These Aplp2 knock-out mice exhibit a phenotype similar to wild-type littermates, but show a slight reduction in weight, decreased forelimb grip strength, and decreased locomotor activity than wild-type littermates.
Dr. David R Borchelt, University of Florida
Mice that are homozygous null for the Aplp2 gene are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. No Aplp2 gene product (mRNA or protein) is detected. This strain may be useful in studies related to Alzheimer's Disease, especially if used in conjunction with other mutant mouse strains (see B6.129S7-Apptm1Dbo, Stock No. 004133).
A targeting vector containing neomycin resistance and herpes simplex virus thymidine kinase genes was used to disrupt a region of the Aplp2 gene encoding the promoter and exon 1. The construct was electroporated into 129S7/SvEvBrd-derived AB2.1 embryonic stem (ES) cells. Correctly targeted ES cells were injected into C57BL/6J blastocysts. The resulting chimeric animals were backcrossed to C57BL/6J mice.
|Allele Name||targeted mutation 1, David R Borchelt|
|Allele Type||Targeted (Null/Knockout)|
|Gene Symbol and Name||Aplp2, amyloid beta (A4) precursor-like protein 2|
|Strain of Origin||129S7/SvEvBrd-Hprtb-m2|
|Molecular Note||Replacement of the promoter region and first exon with a neomycin cassette. Western blot analysis on samples derived from nervous tissue and other peripheral tissues of homozygous mutant mice failed to detect any protein.|
|Mutations Made By|| |
Dr. David Borchelt, University of Florida
This strain originated on a B6;129S7 background and has been backcrossed to C57BL/6J for at least 5 generations (7/01).
When using the APLP2 KO mouse strain in a publication, please cite the originating article(s) and include JAX stock #004142 in your Materials and Methods section.