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Inbred Strains of Mice: SAMP1

SAMP1

Inbr. F?+59 (1993). Origin: Dr. Toshio Takeda, Dept. of Senescence Biology, Chest Disease Research Institute, Kyoto University, Sakyo-ku, Kyoto 606, Japan, from AKR/J mice imported from J in 1968 and crossed (?) with mice of an unknown strain, followed by sib mating since 1975. Albino (c). All SAMP mice have been defined at approx. 20 loci. There is only minor variation among the strains restricted to the Idh1, Mod1 and Car2 loci. The origin, history and characteristics of the SAM family of strains has been summarised by Takeda (1994), Higuchi (1997) and Takeda et al (1997).


Characteristics

All mice over 8 months show amyloid deposition of AApoAII protein (Higuchi et al 1986) due to an amino acid substitution in a precursor of apoA-II (Yonezu et al 1987, Higuchi et al 1991). About 75% of mice over 10 months have kideny defects. Autoimmunity develops early in life (Yoshida et al 1989). There is an age-related increase in the frequency of chromosomal abberations in bone marrow cells (Nisitani et al 1990). Strain has accelerated aging with median survival time of 374 days (Takeda et al 1991).


Higuchi K., Kitagawa K., Naiki H., Hanada K., Hosokawa M., and Takeda T. (1991) Polymorphism of apolipoprotein A-II (apoA-II) among inbred strains of mice. Relationship between the molecular type of apoA-II and mouse senile amyloidosis. Biochem. J. 279, 427-433. \par

Higuchi K. (1997) Genetic characterization of senescence-accelerated mouse (SAM). Exp. Gerontol. 32, 129-138. \par

Nisitani S., Hosokawa M., Sasaki M. S., Yasuoka K., Naiki H., Matsuchita T., and Takeda T. (1990) Acceleration of chromosome abberations in senescence-accelerated strains of mice. Mutation Res. 237, 221-228. \par

Takeda T., Hosokawa M., and Higuchi K. (1991) Senescence-accelerated mouse (SAM): A novel murine model of accelerated senescence. J. Amer. Geriatr. Soc. 39, 911-919. \par

Takeda T., Hosokawa M., and Higuchi K. (1997) Senescence-accelerated mouse (SAM): A novel murine model of senescence. Exp. Gerontol. 32, 105-109. \par

Yonezu T., Tsunasawa S., Higuchi K., Kogishi K., Naiki H., Hanada K., Sakiyama F., and Takeda T. (1987) A molecular-pathologic approach to murine senile amyloidosis. Serum precursor-apolipoprotein A-II variant (Pro5-Gln) present only in the senile amyloidosis-prone SAM-P/2 mice. Lab. Invest. 57, 65-70. \par


INBRED STRAINS OF MICE
Updated 9 Apr. 1998
Michael FW Festing
MRC Toxicology Unit, Hodgkin Building,
University of Leicester, UK

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