K+ efflux in NIH mouse 3T3 cells and transformed derivatives: dependence on extracellular Ca2+ and phorbol esters.
K+ efflux in NIH mouse 3T3 cells and transformed derivatives: dependence on extracellular Ca2+ and phorbol esters.
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NIH 小鼠 3T3 细胞和转化衍生物中的 K 流出：依赖于细胞外 Ca2 和佛波酯。
DOI：
10.1073/pnas.85.14.5097
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发表时间：
1988
影响因子：
11.1
通讯作者：
Martin Lubin
中科院分区：
文献类型：
--
作者：
Martin Lubin
在缺钙的培养液中，NIH小鼠3T3细胞失去K+，获得Na+，停止生长。K+外流速率的显著增加是这种损失的原因；Na+，K+-ATPase泵的活性增加，但不能完全补偿K+外流的增加。佛波酯和放线菌酮可抑制缺钙介质中K+的流失。佛波酯也抑制人成纤维细胞的K+外流，甚至在生理水平的钙离子下也是如此。两株来源于NIH-3T3的细胞株，一株由猴病毒40缺失突变体转化，另一株由编码中等大小肿瘤抗原的多瘤病毒癌基因转化，保留K+，并能在低钙条件下增殖。这些细胞的K+外流对降低的钙离子浓度、佛波醇酯和放线菌酮相对不敏感。结果提示如下假设：当NIH-3T3细胞处于钙离子缺乏的介质中时，一条对K+和Na+非选择性的通道开放；该通道由佛波酯受体(蛋白激酶C)控制，也可能受一种短暂的蛋白调节。
In culture medium deficient in Ca2+, NIH mouse 3T3 cells lose K+, gain Na+, and stop growing. A marked increase in the rate of K+ efflux accounts for this loss; Na+, K+-ATPase pump activity increases but does not fully compensate for enhanced K+ efflux. Phorbol esters and cycloheximide inhibit K+ loss in Ca2+-deficient medium. Phorbol esters inhibit K+ efflux from human fibroblasts as well, even at physiological levels of Ca2+. Two cell lines derived from NIH-3T3, one transformed by a simian virus 40 deletion mutant, the other by the polyoma virus oncogene encoding the middle-sized tumor antigen, retain K+ and can multiply in medium with low Ca2+. Efflux of K+ from these cells is relatively insensitive to reduced Ca2+ concentration, phorbol esters, and cycloheximide. The results suggest the following hypothesis: a channel, nonselective for K+ and Na+, opens when NIH-3T3 cells are in Ca2+-deficient medium; the channel is controlled by the receptor for phorbol ester (protein kinase C) and may also be regulated by a short-lived protein.