Posted 10 June 2005
Transgene:&The FAD mutation N141I was introduced into a human PS2 cDNA. A vector
based on the mouse prion protein gene was used (pPrnpHG). A KpnI-NarI fragment,
encompassing the coding region of the prion protein gene, was deleted and replaced
by a unique SceI site. The presenilin 2 coding sequence was inserted by
blunt-end ligation and verified by sequencing of the insertion sites. Vector-free
linear fragments of Prnp-huPS2 (N141I) constructs were microinjected into pronuclei
of B6D2F1 zygotes. After microinjection, viable zygotes were implanted into the
oviducts of pseudopregnant foster mothers. Transgenic founders were crossed to C57BL/6
to establish lines.
Mutation: Human N141I
Promoter: Murine prion protein genomic fragment (pPrnpHG)
Mouse Strain: (C57BL/6, DBA/2) zygotes
F. Hoffmann-La Roche AG
Building 69/440 Grenzacherstr 124, CH-4070
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J.G. Richards, G.A. Higgins, A.M. Ouagazzal, L. Ozmen, J.N. Kew, B. Bohrmann, P.
Malherbe, M. Brockhaus, H. Loetscher, C. Czech, G. Huber, H. Bluethmann, H. Jacobsen
and J.A. Kemp. PS2APP transgenic mice, coexpressing hPS2mut and hAPPswe, show age-related
cognitive deficits associated with discrete brain amyloid deposition and inflammation,
J. Neurosci. 23:8989-9003, 2003.
von Kienlin M, Künnecke B, Metzger F, Steiner G, J. Richards G, Ozmen L, Jacobsen
H, Loetscher H. Altered metabolic profile in the frontal cortex of PS2APP transgenic
mice, monitored throughout their life span. Neurobiology of Dis. 18(1):32-39, 2005.