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: 7381071
• 负责人: IGOR PRUDOVSKY
• 金额: $ 19.21万
• 依托单位: MAINEHEALTH
• 依托单位国家: 美国
• 财政年份: 2006
• 资助国家: 美国
• 起止时间: 2006-05-01 至 2007-04-30
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/7381071
• 关键词: MECHANISM; NON; CLASSICAL; RELEASE; ANGIOGENESIS

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. The project by I. Prudovsky represents a new direction for his long-term productive interest in non-classical release mechanisms for proteins lacking signal-peptides. These studies have evolved through collaboration with T. Maciag, although the hypothesis and approach were developed independently by Dr. Prudovsky. This project proposes to examine the mechanism of release of the pro-inflammatory cytokine IL1-alpha, and how this mechanism differs from that of the pro-angiogenic factor FGF1. These studies will have translational potential and therapeutic implications for the design of novel inhibitors of IL1-alpha and FGF1 release. It is anticipated that this project will be interactive with Project 2 (L. Liaw) in examining the release of IL1-alpha from GIST tumors or surrounding inflammatory cells. Furthermore it is anticipated that this project will be interactive with both of our senior recruits (Projects 7 and 8), whose area of research interest will involve inflammatory mechanisms in the vessel wall.

该子项目是利用NIH/NCRR资助的中心赠款提供的资源的许多研究子项目之一。子项目和研究者（PI）可能从另一个NIH来源获得主要资金，因此可以在其他CRISP条目中表示。所列机构为中心，不一定是研究者所在机构。该项目由我。Prudovsky代表了他对缺乏信号肽的蛋白质的非经典释放机制的长期生产兴趣的新方向。这些研究是通过与T. Maciag，虽然假设和方法是由Prudovsky博士独立开发的。该项目旨在研究促炎细胞因子IL 1-α的释放机制，以及该机制与促血管生成因子FGF 1的机制有何不同。这些研究对于设计新型IL 1-α和FGF 1释放抑制剂具有潜在的转化潜力和治疗意义。预计该项目将与项目2（L）互动。Liaw）在检查IL 1-α从GIST肿瘤或周围炎性细胞释放中的作用。此外，预计该项目将与我们的两个高级招聘（项目7和8），其研究兴趣的领域将涉及血管壁的炎症机制的互动。