我们前期研究发现SDPR和PTRF除影响膜小窝的功能外，还广泛影响多种细胞膜皱褶的形成。本项目将深入研究SDPR、PTRF调控细胞膜张力、细胞膜的韧性和膜储备的分子机制：研究SDPR引发膜皱褶和SDPR-PTRF复合物相互作用引发特殊膜皱褶的分子机制；分析SDPR和PTRF在介导cavicle与质膜融合过程中的作用模式；阐明SDPR-PTRF引发的膜皱褶对细胞膜张力、内吞、细胞代谢信号传导和细胞运动的影响。本项目研究将阐明控制细胞膜张力的结构性要素和调控机制，有助于解答与癌细胞的迁移和浸润、内分泌激素的释放、脂肪等营养物质的转运和代谢等基本生命活动相关的膜生物学问题。

SDPR and PTRF have been reported to be highly relevant to the caveolae function. However, our preliminary data have suggested that SDPR and/or PTRF perform far beyond caveolae itself on cell membrane. Several kinds of membrane curvature without caveolae even without PTRF were found to exist extensively in cell membrane. So we propose SDPR and/or PTRF were novel components of membrane tension machinery. In this project, we’ll investigate how SDPR and/or SDPR-PTRF mediate different membrane curvature formation, thus closely control cell membrane tension, cell motility, endocytosis and metabolic signal transduction. This project will provide more clues to many biological problems such as tumor cell metastasis, endocrine hormone secretion, energy metabolism and its signal control.