LAT is required for TCR-mediated activation of PLCγ1 and the Ras pathway
LAT is required for TCR-mediated activation of PLCγ1 and the Ras pathway
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DOI：
10.1016/s1074-7613(00)80659-7
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发表时间：
1998-11-01
期刊：
影响因子：
32.4
通讯作者：
Weiss, A
中科院分区：
文献类型：
--
作者：
Finco, TS;Kadlecek, T;Weiss, A
在这项研究中，我们提出了一个突变的Jurkat T细胞系，J.CaM2，这是在TCR介导的信号转导缺陷的进一步表征。虽然初始TOP介导的信号传导事件，如TCR-E链和ZAP-70的诱导型酪氨酸磷酸化在J.CaM2中是完整的，但随后的事件，包括细胞内钙的增加、Pas活化和IL-2基因表达是有缺陷的。随后对J.CaM2的分析表明pp 36/LAT表达严重不足，这是一种最近克隆的与TCR信号传导有关的衔接蛋白。重要的是，LAT在J.CaM2中的再表达恢复了TCR信号传导的所有方面。这些结果表明LAT在T细胞活化中的必要和排他性作用。
In this study, we present the further characterization of a mutant Jurkat T cell line, J.CaM2, that is defective in TCR-mediated signal transduction. Although initial TOP-mediated signaling events such as the inducible tyrosine phosphorylation of the TCR-E, chain and ZAP-70 are intact in J.CaM2, subsequent events, including increases in intracellular calcium, Pas activation, and IL-2 gene expression are defective. Subsequent analysis of J.CaM2 demonstrated a severe deficiency in pp36/LAT expression, a recently cloned adaptor protein implicated in TCR signaling. Importantly, reexpression of LAT in J.CaM2 restored all aspects of TCR signaling. These results demonstrate a necessary and exclusive role for LAT in T cell activation.