Levenson R, Macara I, Cantley L, Housman D
J Cell Biochem. 1983;21(1):1-8. doi: 10.1002/jcb.240210102.
A key event in the initiation of the dimethyl sulfoxide (DMSO)-induced program of murine erythroleukemia (MEL) cell differentiation is a rise in the level of cytoplasmic calcium ions. Our interest in the present study is whether other inducers of the terminal erythroid differentiation program also act via a calcium-dependent pathway. Inhibition of calcium transport has been found to prevent the induction of MEL cell commitment by DMSO, butyric acid (BA), or hypoxanthine (HX). Enhancement of the calcium flux rate with A23187 or elevation of cytoplasmic calcium levels with FCCP stimulates the kinetics of commitment in response to all three inducers. These results suggest that of the inducers we have tested (DMSO, BA, and HX), all three act to initiate commitment via a common mechanism which involves modulation of cytoplasmic calcium levels.
二甲基亚砜（DMSO）诱导小鼠红白血病（MEL）细胞分化过程中的一个关键事件是细胞质钙离子水平的升高。我们在本研究中的兴趣在于，终末红系分化程序的其他诱导剂是否也通过钙依赖性途径起作用。已发现抑制钙转运可阻止DMSO、丁酸（BA）或次黄嘌呤（HX）诱导MEL细胞定向分化。用A23187提高钙通量速率或用FCCP提高细胞质钙水平可刺激对所有三种诱导剂的定向分化动力学。这些结果表明，在我们测试的诱导剂（DMSO、BA和HX）中，所有三种诱导剂都通过一种共同机制启动定向分化，该机制涉及调节细胞质钙水平。
