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Posted 6 March 2005
Transgene: The hBACE cDNA was cloned into the MoPrP.Xho expression vector at the
XhoI restriction site to generate a 15.9-kb NotI linear fragment. DNA was microinjected
into C57B6/C3H mouse.
Mutation: hBACE
Promoter: Mouse prion protein (PrP) promoter
Mouse Strain: C57B6/C3H
Neuropathological Analysis:
Produced three tg lines BACE-L (line 30), BACE-M (line 34), and BACE-H (line 8),
expressing BACE ~7-, 10-, and 20-fold over endogenous levels, respectively. BACE
expression was similar in single BACE and bigenic APPxBACE mice. Monogenic BACE
mice showed no evidence of Aß deposition. Immunostaining showed increased BACE expression
in neuronal cell bodies, axons and synaptic elements such as the mossy fiber terminals
of the hippocampus, puncta within the granule cell layer of the cerebellum, and
neuropil within the spinal cord.
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.
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