脂筏(lipid rafts)是细胞膜上富含胆固醇和鞘磷脂的高度动态膜微区，能够聚集多种信号分子，是细胞信号转导的平台。我们前期研究结果显示，胶质细胞系源性神经营养因子（GDNF）的膜信号转导受体RET，在介导GDNF对多巴胺能神经细胞保护作用时，需要从脂筏外微区转位到脂筏上，但是其转位机制不清楚。新的研究进展表明，肌动蛋白细胞骨架能调控膜分子的侧向运动和脂筏的组装。而且我们发现，GDNF能够诱导RET和肌动蛋白结合；使用latrunculin抑制肌动蛋白聚合后，GDNF诱导的RET向脂筏转位的现象消失。据此我们推测：在GDNF作用下，RET通过招募接头蛋白与肌动蛋白细胞骨架结合，最终通过肌动蛋白的聚合实现RET向脂筏转位。本研究不仅有助于进一步探明GDNF对多巴胺能神经细胞的保护机制，同时也为研究膜受体运动及脂筏的动态组装开辟新思路。

Lipid rafts are highly dynamic, cholesterol and sphingolipid-enriched membrane microdomains which appear to act as signaling platforms. Our preliminary results showed that RET could function as the signal transducing receptor for the GDNF and mediate the protective actions exerted by GDNF upon Dopaminergic neurons. And the efficient GDNF signaling required the translocation of Ret to the lipid rafts. However, the mechanism for directing Ret into lipid rafts remains largely unknown. The latest research advances show that organization of lipid raft and the lateral movement of membrane molecules can be regulated by F-actin cytoskeleton. We also found that GDNF could induce the interaction of RET and F-actin. Inhibition of F-actin polymerization with Latrunculin prevented the translocation of RET to lipid rafts. We hypothesize that in the presence of GDNF, RET can recruit an F-actin-binding protein. Subsequently RET is associated with F-actin cytoskeleton via this adaptor protein. Finally, RET would be translocated to lipid rafts driven by the polymerization and rearrangement of F-actin. This study will not only provide further insight into the mechanism of GDNF protection in DA neurons but also provide a new direction for understanding the lateral movement of membrane proteins and organization of lipid rafts.