Polymorphisms of mouse apolipoprotein A-II: seven alleles found among 41 inbred strains of mice.

In mice, apolipoprotein A-II (apoA-II) associates to form amyloid fibrils in an age-associated manner. We determined the complete nucleotide sequences of the apoA-II gene (Apoa2) cDNA in 41 inbred strains of mice including Mus musculus domesticus (laboratory mouse), Mus musculus castaneus, Mus musculus molossinus, Mus musculus musculus and Mus spretus. Among these strains we identified 7 alleles (Apoa2a1, Apoa2a2, Apoa2b, Apoa2c, Apoa2d, Apoa2e and Apoa2f).

Birth of offspring following transplantation of cryopreserved immature testicular pieces and in-vitro microinsemination.

Background: Fertility protection is an urgent clinical problem for prepubertal male oncology patients who undergo either chemotherapy or radiotherapy. As these patients do not have mature sperm to be frozen, there is as yet no effective method to preserve their fertility.

Methods And Results: Single pieces of immature mouse (1.

Induction of protein conformational change in mouse senile amyloidosis.

Aggregated amyloid fibrils can induce further polymerization of precursor proteins in vitro, thus providing a possible basis for propagation or transmission in the pathogenesis of amyloidoses. Previously, we postulated that the transmission of amyloid fibrils induces conformational changes of endogenous amyloid protein in mouse senile amyloidosis (Xing, Y., Nakamura, A.

Transmission of mouse senile amyloidosis.

In mouse senile amyloidosis, apolipoprotein A-II polymerizes into amyloid fibrils (AApoAII) and deposits systemically. Peripheral injection of AApoAII fibrils into young mice induces systemic amyloidosis (Higuchi et al, 1998). We isolated AApoAII amyloid fibrils from the livers of old R1.

Wild type ApoA-II gene does not rescue senescence-accelerated mouse (SAMP1) from short life span and accelerated mortality.

Biochemical and genetic data suggest that the Apoa2c allele of the apolipoprotein A-II gene causes severe senile amyloidosis (AApoAII) in SAMP1, a mouse model for accelerated senescence. We analyzed the effects of replacement of Apoa2c in SAMP1 mice with non-amyloidogenic Apoa2b on amyloidosis, lipoprotein metabolism, and progression of senescence using a congenic strain, P1.R1-Apoa2b, which has the Apoa2b chromosome region of SAMR1 in the genome of SAMP1.