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首页> 外文期刊>Molecular and Cellular Biology >Altered expression of protein kinase C, lck, and CD45 in a 12-O-tetradecanoylphorbol-13-acetate-dependent leukemic T-cell variant that expresses a high level of interleukin-2 receptor.
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Altered expression of protein kinase C, lck, and CD45 in a 12-O-tetradecanoylphorbol-13-acetate-dependent leukemic T-cell variant that expresses a high level of interleukin-2 receptor.

机译：蛋白激酶C，lck和CD45在表达高水平白介素2受体的12-O-十四烷酰phorbol-13-乙酸依赖性白血病T细胞变体中的表达变化。

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The compound 12-O-tetradecanoylphorbol-13-acetate (TPA) is extremely toxic to the P13 subclone of the Jurkat human T-cell leukemia line. By selecting for growth in the presence of TPA, we have isolated two TPA-resistant variants of these cells, P13-50 and P13-5/A8. Studies of protein kinase C (PKC) enzyme activity, immunoblot analyses, and assays for PKC mRNAs indicate that both of these variants express lower levels of PKC than do the parental P13 cells. We suggest that this protects them from the toxic effects of TPA. The P13-5/A8 cells are of particular interest because not only are they resistant to TPA toxicity but they actually require TPA for optimal growth. These cells have a more profound decrease in PKC expression that do P13-50 cells. In addition, P13-5/A8 cells display very little, if any, surface expression of CD45, a receptor-linked tyrosine protein phosphatase, and lck, a lymphocyte-specific tyrosine kinase. On the other hand, they express a very high level of interleukin-2 receptor. A model is proposed that suggests that these cells are dependent on TPA because they have defects in both the PKC and tyrosine kinase signal transduction pathways, and that TPA compensates for these defects by providing a strong stimulus to the residual level of PKC. This variant may be useful for studying the interactions between tyrosine kinase and PKC pathways in controlling the various functions of T lymphocytes.
机译：化合物12-O-十四烷酰phorbol-13-乙酸盐（TPA）对Jurkat人T细胞白血病细胞株的P13亚克隆有剧毒。通过选择在TPA存在下的生长，我们分离了这些细胞的两个TPA抗性变体P13-50和P13-5 / A8。对蛋白激酶C（PKC）酶活性，免疫印迹分析和PKC mRNA检测的研究表明，这两个变体均比亲本P13细胞表达更低水平的PKC。我们建议，这可以保护他们免受TPA的毒性影响。 P13-5 / A8细胞特别受关注，因为它们不仅对TPA毒性有抵抗力，而且实际上需要TPA才能达到最佳生长。这些细胞在P13-50细胞中的PKC表达上有更深刻的降低。此外，P13-5 / A8细胞几乎没有（如果有的话）表面表达CD45（一种受体连接的酪氨酸蛋白磷酸酶）和lck（一种淋巴细胞特异性酪氨酸激酶）。另一方面，它们表达非常高水平的白介素2受体。提出了一个模型，该模型表明这些细胞依赖于TPA，因为它们在PKC和酪氨酸激酶信号转导途径中均存在缺陷，并且TPA通过对PKC的残留水平提供强烈刺激来补偿这些缺陷。该变体可用于研究酪氨酸激酶和PKC途径之间的相互作用，以控制T淋巴细胞的各种功能。

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