MECHANISM OF NON-CLASSICAL RELEASE OF THE ANGIOGENESIS REGULATOR, IL1-ALPHA

血管生成调节因子 IL1-α 的非经典释放机制

• 批准号: 7720099
• 负责人: IGOR PRUDOVSKY
• 金额: $ 18.87万
• 依托单位: MAINEHEALTH
• 依托单位国家: 美国
• 财政年份: 2008
• 资助国家: 美国
• 起止时间: 2008-03-01 至 2009-02-28
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/7720099
• 关键词: Angiogenic Proteins; Cardiovascular system; Computer Retrieval of Information on Scientific Projects Database; Development; Disease; FGF1 gene; Funding; Goals; Grant; Inflammatory; Institution; Interleukin-1 alpha; Methods; Regulation; Research; Research Personnel; Resources; Role; Signal Transduction; Source; United States National Institutes of Health; angiogenesis; base; carcinogenesis; notch protein; polypeptide

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. This goal of the project is to examine the mechanism of transmembrane translocation of pro-angiogenic polypeptides FGF1 and IL1-alpha and regulation of the non-classical release of these proteins by Notch signaling. This project is interactive with Project 2 (L. Liaw) in examining the role of Notch in the regulation of angiogenesis and carcinogenesis. The project can contribute to the development of new methods of treatment of cardiovascular and oncological disorders, based on targeting non-classical release of pro-inflammatory and pro-angiogenic proteins.

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。 该项目的目标是研究促血管生成多肽 FGF1 和 IL1-α 的跨膜易位机制以及通过 Notch 信号传导调节这些蛋白质的非经典释放。 该项目与项目 2 (L. Liaw) 互动，研究 Notch 在血管生成和癌变调节中的作用。该项目可以基于促炎和促血管生成蛋白的非经典释放，有助于开发治疗心血管和肿瘤疾病的新方法。