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衰老加速小鼠(SAM)的遗传特征分析。

Genetic characterization of senescence-accelerated mouse (SAM).

作者信息

Higuchi K

机构信息

Department of Senescence Biology, Kyoto University, Japan.

出版信息

Exp Gerontol. 1997 Jan-Apr;32(1-2):129-38. doi: 10.1016/s0531-5565(96)00060-5.

Abstract

The Senescence-Accelerated Mouse (SAM) strains are unique and appropriate models for genetic studies on aging because the SAMP strains have an "accelerated senescence" phenotype for which the SAMR strains are controls, and each SAMP strain has a strain-specific age-associated disorder. Furthermore, because they have gone through sufficient generations of sister-brother mating, they can be considered inbred strains, which can be analyzed genetically. There are now 11 SAMP strains and 3 SAMR strains descended from the progenitor litters. Analysis with the Gompertz function shows that the SAMP strains have the same initial mortality rate (IMR) as the SAMR strains but a shorter mortality rate doubling time (MRDT), presumably due to genes that accelerated the rate of senescence in the SAMP strains. This accelerated senescence may also occur in cultured fibroblast-like cells. We performed molecular genetic characterization of all the SAM strains to acquire a base of genetic information from which we could develop hypotheses on the mechanism of development of SAM strains and genetic factors that contribute to accelerated senescence.

摘要

衰老加速小鼠(SAM)品系是衰老遗传研究中独特且合适的模型,因为SAMP品系具有“加速衰老”表型,而SAMR品系作为对照,且每个SAMP品系都有一种特定品系的年龄相关疾病。此外,由于它们已经历了足够多代的同胞交配,它们可被视为近交系,能够进行遗传分析。目前有11个SAMP品系和3个SAMR品系源自始祖窝。用冈珀茨函数分析表明,SAMP品系与SAMR品系具有相同的初始死亡率(IMR),但死亡率加倍时间(MRDT)较短,推测这是由于加速SAMP品系衰老速率的基因所致。这种加速衰老也可能发生在培养的成纤维样细胞中。我们对所有SAM品系进行了分子遗传学特征分析,以获取遗传信息库,从而能够就SAM品系的发育机制以及导致加速衰老的遗传因素提出假设。

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