OXIDATIVE MODIFICATIONS OF THE C-TERMINAL DOMAIN OF TROPOELASTIN PREVENT

原弹性蛋白 C 端结构域的氧化修饰预防

• 批准号: 8361465
• 负责人: TRACY L ADAIR-KIRK
• 金额: $ 0.4万
• 依托单位: WASHINGTON UNIVERSITY
• 依托单位国家: 美国
• 财政年份: 2011
• 资助国家: 美国
• 起止时间: 2011-01-01 至 2011-12-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/8361465
• 关键词: Arteries; Binding; C-terminal; Cell Surface Receptors; Cells; Fetal Lung; Fibroblasts; Funding; Grant; Human; Lung; Mass Spectrum Analysis; Modification; National Center for Research Resources; Principal Investigator; Research; Research Infrastructure; Resources; Source; Tropoelastin; United States National Institutes of Health; biomedical resource; cost; prevent

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. In the present study, we investigated whether oxidative modification of TE has effects on binding to cell surface receptors. These studies show that SMCs and human fetal lung fibroblasts, elastogenic cells in arteries and lung, respectively, bind to TE via different mechanisms.

这个子项目是许多利用资源的研究子项目之一 由NIH/NCRR资助的中心拨款提供。子项目的主要支持 而子项目的主要调查员可能是由其他来源提供的， 包括其它NIH来源。 列出的子项目总成本可能 代表子项目使用的中心基础设施的估计数量， 而不是由NCRR赠款提供给子项目或子项目工作人员的直接资金。 在本研究中，我们研究了TE的氧化修饰是否对与细胞表面受体的结合有影响。这些研究表明，SMC和人胎肺成纤维细胞，动脉和肺中的弹性细胞，分别通过不同的机制与TE结合。