The transmembrane adaptor protein NTAL signals to mast cell cytoskeleton via the small GTPase Rho
The transmembrane adaptor protein NTAL signals to mast cell cytoskeleton via the small GTPase Rho
复制标题
跨膜接头蛋白 NTAL 通过小 GTPase Rho 向肥大细胞骨架发出信号
DOI：
10.1002/eji.201040403
复制
发表时间：
2010
影响因子：
5.4
通讯作者：
P. Dráber
中科院分区：
文献类型：
--
作者：
M. Tůmová;A. Koffer;M. Šimíček;L. Draberova;P. Dráber
跨膜衔接蛋白NTAL（非T细胞活化接头）参与造血细胞中的信号体组装，但其在细胞生理学中的确切作用仍然是个谜。我们在这里报告说，相对于WT细胞，NTAL缺陷小鼠的BM来源肥大细胞对单独的Ag或与SCF联合反应，表现出纤连蛋白上的铺展减少、丝状肌动蛋白解聚增强和向Ag迁移增强。当单独使用SCF作为激活剂时，WT和NTAL−/− BM衍生的肥大细胞之间没有观察到这种差异。我们已经研究了两个小GTP酶，Rac和Rho，这是肌动蛋白聚合的重要调节剂的活动。用Ag和/或SCF刺激增强NTAL-/-和WT细胞中Rac（1，2，3）的活性。相比之下，RhoA活性下降，并且这种趋势在NTAL−/−细胞中更快，更广泛，表明NTAL在RhoA活性恢复中具有积极的调节作用。在将NTAL恢复为NTAL−/−细胞后，扩展和肌动蛋白反应都得到了拯救。这是第一次报道NTAL在信号转导中的关键作用，通过RhoA，肥大细胞细胞骨架。
The transmembrane adaptor protein NTAL (non‐T‐cell activation linker) participates in signalosome assembly in hematopoietic cells, but its exact role in cell physiology remains enigmatic. We report here that BM‐derived mast cells from NTAL‐deficient mice, responding to Ag alone or in combination with SCF, exhibit reduced spreading on fibronectin, enhanced filamentous actin depolymerization and enhanced migration towards Ag relative to WT cells. No such differences between WT and NTAL−/− BM‐derived mast cells were observed when SCF alone was used as activator. We have examined the activities of two small GTPases, Rac and Rho, which are important regulators of actin polymerization. Stimulation with Ag and/or SCF enhanced activity of Rac(1,2,3) in both NTAL−/− and WT cells. In contrast, RhoA activity decreased and this trend was much faster and more extensive in NTAL−/− cells, indicating a positive regulatory role of NTAL in the recovery of RhoA activity. After restoring NTAL into NTAL−/− cells, both spreading and actin responses were rescued. This is the first report of a crucial role of NTAL in signaling, via RhoA, to mast cell cytoskeleton.
影响因子：
3.3
作者：
Arthur, WT;Burridge, K
通讯作者：
Burridge, K
影响因子：
4.8
作者：
Iwaki, Shoko;Spicka, Jiri;Gilfillan, Alasdair M.
通讯作者：
Gilfillan, Alasdair M.