All PI3Kinase signaling is not mTOR: dissecting mTOR-dependent and independent signaling pathways in T cells.
All PI3Kinase signaling is not mTOR: dissecting mTOR-dependent and independent signaling pathways in T cells.
复制标题
所有 PI3Kinase 信号传导均不是 mTOR：剖析 T 细胞中依赖于 mTOR 和独立的信号传导途径。
DOI：
10.3389/fimmu.2012.00312
复制
发表时间：
2012
影响因子：
7.3
通讯作者：
Powell JD
中科院分区：
文献类型：
--
作者：
Gamper CJ;Powell JD
雷帕霉素的机制靶点（mTOR）正在成为调节T细胞活化，分化和功能的核心作用。mTOR整合来自免疫微环境的不同信号以形成T细胞受体（TCR）抗原识别的结果。磷脂酰肌醇3-激酶（PI 3 K）酶是通过其产生第二信使磷脂酰肌醇（3，4，5）三磷酸（PIP 3）而活化T细胞的关键介质。事实上，PIP 3的产生导致蛋白激酶B（PKB，也称为AKT）的活化，其是mTOR的关键活化剂。然而，最近的遗传学研究已经证明了PI 3 K破坏和mTOR表达的丧失在调节效应和调节性T细胞稳态和功能方面的不一致性。在这篇综述中，我们专注于PI 3 K激活如何指导成熟的CD 4 T细胞的激活和效应器功能的途径依赖于和独立的mTOR信号。重要的是，已经清楚的是，靶向mTOR依赖性和mTOR非依赖性PI 3 K诱导的信号传导远端提供了更有选择性地调节T细胞分化和功能的机会。
The mechanistic target of rapamycin (mTOR) is emerging as playing a central role in regulating T cell activation, differentiation, and function. mTOR integrates diverse signals from the immune microenvironment to shape the outcome of T cell receptor (TCR) antigen recognition. Phosphatidylinositol 3-kinase (PI3K) enzymes are critical mediators of T cell activation through their generation of the second messenger phosphatidylinositol (3,4,5) triphosphate (PIP3). Indeed, PIP3 generation results in the activation of Protein Kinase B (PKB, also known as AKT), a key activator of mTOR. However, recent genetic studies have demonstrated inconsistencies between PI3K disruption and loss of mTOR expression with regard to the regulation of effector and regulatory T cell homeostasis and function. In this review, we focus on how PI3K activation directs mature CD4 T cell activation and effector function by pathways dependent on and independent of mTOR signaling. Importantly, what has become clear is that targeting both mTOR-dependent and mTOR-independent PI3K-induced signaling distally affords the opportunity for more selective regulation of T cell differentiation and function.
登录
查看更多内容
影响因子：
4.4
作者：
Deane, JA;Trifilo, MJ;Fruman, DA
通讯作者：
Fruman, DA
影响因子：
4.1
作者：
Currie, RA;Walker, KS;Lucocq, J
通讯作者：
Lucocq, J
影响因子：
11.4
作者：
Brunn, GJ;Williams, J;Abraham, RT
通讯作者：
Abraham, RT
影响因子：
64.5
作者：
Dang EV;Barbi J;Yang HY;Jinasena D;Yu H;Zheng Y;Bordman Z;Fu J;Kim Y;Yen HR;Luo W;Zeller K;Shimoda L;Topalian SL;Semenza GL;Dang CV;Pardoll DM;Pan F
通讯作者：
Pan F
影响因子：
5.2
作者：
Finlay D;Cantrell D
通讯作者：
Cantrell D