Sojar H T, Rothstein M
Mech Ageing Dev. 1986 Jun;35(1):47-57. doi: 10.1016/0047-6374(86)90065-5.
The age-related decrease in protein synthesis by cell-free systems has been traced to a factor which can be obtained by high salt extraction of young polysomes. Such extracts, when added to old ribosomes in young post-ribosomal supernate, stimulate the level of Poly(U)-directed protein synthesis. Extracts of old polysomes have essentially no effect. The deficient factor is not EF-2 and is highly unlikely to be EF-1, as this component resides almost entirely in the post-ribosomal supernates used in the reaction mixture. Since initiation factors are not necessary for Poly(U)-directed protein synthesis and EF-1 and EF-2 do not appear to be involved, the nature of the soluble factor which is deficient in old ribosomes appears to lie outside of proteins which are commonly implicated in the age-related slowing of protein synthesis.
无细胞系统中与年龄相关的蛋白质合成下降已追溯到一种因子，该因子可通过对年轻多核糖体进行高盐提取获得。将此类提取物添加到年轻核糖体后上清液中的旧核糖体中时，可刺激聚尿苷酸（Poly(U)）指导的蛋白质合成水平。旧多核糖体的提取物基本没有作用。缺乏的因子不是延伸因子2（EF-2），而且极不可能是延伸因子1（EF-1），因为该组分几乎完全存在于反应混合物中使用的核糖体后上清液中。由于起始因子对于聚尿苷酸指导的蛋白质合成不是必需的，而且似乎不涉及延伸因子1和延伸因子2，因此旧核糖体中缺乏的可溶性因子的性质似乎不在通常与年龄相关的蛋白质合成减慢有关的蛋白质范围内。
