Gil J, Esteban M
Department of Molecular and Cellular Biology, Centro Nacional de Biotecnología, Consejo Superior de Investigaciones Científicas, (CSIC), Campus Universidad Autónoma, 28049 Madrid, Spain.
Apoptosis. 2000 Apr;5(2):107-14. doi: 10.1023/a:1009664109241.
Interferons are a family of cytokines that exerts antiviral, antitumor and immunomodulatory actions by inducing a complex set of proteins. One of the best known IFN-induced protein is the dsRNA-dependent protein kinase (PKR), that mediates both antiviral and anticellular activities. PKR inhibits translation initiation through the phosphorylation of the alpha subunit of the initiation factor eIF-2 (eIF-2 alpha) and also controls the activation of several transcription factors such as NF-kappa B, p53, or STATs. In addition, PKR mediates apoptosis induced by many different stimuli, such as treatment with LPS, TNF-alpha, viral infection, or serum starvation. The mechanism of apoptosis induction by PKR involves phosphorylation of eIF-2 alpha and activation of NF-kappa B. In this way, expression of different genes is regulated by PKR. Among the genes upregulated in response to PKR are Fas, Bax and p53. The pathway of PKR-induced apoptosis involves FADD activation of caspase 8 by a mechanism independent of Fas and TNFR. Since IFNs are used as drugs for different disorders such as viral infection and cancer, understanding the pathway of apoptosis induction triggered by PKR should be useful in the rational design of IFN therapies.
干扰素是一类细胞因子,通过诱导一系列复杂的蛋白质发挥抗病毒、抗肿瘤和免疫调节作用。最著名的干扰素诱导蛋白之一是双链RNA依赖性蛋白激酶(PKR),它介导抗病毒和抗细胞活性。PKR通过起始因子eIF-2的α亚基(eIF-2α)磷酸化抑制翻译起始,还控制多种转录因子如NF-κB、p53或信号转导和转录激活因子(STATs)的激活。此外,PKR介导由许多不同刺激诱导的细胞凋亡,如用脂多糖、肿瘤坏死因子-α、病毒感染或血清饥饿处理。PKR诱导细胞凋亡的机制涉及eIF-2α磷酸化和NF-κB激活。通过这种方式,不同基因的表达受PKR调控。响应PKR而上调的基因包括Fas、Bax和p53。PKR诱导的细胞凋亡途径涉及FADD通过一种独立于Fas和肿瘤坏死因子受体(TNFR)的机制激活半胱天冬酶8。由于干扰素被用作治疗病毒感染和癌症等不同疾病的药物,了解PKR触发的细胞凋亡诱导途径对于干扰素疗法的合理设计应该是有用的。