Pani A, Julian M, Lucas-Lenard J
J Virol. 1986 Dec;60(3):1012-7. doi: 10.1128/JVI.60.3.1012-1017.1986.
Infection of mouse L929 cells by mengovirus resulted in the expression of a kinase activity that selectively phosphorylated the small, 38,000-molecular-weight subunit of eucaryotic initiation factor 2 and histone H2. This kinase activity was independent of host cell RNA synthesis and was located in the postribosomal supernatant (S-100 fraction) early after infection (up to 3 h). At later times after infection (5 h), kinase activity was also associated with the polysome fraction. The kinase present in the S-100 fraction bound strongly to DEAE-cellulose, its peak activity eluting at 0.5 M KCl. Kinase activity was independent of the presence of exogenous double-stranded RNA, and KCl at concentrations greater than 0.1 M inhibited eucaryotic initiation factor 2 phosphorylation. The 67,000-molecular-weight phosphoprotein activated in interferon-treated cells by double-stranded RNA was not detected by standard phosphorylation assays in lysates from mengovirus-infected cells. Labeling of this protein in vivo during 5 h of infection was also not detected. The DEAE-cellulose-purified mengovirus kinase inhibited protein synthesis in reticulocyte lysates, and the inhibition was not reversible by high concentrations of poly(I).poly(C).
脑心肌炎病毒感染小鼠L929细胞后,会导致一种激酶活性的表达,该激酶可选择性地磷酸化真核起始因子2的38,000分子量小亚基和组蛋白H2。这种激酶活性独立于宿主细胞RNA合成,在感染后早期(长达3小时)位于核糖体后上清液(S-100组分)中。感染后期(5小时),激酶活性也与多核糖体组分相关。S-100组分中的激酶与DEAE-纤维素强烈结合,其峰值活性在0.5M KCl浓度下洗脱。激酶活性独立于外源双链RNA的存在,浓度大于0.1M的KCl会抑制真核起始因子2的磷酸化。在经干扰素处理的细胞中由双链RNA激活的67,000分子量磷蛋白,在脑心肌炎病毒感染细胞的裂解物中通过标准磷酸化测定未检测到。在感染5小时期间体内对该蛋白的标记也未检测到。经DEAE-纤维素纯化的脑心肌炎病毒激酶抑制网织红细胞裂解物中的蛋白质合成,且高浓度的聚肌苷酸-聚胞苷酸不能使其抑制作用逆转。