STRUCTURAL STUDIES OF NUCLEOTIDE EXCISION REPAIR ENZYMES

核苷酸切除修复酶的结构研究

• 批准号: 8169208
• 负责人: GREGORY Lawrence VERDINE
• 金额: $ 0.35万
• 依托单位: CORNELL UNIVERSITY
• 依托单位国家: 美国
• 财政年份: 2010
• 资助国家: 美国
• 起止时间: 2010-04-01 至 2011-03-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/8169208
• 关键词: Bacteria; Binding; Complex; Computer Retrieval of Information on Scientific Projects Database; DNA; DNA Damage; DNA Repair; DNA Sequence; DNA lesion; Funding; Goals; Grant; Institution; Left; Lesion; Molecular; Monitor; Nucleotide Excision Repair; Process; Proteins; Research; Research Personnel; Resources; Source; Surgical incisions; United States National Institutes of Health; insight; repair enzyme; repaired

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. Among the various DNA repair mechanisms, nucleotide excision repair (NER) is unique in its ability to process a wide range of structurally unrelated DNA lesions. In bacteria, the initial steps of NER are performed by three proteins: UvrA, UvrB, and UvrC. The UvrA+UvrB complex monitors DNA and recognizes damage. After the lesion is encountered, UvrA dissociates from the complex and leaves UvrB bound to the damaged DNA. Damage searching and formation of the UvrB+DNA pre-incision complex are regulated by ATP. UvrB subsequently cooperates with UvrC and other factors to restore the original DNA sequence. The overall goal of our project is to achieve a molecular understanding of damage recognition and repair by bacterial NER proteins. Specifically, we are performing structural studies to gain insights into how UvrA and UvrB can cooperate to recognize a large number of structurally diverse DNA lesions, and how UvrB+DNA complex presents the damaged DNA for cleavage and additional processing.

该子项目是利用该技术的众多研究子项目之一 资源由 NIH/NCRR 资助的中心拨款提供。子项目和 研究者 (PI) 可能已从 NIH 的另一个来源获得主要资金， 因此可以在其他 CRISP 条目中表示。列出的机构是 对于中心来说，它不一定是研究者的机构。 在各种 DNA 修复机制中，核苷酸切除修复 (NER) 的独特之处在于它能够处理各种结构上不相关的 DNA 损伤。在细菌中，NER 的初始步骤由三种蛋白质执行：UvrA、UvrB 和 UvrC。 UvrA+UvrB 复合物监测 DNA 并识别损伤。遇到损伤后，UvrA 从复合物中解离，留下 UvrB 与受损的 DNA 结合。 UvrB+DNA 切口前复合物的损伤搜索和形成受 ATP 调节。 UvrB 随后与 UvrC 等因子配合，恢复原始 DNA 序列。我们项目的总体目标是通过细菌 NER 蛋白实现对损伤识别和修复的分子理解。具体来说，我们正在进行结构研究，以深入了解 UvrA 和 UvrB 如何合作识别大量结构多样的 DNA 损伤，以及 UvrB+DNA 复合物如何呈现受损的 DNA 以进行切割和额外加工。