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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >Unphosphorylated STAT1 prolongs the expression of interferon-induced immune regulatory genes
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Unphosphorylated STAT1 prolongs the expression of interferon-induced immune regulatory genes

机译：未磷酸化的STAT1延长干扰素诱导的免疫调节基因的表达

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In normal human cells treated with interferons (IFNs), the concentration of tyrosine-phosphorylated STAT1 (YP-STAT1), which drives the expression of a large number of genes, increases quickly but then decreases over a period of several hours. Because the 5TAT1 gene is activated by YP-STAT1, IFNs stimulate a large increase in the concentration of unphosphorylated STAT1 (U-STAT1) that persists for several days. To test the significance of high U-STAT1 expression, we increased its concentration exogenously in the absence of IFN treatment. In response, the expression of many immune regulatory genes (e.g., IFI27, IFI44, OAS, and BST2) was increased. In human f ibroblasts or mammary epithelial cells treated with low concentrations of IFN-β or IFN-y, the expression of the same genes increased after 6 h and continued to increase after 48 or 72 h, long after the concentration of YP-STAT1 had returned to basal levels. Consistent with its activity as a transcription factor, most U-STAT1 was present in the nuclei of these cells before IFN treatment, and the fraction in nuclei increased 48 h after treatment with IFN. We conclude that the nuclear U-STAT1 that accumulates in response to IFNs maintains or increases the expression of a subset of IFN-induced genes independently of YP-STAT1, and that many of the induced proteins are involved in immune regulation.
机译：在用干扰素（IFN）处理的正常人细胞中，驱动大量基因表达的酪氨酸磷酸化STAT1（YP-STAT1）的浓度迅速增加，然后在数小时内下降。因为5TAT1基因被YP-STAT1激活，所以IFN刺激了持续数天的未磷酸化STAT1（U-STAT1）浓度的大幅增加。为了测试高U-STAT1表达的重要性，我们在没有IFN治疗的情况下外源性地增加了其浓度。作为响应，许多免疫调节基因（例如，IFI27，IFI44，OAS和BST2）的表达增加。在用低浓度的IFN-β或IFN-γ处理的人成纤维细胞或乳腺上皮细胞中，相同的基因的表达在YP-STAT1浓度达到6h后的6h后增加，并在48或72h后继续增加。回到基础水平。与它作为转录因子的活性一致，大多数U-STAT1在IFN处理之前存在于这些细胞的细胞核中，而在用IFN处理后48 h细胞核中的比例增加。我们得出的结论是，响应于IFN积累的核U-STAT1维持或增加了IFN诱导基因的一个子集的表达，而与YP-STAT1无关，并且许多诱导的蛋白质都参与了免疫调节。

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