CD99的激活引发神经节苷脂GM1的胞吐转运以及肌动蛋白细胞骨架的重组。
Engagement of CD99 triggers the exocytic transport of ganglioside GM1 and the reorganization of actin cytoskeleton.
作者信息
Yoon Sang Soon, Jung Kyung In, Choi Yoon-La, Choi Eun Young, Lee Im-Soon, Park Seong Hoe, Kim Tae Jin
机构信息
Department of Pathology and Center for Molecular Medicine, Samsung Biomedical Research Institute, Sungkyunkwan University School of Medicine, Suwon, South Korea.
出版信息
FEBS Lett. 2003 Apr 10;540(1-3):217-22. doi: 10.1016/s0014-5793(03)00268-0.
We studied the role of lipid rafts and actin cytoskeleton in CD99-mediated signaling to elucidate the mechanism of protein transport upon CD99 engagement. CD99 engagement in Jurkat cells elicited the exocytic transport of GM1 as well as several surface molecules closely related with CD99 functions. In addition, CD99 molecules were rapidly incorporated into lipid rafts and appeared to rearrange the actin cytoskeleton upon CD99 stimulation. Association of CD99 with actin cytoskeleton was inhibited by methyl-beta-cyclodextrin, while CD99-mediated GM1 clustering was inhibited by cytochalasin D. Therefore, we suggest that CD99 may play a role in the vesicular transport of transmembrane proteins and lipid rafts from the intracellular location to the cell surface, possibly by effecting actin cytoskeleton reorganization.
我们研究了脂筏和肌动蛋白细胞骨架在CD99介导的信号传导中的作用，以阐明CD99激活后蛋白质转运的机制。Jurkat细胞中CD99的激活引发了GM1的胞吐转运以及与CD99功能密切相关的几种表面分子的转运。此外，CD99分子迅速整合到脂筏中，并且在CD99刺激后似乎会重新排列肌动蛋白细胞骨架。甲基-β-环糊精可抑制CD99与肌动蛋白细胞骨架的结合，而细胞松弛素D可抑制CD99介导的GM1聚集。因此，我们认为CD99可能在跨膜蛋白和脂筏从细胞内位置到细胞表面的囊泡转运中发挥作用，可能是通过影响肌动蛋白细胞骨架的重组来实现的。
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