Genoud
Fakultäten » Medizinische Fakultät » Neuropathologie, Institut für » Prof. Dr. Adriano Aguzzi » Genoud
Completed research project
| Title / Titel | Generation and functional analysis of mice lacking Dpl and PrP/Dpl | ||||
|---|---|---|---|---|---|
| Abstract (PDF, 14 KB) | |||||
| Summary / Zusammenfassung | The agent that causes prion diseases is thought to be identical with PrPSc, a conformer of the normal prion protein PrPC. PrPC deficient mice do not exhibit major pathologies, perhaps because they express a protein termed Dpl, that shares significant biochemical and structural homology with PrPC. To investigate the physiological function of Dpl, we generated mice harbouring a homozygous disruption of the Prnd gene that encodes Dpl. Dpl deficiency did not interfere with embryonic and postnatal development, but resulted in male sterility. In order to exclude any redundant functions between PrP and Dpl, we are also generating mice lacking both Dpl and PrP. The Tamere technology, which has been used so far only with the Hox genes, will be used to generate double mutant mice. | ||||
| Publications / Publikationen | Behrens, A., Brandner, S., Genoud, N., and Aguzzi, A. (2001). Normal neurogenesis and scrapie pathogenesis in neural grafts lacking the prion protein homologue Doppel. EMBO Rep 2, 347-352.Behrens, A., Genoud, N., Naumann, H., Rulicke, T., Janett, F., Heppner, F. L., Ledermann, B., and Aguzzi, A. (2002). Absence of the prion protein homologue Doppel causes male sterility. Embo J 21, 3652-3658 | ||||
| Project leadership and contacts / Projektleitung und Kontakte |
|
||||
| Funding source(s) / Unterstützt durch |
Foundation Betty and David Koetser Foundation |
||||
| Duration of Project / Projektdauer | Jan 2001 to Dec 2003 |