Robinson R A, Volkenant M E, Ryan R J, Moses H L
J Cell Physiol. 1981 Dec;109(3):517-24. doi: 10.1002/jcp.1041090318.
Previous studies have shown that the nontransformed AKR-2B mouse embryo derived cell line may growth arrest by two separate mechanisms in the G1 phase of the cell cycle--growth factor deficiency arrest (G0) and low molecular weight nutrient deficiency arrest. An examination of epidermal growth factor (EGF) receptors under the different resting or growth conditions has shown that rapidly growing cells or cells arrested due to growth factor deficiency have the expected amount of 125I-EGF binding with approximately 10(5) receptors per cell being present in G0 arrested cells. In contrast, cells arrested due to nutrient deficiency show a reduction in 125I-EGF binding to 10-20% of that observed under the other conditions. This effect appears to be due to decreased receptor number and not to a change in the affinity of the receptor. Stimulation of DNA synthesis by nutrient replenishment causes a tenfold increase in EGF binding 20 hours later, with some increase in binding being detectable as early as six hours. The increase in binding is inhibited by cycloheximide and actinomycin D. This suggests that new mRNA synthesis as well as increased protein synthesis is required for the increase in EGF binding.
先前的研究表明，未转化的AKR - 2B小鼠胚胎衍生细胞系可能在细胞周期的G1期通过两种不同机制发生生长停滞——生长因子缺乏停滞（G0）和低分子量营养物质缺乏停滞。对处于不同静止或生长条件下的表皮生长因子（EGF）受体进行检测发现，快速生长的细胞或因生长因子缺乏而停滞的细胞具有预期数量的125I - EGF结合，G0期停滞细胞中每个细胞约有10⁵个受体。相比之下，因营养物质缺乏而停滞的细胞显示125I - EGF结合减少至其他条件下观察到的10% - 20%。这种效应似乎是由于受体数量减少，而非受体亲和力改变。营养物质补充刺激DNA合成会在20小时后使EGF结合增加10倍，早在6小时就可检测到结合有所增加。结合的增加受到环己酰亚胺和放线菌素D的抑制。这表明EGF结合增加需要新的mRNA合成以及蛋白质合成增加。
