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
Laurence Ozmen
F. Hoffmann-La Roche AG
Building 69/440 Grenzacherstr 124, CH-4070 Basel, Switzerland
Phone: +41 61 6870248
Fax: +41 61 688 4575
Email: Laurence.ozmen@roche.com
Primary:
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. Abstract.
Associated:
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. Abstract.
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