Paddon H B, Vance D E
Biochim Biophys Acta. 1980 Dec 5;620(3):636-40. doi: 10.1016/0005-2760(80)90156-3.
Studies have been performed on the mechanism by which 12-O-tetradecanoyl-phorbol-13-acetate (TPA) stimulates phosphatidylcholine biosynthesis in HeLa cells. The phorbol acetate did not alter the transport of choline into the cells, nor did it stimulate choline phosphorylation. When [methyl-3H]choline was added to HeLa cells for a 1 h pulse, virtually all of the radioactivity in the aqueous phase of the cell extracts became associated with phosphocholine. The addition of the phorbol ester caused an accelerated disappearance of radioactivity from phosphocholine and a concomitant increase in the incorporation into phosphatidylcholine. The radioactivity associated with CDPcholine remained low and constant throughout the experiment. These results provide strong evidence that TPA accelerates phosphatidylcholine biosynthesis in HeLa cells by stimulation of the reaction catalyzed by CTP:phosphocholine cytidylyltransferase.
针对12 - O - 十四烷酰佛波醇 - 13 - 乙酸酯（TPA）刺激HeLa细胞中磷脂酰胆碱生物合成的机制进行了研究。佛波醇乙酸酯并未改变胆碱进入细胞的转运过程，也未刺激胆碱磷酸化。当向HeLa细胞中加入[甲基 - ³H]胆碱进行1小时脉冲时，细胞提取物水相中的几乎所有放射性都与磷酸胆碱相关联。佛波醇酯的添加导致磷酸胆碱中放射性的加速消失，并伴随着磷脂酰胆碱掺入量的增加。在整个实验过程中，与CDP胆碱相关的放射性保持低水平且恒定。这些结果提供了有力证据，表明TPA通过刺激CTP：磷酸胆碱胞苷转移酶催化的反应来加速HeLa细胞中磷脂酰胆碱的生物合成。
