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

这个子项目是许多利用 由NIH/NCRR资助的中心赠款提供的资源。子项目和 研究者（PI）可能从另一个NIH来源获得了主要资金， 因此可以在其他CRISP条目中表示。所列机构为 研究中心，而研究中心不一定是研究者所在的机构。 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。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。该项目可以促进心血管和肿瘤疾病治疗新方法的开发，其基础是靶向促炎和促血管生成蛋白的非经典释放。

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. 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. 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.