Wild type ApoA-II gene does not rescue senescence-accelerated mouse (SAMP1) from short life span and accelerated mortality.
Wild type ApoA-II gene does not rescue senescence-accelerated mouse (SAMP1) from short life span and accelerated mortality.
复制标题
野生型 ApoA-II 基因不能挽救加速衰老小鼠 (SAMP1) 的寿命缩短和死亡率加快。
DOI:
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复制
发表时间:
2000
期刊:
影响因子:
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通讯作者:
K. Higuchi
中科院分区:
文献类型:
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作者:
J. Wang;T. Matsushita;K. Kogishi;C. Xia;A. Ohta;T. Chiba;A. Nakamura;H. Kondo;M. Mori;M. Hosokawa;K. Higuchi
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. Age-associated amyloid deposition was not observed, but plasma concentrations of apoA-II protein and HDL-cholesterol decreased with age in P1.R1-Apoa2b. P1.R1-Apoa2b showed lower scores of senescence than did SAMP1. However, the life span and mortality rate doubling time were similar in P1.R1-Apoa2b and SAMP1. These results suggest that replacement of Apoa2c with non-amyloidogenic Apoa2b does not rescue SAMP1 mice from a short life span and accelerated mortality.
DOI:
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发表时间:
1990
期刊:
The Journal of biological chemistry
影响因子:
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作者:
Doolittle,MH;LeBoeuf,RC;Warden,CH;Bee,LM;Lusis,AJ
通讯作者:
Lusis,AJ
DOI:
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发表时间:
1983
期刊:
The Journal of biological chemistry
影响因子:
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作者:
Lusis,AJ;Taylor,BA;Wangenstein,RW;LeBoeuf,RC
通讯作者:
LeBoeuf,RC