Prywes R, Roeder R G
Cell. 1986 Dec 5;47(5):777-84. doi: 10.1016/0092-8674(86)90520-9.
We have identified a factor in nuclear extracts that binds to the c-fos enhancer. Treatment of A431 cells with epidermal growth factor results in a rapid increase in the level of transcription and a concomitant increase in binding of the factor to the enhancer. Surprisingly, as transcription decreases rapidly, the enhancer-binding activity remains elevated. In addition, although HeLa cells exhibit no detectable transcription of the c-fos gene, they contain significant amounts of binding activity, comparable to those in induced A431 cells. These results suggest that regulation of c-fos transcription involves more than simply an increased level of a factor capable of binding the enhancer. Finally, transcription of c-fos in A431 cells is markedly induced by the tumor promoter TPA and the calcium ionophore A23187, yet neither induced an increased level of the enhancer-binding activity. These agents thus appear to activate c-fos transcription via a mechanism distinct from that used by epidermal growth factors.
我们已经在核提取物中鉴定出一种与c-fos增强子结合的因子。用表皮生长因子处理A431细胞会导致转录水平迅速增加，同时该因子与增强子的结合也会增加。令人惊讶的是，随着转录迅速下降，增强子结合活性仍然升高。此外，尽管HeLa细胞未表现出可检测到的c-fos基因转录，但它们含有大量的结合活性，与诱导的A431细胞中的结合活性相当。这些结果表明，c-fos转录的调控不仅仅涉及能够结合增强子的因子水平的增加。最后，肿瘤启动子TPA和钙离子载体A23187可显著诱导A431细胞中c-fos的转录，但两者均未诱导增强子结合活性水平的增加。因此，这些试剂似乎通过一种不同于表皮生长因子的机制激活c-fos转录。
