Reem G H, Friend C
Proc Natl Acad Sci U S A. 1975 Apr;72(4):1630-4. doi: 10.1073/pnas.72.4.1630.
Purine metabolism was studied in murine virus-induced erythroleukemia cells stimulated to differentiate in vitro in the presence of dimethylsulfoxide. The activities of the enzymes that catalyze the synthesis of the first intermediate of the de novo purine pathway, phosphoribosyl-1-amine, were decreased while the enzymes that catalyze the conversion of purine bases to purine ribonucleotides remained unchanged at the time the cells acquired the specialized function of hemoglobin synthesis. In addition, cytidine deaminase (cytidine aminohydrolase, EC 3.5.4.5) activity increased with erythropoietic maturation, as it does during murine erythropoiesis in vivo. Stimulation of cellular proliferation of stationary erythroleukemic cells resulted in a marked increase in the activities of purine biosynthetic enzymes. These data provide a convincing example of repression and derepression of the PRA synthesizing enzymes in mammalian cells in vitro, and further evidence that the regulatory mechanisms operative in the normal development of erythrocytes can be activated by exposure of erythroleukemic cells to dimethylsulfoxide.
在存在二甲基亚砜的情况下,对体外诱导分化的鼠病毒诱导性红细胞白血病细胞中的嘌呤代谢进行了研究。在细胞获得血红蛋白合成的特殊功能时,催化从头嘌呤途径第一个中间体磷酸核糖胺合成的酶活性降低,而催化嘌呤碱基转化为嘌呤核糖核苷酸的酶活性保持不变。此外,胞苷脱氨酶(胞苷氨基水解酶,EC 3.5.4.5)活性随着红细胞生成的成熟而增加,这与体内小鼠红细胞生成过程中的情况相同。静止的红细胞白血病细胞的细胞增殖刺激导致嘌呤生物合成酶活性显著增加。这些数据为体外哺乳动物细胞中磷酸核糖胺合成酶的阻遏和去阻遏提供了一个有说服力的例子,并进一步证明,通过将红细胞白血病细胞暴露于二甲基亚砜,可以激活在红细胞正常发育过程中起作用的调节机制。