• 主题
高级搜索  >
历史搜索 清空历史
首页> 外文学位 >A role for the Herpesvirus saimiri U RNAs in latently infected T cells.
【24h】

A role for the Herpesvirus saimiri U RNAs in latently infected T cells.

机译：疱疹病毒Saimiri U RNA在潜在感染的T细胞中的作用。

获取原文
获取原文并翻译 | 示例
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

Herpesvirus saimiri (HVS), a gamma-Herpesvirus that causes aggressive T cell leukemias and lymphomas in New World primates, encodes seven small nuclear RNAs of the Sm class called HSURs, for H&barbelow;erpesvirus s&barbelow;aimiri U&barbelow; R&barbelow;NAs. The HSURs are abundantly expressed in T cells transformed by HVS both in vivo and in vitro.; HSURs 1, 2 and 5 have highly conserved 5' end AU-rich sequences containing the AUUUA pentamer characteristic of AU-rich elements (AREs) that regulate the stability of many host mRNAs, including those of most proto-oncogenes and cytokines, and have been proposed to alter the stability of these mRNAs by sequestering host proteins that regulate their decay. We show that the ARE-containing HSURs interact with the ARE-binding proteins hnRNP D and HuR in HVS-transformed T cells using a novel in vivo UV cross-linking assay and with TTP in activated T cells by in vitro UV cross-linking. Comprehensive Northern and microarray analyses revealed, however, that the absence of HSURs 1 and 2 does not alter the levels of endogenous ARE-containing mRNAs in latently infected T cells. Instead, HSUR 1 itself is degraded by an ARE-dependent pathway in HVS-transformed T cells, suggesting that HVS may take advantage of the host ARE-mediated mRNA decay pathway to regulate HSUR expression. This is the first example of post-transcriptional regulation of the expression of an Sm snRNA.; We further investigated HSUR function by an extensive comparison of host gene expression in common marmoset T cells transformed with wild-type HVS and a mutant HVS lacking HSURs 1 and 2 by both microarray and Northern analyses. We demonstrate that expression of the most highly conserved HSURs, HSURs 1 and 2, correlates with increased expression of T cell receptors and other T cell and natural killer (NK) cell surface receptors, including CD52 and DAP10. Intracellular genes linked to T cell and NK cell activation, including SKAP55, granulysin, and NKG7, were also upregulated in the presence of HSURs 1 and 2. These are the first phenotypic changes attributable to expression of the HSURs and suggest that the HSURs enhance the activation state of HVS-transformed T cells during latency.
机译：疱疹病毒赛米里病毒（HVS）是一种在新大陆灵长类动物中引起侵袭性T细胞白血病和淋巴瘤的伽马疱疹病毒，它编码7个Sm类小核RNA，称为HSURs，用于H＆barbelow; erpesvirus s＆barbelow; R＆barbelow; NA。 HSUR在体内和体外均在被HVS转化的T细胞中大量表达。 HSUR 1、2和5具有高度保守的5'末端富含AU的序列，其中包含AUUUA五聚体的特征，该AUUUA五聚体具有调节许多宿主mRNA（包括大多数原癌基因和细胞因子）的稳定性的AU-富集元件（ARE）的特征。已提出通过隔离调节其衰变的宿主蛋白来改变这些mRNA的稳定性。我们显示，含有ARE的HSURs与ARE结合蛋白hnRNP D和HuR在HVS转化的T细胞中使用一种新型的体内UV交联测定，并与TTP在激活的T细胞中通过体外UV交联相互作用。全面的Northern和微阵列分析显示，但是，HSURs 1和2的缺失不会改变潜伏感染的T细胞中内源性含ARE的mRNA的水平。而是，HSUR 1本身在HVS转化的T细胞中通过ARE依赖性途径降解，这表明HVS可以利用宿主ARE介导的mRNA衰变途径来调节HSUR表达。这是转录后调控Sm snRNA表达的第一个例子。我们通过广泛比较宿主基因在通过野生型HVS和缺乏HSURs 1和2的芯片和Northern分析的野生型HVS和缺乏HSURs 1和2的突变型HVS转化的宿主基因表达中进一步研究了HSUR功能。我们证明，最高度保守的HSURs，HSURs 1和2的表达与T细胞受体和其他T细胞和自然杀伤（NK）细胞表面受体（包括CD52和DAP10）的表达增加有关。在HSURs 1和2的存在下，与T细胞和NK细胞活化相关的细胞内基因（包括SKAP55，颗粒溶素和NKG7）也被上调。这是可归因于HSURs表达的第一个表型变化，提示HSURs增强了潜伏期中HVS转化T细胞的活化状态。

著录项

  • 作者

    Cook, Heidi L.;

  • 作者单位

    Yale University.;

  • 授予单位 Yale University.;
  • 学科 Biology Cell.; Biology Microbiology.; Biology Molecular.
  • 学位 Ph.D.
  • 年度 2005
  • 页码 110 p.
  • 总页数 110
  • 原文格式 PDF
  • 正文语种 eng
  • 中图分类 细胞生物学;微生物学;分子遗传学;
  • 关键词

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