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首页> 外文期刊>Molecular membrane biology >Regulation of expression and function of Lck tyrosine kinase by high cell density.
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Regulation of expression and function of Lck tyrosine kinase by high cell density.

机译：高细胞密度调节Lck酪氨酸激酶的表达和功能。

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摘要

For many types of cells, an increase in cell density leads to characteristic changes in intracellular signalling and cell function. It is unknown, however, whether cell density affects the function of T lymphocytes. It is presented here that aggregation of Jurkat T cells, murine thymocytes or human peripheral blood T cells, results in gradual modification of the Lck tyrosine kinase. Within one hour of aggregation, Lck in the detergent-insoluble lipid raft fraction is dephosphorylated mainly at the carboxy-terminal tyrosine. Further aggregation leads to gradual loss of Lck protein from both lipid raft and non-raft fractions which is accompanied by increased protein ubiquitination, a process that is more evident in the detergent-soluble fraction. In contrast, the expression of LAT, which like Lck distributes to raft and non-raft membrane, or Csk, a kinase with a structure similar to Lck, is not affected by cell aggregation. Dephosphorylation of lipid raft-associated Lck, albeit with reduced kinetics, is observed in aggregated Jurkat CD45-deficient cells as well, suggesting involvement of additional tyrosine phosphatases. Changes in Lck structure and expression correlate with reduced ability of aggregated cells to fully activate protein tyrosine phosphorylation after stimulation of the TCR, and with changes in the activation of down-stream signalling cascades.
机译：对于许多类型的细胞，细胞密度的增加导致细胞内信号传导和细胞功能的特征性变化。但是，细胞密度是否影响T淋巴细胞的功能尚不清楚。这里提出Jurkat T细胞，鼠胸腺细胞或人外周血T细胞的聚集导致Lck酪氨酸激酶的逐渐修饰。在聚集的一小时内，不溶于洗涤剂的脂质筏部分中的Lck主要在羧基末端的酪氨酸上被去磷酸化。进一步的聚集导致脂筏和非筏部分中Lck蛋白的逐渐丧失，同时伴随着蛋白质泛素化的增加，这一过程在去污剂可溶部分中更为明显。相反，像Lck一样分布在筏和非筏膜上的LAT或Csk（一种与Lck类似的结构的激酶）的表达不受细胞聚集的影响。在聚合的Jurkat CD45缺陷型细胞中也观察到了脂筏相关Lck的去磷酸化，尽管动力学降低了，这表明还存在其他酪氨酸磷酸酶。 Lck结构和表达的变化与刺激TCR后聚集细胞完全激活蛋白酪氨酸磷酸化能力降低以及下游信号级联反应激活的变化有关。

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