Updated 28 January 2005
Mouse Pin1 gene comprising a 997bp fragment upstream of first coding exon and a
6.5 fragment downstream of last exon was inserted into pLNTK carrying the neomycin
resistance, thymidine kinase and Lox-P genes.
Background: Backcross to C57BL/6, N 11
Progressive age-dependent neuropathy: tau hyperphosphorylation, tau filament formation
and neuronal degeneration. Pin1-/- neurons have NFT-like pathologies.
Total MPM-2 reactivity was 3x higher in Pin1-/-
brain lysates compared to control brain lysates.
Normal development but showed progressive age-dependent motor and behavioral deficits,
including abnormal limb-clasping reflexes, hunched postures, reduced mobility and
Center for Interdisciplinary Research/Institute of Development, Aging and Cancer
Aramaki Aza-Aoba, Aoba, Sendai, 980-8578 Japan.
Fujimori F, Takahashi K,Uchida C, Uchida T. Mice Lacking Pin1 Develop Normally,
but Are Defective in Entering Cell Cycle from G0 Arrest. Biochm Biophy Res Comm
Y.C. Liou, R. Ryo, H.K. Huang, P.J. Lu, R. Bronson, F. Fujimori, U. UchidaÞ, T.
Hunter and K.P. Lu, Loss of Pin1 function in the mouse causes phenotypes resembling
cyclin D1-null phenotypes, Proc. Natl. Acad. Sci. USA. 99:1335-1340, 2002.
Liou Y-C, Sun A, Ryo A, Zhou X Z, Yu Z-X, Huang H-K, Uchida T, Bronson R, Bing G,
Li X, Hunter T & Lu K P. Role of the prolyl isomerase Pin1 in protecting against
age-dependent neurodegeneration. Nature 424, 556 - 561, 2003.