THE INVOLVEMENT OF NF-KAPPAB IN BETA-INTERFERON GENE-REGULATION REVEALS ITS ROLE AS WIDELY INDUCIBLE MEDIATOR OF SIGNAL TRANSDUCTION
THE INVOLVEMENT OF NF-KAPPAB IN BETA-INTERFERON GENE-REGULATION REVEALS ITS ROLE AS WIDELY INDUCIBLE MEDIATOR OF SIGNAL TRANSDUCTION
复制标题
DOI：
10.1016/0092-8674(89)90966-5
复制
发表时间：
1989-04-21
期刊：
影响因子：
64.5
通讯作者：
BALTIMORE, D
中科院分区：
文献类型：
--
作者：
LENARDO, MJ;FAN, CM;BALTIMORE, D
DNA结合蛋白NF-.KAPPA.B参与了B和T淋巴细胞的基因调控。我们已经发现，核因子-KAPPA.B在病毒诱导的人β-干扰素(β-干扰素)基因表达中也起着核心作用。该基因的一个关键的病毒诱导元件PRDII，在B淋巴细胞和病毒感染的成纤维细胞中，与Ig kappa增强子的NF-.KAPPA.B结合部位可以互换。在体内削弱β-干扰素基因诱导性的单碱基替换在体外也会减少核因子-KAPPA.B与PRDII的结合。病毒感染能有效地激活核因子-KAPPA.B的结合和核定位，并在前B淋巴细胞中导致β-干扰素基因和Ig-kappa基因的表达。可诱导β-干扰素的多种细胞类型和涉及核因子-KAPPA.B的一套不同的基因诱导过程表明，该转录因子作为可诱导信号转导的中介在基因调控中发挥着广泛的作用。
The DNA binding protein NF-.KAPPA.B has been implicated in gene regulation in B and T lymphocytes. We have found that NF-.KAPPA.B also has a central role in virus induction of human .beta.-interferon (.beta.-IFN) gene expression. A critical virus-inducible element of this gene, PRDII, behaves interchangeably with the NF-.KAPPA.B binding site from the Ig kappa enhancer in both B lymphocytes and virus-infected fibroblasts. Single base substitutions that impair inducibility of the .beta.-IFN gene in vivo also reduce the binding of NF-.KAPPA.B to PRDII in vitro. Virus infection potently activates the binding and nuclear localization of NF-.KAPPA.B and, in pre-B lymphocytes, results in the expression of both the .beta.-IFN gene and the Ig kappa gene. The wide variety of cell types in which .beta.-interferon can be induced and the divergent set of gene induction processes involving NF-.KAPPA.B suggest that this transcription factor plays a broad role in gene regulation as a mediator of inducible signal transduction.