文章基本信息

标题：Unphosphorylated STAT1 prolongs the expression of interferon-induced immune regulatory genes
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作者：HyeonJoo Cheon ; George R. Stark
期刊名称：Proceedings of the National Academy of Sciences
印刷版ISSN：0027-8424
电子版ISSN：1091-6490
出版年度：2009
卷号：106
期号：23
页码：9373-9378
DOI：10.1073/pnas.0903487106
语种：English
出版社：The National Academy of Sciences of the United States of America
摘要：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 STAT1 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 fibroblasts or mammary epithelial cells treated with low concentrations of IFN-{beta} or IFN-{gamma
关键词：innate immunity ; interferon response ; STAT1 gene