...
  • 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Molecular and Cellular Biology >The dual effect of adenovirus type 5 E1A 13S protein on NF-kappaB activation is antagonized by E1B 19K.
【24h】

The dual effect of adenovirus type 5 E1A 13S protein on NF-kappaB activation is antagonized by E1B 19K.

机译：E1B 19K拮抗5型腺病毒E1A 13S蛋白对NF-κB活化的双重作用。

获取原文
           
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

The genomes of human adenoviruses encode several regulatory proteins, including the two differentially spliced gene products E1A and E1B. Here, we show that the 13S but not the 12S splice variant of E1A of adenovirus type 5 can activate the human transcription factor NF-kappaB in a bimodal fashion. One mode is the activation of NF-kappaB containing the p65 subunit from the cytoplasmic NF-kappaB-IkappaB complex. This activation required reactive oxygen intermediates and the phosphorylation of IkappaBalpha at serines 32 and 36, followed by IkappaBalpha degradation and the nuclear uptake of NF-kappaB. In addition, 13S E1A stimulated the transcriptional activity of the C-terminal 80 amino acids of p65 at a core promoter with either a TATA box or an initiator (INR) element. The C-terminal 80 amino acids of p65 were found to associate with E1A in vitro. The activation of NF-kappaB-dependent reporter gene transcription by E1A was potently suppressed upon coexpression of the E1B 19-kDa protein (19K). E1B 19K prevented both the activation of NF-kappaB and the E1A-mediated transcriptional enhancement of p65. These inhibitory effects were not found for the 55-kDa splice variant of the E1B protein. We suggest that the inductive effect of E1A 13S on the host factor NF-kappaB, whose activation is important for the transcription of various adenovirus genes, must be counteracted by the suppressive effect of E1B 19K so that the adenovirus-infected cell can escape the immune-stimulatory and apoptotic effects of NF-kappaB.
机译：人腺病毒的基因组编码几种调节蛋白，包括两个不同剪接的基因产物E1A和E1B。在这里，我们显示腺病毒5型E1A的13S而非12S剪接变体可以双峰方式激活人类转录因子NF-κB。一种模式是从细胞质NF-κB-IkappaB复合物中激活含有p65亚基的NF-κB。该活化需要活性氧中间体和在丝氨酸32和36处的IkappaBalpha的磷酸化，随后IkappaBalpha降解和NF-kappaB的核吸收。此外，13S E1A通过TATA盒或启动子（INR）元件在核心启动子上刺激了p65的C端80个氨基酸的转录活性。发现p65的C末端80个氨基酸在体外与E1A缔合。在E1B 19-kDa蛋白（19K）共表达时，有效抑制了E1A对NF-kappaB依赖的报告基因转录的激活。 E1B 19K既阻止了NF-κB的活化，又阻止了E1A介导的p65转录增强。对于E1B蛋白的55 kDa剪接变体没有发现这些抑制作用。我们建议，E1A 13S对宿主因子NF-kappaB的诱导作用（其激活对于各种腺病毒基因的转录很重要）必须通过E1B 19K的抑制作用来抵消，以便感染腺病毒的细胞可以逃避免疫-NF-κB的刺激和凋亡作用。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱：kefu@zhangqiaokeyan.com

京公网安备：11010802029741号 ICP备案号：京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有

  • 客服微信

  • 服务号