|
Posted 6 March 2005
Transgene: To generate bigenic mice, APPSw mice Tg2576 (see TAC #001349) were crossed with
BACE Tg lines to generate double heterozygous offspring.
Mutation: hBACE, APPSw(KM670/671NL)
Promoter: Mouse prion promoter (moPrP)
Mouse Strain: C57BL/6/C3H/SJL
Neuropathological Analysis:
BACE expression was similar in single BACE and bigenic APPxBACE mice. In bigenic
mice high BACE overexpression inhibited amyloid formation despite increased ß-cleavage
of APP. Also the high BACE expression shifted the subcellular location of APP cleavage
to the neuronal perikarya early in the secretory pathway thereby depleting APP destined
for axonal transport.
Behavioral:
N/A
Contact:Virginia M-Y Lee
The Center for Neurodegenerative Disease Research, Department of Pathology and Laboratory
Medicine
Institute on Aging, University of Pennsylvania School of Medicine, Philadelphia,
PA 19104
Phone: 215-662-6427
Fax: 215-349-5909
Email: vmylee@mail.med.upenn.edu
Patents: None
Primary:
Lee EB, Zhang B, Liu K, Greenbaum EA, Doms RW, Trojanowski JQ, LeeVM-Y. BACE overexpression
alters the subcellular processing of APP and inhibits Aβ deposition in vivo
J. Cell Biol. 168: 291 - 302, 2005.
Abstract.
|