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.

该副本是利用众多研究子项目之一 由NIH/NCRR资助的中心赠款提供的资源。子弹和 调查员（PI）可能已经从其他NIH来源获得了主要资金， 因此可以在其他清晰的条目中代表。列出的机构是 对于中心，这不一定是调查员的机构。 首先将再生肝脏（PRL-1）的磷酸酶（PRL-1）鉴定为受损的肝组织中的早期反应基因，但此后已被证明是在许多细胞组织的开发和修复过程中专门表达的必不可少的蛋白质。有趣的是，当以升高水平表达时，还发现该蛋白质可以促进细胞的癌症和触发转移。我们的研究旨在确定在受控再生生长过程中调节PRL-1的机制，并最终确定如何恢复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，但是与癌细胞和转移性细胞相比，该蛋白位于细胞内并且活性时似乎在再生组织中有所不同。这种类型的差异通常是从化学修饰到蛋白质的，这改变了它们与其他分子相互作用的能力。