Stathmin regulates microtubule dynamics and microtubule organizing center polarization in activated T cells.
Stathmin regulates microtubule dynamics and microtubule organizing center polarization in activated T cells.
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DOI：
10.4049/jimmunol.1200242
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发表时间：
2012-06-01
期刊：
影响因子：
--
通讯作者：
Shaw AS
中科院分区：
文献类型：
--
作者：
Filbert EL;Le Borgne M;Lin J;Heuser JE;Shaw AS
T细胞的极化涉及微管组织中心（MTOC）的重新定向。由于激活的ERK定位于免疫突触，我们研究了它的作用，表明ERK激活是重要的MTOC极化。我们怀疑ERK磷酸化微管的调节剂，接下来专注于stathmin，一种已知的ERK底物。我们的工作表明，在T细胞活化过程中，ERK被募集到突触，使其磷酸化免疫突触附近的stathmin分子。支持stathmin磷酸化在T细胞活化中的重要作用，我们表明T细胞活化导致依赖于stathmin存在的微管生长速率增加。这一发现的重要性通过以下结果得到了证明：来自stathmin−/−小鼠的CTL显示出缺陷的MTOC极化和缺陷的靶细胞溶解。这些数据暗示stathmin作为T细胞活化期间微管网络的调节剂。
Polarization of T cells involves reorientation of the microtubule-organizing center (MTOC). Because activated ERK is localized at the immunological synapse, we investigated its role by showing that ERK activation is important for MTOC polarization. Suspecting that ERK phosphorylates a regulator of microtubules, we next focused on stathmin, a known ERK substrate. Our work indicates that during T cell activation, ERK is recruited to the synapse allowing it to phosphorylate stathmin molecules near the immunological synapse. Supporting an important role of stathmin phosphorylation in T cell activation, we showed that T cell activation results in increased microtubule growth rate dependent on the presence of stathmin. The significance of this finding was demonstrated by results showing that CTL from stathmin−/− mice displayed defective MTOC polarization and defective target cell cytolysis. These data implicate stathmin as a regulator of the microtubule network during T cell activation.
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影响因子：
3.5
作者：
LEGOUVELLO, S;CHNEIWEISS, H;SOBEL, A
通讯作者：
SOBEL, A
影响因子：
4.3
作者：
LEIGHTON, IA;CURMI, P;SOBEL, A
通讯作者：
SOBEL, A
影响因子：
--
作者：
KNOX, JD;MITCHEL, REJ;BROWN, DL
通讯作者：
BROWN, DL
DOI：
10.1073/pnas.0604236103
发表时间：
2006-07-05
影响因子：
11.1
作者：
Chen, Xi;Allan, David S. J.;Strominger, Jack L.
通讯作者：
Strominger, Jack L.
影响因子：
3.5
作者：
DiPaolo, G;Antonsson, B;Grenningloh, G
通讯作者：
Grenningloh, G