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钙离子在超微量注射后对弗氏红白血病细胞活力的维持作用。

Role of Ca2+ in preserving viability of Friend erythroleukaemic cells after ultramicroinjection.

作者信息

Wasserman M, Loyter A, Kulka R G

出版信息

J Cell Sci. 1977;27:157-65. doi: 10.1242/jcs.27.1.157.

Abstract

Ca2+ facilitated the fusion by Sendai virus of Friend erythroleukaemic cells and Ehrlich ascites tumour cells but not that of hepatoma tissue culture cells. In the absence of Ca2+ Sendai virus caused the complete depletion of ATP and abolished protein synthesis in Friend erythro-leukaemic cells fused with each other. Addition of high concentrations of Ca2+ (10-20 mM) partially protected the cells from ATP depletion. After a further incubation of cells in complete medium plus 0.2 mM adenine, ATP levels and protein synthesis were restored to 60-85% of those of the untreated control. The protective effect of Ca2+ was used to improve the ultramicroinjection method which involves the fusion of human erythrocyte ghosts with cells. When human erythrocyte ghosts containing high K+ were fused with Friend erythroleukaemic cells in the presence of 10 mM Ca2+ ATP levels and protein synthesis after recovery were about 60-85% of the control. Friend erythroleukaemic cells subjected to ultramicroinjection under these conditions had a cloning efficiency of 75-95% of that of the untreated controls. In these experiments 70-100% of the cells had fused with ghosts. Induction of haemoglobin synthesis by dimethylsulphoxide was unimpaired in cells subjected to ultramicroinjection under the same conditions.

摘要

钙离子促进仙台病毒介导的Friend红白血病细胞与艾氏腹水瘤细胞的融合,但不促进肝癌组织培养细胞的融合。在没有钙离子的情况下,仙台病毒会使相互融合的Friend红白血病细胞中的ATP完全耗尽,并使蛋白质合成停止。添加高浓度的钙离子(10 - 20 mM)可部分保护细胞免受ATP耗尽的影响。在完全培养基中加入0.2 mM腺嘌呤进一步孵育细胞后,ATP水平和蛋白质合成恢复到未处理对照的60 - 85%。钙离子的保护作用被用于改进涉及人红细胞膜泡与细胞融合的超显微注射方法。当含有高钾的人红细胞膜泡在10 mM钙离子存在下与Friend红白血病细胞融合时,恢复后的ATP水平和蛋白质合成约为对照的60 - 85%。在这些条件下接受超显微注射的Friend红白血病细胞的克隆效率为未处理对照的75 - 95%。在这些实验中,70 - 100%的细胞与膜泡发生了融合。在相同条件下接受超显微注射的细胞中,二甲基亚砜诱导的血红蛋白合成未受损害。

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