Interferon action against reovirus: activation of interferon-induced protein kinase in mouse L929 cells upon reovirus infection.
Interferon action against reovirus: activation of interferon-induced protein kinase in mouse L929 cells upon reovirus infection.
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干扰素对呼肠孤病毒的作用：呼肠孤病毒感染后小鼠 L929 细胞中干扰素诱导的蛋白激酶的激活。
DOI：
10.1016/0042-6822(82)90051-4
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发表时间：
1982
期刊：
影响因子：
3.7
通讯作者：
Mehra,LL
中科院分区：
文献类型：
--
作者：
Gupta,SL;Holmes,SL;Mehra,LL
实验表明呼肠孤病毒感染导致小鼠L929细胞中干扰素（IFN）诱导的蛋白激酶的激活。这可以通过(i)呼肠孤病毒感染经ifn处理的小鼠L929细胞后数小时内，67000mr （67K）多肽（ifn诱导的蛋白激酶的特征）的体内磷酸化来证明。（ii）在ifn处理的呼肠孤病毒感染细胞的提取物中，67K多肽以及外源添加的起始因子eIF-2的α-亚基的磷酸化，而在未感染细胞的类似提取物中则需要添加双链RNA。在NIH 3T3细胞中，缺乏（2 ',5 '）寡聚腺苷酸激活的内切酶，IFN处理可抑制呼肠孤病毒的复制，而EMC病毒的复制不敏感。提示在呼肠孤病毒感染时观察到的这种激酶激活可能在IFN对呼肠孤病毒的抗病毒作用中起作用。
Experiments are presented which indicate that reovirus infection results in an activation of the interferon (IFN)-induced protein kinase in mouse L929 cells. This is indicated by (i) the phosphorylationin vivoof a 67,000Mr(67K) polypeptide, which is characteristic of the IFN-induced protein kinase, within a few hours after reovirus infection of IFN-treated mouse L929 cells, and (ii) the phosphorylationin vitroof the 67K polypeptide as well as the α-subunit of exogenously added initiation factor eIF-2 in extracts of IFN-treated reovirus-infected cells without the addition of double-stranded RNA which is required in similar extracts from uninfected cells. In NIH 3T3 cells, which are deficient in (2′,5′)oligoadenylate-activated endonuclease, the replication of reovirus is inhibited by IFN treatment, though EMC virus replication is insensitive. It is suggested that this kinase activation observed upon reovirus infection may play a role in the antiviral action of IFN against reovirus.