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  • 标题:Unphosphorylated STAT1 prolongs the expression of interferon-induced immune regulatory genes
  • 本地全文:下载
  • 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
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