrupted PrP geneH Bueler
Institut für Molekularbiologie I, Universitat Zurich, Switzerland
Mol Med 1:19-30. 1994..We showed previously that mice devoid of PrPC (Prn-p0/0) are completely resistant to scrapie. We now report on the unexpected response of heterozygous (Prn-p0/+) mice to scrapie infection... - Mice devoid of PrP are resistant to scrapieH Bueler
Institut für Molekularbiologie I, Universitat Zurich, Switzerland
Cell 73:1339-47. 1993..These experiments show that PrPC, possibly at close to normal levels, is required for the usual susceptibility to scrapie and that lack of homology between incoming prions and the host's PrP genes retards disease... - Neuroinvasion of prions: insights from mouse modelsS Brandner
Institute of Neuropathology, Department of Pathology, University Hospital, Zurich, Switzerland
Exp Physiol 85:705-12. 2000..The latter studies have allowed us to clarify some of the mechanisms of prion spread and disease pathogenesis... - Expression of amino-terminally truncated PrP in the mouse leading to ataxia and specific cerebellar lesionsD Shmerling
Institut fur Molekularbiologie, Abteilung I, Universitat Zurich, Switzerland
Cell 93:203-14. 1998..The defect was completely abolished by introducing one copy of a wild-type PrP gene. We speculate that these truncated PrPs may be nonfunctional and compete with some other molecule with a PrP-like function for a common ligand... - Normal host prion protein necessary for scrapie-induced neurotoxicityS Brandner
Department of Pathology, University Hospital, Zurich, Switzerland
Nature 379:339-43. 1996..Therefore, in addition to being resistant to scrapie infection, brain tissue devoid of PrPC is not damaged by exogenous PrPSc... - Transgenic and knockout mice in research on prion diseasesA J Raeber
Institute of Neuropathology, Department of Pathology, University Hospital, Zurich, Switzerland
Brain Pathol 8:715-33. 1998..Such studies have shed new light onto the mechanisms of prion spread and disease pathogenesis... - Studies on prion replication in spleenA J Raeber
Institute of Neuropathology, University Hospital, Zurich, Switzerland
Dev Immunol 8:291-304. 2001..These results imply that splenic lymphocytes can acquire prions, possibly from FDC's, but only if they express PrP... - Susceptibility to scrapie in mice is dependent on PrPCC Weissmann
Institut für Molekularbiologie I, Universitat Zurich, Switzerland
Philos Trans R Soc Lond B Biol Sci 343:431-3. 1994..These experiments show that PrPC, possibly at close to normal levels, is required for the usual susceptibility to scrapie and that lack of homology between incoming prions and the host's PrP genes retards disease... - Role of the PrP gene in transmissible spongiform encephalopathiesC Weissmann
Institut für Molekularbiologie I, Universitat Zurich, Switzerland
Intervirology 35:164-75. 1993..Prn-p0/0, Prn-p+/+ and Prn-p0/+ mice were inoculated with scrapie agent; the clinical response as well as the prion titer at different time points are being determined... - Deficient signaling in mice devoid of double-stranded RNA-dependent protein kinaseY L Yang
Institut für Molekularbiologie I, Universitat Zurich, Switzerland
EMBO J 14:6095-106. 1995..Thus, PKR is not directly essential for responses to pIC, and a pIC-responsive system independent of PKR is induced by IFN. No evidence of the tumor suppressor activity of PKR was demonstrated... - A 'unified theory' of prion propagationC Weissmann
Institut für Molekularbiologie I, Universitat Zurich, Switzerland
Nature 352:679-83. 1991..Can the two views be reconciled?.. - Behavioral and anatomical deficits in mice homozygous for a modified beta-amyloid precursor protein geneU Muller
Institut für Molekularbiologie I, Universitat Zurich, Switzerland
Cell 79:755-65. 1994..The brain contained shortened beta APP-specific protein at a low level. Mutant mice were severely impaired in spatial learning and exploratory behavior and showed increased incidence of agenesis of the corpus callosum... - Normal development and behaviour of mice lacking the neuronal cell-surface PrP proteinH Bueler
Institut für Molekularbiologie I, Universitat Zurich, Switzerland
Nature 356:577-82. 1992..It is now feasible to determine whether mice devoid of PrPC can propagate prions and are susceptible to scrapie pathogenesis... - Mice devoid of interferon regulatory factor 1 (IRF-1) show normal expression of type I interferon genesL F Reis
Institut für Molekularbiologie I, Universitat Zurich, Switzerland
EMBO J 13:4798-806. 1994..There was also no impairment in the response of type I IFN-inducible genes. Therefore, IRF-1 is not essential for these processes in vivo... - B lymphocyte-restricted expression of prion protein does not enable prion replication in prion protein knockout miceF Montrasio
Institute of Molecular Biology, University of Zurich, Winterthurerstrasse 190, CH 8057 Zurich, Switzerland
Proc Natl Acad Sci U S A 98:4034-7. 2001..We conclude that splenic B lymphocytes are not prion-replication competent and that they acquire prions from other cells, most likely follicular dendritic cells with which they closely associate and whose maturation depends on them... - PrP knock-out and PrP transgenic mice in prion researchC Weissmann
MRC Prion Unit, Department of Neurodegenerative Disease, Institute of Neurology, London, UK
Br Med Bull 66:43-60. 2003..In addition, the availability of PrP knock-out mice provided an approach to carry out reverse genetics on PrP, both in regard to prion disease and to its physiological role... - Molecular genetics of transmissible spongiform encephalopathiesC Weissmann
, Abteilung I, Winterthurerstrasse 190, , Switzerland
J Biol Chem 274:3-6. 1999 - The role of PrP in health and diseaseE Flechsig
Institut fur Virologie und Immunbiologie, Versbacherstrasse 7, D 97078 Wurzburg, Germany
Curr Mol Med 4:337-53. 2004..Many questions regarding the role of PrP in susceptibility to prions have been elucidated, however the physiological role of PrP and the pathological mechanisms of neurodegeneration in prion diseases are still elusive... - Perspectives: neurobiology. PrP's double causes troubleC Weissmann
MRC Prion Unit/Neurogenetics, Imperial College School of Medicine at St. Mary's, London W2 1PG, UK
Science 286:914-5. 1999 - Ethical issues in human prion diseasesS J Tabrizi
Department of Neurodegenerative Disease/MRC Prion Unit, Institute of Neurology, London, UK
Br Med Bull 66:305-16. 2003..In this chapter, we outline ethical questions posed by research, diagnostic procedures and therapy in the field of prion diseases... - Structure and expression of cloned murine IFN-alpha genesG D Shaw
Nucleic Acids Res 11:555-73. 1983..coli under the control of the ampicillinase promoter. MuIFN-alpha 1 had no detectable activity on human cells, while MuIFN-alpha 2 was 20% as active on human as on mouse cells... - A quantitative, highly sensitive cell-based infectivity assay for mouse scrapie prionsP C Klöhn
Medical Research Council Prion Unit, Department of Neurodegenerative Disease, Institute of Neurology, National Hospital for Neurology and Neurosurgery, Queen Square, London WC1N 3BG, United Kingdom
Proc Natl Acad Sci U S A 100:11666-71. 2003..SC assays performed in a more time-consuming end point titration format extend the sensitivity and show that infectivity titers measured in tissue culture and in the mouse are similar... - Transmission of prionsC Weissmann
Medical Research Council Prion Unit, Department of Neurodegenerative Disease, Institute of Neurology, Queen Square, London WC1N 3BG, UK
J Infect Dis 186:S157-65. 2002..This property, first observed in a clinical setting, is now being investigated in experimental settings, both in animals and in cell culture... - Transmission of prionsC Weissmann
Medical Research Council Prion Unit, Department of Neurodegenerative Disease, Institute of Neurology, Queen Square, London WC1N 3BG, United Kingdom
Proc Natl Acad Sci U S A 99:16378-83. 2002..This property, first observed in a clinical setting, is now being investigated in experimental settings, both in animals and in cell culture... - No propagation of prions in mice devoid of PrPA Sailer
, , Switzerland
Cell 77:967-8. 1994 - Prion protein (PrP) with amino-proximal deletions restoring susceptibility of PrP knockout mice to scrapieM Fischer
Institut für Molekularbiologie der Universität Zürich, Switzerland
EMBO J 15:1255-64. 1996.... - Onset of ataxia and Purkinje cell loss in PrP null mice inversely correlated with Dpl level in brainD Rossi
MRC Prion Unit Neurogenetics, Imperial College School of Medicine at St Mary s, London W2 1PG, UK
EMBO J 20:694-702. 2001..Zürich II mice transgenic for a PRND:-containing cosmid expressed Dpl at twice the level and became ataxic approximately 5 months earlier. Thus, Dpl levels in brain and onset of the ataxic syndrome are inversely correlated... - Astrocyte-specific expression of hamster prion protein (PrP) renders PrP knockout mice susceptible to hamster scrapieA J Raeber
Institut fur Molekularbiologie, Abteilung I, University of Zurich, H onggerberg, 8093 Z urich, Switzerland
EMBO J 16:6057-65. 1997..Interestingly, mice expressing the same transgenes but also endogenous murine PrP genes propagated infectivity without developing disease...