一个Actin网络将状GPCRs发送到细胞外囊中以调节信号
Andrew R Nager1, Jaclyn S Goldstein1, Vicente Herranz-Pérez2
1Department of Molecular and Cellular Physiology, Stanford University School of Medicine, Stanford, CA 94305-5345, USA.
Cell
|December 27, 2016
概括
激活的G蛋白合受体 (GPCRs) 可以通过外细胞分裂 (ectocytosis) 从乳毛中释放出来,这是一种涉及actin的过程. 这条通道补偿缺陷并调节状信号.
科学领域:
- 细胞生物学
- 分子信号
- 细胞的生物学
背景情况:
- 已知信号受体,包括G蛋白合受体 (GPCRs),在激活时会离开乳毛.
- BBSome复合体调解激活的受体从乳毛回细胞.
研究的目的:
- 在BBSome介导检索失败时,研究从乳毛中激活GPCR释放的机制.
- 确定参与释放过程的细胞机械.
- 了解这种替代性清除途径的生理和病理影响.
主要方法:
- 使用先进显微镜观察眼尖的GPCR行为.
- 在受体释放中分析actin和相关蛋白 (drebrin,myosin 6) 的作用.
- 一些BBS功能和受体检索决定者的遗传操纵.
- 在野生类型和突变环境中评估的信号通路活动.
主要成果:
- 能够逃避BBSome检索的激活GPCRs会积聚在尖芽中,并被释放为ectosomes.
- 乙烯酸,德布林和肌肉素6对于体释放过程 (细胞分裂) 是必不可少的.
- 信号依赖性外细胞分裂选择性地从乳毛中去除激活的信号分子.
- 细胞外化补偿了一些BBS缺陷,使Bbs突变者能够传递信号.
- 缺少检索信号的细胞受体即使在野生类型细胞中也会发生细胞外化.
结论:
- 信号依赖性细胞外移是一种新的选择性机制,用于从乳毛中去除激活的信号受体.
- 这一过程在正常生理和疾病状态中起着调节状信号的作用.
- 当正规检索机制受到损害时,细胞外形成了支受体清除的途径.
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