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首页> 外文期刊>Journal of Cellular Physiology >Deoxyadenosine blockade of G0 to G1 transition in lymphocytes: possible involvement of protein kinases.
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Deoxyadenosine blockade of G0 to G1 transition in lymphocytes: possible involvement of protein kinases.

机译：脱氧腺苷的封锁G0 G1过渡淋巴细胞:蛋白质参与的可能性激酶。

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摘要

Immunodeficiency in adenosine deaminase deficiency has been attributed to the lymphotoxicity of deoxyadenosine that accumulates to high levels in patients. To gain insight into the mechanism of deoxyadenosine toxicity, we investigated the dose-response and time course of its toxic effects on concanavalin A-stimulated mouse splenic lymphocytes by thymidine incorporation and flow cytometry. Deoxyadenosine at a level as low as 0.3 microM inhibited the progression of G0. In contrast, higher concentrations of the nucleoside, i.e., in the range of 1 to 3 microM, were needed to block transition of the stimulated lymphocytes from G0 to G1. The inhibition of their S entry and progression required even higher concentrations. Furthermore, staurosporine, a potent inhibitor of protein kinases, was found to potentiate the toxicity of deoxyadenosine in mitogen-stimulated lymphocytes. Calcium mobilization in mitogen-activated lymphocytes was inhibited by deoxyadenosine. Our data suggest that, while ribonucleotide reductase inhibition by dATP could explain the blockade of S entry and progression by deoxyadenosine in cycling lymphocytes or leukemic cells, more important effects of this compound on antigen-activated lymphocytes occur at the early G0 phase. A possible mechanism of deoxyadenosine lethality is its inhibition of protein phosphorylation.
机译：免疫缺陷的腺苷脱氨酶缺乏症被归因于lymphotoxicity的脱氧腺苷,积累的高水平病人。脱氧腺苷毒性,我们调查了有毒的剂量反应和时间影响伴刀豆球蛋白模拟鼠标脾淋巴细胞的胸腺嘧啶核苷掺入和流式细胞术。低至0.3 microM抑制病情发展G0。核苷,即在1到3 microM的范围,需要阻止过渡刺激吗淋巴细胞G0 G1。甚至他们年代进入和发展需要更高的浓度。staurosporine,一种蛋白质的有效抑制剂激酶,发现加强的毒性脱氧腺苷mitogen-stimulated淋巴细胞。钙动员增殖作用淋巴细胞是由脱氧腺苷抑制的。数据表明,核苷酸还原酶抑制dATP可以解释的封锁脱氧腺苷年代进入和发展多骑自行车或白血病细胞,淋巴细胞这种化合物的重要影响antigen-activated淋巴细胞发生在早期G0期。杀伤力是其抑制作用的蛋白质磷酸化。

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