Ikuta K, Coward J, Luftig R B
Virology. 1986 Oct 15;154(1):207-13. doi: 10.1016/0042-6822(86)90442-3.
The effect of cerulenin, an inhibitor of de novo fatty acid (and cholesterol) biosynthesis, on the synthesis of the precursor gag polyprotein, Pr65gag in a defective murine leukemia virus (334C) producing murine cell line (3JE) and a defective murine sarcoma virus (Gazdar) producing hamster cell line (HTG-2) was examined. In contrast to Moloney murine leukemia virus (M-MuLV) producing cell lines (MJD-54, clone 2) the amount of the Pr65gag remaining in the presence of cerulenin (20 micrograms/ml) was greatly reduced in both defective virus-infected cells. This effect appears specific for the Pr65gag polyprotein, since the env precursor polyprotein Pr80env was normally synthesized and remained undegraded in cerulenin-treated 3JE-infected cells. Thin-section electron micrographs showed an increased accumulation of virion particles in vesicles of treated HTG-2 cells.
对脂肪酸(和胆固醇)从头生物合成抑制剂浅蓝菌素,在产生缺陷型小鼠白血病病毒(334C)的小鼠细胞系(3JE)和产生缺陷型小鼠肉瘤病毒(Gazdar)的仓鼠细胞系(HTG-2)中,对前体gag多聚蛋白Pr65gag合成的影响进行了检测。与产生莫洛尼氏小鼠白血病病毒(M-MuLV)的细胞系(MJD-54,克隆2)不同,在浅蓝菌素(20微克/毫升)存在的情况下,在这两种缺陷病毒感染的细胞中,剩余的Pr65gag量都大大减少。这种作用似乎对Pr65gag多聚蛋白具有特异性,因为env前体多聚蛋白Pr80env在经浅蓝菌素处理的3JE感染细胞中正常合成且未被降解。超薄切片电子显微镜照片显示,在处理过的HTG-2细胞的囊泡中病毒粒子的积累增加。