Modification: APLP2: Knock-Out
Disease Relevance: Alzheimer's Disease
Strain Name: B6.129S7-Aplp2tm1Dbo/J
Genetic Background: 129S7,C57BL/6J; backcrossed to C57BL/6J
Availability: The Jackson Lab: Stock# 004142; Cryopreserved
These mice have a targeted deletion of the Amyloid β (A4) precursor-like protein 2 (APLP2), a member of the APP gene family with sequence homology to APP. No APLP2 gene product (mRNA or protein) is detected in homozygous null animals. Homozygous null animals are viable, normal in size, fertile, and do not display any gross physical or behavioral abnormalities up to 22 months of age. No impairments in axonal outgrowth of olfactory sensory neurons following bulbectomy were observed (von Koch et al., 1997).
Inactivation of the mouse APLP2 gene by deletion of a 1.1 kb region containing the promoter and exon 1 using a targeting vector containing a PGK-neomycin expression cassette for positive selection and a MC1-TK cassette for negative selection.
- von Koch CS, Zheng H, Chen H, Trumbauer M, Thinakaran G, van der Ploeg LH, Price DL, Sisodia SS. Generation of APLP2 KO mice and early postnatal lethality in APLP2/APP double KO mice. Neurobiol Aging. 1997 Nov-Dec;18(6):661-9. PubMed.
- Yang G, Gong YD, Gong K, Jiang WL, Kwon E, Wang P, Zheng H, Zhang XF, Gan WB, Zhao NM. Reduced synaptic vesicle density and active zone size in mice lacking amyloid precursor protein (APP) and APP-like protein 2. Neurosci Lett. 2005 Aug 12-19;384(1-2):66-71. PubMed.