REDOX EFFECTS ON THE STRUCTURE AND DYNAMICS OF PRL-1

氧化还原对 PRL-1 结构和动力学的影响

• 批准号: 7720681
• 负责人: Jennifer S. Laurence
• 金额: $ 11.73万
• 依托单位: UNIVERSITY OF KANSAS LAWRENCE
• 依托单位国家: 美国
• 财政年份: 2008
• 资助国家: 美国
• 起止时间: 2008-05-15 至 2009-03-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/7720681
• 关键词: Cancerous; Cells; Chemicals; Computer Retrieval of Information on Scientific Projects Database; Development; ERG gene; Funding; Grant; Growth; Institution; Liver; Malignant Neoplasms; Modification; Natural regeneration; Neoplasm Metastasis; Oxidation-Reduction; Phosphoric Monoester Hydrolases; Proteins; Research; Research Personnel; Resources; Source; Structure; Tissues; United States National Institutes of Health; cell growth; 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. Phosphatase of Regenerating Liver (PRL-1) was identified first as an immediate early response gene in damaged liver tissue but has since been shown to be an essential protein expressed specifically during the development and repair of many cellular tissues. Interestingly, this protein also has been found to promote cancer and trigger metastasis of cells when expressed at elevated levels. Our research aims to identify the mechanisms by which PRL-1 is regulated during controlled regenerative growth, and ultimately to determine how regulatory control of aberrant cells might be regained. The phosphatase activity of PRL-1 is required for cell growth, but where this protein is located inside the cell and when it is active appears to differ in regenerating tissues compared to cancerous and metastatic cells. Differences of this type commonly result from chemical modifications to a protein, which alter their ability to interact with other molecules.

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。 肝脏再生磷酸酶 (PRL-1) 首先被鉴定为受损肝组织中的立即早期反应基因，但后来被证明是在许多细胞组织的发育和修复过程中特异性表达的必需蛋白质。有趣的是，这种蛋白质还被发现在表达水平升高时会促进癌症并引发细胞转移。我们的研究旨在确定 PRL-1 在受控再生生长过程中的调节机制，并最终确定如何重新获得对异常细胞的调节控制。 PRL-1 的磷酸酶活性是细胞生长所必需的，但与癌细胞和转移细胞相比，该蛋白质在细胞内的位置以及其活性的时间在再生组织中似乎有所不同。这种类型的差异通常是由蛋白质的化学修饰引起的，这改变了它们与其他分子相互作用的能力。