| First Author | Müller U | Year | 1994 |
| Journal | Cell | Volume | 79 |
| Issue | 5 | Pages | 755-65 |
| PubMed ID | 8001115 | Mgi Jnum | J:21937 |
| Mgi Id | MGI:69837 | Doi | 10.1016/0092-8674(94)90066-3 |
| Citation | Muller U, et al. (1994) Behavioral and anatomical deficits in mice homozygous for a modified beta-amyloid precursor protein gene. Cell 79(5):755-65 |
| abstractText | 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. |
