Koopman P, Thomas C, Fowler K J, McArdle H J, Cotton R G
Murdoch Institute for Research into Birth Defects, Royal Children's Hospital, Parkville, Australia.
Differentiation. 1987;34(3):216-21. doi: 10.1111/j.1432-0436.1987.tb00069.x.
A concanavalin-A(Con A)-resistant variant of the pluripotent mouse embryonal carcinoma cell line, PSA1-NG2, was isolated. This variant, designated NG2-2.16, fails to exhibit the extensive spontaneous differentiation displayed by PSA1-NG2 in colonies in vitro and in tumours in vivo. The molecular nature of the defect in NG2-2.16 cells was not revealed by quantitative studies of the binding, uptake and metabolism of tritiated Con A, or by Western blotting of membrane and whole cell homogenates, thus indicating the defect to be the result of a more subtle molecular alteration. Statistical evidence suggests that the same mutation is responsible for both the Con A resistance and the lack of spontaneous differentiation. NG2-2.16 cells were induced to differentiate by exposure to retinoic acid, suggesting that the mutation affects the regulation of differentiation rather than the potential for differentiation.
分离出了多能性小鼠胚胎癌细胞系PSA1-NG2的一种刀豆球蛋白A（Con A）抗性变体。这种变体命名为NG2-2.16，在体外集落和体内肿瘤中均未表现出PSA1-NG2所呈现的广泛自发分化。对氚标记的Con A的结合、摄取和代谢进行定量研究，以及对膜和全细胞匀浆进行蛋白质免疫印迹分析，均未揭示NG2-2.16细胞中缺陷的分子本质，因此表明该缺陷是更细微分子改变的结果。统计证据表明，相同的突变导致了对Con A的抗性和自发分化的缺乏。通过暴露于视黄酸诱导NG2-2.16细胞分化，这表明该突变影响分化的调控而非分化潜能。
