POLYOMA VIRUS REPLICATION

多瘤病毒复制

• 批准号: 8362556
• 负责人: Robert L Garcea
• 金额: $ 3.19万
• 依托单位: UNIVERSITY OF COLORADO
• 依托单位国家: 美国
• 财政年份: 2011
• 资助国家: 美国
• 起止时间: 2011-05-01 至 2012-04-30
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/8362556
• 关键词: 3T3 Cells; Apoptosis; Caliber; Capsid; Capsid Proteins; Cell Cycle Progression; Cell Nucleus; Cell physiology; Cells; Cellular Structures; Collaborations; DNA biosynthesis; Data; Funding; Gene Expression; Goals; Grant; Large T Antigen; Mus; National Center for Research Resources; Nuclear; Phase; Polyomavirus; Principal Investigator; Process; Proteins; Research; Research Infrastructure; Resources; S Phase; Source; Structural Protein; United States National Institutes of Health; Viral; Viral Nonstructural Proteins; Virion; Virus; Virus Replication; cost; immunocytochemistry; migration; particle; prevent; viral DNA

This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. Primary support for the subproject and the subproject's principal investigator may have been provided by other sources, including other NIH sources. The Total Cost listed for the subproject likely represents the estimated amount of Center infrastructure utilized by the subproject, not direct funding provided by the NCRR grant to the subproject or subproject staff. Murine PyV is a double stranded, none enveloped virus. Its capsid (50 nm in diameter) is composed of 72 pentamers of the major coat protein VP1 and of VP2 and VP3 proteins buried within the capsid. After entry and migration to the cell host nucleus, the mPyV gene expression can be divided into two phases (3, 4). The early phase sees nonstructural viral proteins such as small, middle and large T antigen to be synthesized. Those proteins highly interact with the host cell key proteins. As a result, the virus takes control of cellular mechanisms like; cell cycle progression towards S-phase as well as preventing the cell to engage apoptosis process. The early phase leads to viral DNA replication exploiting the host nuclear machinery. During the later phase, the structural proteins (VP1, VP2, VP3) are expressed and de novo viral particles are assembled in the nucleus. The goal of the collaboration is to combine immunocytochemistry data on EM prepared infected 3T3 cells coming from the Garcea lab and ultrastructural information collected in the facility to understand better the way Polyoma virus particles assembled in the cell nucleus as well as how PML bodies are involved in this process.

这个子项目是利用资源的许多研究子项目之一。 由NIH/NCRR资助的中心拨款提供。对子项目的主要支持 子项目的首席调查员可能是由其他来源提供的， 包括美国国立卫生研究院的其他来源。为子项目列出的总成本可能 表示该子项目使用的中心基础设施的估计数量， 不是由NCRR赠款提供给次级项目或次级项目工作人员的直接资金。 小鼠PYV是一种双链、无包膜的病毒。它的衣壳(直径50 nm)由72个主要外壳蛋白VP1的五聚体以及埋在衣壳内的VP2和VP3蛋白组成。在进入和迁移到细胞宿主核后，mPyV基因的表达可以分为两个阶段(3，4)。早期阶段将合成非结构性病毒蛋白，如小T抗原、中T抗原和大T抗原。这些蛋白质与宿主细胞的关键蛋白质高度相互作用。因此，病毒控制了细胞机制，如细胞周期向S期的进展以及阻止细胞参与凋亡过程。早期阶段导致利用宿主核机制进行病毒DNA复制。在后期，表达结构蛋白(VP1、VP2、VP3)，并在细胞核内组装新生的病毒颗粒。合作的目标是结合来自Garcea实验室的EM准备的受感染3T3细胞的免疫细胞化学数据和在该设施中收集的超微结构信息，以更好地了解多瘤病毒颗粒在细胞核中组装的方式，以及PML小体如何参与这一过程。