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PMID:8001115

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Citation

Müller, U, Cristina, N, Li, ZW, Wolfer, DP, Lipp, HP, Rülicke, T, Brandner, S, Aguzzi, A and Weissmann, C (1994) Behavioral and anatomical deficits in mice homozygous for a modified beta-amyloid precursor protein gene. Cell 79:755-65

Abstract

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.

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PubMed

Keywords

Amyloid beta-Protein Precursor/genetics; Animals; Base Sequence; Behavior, Animal; Brain/pathology; Exons/genetics; Exploratory Behavior; Female; Gene Expression; Homozygote; Learning; Male; Mice; Mice, Mutant Strains; Molecular Sequence Data; Mutagenesis, Insertional; RNA, Messenger/analysis; Spatial Behavior

Significance

Annotations

Gene product Qualifier GO ID GO term name Evidence Code with/from Aspect Notes Status


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References

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