Characterization of a specific kinase inhibitory factor produced by vaccinia virus which inhibits the interferon-induced protein kinase.
Characterization of a specific kinase inhibitory factor produced by vaccinia virus which inhibits the interferon-induced protein kinase.
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DOI：
10.1016/0042-6822(84)90020-5
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发表时间：
1984-08
期刊：
影响因子：
3.7
通讯作者：
P. Whitaker-Dowling;J. Youngner
中科院分区：
文献类型：
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作者：
P. Whitaker-Dowling;J. Youngner
当小鼠L细胞被牛痘病毒感染时，产生一种特异性的激酶抑制因子，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）病毒学131,128-136）。这种抑制因子在牛痘感染早期出现（90分钟），其产生需要蛋白质合成。它抑制蛋白合成起始因子eIF-2 α亚基的磷酸化，并在ifn处理细胞和牛痘感染细胞的混合提取物中具有活性。牛痘介导的对ifn诱导的蛋白激酶的抑制不是由于特定的磷酸酶或特定的蛋白酶，可以通过添加过量的双链RNA来逆转。有证据表明，特定的激酶抑制因子以化学计量的方式与双链RNA相互作用，这是激活干扰素诱导的蛋白激酶所必需的。
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 α 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.