COORDINATED CONTROL OF HPV TRANSCRIPTION AND REPLICATION

HPV 转录和复制的协调控制

• 批准号: 6513536
• 负责人: KENNETH A ALEXANDER
• 金额: $ 20.79万
• 依托单位: DUKE UNIVERSITY
• 依托单位国家: 美国
• 财政年份: 2000
• 资助国家: 美国
• 起止时间: 2000-07-01 至 2004-06-30
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/6513536
• 关键词: DNA directed DNA polymerase; DNA replication; enzyme activity; genetic transcription; helicase; human papillomavirus; intermolecular interaction; tissue /cell culture; transcription factor; virus DNA; virus protein

DESCRIPTION: (Adapted from the Investigator's abstract): In this revised new application from a young independent investigator, a series of biophysical studies are proposed to investigate the mechanisms underlying the hypothesized coordinate regulation of papillomaviral transcription and papillomaviral DNA replication. The PI, Dr. Alexander, hypothesizes that this coordinate regulation is a consequence of competition between cellular transcription and replication factors and the viral E1 and E2 protein that regulate and contribute to transcription and replication. The aims of this proposal are to evaluate the influence of these factors on each other's DNA binding, protein binding and enzymatic activities. The data gained from this study will be used to create a dynamic model of HPV transcription and replication control that will be broadly applicable to transcription and replication control in DNA viruses.

描述：（改编自研究者摘要）：在此修订的新 一位年轻的独立研究者的申请，一系列的生物物理 研究提出了调查的机制，假设 乳头瘤病毒转录与DNA协同调控 复制的PI，亚历山大博士，假设这个坐标 调节是细胞转录和转录之间竞争的结果。 复制因子和病毒E1和E2蛋白， 有助于转录和复制。这项建议的目的是 评估这些因素对彼此DNA结合、蛋白质 结合和酶活性。将使用本研究获得的数据 建立HPV转录和复制控制的动态模型， 将广泛应用于DNA的转录和复制控制 病毒

项目成果

Human TATA binding protein inhibits human papillomavirus type 11 DNA replication by antagonizing E1-E2 protein complex formation on the viral origin of replication.

人 TATA 结合蛋白通过拮抗病毒复制起点上 E1-E2 蛋白复合物的形成来抑制人乳头瘤病毒 11 型 DNA 复制。

• DOI: 10.1128/jvi.76.10.5014-5023.2002
• 发表时间: 2002
• 期刊: Journal of virology
• 影响因子: 5.4
• 作者: Hartley,KellyA;Alexander,KennethA
• 通讯作者: Alexander,KennethA