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中文摘要
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这个子项目是许多研究子项目中的一个 由NIH/NCRR资助的中心赠款提供的资源。子项目和 研究者(PI)可能从另一个NIH来源获得了主要资金, 因此可以在其他CRISP条目中表示。所列机构为 研究中心,而研究中心不一定是研究者所在的机构。 在张博士的实验室里,我继续研究爱泼斯坦巴尔病毒和癌症之间的关系。EB病毒(Epstein-Barr virus,EBV)是一种人类疱疹病毒,在哺乳动物细胞的肿瘤发生中起着重要作用。 转化过程主要由EBV潜伏膜蛋白1(LMP-1)引起。在体外,EBV不能在不表达LMP-1的情况下转化原代B细胞。 已经产生了LMP-1的显性负突变体,称为LMP-DM。 LMP-DM蛋白具有抑制通常由LMP-1调节的细胞信号传导分子的能力,特别是那些参与癌症形成的细胞信号传导分子。 本研究的目的是检测LMP-DM是否具有阻断LMP-1在EBV转化细胞中的转化功能的能力。我参与的第二个项目(2004年5月至2004年12月)是研究人类疱疹病毒8型(HHV-8)、爱泼斯坦巴尔病毒(EBV)和体腔肿瘤形成之间的关系。 使用含有来自HHV-8和EBV的DNA的载体进行共转染实验沿着免疫沉淀实验,以确定HHV-8和EBV是否引起肿瘤形成,特别是通过引起体内肿瘤特异性蛋白质的表达。
英文摘要
This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. In Dr. Zhang's lab I have continued researching the relationship between the Epstein Barr Virus and cancer. Epstein-Barr virus (EBV), a human herpesvirus, plays a critical role in oncogenesis of mammalian cells. The transformation process is primarily caused by the EBV latent membrane protein 1 (LMP-1). In vitro, EBV cannot transform primary B-cells without the expression of LMP-1. A dominant negative mutant of LMP-1 referred to as LMP-DM has been generated. The LMP-DM protein has the ability to inhibit cell signaling molecules which are normally regulated by LMP-1, specifically those involved in cancer formation . The purpose of this research was to test if LMP-DM has the ability to block the transformation function of LMP-1 in EBV transformed cells. A second project (May 2004-Dec2004) that I have worked on is looking at the relationship between the Human Herpesvirus 8 (HHV-8), Epstein Barr Virus (EBV), and body cavity tumor formation. Co-transfection experiments using vectors containing DNA from HHV-8 and EBV along with immunoprecipitation experiments were done to determine if HHV-8 and EBV cause tumor formation, specifically by causing the expression of tumor specific proteins in vivo.
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