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: 7381965
• 负责人: Jennifer S. Laurence
• 金额: $ 12.26万
• 依托单位: UNIVERSITY OF KANSAS LAWRENCE
• 依托单位国家: 美国
• 财政年份: 2006
• 资助国家: 美国
• 起止时间: 2006-07-01 至 2007-06-30
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/7381965
• 关键词: REDOX; EFFECTS; STRUCTURE; DYNAMICS; PRL

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.

这个子项目是利用由NIH/NCRR资助的中心拨款提供的资源的许多研究子项目之一。子项目和调查员(PI)可能从另一个NIH来源获得了主要资金，因此可能会出现在其他CRISE条目中。列出的机构是针对中心的，而不一定是针对调查员的机构。再生肝磷酸酶(PRL-1)最先在受损的肝组织中被鉴定为即刻早期反应基因，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表达的必需蛋白。有趣的是，这种蛋白还被发现在高水平表达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控机制，并最终确定如何重新获得对异常细胞的调控。PRL-1的磷酸酶活性是细胞生长所必需的，但与癌症和转移细胞相比，再生组织中该蛋白位于细胞内的位置和何时被激活似乎是不同的。这种类型的差异通常是由于对蛋白质进行化学修饰而导致的，这种修饰改变了蛋白质与其他分子相互作用的能力。