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T 细胞中的中心体极化:formin 的任务。

Centrosome polarization in T cells: a task for formins.

机构信息

Centro de Biología Molecular Severo Ochoa, Consejo Superior de Investigaciones Científicas and Universidad Autónoma de Madrid , Madrid , Spain.

出版信息

Front Immunol. 2013 Jul 11;4:191. doi: 10.3389/fimmu.2013.00191. eCollection 2013.

Abstract

T-cell antigen receptor (TCR) engagement triggers the rapid reorientation of the centrosome, which is associated with the secretory machinery, toward the immunological synapse (IS) for polarized protein trafficking. Recent evidence indicates that upon TCR triggering the INF2 formin, together with the formins DIA1 and FMNL1, promotes the formation of a specialized array of stable detyrosinated MTs that breaks the symmetrical organization of the T-cell microtubule (MT) cytoskeleton. The detyrosinated MT array and TCR-induced tyrosine phosphorylation should coincide for centrosome polarization. We propose that the pushing forces produced by the detyrosinated MT array, which modify the position of the centrosome, in concert with Src kinase dependent TCR signaling, which provide the reference frame with respect to which the centrosome reorients, result in the repositioning of the centrosome to the IS.

摘要

T 细胞抗原受体 (TCR) 结合触发中心体的快速重定向,该重定向与分泌机制一起朝向免疫突触 (IS) 进行极化蛋白运输。最近的证据表明,在 TCR 触发 INF2 formin 后,formin DIA1 和 FMNL1 一起促进了一组特殊的稳定去酪氨酸化 MT 的形成,该 MT 破坏了 T 细胞微管 (MT) 细胞骨架的对称组织。去酪氨酸化 MT 阵列和 TCR 诱导的酪氨酸磷酸化应该同时发生以实现中心体极化。我们提出,去酪氨酸化 MT 阵列产生的推动力改变了中心体的位置,与 Src 激酶依赖性 TCR 信号协同作用,为中心体重新定向提供了参考框架,导致中心体重新定位到 IS。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fe68/3708132/4d8493eb4943/fimmu-04-00191-g001.jpg

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