NR AHTZ
AU Manson,J.C.; Clarke,A.R.; Hooper,M.L.; Aitchison,L.; McConnell,I.; Hope,J.
TI 129/Ola mice carrying a null mutation in PrP that abolishes mRNA production are developmentally normal
QU Molecular Neurobiology 1994 Apr-Jun; 8(2-3): 121-7
PT journal article
AB The neural membrane glycoprotein PrP is implicated in the pathogenesis of the transmissible spongiform encephalopathies; however, the normal function of PrP and its precise role in disease are not understood. Recently, gene targeting has been used to produce mice with neo/PrP fusion transcripts, but no detectable PrP protein in the brain (1). Here we report the use of a different targeting strategy, to produce inbred mice with a complete absence of both PrP protein and mRNA sequences. At 7 mo of age, these mice show no overt phenotypic abnormalities despite the normal high levels of expression of PrP during mouse development. The mice are being used in experiments designed to address the role of PrP in the pathogenesis of scrapie and the replication of infectivity.
IN Mäuse, die aufgrund einer gentechnisch eingeführten Mutation weder das Prionprotein, noch seine mRNA exprimieren, zeigen im Alter von 7 Monaten keine offensichtlichen phänotypischen Beeinträchtigungen.
MH Aging/physiology; Animal; Blotting, Northern; Brain/*metabolism; Chimera; Embryo; *Gene Expression; Genetic Vectors; Heterozygote; Homozygote; Mice; Mice, Inbred C57BL; Mice, Inbred CBA; Mice, Mutant Strains; Mutation; Prions/*biosynthesis/*genetics; RNA, Messenger/biosynthesis; Reference Values; Scrapie/genetics/*physiopathology
AD J.C. Manson, Afrc, Institute for Animal Health, Ogston Bldg, W Mains Rd, Edinburgh EH9 3JF, Midlothian, Scotland
SP englisch
PO USA