6 research outputs found
Transfer of137Cs and90Sr to flour, bran and straw from wheat, rye, barley and oats during the years 1982, 1986 (reactor accident at Chernobyl) and 1987 by field measurements
Fermentaktivit�ten und Konzentration von Stoffwechselzwischenprodukten im Blut bei Leber- und Herzkrankheiten
Delayed Seroconversion and Rapid Onset of Lymphoproliferative Disease After Transmission of Human T-Cell Lymphotropic Virus Type 1 From a Multiorgan Donor
Immune recognition of genetically diverse simian T-cell lymphotropic virus type I isolates
Disruption of Doppel prevents neurodegeneration in mice with extensive Prnp deletions
The Prnp gene encodes the cellular prion protein PrP(C). Removal of its ORF does not result in pathological phenotypes, but deletions extending into the upstream intron result in cerebellar degeneration, possibly because of ectopic cis-activation of the Prnd locus that encodes the PrP(C) homologue Doppel (Dpl). To test this hypothesis, we removed Prnd from Prnp(o/o) mice by transallelic meiotic recombination. Balanced loxP-mediated ablation yielded mice lacking both PrP(C) and Dpl (Prn(o/o)), which developed normally and showed unimpaired immune functions but suffered from male infertility. However, removal of the Prnd locus abolished cerebellar degeneration, proving that this phenotype is caused by Dpl upregulation. The absence of compound pathological phenotypes in Prn(o/o) mice suggests the existence of alternative compensatory mechanisms. Alternatively, Dpl and PrP(C) may exert distinct functions despite having partly overlapping expression profiles