STRUCTURAL STUDIES OF NUCLEOTIDE EXCISION REPAIR ENZYMES

核苷酸切除修复酶的结构研究

• 批准号: 8361603
• 负责人: GREGORY Lawrence VERDINE
• 金额: $ 0.29万
• 依托单位: CORNELL UNIVERSITY
• 依托单位国家: 美国
• 财政年份: 2011
• 资助国家: 美国
• 起止时间: 2011-04-01 至 2012-03-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/8361603
• 关键词: Bacteria; Binding; Complex; DNA; DNA Damage; DNA Repair; DNA Sequence; DNA lesion; Funding; Goals; Grant; Lesion; Molecular; Monitor; National Center for Research Resources; Nucleotide Excision Repair; Principal Investigator; Process; Proteins; Research; Research Infrastructure; Resources; Source; United States National Institutes of Health; cost; insight; repair enzyme; repaired; structural biology

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. 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 preincision 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.

该副本是利用资源的众多研究子项目之一 由NIH/NCRR资助的中心赠款提供。对该子弹的主要支持 而且，副投影的主要研究员可能是其他来源提供的 包括其他NIH来源。 列出的总费用可能 代表subproject使用的中心基础架构的估计量， NCRR赠款不直接向子弹或副本人员提供的直接资金。 在各种DNA修复机制中，核苷酸切除修复（NER）在处理各种结构无关的DNA病变的能力方面是独一无二的。在细菌中，NER的初始步骤由三种蛋白质进行：UVRA，UVRB和UVRC。 UVRA+UVRB复合物监视DNA并识别损伤。遇到病变后，UVRA从复合物中分离，并使UVRB与受损的DNA结合。 UVRB+DNA前络合物的损伤搜索和形成由ATP调节。 UVRB随后与UVRC和其他因素合作，以恢复原始的DNA序列。我们项目的总体目标是对细菌NER蛋白的损害识别和修复进行分子理解。具体而言，我们正在进行结构研究，以了解UVRA和UVRB如何合作以识别大量结构上不同的DNA病变，以及UVRB+DNA复合物如何呈现损坏的DNA进行裂解和其他处理。