Oren M, Reich N C, Levine A J
Mol Cell Biol. 1982 Apr;2(4):443-9. doi: 10.1128/mcb.2.4.443-449.1982.
F9 embryonal carcinoma cells express high levels of a 53,000-molecular-weight cellular tumor antigen called p53. When F9 cell cultures are treated with retinoic acid and dibutyryl adenosine 3',5'-phosphate, they differentiate, predominantly into endoderm-like cells. This differentiation is accompanied by a marked decrease in the levels of p53. The mechanism(s) responsible for this decline in the level of p53 in differentiated cells was investigated. The results demonstrate that the high levels of p53 in F9 cells relative to their differentiated progeny were not due to alterations in the stability or turnover of this protein. Rather, the regulation during differentiation involved a marked decrease in the amount of in vitro translatable p53 mRNA detected in the differentiated cell cultures. This mechanism is unlike the one operating during the simian virus 40 infection or transformation, where the increased levels of p53 are largely due to the increased stability of the p53 protein.
F9胚胎癌细胞表达高水平的一种名为p53的53,000分子量的细胞肿瘤抗原。当用视黄酸和二丁酰腺苷3',5'-磷酸处理F9细胞培养物时，它们主要分化为内胚层样细胞。这种分化伴随着p53水平的显著降低。研究了分化细胞中p53水平下降的机制。结果表明，F9细胞中p53水平相对于其分化后代较高，并非由于该蛋白质稳定性或周转的改变。相反，分化过程中的调节涉及分化细胞培养物中检测到的体外可翻译p53 mRNA量的显著减少。这种机制不同于猿猴病毒40感染或转化过程中起作用的机制，在猿猴病毒40感染或转化过程中，p53水平的升高主要是由于p53蛋白稳定性的增加。
