Whitaker-Dowling P, Youngner J S
Virology. 1984 Aug;137(1):171-81. doi: 10.1016/0042-6822(84)90020-5.
When mouse L cells are infected by vaccinia virus, a specific kinase inhibitory factor is produced which inhibits the interferon-induced, double-stranded RNA-dependent protein kinase (P. Whitaker-Dowling and J. S. Youngner (1983) Virology 131, 128-136). This inhibitory factor appears early in vaccinia infection (90 min) and its production requires protein synthesis. It inhibits the phosphorylation of the alpha subunit of protein synthesis initiation factor eIF-2 and it is active in mixed extracts of IFN-treated cells and vaccinia-infected cells. The vaccinia-mediated inhibition of the IFN-induced protein kinase is not due to a specific phosphatase or a specific protease and can be reversed by the addition of excess double-stranded RNA. Evidence is presented which suggests that the specific kinase inhibitory factor interacts in a stoichiometric manner with the double-stranded RNA which is required for the activation of the interferon-induced protein kinase.
当小鼠L细胞被痘苗病毒感染时，会产生一种特异性激酶抑制因子，该因子可抑制干扰素诱导的双链RNA依赖性蛋白激酶（P. Whitaker-Dowling和J. S. Youngner（1983年），《病毒学》131卷，第128 - 136页）。这种抑制因子在痘苗感染早期（90分钟）出现，其产生需要蛋白质合成。它抑制蛋白质合成起始因子eIF-2的α亚基的磷酸化，并且在经干扰素处理的细胞和痘苗感染细胞的混合提取物中具有活性。痘苗介导的对干扰素诱导蛋白激酶的抑制作用并非由于特异性磷酸酶或特异性蛋白酶，并且可以通过添加过量的双链RNA来逆转。有证据表明，特异性激酶抑制因子与激活干扰素诱导蛋白激酶所需的双链RNA以化学计量方式相互作用。
