Clairmont A, Tessmann D, Sies H
Institut für Physiologische Chemie I and Biologisch-Medizinisches Forschungszentrum, Heinrich-Heine-Universität Düsseldorf, Germany.
FEBS Lett. 1996 Nov 11;397(1):22-4. doi: 10.1016/s0014-5793(96)01129-5.
All-trans retinoic acid (10(-7) M) induces cell-cell communication and expression of the gap junction protein connexin43 in mouse F9 teratocarcinoma cells. Northern blot analysis revealed an increase of connexin43 mRNA after treatment with retinoic acid, accompanied by an increase of the mRNA of collagen IV, a differentiation marker. To address the question at what level gene expression is enhanced by retinoic acid, nuclear run-on experiments were carried out. There was no detectable change in the level of newly transcribed connexin43 mRNA. Therefore, we postulate a post-transcriptional mechanism responsible for the regulation of connexin43 mRNA levels by retinoic acid.
全反式维甲酸(10^(-7) M)可诱导小鼠F9畸胎瘤细胞中的细胞间通讯及缝隙连接蛋白连接蛋白43的表达。Northern印迹分析显示,用维甲酸处理后连接蛋白43 mRNA增加,同时伴有分化标志物IV型胶原mRNA的增加。为了探讨维甲酸在何种水平增强基因表达这一问题,进行了核转录实验。新转录的连接蛋白43 mRNA水平未检测到变化。因此,我们推测存在一种转录后机制负责维甲酸对连接蛋白43 mRNA水平的调控。