Suppr超能文献

衰老小鼠的核糖体在无细胞蛋白质合成方面通常并不缺乏。

Ribosomes from aging mice are not generally deficient in cell-free protein synthesis.

作者信息

Shmookler Reis R J

出版信息

Mech Ageing Dev. 1981 Dec;17(4):311-20. doi: 10.1016/0047-6374(81)90049-x.

Abstract

Cell-free protein synthesis by mouse liver ribosomes was examined as a function of the age of individual ribosome donors. In two strains of mouse, one long-lived and one short-lived, both the fraction of polyribosomes and the rate of in vitro ribosomal protein synthesis remained essentially constant throughout the lifespan, although in each "old" group one of three mice fell below the range of values observed for all other mice. Poly(U) stimulation of preincubated ribosome preparations similarly did not change with senescence; whereas poly(U)-directed synthesis by washed monosomes, pelleted after messenger run-off, increased two-fold for old mice. These results indicate that ribosomes of old mice are not necessarily defective in protein-synthesizing capacity, as previously reported, but may become defective in particular individuals.

摘要

研究了从小鼠肝脏核糖体进行的无细胞蛋白质合成作为个体核糖体供体年龄的函数。在两种小鼠品系中,一种寿命长,一种寿命短,多核糖体的比例和体外核糖体蛋白质合成速率在整个寿命期间基本保持恒定,尽管在每个“老年”组中,三只小鼠中有一只低于所有其他小鼠观察到的值范围。对预孵育的核糖体制剂的聚尿苷酸(Poly(U))刺激同样不会随着衰老而改变;而在信使RNA洗脱后沉淀的洗涤单体进行的聚尿苷酸指导的合成,老年小鼠增加了两倍。这些结果表明,老年小鼠的核糖体不一定如先前报道的那样在蛋白质合成能力上存在缺陷,而是可能在特定个体中出现缺陷。

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验