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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 

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Behavioral and anatomical deficits in mice homozygous for a modified beta-amyloid precursor protein gene.

The beta-amyloid precursor protein (beta APP) gene of the mouse was disrupted by inserting into exon 2 a cassette containing a neomycin resistance gene and a putative transcription termination sequence. Contrary to expectation, brain and other tissues from mice homozygous for the insertion still contained beta APP-specific RNA, albeit at a level 5- to 10-fold lower than wild type and lacking the disrupted exon, which had been spliced out. The brain contained shortened beta APP-specific protein at a low level. Mutant mice were severely impaired in spatial learning and exploratory behavior and showed increased incidence of agenesis of the corpus callosum.[1]

References

  1. Behavioral and anatomical deficits in mice homozygous for a modified beta-amyloid precursor protein gene. Müller, U., Cristina, N., Li, Z.W., Wolfer, D.P., Lipp, H.P., Rülicke, T., Brandner, S., Aguzzi, A., Weissmann, C. Cell (1994) [Pubmed]
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